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Gastrointestinal Disorders

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CHIEF ASSESSMENT FACTORS

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Abdominal Pain or Distention Appetite, Anorexia • Ascites, Jaundice Bezoars (Undigested Foreign Matter, Usually in Stomach) Change in Eating or Bowel Habits • Change in Stools, Consistency, and Frequency; Fecal Incontinence Constipation • Dentition Diarrhea (bloody, explosive) Dysphagia • Easy Fatigue • Edema of Extremities • Feeding Method for Digestive or Absorptive Problems • Hemorrhoids, Rectal Bleeding or Polyps • Indigestion, Heartburn, Reflux • Nausea, Vomiting, Regurgitation • Painful or Cramping Abdomen, Flatulence • Painful Oral Tissues, Tongue • Use of Antacids, Stool Softeners, Diuretics, Laxatives, Histamine Blockers Weight Loss


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INTRODUCTION AND BACKGROUND FOR GASTROINTESTINAL DISORDERS Digestion Digestion is a process that physically and chemically breaks down food in preparation for absorption. It begins with mastication and mixing of food with salivary fluid and enzymes (oral phase). In the gastric phase, pepsin and gastric acid begin to work. Chyme is then delivered to the small intestine for mixing with pancreatic and biliary juices. The pancreatic phase involves pancreatic amylase and lipase, proteases, and phospholipase. The intestinal phase involves disaccharidases (maltase, lactase, and sucrase), peptidases, and cholecystokinin for bile salts. Maldigestion involves the interference at any of these stages, including abnormal emptying of the stomach and pancreatic insufficiency.

Absorption Passage of molecular nutrients into the bloodstream from the intestinal cells, starts primarily in the duodenum, with monosaccharides, amino acids and small peptides, monoglycerides, and free fatty acids. Water is also absorbed to maintain isotonicity of blood and cells. Bile and fat are needed to absorb fat-soluble vitamins A, D, E, and K. Watersoluble vitamins C and B-complex are usually absorbed in the intestinal mucosa with some storage in the liver. Malabsorption can result from dysfunction from any of the above steps.

Small Intestine It is approximately 3.8 cm in diameter and 4.8-m long, covered with villi projections to increase absorptive surface. Villi cells have a rapid turnover rate of 2–5 days. Fecal fat is a valuable test of lipid digestion/absorption.

TABLE 7-1 Gastrointestinal Conditions That May Lead to Malnutrition Malabsorption Celiac disease

Pancreatic insufficiency

Crohn’s disease

Short bowel syndrome

Disaccharidase deficiencies

Ulcerative colitis

Dumping syndrome HIV infection or AIDS Mechanical Function Achalasia or esophageal hypomotility

Esophageal obstruction

Adynamic ileus

Hirschsprung’s disease

Bezoar formation after gastric surgery

Pyloric stenosis

Bowel obstruction

Tracheoesophageal fistula

Esophageal stricture Conditions that May Cause Fear of Eating Aspiration risk

Crohn’s disease

Bloating/obstruction/ distension/pain

Dental disease

Cholelithiasis and other biliary diseases

Diarrhea

Diverticulitis

Irritable bowel syndrome

Dumping syndrome

Lactose intolerance

Dysphagia

Pancreatitis (acute or chronic)

Esophageal spasm

Peptic ulcer

Flatulence

Proctitis

Food allergies

Rectal fissures

Gastritis

Reflux esophagitis

Ill-fitting dentures

Ulcerative colitis

Large Intestine It is approximately 5 cm in diameter and 1.5-m long, with two sections (colon and rectum) forming a frame around a highly convoluted small intestine. A diet high in whole and unrefined foods (whole grains, dark green and yellow/orange vegetables and fruits, legumes, nuts, and seeds) is high in antioxidant phenolic compounds, fibers, and other phytochemicals, all of which are beneficial.

Rectum It is approximately 12-cm long. The area is susceptible to polyps and tumors. The entire process of digestion/absorption takes about 24 hours, with large variations among individuals. Digestive problems such as abdominal pain, diarrhea, nausea, and vomiting result in approximately millions of physician visits, billions in direct U.S. medical costs annually, and frequent use of prescription medications. Table 7-1 lists gastrointestinal (GI) conditions that may lead to malnutri-

tion. The enteric nervous system (ENS) consists of many different types of enteric neurons forming complex reflex circuits that underlie or regulate many gut functions (Young, 2008). The identification of the genetic, molecular, and cellular mechanisms responsible for the colonization of the gut by enteric neuron precursors provides an exciting future management for GI disorders. The GI tract does not respond well to inflammation where digestion, absorption, and gut barrier protection is impaired (Tappenden, 2008). Arachidonic acid (AA) is the precursor of inflammatory eicosanoids-like prostaglandin E(2) and leukotriene B(4); the n-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are antiinflammatory. Fish oil supplementation in patients with inflammatory bowel diseases (IBD) results in n-3 PUFA incorporation into gut mucosal tissue with the potential for modified inflammation, improved gut histology, decreased disease activity, reduced use of corticosteroids (Calder, 2008), and decreased risk of colorectal cancer (Habermann et al, 2009). Glutamine (an amino acid needed in stress or


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SECTION 7 • GASTROINTESTINAL DISORDERS

TABLE 7-2 Enteral Nutrition, Prebiotics, Probiotics, and Synbiotics in Gastrointestinal Tract Function

TABLE 7-3 Conditions That May Benefit from Use of Intestinal Fuelsa

When an oral diet is not feasible, enteral nutrition (EN) is needed to avoid prolonged starvation, to prevent deterioration of intestinal integrity, and to avoid translocation of gut bacteria. One or two basic formulas can meet most patients’ needs. Prebiotics: Low-digestible carbohydrates that are not digested in the upper GI tract become fermented in the large intestine. They have physiological benefits similar to those of dietary fiber. Short-chain fatty acids (SCFAs) are produced from fermentation of fiber; the SCFAs are fuel for mucosal cells, so they benefit the gut tissue. Fermentation leads to the selective stimulation and growth of beneficial gut bacteria such as bifidobacteria (prebiotics). Carbohydrates that offer desirable physiological properties are resistant starch (RS), oligofructose, and polydextrose. Probiotics are live microbial food supplements; they support balance in the intestinal tract. Probiotics have the ability to modify gut pH, antagonize pathogens, produce lactase, and stimulate immunomodulatory cells. Functional foods such as yogurt with live cultures may decrease the incidence of cancer, allergic reactions, and lactose intolerance. Probiotics also have immunomodulating properties and enhance the mucosal barrier in inflammatory bowel disease, pancreatitis, liver transplantation, and diarrhea (Jenkins et al, 2005). Synbiotics are combinations of prebiotics and probiotics. By combining specific prebiotics and plant fibers into multifiber synbiotics, immunosupportive effects are possible (Bengmark and Martindale, 2005). The use of these products may become common practice in intensive care and GI units. Crohn’s disease and ulcerative colitis are caused by overly aggressive immune responses to a nonpathogenic enteric bacteria in genetically predisposed individuals; administration of probiotics, prebiotics, or synbiotics can restore a predominance of beneficial Lactobacillus and Bifidobacterium. They may be protective against colon cancer as well (Pool-Zobel, 2005).

Bowel resection

REFERENCES Bengmark S, Martindale R. Prebiotics and synbiotics in clinical medicine. Nutr Clin Pract. 20:244, 2005. Jenkins B, et al. Probiotics: a practical review of their role in specific clinical scenarios. Nutr Clin Pract. 20:262, 2005. Pool-Zobel BL. Inulin-type fructans and reduction in colon cancer risk: review of experimental and human data. Br J Nutr. 93:S73, 2005.

TABLE 7-4

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Constipation Diarrhea Diverticulosis Dumping syndrome Inflammatory bowel disease (IBD) Irritable bowel syndrome (IBS) Parenteral nutrition–induced bowel atrophy Radiation/chemotherapy damage to the GI tract Tube feeding a

Glutamine, short-chain fatty acids, soy, fermentable fiber, prebiotics, probiotics

sepsis) requires GI processing to become effective; this is likely true for other nutrients. Threonine is an essential amino acid that is abundantly present in intestinally produced glycoproteins; studies in infants suggest a high obligatory visceral need for it in protein synthesis (van der Schoor et al, 2007). Lysine, arginine, and other amino acids are also used in intestinal health, providing support for early enteral feeding whenever possible. Table 7-2 gives details about the role of enteral nutrition, prebiotics, probiotics, and synbiotics in GI health. The right product and the right ingredients can make a big difference. Therefore, it is beneficial to employ a nutrition support specialist or team in facilities where many patients need enteral or parenteral support. Table 7-3 lists GI conditions that may benefit from nutritional enhancements and Table 7-4 describes the role of dietitians in the GI specialty area.

Knowledge and Skills of Dietitians in Gastrointestinal Specialty

The GI dietetics practitioner: Knows sites of digestion and absorption of macronutrients and micronutrients Understands normal digestion, nutrient secretion, and absorption Identifies key nutritional screening factors for persons with GI disease Explains the association between diet and other therapies in treating GI disorders Knows the value and limitations of enteral and parenteral nutrition formulas and common functional food ingredients Knows how to handle complex GI problems in conditions as diverse as cystic fibrosis (Mascarenhas, 2003) and celiac disease (Niewinski, 2008) Recognizes extremes of dietary intake and the effects of diet on GI function and symptoms Understands how GI dysfunction, surgical resections, and diseases affect nutritional status Understands how other diseases and conditions can affect GI function, such as diabetes and gastroparesis, postanesthetic ileus, neurological injury, and hormonal changes Understands the consequences of eating patterns in both healthy persons and in those who have GI disease REFERENCES Beyer PL. Gastrointestinal disorders: roles of nutrition and the dietetics practitioner. J Am Diet Assoc. 98:272, 1998. Mascarenhas MR. Treatment of Gastrointestinal Problems in Cystic Fibrosis. Current Treat Options Gastroenterol. 6:427, 2003. Niewinski MM. Advances in celiac disease and gluten-free diet. J Am Diet. 108:661, 2008.


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For More Information

Society of Gastroenterology Nurses and Associates http://www.sgna.org

World Organization for Digestive Endoscopy http://www.omed.org

American College of Gastroenterology http://www.acg.gi.org/

American Digestive Health Foundation http://www.fdhn.org/

American Gastroenterological Association http://www.gastro.org

CITED REFERENCES

American Society of Gastrointestinal Endoscopy http://www.asge.org

Cleveland Clinic Foundation http://www.clevelandclinic.org/gastro/

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://www.niddk.nih.gov/

Society of American Gastrointestinal Endoscopic Surgeons http://www.sages.org

Calder PC. Polyunsaturated fatty acids, inflammatory processes and inflammatory bowel diseases. Mol Nutr Food Res. 52:885, 2008. Habermann N, et al. Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells. Genes Nutr. 4:73, 2009. Tappenden KA. Inflammation and intestinal function: where does it start and what does it mean? JPEN J Parenter Enter Nutr. 32:648, 2008. van Der Schoor SR, et al. The gut takes nearly all: threonine kinetics in infants. Am J Clin Nutr. 86:1132, 2007. Young HM. Functional development of the enteric nervous system—from migration to motility. Neurogastroenterol Motil. 20:20S, 2008.

UPPER GI: ESOPHAGUS

DYSPHAGIA NUTRITIONAL ACUITY RANKING: LEVEL 3–4

Nasal cavity Tongue Oropharynx

Esophagus

Aorta Liver

Gallbladder Portal vein

Celiac trunk Stomach

Esophagus Diaphragm

Stomach

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TABLE 7-5 Standard Questions in the Evaluation of Dysphagia Describe any difficulty swallowing that you have. Is the swallowing difficulty greater for solids or liquids? How long have you had this swallowing difficulty? Do you have heartburn along with this difficulty swallowing? Is swallowing painful? Do you get chest pain? Does food get stuck when you swallow? Do you choke or cough with swallowing? Do you have temperature sensitivity (especially cold foods and beverages)? Has there been any weight loss? Adapted from: http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?bookcm&part A2747, accessed July 25, 2009.

DEFINITIONS AND BACKGROUND Anatomic or physiological swallowing problems of dysphagia create a disturbance in the normal transfer of food from the oral cavity to the stomach. Swallowing requires 5–10 seconds and three phases for completion—oral phase, pharyngeal phase, and esophageal phase. All must be adequate to prevent choking and/or aspiration into the lung. Signs of possible dysphagia include coughing with meals, choking, drooling, or pocketing of foods. Consult speech therapist for a full evaluation; a barium swallow may reveal silent aspiration. Videofluoroscopy (VF) is the gold standard. Questions to ask about swallowing difficulty are listed in Table 7-5. Progress diet when possible, under guidance of the therapist. Inadequate dietary intake, weight loss, nutrient deficiencies, protein-energy malnutrition, and dehydration may result from prolonged dysphagia. In children with developmental disabilities, diagnosis-specific treatment of feeding disorders results in significantly improved energy consumption and nutritional status. Dysphagia is classified into oropharyngeal dysphagia due to malfunction of the pharynx and upper esophageal sphincter, or esophageal dysphagia due to malfunction of the esophagus. Common causes of dysphagia are listed in Table 7-6.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS

Videofluoroscopic swallowing study Esophagoscopy Barium swallow Cookie swallow test Pocketing of food under tongue or in cheeks Spitting food out of mouth Facial weakness Slow oral transit time Choking Coughing before, during, or after swallowing Excessive eating time

TABLE 7-6

Wet, gurgly voice after drinking or eating Slurred speech Poor tongue control or excessive movement Hoarseness, breathy voice Recurrent pneumonia Mealtime resistance— clenching teeth or throat Regurgitation of food through nose or mouth

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Upper GI bleeding Blood pressure (BP) Lab Work Hemoglobin and hematocrit (H & H) Blood urea nitrogen (BUN) Albumin (Alb) C-reactive protein (CRP) Na, K, Cl Ca, Mg Other labs specific for the disorder

Common Causes of Dysphagia

Achalasia

Head trauma

Aging

Hiatal hernia

Alzheimer’s disease

Huntington’s disease

Amyotrophic lateral sclerosis

Lung cancer

Cerebral palsy

Meningitis

Cerebrovascular accident (stroke)

Multiple sclerosis

Chronic obstructive lung disease

Muscular dystrophy

Cleft lip or palate

Myasthenia gravis

Closed head injury

Myotonic dystonia

Dehydration from medications

Parkinson’s disease

Diabetes, type 1 (long term)

Pneumonia with aspiration history

Encephalopathy

Poliomyelitis

Esophageal inflammation

Prematurity

Esophageal fistula

Pulmonary disorders

Genetic Markers: Mutations in the PABPN1 gene can cause an oculopharyngeal muscular dystrophy.

Esophageal obstruction or stricture

Radiation treatment to head/neck

Esophageal trauma

Sjögren’s disease

Weight changes Fiberoptic endoDiet history and scopic evaluaHeight swallowing tion of Weight problems— swallowing Body mass index current, his(FEES) (BMI) tory, duration

Gastroparesis

Spinal cord injury

Gastroesophageal reflux (GERD)

Throat cancer or injury

Clinical/History

Goiter

Tongue cancer

Guillain-Barré syndrome

Tracheoesophageal fistula

Head or neck cancer

Zenker’s diverticulum


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SAMPLE NUTRITION CARE PROCESS STEPS Dysphagia Assessment Data: Weight loss, dysphagia and jaw pain, throbbing headache

• •

Nutrition Diagnoses (PES): Dysphagia related to progression of Parkinson’s disease as evidenced by weight loss, difficulty swallowing solids, and choking on thin liquids.

Interventions: Education about blending foods and simplifying meal planning to increase intake. Swallowing evaluation for determination of appropriate textures and thickening of liquids. Counseling on positioning at mealtime to reduce likelihood of aspiration.

Monitoring and Evaluation: Improved intake for meals and snacks; fewer complaints of difficulty swallowing. No further weight loss.

INTERVENTION

OBJECTIVES • Prevent choking and aspiration of foods and beverages. • Promote weight maintenance or gain if losses have occurred. In head and neck cancer patients, anorexia and dysphagia are factors that adversely affect outcome of treatments (Kubrak et al, 2010). • Individualize diet based on patient needs and preferences. Refer to speech therapist, who will help to determine the level of consistency that is required (e.g., nectar or syrup, honey, pudding). Monitor for pocketing of food. • For some patients, thin liquids may be needed. Modify levels of dysphagia diets as impairment level changes; upgrade when and if safe for the patient. • Support independence in eating whenever possible. Provide foods that stimulate the swallowing reflex. • For persons who have viscous oral secretions or dry mouth, liquefy foods before serving by adding broth, juice, or water. Provide moistened foods or thickened beverages for adequate hydration. • Correct any nutrient deficits. Prevent pressure ulcers, if relevant.

FOOD AND NUTRITION

• • • • •

• • • •

• The patient may be fed enterally if needed. Results from the FOOD (Feed or Ordinary Food) Collaboration Trials showed that nasogastric (NG) tube feeding (TF) was favored over percutaneous endoscopic gastrostomy (PEG) as the early route of feeding in dysphagic stroke patients (Prosser-Loose and Paterson, 2006). • If needed, jejunostomy feedings may be more appropriate for the patient’s condition. Home TF may be needed,

• •

depending on the medical condition and cause of dysphagia. If central parenteral nutrition (CPN) is needed, monitor closely for ability to progress back to TF or oral diet. Following a protocol, clinical guideline, or algorithms improves dysphagia management. Calculate needs at 30–35 kcal/kg. Use a 1- to 1.5-g protein intake per kilogram to assure adequacy and to prevent loss of lean body mass. Monitor cardiac, hepatic, and renal status accordingly. Prevent aspiration by careful selection of foods and beverages, such as thick, soft, pureed foods instead of thin liquids. Thickening may be at honey, nectar, or pudding consistency; the label on the thickener will indicate the amount required for the differing levels. When a thickened liquid diet is ordered, foods such as gelatin should not be used because they liquefy at body temperature. Thicken foods and beverages with special products such as Thick-It, Thicken-Up, and Thick ‘n Easy; these products use thickeners to make semisolids out of coffee, soup, beverages, juices, and shakes. It is possible to use mashed potato flakes to thicken some meat and casserole dishes. Baby rice cereal is an inexpensive thickener as well. Fruit purees are also helpful in thickening juices and some desserts. Progress over time to a soft diet. With a decreased saliva production, moisten foods with small amounts of liquid and use extra fats, mild sauces, and gravies. Monitor for deficiencies in fiber, vitamins A and C if whole grains, fruits, and vegetables are not consumed. Avoid alcoholic and extremely hot or cold liquids and beverages. Avoid foods that cause choking or are hard to manage: tart juices and foods, dry or crisp foods such as crackers and chips, bony fish, chewy meats such as steak, sticky foods such as peanut butter or bananas, thinly pureed foods that are easily aspirated, foods with varying consistency, excessively sweet drinks that aggravate drooling, carbonated beverages, dry bread in sandwiches. Avoid foods that are easily aspirated: popcorn, bran cereals, nuts, dry mashed potatoes, cottage cheese, corn, celery, pineapple, other fruits or vegetables with skins or fibrous pulp. Where there is reduced oral sensation, position food in the most sensitive area and use cold foods. To form a more cohesive bolus of food in the mouth, serve semisolid consistencies. For a severely sore mouth, avoid acidic foods and use soft foods at moderate temperatures. For delayed or absent swallowing reflex, temperature extremes and spicy foods may help excite the nerves necessary to function better. Some thickened liquids may actually be beneficial. Use cohesive foods that do not fall apart. Finely crushed bran on cereal, powdered fiber, or highfiber tube-feeding products can help alleviate constipation. An interdiscplinary care plan is available for use.


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INTERDISCIPLINARY NUTRITION CARE PLAN Dysphagia Client Name:

#:

Initiated by:

Date:

SCREEN Nutrition Screen diagnosis: Dysphagia

GOALS (Check any/all):

Signed:

❑ Safely eat and drink without risk in ____ (goal time).

Date:

❑ Swallow efficiently to maintain nutrition and hydration in ____ (goal time).

Weight ❑ maintained, or ❑ loss/ ❑ gain of ____ lb in ____ (goal time).

Date: 1 or more

Signed:

Date: Next visit

1 or more

HIGH-RISK INTERVENTIONS (Check any/all) ❑ Foods that are easy to swallow provided and explained ❑ Food record provided and explained Obtain Dr. orders as needed: ❑ RD referral for home visit(s) ❑ SLP referral for home visit(s) ❑ OT referral for home visit(s) ❑ Monitor weight q:_____ ❑ Monitor I & O q: _____ ❑ BID/TID supplements ❑ Medication adjustment ❑ Other:________________________ (See notes for documention.) Signed:

MODERATE RISK INTERVENTIONS (Check any/all) ❑ Foods that are easy to swallow provided and explained ❑ Food record provided and explained Obtain Dr. orders as needed: ❑ RD chart consult ❑ SLP chart consult ❑ OT chart consult ❑ Monitor weight q:_____ ❑ Monitor I & O q:_____ ❑ BID/TID supplements ❑ Other:________________________ (See notes for documention.)

ASSESS RESPONSE (Check any/all) ❑ Further food/liquid texture modification required ❑ Weight change not appropriate per goal ❑ Dehydration ❑ Onset of pulmonary infection ❑ Exhibiting Poor Oral Intake Symptoms ❑ Other:________________________ (See notes for documention.)

None

Signed:

❑ Advance to normal texture of food in ____ (goal time).

None

ASSESS (Check any/all) ❑ Food/liquid texture modification Weight/BMI ❑ Weight loss >3 lb/wk or >5%/mo or >10%/6 mo ❑ BMI <20 (High risk) ❑ BMI <27 ❑ Medications ❑ Infection (e.g., pneumonia) ❑ Pressure ulcers/wounds Poor oral intake symptoms ❑ Complex diet order ❑ Nausea/vomiting ❑ Poor appetite/early satiety ❑ Problems chewing/swallowing ❑ Depression/anxiety ❑ GI distress

OUTCOMES ACHIEVED ❑ Food/liquid texture advanced toward normal ❑ Weight maintained or improved ❑ Hydration status maintained or improved ❑ Other:________________________ (See notes for documention.) ❑ Repeat Nutrition Risk Screen in ____ days

Signed: Signed:

Date:

Date:

Date:

ASSESS RESPONSE (Check any/all) ❑ Further food/liquid texture modification required ❑ Continued poor oral intake symptoms ❑ Weight change not appropriate per goal ❑ Dehydration ❑ Onset of pulmonary infection ❑ Other:________________________ (See notes for documention.)

None

Next visit OUTCOMES ACHIEVED ❑ Food/liquid texture advanced toward normal ❑ Weight maintained or improved ❑ Hydration status maintained or improved ❑ Other:________________________ (See notes for documention.) ❑ Repeat Nutrition Risk Screen in ____ days

Signed: Signed:

Date:

Date: 1 or more

OUTCOMES NOT ACHIEVED Reassess/evaluate need for EN/PN (refer to Tube Feeding Nutrition Care Plan). Document on Nutrition Variance Tracking form. Adapted with permission from www.RD411.com, Inc.

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Common Drugs Used and Potential Side Effects • For thick saliva and gagging, artificial saliva such as lemon glycerin may be useful. • Papain or citrus juices may be useful for thinning secretions.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • It is important to stress that no supplement or diet can cure dysphagia.

• Encourage regular review of changes in swallowing abilities to identify early decline or to lessen restrictions when possible. • Monitor for quality of life factors and adjust where possible.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Dysphagia On-Line (Nestle) http://www.dysphagiaonline.com/en/pages/01_what_is_dysphagia.aspx

E-medicine http://emedicine.medscape.com/article/324096-overview

NIH—Dysphagia http://www.nidcd.nih.gov/health/voice/dysph.asp

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT DYSPHAGIA—CITED REFERENCES • Follow meals by brushing teeth to reduce dental caries; encourage optimal mouth care. • Offer suggestions for specific changes in food preparation (e.g., adding moistening sauces, gravies, etc.) and cutting or mincing foods to increase control of the swallowing process.

Kubrak C, et al. Nutrition impact symptoms: key determinants of reduced dietary intake, weight loss, and reduced functional capacity of patients with head and neck cancer before treatment [published online ahead of print July 22, 2009]. Head Neck. 32:290, 2010. Prosser-Loose EJ, Paterson PG. The FOOD Trial Collaboration: nutritional supplementation strategies and acute stroke outcome. Nutr Rev. 64:289, 2006.

ESOPHAGEAL STRICTURE OR SPASM, ACHALASIA, OR ZENKER’S DIVERTICULUM NUTRITIONAL ACUITY RANKING: LEVEL 3, STRICTURE; LEVEL 2 ACHALASIA

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DEFINITIONS AND BACKGROUND Esophageal stricture is caused by injury or chemical ingestion (such as lye), sliding hiatal hernia, esophageal cancer, reflux esophagitis (RE), peptic ulcer disease, or prolonged use of an NG tube. Another cause is eosinophilic esophagitis, with solid food dysphagia on presentation. Scar tissue builds up and prevents normal swallowing.

In esophageal spasm, segmented, concentric contractions occur simultaneously in the lower two thirds of the esophagus. Barium and manometric studies are useful in the evaluation. Achalasia and diffuse esophageal spasm are associated with hypertrophy of circular and longitudinal muscle layers (Mittal et al, 2005). Chemical denervation with Clostridium botulinum toxin (Botox) is effective in relieving spasm. Achalasia is failure of the cardiac sphincter to relax, with obstruction of food passage into the stomach. In addition, the esophagus does not demonstrate normal waves of contraction after swallowing. The mechanisms remain poorly understood (Kraichely and Farrugia, 2006; Sonnenberg, 2009). Esophageal dilatation or surgical myotomy is common. Laparoscopic procedures are preferred (Pastor et al, 2009). Zenker’s diverticulum (ZD, or pharyngeal pouch) generally presents after 60 years of age, but patients may have years of dysphagia symptoms. Regurgitation of undigested food when patient bends over or lies down may occur. Serious complications include aspiration and malnutrition (Ferreira et al, 2008). Diagnosis is by barium swallow, and treatment is open surgical diverticulectomy. Minimally invasive (endoscopic stapling) devices are often used. Oral feeding is usually possible the day after surgery as general anesthesia is not needed.


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ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Achalasia is usually of idiopathic origin but may be secondary to cancer or mast cell disorders. Esophageal stricture secondary to radiation treatment may show signs of altered interleukin or tumor necrosis factor (TNF). Clinical/History Height Weight Weight loss? BMI Diet history Intake and output (I & O) Dysphagia Substernal pain after meals

Regurgitation, halitosis Heartburn or other specific symptoms Endoscopy Esophageal manometry Esophagoscopy Cineesophagography BP

Lab Work Glucose (Gluc) Alb CRP Gastrin H&H Na, K, Cl Ca, Mg

391

FOOD AND NUTRITION • Esophageal stricture: Begin with liquid diet and progress to soft diet as tolerance increases. Adequate calories are needed. Gastrostomy may be needed. Antireflux regimen (no alcohol, weight loss) may be helpful. Avoid sticky and dry foods. Use thin liquids and pureed or soft foods. • Esophageal spasm: Use diet as tolerated with modified temperatures for foods and beverages. • Achalasia: Patients should take smaller bites of food, chew well, and eat slowly. Provide large volumes of fluids with each meal, unless dysphagia prevents appropriate swallowing of liquids. Tube feed if needed; may need to use gastrostomy TF.

Common Drugs Used and Potential Side Effects • Antacids: Check the label for aluminum, calcium, magnesium, or sodium if other medical problems exist. Beware of long-term side effects. • Isosorbide dinitrate and calcium channel blockers such as nifedipine may be needed 30 minutes before meals. • Nitroglycerin often helps spasm. Headache is one possible side effect.

INTERVENTION Herbs, Botanicals, and Supplements OBJECTIVES • Esophageal stricture: Avoid large boluses of food. Provide adequate nutrition. Prevent weight loss. Remove cause or dilate, if necessary. • Esophageal spasm: Avoid either very cold or very hot foods or beverages. Monitor dysphagia. • Achalasia: Individualize diet according to patient tolerances and preferences. Monitor chronic dysphagia. Avoid aspiration.

SAMPLE NUTRITION CARE PROCESS STEPS Dysphagia and Esophageal Stricture Assessment Data: Weight loss, choking after swallowing, regurgitation, heartburn and chest pain after eating. Nutrition Diagnoses (PES): Dysphagia related to altered GI function and esophageal stricture as evidenced by difficulty swallowing, abnormal barium swallow, and weight loss of 10 lb in last month. Interventions: Education about blending foods and simplifying meal planning to increase intake. Swallowing evaluation for determination of appropriate textures and thickening of liquids. Counseling on positioning at mealtime; preparation for surgery Monitoring and Evaluation: Improved intake of meals and snacks. Resolution of esophageal structure after surgery with no further weight loss.

• Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Emphasize the importance of spacing meals and achieving relaxation. Recommend intake of food at moderate temperature only. • Elevate head of bed for 30–45 minutes after meals and at bedtime. • Encourage fluids at mealtimes. • Avoid foods that aggravate dysphagia. • Bland foods are not clearly beneficial and not required.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Achalasia http://www.medicinenet.com/achalasia/article.htm

Baylor College of Medicine—Zenker’s diverticulum http://www.bcm.edu/oto/grand/05_06_04.htm

Esophagitis http://chorus.rad.mcw.edu/doc/00858.html


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ESOPHAGEAL STRICTURE OR SPASM, ACHALASIA, AND ZENKER’S DIVERTICULUM—CITED REFERENCES Ferreira LE, et al. Zenker’s diverticula: pathophysiology, clinical presentation, and flexible endoscopic management. Dis Esophagus. 21:1, 2008. Kraichely RE, Farrugia G. Achalasia: physiology and etiopathogenesis. Dis Esophagus. 19:213, 2006.

Mittal RK, et al. Sensory and motor function of the esophagus: lessons from ultrasound imaging. Gastroenterology. 128:487, 2005. Pastor AC, et al. A single center 26-year experience with treatment of esophageal achalasia: is there an optimal method? J Pediatr Surg. 44:1349, 2009. Sonnenberg A. Hospitalization for achalasia in the United States 1997–2006. Dig Dis Sci. 54:1680, 2009.

ESOPHAGEAL TRAUMA NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Esophageal trauma is a major traumatic condition that affects the esophagus; it is often caused by chemical burns, ingestion of foreign bodies, or injury. Diagnosis of penetrating pharyngeal and esophageal injuries is difficult when the patient has severe facial injuries, is obese, intubated, or hemodynamically unstable (Ahmed et al, 2009). Boerhaave syndrome involves complete laceration of the esophagus, sometimes spontaneously from alcohol abuse with retching or secondary to endoscopy or vagotomy. Mallory– Weiss syndrome involves a mucosal gastric tear that can occur at the gastroesophageal (GE) junction or proximal stomach; it is also associated with retching or alcohol abuse.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Esophageal trauma is acquired, not genetic. Na, K TLC Height H&H Weight Serum Fe, BMI ferritin, Weight changes ferritin Videoendoscopy Alb or I&O Lab Work transthyretin Nausea, Transferrin Gluc vomiting   BUN, creatinine Ca , Mg Loss of (Creat) consciousness Clinical/History

Respiratory distress Esophageal perforation? Dysphagia Temperature

• Allow the esophagus to rest and heal. Prepare for esophageal surgery if necessary. • Keep the patient adequately hydrated. • Improve swallowing capacity as rapidly as possible; prevent aspiration. • Prevent malnutrition, weight loss, sepsis, constipation, fluid loss from exudates, and other complications. • For serious injuries with permanent damage, it may be necessary for a gastrostomy TF to be used.

FOOD AND NUTRITION • Nothing by mouth (NPO) as needed. Provide CPN, gastrostomy, or jejunostomy feedings as appropriate for the patient’s condition. • Calculate needs with extra protein, if applicable. Monitor cardiac, hepatic, and renal status. • Progress over time to a soft diet. Avoid alcoholic beverages, extremely hot liquids and beverages, caffeine, and spicy foods if not tolerated.

SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment: Prior gunshot wound to the neck that required esophageal repair. Loss of 10 lb this year even though eating “a lot.” Nutrition Diagnosis (PES): Inability to digest/absorb nutrients (NC-1.4) related to surgical alteration in GI anatomical structure as evidenced by weight loss, albumin indicative of malnutrition. Interventions: Food and Nutrient Delivery: ND 1.2—Alter diet as tolerated. ND 32.3 and 32.4—Initiate vitamin and mineral supplementation. Education: E-1.2—Discuss ways to increase energy and nutrient density in food choices.

INTERVENTION OBJECTIVES • Emergency care, such as adequate ventilation, is given as needed.

Counseling: C-2.3—Keep a food diary for 1 month. C-2.2—Set goal of only nutrient and energy-dense meals for 1 month if tolerated. Monitoring and Evaluation: Review food diary after 1 month. Monitor weight for resolution of unintentional weight loss; goal is gain of 1–2 lb weekly.


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• Provide adequate fluids but avoid overhydration. • When able to eat orally, monitor for signs of dysphagia. Work with a speech therapist for proper consistency evaluations. Use appropriately thickened or thinned liquids and pureed foods until swallowing ability returns. • Home TF may be needed, for which either a gastrostomy or jejunostomy will be used, depending on location and extent of injury and surgical repair.

Common Drugs Used and Potential Side Effects • Liquid topical anesthetizing agents (such as lidocaine) may be used before meals to reduce pain. • Antibiotics may be used in bacterial infections.

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • When the patient can swallow, discuss the need to chew well and swallow carefully. The patient should also learn to eat slowly to prevent aspiration. • Discuss the appropriate food textures for different stages of progress. This plan will be developed in accordance with the speech therapist and the physician.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Esophageal trauma http://emedicine.medscape.com/article/775165-overview

Herbs, Botanicals, and Supplements ESOPHAGEAL TRAUMA—CITED REFERENCES • Herbs and botanical supplements should not be used without discussing with the physician.

Ahmed N, et al. Diagnosis of penetrating injuries of the pharynx and esophagus in the severely injured patient. J Trauma. 67:152, 2009.

ESOPHAGEAL VARICES NUTRITIONAL ACUITY RANKING: LEVEL 2–3 DEFINITIONS AND BACKGROUND Acute bleeding from esophageal varices due to portal hypertension is a frequent and severe complication of liver cirrhosis (Lata et al, 2006). Esophageal varices occur in about half of all people with alcoholic cirrhosis and one third of these will experience variceal hemorrhage, a life-threatening event (Smith, 2010). Portal hypertension is defined as a portal pressure gradient exceeding 5 mm Hg where portosystemic collaterals decompress the portal circulation and give rise to varices (Toubia and Sanyal, 2008). Small esophageal veins become distended and may rupture due to increased pressure in the portal system. Thrombocytopenia and splenomegaly are independent predictors of large esophageal varices. All cirrhotic patients should undergo endoscopic screening to detect varices. Severe fibrosis and esophageal varices may be diagnosed through a prothrombin index of less than 60%, alkaline phosphatase activity greater than 110 IU/L, and hyaluronate greater than 100 g/L in alcoholic patients (Vanbiervliet et al, 2005). Maintenance of a good renal function is essential in these patients (Lata et al, 2006). Fortunately, great strides have been made because of noninvasive imaging and pressure measurement. Mortality has been substantially reduced. Band ligation is the first-line endoscopic treatment. If this fails, the more invasive surgical shunt may be needed.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Cirrhotic patients have an increased risk for thrombosis because of portal blood flow stasis; known risk factors include G20210 A mutation of prothrombin or factor V Leiden (Amitrano et al, 2007). Clinical/History Height Weight BMI Diet history Weight changes Esophagoscopy Edema Melena Upper GI bleeding BP Respiratory distress Aspiration of emesis

Transferrin Confusion Abdominal dis- Bilirubin (20 tention, mg/dL) Jaundice or hepatic coma Platelet count (200,000/ Lab Work mm3) Prothrombin H&H index Serum Fe, (60%) ferritin Hyaluronate Ammonia (NH3) (100 g/L) BUN Alkaline Alb (4.0 g/dL) phosphatase Ascites (Alk phos)    Na , K , Cl (110 IU/L)   Ca , Mg


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Assessment: Intake history revealing poor intake of nutrientdense foods and frequent meal skipping with use of one fifth of rum daily for 12 years. Lab results showing elevated ammonia level, blood in stool, low H & H with documented anemia.

• Beta-blockers; propranolol reduces the risk of bleeding, especially in cirrhosis (Suzuki et al, 2005). However, the combination of beta-blockers with mononitrate of isosorbide is superior to beta-blockade alone (Kravetz, 2007). • Vasoactive agents, such as somatostatin analog and terlipressin, are useful. • Vitamin K may be needed to help with clotting.

Nutrition Diagnoses (PES): Excessive alcohol intake related to intake of rum instead of meals as evidenced by bleeding and varices, diet history, altered hepatic labs.

Herbs, Botanicals, and Supplements

Interventions: Enhance oral intake, or offer PEG TF as needed. Remove access to alcohol and coordinate care for referral to rehabilitation center when feasible.

• Herbs and botanical supplements should not be used without discussing with the physician.

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Alcohol Intake

Monitoring and Evaluation: No rebleeding. Adequate intake from TF and slow progression back to oral diet. Improved intake of all macro- and micronutrients, and improvement in labs. Corrected anemia.

INTERVENTION OBJECTIVES • Promote healing and recovery. • Prevent variceal rebleeding, which is a very frequent and severe complication in cirrhotic patients (Kravetz, 2007). • Avoid constipation or straining with stool. • Prevent or correct hepatic encephalopathy or coma; see Section 8.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The importance of good nutrition with proper consistency should be addressed. Avoid rough or crunchy foods that are fibrous or sharp; chew all foods well before swallowing. • If gastrostomy is needed, discuss how to manage the process. • If relevant, discuss the role of alcohol in contributing to the disease process with the patient and family. Advise the patient to avoid mouthwashes, cough syrups, and other products that contain alcohol.

Patient Education—Foodborne Illness

FOOD AND NUTRITION • Generally, unless comatose, the patient can tolerate five to six small meals of soft foods. Avoid foods such as tacos, tortilla chips, or large pieces of raw fruits and vegetables. • Alter carbohydrate, protein, and fat intake according to hepatic function and state of consciousness. Monitor micronutrient needs, such as iron if patient is anemic. • Provide adequate fluid as allowed or controlled. • To prevent constipation and straining, use foods such as prune juice or formulas with added fiber. • Consider use of branched-chain amino acid formula for cirrhosis.

Common Drugs Used and Potential Side Effects • Antacids may be beneficial to buffer gastric acidity. Extended use can cause problems with pH, altered mineral and nutrient use, and other imbalances.

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Esophageal Varices http://www.nlm.nih.gov/medlineplus/ency/article/000268.htm

ESOPHAGEAL VARICES—CITED REFERENCES Amitrano L, et al. Coagulation abnormalities in cirrhotic patients with portal vein thrombosis. Clin Lab. 53:583, 2007. Kravetz D. Prevention of recurrent esophageal variceal hemorrhage: review and current recommendations. J Clin Gastroenterol. 41:318S, 2007. Lata J, et al. Factors participating in the development and mortality of variceal bleeding in portal hypertension—possible effects of the kidney damage and malnutrition. Hepatogastroenterology. 53:420, 2006. Smith MM. Emergency: Variceal hemorrhage from esophageal varices associated with alcoholic liver disease. Am J Nurs. 110:32, 2010. Suzuki A, et al. Diagnostic model of esophageal varices in alcoholic liver disease. Eur J Gastroenterol Hepatol. 17:307, 2005. Toubia N, Sanyal AJ. Portal hypertension and variceal hemorrhage. Med Clin North Am. 92:551, 2008. Vanbiervliet G, et al. Serum fibrosis markers can detect large oesophageal varices with a high accuracy. Eur J Gastroenterol Hepatol. 17:333, 2005.


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ESOPHAGITIS, GASTROESOPHAGEAL REFLUX DISEASE AND HIATAL HERNIA NUTRITIONAL ACUITY RANKING: LEVEL 2–3

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Esophagitis results from gastric juice being forced into the esophagus from the stomach. Pill-induced esophageal injury may occur from use of aspirin, tetracycline, vitamin C, ferrous sulfate, potassium chloride, or nonsteroidal antiinflammatory drugs (NSAIDs). Take these with plenty of liquid. Eosinophilic esophagitis (EoE or EE) is a disorder characterized by a severe, isolated eosinophilic infiltration of the esophagus that is unresponsive to aggressive acid blockade but responsive to the removal of dietary antigens (Liacouras et al, 2005). Adult patients usually present with dysphagia, food impaction and reflux-like symptoms (Gupte and Draganov, 2009). Known causes of tissue eosinophilia include GE reflux disease (GERD), infections, malignancy, collagen vascular diseases, hypersensitivity, and IBD (Gupte and Draganov, 2009). It is highly associated with atopic disease.

Barrett’s esophagus is a condition that affects men more than women, and length of impact is greater in men than in women (Falk et al, 2005). It is also more common in Caucasians and in persons older than age 50. Symptoms are similar to GERD, but Barrett’s esophagus is more likely to precede esophageal adenocarcinoma. Upper endoscopy and surveillance biopsies may be needed (Liu and Saltzman, 2006). Antioxidants (vitamins C, E, and betacarotene) are important protective factors (Kubo et al, 2008), whereas obesity and the western diet may be promoters of cancer. GERD and peptic ulcer disease are common in elderly individuals. GERD affects approximately 19 million Americans; prevalence is as high as 80% among asthma patients. There is a significantly higher prevalence of RE in an Helicobacter pylori-infected individuals of any age or sex (Moon et al, 2009). Distal esophageal cancer is associated with symptomatic GI reflux disease and Barrett’s esophagus; surveillance programs are identifying patients early for curable esophageal adenocarcinoma (Demeester, 2006). GERD may occur in infants but usually resolves by 6–12 months of age. Management involves thickened feedings and positioning. The recommended approach for infants with uncomplicated regurgitation is the reassurance of the parents about the physiological nature of excessive regurgitation and dietary recommendations for formula feeding. Symptoms of pediatric GERD include colic, inconsolable crying, frequent spitting up or vomiting, food refusal, failure to thrive, heartburn, stomach pains, chronic sore throat, chronic respiratory problems, asthma, and apnea. GERD diagnosis in older children warrants review for upper GI tract disorders, cow’s milk allergy, or metabolic, infectious, renal, or central nervous system diseases. Treatment guidelines address lifestyle changes, patientdirected (over the counter) therapy, acid suppression, promotility therapy, maintenance therapy, and antireflux surgery (DeVault and Castell, 2005). Intractable GERD may require minor surgery to strengthen a weak sphincter. Laparoscopic antireflux surgery is highly effective as a longterm treatment for severe GERD. Hiatal hernia is caused by protrusion of part of the stomach through the diaphragm muscle, which separates the chest from the abdomen. This causes an enlarged diaphragm opening (hiatus) through which the esophagus passes to join the stomach. An increase in BMI is associated with the increased prevalence of hoatal hernia, esophageal mucosal injury, and complications because of increased intragastric pressure and increased GE pressure gradient (Fass, 2008). Hiatal hernia may show no symptoms or may contribute to heartburn, swallowing difficulty, reflux, or vomiting. Hiatal hernia surgery has evolved from anatomic repair to physiological restoration (Stylopoulos and Rattner, 2005).


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INTERVENTION OBJECTIVES

CLINICAL INDICATORS Genetic Markers: Proton pump inhibitors (PPIs), such as omeprazole, lansoprazole, and rabeprazole are metabolized by CYP2C19 in the liver; there are genetic differences in the activity of this enzyme (Furuta et al, 2010). These genotypic differences influence the healing and eradication rates for GERD and H. pylori infection (Furuta et al, 2010). The pathogenesis of EE involves multiple tissues, cell types, and genes, and derives from complex genetic and environmental factors (Blanchard and Rothenberg, 2008). Clinical/History

Reactive airway disease or nocturnal asthma Choking attacks Dental erosion or caries

H. pylori infection? Height Cholesterol Weight (Chol) BMI Triglycerides Diet history (Trig) Weight Transferrin changes Total ironUpper GI Lab Work binding endoscopy capacity Esophagoscopy H & H (TIBC) PillCAM (nonin- Mean cell Bernstein test: volume vasive visualiHCl solution (MCV) zation) is dripped   Na , K Manometry into the distal   Feeding difficul- Ca , Mg esophagus; Gluc ties in positive Gastrin children test mimics Alb, transthyretin Recurrent patient CRP vomiting symptoms

SAMPLE NUTRITION CARE PROCESS STEPS Gastroesophageal Reflux Disease (GERD) Assessment: Knowledge about the role of diet in GERD; food diary; timing of meals and related symptoms. Use of antacids with every meal and at bedtime. Nutrition Diagnosis (PES): Undesirable food choices related to lack of knowledge regarding role of diet in GERD symptoms and complications as evidenced by frequent consumption of large, high-fat meals and alcoholic beverages. Intervention: Teach about dietary changes that will alleviate GERD symptoms and possibly prevent complications. Counsel about lifestyle changes, such as weight loss, loose clothing, and upright posture during and after eating. Monitoring and Evaluation: Report of relief from symptoms. No complications from GERD. Gradual reduction in need for antacids and medication.

• In stage 1, simple lifestyle modifications may be successful: elevate head of the bed, decrease fat intake, stop smoking, lose excess weight, avoid eating large meals, and do not eat 3 hours before lying down. Large meals increase gastric pressure and alter pressure on the lower esophageal sphincter (LES), thereby allowing reflux or aspiration to occur. Avoid tightly fitted garments around the abdomen. • In stage 2, add pharmacological treatments, such as histamine-receptor blockers or antacids. • In stage 3 with erosive esophagitis, it may be necessary to add a PPI as first-line therapy. • In stage 4, maintenance therapy, use the lowest possible dose of medications to manage symptoms. • In severe stage 5, surgery may be needed. This may include laparoscopic Nissan fundoplication.

FOOD AND NUTRITION • Provide an individual diet reflecting patient needs. Assess intake of fat, alcohol, spices, and caffeine. • If needed, a reduced-energy diet should be used to promote weight loss. • During acute episodes, provide small, frequent feedings of soft foods. • Diet should be high in protein to stimulate gastrin secretion and to increase LES pressure. Avoid foods that decrease LES pressure, including chocolate, peppermint, onions, garlic, and spearmint. • Use fewer fried foods, cream sauces, gravies, fatty meats, pastries, nuts, potato chips, butter, and margarine. • Dietary fiber and physical exercise may be protective. Increased fiber intake benefits a number of GI disorders including GERD (Anderson et al, 2009). Dietary fiber intakes for children and adults should be calculated as 14 g/1000 kcal. • Avoid foods that may irritate the esophagus, such as citrus juices, tomatoes, and tomato sauce. Other spicy foods are to be eliminated according to individual experience. • If there is EoE, try a dietary elimination diet and add back foods one at a time to identify potential allergens (Liacouras et al, 2005). • Fluids can be taken between meals to reduce abdominal distention and discomfort. • Preterm infants may benefit from transpyloric feedings if they show signs suggestive of reflux and apnea (Malcolm et al, 2009).

Common Drugs Used and Potential Side Effects • Antacids neutralize gastric contents. They destroy thiamin and may provide excess sodium for the body; check labels carefully. If the antacid contains calcium (e.g., Tums, which contains calcium carbonate), excess calcium may decrease levels of magnesium and phosphorus. Aluminum hydroxide (Maalox) depletes phosphorus, which is acceptable for patients with certain types of renal diseases, but otherwise this is not desirable for the long term. When


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used as an antacid, sodium bicarbonate can decrease iron absorption and causes sodium retention; use with caution. • Calcium glycerophosphate (Prelief) is somewhat useful for relief of heartburn by neutralizing the acid in foods; it is available over the counter. • PPIs, such as lansoprazole (Prevacid), omeprazole (Prilosec), and esomeprazole (Nexium) are popular treatments. When clarithromycin-resistant H. pylori (CRHP) occur, PPIs tend to inhibit the growth and motility of CRHP. Omeprazole is useful for refractory RE. Because CYP2C19 genotypes affect the recurrence rate of GERD symptoms during PPI maintenance therapy, genotype-based tailored therapy is needed (Furuta et al, 2010; Saitoh et al, 2009).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Chamomile, fennel, cardamom, cinnamon, dill, and licorice have been recommended for this condition, but no clinical trials have proven efficacy.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Encourage the patient to avoid late evening meals and snacks and to avoid lying down or sleeping or swimming soon after a meal to guard against reflux. • Teach the proper measures for controlling weight, including small, frequent feedings. • Instruct the patient about lifestyle modifications listed in the Objectives. Patients with heartburn probably should not sleep in a waterbed. • Chewing sugarless gum after meals may reduce reflux somewhat because of the saliva production. • More effective communication and consumer education is required to enhance fiber consumption from foods or supplements (Anderson et al, 2009).

Patient Education—Foodborne Illness • Careful food handling and washing hands before eating are useful recommendations.

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• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

International Foundation for Gastrointestinal Disorders http://www.aboutgerd.org/

Heartburn and Regurgitation Algorithm http://www.uwgi.org/guidelines/ch_03/ch03.htm

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/

Prelief http://www.akpharma.com/prelief/preliefindex.html

HIATAL HERNIA, ESOPHAGITIS, AND GERD—CITED REFERENCES Anderson JW, et al. Health benefits of dietary fiber. Nutr Rev. 67:188, 2009. Blanchard C, Rothenberg ME. Basic pathogenesis of eosinophilic esophagitis. Gastrointest Endosc Clin N Am. 18:133, 2008. Demeester SR. Adenocarcinoma of the esophagus and cardia: a review of the disease and its treatment. Ann Surg Oncol. 13:12, 2006. DeVault K, Castell D. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 100:190, 2005. Falk GW, et al. Barrett’s esophagus in women: demographic features and progression to high-grade dysplasia and cancer. Clin Gastroenterol Hepatol. 3:1089, 2005. Fass R. The pathophysiological mechanisms of GERD in the obese patient. Dig Dis Sci. 53:2300, 2008. Furuta T, et al. Influences of different proton pump inhibitors on the antiplatelet function of clopidogrel in relation to CYP2C19 genotypes. Br J Clin Pharmacol. 70:383, 2010. Gupte AR, Draganov PV. Eosinophilic esophagitis. World J Gastroenterol. 15:17, 2009. Kubo A, et al. Dietary antioxidants, fruits, and vegetables and the risk of Barrett’s esophagus. Am J Gastroenterol. 103:1614, 2008. Liacouras CA, et al. Eosinophilic esophagitis: a 10-year experience in 381 children. Clin Gastroenterol Hepatol. 3:1198, 2005. Liu JJ, Saltzman JR. Management of gastroesophageal reflux disease. South Med J. 99:735, 2006. Malcolm WF, et al. Transpyloric tube feeding in very low birthweight infants with suspected gastroesophageal reflux: impact on apnea and bradycardia. J Perinatol. 29:372, 2009. Moon A, et al. Positive association between helicobacter pylori and gastroesophageal reflux disease in children [published online ahead of print 9 June 2009]. J Pediatr Gastroenterol Nutr. 49:283, 2009. Saitoh T, et al. Influences of CYP2C19 polymorphism on recurrence of reflux esophagitis during proton pump inhibitor maintenance therapy. Hepatogastroenterology. 56:703, 2009. Stylopoulos N, Rattner DW. The history of hiatal hernia surgery: from Bowditch to laparoscopy. Ann Surg. 241:185, 2005.

STOMACH

DYSPEPSIA/INDIGESTION OR BEZOAR FORMATION NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND Indigestion (dyspepsia) may be secondary to other systemic disorders such as atherosclerotic heart disease, hypertension, liver disease, or renal disease. It may have psychogenic causes as well, such as during periods of anxiety. Symptoms may be graded from mild to severe for the individual patient. Gastric hypersensitivity is an important factor.

In rare cases, a patient may exhibit signs of bezoar formation, such as after gastric surgery or chronic use of medications that do not dissolve easily for that individual. A bezoar (foreign matter accumulation) may be made of plant material, medications, or swallowed foreign objects. The patient complains of vague abdominal pain or indigestion and may experience nausea or vomiting. An x-ray of the GI tract may be useful for a clarifying diagnosis.


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CLINICAL INDICATORS Genetic Markers: Genetic factors in indigestion would be related to the primary disorder. Clinical/History Height Weight Weight changes BMI Diet history Gastric burning sensation Bloating, heartburn, nausea Burping, vomiting Early satiety, postprandial fullness

Anorexia Nausea or vomiting Epigastric pain or burning Postprandial fullness, early satiation Gastric barostat tests Endoscopy I&O Bezoar formation?

Lab Work Gluc H. pylori infection H&H Serum Fe, ferritin MCV Alb, transthyretin CRP BUN, Creat Na, K Ca, Mg

INTERVENTION OBJECTIVES • Determine whether the problem is psychogenic or organic in etiology. Do not oversimplify the patient’s discomfort. • If the patient has a bezoar, alter food and beverage consistencies. • If the patient has irritable bowel or other GI condition, work closely with the medical team to manage dietary changes and reduce excessive use of medications.

SAMPLE NUTRITION CARE PROCESS STEPS Dyspepsia Assessment Data: Weight, BMI; recent GI surgery for extensive peptic ulcer disease; positive hx of H. pylori infection; heartburn with every meal and complaints of indigestion. Nutrition Diagnoses (PES): Inadequate oral food and beverage intake related to frequent bouts of indigestion after GI surgery as evidenced by unplanned weight loss, reports of heartburn and indigestion with meals. Interventions: Alter foods served to decrease use of acidic foods or stimulants such as caffeine and alcoholic beverages. Educate about simplifying meals and small snacks to increase intake. Counseling on food choices and lifestyle changes to improve intake and decrease discomfort. Monitoring and Evaluation: Improved intake for meals and snacks. Fewer complaints of dyspepsia. No further weight loss. Reduced need for use of antacids for heartburn.

FOOD AND NUTRITION • Diet should make use of well-cooked foods that are adequate in amount but not overly seasoned. • Evaluate for any undetected food allergies and manage accordingly. • A relaxed atmosphere is helpful, and small meals may be better tolerated. • If the dyspepsia is organic in etiology, a soft, low-fat diet may be helpful. • If there is irritable bowel as well, discuss fiber from fruits and vegetables (American Dietetic Association, 2008). Bran is not always well tolerated. • If the patient has an obstruction or bezoar, a liquid diet may be useful until resolved.

Common Drugs Used and Potential Side Effects • Antacids: Beware of nutritional side effects resulting from chronic use or dependency. • Antisecretory drugs are useful (Suzuki et al, 2006). PPIs may be used, especially if reflux also exists. Lansoprazole (Prevacid), omeprazole (Prilosec), and esomeprazole (Nexium) are commonly used. • NSAIDs are nonselective cyclooxygenase-1 (COX-1) and COX-2 inhibitors and may be associated with dyspepsia. Other anti-inflammatory medicines such as ibuprofen, aspirin, and naproxen (Aleve) can irritate the stomach. Acetaminophen (Tylenol) is a better choice for pain.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Ginger is often used as an antinauseant. Do not use large doses with warfarin, aspirin, other antiplatelet drugs, antihypertensive drugs, and hypoglycemic drugs. Additive effects can cause unpredictable changes in BP and decreases in blood glucose levels and may decrease platelet aggregation and thus increase bleeding. Ginger ale has few side effects. • Chamomile, peppermint, red pepper, angelica, and coriander have been recommended, but no clinical trials have proven efficacy.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Encourage the patient to eat in a relaxed atmosphere. • Yoga and other stress-relieving lifestyle changes may be beneficial. • Discuss the role of fiber in maintaining bowel regularity. • Discuss tips for preparing meals that are lower in acid, stimulants, or other irritants.


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Patient Education—Food Safety

• Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the diet of the individual. Preparation and storage techniques are also essential. • If home TF is needed, teach appropriate sanitation and food handling procedures.

DYSPEPSIA/INDIGESTION—CITED REFERENCES

For More Information •

Dyspepsia http://familydoctor.org/474.xml

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Dyspepsia Algorithm http://www.uwgi.org/guidelines/ch_02/ch02.htm

American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Suzuki H, et al. Therapeutic strategies for functional dyspepsia and the introduction of the Rome III classification. J Gastroenterol. 41:513, 2006.

GASTRECTOMY AND VAGOTOMY NUTRITIONAL ACUITY RANKING: LEVEL 3–4 Fundus Vagotomy

Antrum of stomach is removed Body Antrectomy Duodenum

Jejunal anastomosis

Stump closed

Jejunal loop

Stomach sutured to jejunum Fundus

Vagotomy

Vagus nerve

Longitudinal incision

Body Antrectomy

Duodenum 75–80% of stomach is removed

Remaining stomach Incision aligned transversely

Transverse closure

Duodenal anastomosis

Adapted from: Nettina, Sandra M., MSN, RN, CS, ANP, The Lippincott Manual of Nursing Practice, 7th ed. Lippincott, Williams & Wilkins, 2001.

DEFINITIONS AND BACKGROUND Gastrectomy and vagotomy are surgical procedures that are used for gastric cancer, when medical management for peptic ulcer has failed, or for perforation. The frequency with which elective gastric surgeries are performed has decreased in the past 20 years as drugs have become increasingly effective in treating ulcers. Laparoscopic-assisted gastrectomy is an increasingly common procedure for gastric cancer, with fewer side effects (Mochiki et al, 2005).

Billroth I (gastroduodenostomy) is an anastomosis between the stomach and duodenum after removal of the distal portion of the stomach. Billroth II (gastrojejunostomy) is an anastomosis between the stomach and jejunum after removal of two thirds to three fourths of the stomach; iron loss can occur. While the Billroth I and Billroth II operations have been used for reconstruction after a distal gastrectomy for gastric cancer, a Roux-en-Y reconstruction is increasingly performed to prevent duodenogastric reflux (Hoya et al, 2009).


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Vagotomy is a procedure in which the vagus nerve is cut to reduce pain; much less nutritional intervention is required. Gastrectomy or vagotomy may lead to reactive hypoglycemia, which may drop plasma glucose levels to as low as 30–40 mg/dL due to rapid digestion and absorption of food, especially carbohydrates. Gastric emptying rate for solids may increase in some patients. In most of them, however, there is a normal to decreased emptying rate.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Gastrectomy and vagotomy are surgical procedures. Any genetic relationships would be from the original problem. Na, K, Cl Blood guaiac Height H&H Urine acetone Weight Serum Fe, White blood cell BMI ferritin (WBC) count Diet history Gluc BUN BP Glucose Alb, Temperature, tolerance test transthyretin fever (GTT) Serum amylase ElectrogastroChol, Trig Serum B12 gram (EGG) Pro-time (PT) or Ca, Mg Dual-energy x-ray International Serum folate absorptiomeNormalized TIBC try (DEXA) Ratio (INR) scan Clinical/History

Lab Work

INTERVENTION OBJECTIVES Preoperative • Empty the stomach and upper intestines. • Ensure high-calorie intake for glycogen stores and weight maintenance or weight gain if needed. Ensure adequate nutrient storage to promote postoperative wound healing. • Maintain normal fluid and electrolyte balance.

Postoperative • Prevent distention and pain. Reduce the likelihood of the dumping syndrome: nausea, vomiting, abdominal distention, diarrhea, malaise, profuse sweating, hypoglycemia, hypotension, increased bowel sounds, and vertigo. Additional use of soy and fermentable fiber may be useful; liquid pectin may prolong gastric emptying time and reduce the onset of dumping. • Compensate for loss of storage/holding space and lessen dumping of large amounts of chyme into the duodenum/ jejunum at one time. Overcome effects of decreased hormonal output (secretin, pancreozymin, and cholecystokinin). • Overcome negative nitrogen balance after surgery; restore healthy nutritional status. • Prevent or correct iron malabsorption; steatorrhea, calcium malabsorption, and vitamin B12 or folacin anemias. • Prevent or treat metabolic bone disease, which can occur over time. • Prevent or treat problems such as bezoars, gastric stasis, or gastroparesis.

FOOD AND NUTRITION Preoperative • Use a soft diet that is high in calories with adequate protein and vitamins C and K. • Regress to soft diet with full liquids and then NPO about 8 hours before surgery.

SAMPLE NUTRITION CARE PROCESS STEPS Inconsistent Carbohydrate Intake Assessment Data: Weight loss, frequent emesis after meals, irregular blood glucose levels with reactive hypoglycemia several times weekly. Nutrition Diagnoses (PES): Inconsistent carbohydrate intake related to lack of knowledge about nutrition after gastrectomy as evidenced by weight loss, complaints of profuse sweating, diarrhea, and vomiting after meals high in carbohydrate, and blood glucose levels that vary with bouts of reactive hypoglycemia. Interventions: (ND-1) Order diet that is low fat, high protein, no concentrated sweets (NCS). Educate about foods that are high in simple carbohydrate and those that are complex. Counsel on eating slowly and drinking beverages between meals. Monitoring and Evaluation: Improved intake for meals and snacks; fewer complaints of dumping syndrome. No further weight loss.

Postoperative • Within a total quantity limit, intake of complex carbohydrates such as bread, rice, and vegetables should be liberal (50–60%). To lessen the hyperosmolar load, use only 0–15% of diet from foods made with sucrose, fructose, and glucose. Initial diet may need to be 20 mL of liquid nutritional supplement every few hours, progressing as tolerated. Gastrectomy patients will be limited by the size of the remaining stomach as well. • A protein-rich food should be consumed with each meal. Include eggs, cheese, dried beans or peas, tender meat or poultry, boneless fish, yogurt, peanut butter, nuts, tofu, and cottage cheese. • Lactose intolerance is common in patients with these conditions; use less milk or omit if needed. Monitor calcium intake carefully. • Use a moderate fat intake (about one third of energy intake). If needed, medium-chain triglycerides (MCTs) may be beneficial with fat maldigestion, and pancreatic enzymes may also be needed in some cases.


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• The diet should also provide adequate chromium, vitamin B12, riboflavin, iron, folacin, calcium, and vitamin D. A liquid multivitamin–mineral supplement may be needed. • If weight loss becomes a problem, a liquid supplemental beverage may be useful between meals and can be sipped throughout the day and evening. • Diet should provide a moderate sodium intake; excess salt draws fluid into the duodenum. If there is diarrhea, losses of sodium in the stool may occur. • Fluids should be taken 1 hour before or after meals, rather than with meals; assure adequate fluid intake overall. • Sit upright while eating. Encourage slow eating and adequate chewing for all meals and snacks. • Diet should provide frequent, small meals. Avoid extremes in food temperature.

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Stress the importance of self-care and optimal functioning— what to do for illness, episodes of vomiting, eating away from home, and how to read labels for carbohydrate (CHO) content. • Discuss the use of artificial sweeteners. • Instruct the patient to eat slowly in an upright position and to remain upright for awhile after meals. • Help the patient to overcome reluctance and the fear of eating. Discuss the dumping syndrome and its effects on nutrient absorption if untreated.

Patient Education—Foodborne Illness

Common Drugs Used and Potential Side Effects • Antibiotics may be used to control bacterial overgrowth. • Antidiarrheals such as Kaopectate and loperamide may be useful. Dry mouth, nausea, vomiting, and bloating may occur. Use plenty of fluids. • For reactive hypoglycemia, use of an alpha-glucosidase inhibitor, acarbose, may be beneficial. GI side effects are common. • Pancreatic enzymes may be useful; the usual dose provides two to three capsules with meals. • If vitamin B12 deficiency occurs, shots may be needed. • If bone density loss occurs, the use of calcium, vitamin D, or bisphosphonates may be prescribed, and these should be taken as directed.

Herbs, Botanicals, and Supplements

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Anti-Dumping Syndrome Diet http://www.gicare.com/Diets/Dumping.aspx

Gastrectomy—Surgical Channel http://www.surgerychannel.com/gastrectomy/index.shtml

Medline http://www.nlm.nih.gov/medlineplus/ency/article/002945.htm

GASTRECTOMY AND VAGOTOMY—CITED REFERENCES Hoya Y, et al. The advantages and disadvantages of a Roux-en-Y reconstruction after a distal gastrectomy for gastric cancer. Surg Today. 39:647, 2009. Mochiki E, et al. Laparoscopic assisted distal gastrectomy for early gastric cancer: Five years’ experience. Surgery. 137:317, 2005.

• Herbs and botanical supplements should not be used without discussing with the physician.

GASTRITIS AND GASTROENTERITIS NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Gastritis involves inflammation of the stomach. Types of gastritis include bacterial (from H. pylori), autoimmune gastritis with pernicious anemia, erosive gastritis (from aspirin or NSAID use), alcohol-induced gastritis, bile reflux gastritis, or atrophic gastritis. The treatment of gastritis will depend on its cause; reduction of stomach acid by medication is often most helpful. Helicobacter pylori infects half the world’s population, causing chronic gastritis (Shanks and El-Omar, 2009). Bacterial, environmental and host genetic factors combine to define the degree of gastric damage in gastritis (Shanks and ElOmar, 2009). Hemorrhagic gastritis may result from chronic intake of alcohol or medications, Crohn’s disease or HIV

infection. Atrophic gastritis is chronic inflammation of the gastric mucosa without erosion but with hypochlorhydria or achlorhydria; it is important to monitor vitamin B12, calcium, and ferric iron intake. Gastroenteritis (GE) is an inflammation of the stomach and intestinal lining that may occur from eating chemical toxins in food (such as seafood, mushrooms, arsenic, or lead), drinking excessive alcohol, foodborne illness and viruses, cathartics or other drugs. GE produces malaise, nausea, vomiting, intestinal rumbles, diarrhea with or without blood and mucus, fever and prostration. Viral gastroenteritis is contagious. Many different viruses can cause gastroenteritis, including rotaviruses or adenoviruses. Norovirus infection is associated with 90% of nonbacterial acute gastroenteritis (Sala et al, 2005).


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Contaminated shellfish and raw oysters are major contributors. People who get viral gastroenteritis almost always recover completely if they consume adequate fluids to replace what they lose through vomiting or diarrhea. Because the intestinal epithelium constitutes the largest and most important barrier against intraluminal toxins, antigens, and enteric flora, its dysfunction is a major factor contributing to the predisposition to inflammatory diseases (Groschwitz and Hogan, 2009). Post-infectious irritable bowel syndrome (PI-IBS) is a disorder where symptoms begin after an episode of acute GE with persistent subclinical inflammation, changes in intestinal permeability and alteration of gut flora (Thabane and Marshall, 2009). Some children acquire functional GI disorders after an episode of acute bacterial gastroenteritis (AGE) from Salmonella (54%), Campylobacter, or Shigella (Saps et al, 2008). Other issues related to intestinal dysfunction include food allergy, IBD, and celiac disease (Groschwitz and Hogan, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Gastroenteritis is acquired and not genetic. Host genetic factors define the severity and extent of Helicobacter-induced gastritis; interleukin-1 and TNF-A gene clusters are involved (Shanks and ElOmar, 2009). Barium swallow study Height Upper GI Weight endoscopy BMI Gastric biopsy Diet history Diarrhea Anorexia, nausea Stool culture Upset stomach Blood in stool? Hiccups I&O Lab Work Signs of dehydration? Na, K, Cl H&H Fever? Serum Fe, Esophageal ferritin manometry Clinical/History

MCV Serum folate Serum B12 Gluc Alb, transthyretin Ca, Mg Hydrogen breath test BUN, creatinine

INTERVENTION OBJECTIVES • Prevent or correct dehydration, shock, hypokalemia, and hyponatremia. • If hemorrhage occurs, consider a medical emergency. • Allow the stomach and GI tract to rest. Empty stomach to permit mucous lining to heal. • Omit lactose if not tolerated during bouts of gastroenteritis.

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function—Diarrhea Assessment Data: Diarrhea, GI pain, slight fever; recent intake of undercooked beef and sushi while traveling. Nutrition Diagnoses (PES): Altered GI function (NC-1.4) with foodborne illness as evidenced by diarrhea, slight fever (100F) for 7 days and stool culture positive for Escherichia coli O157:H7. Interventions: Alter diet as tolerated; soft diet or liquids may be accepted. Provide oral rehydration products. Educate about foodborne illness related to E. coli O157:H7 including food sources. Counseling about safe food-handling procedures and better choices at restaurants while traveling. Monitoring and Evaluation: Resolution of diarrhea. Stool cultures free from E. coli O157:H7. Improved knowledge about food safety as documented by correct responses to questions.

FOOD AND NUTRITION • Gastritis: Omit foods that are poorly tolerated. Provide adequate hydration. If chronic, mucosal atrophy can lead to nutritional deficits (e.g., pernicious anemia, achlorhydria). Alter diet accordingly. • Acute gastroenteritis: Patient will be NPO or on partial parenteral nutrition (PPN) for the first 24–48 hours to rest stomach. Use crushed ice to relieve thirst. Oral rehydration therapy may be useful. Progress to a soft diet, if desired. Alcohol is prohibited. Omit lactose if needed. Gradually add fiber-containing foods as tolerance improves. Rehydration solutions may be effective. • Chronic gastritis: Use small, frequent feedings of easily tolerated foods. Progress with larger amounts and greater variety of foods, as tolerated. Restrict fat intake, which depresses food motility, and alcohol intake. Monitor lactose intolerance. Add fiber-containing foods as tolerated.

Common Drugs Used and Potential Side Effects • Antacids: Watch for constipation caused by aluminum and calcium agents. Watch for diarrhea caused by magnesium agents. • Antibiotics are used for infection. If used in excess over a long period of time, they may cause or aggravate gastroenteritis. Monitor carefully and suggest use of probiotics such as yogurt with live and active cultures. • Sucralfate may be useful. Take separately from calcium or magnesium supplements by 30 minutes. Constipation may occur. • Early postoperative medication with a PPI is effective in preventing gastritis after open-heart surgery (Hata et al, 2005). Lansoprazole (Prevacid), omeprazole (Prilosec), and esomeprazole (Nexium) are commonly used. • Eliminate use of aspirin and other agents that may aggravate gastritis. • If the gastritis is caused by pernicious anemia, B12 vitamin shots will be given.


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Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. Products such as ginger and ginger ale may alleviate some nausea. • The Polynesian traditional food, poi, is a starchy paste made from taro plants (Brown et al, 2005). It may be useful as a probiotic.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Omit offenders in chronic conditions: alcohol, caffeine, and aspirin. • Patients with chronic gastritis should be assessed for folate and vitamin B12 status. Atrophy of the stomach and intestinal lining interferes with folate and vitamin B12 absorption. • Discuss calcium and riboflavin food sources if dairy products must be omitted. • Discuss the role of fiber in achieving or maintaining bowel integrity. • Discuss foodborne illness and its prevention (e.g., avoiding raw shellfish). • Oral rehydration therapy (ORT) is recommended as firstline therapy for both mildly and moderately dehydrated children with gastroenteritis (Spandorfer et al, 2005).

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

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• Careful food handling will be important. To prevent gastroenteritis, cook all foods to proper temperatures; wash all produce before cutting or eating; use careful hand washing.

For More Information •

Gastritis http://digestive.niddk.nih.gov/ddiseases/pubs/gastritis/

Gastroenteritis http://www.cdc.gov/ncidod/dvrd/revb/gastro/faq.htm

Merck manual http://www.merck.com/mmpe/sec02/ch013/ch013c.html

GASTRITIS AND GASTROENTERITIS—CITED REFERENCES Brown AC, et al. A non-dairy probiotic’s (poi) influence on changing the gastrointestinal tract’s microflora environment. Altern Ther Health Med. 11:58, 2005. Groschwitz KR, Hogan SP. Intestinal barrier function: molecular regulation and disease pathogenesis. J Allergy Clin Immunol. 124:3, 2009. Hata M, et al. Prospective randomized trial for optimal prophylactic treatment of the upper gastrointestinal complications after open heart surgery. Circ J. 69:331, 2005. Sala MR, et al. An outbreak of food poisoning due to a genogroup I norovirus. Epidemiol Infect. 133:187, 2005. Saps M, et al. Post-infectious functional gastrointestinal disorders in children. J Pediatr. 152:812, 2008. Shanks AM, El-Omar EM. Helicobacter pylori infection, host genetics and gastric cancer. J Dig Dis. 10:157, 2009. Spandorfer PR, et al. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics. 115:295, 2005. Thabane M, Marshall JK. Post-infectious irritable bowel syndrome. World J Gastroenterol. 15:3591, 2009.

GASTROPARESIS AND GASTRIC RETENTION NUTRITIONAL ACUITY RANKING: LEVEL 2–3 Etiologies of Gastroparesis 6% 5% 8% 36%

14%

31% Post-surgical

Miscellaneous

Diabetes

Pseudo-obstruction

Idiopathic

Parkinsons Disease

DEFINITIONS AND BACKGROUND Phases of normal digestion include: phase I (45–60 minutes of inactivity), phase II (30–45 minutes of intermittent peristaltic contractions), phase III (10 minutes of intense, regular contractions), and phase IV (brief transition between cycles). Gastric retention is caused by a partial obstruction at the outlet of the stomach into the small bowel. Gastric retention may result from diabetes, prolonged hyperglycemia, vagal autonomic neuropathy, scleroderma, Parkinson’s disease, hypothyroidism, postviral syndromes, gastric surgery, or vascular insufficiencies. Gastroparesis is a chronic disorder of gastric motility that is characterized by delayed emptying of either solids or liquids from the stomach in the absence of any mechanical obstruction; diabetes mellitus and postsurgical states cause the majority of these problems Complications include ketoacidosis, infection, and bezoar formation (Feigenbaum, 2006). Bezoars further obstruct the flow from the stomach to the small intestine. Gastroparesis may occur as a


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complication of end-stage liver disease and portal hypertension. Idiopathic gastroparesis is characterized by severely delayed gastric emptying of solids without obvious underlying organic cause (Karamanolis et al, 2007). Because ghrelin is produced by enteroendocrine cells in the gastric mucosa, vagal function and regulation of ghrelin are impaired in gastroparesis (Gaddipati et al, 2006; Levin et al, 2006). Severe gastroparesis can result in recurrent hospitalizations, malnutrition, and even death (McKenna et al, 2008). Gastroparesis can be difficult to treat. Prokinetic drugs are commonly used. Treatment may involve use of an implantable gastric electrical stimulation (GES) device or endoscopic botolinium toxin injection (Gumaste and Baum, 2008; Monnikes and van der Voort, 2006; Vittal and Pasricha, 2006). The surgical procedure has been found to be effective in reducing symptoms within 6 weeks (McKenna et al, 2008).

ASSESSMENT, MONITORING, AND EVALUATION

Genetic Markers: No specific genetic disorder predicts the onset of gastric retention or gastroparesis. Flatulence Early satiety Gastric x-rays– EGG Gastric emptying test (slow emptying of liquids and/or solids)

Height Weight Weight changes BMI Diet history I&O Nausea, vomiting Abdominal pain Lab Work after eating Gluc (poorly conHeartburn trolled, over Belching, 200 mg/dL?) bloating

Phytobezoar Assessment Data: Weight loss. Abdominal pain. Swallowing evaluation showing gastroparesis and GI obstruction from phytobezoar. Nutrition Diagnoses (PES): Altered GI function (NC-1.4) related to phytobezoar as evidenced by delayed gastric emptying, abdominal pain and vomiting, and labs showing glucose levels of 250–300 mg/dL. Interventions: Food and Nutrient Delivery: Use a liquid, low residue diet until bezoar is resolved. Educate: Blending foods to improve intake. Coordinate care: insulin as needed to improve serum glucose control; try doses of coca cola to dissolve phytobezoar. Monitoring and Evaluation: Improved intake for meals and snacks. Improved glucose management. No further abdominal pain or vomiting. Resolution of phytobezoar.

• Monitor use of, or avoid where possible, medications that cause gastric stasis.

CLINICAL INDICATORS

Clinical/History

SAMPLE NUTRITION CARE PROCESS STEPS

H&H BUN, Creat Alb, transthyretin CRP Gastrin Ghrelin levels Na, K, Cl Ca, Mg Serum folate and B12

INTERVENTION OBJECTIVES • Decrease volume of meals served. Use liquids or foods that liquefy at body temperature so they are able to pass by a partial obstruction before or during digestion. Bypass or correct obstruction or other causes of retention. • If diabetes is present, manage control of blood glucose. Differentiate from ketoacidosis, which has similar symptoms of nausea and vomiting. Pernicious vomiting may occur; distinguish from bulimia. • Correct dehydration and electrolyte abnormalities. • Reduce or control pain, diarrhea, or bouts of constipation. • Ensure adequate intake of diet as prescribed to prevent weight loss and control malnutrition. • Prevent or correct bezoar formation of indigestible solids.

FOOD AND NUTRITION • A soft-to-liquid diet lower in fat may be useful to prevent delay in gastric emptying. Isotonic liquids empty more quickly than hypertonic liquids. • Six small meals may be better tolerated than large meals. • Calculate protein and energy requirements according to underlying medical condition(s). • Alter fiber intake according to needs (more to alleviate diarrhea, constipation; less with a history of bezoar formation). • If patient complains of dry mouth, add extra fluids and moisten foods with broth or allowed sauces or gravies. • For patients with a lesser obstruction of the stomach, progress to a mechanical soft diet. • For patients with greater obstruction of the stomach, use a low-fiber diet or tube feed, checking residuals frequently. • A jejunostomy TF may be indicated for persistent problems, even temporarily if needed to correct malnutrition. Consider if there is a history of significant weight loss, cyclical nausea and vomiting, or repeated hospitalizations for gastroparesis. • Ensure that the patient sits upright during meals.

Common Drugs Used and Potential Side Effects • Medications that may cause or aggravate gastric emptying include: alcohol, antacids containing aluminum, anticholinergics, calcitonin, calcium channel blockers, glucagon, interleukin-1, levodopa, lithium, octreotide, narcotics, nicotine, potassium salts, progesterone, sucralfate, tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs) including Celexa, Paxil, Prozac, and Zoloft. • Dopamine antagonists, such as metoclopramide and domperidone, and the motilin receptor agonist erythromycin have been the cornerstones in drug treatment of severe gastroparesis for more than a decade (Abrahamsson, 2007).


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These drugs are less than ideal (Gumaste and Baum, 2008). Give metoclopramide (Reglan) 30 minutes before meals to increase gastric contractions and to relax the pyloric sphincter. Dry mouth, sleepiness, anxiety, and nausea can be side effects. • If there is hyperglycemia, oral agents or insulin may be needed. • Ghrelin receptor agonists may have a role as prokinetic agents (Levin et al, 2006).

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Association of Gastrointestinal Motility Disorders, Inc. http://www.agmd-gimotility.org

Cyclic Vomiting Association http://www.cvsaonline.org

Gastroparesis and Dysmotilities Association http://gpda.net

International Foundation for Functional Gastrointestinal Disorders http://www.iffgd.org

Herbs, Botanicals, and Supplements • Products such as ginger and ginger ale may alleviate some nausea. Use of herbal remedies is common in the Hispanic population. Herbs and botanical supplements should not be used without discussing with the physician. • Cuminum cyminum is widely used in Ayurvedic medicine for the treatment of dyspepsia. • Adolph’s Meat Tenderizer (1 teaspoonful in 8 oz of water before each meal for 7 days) provides papain, a proteolytic enzyme that is a safe treatment for bezoars (Baker et al, 2007). Other studies suggest the use of coca cola.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Help the patient determine a specific dietary regimen. If there is diabetes, optimize glycemic control. • Discuss methods for liquefying foods as needed. • Bezoar formation may occur after eating oranges, coconuts, green beans, apples, figs, potato skins, Brussels sprouts, broccoli, and sauerkraut in a vulnerable individual.

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GASTROPARESIS AND GASTRIC RETENTION—CITED REFERENCES Abrahamsson H. Severe gastroparesis: new treatment alternatives. Best Pract Res Clin Gastroenterol. 21:645, 2007. Baker EL, et al. Resolution of a phytobezoar with Aldoph’s Meat Tenderizer. Pharmacotherapy. 27:299, 2007. Feigenbaum K. Update on gastroparesis. Gastroenterol Nurs. 29:239, 2006. Gaddipati KV, et al. Abnormal ghrelin and pancreatic polypeptide responses in gastroparesis. Dig Dis Sci. 51:1339, 2006. Gumaste V, Baum J. Treatment of gastroparesis: an update. Digestion. 78:173, 2008. Karamanolis G, et al. Determinants of symptom pattern in idiopathic severely delayed gastric emptying: gastric emptying rate of proximal stomach dysfunction. Gut. 56:29, 2007. Levin F, et al. Ghrelin stimulates gastric emptying and hunger in normal weight humans. J Clin Endocrinol Metab. 91:3296, 2006. McKenna D, et al. Gastric electrical stimulation is an effective and safe treatment for medically refractory gastroparesis. Surgery. 144:566, 2008. Monnikes H, Van Der Voort IR. Gastric electrical stimulation in gastroparesis: where do we stand? Dig Dis. 24:260, 2006. Vittal H, Pasricha PF. Botulinum toxin for gastrointestinal disorders: therapy and mechanisms. Neurotox Res. 9:149, 2006.

GIANT HYPERTROPHIC GASTRITIS AND MÉNÉTRIER’S DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND

Adapted from: Ronald L. Eisenberg, An Atlas of Differential Diagnosis. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

Giant hypertrophic gastritis (GHG) is a pathological condition with increased loss of plasma proteins, resulting in hydrolysis by the proteolytic enzymes of the gut. The hydrolyzed proteins are then reabsorbed as amino acids. Ascites or edema occur if the liver cannot produce sufficient albumin rapidly enough. The condition may precede stomach cancer. The disease is rare and diagnosed in patients with giant gastric folds, dyspeptic symptoms, and hypoalbuminemia due to GI protein loss. Ménétrier’s disease is a form of hyperplastic gastropathy and not a form of gastritis because inflammation is minimal. Overexpression of transforming growth factor (TGF)-alpha results in selective expansion of surface mucous cells in the body and fundus of the stomach. Ménétrier’s disease is often associated with H. pylori infection. Most patients with


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Ménétrier’s disease are treated nonoperatively with nutritional support, antacids, and pain medications (Sanchez et al, 2007). Gastric resection provides permanent relief if needed.

• Promote normal dietary intake with a return to wellness. • Delay or prevent onset of stomach cancer if possible.

FOOD AND NUTRITION ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: The H. pylori strain with Ménétrier’s disease has high hepatocyte growth factor (HGF) and TNF-alpha mRNA expressions from gastric fibroblasts (Ishikawa et al, 2008). Clinical/History Height Weight BMI Diet history Weight changes Abdominal pain Blood in vomit Gastroscopy Gastric biopsy Abdominal ultrasound

CRP Gluc Na, K Ca, Mg Nitrogen (N) balance Transferrin Lab Work H&H Serum Fe, Pepsin levels ferritin H. pylori bacteria Serum folate Alb, transthyretin and B12 Globulin BUN, Creat A:G ratio Fecal occult blood test Steatorrhea Generalized edema Stomach ulcers?

INTERVENTION OBJECTIVES

• Use a high-protein/high-calorie diet. The protein level should be approximately 20% of total kilocal unless contraindicated for renal or hepatic problems. • Omit any food intolerances. • Include adequate sources of micronutrients in the diet; a basic supplement may be warranted.

Common Drugs Used and Potential Side Effects • Ménétrier disease patients have been effectively treated with a specific blocking monoclonal antibody (Coffey et al, 2007). This reduces the frequency of nausea and vomiting, improves serum albumin concentration, and improves abnormalities of the stomach. • For eradication of H. pylori, 2 weeks of treatment with an acid-suppressing drug (one time daily), Pepto-Bismol (four times daily), and antibiotics (three to four times daily) are prescribed. This therapy often must be used more than once. Other combinations may include the antibiotics omeprazole, clarithromycin, and ranitidine bismuth (Tritec). • Lansoprazole (Prevacid), omeprazole (Prilosec), and esomeprazole (Nexium) may be prescribed. • If prednisone is used for a long period of time, monitor for changes in glucose levels.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

• Replace protein; maintain adequate nitrogen balance. • Reduce edema. • Spare protein for tissue synthesis and repair.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Protein Intake Assessment Data: Diagnosis of GHG with giant gastric folds, dyspepsia, hypoalbuminemia (serum levels 2.0). Nutrition Diagnoses (PES): Inadequate protein intake (NI-52.1) related to GI protein loss as evidenced by serum albumin 2.0 g/dL.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Eliminate aggravating foods specific to the patient. • Teach the patient about use of high biological value (HBV) proteins to replenish protein levels from GI losses. • During recovery, the use of probiotics such as yogurt with live and active cultures may be helpful.

Patient Education—Foodborne Illness

Interventions: Alter diet to increase protein intake orally, or tube feed if necessary. Educate patient and family about the role of protein in alleviating edema and correcting low albumin levels.

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

Monitoring and Evaluation: Improvements in serum albumin from diet or transfusion (if needed). Transthyretin levels showing improvement over several weeks. Resolution of edema and improved quality of life.

For More Information •

Giant hypertrophic gastritis http://www.cancer.gov/templates/db_alpha.aspx?CdrID589414

Medical terms on line http://www.medicaltermsonline.org/index.php?sectionpages&item Giant-hypertrophic-gastritis


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GIANT HYPERTROPHIC GASTRITIS AND MÉNÉTRIER’S DISEASE—CITED REFERENCES Coffey RJ, et al. Ménétrier disease and gastrointestinal stromal tumors: hyperproliferative disorders of the stomach. J Clin Invest. 117:70, 2007.

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Ishikawa T, et al. Helicobacter pylori isolated from a patient with Ménétrier’s disease increases hepatocyte growth factor mRNA expression in gastric fibroblasts: comparison with Helicobacter pylori isolated from other gastric diseases. Dig Dis Sci. 53:1785, 2008. Sanchez C, et al. Laparoscopic total gastrectomy for Ménétrier’s disease. J Laparoendosc Adv Surg Tech A. 17:32, 2007.

PEPTIC ULCER DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 2 Dark, altered blood in base of ulcer

Muscular wall of stomach

tend to have a higher risk for peptic ulcer disease (PUD). Bland diets neither heal ulcers nor cause a decrease in gastric acid secretion. Drug therapy is most effective in preventing ulcer recurrence and primarily consists of antibiotics and antacids. A vaccine to prevent H. pylori infection is being developed. In the meantime, vitamin B12 tends to be lower in patients who have peptic ulcers; anemia should be monitored. The decline in duodenal ulcer disease and the established relation of peptic ulcer to H. pylori have eliminated the need for elective ulcer surgery. Options for refractory and complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II).

ASSESSMENT, MONITORING, AND EVALUATION

Stomach

Sharp edge of ulcer

Adapted from: Thomas H. McConnell, The Nature Of Disease Pathology for the Health Professions, Philadelphia: Lippincott Williams & Wilkins, 2007.

DEFINITIONS AND BACKGROUND A peptic ulcer suggests an imbalance between digestive fluids in the stomach and duodenum, with erodion by gastric acid and pepsin and exposed nerves. Most ulcers are duodenal, within the first 25–30 cm. One of 10 Americans suffers from peptic ulcer disease. H. pylori bacteria play a role in the etiology of 75% or more of peptic ulcers. Helicobacter pylori can be transmitted from person to person through close contact, exposure to vomit, or fecal–oral contamination. It can also be found in well water. Because the bacterium is one of the most genetically diverse bacterial species, more than half of the world population in both developed and developing countries are infected (Dube et al, 2009). It has been implicated in stomach cancer. Hand washing is an important preventive measure. In addition, sulforaphane (SF) from broccoli is a powerful bactericidal agent against H. pylori (Yanaka et al, 2009) and intake of soy products may help reduce the effects of inflammation-related IL-10 genetic polymorphisms (Ko et al, 2009). Individuals who have cirrhosis, chronic obstructive pulmonary disease, renal failure, and organ transplantation

CLINICAL INDICATORS Genetic Markers: H. pylori infection tends to run in families. This pathogen has been shown to follow the routes of human migration; the global H. pylori population has been divided into six ancestral populations, three from Africa, two from Asia, and one from Europe (Tay et al, 2009). In addition, the interleukin 1B gene has been identified as a factor, especially inflammation-related IL-10 genetic polymorphisms. GI bleeding or black, tarry Height stools Weight Nausea, BMI vomiting Diet history Frequent bloatWeight and ing appetite Chronic changes idiopathic Sharp and sudurticaria or den abdomiatopic nal pain dermatitis Burning or gnawStool test for ing pain (betH. pylori ter with meals Endoscopy but returns) Clinical/History

Lab Work Red blood cell (RBC) count Anti-H. pylori immunoglobulin G antibody titer C-Urea breath test for H. pylori Chol, Trig BUN, Creat Alb, transthyretin


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Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Blood guaiac Amylase (increased in

perforated ulcers) Serum gastrin (increased) Alk phos (increased) H&H Serum Fe, ferritin

Serum folate PT or INR Transferrin Ca, Mg Serum B12 TIBC Na, K, Cl Ca, Mg

INTERVENTION OBJECTIVES • Eradicate any H. pylori infection where present. Take medications as directed. Rest during healing stages. • Reduce pain. Avoid distention from large meals. • Dilute stomach contents and provide buffering action. • Correct anemia, if present. Vitamin B12 deficiency may be corrected after effective H. pylori treatment. • Monitor and prevent steatorrhea, bone disease, dumping syndrome, and complications such as perforation and obstruction.

FOOD AND NUTRITION • Use small feedings, frequently if preferred. Include highprotein foods and vitamin C to speed healing. • Avoid personal intolerances. Citrus and acidic juices may cause pain during exacerbations. If a particular food bothers an individual, it should be avoided. • Use broccoli and cruciferous vegetables often to enhance chemoprotection of the gastric mucosa against H. pyloriinduced oxidative stress (Yanaka et al, 2009). • Encourage soybean intake (Ko et al, 2009). • Limit gastric stimulants if not tolerated, such as caffeine, alcohol, peppermint, black pepper, garlic, cloves, and chili powder. This is a “liberal bland” diet. See Table 7-7 regarding caffeine in beverages and medications.

TABLE 7-7 Typical Caffeine Content of Beverages and Medications Beverages/Medications

Measure

Caffeine (mg)

Coffee, brewed

5 oz

65–120 (average, 85)

Coffee, instant

5 oz

60–85 (average, 75)

Coffee, Starbucks Frappucino

8 oz

83

Espresso coffee

1 oz

30–50 (average, 40)

Decaffeinated coffee

5 oz

2–4

Black tea, brewed (most U.S. brands)

5 oz

20–50

Black tea, brewed (imported)

5 oz

25–60

Tea, instant

6 oz

28–30

Mountain Dew

12 oz

54

Cola drinks

12 oz

36–47

Coffee ice cream

4 oz

28

Baker’s chocolate

1 oz

26

Dark chocolate

1 oz

5–35 (average, 20)

Milk chocolate

1 oz

1–15 (average, 6)

Cocoa beverage

8 oz

3–32 (average, 6)

Chocolate milk

8 oz

2–7 (average, 5)

Analgesic

1 tablet

30–66

Cold preparation

1 tablet

30

Chocolate syrup

1 oz

4

7-Up or Sprite

12 oz

0

Ovaltine

8 oz

0

Data from Leonard T, et al. The effects of caffeine on various body systems: a review. J Am Diet Assoc. 87:1048, 1987.

• Use fewer saturated fats and more polyunsaturated fats if increased lipid levels are found. AA metabolites may play a role in peptic ulcer disease. • Monitor water supply as a potential source of H. pylori.

Common Drugs Used and Potential Side Effects (see Table 7-8)

SAMPLE NUTRITION CARE PROCESS STEPS Undesirable Food Choices Assessment: Food and symptoms diary. Positive stool guaic test. Altered GI lab results. No H. pylori present. Nutrition Diagnosis (PES): Undesirable food choices related to chronic alcohol intake (beer and wine, 10 drinks/wk) as evidenced by nausea, sharp stomach pains, abdominal discomfort, black tarry stools and altered GI labs. Intervention: Teach about role of alcohol in GI mucosal damage. Counsel about alternative lifestyle changes that will help alleviate GI pain. Encourage intake of broccoli for its chemoprotective effects. Monitoring and Evaluation: Report of decreased alcohol consumption and less GI discomfort and pain. Resolution of peptic ulcer symptoms; improved lab results. No further tarry stools.

• Most patients with PUD should avoid NSAIDs. Analgesics and corticosteroids, when taken over a long time, may cause GI bleeding and ulceration and should be taken with food. High doses of Advil or Motrin (ibuprofen), even for a few days, can significantly increase the risk of GI bleeding. • For eradication of H. pylori, 2 weeks of treatment with an acid-suppressing drug (once daily), Pepto-Bismol (four times daily), and antibiotics (three to four times daily) are prescribed. A 1- to 2-week course of H. pylori eradication therapy is an effective treatment (Ford et al, 2006); triple therapy often must be used more than once. Quadruple therapy is also being tested (Feng et al, 2005). Some FDA-approved combinations include the antibiotics omeprazole, clarithromycin, and ranitidine bismuth (Tritec). Other antibiotics include amoxicillin, metronidazole, and tetracycline. Suggest use of probiotics, such as yogurt with live and active cultures.


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TABLE 7-8

409

Medications Used in Peptic Ulcer Disease

Medication Type

Description

Specific Drugs

Antacids

Aluminum-containing and magnesium-containing antacids can be helpful in relieving symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe. Aluminum ions inhibit smooth muscle contraction, thus inhibiting gastric emptying. Use aluminum-containing antacids cautiously with upper GI hemorrhage. Magnesium and aluminum antacid mixtures are used to avoid bowel function changes.

Gaviscon contains magnesium as well as aluminum and may decrease absorption of thiamine, phosphate, and vitamin A.

These drugs inhibit the action of histamine on the parietal cell, which inhibits acid secretion. The drugs in this class are all equally effective and are available over the counter in half prescription strength for heartburn treatment. Histamine H2 blockers should be taken with food. Since acid secretion and ulcer pain are most prevalent at night, taking Zantac or Tagamet before bed may be helpful. These drugs can elevate AST/ALT and creatinine, cause confusion in elderly individuals, and cause diarrhea, constipation, or urticaria.

Cimetidine (Tagamet) inhibits histamine at H2 receptors of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

H2-receptor antagonists

Proton pump inhibitors (PPIs)

PPIs bind to the proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. PPIs relieve pain and heal peptic ulcers more rapidly than H2 antagonists do. Drugs in this class are equally effective. All PPIs decrease serum concentrations of drugs that require gastric acidity for absorption, such as ketoconazole or itraconazole. PPIs are used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 weeks to treat all grades of erosive esophagitis.

Gelusil contains magnesium, aluminum, and simethicone; it may have side effects similar to those of Gaviscon. Mylanta and Amphogel (aluminum hydroxide) may cause nausea, vomiting, and lowered vitamin A, calcium, and phosphate absorption. Take between meals, followed by water. Milk of magnesia (magnesium hydroxide) is a laxative–antacid and can deplete phosphorus and calcium over time. Magaldrate (Riopan) decreases serum vitamin A but can be used on a low-sodium diet.

Famotidine (Pepcid) competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations. Nizatidine (Axid) competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations. Ranitidine (Zantac) competitively inhibits histamine at the H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations. Ranitidine can cause nausea, constipation, and vitamin B12 malabsorption; may alter serum levels of serum iron. Lansoprazole (Prevacid) decreases gastric acid secretion by   inhibiting the parietal cell H /K ATP pump. Omeprazole (Prilosec) decreases gastric acid secretion by   inhibiting the parietal cell H /K ATP pump. Omeprazole is now available over the counter. Esomeprazole (Nexium) is the S-isomer of omeprazole. It decreases gastric acid secretion by inhibiting the parietal   cell H /K ATP pump. May increase absorption of digoxin; may decrease absorption of iron. Rabeprazole (Aciphex, Alfence, Pariet) decreases gastric acid   secretion by inhibiting the parietal cell H /K ATP pump. It is used for short-term (4–8 weeks) treatment and symptomatic relief of gastritis. Pantoprazole (Protonix) decreases gastric acid secretion by   inhibiting the parietal cell H /K ATP pump. It is used for short-term (4–8 weeks) treatment and symptomatic relief of gastritis.

Gastrointestinal agents

These agents are effective in the treatment of peptic ulcers and in preventing relapse. Their mechanism of action is not clear. Multiple doses are required, and they are not as effective as the other options.

Sucralfate (Carafate) binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Used for short-term management of ulcers. Sucralfate may cause constipation as one side effect.

Stomach acid protector

Bismuth subsalicylate

Bismuth is a component of Pepto-Bismol and is used to protect the stomach lining from acid; it kills Helicobacter pylori.

Adapted from: Shayne P. Gastritis and peptic ulcer disease, http://www.emedicine.com/emerg/topic820.htm, accessed February 28, 2005.


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Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Ginger may be used as an antinauseant. Do not use large doses with warfarin, aspirin, or other antiplatelet drugs, antihypertensive drugs, and hypoglycemic drugs. Additive effects can cause unpredictable changes in BP and decreases in blood glucose levels and may decrease platelet aggregation and thus increase bleeding. Ginger ale is commonly used with few side effects. • Licorice root may be recommended for gastric and duodenal ulcers. Do not take with digoxin, because it may cause potassium loss and digoxin toxicity. Licorice root may potentiate the effects of steroids, especially hydrocortisone, progesterone, and estrogens. Also avoid taking with thiazide diuretics and antihypertensive medications because of increased sodium and water retention, along with potential hypokalemia; spironolactone is especially antagonized by licorice root. • Banana, garlic, cabbage, and yellow root have no clinical trials proving efficacy. Broccoli and soy products may be beneficial.

• As a preventive measure, recommend endoscopy early in patients older than 45–50 years who have dysphagia, recurrent vomiting, weight loss, or bleeding.

Patient Education—Foodborne Illness • Careful food handling will be important. Hand washing is important to reduce the spread of H. pylori. Always wash hands after using the bathroom and before eating. • If home TF is needed, teach appropriate sanitation and food handling procedures.

For More Information •

Centers for Disease Control and Prevention—Peptic Ulcer http://www.cdc.gov/ulcer/md.htm

Foundation for Digestive Health http://www.fdhn.org/html/education/ulcer/facts.html

Helicobacter Foundation http://www.helico.com/

Medline—Peptic Ulcer http://www.nlm.nih.gov/medlineplus/pepticulcer.html

Web MD—Peptic Ulcer http://www.webmd.com/digestive-disorders/digestive-diseasespeptic-ulcer-disease

PEPTIC ULCER DISEASE—CITED REFERENCES NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • As needed by the individual, offer guidance about dietary alterations that may be useful. • Discuss the need to complete treatments for eradication of H. pylori bacteria, where present. One treatment is usually not sufficient. Suggest increasing intake of broccoli and soy products. • Reduce intake of alcoholic beverages; stop smoking; and monitor any family history of ulcer disease to address it as quickly as possible.

Dube C, et al. Helicobacter pylori in water sources: a global environmental health concern. Rev Environ Health. 24:1, 2009. Feng LY, et al. Effects of killing Helicobacter pylori quadruple therapy on peptic ulcer: a randomized double-blind clinical trial. World J Gastroenterol. 11:1083, 2005. Ford AC, et al. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2:CD003840, 2006. Ko KP, et al. Soybean product intake modifies the association between interleukin-10 genetic polymorphisms and gastric cancer risk. J Nutr. 139: 1008, 2009. Tay CY, et al. Population structure of Helicobacter pylori among ethnic groups in Malaysia: recent acquisition of the bacterium by the Malay population. BMC Microbiol. 9:126, 2009. Yanaka A, et al. Dietary sulforaphane-rich broccoli sprouts reduce colonization and attenuate gastritis in Helicobacter pylori-infected mice and humans. Cancer Prev Res. 2:353, 2009.

VOMITING, PERNICIOUS NUTRITIONAL ACUITY RANKING: LEVEL 3 (LONGER THAN 7 DAYS) DEFINITIONS AND BACKGROUND Pernicious, uncontrolled vomiting may occur in any of several disorders, including concussion or brain trauma, meningitis or encephalitis, intestinal blockage, migraine headaches, brain tumor or other forms of cancer, foodborne illness, gastroparesis, and pregnancy (hyperemesis gravidarum, see Pregnancy in Section 1). Hyperemesis gravidarum involves pregnancy-induced hormonal changes, often associated with concurrent H. pylori infection. The presence of weight loss, GI bleeding, persistent fever,

chronic severe diarrhea, and significant vomiting is associated with a higher prevalence of organic disease in children and should be carefully assessed (American Academy of Pediatrics, 2005). The biggest immediate risk with pernicious vomiting is dehydration, where losses of water, potassium, and sodium can affect the brain, kidneys, and heart. Watch for signs such as dry mouth membranes, dry lips, sunken eyes, rapid but weak pulse, rapid breathing, cold hands and feet, confusion, and difficulty with arousal. Nutritional deficits are possible when the vomiting is prolonged.


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ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Pernicious vomiting in itself is a symptom of an underlying condition and is not genetic. Clinical/History Height Weight Weight changes BMI Diet history Temperature (fever?) Dehydration?

N balance Orthostatic hypotension? Gluc H&H GI bleeding? Serum Fe, Lab Work ferritin Serum folate or    Na , K , Cl B12 Ca, Mg Gastric emptying Alb, transthyretin tests BUN, Creat

411

FOOD AND NUTRITION • For patients with an acute condition, NPO for 24 hours with intravenous (IV) glucose is common. Oral rehydration solution may be needed. (See Diarrhea entry.) • When tolerated, gastrostomy TF or jejunostomy may be warranted. An isotonic formula is desirable to reduce imbalances between solute and solvent. CPN may also be a consideration if the condition is prolonged. • As the patient progresses to an oral diet, clear liquids such as cranberry juice or boullion may be helpful. Gradually add toast, crackers, jelly, and simple carbohydrates in small, frequent meals. • Give fluids between meals (a “dry diet”). Avoid acidic fruit and vegetable juices if not tolerated. • Consider avoiding foods that delay gastric emptying (high-fat, hypertonic, or highly fibrous foods). • Gradually have the patient resume a normal diet. Decrease fatty foods if not tolerated.

Common Drugs Used and Potential Side Effects INTERVENTION OBJECTIVES • Correct electrolyte and fluid imbalances and unintentional weight loss • Modify oral intake until vomiting resolves. • Distinguish symptoms that could be related to bulimia nervosa. • If there is hyperglycemia or diabetes, return to normal blood glucose levels as quickly as possible; insulin may be needed. • For cancer patients, depending on the type of treatment (either curative or palliative) and on the patient’s nutritional status, provide patient-tailored nutritional intervention such as oral supplementation, enteral or total PN (Marin Caro et al, 2007).

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function—Vomiting Assessment: Food records, I & O reports, chemotherapy schedule and frequency. Uncontrollable vomiting three to four times daily for past week. Signs of dehydration. Nutrition Diagnosis (PES): Inadequate food and beverage intake related to intolerance to oral diet and chemotherapy treatment as evidenced by dehydration and vomiting after meals, with weight loss of 5 lb over past week. Intervention: Coordinate care: Alter meal pattern according to chemotherapy medications and timing, review timing of fluid intake related to meals. Offer sips of fluid every 1–2 hours while awake. Monitoring and Evaluation: Food records, I & O reports, weight recovery. Resolution of vomiting episodes.

• Anti-emetic agents may be indicated for some conditions. Meclizine or cyclizine may be prescribed; they are antihistamines and powerful antinausea agents. • Selective serotonin 5-hydroxytryptamine-3 (5-HT3) receptor antagonists have proven to be safe and effective for postoperative nausea and vomiting; these include dolasetron, granisetron, ondansetron, and tropisetron, which bind to 5-HT3 receptors, blocking serotonin binding at vagal afferents in the gut and in the regions of the CNS involved in emesis (Gan, 2005). • Insulin or oral agents may be needed if diabetes is also present. • Peristaltic agents may be used in cases of gastroparesis. • Chronic use of cannabinoids can lead to hyperemesis; this includes oral use of marijuana for cancer, multiple sclerosis, or social purposes.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Ginger is often used as an antinauseant. Do not use large doses with warfarin, aspirin, other antiplatelet drugs, antihypertensive drugs, and hypoglycemic drugs. Additive effects can cause unpredictable changes in BP, blood glucose levels, platelet aggregation, and bleeding. • Ginger ale has few side effects and may help.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain why fluids should be taken between meals. Identify adequate amounts of fluids to be consumed every day. Sips of 1–2 oz every few hours can be tolerated; this may include water, sports drinks, gelatin, and clear broth. • There are many suitable oral rehydration products available from a pharmacy; discuss appropriate products with


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the pharmacist. If needed, share the ingredient recipe if it is to be made at home. Do not force eating. Eat and drink slowly; stop when full. Make up lost calories at another time. Eat meals in a well-ventilated area free from odors. Do not lie down for 2 hours after eating. Do not overeat. Discuss the role of carbohydrates and fiber in maintaining blood glucose levels. Discuss reasons to seek immediate medical attention, including severe abdominal pain, severe headache, stiff neck, fever over 101F, vomiting of blood, rapid breathing or pulse. In palliative care, nutritional support aims at improving patient’s quality of life by controlling symptoms such as nausea, vomiting, and pain related to food intake (Marin Caro et al, 2007).

Patient Education—Food Safety • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the diet of the individual.

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Medicine Net http://www.medicinenet.com/nausea_and_vomiting/article.htm

Nausea and Vomiting Algorithm http://www.uwgi.org/guidelines/ch_01/ch01txt.htm

VOMITING, PERNICIOUS—CITED REFERENCES American Academy of Pediatrics. Subcommittee on Chronic Abdominal Pain; North American Society for Pediatric Gastroenterology Hepatology, and Nutrition. Chronic abdominal pain in children. Pediatrics. 115:370, 2005. Gan TJ. Selective serotonin 5-HT(3) receptor antagonists for postoperative nausea and vomiting: are they all the same? CNS Drugs. 19:225, 2005. Marin Caro MM, et al. Nutritional intervention and quality of life in adult oncology patients. Clin Nutr. 26:289, 2007.

LOWER GI: INTESTINAL DISORDERS

CARCINOID SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Carcinoid tumors are part of a group of GI and pancreatic endocrine tumors that secrete hormones, 5-HT, tachykinins, and other mediators (Druce et al, 2009). The rare neuroendocrine growth develops in the wall of the intestine and is usually discovered in x-rays or during surgery performed for other reasons. GI carcinoid tumors are difficult to diagnose (Gore et al, 2005). Carcinoid cancer patients often have elevated levels of serotonin or its precursor 5-hydroxytryptophan (Shah et al, 2005). Octreotide scanning has a sensitivity of primary tumor detection of 90% (Northrup and Lee, 2007). GI carcinoids comprise 90% of all carcinoid tumors and all carcinoids have malignant potential (Northrup and Lee, 2007). Sometimes, the growth occurs in the appendix area. The growths can be large enough to cause intestinal obstruction. Some growths metastasize to the liver, creating hormone-producing tumors with flushing of the head and neck (usually triggered by alcohol or exercise). Flushing symptoms can last for several hours from the release of vasoactive serotonin, histamine, and prostaglandins. Other symptoms include swollen or watery eyes, explosive diarrhea, abdominal cramps, wheezing, breathlessness, and symptoms similar to heart failure. Cardiac lesions are also seen; up to one third of patients develop cardiac valvulopathy. Patients may benefit from a valve replacement. If liver involvement occurs, liver resection or transplantation may be needed. Diversion of tryptophan to 5-HT synthesis occurs, resulting in less tryptophan for protein and nicotinamide synthesis. Pellagra and psychiatric symptoms result from depletion of tryptophan, which is consumed by the tumor for serotonin

synthesis (van der Horst-Schrivers et al, 2004). Psychiatric symptoms should be evaluated carefully. The malignant carcinoid syndrome is caused by circulating neuroendocrine mediators produced by the tumor and occurs in less than 10% of patients (Bell et al, 2005). Surgery is combined with continuous biotherapy with long-acting somatostatin analogs and interferon, which may alleviate symptoms and slow the disease progression (Akerstrom et al, 2005). Survival ranges from 3 to 20 years after diagnosis.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Carcinoid tumor fibrosis is a CTGF/ TGFbeta1-mediated stellate cell-driven fibrotic response (Kidd et al, 2007). Clinical/History Height Weight BMI Diet history Diarrhea, flushing, wheezing

(carcinoid syndrome) Breathlessness Number of stools, consistency Biopsy Endoscopy

Octreotide scanning X-rays of GI tract Skin changes (scleroderma, pellagra)? Psychiatric symptoms?


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Magnetic resonance imaging (MRI) Lab Work 5-HIAA test (urine S-HIAA)

Serum histamine Serum serotonin (elevated) Alb, transthyretin Transferrin

TLC H&H Serum Fe, ferritin Na, K Ca, Mg

413

Common Drugs Used and Potential Side Effects • Subcutaneous injections of the somatostatin analog octreotide are used. This is expensive, and treatment may be for many years. Newer somatostatin analogs (such as lanreotide) are being tested. Vasoconstricting interleukin or cytotoxic drugs may control side effects. • If kaolin (Kaopectate) and other medications are used to control diarrhea, constipation is a possible side effect. • Bronchodilators may be used to control wheezing. Evaluate for potential side effects.

INTERVENTION OBJECTIVES • Ease symptoms of secretory diarrhea and reduce any pain. • Slow progression of the disease, which is not cured by surgery. • Control side effects of medications. • Replenish electrolyte and fluid losses. • Correct niacin deficiency. Biochemical niacin deficiency is prevalent among newly diagnosed carcinoid syndrome patients (Shah et al, 2005).

FOOD AND NUTRITION • Decrease fiber intake during acute stages of diarrhea. Add pectin and ensure adequate fluid intake during those periods. • Avoid alcoholic beverages. Limit caffeine intake to a controlled amount. • During testing, omit foods that contain 5-HIAA: avocados, pineapple, bananas, kiwi fruit, plums, eggplant, walnuts, hickory nuts, and pecans. • Omega-3 fatty acids may used for their role in reduction of inflammation; include fish such as salmon, sardines, tuna, and herring often. • Since tryptophan is not adequately converted to niacin, a daily supplement with DRI levels may be suggested. Avoid excesses.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Monitor side effects if large doses of niacin are taken.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss measures specifically designed for the patient’s status and tolerance levels. • Suggest ways to make meals more appetizing if appetite is poor. • Describe techniques for management of diarrhea, abdominal pain, or cramping by reducing fiber and fat intake during those times of flare. • Probiotics such as acidophilus milk and yogurt with live and active cultures may be useful in the diet.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Carcinoid Syndrome http://www.emedicine.com/med/topic2649.htm

SAMPLE NUTRITION CARE PROCESS STEPS Altered GI Function Assessment Data: Explosive diarrhea, flushing, fear of eating. Nutrition Diagnoses (PES): Altered GI function related to release of vasoactive substances as evidenced by explosive diarrhea and altered labs with diagnosis of carcinoid syndrome. Interventions: Education about foods or alcohol that may aggravate symptoms. Counseling about postsurgical wound healing, if required. Discuss use of probiotics, adequate fluid, omega-3 fatty acid sources. Avoid alcohol if symptoms are aggravated by intake. Monitoring and Evaluation: Fewer complaints of diarrhea, flushing, GI discomfort, and fear of eating.

CARCINOID SYNDROME—CITED REFERENCES Akerstrom G, et al. Management of midgut carcinoids. J Surg Oncol. 89:161, 2005. Bell HK, et al. Cutaneous manifestations of the malignant carcinoid syndrome. Br J Dermatol. 152:71, 2005. Druce M, et al. Fibrosis and carcinoid syndrome: from causation to future therapy. Nat Rev Endocrinol. 5:276, 2009. Gore RM, et al. GI carcinoid tumours: appearance of the primary and detecting metastases. Best Pract Res Clin Endocrinol Metab. 19:245, 2005. Kidd M, et al. CTGF, intestinal stellate cells and carcinoid fibrogenesis. World J Gastroenterol. 13:5208, 2007. Northrup JA, Lee JH. Large bowel carcinoid tumors. Curr Opin Gastroenterol. 23:74, 2007. Shah GM, et al. Biochemical assessment of niacin deficiency among carcinoid cancer patients. Am J Gastroenterol. 100:2307, 2005. Van Der Horst-Schrivers AN, et al. Complications of midgut carcinoid tumors and carcinoid syndrome. Neuroendocrinology. 80:28S, 2004.


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CELIAC DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND

Adapted from: Rubin E MD and Farber JL MD. Pathology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999.

Celiac disease (CD) is a common, lifelong, genetically based autoimmune disorder that causes inflammation of the proximal small intestine (See and Murray, 2006). CD is characterized by inappropriate T cellâ&#x20AC;&#x201C;mediated immune response to ingested gluten from wheat, rye, and barley that leads to inflammation, villous atrophy, and crypt hyperplasia in the small intestine. Intestinal villi decrease in number, with less absorptive surface and fewer enzymes. Crypts are markedly elongated, causing mucosal malabsorption. Other names for this disorder include celiac sprue, gluten enteropathy, or nontropical sprue. A major consensus panel determined that 1% of Caucasians (upwards of 3 million people) may have CD (See and Murray, 2006). While screening suggests that one in 133 people have it, the frequency may be closer to one in 100; undiagnosed CD seems to have increased dramatically in the United States during the past 50 years (Rubio-Tapia et al, 2009). Diagnosis can occur at any age (infancy through old age) and often occurs after stress, pregnancy, or viral infections. Infants may present with impaired growth, diarrhea, pica, abdominal distention, pallor, edema, or vomiting. Children may have frequent, strong-smelling stools that are pale and foamy, diarrhea, irritability, a distended abdomen, easy fatigue, pallor, weight loss, vomiting, and anemia. Increased intestinal permeability plays a pathogenic role in various autoimmune diseases including CD and type 1 diabetes (T1D) (Visser et al, 2009). Gliadin may also be involved in the pathogenesis of T1D (Visser et al, 2009). All persons with GI symptoms should be tested for CD, as should individuals with type 1 diabetes (T1D), unexplained iron deficiency anemia, elevated levels of transaminases, thyroid disorders, short stature, delayed puberty, fetal loss, and in relatives of patients who have CD (Thompson, 2005). Screening studies have revealed that CD may be asymptomatic in adults (Niewinski, 2008), or they may have episodic or nocturnal diarrhea, flatulence, intestinal bloating that mimics IBS, steatorrhea, weight loss, recurrent stomatitis, anemias or peripheral neuropathy. Tissue transglutaminase is the main antigen for the antiendomysial antibodies used to diagnose CD. Deamidated gliadin antibodies (DGP) have shown promising results as serological markers for CD (Setty et al, 2008). False-negative test results can occur in children under age 2 years or in patients who have followed a gluten-free (GF) diet for a month or longer. The diagnostic criteria for CD need re-evaluation; endomysial antibody positivity without atrophy belongs to the spectrum of genetic gluten intolerance, and warrants dietary treatment (Kurppa J, et al. 2010). Early diagnosis and treatment, together with regular followup visits with a dietitian, are necessary to ensure nutritional adequacy and to prevent malnutrition while adhering to the GF diet for life (Niewinski, 2008). Longer duration of exposure to gluten can increase the risk of other autoimmune diseases, including non-Hodgkinâ&#x20AC;&#x2122;s or intestinal lymphoma,


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squamous cell cancer of the esophagus, type 1 diabetes, autoimmune thyroid disease, Addison’s disease, lupus, primary biliary cirrhosis, osteoporosis, psoriasis, Sjogren’s syndrome, and rheumatoid arthritis (National Institutes of Health, 2004). Dermatitis herpetiformis (DH) is the skin manifestation, with intensely pruritic lesions that occur over the surface of the elbows, knees, legs, buttocks, trunk, neck, or scalp. Abnormal biopsy is evident, but GI symptoms are not always present. There may be immunoglobulin (IgA) deposits around the lesions, and large intake of iodine may trigger flares of DH. When wheat, rye, and barley grains are consumed, they damage the mucosa of the small intestine, eventually leading to nutrient malabsorption. Moderate amounts of pure oats can be consumed. However, since much of the commercially available oat flour may be contaminated with wheat gluten, caution is advised for new patients. Response to GF diets in children with autism may be related to amelioration of nutritional deficiency resulting from undiagnosed gluten sensitivity. Therefore, it is recommended that all children with neurodevelopmental problems be assessed for CD (Genius and Bouchard, 2009). Children and adolescents with symptoms of or an increased risk for CD should have the blood test for antibody to tissue transglutaminase (TTG). Those with an elevated TTG should be referred to a pediatric gastroenterologist for an intestinal biopsy. If tests prove positive, a GF diet is needed. Then, a gastroenterologist should follow all patients with CD. Because oxidative stress plays an important role in the inflammatory process of CD, increased use of lycopene, quercertin, and tyrosol can be recommended (DeStefano et al, 2007). New forms of treatment propose the use of gluten-degrading enzymes to be ingested with meals, the development of GF grains by genetic modification, the use of substrates regulating intestinal permeability to prevent gluten entry across the epithelium, and different forms of immunotherapy (Setty et al, 2008). Since the defect is permanent, the GF diet is curative and must be a permanent change. Surface cells of the mucosa are replaced within 5 days; swelling is reduced within 14 days; and villi improve within 6 months or up to 5 years. Consultation with a dietetics professional knowledgeable in CD is essential. An individualized, team approach is best because symptoms change over time.

ASSESSMENT, MONITORING, AND EVALUATION

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Single-nucleotide polymorphisms (SNPs) in the chromosome 4q27 region containing IL2 and IL21 are associated with CD; this is similar to other autoimmune diseases such as rheumatoid arthritis, type 1 diabetes, Graves’ disease, psoriatic arthritis, and ulcerative colitis (UC, Glas et al, 2009). Multiple small bowel Height biopsies Weight showing flat BMI villi Diet history Abdominal comFailure to thrive puted tomogor weight loss raphy (CT) Aphthous stomor MRI scan atitis Capsule Fatigue, endoscopy lassitude, Small bowel depression biopsy Recurrent abdominal Lab Work pain, bloating Strong-smelling Anti-TTG antibodies stools that are (tTG)—IgA pale and and IgG foamy (95–100% Distended sensitive and abdomen specific) Irritability, Antipallor endomysium Steatorrhea, antibodieschronic diarIgA rhea (EMA)–100% DH specificity, Enamel defects 90% of permanent sensitivity teeth HLA-DQ2 and Headaches? HLA-DQ8 Osteopenia, haplotype bone pain? H&H Infertility, frequent mis- Serum Fe, ferritin (anemia is carriages? common) Short stature? Clinical/History

Macrocytic anemia (low vitamin B12 or folate?) Serum homocysteine (tHcy) Serum carotene for vitamin A Serum vitamins D, E, and K Serum copper (decreased) Serum phosphorus (decreased) Serum zinc (decreased) Ca (often low) Na, K Mg Alb, transthyretin CRP Transferrin, TIBC Lactic acid dehydrogenase (increased) Xylose absorption DEXA scan Fecal chymotrypsin level Fecal fat study Liver function tests (mildly abnormal)

INTERVENTION OBJECTIVES

CLINICAL INDICATORS Genetic Markers: Like an IBD, gliadin peptides are presented on the Human Leukocyte Antigen DQ2 or DQ-8 molecules of antigen-presenting cells to T helper cells, provoking a T helper 1 response that leads to damage by pro-inflammatory cytokines and interleukins (Festen et al, 2009; Visser et al, 2009). CD is more common among people with other genetic disorders including Down syndrome.

There are six elements required for the management of CD (Thompson, 2005): 1. Consult a skilled dietetics professional. Medical nutrition therapy (MNT) to promote provided by a registered dietitian is strongly recommended improved self-management (American Dietetic Association, 2009). 2. Educate about the disease. 3. Adhere to a GF diet. Remove the offending protein (gliadin fraction) from the diet; glutenin is harmless. Improvement is noted within 4–5 days.


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SAMPLE NUTRITION CARE PROCESS STEPS

TABLE 7-9 Grains and Starches to Use Freely in Celiac Disease

Altered Nutrient Utilization—Celiac Disease Assessment Data: Weight loss over the past year. I & O records; stool patterns and frequency; abdominal distention and bloating; DH. GI biopsies reveal CD; positive tTG test. Nutrition Diagnosis (PES): Altered nutrient utilization related to flattened intestinal villi from CD as evidenced by positive biopsies and tTG test, presence of DH, frequent bouts of abdominal distention, bloating, diarrhea and weight loss.

Amaranth

Nut flours

Arrowroot

Quinoa

Beans (black, garbanzo, kidney, northern, pinto)

Poha flakes

Black-eyed peas, lentils, split peas

Potato

Buckwheat

Potato starch, potato flour

Intervention: Education about the sources of gluten from diet and food and nonfood products. Provision of recipes for managing the GF diet. Supplier sources of GF foods and flours or grain products. Counseling about fluid sources and ways to incorporate fluids into meals and nourishments. Meal planning tips for the family.

Cassava

Rice

Monitoring and Evaluation: Improved I & O records and weight gain. Normalized stool patterns and frequency. Fewer complaints of GI distress, bloating and diarrhea associated with meals. No signs of protein-energy malnutrition.

4. Identify and treat nutritional deficiencies: • Deficiencies of iron, folate, calcium, and vitamin D may be found. • Replace nutrients lost from diarrhea and steatorrhea. • Reverse bone demineralization, hypoalbuminemia, and hypoprothrombinemia where present. • Whole-body protein breakdown is common in CD, contributing to a high level of protein–calorie malnutrition. • Glutamine is an important fuel for the health of intestinal epithelial cells. Replenish as needed. 5. Provide access to an advocacy group. A local celiac support chapter is most helpful. 6. Provide continuous long-term follow-up care by a multidisciplinary team.

Corn, corn bran, hasa marina

Sorghum

Gluten-free bread

Soy

Hominy, grits

Tapioca

Indian rice grass

Tef

Montina

Wild rice

• •

FOOD AND NUTRITION • A GF diet excludes wheat, rye, and barley. Avoid products such as breading, stuffing, croutons, graham, bulgur, matzo, broth, breading or coating mixes, communion wafers, pastas, cracked wheat, semolina, farina, malt, malt flavoring, brown rice syrup, commercial soups, imitation bacon, imitation seafood, marinades, processed meats, roux, sauces, seasonings, self-basting poultry, soups and soup bases, thickeners, vegetarian meat substitutes, and commercial potato and rice mixes. Soy sauce, white or nonmalt vinegars, and wheat starch must be pure; read labels. • Plan a diet that includes acceptable grains and starches; see Table 7-9. • A Greek-Mediterranean dietary pattern with olive oil, nuts, fruits, and vegetable intake can be recommended. Lycopene, quercetin, and tyrosol may control the proinflammatory genes involved in CD (DeStefano et al, 2007). Tyrosol is found in wine and extra virgin olive oil;

• •

lycopene in tomato products, watermelon, pink grapefruit; quercetin in apples, citrus fruit, tea, capers, buckwheat, red grapes, broccoli, and red onions. Buckwheat contains rutin (quercetin-3-O-rutinoside) which produces a catabolite (3,4-dihydroxyphenylacetic acid) with significant reducing power, free-radical scavenging activity and enhanced antioxidant capacity of the colonic lumen (Jaganath et al, 2009). Because oats are sometimes contaminated with wheat during processing, avoid in initial stages of treatment. Include small-to-moderate amounts if tolerated after the first few months. Diet for adults should provide 1–2 g of protein/kg body weight from fresh meat, fresh fish, milk, cheese, and eggs. Examine processed items carefully since there is often gluten added. Diet should provide 35–40 kcal/kg body weight for adults. For infants with diarrhea, provide fluids, electrolytes, and a formula that is not high in fat content. Infants may tolerate banana powder; adults and children can eat starchy-type carbohydrates, bananas, leans meats, and fish. Rehydrate with oral rehydration solution or other fluids. Initially, the diet should include low amounts of fiber because of flattened mucosal villi; increase as tolerated. Fruits and vegetables are naturally low in gluten and should be included regularly. If TF is used, a glutamine-enriched product may be useful. Monitor ingredients carefully to avoid gluten. Lactose intolerance may be either temporary or permanent. Initially, dairy products (primarily milk and products made with milk) should be avoided. After 3– 6 months of treatment, dairy products may be gradually reintroduced. GF products are often low in B vitamins, calcium, vitamin D, iron, zinc, magnesium, and fiber. Few GF products are enriched or fortified, adding to the risk of nutrient deficiencies. Correction of vitamin and mineral deficiencies is important. Supplements to the diet should include water-miscible vitamins A, D, E, and K, iron, calcium,


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folic acid, vitamin B12, thiamine, and other B-complex vitamins. • Products containing MCTs are often used when fat malabsorption is present, especially in adults. • Foods that often are not allowed include commercial cream soups, creamed vegetables, ice cream (labels should be checked for thickening agents), cakes, cookies, and breads unless made with rice, corn, or potato flours. For toddlers, mixed infant dinners and junior dinners that contain flour thickeners, spaghetti, macaroni, and other pastas should not be used.

• •

Common Drugs Used and Potential Side Effects

• No drug therapy has been proven to suppress the disease. • Check all labels each time for gluten-containing ingredients. GF laxatives include psyllium seed laxatives (Metamucil, Naturacil), docusate sodium (Surfak), and bisacodyl (Dulcolax). Gliadins are often impurities in medications, including acetaminophen; check carefully. • Corticosteroids may be used with numerous side effects. Take with food. Monitor for negative nitrogen or calcium balances, and for weight gain.

• • •

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Avoid aloe, cascara, senna, and yellow dock because of enhancing effects when using bisacodyl. • A B-complex supplement may be warranted if serum tHcy levels are elevated (Hadithi et al, 2009; Hallert et al, 2009). A general multivitamin–mineral supplement may be beneficial. • With antibiotics, quercertin may interfere with fluroquinolones. Advise the physician if used in large amounts. • Studies are ongoing about the need for carnitine supplementation in CD.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Strict lifelong elimination of gluten and dietary adherence are essential (Chand and Mihas, 2006). If strictly followed, improvement will occur in most patients within 2 weeks. If results are not seen after 6–9 months of diet therapy, a new diagnosis should be sought. • Endomysial antibodies are specific in predicting villous atrophy; patients with endomysial antibodies benefit from a GFD regardless of the degree of enteropathy (Kurppa et al, 2010). • Intense expert dietary counseling is needed for all patients with CD because the diet is complex (American Dietetic Association, 2009; Niewinski, 2008). An effective plan requires extensive, repeated counseling and instruction of the patient by a skilled dietitian. • Instruct the patient or family to read food labels each time for cereal, starch, flour, thickening agents, emulsifiers,

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gluten, stabilizers, hydrolyzed vegetable proteins, semolina, durum, triticale, bulgur, farina, couscous, broth, caramel coloring and monosodium glutamate (MSG). The Food Allergen Labeling and Consumer Protection Act (FALCPA) requires food labels to clearly identify wheat and other common food allergens in the list of ingredients. A GF symbol is now widely used by food manufacturers. Contact the manufacturer if there are questionable ingredients. “Wheat free” is not the same as gluten free; products may contain rye or barley. Because of possible contamination with wheat, oats should be avoided in new patients. “Wheat starch” is acceptable because the gliadin/gluten has been removed. Toothpaste, mouthwash, lipstick or chapstick, glue on envelopes or teabags, boxed candy, chewing gum wrappers, utensils in buffet lines, toasters, bulk food bins, jars used for various purposes, and other related items should be checked carefully and avoided if gluten is present. A Greek–Mediterranean dietary pattern high in olive oil, nuts, fruits and vegetable may be recommended. For children at school, it may be necessary to educate the staff, nurses and teachers about the GF diet to enhance compliance. Quality of life improves for most individuals with CD who follow the GF diet for at least a year (American Dietetic Association, 2009).

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related GI discomfort. • If home TF is needed, teach appropriate sanitation and food handling procedures.

For More Information •

Celiac Disease and Gluten-Free Diet Support Group http://www.celiac.com/

Celiac Disease Foundation http://www.celiac.org

Celiac Sprue Association http://www.csaceliacs.org/

Children’s Digestive Health and Nutrition Foundation http://www.cdhnf.org/wmspage.cfm?parm140

Freeda Vitamins http://www.freedavitamins.com

Gluten-Free Diet by Shelley Case http://www.glutenfreediet.ca

Gluten Free Guide http://www.cdhnf.org/user-assets/documents/pdf/ GlutenFreeDietGuideWeb.pdf

Gluten-Free Pantry http://www.glutenfree.com/

Gluten Intolerance Group of North America http://www.gluten.net/

Guidelines for a Gluten-Free Lifestyle http://www.celiac.org/newsEvents.php

National Celiac-Sprue Society http://www.csaceliacs.org

NIDDK http://digestive.niddk.nih.gov/ddiseases/pubs/celiac/


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CELIAC DISEASE—CITED REFERENCES American Dietetic Association. Evidence analysis library: Celiac disease. Web site accessed November 8, 2009. at, http://www.adaevidencelibrary.com/ topic.cfm?cat3677&libraryEBG. Chand N, Mihas AA. Celiac disease: current concepts in diagnosis and treatment. J Clin Gastroenterol. 40:3, 2006. DeStefano D, et al. Lycopene, quercetin and tyrosol prevent macrophage activation induced by gliadin and IFN-gamma. Eur J Pharmacol. 566:192, 2007. Festen EA, et al. Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets. Endocr Metab Immune Disord Drug Targets. 9:199, 2009. Genius SJ, Bouchard TP. Celiac Disease Presenting as Autism [published online ahead of print 29 June 2009]. J Child Neurol. 25:114, 2009. Glas J, et al. Novel genetic risk markers for ulcerative colitis in the IL2/IL21 region are in epistasis with IL23R and suggest a common genetic background for ulcerative colitis and celiac disease. Am J Gastroenterol. 104:1737, 2009. Hadithi M, et al. Effect of B vitamin supplementation on plasma homocysteine levels in celiac disease. World J Gastroenterol. 15:955, 2009. Hallert C, et al. Clinical trial: B vitamins improve health in patients with coeliac disease living on a gluten-free diet. Aliment Pharmacol Ther. 29:811, 2009.

Jaganath IB, et al. In vitro catabolism of rutin by human faecal bacteria and the antioxidant capacity of its catabolites [published online ahead of print 30 July 2009]. Free Radic Biol Med. 47:1180, 2009. Kurppa J, et al. Celiac disease without villous atrophy in children: a prospective study. J Pediatr. 157:373, 2010. National Institutes of Health. National Institutes of Health Consensus Development Conference Statement: Celiac disease, 2004. Accessed July 22, 2009 at http://consensus.nih.gov/2004/2004CeliacDisease118html. htm. Niewinski MM. Advances in celiac disease and gluten-free diet. J Am Diet Assoc. 108:661, 2008. Rubio-Tapia A, et al. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. 137:88, 2009. See J, Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutr Clin Pract. 21:1, 2006. Setty M, et al. Celiac disease: risk assessment, diagnosis, and monitoring. Mol Diagn Ther. 12:289, 2008. Thompson T. National Institutes of Health consensus statement on celiac disease. J Am Diet Assoc. 105:194, 2005. Visser J, et al. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 1165:195, 2009.

CONSTIPATION NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND Constipation occurs when the fecal mass remains in the colon longer than the normal 24–72 hours after meal ingestion or when the patient strains to defecate. Stool type and frequency could be used to determine another problem, such as IBS. Constipation and fecal incontinence are common symptoms in patients with cerebral palsy, traumatic spinal cord injuries, spina bifida, multiple sclerosis, diabetic polyneuropathy, Parkinson’s disease, and stroke. Intestinal obstruction, tumors and diverticulosis may narrow the intestine, which can also lead to constipation. Atonic constipation (“lazy bowel”) occurs when musculature of the bowel no longer functions properly, sometimes from laxative overuse or poor bowel habits. Spastic constipation entails increased narrowing of the colon with small, ribbon-like stools caused by inactivity, immobility, or obstruction; increasing physical activity may be useful. TF constipation occurs with use of low-fiber products, medications, or other products. In infants and children, chronic constipation is a concern, with encopresis from poor bowel habits and poor fiber intake. There may be food allergies, such as to milk or wheat, which should also be addressed. Treatment modalities for constipation include prokinetic agents, enemas administered through the enema continence catheter, and biofeedback. For chronic problems, bowel retraining may be necessary. There is limited evidence that constipation can successfully be treated by increasing fluid intake unless there is dehydration (Muller-Lissner et al, 2005). Increasing physical activity may be helpful (Muller-Lissner et al, 2005). Some patients may be helped by a fiber-rich diet (American Dietetic Association, 2008). Water-soluble fibers (e.g., pectins, gums, mucilages, and some hemicelluloses) slow down intestinal transit while insoluble fibers from lignin, cellulose, and hemicellulose accelerate intestinal transit. Patients with more severe consti-

pation may get increased bloating or distention when increasing dietary fiber intake; proceed slowly when making a change in fiber intake. Fiber supplements may also help. Conservative therapies focus on a holistic approach in tandem with evolving drug therapies that target intestinal secretion and transit (Chatoor and Emmanuel, 2009). Chronic constipation decreases quality of life. A Constipation-Related Quality of Life measure is available but should be validated with different treatment methods used for chronic constipation (Wang et al, 2009). Surgical correction of rectocele and intussusception benefit those with anatomical symptoms; for those with predominantly functional features, surgery is best avoided (Chatoor and Emmanuel, 2009).

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS Genetic Markers: Chronic constipation may have a genetic basis; research is underway. Clinical/History Height Weight Recent weight changes BMI Diet history Defecation longer than every 3 days

Bowel habits Stool color and number Hard, lumpy stools I&O BP Headaches Abdominal distention, pain, spasms

Gas pain, flatulence Heartburn, indigestion Straining at stool Feeling of obstruction or incomplete evacuation


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Colorectal tran- Constipation sit study Severity Index Anorectal funcLab Work tion test Colonoscopy or Alb, transthyretin sigmoidoscopy BUN, Creat

H&H Serum Fe, ferritin Gluc Na, K Ca, Mg Stool guaiac

INTERVENTION OBJECTIVES • Atonic constipation (“lazy bowel”): Stimulate peristalsis, provide bulk, and retain water in the feces. • Spastic constipation: Undue distention and stimulation of the bowel should be prevented during exacerbations. After the patient is well, fiber should be increased. • TF constipation: Check for obstruction (nausea, vomiting, distention, and dehydration). Record I & O, along with activity levels. • Pediatric constipation and encopresis: Provide laxatives and lubricants initially, followed by improved fiber and fluid intakes.

SAMPLE NUTRITION CARE PROCESS STEPS Altered GI Function—Constipation Assessment Data: Fluid intake records (I & O), medication history and recent changes, stool patterns and frequency. No food allergies or intolerances noted. Limited fluid intake recently. Nutrition Diagnosis (PES): Altered GI function related to very low fluid intake and use of constipating medications as evidenced by patient complaints of hard, dry, infrequent stools, low intake of fluids, and poor nutritional quality of life. Intervention: Food-Nutrient Delivery: Incorporate more fluids into meals and nourishments, discussion of fluid tracking with staff or family as well as patient. Offer hot or caffeinated beverages, such as coffee or hot tea. Try prune juice mixed with bran and applesauce, especially for the elderly. Education: Discuss role of fiber, fluid and physical activity in maintenance of normal bowel activity. Counseling: Discuss food sources and ways to increase fiber content in recipes and meals. Coordination of Care: Discuss need for stool softener with doctor or nursing staff. Avoid mineral oil that interferes with nutrient absorption. Monitoring and Evaluation: Fluid intake records, stool patterns and frequency records. Review medication changes or addition of stool softener. Note fewer complaints of incidents of hard, dry, and infrequent stools or straining. Note more GI comfort and improved nutritional quality of life.

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FOOD AND NUTRITION • In general, it may be helpful to consume more fruits and vegetables and more servings from the bread/cereal group each day, especially whole grains, root vegetables such as carrots or potatoes, stewed dried fruit, and cabbage. Gradually increase fiber, maintain an adequate fluid intake, and exercise regularly. • Atonic constipation: The diet should contain 20–35 g of fiber, with liberal use of whole grains, fruits, and vegetables. Adding a few carrots and whole-grain breads and cereal may be an easy solution. Use adequate fluid (30–35 mL/Kg). • Spastic constipation: Decrease fiber during painful episodes. Then, increase use of prune juice, dried fruits, raw fruits and vegetables, nuts, and whole grains. If wheat allergy is a concern for a patient, do not promote use of bran. • TF constipation: Use a fiber-containing formula if appropriate. Use adequate flushes. • Pediatric constipation and encopresis: Add more fruits and vegetables to the diet; increase whole-grain fiber and fluid intake.

Common Drugs Used and Potential Side Effects • There is limited evidence about efficacy of treatments used for constipation. Good evidence supports the use of polyethylene glycol and tegaserod. Moderate evidence supports the use of psyllium and lactulose. Limitedquality data exist for milk of magnesia, senna, bisacodyl, and stool softeners (Kamm et al, 2005; Ramkumar and Rao, 2005). • Discourage overuse or dependence on laxatives and cathartics; see Table 7-10. • Prescription medications that may cause constipation include opiates, anticholinergics, tricyclic antidepressants, calcium channel blockers, antiparkinsonian drugs, antipsychotics, diuretics and antihistamines. • Over the counter drugs that can cause constipation include calcium-containing antacids, calcium supplements, iron supplements, NSAIDs, and antidiarrheal agents.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Flax, aloe (anthraquinones), fenugreek, and rhubarb have been recommended for constipation, but no clinical trials have proven efficacy. • With use of bisacodyl, avoid aloe, cascara, senna, and yellow dock because of enhancing effects. • A herbal tea (Smooth Move) increases bowel movements naturally (Bub et al, 2006). • More studies on probiotic products are needed, but they have possibility.


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TABLE 7-10

Medications for Constipation

Medication

Description

Bulking agents Psyllium (Metamucil, Effersyllium, Perdiem Fiber), Benefiber (with guar gum), methylcellulose (Citrucel), calcium polycarbophil (FiberCon), Fiberall, Fiber-Lax,Equilactin, Konsyl, Serutan

Fiber supplements that retain water and are safe choices. Take with plenty of water or juice (8 oz per teaspoonful). Results may require 1–4 teaspoons of the product.

Chloride channel activators Lubiprostone (Amitiza)

Activators increase intestinal motility and fluid to ease passage of stool. Not recommended for use longer than 12 months without doctor’s evaluation.

Lubricant laxatives (Fleet Mineral Oil, Zymenol)

Lubricant laxatives coat the intestinal lining to allow easier passage of stool but may also interfere with absorption of calcium and fat-soluble vitamins.

Osmotic or Hyperosmolar laxatives (Cephulac, Fleet Phospho-Soda, Milk of Magnesia or MOM, Kristalose) or Lactulose (Chronulac) or Polyethylene Glycol 3350 (Miralax, Glycolax)

Osmoticsand saline laxatives draw fluid, cause bowel distention, and may be useful for idiopathic constipation. “The wetter the better.” Take with plenty of fluid. Monitor for electrolyte imbalances. Use caution in diabetes. Miralax is safe and effective in pediatrics and pregnancy.

Prebiotics and probiotics

Use of probiotics such as yogurt with active cultures, lactobacilli and bifidobacteria, and prebiotics (nondigestible oligosaccharides) may be beneficial for gut integrity.

Stimulant laxatives Bisacodyl (Fleet Stimulant Laxative, Correctol, Dulcolax)

Stimulant laxatives irritate the intestine, causing bowel contractions. They can cause severe cramping, diarrhea, nausea, and electrolyte imbalances. Avoid using bisacodyl (Dulcolax) with dairy products; take with a highfiber diet. Not recommended for daily or regular use as they can deplete vitamin D and calcium.

Ex-Lax or Senokot (with senna) Herbal Authority Aloe Vera, Purge, Feen-a-Mint. Prunes (dried plums) are a natural stimulant laxative. Stool softeners (Emollient laxatives) Docusate sodium (Colace, Fleet Sof-lax, Peri-Colace, Surfak) Tegaserod (Zelnorm)

Stool softeners are short-term solutions; they allow more water to penetrate stool and to facilitate elimination. Docusate sodium (Colace) should be taken with milk or juice. Long-term use can deplete electrolytes. Tegaserod was removed from the market in 2007.

See also: Drug Class Review on constipation Drugs at http://www.ncbi.nlm.nih.gov/books/bv.fcgi?ridconstip, accessed August 11, 2009.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain that proper diet can produce relief but cannot cure the condition. A normal bowel routine is needed, but daily fecal evacuation is not needed by everyone. • Specifically identify foods that have a laxative effect for the patient. Explain why fiber should be increased on a gradual basis only and that items such as prune juice may help. For every gram of cereal fiber, stool weight increases by 3–9 g. For some, a cup of hot prune juice may be useful. • Have the patient drink 8–10 glasses of water daily, as permitted. Warm fluids are especially useful. • Exercise may be beneficial in maintaining regularity, especially abdominal-strengthening exercises. • Discuss foods that have caused constipation, flatus, and GI distress; offer relevant suggestions. • Medical assistance is needed for diarrhea, bleeding, infection, or other changes in bowel habits. • Bowel retraining programs may be helpful and may include increasing exercise, including more fiber in the diet, drinking more liquids, and setting aside 15 minutes to spend on the toilet after breakfast. Regular practices may help reestablish a healthy pattern.

• In a pediatric population, dietary changes, corn syrup, or both may resolve constipation in 25% of children. Laxatives such as milk of magnesia and polyethylene glycol are efficient and safe for almost all cases (Loening-Baucke, 2005).

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures. • Hand washing is extremely important after toileting.

For More Information •

Constipation http://digestive.niddk.nih.gov/ddiseases/pubs/constipation/

Constipation Algorithm http://www.uwgi.org/guidelines/ch_05/AlgA.htm

Emedicine http://www.emedicine.com/med/topic2833.htm

International Foundation for Functional Gastrointestinal Disorders http://www.aboutconstipation.org/

Med Info http://www.medinfo.co.uk/conditions/constipation.html

Web MD—Chronic Constipation http://www.webmd.com/digestive-disorders/ chronic-constipation-7/default.htm


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CONSTIPATION—CITED REFERENCES American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Bub S, et al. Efficacy of an herbal dietary supplement (Smooth Move) in the management of constipation in nursing home residents: a randomized, double-blind, placebo-controlled study. J Am Med Dir Assoc. 7:556, 2006. Chatoor D, Emmanuel A. Constipation and evacuation disorders. Best Pract Res Clin Gastroenterol. 23:517, 2009.

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Kamm MA, et al. Tegaserod for the treatment of chronic constipation: a randomized, double-blind, placebo-controlled multinational study. Am J Gastroenterol. 100:362, 2005. Loening-Baucke V. Prevalence, symptoms and outcome of constipation in infants and toddlers. J Pediatr. 146:359, 2005. Muller-Lissner SA, et al. Myths and misconceptions about chronic constipation. Am J Gastroenterol. 100:232, 2005. Ramkumar D, Rao SS. Efficacy and safety of traditional medical therapies for chronic constipation: systematic review. Am J Gastroenterol. 100:936, 2005. Wang JY, et al. A valid and reliable measure of constipation-related quality of life. Dis Colon Rectum. 52:1434, 2009.

DIARRHEA, DYSENTERY, AND TRAVELER’S DIARRHEA NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Diarrhea (acute enteritis) is a symptom of many disorders in which there is usually an increased peristalsis with decreased transit time through the GI tract. In Table 7-11, etiologies and comments related to diarrhea are given. Reduced reabsorption of water and watery stools result; see Table 7-12. Bacterial diarrhea is caused from food or water contaminated with Campylobacter, Salmonella, Shigella, and E. coli. Chronic diarrhea involves production of loose stools with or without increased frequency for more than a month. An individualized approach, knowledge of GI physiology, and awareness of the physiological effects of foods or medications are best used to design an effective dietary plan

TABLE 7-11

(Schiller, 2006). Dehydration is a common problem; watch for decreased skin turgor, dry mucous membranes, thirst, 2% weight loss or more, low BP, postural hypotension, increased BUN and hematocrit, and decreased urinary output. Early childhood diarrhea can come from or lead to malnutrition. Diarrhea is the leading cause of death in children younger than 5 years of age, especially in developing countries. Early rehydration may prevent many deaths in highrisk infants if mothers seek medical attention and offer proper rehydration solutions as soon as diarrhea begins. Oral rehydration solutions (ORS) are well tolerated and shorten illness and decrease fluid losses. Diarrhea can be prevented by breastfeeding, by immunizing all children

Diarrhea: Etiologies, Comments and Bristol Stool Chart

Diarrhea Type

Cause

Comments

Antibiotic-induced

Clostridium difficile is the gram-positive anaerobic bacterium most often responsible.

Clindamycin or cephalosporin often causes diarrhea.

Chronic diarrhea

Celiac disease, cow’s milk allergy, bacterial and parasitic factors, cystic fibrosis, or post-infectious gastroenteritis

Manage the underlying condition and often the diarrhea resolves. Celiac disease or food allergy should be considered.

Dysentery

Dysentery is from poor sanitation; causes range from contact with feces to contamination by houseflies.

Dysentery may involve diarrhea, with blood and mucus, intestinal rumbling, cramps, fever, and pus in stools.

Functional

From irritation or stress

Often resolves on its own

Organic

From intestinal lesion

May require further medical evaluation

Osmotic

From carbohydrate intolerance

Lactose, fructose, or sorbitol malabsorption may be a cause

Secretory

From bacteria, viruses, bile acids, laxatives, or hormones

This is typically a more serious condition.

TD is from contaminated food or water.

TD is usually caused by enterotoxic bacteria (E. coli, Campylobacter, Shigella, Salmonella, or Yersinia) or viruses or protozoa, Giardia is less common.

Rotavirus and Norwalk virus commonly affect infants and school-aged children; vomiting and watery diarrhea may occur. Norwalk-like viruses may also affect the frail elderly.

Traveler’s diarrhea (TD)


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TABLE 7-12

Bristol Stool Scalea

Type 1

Separate hard lumps, like nuts (hard to pass)

Type 2

Sausage-shaped but lumpy

Type 3

Like a sausage but with cracks on its surface

Type 4

Like a sausage or snake, smooth and soft

Type 5

Soft blobs with clear-cut edges (passed easily)

Type 6

Fluffy pieces with ragged edges, a mushy stool

Type 7

Watery, no solid pieces. Entirely Liquid

a

This medical aid was designed to classify feces into seven groups, developed by Heaton and Lewis at the University of Bristol, and first published in the Scandinavian Journal of Gastroenterology in 1997. The form of the stool depends on the time it spends in the colon. For more information, see www.continence.org.au. Accessed August 1, 2009.

against measles, by keeping food safe and water clean, and by washing hands before touching food. Clostridium difficile infection (CDI) diarrhea can be caused by use of most antibiotics. There may be profuse watery diarrhea that may be foul smelling; abdominal pain, cramping, and tenderness; stools that may be guaiac positive and grossly bloody; and fever or WBC count of 12,000–20,000/L. In severe cases, toxic megacolon, colonic perforation, peritonitis, hypovolemic shock, sepsis, and hemorrhage might occur. Symptoms may develop within a few days or even 6–10 weeks after antibiotic therapy is completed. Because C. difficile may be a normal bowel organism (especially in children), simply culturing the organism does not mean that diarrhea is caused by C. difficile. In mild cases, symptoms will usually resolve spontaneously once the causative antibiotic is withdrawn. More severe cases warrant therapy with vancomycin and metronidazole for 10 days. Tapered-dose oral vancomycin followed by a pulsed-dose regimen, probiotic approaches, restoration of the normal flora, immunological approaches, toxin-binding approaches, and serial therapy with vancomycin followed by rifaximin may be needed for recurrent infections (Johnson, 2009). See Section 15 for more information. Dysentery involves severe diarrhea containing mucus or blood. Vomiting of blood occurs. If left untreated, it may be fatal. Oral rehydration therapy is needed, and medication to treat any parasitic or bacterial infection. For traveler’s diarrhea (TD), high-risk destinations include most countries in Latin America, Africa, the Middle East, and Asia. Both cooked and uncooked foods are a concern if they have been improperly handled. Risky foods include raw or undercooked meat and seafood and raw

fruits and vegetables. Tap water, ice, and unpasteurized milk and dairy products can be associated with increased risk. Daily doses of rifaximin (Xifaxan) appear to significantly decrease the incidence of TD from E. coli.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Diarrhea is a symptom rather than a disease. Identify the cause and whether or not there is a genetic origin. I & O; dehydra- Lactose tolerance test tion? Height Hydrogen Temperature Weight breath test Abdominal pain Weight changes Stool culture BMI Lab Work such as for C. Diet history difficile  Na (decreased) Number of BUN:Creat ratio   K , Cl stools daily Gluc Stool consistency Ca, Mg Alb, transthyretin H&H (see Stool CRP Serum Fe, Chart) Serum copper ferritin BP N balance Clinical/History


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SAMPLE NUTRITION CARE PROCESS STEPS •

Altered GI Function with Diarrhea Assessment: Food diary, bowel patterns. Medical history or genetic etiology of diarrheal disorders. Nutrition Diagnosis (PES): Altered GI function related to excessive intake of poorly absorbed CHOs as evidenced by frequent intake of apple juice and sorbitol-containing dietetic products with cramping and loose stools. Intervention: Food and Nutrient Delivery: change diet as needed. Educate about impact of poorly absorbed CHO on bowel function. Monitoring/Evaluation: Reports of less abdominal cramping and loose stools.

INTERVENTION •

OBJECTIVES • Determine cause and apply an appropriate treatment. • Prevent or alleviate dehydration, electrolyte imbalances, anemia, weight loss, and hypoglycemia. • Avoid refeeding syndrome. CPN may lead to reduction in nutrient intake and atrophy of the gut. • Restore normal bowel motility. Alter stool consistency and quantity; up to 200 g of stool per day is normal. • Avoid extremes in food and beverage temperatures, which may stimulate extra colonic activity. • Correct intolerances for CHO and protein. Ensure adequate fat intake. Short-chain fatty acids enhance sodium reabsorption; include adequate fiber (American Dietetic Association, 2008). • Probiotic foods may be useful, such as yogurt with live and active cultures.

FOOD AND NUTRITION • It may be useful to hold food for 12 hours with use of IV fluids and electrolytes. Start oral fluids as soon as allowed. Use oral rehydration therapy, shown in Table 7-13, or prepared products such as CeraLyte. • Infants: Use rehydration solutions if allowed. Breastfeeding may be continued, or return to lactose-containing

TABLE 7-13

formula when feasible. Cut back on use of sorbitol (as in apple juice). Adults: Start with broth, tea, toast, and gradually add foods to a normal diet as tolerance progresses. Three to four small meals may be better tolerated. Products such as Gatorade may be useful. Banana flakes may be a safe, cost-effective treatment for diarrhea in critically ill patients on TFs. Use products containing probiotics. For potassium, include bananas, orange juice, fruits, and vegetables in the diet. Cocoa beans contain a large amount of flavonoids; dark chocolate may offer mild relief from diarrhea (Schuier et al, 2005). If TF is used, check tube placement and medications, presence of bloody stools, and endoscopic exams. Treatment includes changing medications, decreasing rate of feeding, changing to a high formula, antibiotic therapy, or using antidiarrheal medications. A jejunal placement may be too far for some patients and may actually cause some diarrhea. Use CPN only for intractable diarrhea. Osmotic diarrhea abates with NPO. Short-chain fatty acids from high-fiber sources may be useful. Use multivitamin–mineral supplements to replace vitamins A and C, zinc, iron, and other nutrients.

Common Drugs Used and Potential Side Effects • Every patient should receive a careful medication review. Magnesium-containing antacids, digoxin, broad-spectrum antibiotics, antifungal agents, colchicine, thiazide diuretics and other antihypertensives, Azulfidine, methotrexate and other anticancer agents, cholinergic stimulants, antiemetics such as metoclopramide, and laxatives such as mineral oil or methylcellulose may cause drug-induced diarrhea. Sorbitol may cause diarrhea; it is found in many medications. Megadoses of vitamin C (1 g daily) may cause diarrhea. • Antibiotics are used if shigellae or amoebae are causing the problem. Suggest use of probiotics with antibiotic therapy. Intestinal flora modifiers (e.g., Lactobacillus acidophilus, Lactinex, Bacid) also help recolonize normal intestinal flora. A common prescription is three to four packages every day for 3 days in adults. Modifiers may be mixed with water for tube-fed patients. • Antidiarrheal drugs are used to slow peristalsis or thicken stools. Kaolin (Kaopectate) has no major side effects but

UNICEF/WHO Oral Rehydration Therapya

Ingredients

Original ORS

New Reduced Osmolarity ORS

Sodium chloride

3.5 g/L

2.6 g/L

Potassium chloride

1.5 g

1.5 g/L

Sodium

2.5 g sodium bicarbonate

2.9 g/L trisodium citrate

Glucose

20 g /L of clean drinking water

13.5 g/L of clean drinking water

a

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Where ORS is not available, home-prepared solutions may use 1 teaspoon of salt, 8 teaspoons of sugar, and 4 oz of orange juice mixed into 1 L of water. From WHO Rehydration Project. Accessed August 1, 2009, at http://www.rehydrate.org/ ors/ort_how_it_works.htm.


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is not useful with infants. Lomotil should be taken with food; it may cause bloating, constipation, dry mouth, swollen gums, dizziness, nausea, and vomiting. Avoid using it with alcohol. Psyllium ingestion reduces stool looseness. Cholestyramine (Questran) may be used for bile acid diarrhea. Nausea, belching, or constipation may result. Replace fat-soluble vitamins. Ciprofloxacin is used for TD; one dose is often sufficient. It is a quinolone-class antibiotic. Avoid milk or yogurt. Nausea is one side effect. Vancomycin is used for treating C. difficile. Anorexia, GI distress, diarrhea, and nausea may result. Daily doses of rifaximin (Xifaxan) may significantly decrease TD from E. coli. It is not known yet if this same treatment is effective against TD from Salmonella and other bacteria.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. Apple, carrot, blackberry, carob, bilberry, and tea have been recommended, but no clinical trials have proven efficacy. • Probiotic medications may be helpful: for children, Lactobacillus GG or Culturelle; and for adults, Saccharomyces boulardii. Probiotics in foods can help to maintain good bacteria in the GI tract of those taking antibiotics. Yogurt may help to reculture the GI tract; check labels for live and active cultures. Acidophilus milk is also useful.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Describe the effects of pectin as a thickening agent (as in apples and bananas), and inform about yogurt or acidophilus milk or other specific probiotic foods/supplements. • Avoid sweetened carbonated beverages because their electrolyte content is low and osmolality is high. Caffeine, apple juice, and milk can aggravate diarrhea; omit until resolved. • Limit fruit juice to 6 oz daily in children. • Partially hydrolyzed guar gum (Benefiber) added to a diet ferments in the colon and produces short-chain fatty acids. This improves intestinal function, including colonic salt and water absorption (Alam et al, 2005). It may be a useful addition until diarrhea resolves. • Newly formulated oral rehydration salts contain lower concentrations of glucose, and salt and zinc supplementation can drastically reduce the number of child deaths. • Teach about the prevention and treatment of dehydration with appropriate fluids, breastfeeding of infants, and selective use of antibiotics to reduce the duration and severity of diarrheal episodes. • Signs of dehydration include increased thirst, dark urine, light headedness, dry skin and less-frequent urination. Children may have no tears when crying, dry mouth and tongue, sunken abdomen or eyes.

Patient Education—Foodborne Illness • The World Health Organization (2009) states the following facts: A total of 1.8 million people die every year from diarrheal diseases (including cholera); 90% are children under 5 who live in developing countries. Nearly all diarrheal disease is attributed to unsafe water supply, inadequate sanitation, and poor hygiene. Improved water supply reduces diarrhea morbidity by 21%, improved sanitation by 37.5%. Simply washing hands at critical times can reduce diarrheal cases by up to 35%. Improvement of drinking water quality, such as point of use disinfection, would lead to a reduction of diarrheal episodes by half. • To prevent TD, follow these guidelines: Use safe, bottled water for drinking and brushing teeth. Wash hands before eating, using antiseptic gel or hand wipes. Avoid ice in drinks. Do not eat raw vegetables or salads, raw fruits, or unpasteurized dairy products. Avoid swimming in streams and lakes. Use only cooked foods and bottled beverages (e.g., water, juices, beer, etc.). Brush teeth with bottled water only. Use caution with fresh foods that may have been washed in contaminated water and foods prepared with unheated water (e.g., jello) or ice cubes made with contaminated water. If symptoms persist, medical attention should be sought.

For More Information •

CeraLyte http://www.ceraproductsinc.com/productline/ceralyte.html

Centers for Disease Control and Prevention (CDC) Division of Parasitic Diseases http://www.cdc.gov/ncidod/dpd/

Diarrhea http://digestive.niddk.nih.gov/ddiseases/pubs/diarrhea/

Medicine Net—Diarrhea http://www.medicinenet.com/diarrhea/article.htm

Diarrhea Algorithm http://www.uwgi.org/guidelines/ch_04/ch04.htm

Giardiasis http://www.cdc.gov/ncidod/dpd/parasites/giardiasis/factsht_giardia.htm

Rehydration Formula http://www.rehydrate.org/

Travelers’ Health (CDC) http://www.cdc.gov/travel/diarrhea.htm

World Health Organization—Dysentery http://www.who.int/topics/dysentery/en/

DIARRHEA, DYSENTERY, AND TRAVELER’S DIARRHEA—CITED REFERENCES Alam NH, et al. Partially hydrolysed guar gum supplemented comminuted chicken diet in persistent diarrhoea: a randomised controlled trial. Arch Dis Child. 90:195, 2005. American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Johnson S. Recurrent Clostridium difficile infection: causality and therapeutic approaches. Int J Antimicrob Agents. 33:33S, 2009.


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Schiller LR. Nutrition management of chronic diarrhea and malabsorption. Nutr Clin Pract. 21:34, 2006. Schuier M, et al. Cocoa-related flavonoids inhibit CFTR-mediated chloride transport across T84 human colon epithelia. J Nutr. 135:2320, 2005.

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World Health Organization. Rehydration Project. Accessed August 1, 2009, at http://rehydrate.org/diarrhoea/index.html.

DIVERTICULAR DISEASES NUTRITIONAL ACUITY RANKING: LEVEL 2–3 DEFINITIONS AND BACKGROUND Diverticular disease results from formation of small pouches (diverticula) in the colon wall and lining due to chronic constipation. Diverticular disease occurs in Westernized countries because of low-fiber diets but is rare in societies that subscribe to high-fiber patterns. Lower GI bleeding from diverticulosis is a common reason for hospital admission, particularly in the elderly (Strate, 2005). A high-fiber diet is the mainstay of management for diverticulosis (American Dietetic Association, 2008). Diverticulitis (inflammation) develops when bacteria or other irritants are trapped in the pouches, causing spasm and pain in the lower left side of the abdomen, as well as distention, nausea, vomiting, constipation or diarrhea, chills, and fever. Bowel cancer has been associated with the presence of diverticular disease. Serotonin is widely distributed throughout the gut in both the enteric nerves and enterochromaffin cells, where they act as signal transducers and respond to bacterial or dietary substances with an inflammatory response and associated diarrheal symptoms respond well to 5-HT(3) receptor antagonists (Spiller, 2008). Probiotics and prebiotics are being tested for relief of pain and inflammation. Prebiotics such as guar gum are fermented into short chain fatty acids in the colon, where they stimulate water and sodium absorption. Probiotics are used to prevent or treat diarrhea; they are live organisms that eliminate toxins and inhibit proliferation of pathogens.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS

Height Weight BMI

Diet history Obesity? Physical inactivity? Stool number, frequency

Lab Work H&H Serum Fe, ferritin

Transferrin, Na, K TIBC Ca, Mg CRP WBC Erythrocyte sedi(increased) mentation rate (increased) Alb, transthyretin

INTERVENTION OBJECTIVES Diverticulitis (Inflamed State) • Allow complete bowel rest to prevent perforation by avoiding the laxative effect of excess fiber. • Eliminate food particles that accumulate in sacs as they may cause bacterial contamination.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Fiber Intake Assessment: Dietary recall of food intake with calculation of average fiber intake 8 g based on 24-hour recall and food frequency. Nutrition Diagnoses (PES): Inadequate fiber intake (NI 5.8.5) related to nutrition-related knowledge deficit as evidenced by inability to list five foods high in fiber and average daily fiber intake less than 3 g/d. Altered GI function (NC 1.4) related to diarrhea for 3 days, frequent pain, and increased flatus over 3 months. Interventions: Food-Nutrient Delivery—ND 1.2—soft diet, lowfiber foods until pain subsides.

Genetic Markers: Altered motility is an important feature of the pathogenesis of diverticular disease, and serotonin (5-HT) release is a primary trigger of gut motility (Costedio et al, 2008). Clinical/History

Abdominal ultrasound CT scan Barium enema

BP Abdominal pain Blood in stool? Sigmoidoscopy

Education—E 2.2—current diet order for soft, low fiber. Education on gradual introduction of fiber to diet to goal daily amount of 25–35 g; adequate fluid intake; increasing physical activity if possible. Provide list of high-fiber foods for inclusion in the diet, discuss the importance of fiber in diverticulosis. Counseling: Discuss foods to avoid when there is discomfort. Monitoring and Evaluation: Reassess dietary intake of fiber at next visit in 3 months; goal is to increase intake to 25–35 g/d. Evaluate daily dietary fiber intake using food recall/diary. Fewer complaints of pain, flatus, or diarrhea.


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• Prevent peritonitis and abscess. • Correct any GI bleeding, hypoalbuminemia, or anemia. • Each person differs in the amounts and types of foods they can eat; keep a food diary to identify any foods that may cause symptoms or discomfort.

Diverticulosis (Convalescent State) • Improve stool quality and increase volume, mostly from fiber. • Relieve intraluminal pressure; decrease the contractions of colonic circular smooth muscle. • Distend the bowel wall to prevent development of highpressure segments and inflammation. • Elimination of specific foods is not necessary.

FOOD AND NUTRITION Diverticulitis (Inflamed State) • As treatment begins, use a soft diet with low fiber. Gradually add fiber as inflammation and pain decrease. • Ensure adequate intake of protein and iron sources. • A low-fat diet may be better tolerated.

Diverticulosis (Convalescent State) • Diet should be high in fiber; 25–35 g/d is desirable. Whole grains, stewed or dried fruits, potato skins, raw carrots, or celery may be used; see Table 7-14. No evidence supports the common advice to avoid nuts and seeds (Strate et al, 2008). Eating nuts, corn, and popcorn does not increase the risk; in fact, nuts and popcorn may have a protective effect (Weisberger and Jamieson, 2009). Increase fiber gradually; avoid large excesses of fiber that may interfere with mineral absorption. Seeds in fruits or vegetables, and sunflower, pumpkin, caraway, poppy and sesame seeds do not enter, block, or irritate the diverticula and may be consumed. • Adequate fluid is recommended. • A vegetarian, plant-based diet is beneficial (Leitzmann, 2005) and a low-fat diet may reduce intracolonic pressure.

TABLE 7-14 •

How to Eat More Fiber

To get adequate fiber in the diet, follow the U.S. Department of Agriculture Food Guidance System (MyPyramid), which recommends eating 2–4 servings of fruit, 3–5 servings of vegetables, and 6–11 servings of cereal and grain foods each day. 1. Be smart by eating a whole-grain cereal that contains at least 5 g of fiber per serving. 1/2 cup of bran cereal contains 10 g of fiber. 2. Beans, peas, and lentils contain 6–9 g per 1/2 cup portion. Add them to soups, stews, and salads. 3. Eat raw vegetables as much as possible because cooking may reduce fiber content. A baked potato with skin, broccoli, shredded carrots, and cauliflower are great choices. 4. Eat the peel on fruits (such as apples, pears), and vegetables (such as cucumbers) because much of the fiber is found in the skin. 5. Eat fresh and dried fruits as snacks. Pears, apples, oranges, strawberries, other berries, prunes, bananas, and figs are all good choices. 6. Read food labels. Select foods that contain fiber whenever possible.

Sources: U.S. Department of Agriculture Nutrient Database, Release 17, 2004; and Medline Plus. Dietary fiber. 2009. Accessed at http://www.nlm.nih.gov/medlineplus/dietaryfiber.html

Common Drugs Used and Potential Side Effects • Antibiotics: For patients with severe and complicated diverticulitis, ampicillin, gentamicin, metronidazole, piperacillin, and tazobactam are used. Ciprofloxacin, metronidazole, and rifaximin are used for uncomplicated diverticular disease. Side effects may include nausea, vomiting, stomatitis, and other GI effects. • There is not enough evidence to recommend the antiinflammatory drug mesalamine or a polybacterial lysate for immunostimulation (Weisberger and Jamieson, 2009). • Pain medicine may be needed when cramping or bloating is significant. • Overusing laxatives may result in dependence on them. • Probiotics seem to be beneficial.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Flax, wheat, wild yam, slippery elm, and chamomile have been recommended for this condition, but no clinical trials have proven efficacy.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient concerning dietary fiber: Some ingested plant material is not digested by GI enzymes, including cellulose, pectin, lignin, and hemicelluloses. Some dietary fibers (whole grains) resist intestinal disintegration, whereas others (fruits and vegetables) are more or less disintegrated. In general, increased fiber increases stool volume, frequency, and transit rate and decreases intracolonic pressure (American Dietetic Association, 2008). Increased stool volume and decreased intracolonic pressure improve transit time. Take a fiber product such as methylcellulose (Citrucel) or psyllium (Metamucil) one to three times a day with at least 8 oz of water. • Instruct patient to chew slowly and to avoid constipation and straining. • If flatulence is a problem, advise that approximately 6 weeks will be needed to allow bacterial flora to adapt to increased fiber intakes. • Adequate physical activity is beneficial.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort. • If home TF is needed, teach appropriate sanitation and food-handling procedures.


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For More Information •

Diverticular Diseases http://emedicine.medscape.com/article/774922-overview

International Foundation for Functional Gastrointestinal Disorders http://www.iffgd.org/

Merck Manual—Diverticular disease http://www.merck.com/mmhe/sec09/ch128/ch128c.html

NIDDK http://digestive.niddk.nih.gov/ddiseases/pubs/diverticulosis/

Web MD http://www.webmd.com/digestive-disorders/diverticular-disease

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DIVERTICULAR DISEASES—CITED REFERENCES American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Costedio MM, et al. Serotonin signaling in diverticular disease. J Gastrointest Surg. 12:1439, 2008. Leitzmann C. Vegetarian diets: what are the advantages? Forum Nutr. 57:147, 2005. Spiller R. Serotonin and GI clinical disorders. Neuropharmacology. 55:1072, 2008. Strate LL. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am. 34:643, 2005. Strate LL, et al. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 300:907, 2008. Weisberger L, Jamieson B. Clinical inquiries: How can you help prevent a recurrence of diverticulitis? J Fam Pract. 58:381, 2009.

FAT MALABSORPTION SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 3

Adapted from: Rubin E MD and Farber JL MD. Pathology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999.


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TABLE 7-15

Altered Stools and Related Disorders

TABLE 7-16

Fecal Fat Study

Characteristic

Disorder

Fat absorption is tested by quantitative measurement of total fat in the stool.

Yellow or silver color

Fat malabsorption

Pale, foamy, mushy, or floating

Pan malabsorption

Normal excretion:

Less than 7 g (5% of a 60–100 g intake)

Formed in morning

Diarrhea

Mild malabsorption:

7–25 g (defects in micelle formation)

Formed in evening

Bile salt malabsorption

Moderate malabsorption:

25–30 g (intestinal mucosal disease)

Severe malabsorption:

More than 40 g (massive ileal resection or pancreatic disease)

Preparation:

Consume 100 g of long-chain triglycerides (LCT) over 3 days

DEFINITIONS AND BACKGROUND Adapted from Hermann-Zaidins M. Malabsorption. J Am Diet Assoc. 86:1171, 1986.

Fat malabsorption syndrome is caused by functional or organic causes. There may be fatigue, weight changes, steatorrhea, abdominal distention with cramps and gas, explosive diarrhea with foul-smelling stools, malnutrition and weight loss, and biochemical abnormalities. Exocrine pancreatic insufficiency is the principal cause. Other causes may include: postgastrectomy, blind loop syndrome, Crohn’s disease, small bowel resection; cystic fibrosis, chronic pancreatitis, pancreatic cancer, pancreatectomy; biliary atresia or steatorrhea; CD, lipoprotein deficiency, or HIV infection. The individual with malabsorption syndrome must be monitored for dehydration (dry tongue, mouth, and skin; increased thirst; low, concentrated urine output; weakness or dizziness when standing). Signs of nutrient depletion include nausea, vomiting, fissures at corner of mouth, fatigue, weakness, and dry, pluckable hair. Long-term nutritional monitoring is necessary after operations for morbid obesity, which can lead to fat malabsorption and vitamin deficiencies for vitamins A, D, and K (Malinowski, 2006). Malabsorption can have severe clinical consequences, including a decline in bone health.

To avoid nutritional deterioration, early screening for fat malabsorption should be recommended. Low total cholesterol (120 mg/dL) or low serum carotene levels may be typical of fat malabsorption but are not necessarily diagnostic. Altered stools characterize different types of malabsorption, as shown in Table 7-15. In patients with bile acid malabsorption, a larger amount of bile acids is spilled into the colon, where the acids stimulate electrolyte and water secretion, which results in loose to watery stools (Westergaard, 2007). Patients with more severe bile acid malabsorption have both diarrhea and steatorrhea; these patients are best treated with a low-fat diet supplemented with MCTs (Westergaard, 2007). A fecal fat study, though now uncommon, may be ordered; see Table 7-16. Enteric hyperoxaluria is the major risk factor for fat malabsorption, especially with IBD. In UC after restorative proctocolectomy, an increase of serum AA occurs with lower utilization for inflammatory processes, and reduced LDL cholesterol occurs as an index of malabsorption (Scarpa et al, 2008). Probiotics are being studied.

FAT MALABSORPTION

Loss of food energy

Loss of essential fatty acids

Loss of fat-soluble vitamins

Loss of food energy

Loss of essential fatty acids

Loss of fat-soluble vitamins

Loss of minerals

Calcium and magnesium deficiencies

Increased risk of bone loss

Increased absorption of oxalate

Increased urinary excretion of oxalate

Increased urinary excretion of oxalate

Adapted from: Merck Manual. Malabsorption syndromes. http://www.merck.com/media/mmpe/pdf/ Figure_ 017-1.pdf. Website accessed 9/1/09.


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ASSESSMENT, MONITORING, AND EVALUATION

TABLE 7-17 • •

CLINICAL INDICATORS •

Genetic Markers: Fat malabsorption is typically a symptom of an underlying disorder that may be either genetic or acquired. D-xylose test (decreased Height Tryptophan load excretion?) Weight test for Serum vitamin E BMI vitamin B6 Schilling test for Fecal Ca Diet history vitamin B12 BP (may be low) Acid steatocrit Na, K, Cl (may Malabsorption Signs of be low from blood test dehydration? diarrhea) 14 C-triolein Failure to thrive Ca, Mg breath test in children (may be low) Perianal itching Fecal fat study: Chol (may be 72-hour stool or soreness decreased) collection Frequent, foulTrig smelling stools Labeled carbon H&H breath test Small intestine Serum Fe, ferritin Sudan stain test biopsy Gluc CT scan or MRI Serum carotene, Alb, transthyretin vitamin A Barium enema (may be low) (may be low) or x-rays CRP Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Monitor for malabsorption of fat-soluble vitamins (A, D, E, and K). Long-term consequences of vitamin deficiency results if fat malabsorption is not corrected.

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal Nutrient (FAT) Utilization Assessment: I & O, abnormal nutritional labs for cholesterol, albumin, electrolytes. Fecal fat test results showing excesses of 20 g fat in stool; stools of yellowish hue. Abdominal pain. Nutrition Diagnoses (PES): Abnormal fat utilization related to malabsorption as evidenced by fecal fat study showing fat in stool of 20 g/d, yellowish stools, and abdominal pain. Interventions: Food and nutrient delivery: alter diet to include products containing MCT oil until condition can be resolved. Education: Discuss how fat malabsorption affects metabolism and absorption of nutrients. Counseling: Inclusion of water-miscible forms of fat-soluble vitamins, more calcium and water-soluble vitamins. Monitoring and Evaluation: Improvement in nutritional labs; fewer yellowish or abnormal stools. Fecal fat study showing less than 7 g fat. Less abdominal discomfort.

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Medium-Chain Triglycerides (MCTs)

Many products now contain MCTs as the primary fat source. MCTs use portal (albumin-free fatty acids) rather than lymphatic system transport and absorption (using less lipase and bile). MCTs have an 8- to 10-carbon source of fat and are useful when longer chain fatty acids (16–18 carbons) cannot be efficiently digested or absorbed. MCTs have concentrated calories made from coconut oil for adjunct therapy. MCT oil has 230 kcal/30 mL (6–7 kcal/g). Use instead of vegetable oil in recipes.

• Prevent calcium oxalate stone formation, or correct where present. • Correct all other nutrient deficiencies. • Alleviate steatorrhea and reduce intake of fat sources that are not tolerated. MCTs are useful. See Table 7-17.

FOOD AND NUTRITION • Initial treatment should consist of parenteral solutions or liquid formulas that contain MCT. MCTs alleviate steatorrhea in some cases; start with 20–60 g and increase gradually in an adult. • For mild cases, oral feeding is preferred because it stimulates brush-border activity. For moderate-to-severe cases, tube feed if necessary (50 mL/hr full strength initially; advance gradually). • Dietary fat may be limited to one egg and 4–6 oz of meat, poultry, or fish. Gradually check tolerance for long-chain triglycerides (LCTs) and work up to 30–40 g. • Increase intake of protein, which may be in the form of skim milk, egg white, cereals, or legumes. • Complex carbohydrates may be better tolerated than simple sugars. Lactose may not be tolerated. • A multivitamin–mineral supplement may be necessary to offset fecal losses of nutrients, vitamins, and water in patients with malabsorption syndromes—especially zinc, folate, vitamin B12, calcium, magnesium, iron, and fat-soluble vitamins (A, D, E, and K). • Monitor or decrease dietary oxalate intake to prevent renal stones. Use of probiotics may be helpful.

Common Drugs Used and Potential Side Effects • Antibiotics are used for bacterial overgrowth. Suggest use of yogurt with live and active cultures with antibiotic therapy. Intestinal flora modifiers (e.g., Lactobacillus acidophilus, Lactinex, Bacid) also help recolonize normal intestinal flora, perhaps three to four packages every day for 3 days in adults. They may be mixed with water for TFs. • Antidiarrheals may be used, such as kaolin (Kaopectate). Cholestyramine may be needed for bile salt diarrhea; fatsoluble vitamins can be depleted. • Cholylsarcosine (CS) is a semisynthetic bile salt replacement. If used properly, no side effects occur. • Orlistat inhibits pancreatic lipase and blocks the absorption of 30% of ingested fat in patients seeking weight loss.


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By its nature, it has the potential to create fat malabsorption syndrome, and use should be carefully monitored to assure that nutrient deficiencies do not occur. • Pancreatic enzymes may be needed if there is pancreatic insufficiency. • Patients with mild-to-moderate bile acid malabsorption present with watery diarrhea and generally respond very well to treatment with bile acid binders such as cholestyramine (Westergaard, 2007).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Caution the patient about a rapid consumption of MCTs. If they are consumed too rapidly, hyperosmolar diarrhea may result. Abdominal discomfort, flatulence, diarrhea, or steatorrhea may indicate continued malabsorption; the physician should be contacted. • Encourage several small, frequent meals throughout the day, avoiding fluids and foods that promote diarrhea. Monitor I & O of fluids, along with the number, color, and consistency of stools.

• Remember that a source of essential fatty acids may be needed if MCTs are used with a low-fat diet.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to this individual who may be experiencing diarrhea and related discomfort. • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Fat Malabsorption Syndrome http://www.merck.com/mrkshared/mmanual/section3/chapter30/30a.jsp

E-medicine http://www.emedicine.com/PED/topic1356.htm

Merck manual—malabsorption http://www.merck.com/mkgr/mmg/sec13/ch111/ch111a.jsp

FAT MALABSORPTION SYNDROME—CITED REFERENCES Malinowski SS. Nutritional and metabolic complications of bariatric surgery. Am J Med Sci. 331:219, 2006. Scarpa M, et al. Restorative proctocolectomy for ulcerative colitis: impact on lipid metabolism and adipose tissue and serum fatty acids. J Gastrointest Surg. 12:279, 2008. Westergaard A. Bile Acid malabsorption. Curr Treat Options Gastroenterol. 10:28, 2007.

INFLAMMATORY BOWEL DISEASE: CROHN’S DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 3–4 Crohn disease • Both large and small bowel involved

Wall thickened

• Areas of normal bowel skipped

• Strictures • Linear ulcerations

Stricture Ulcerative colitis • Small bowel not involved • Continuous involvement –No skipped areas of normal bowel

Linear ulcerations

Deep ulcers

Inflammation through full thickness of colon wall

Wall remains thin Pseudopolyp Superficial ulcer

• Superficial inflammation • No strictures • Patchy, nonlinear ulceration Superficial inflammation

Adapted from: Thomas H. McConnell, The Nature Of Disease Pathology for the Health Professions, Philadelphia: Lippincott Williams & Wilkins, 2007.


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DEFINITIONS AND BACKGROUND Crohn’s disease involves acute and chronic granulomatous, IBD with a cobblestone effect. Onset is generally between 15 and 30 years of age. Crohn’s disease differs from UC by affecting mucosal tissue of GI tract from oral cavity to rectum. In 33%, only the ileum is involved; in 45%, both the ileum and the large intestine are affected. As many as 1.4 million persons in the United States and 2.2 million persons in Europe suffer from with IBD. Macroscopic cobblestoning, segmental colitis, ileal stenosis and ulceration, perianal disease, and multiple granulomas in the small bowel or colon strongly suggest a diagnosis of CD. The causative antigen in IBD is the microflora in the intestinal lumen, facilitated by an impaired innate immune system; these provoke T helper 1 and T helper 17 responses in Crohn’s disease and a T helper 2 response in UC, resulting in pro-inflammatory cytokines and interleukins (Festen et al, 2009). Increased numbers of mucosa-associated E. coli are observed (Willing et al, 2009). Patients with CD exhibit a profound systemic failure of the acute inflammatory response that results in markedly delayed clearance of bacteria from the tissues, leading to local chronic granulomatous inflammation and compensatory adaptive changes (Sewell et al, 2009). Environmental triggers include smoking, northern geographic residence, allergic and autoimmune responses. Both passive and active smoke exposure in childhood predisposes children to IBD (Mahid et al, 2007). In addition, the pathways for amino acids, fatty acids, bile acids and AA are altered (Jansson et al, 2009). The intestinal lumen decreases; peristalsis from food intake causes cramping pain, especially in the right lower quadrant. Only 25% of Crohn’s disease cases present with the classic triad of abdominal pain, weight loss, and diarrhea (Beattie et al, 2006). Chronic watery diarrhea results from edema, bile salt malabsorption, bacterial overgrowth, and ulceration. Children may present with growth failure, inflammation, fever, pallor, and anemia. Stricture may precipitate bowel obstruction. Fever, weight loss, nausea, mouth sores, anal fissures, vomiting, abdominal pain, intestinal bleeding, arthritis, iritis or uveitis, conjunctivitis, jaundice, or pruritus may also be present. Elevated plasma tHcy is common. Nutritional therapy is an essential adjunctive treatment. In cases of short bowel syndrome (SBS), longterm CPN may be essential. Anti-TNF alpha (anti-TNF ) therapies have been used. Complications associated with Crohn’s disease include arthritis, skin problems, inflammation in the eyes or mouth, kidney stones, gallstones, or other diseases of the hepatobiliary system. If medical management fails, surgery may be indicated for continuous bleeding; recurrent ileus, abscesses, or fistulae. After total proctocolectomy, patients have less morbidity and are more likely to be weaned off all Crohn’s-related medications (Fichera et al, 2005). Persons with Crohn’s disease are at increased risk for colon cancer, obstruction, anorectal fistulas, and abscesses. Chronic inflammatory processes cause overproduction of reactive oxygen and nitrogen species, overproduction or activation of key AA metabolites and cytokines/growth factors, and immunity system dysfunction (Yang et al, 2009). Researchers are looking at genetically altering Bacteroides ovatus, naturally in the gut, to secrete human growth factor

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KGF-2 protein when exposed to xylan sugar and to heal the damage caused by inflammation (Hamady et al, 2008).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Crohn’s disease is associated with multiple mutations in the CARD15, the interleukin 23 receptor (IL23R) and autophagy-related 16-like 1 (ATG16L1) genes. The G allele of SNP rs2241880 confers strong risk for CD with a coding variant, threonine-to-alanine substitution at amino acid position 300 of the ATG16L1 protein (Grant et al, 2008). Transferrin, TIBC Height N balance Weight Serum tHcy BMI Serum folate Weight loss? Serum B12 and Stunted growth? Lab Work Schilling test Diet history Ca, Mg WBC, ESR BP (fever?) Serum B12 (increased) Temperature Total protein Rectal bleeding Crohn’s disease BUN, Creat activity factor Diarrhea Serum carotene (CDAI) Number of bowel Serum zinc CRP movements, (decreased) H&H frequency TLC Serum Fe, ferritin Barium upper Serum Cu (decreased) GI series with Hydrogen   Na , K small bowel breath test Alb, transthyretin follow(low) through Clinical/History

Abdominal CT Upper endoscopy Colonoscopy with biopsies

INTERVENTION OBJECTIVES • Replace fluid and electrolytes lost through diarrhea and vomiting. Lessen mechanical irritation and promote rest, especially with diarrhea. • Replenish nutrient reserves; correct malabsorption or anemia. Poor nutritional status may be related to decreased intake from anorexia, nausea or vomiting, abdominal pain, restrictive diets, side effects of medications, protein losses from ulcerated mucosal lesions, blood loss or wound-healing requirements, bacterial overgrowth, and malabsorption. • Monitor lactose and gluten intolerances, which may be present. • Promote healing; rest bowel from offending agents. Provide foods that contain short-chain fatty acids and glutamine to promote healing. • Prevent peritonitis, obstruction, renal calculi, and fistulas.


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SAMPLE NUTRITION CARE PROCESS STEPS Food and Nutrition Knowledge Deficit Assessment: Food diary, x-ray reports, biopsy. Nutrition Diagnosis (PES): Food and nutrition-related knowledge deficit (NB 1.1) related to management of Crohn’s as evidenced by new diagnosis and request for information from patient and family. Altered GI function (NC 1.4) related to inflammation in newly diagnosed Crohn’s disease as evidenced by diarrhea for 2 weeks; abdominal pain and cramping after meals. Involuntary weight loss (NC 3.2) related to diarrhea and inability to consume and digest adequate daily kilocal as evidenced by weight loss of 15 lb in last 60 days.

• •

Interventions: Food and Nutrient Delivery: ND 3.2.1 Multivitamin/ mineral supplement. Clear liquids advancing to low residue diet prior to discharge. Educate on low residue diet as needed, use of probiotic foods, and small frequent meals with lactose-free foods as needed.

Coordinate Care: Refer to gastroenterology dietitian specialist for outpatient follow-up. Monitoring and Evaluation: Improved intake and type of foods; symptoms resolved or improved. Monitor Hgb, Alb, Na, K for improvements while inpatient; weight for maintenance and eventual regain to usual body weight; bowel health with regard to decreased cramping and diarrhea after meals.

• •

35–45 kcal/kg; a BMI of 15–19 may require 30–35 kcal/kg; a BMI of 20–29 may require 25–30 kcal/kg; and a high BMI (30) may only require 15–25 kcal/kg. Estimate needs at the high end of normal for growth and repair in infants or children. With strictures or fistulas, use a low-fiber diet that is high in energy with a high protein content of 1–1.5 g/kg. For some patients, TF with added glutamine may be useful. Polymeric formulas are acceptable; elemental products are not required. Randomized controlled trials show that enteral nutrition is effective. Perioperative PN may reverse malnutrition and facilitate rehabilitation (Yao et al, 2005). If CPN is needed after total colectomy, use indirect calorimetry to estimate needs. A diet relatively high in fat may improve energy balance. Limit fat intake only if steatorrhea is present, in which case MCTs may be better tolerated. Omega-3 fatty acids may be indicated. Supplement the diet with multivitamins and minerals, especially thiamine, folacin, vitamin B12, vitamin E, zinc, vitamin D, calcium, magnesium, and iron. Vitamins A and K should be given every other day. With resection greater than 200 cm, selenium may become deficient; monitor carefully. Reduce lactose intake if not tolerated. Check for wheat and gluten tolerances. Monitor progress carefully; patients may be finicky. Small, frequent meals may be better tolerated.

Common Drugs Used and Potential Side Effects • Promote weight gain or prevent losses from exudates or inadequate intake. • Prepare for surgery if necessary after failed medical management, obstruction, fistula, or peritonitis. A total colectomy or a right-sided ileocolectomy may be necessary. • In a child, promote growth. Growth spurts follow sustained weight gain. • Reduce inflammatory process; fish oil intake may reduce severity of symptoms. • Monitor mineral and trace element levels carefully to ensure adequacy. Iron tends to be low. Antioxidant intake should be increased. • Prevent or correct metabolic bone disease (e.g., osteopenia, arthropathies) caused by disease itself, nutrient malabsorption, side effects of medications, or lifestyle factors. • Because tHcy production within the intestinal mucosa may contribute to the inflammatory response and endothelial cell dysfunction, treat folate and vitamin B12 deprivation as well as methylenetetrahydrofolate reductase (MTHFR) polymorphisms (Peyrin-Biroulet et al, 2007). Prevent thrombotic events.

FOOD AND NUTRITION • For adult energy requirements, estimate needs according to current BMI. A low BMI (15) may require

• Therapies for CD typically include aminosalicylates and antibiotics (for mild mucosal disease), nutritional therapy (including elemental or polymeric formulas), corticosteroids (for moderate disease), and infliximab for corticosteroid-resistant or fistulizing disease (Rufo and Bousvaros, 2006). Standard treatments with 5-aminosalicylic acid, antibiotics, corticosteroids, and immunosuppressives have serious and potentially adverse events (Krygier et al, 2009). • Anti-inflammation drugs are first-line treatments, with mesalamine in 5-ASA agents (Asacol, Canasa, Pentasa) or sulfasalazine (Azulfidine). Side effects include nausea, vomiting, heartburn, diarrhea, headache, folate depletion. • Antibiotics reduce bacterial overgrowth and vitamin K may be needed for fistulas. Ampicillin, sulfonamide, cephalosporin, tetracycline, or metronidazole are common choices. Metronidazole may be used when there is anal involvement; nausea, vomiting, anorexia, or diarrhea may occur. • Anti-diarrheal agents are needed, such as diphenoxylate, loperamide, and codeine. • Corticosteroids such as Budesonide (Entocort) are used in large doses at first. They are most effective with colon involvement. Patients will need a diet that provides sodium restriction, with extra protein, calcium, and potassium. Corticosteroids are more effective than enteral nutrition (Zachos et al, 2007).


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• Anti-TNF therapy is beneficial. Infliximab (Remicade) was the first treatment approved specifically to reduce inflammation in Crohn’s disease. The anti–TNF alpha agents are effective in the induction and maintenance of remission in luminal and fistulizing Crohn’s disease; early use with immunosuppressives may alter progression of the disease and prevent late complications (Krygier et al, 2009). • Some neuroregulatory peptides act as endogenous immune factors with anti-inflammatory effects; selective peptide analogs are being developed as novel therapeutic strategies for IBD patients (Motilva et al, 2008). • Retinoic acid and vitamin D are being studied for their possible effects in gut immunity and Crohn’s disease (O’Sullivan, 2009). • In MTHFR polymorphisms, use of L-methylfolate may be useful; Deplin is one prescription drug.

Herbs, Botanicals, and Supplements • Use of complementary medicine is common in this population (Langhorst et al, 2005). Omega-3 fatty acids help to reduce symptoms of Crohn’s disease. Alpha linoleic acid (ALA) works better at decreasing bowel inflammation than EPA and DHA. Fish oil supplements can cause side effects such as flatulence and diarrhea. • Phytochemicals such as turmeric (curcumin), red pepper (capsaicin), cloves (eugenol), ginger (gingerol), cumin, anise, and fennel (anethol), basil and rosemary (ursolic acid), garlic (diallyl sulfide, S-allylmercaptocysteine, ajoene), and pomegranate (ellagic acid) can suppress some inflammatory pathways (Aggarwal and Shishodia, 2004). • Probiotics may be beneficial; clinical studies are needed to verify the specific bacteria to be recommended. Studies have been performed with a variety of antioxidants, glutamine, short-chain fatty acids and prebiotics.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Encourage patient to eat. Discuss fiber, fluid, and supplements. • Periodic assistance or reevaluation by a qualified dietitian may be helpful. Alleviate fears associated with mealtimes. • Ensure that sources of potassium are increased during periods of diarrhea. • Instruct patient to chew foods well and avoid swallowing air. • Bone density should be monitored yearly (Sylvester et al, 2007). Highlight calcium and vitamin D and discuss alternate sources when milk cannot be used. Promote exercise as well. • Nocturnal TFs have been useful to regain weight or to promote growth. Total enteral nutrition with a liquid formula can suppress gut inflammation and induce remission in active Crohn’s disease (Johnson et al, 2006; Newby et al, 2005).

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Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort. • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Colon Cancer Screening http://www.uwgi.org/guidelines/ch_08/ch08txt.htm

Crohn’s Disease http://digestive.niddk.nih.gov/ddiseases/pubs/crohns/

Crohn’s and Colitis Foundation of America http://www.ccfa.org/

HealingWell Crohn’s Disease Resource Center http://www.healingwell.com/ibd/

National Association for Colitis and Crohn’s Disease http://www.nacc.org.uk/content/home.asp

Reach Out for Youth with Ileitis and Colitis http://www.reachoutforyouth.org/

CROHN’S DISEASE—CITED REFERENCES Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 1030:434, 2004. Beattie RM, et al. Inflammatory bowel disease. Arch Dis Child. 91:426, 2006. Festen EA, et al. Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets. Endocr Metab Immune Disord Drug Targets. 9:199, 2009. Fichera A, et al. Long-term outcome of surgically treated Crohn’s colitis: a prospective study. Dis Colon Rectum. 48:963, 2005. Grant SF, et al. Classification of genetic profiles of Crohn’s disease: a focus on the ATG16L1 gene. Expert Rev Mol Diagn. 8:199, 2008. Hamady ZZ, et al. Identification and use of the putative Bacteroides ovatus xylanase promoter for the inducible production of recombinant human proteins. Microbiology. 154:3165, 2008. Jansson J, et al. Metabolomics reveals metabolic biomarkers of Crohn’s disease. PLoS One. 4:e6386, 2009. Johnson T, et al. Treatment of active Crohn’s disease in children using partial enteral nutrition with liquid formula: a randomised controlled trial. Gut. 55:356, 2006. Krygier DS, et al. How to manage difficult Crohn’s disease: optimum delivery of anti-TNFs. Expert Rev Gastroenterol Hepatol. 3:407, 2009. Langhorst J, et al. Amount of systemic steroid medication is a strong predictor for the use of complementary and alternative medicine in patients with inflammatory bowel disease: results from a German national survey. Inflamm Bowel Dis. 11:287, 2005. Mahid SS, et al. Active and passive smoking in childhood is related to the development of inflammatory bowel disease. Inflamm Bowel Dis. 13:431, 2007. Motilva V, et al. Intestinal immunomodulation. Role of regulative peptides and promising pharmacological activities. Curr Pharm Des. 14:71, 2008. Newby EA, et al. Interventions for growth failure in childhood Crohn’s disease. Cochrane Database Syst Rev. 3:CD003873, 2005. O’Sullivan M. Symposium on ‘The challenge of translating nutrition research into public health nutrition’. Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’. Nutrition in Crohn’s disease. Proc Nutr Soc. 68:127, 2009. Peyrin-Biroulet L, et al. Vascular and cellular stress in inflammatory bowel disease: revisiting the role of homocysteine. Am J Gastroenterol. 102:1108, 2007. Rufo PA, Bousvaros A. Current therapy of inflammatory bowel disease in children. Pediatr Drugs. 8:279, 2006. Sewell GW, et al. The immunopathogenesis of Crohn’s disease: a three-stage model [published online ahead of print 7 Aug 2009]. Curr Opin Immunol. 21:506, 2009.


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Sylvester FA, et al. Natural history of bone metabolism and bone mineral density in children with inflammatory bowel disease. Inflamm Bowel Dis. 13:42, 2007. Willing B, et al. Twin studies reveal specific imbalances in the mucosa-associated microbiota of patients with ileal Crohn’s disease. Inflamm Bowel Dis. 15:653, 2009.

Yang GY, et al. Inflammatory bowel disease: a model of chronic inflammation-induced cancer. Methods Mol Biol. 511:193, 2009. Yao GX, et al. Role of perioperative parenteral nutrition in severely malnourished patients with Crohn’s disease. World J Gastroenterol. 11:5732, 2005. Zachos M, et al. Enteral nutritional therapy for induction of remission in Crohn’s disease. Cochrane Database Syst Rev. (1):CD000542, 2007.

INFLAMMATORY BOWEL DISEASE: ULCERATIVE COLITIS NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND UC is a chronic inflammatory disease of the mucosa of the colon. Complications can include arthritis, severe skin rashes, endocarditis, cirrhosis, splenomegaly, and stomatitis. Patients with UC may have histological features such as microscopic inflammation of the ileum, histological gastritis, periappendiceal inflammation, patchiness, and relative rectal sparing at the time of diagnosis (North American Society for Pediatric Gastroenterology, 2007). UC usually begins in the rectum or sigmoid colon. When UC affects only the rectum, it is called ulcerative proctitis. If the disease affects only the left side of the colon, it is called distal colitis; and if it permeates the entire colon, it is termed pancolitis. The condition is often a relentless, continuous lesion of the colon with some involvement of the terminal ileum. It does not affect full thickness of the intestine and never affects the small intestine. UC may be acute, mild, or chronic. Indeterminate colitis may be diagnosed with features of both UC and Crohn’s disease; this is called colitis of uncertain type or etiology (Geboes et al, 2008). The pathogenesis is complex and involves environmental, genetic, microbial, and immune factors. Onset of UC is usually between 15 and 35 years of age. There is a second, lesser peak of onset between ages 50 and 70 years. Intestinal microvascular ischemia usually precedes the onset of UC (Ibrahim et al, 2009). Blood in the stool is the most common symptom (Beattie et al, 2006) but children who present with UC may also have growth failure. Remissions occur, and there may be long periods between exacerbations. Flares often involve non-GI symptoms such as arthritis, uveitis, and ankylosing spondylitis. Because increased risk of colon cancer exists for the more extensive disease, patients with UC should be enrolled in a colonoscopy surveillance program after 8–10 years of disease duration (Rufo and Bousvaros, 2006). Probiotic bacterial mixtures provide relief in mild-tomoderate UC by reducing the number of “bad” bacteria, reducing the amount of inflammation, increasing the mucus layer of the gut, and increasing the number of anti-inflammatory molecules in the intestine (Bibiolni et al, 2005). Researchers are looking at genetically altering Bacteroides ovatus, naturally in the gut, to secrete human growth factor KGF2 protein when exposed to xylan sugar (Hamady et al, 2008). This may help to heal the damage caused by inflammation.

Both nutritional deficiencies and nutritional excesses impair GI responses and alter susceptibility to inflammation and other diseases. Enhancement of micronutrient nutrition is an important determinant of immunity and treatment of side effects in UC (Scrimgeour and Condlin, 2009). Approximately 15% of patients with UC will develop a severe exacerbation requiring hospitalization (Doherty and Cheifiz, 2009). If medical management fails, surgical colectomy to remove the colon and rectum is curative. The ileocecal valve should be preserved where possible. Colectomy with creation of an ileal pouch anal anastomosis (J pouch) is standard for patients with severe or refractory colitis, resulting in an improved quality of life in most patients (Rufo and Bousvaros, 2006).

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS Genetic Markers: IBD is associated with inheritance of several specific SNPs and gene variants that disrupt bacterial homeostasis mechanisms (Ferguson et al, 2007) and promote venous thrombosis (Bernstein et al, 2006). The ECM1 gene is found in UC (Jung and Hugit, 2009). Methionine synthase and MTHFR C677 T are also associated with extent of UC (Chen et al, 2008). Microflora in the intestinal lumen and an impaired innate immune system provoke a T helper 2 response, resulting in pro-inflammatory cytokines and interleukins (Festen et al, 2009). The IL-12-related cytokine, designated IL-23, establishes chronic inflammation and in the development of a Th cell subset producing IL-17, designated Th17 (Boniface et al, 2008; Shih and Targan, 2008). Clinical/History Height Weight BMI Diet history

Temperature Pus or mucus Stool sample discharged Bloody or explobetween sive diarrhea stools Crampy abdomi- Anemia, fatigue nal pain Anorexia


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Biopsy Anti–SacchaSigmoidoscopy romyces Colonoscopy cerevisiae Capsule antibody endoscopy to (ASCA) rule out Bilirubin Crohn’s Chol, Trig Na, K, Cl Lab Work BUN, Creat Alb, RBP CRP Ca, Mg ESR Serum phosphoPerinuclear antirus, Alk phos neutrophilic PT or INR cytoplasmic Transferrin, antibody TIBC (pANCA) N balance

Serum tHcy Serum folate Serum B12 and Schilling test Genetic testing for ECM1 and MTHFR H&H Serum Fe, ferritin Gluc Complete blood count (CBC), ESR WBC Hydrogen breath test Fecal fat study

INTERVENTION OBJECTIVES • In acute stages, allow the bowel to heal and use products that include short-chain fatty acids and glutamine to prevent a decline in nutritional status. Correct fluid and electrolyte imbalance. • Develop an optimal regimen of pharmacologic therapies, nutritional management, psychologic support, and properly timed surgery (when necessary) to maintain disease remission, minimize disease and drug-induced adverse effects, and optimize growth and development (Rufo and Bousvaros, 2006).

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Nutrient Intake Assessment Data: BMI 19, recent weight loss of 10 lb in 3 months, abdominal pain and bloody diarrhea at least once daily for 2 weeks. Diet hx reveals intolerance for high fiber fruits and vegetables and poor intake of protein-rich foods. Nutrition Diagnoses (PES): Inadequate nutrient intake related to GI discomfort and maldigestion as evidenced by weight loss 10 lb in 3 months, intolerance of fruits and vegetables, poor intake of protein-rich foods. Interventions: Food and nutrient delivery—change diet to low residue during flare. Educate about the role of diet in reducing inflammation; add omega-3 fatty acids and a multivitamin–mineral supplement once daily. Counsel about fiber-rich foods and when to avoid them (such as during times of GI distress). Discuss use of frequent small meals and intake of fruit and vegetable juices. Provide tips for adding protein and kilocals into the diet to regain lost weight. Discuss the option of using probiotic food sources. Monitoring and Evaluation: Weight status; diet hx revealing improved intake from all food groups; fewer incidents of GI distress with use of the low residue diet, omega-3 fatty acid supplements, and appropriate medicines.

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• Replenish depleted stores and correct poor nutritional status. Poor nutritional status may be related to decreased intake from anorexia, nausea or vomiting, abdominal pain, restrictive diets, side effects of medications, protein losses from ulcerated mucosal lesions, blood loss or wound-healing requirements, bacterial overgrowth, or malabsorption. • Avoid further irritation of the bowel by managing fiber intake. Large fecal volume distends the bowel and could create obstruction. Correct for diarrhea, steatorrhea, obstruction, and related anemias. • Provide sufficient dietary antioxidants and omega-3 fatty acids, which play a role in inflammatory processes. UC patients may be able to reduce steroid doses and achieve good symptom control by drinking a nutritionally balanced cocktail of fish oil, soluble fiber, and antioxidants daily. • Prolonged use of corticosteroids, calcium and vitamin D deficiency, and a low BMI are some of the possible contributing factors to bone disease. Replenish as needed. • Production of tHcy within the intestinal mucosa may contribute to the inflammatory response and endothelial cell dysfunction; treat folate and vitamin B12 deprivation as well as MTHFR polymorphisms, history of intestinal resection, or treatment with methotrexate (PeyrinBiroulet et al, 2007). Prevent thrombotic events.

FOOD AND NUTRITION • For adult energy requirements, estimate needs according to current BMI. A low BMI (15) may require 35– 45 kcal/kg; a BMI of 15–19 may require 30–35 kcal/kg; a BMI of 20–29 may require 25–30 kcal/kg; and a high BMI (30) may only require 15–25 kcal/kg. • Estimate needs at the high end of normal for growth and tissue repair in infants or children. • To treat the condition in its acute state, a low-fiber diet is needed to minimize fecal volume. A nutritional supplement that contains fish oil, soluble fiber, and antioxidants reduces reliance on traditional therapies and lessens the need to start on corticosteroid therapy (Seidner et al, 2005). • Persons with this condition often have lactose, wheat, or gluten intolerance. Alter diet accordingly. • Dietary changes that have been suggested include use of less red meat, dairy products, artificial sweeteners, and caffeine. Controlled trials are needed to confirm efficacy of these changes. • Diet should limit nuts, seeds, legumes, and coarse whole grains during a flare. Fresh fruits and vegetables may not be tolerated if they are highly fibrous; monitor carefully. A low-residue diet is useful during exacerbations. • CPN is useful when needed, often for 2 weeks or longer during acute stages. CPN may be needed in long term if there is short-gut syndrome. • As the patient progresses, a high-protein diet (1–1.5 g/kg) with high energy intake, given in six small feedings, is recommended. Protein may have to be restricted in patients with renal disease. • Vitamin–mineral supplementation may be needed. Supplement the diet with multivitamins and minerals,


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especially zinc, thiamin, folic acid, vitamin B12, vitamin E, vitamin D, calcium, magnesium, and iron. Vitamins A and K can be given every other day. With resection greater than 200 cm, selenium may become deficient; monitor carefully. • MCTs may be helpful. Use omega-3 fatty acid sources, such as salmon, mackerel, and tuna; supplements also may be beneficial. • After colectomy with ileostomy: IV feeding should continue for 1–2 days. Diet should progress slowly to a lowfiber, high-protein regimen with high energy, vitamins, and minerals (especially sodium and potassium). The patient will need vitamin B12 injections and adequate fluid. CPN may be needed if progress is slow. Once liberalized, foods are added one at a time. Avoid gas-forming foods that may cause increased peristalsis; products to reduce flatulence may be helpful.

Common Drugs Used and Potential Side Effects • The principal medical therapies used to induce disease remission in patients with UC are aminosalicylates for mild disease, corticosteroids for moderate disease, and cyclosporine for severe disease (Rufo and Bousvaros, 2006). Maintenance therapies that are used to prevent disease relapse include aminosalicylates, mercaptopurine, and azathioprine (Rufo and Bousvaros, 2006). • Aminosalicylates (mesalamine, olsalazine, and sulfasalazine) contain 5-aminosalicylic acid (5-ASA) and reduce inflammation. Extra fluid intake is needed to avoid renal stone formation. anorexia, nausea, vomiting, and GI distress may occur. Folic acid supplements also may be required. • Antibiotics such as metronidazole and ciprofloxacin reduce intestinal bacteria and directly suppress the intestine’s immune system. They should be used with probiotics such as yogurt containing live and active cultures. • Corticosteroids (prednisone, methylprednisolone, and budesonide) are used for patients with moderate-tosevere disease to reduce inflammation also. Although steroids can be quite effective for short-term control of acute episodes of colitis (flare-ups), they are not recommended for long-term use due to side effects. Negative nitrogen and calcium balances may result. Monitor the need for extra vitamins and minerals. • Immunomodulatory medicines including azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG), and cyclosporine alter the immune cell interaction with the inflammatory process. They are used for patients when aminosalicylates and corticosteroids have been ineffective. Azathioprine and 6-MP may be useful in reducing dependence on corticosteroids and in maintaining remission in some patients. These medications take several months before their beneficial effects begin to work. • Psyllium laxatives (Metamucil) can help with constipation and diarrhea. Long term use alters electrolytes. Flatulence or steatorrhea may occur. • TNF-neutralizing agent infliximab (Remicade) appears to be an effective option for patients with UC that are not responding to conventional treatment.

• Therapies under investigation include tacrolimus and novel biologic drugs. However, there is the challenge of addressing potential safety issues, while more traditional drugs should be further developed to facilitate patient compliance (Pastroelli et al, 2009). The delivery system and frequency of medication administration should be resolved (Tindall, 2009).

Herbs, Botanicals, and Supplements • Probiotics may be beneficial. Inulin and oligofructose have been suggested to increase the number of natural intestinal flora. • Use of complementary medicine is common in this population (Langhorst et al, 2005). Further study is needed to evaluate whether glutathione or coenzyme Q10 affects prevention or treatment of IBD. • Herbs and botanical supplements should not be used without discussing with the physician. Onion, cat’s claw, boswellia, honeysuckle, peppermint, valerian, and tea have been recommended for this condition, but no clinical trials have proven efficacy. • Omega-3 fatty acids may help to reduce symptoms of UC. ALA works better at decreasing bowel inflammation than EPA and DHA. Fish oil supplements may cause flatulence and diarrhea.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Ensure that the patient avoids foods that are known to cause diarrhea. Avoid extremes in food or beverage temperatures. • Pleasant mealtimes are an important part of treatment. Frequent, small meals may increase the total nutritional intake. Discontinue eating 2–3 hours before bedtime. • Avoid iced or carbonated beverages, which may stimulate peristalsis in times of discomfort. • Instruct the patient to eat slowly and chew foods well. Discuss fears related to eating. • Frequent counseling by a dietitian may be helpful. • It has been noted that women with IBD tend to be childless or have fewer children. However, fears should be discussed, as adverse reproductive problems are not common (Mountifield et al, 2009).

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to this individual who may be experiencing diarrhea and related discomfort. • Avoid excessive use of hand sanitizers, as a healthy gut contains some bacteria. • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Crohn’s and Colitis Foundation of America http://www.ccfa.org/research/info/aboutcd http://www.ccfa.org/info/diet?LMI4.2


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FACSR http://www.fascrs.org/patients/conditions/ulcerative_colitis/

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://digestive.niddk.nih.gov/ddiseases/pubs/colitis/index.htm

National Institutes of Health—Ulcerative Colitis http://www.nlm.nih.gov/medlineplus/ulcerativecolitis.html

ULCERATIVE COLITIS—CITED REFERENCES Beattie RM, et al. Inflammatory bowel disease. Arch Dis Child. 91:426, 2006. Bernstein CN, et al. Mutations in clotting factors and inflammatory bowel disease. Am J Gastroenterol. 102:338, 2006. Bibiolni R, et al. VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis. Am J Gastroenterol. 100:1539, 2005. Boniface K, et al. From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited. Immunol Rev. 226:132, 2008. Chen M, et al. Methionine synthase A2756G polymorphism may predict ulcerative colitis and methylenetetrahydrofolate reductase C677 T pancolitis, in Central China. BMC Med Genet. 9:78, 2008. Doherty GA, Cheifiz AZ. Management of acute severe ulcerative colitis. Expert Rev Gastroenterol Hepatol. 3:395, 2009. Ferguson LR, et al. Nutrigenomics and gut health. Mutat Res. 622:1, 2007. Festen EA, et al. Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets. Endocr Metab Immune Disord Drug Targets. 9:199, 2009. Geboes K, et al. Indeterminate colitis: a review of the concept—what’s in a name? Inflamm Bowel Dis. 14:850, 2008. Hamady ZZ, et al. Identification and use of the putative Bacteroides ovatus xylanase promoter for the inducible production of recombinant human proteins. Microbiology. 154:3165, 2008.

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Ibrahim CB, et al. On the role of ischemia in the pathogenesis of IBD: A review [published online ahead of print 14 August 2009]. Inflamm Bowel Dis. 16:696, 2009. Jung C, Hugit JP. Inflammatory Bowel Diseases: the genetic revolution. Gastroenterol Clin Biol. 33:123S, 2009. Langhorst J, et al. Amount of systemic steroid medication is a strong predictor for the use of complementary and alternative medicine in patients with inflammatory bowel disease: results from a German national survey. Inflamm Bowel Dis. 11:287, 2005. Mountifield R, et al. Fear and fertility in inflammatory bowel disease: a mismatch of perception and reality affects family planning decisions. Inflamm Bowel Dis. 15:720, 2009. North American Society for Pediatric Gastroenterology. Differentiating ulcerative colitis from Crohn disease in children and young adults: report of a working group of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the Crohn’s and Colitis Foundation of America. J Pediatr Gastroenterol Nutr. 44:563, 2007. Pastorelli L, et al. Emerging drugs for the treatment of ulcerative colitis [published online ahead of print 5 August 2009]. Expert Opin Emerg Drugs. 14:505, 2009. Peyrin-Biroulet L, et al. Vascular and cellular stress in inflammatory bowel disease: revisiting the role of homocysteine. Am J Gastroenterol. 102:1108, 2007. Rufo PA, Bousvaros A. Current therapy of inflammatory bowel disease in children. Pediatr Drugs. 8:279, 2006. Scrimgeour AG, Condlin ML. Zinc and micronutrient combinations to combat gastrointestinal inflammation [published online ahead of print 13 August 2009]. Curr Opin Clin Nutr Metab Care. 12:653, 2009. Seidner DL, et al. An oral supplement enriched with fish oil, soluble fiber, and antioxidants for corticosteroid sparing in ulcerative colitis: a randomized, controlled trial. Clin Gastroenterol Hepatol. 3:358, 2005. Shih DQ, Targan SR. Immunopathogenesis of inflammatory bowel disease. World J Gastroenterol. 14:390, 2008. Tindall WH. New approaches to adherence issues when dosing oral aminosalicylates in ulcerative colitis. Am J Health Syst Pharm. 66:451, 2009.

INTESTINAL FISTULA NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND An intestinal fistula is an unwanted pathway from intestines to other organs (e.g., the bladder). External fistulas are between the small intestine and the outside (e.g., skin). Internal fistulas are between two internal organs. Most fistulas occur secondary to abdominal surgery, and a high proportion occurs in association with IBD, intestinal cancer, or trauma. In patients with a suspected fistula, CT followed by a colonoscopy helps to rule out malignancy. Nutrition support may support spontaneous fistula closure. If spontaneous (nonoperative) closure does not occur in 5–6 weeks, it is unlikely to occur and an operation will be required (Osborn and Fischer, 2009). GI cutaneous fistulas are among the more complex surgical conditions, with mortalities between 6% and 20%, and even up to 40% (Osborn and Fischer, 2009). Substantial morbidity is related to large fluid and electrolyte losses and metabolic disturbances; mortality is most often related to sepsis and malnutrition (Slater, 2009). Hypertriglyceridemia (266 mg/dL) is commonly observed with enterocutaneous fistulas; it is associated with sepsis, a high output small bowel fistula, nutrition by the parenteral route, and primary diseases with inflammatory etiology (Visschers et al, 2009). Laparoscopic surgery may be a safe and effective procedure (Laurent et al, 2005), but surgery is performed only

after 4–6 months of medical therapy. Fistuloclysis is a procedure in which nutrition is provided via an enteral feeding tube placed directly into the distal lumen of a high output fistula (Slater, 2009). The primary determinant of mortality after enterocutaneous fistula (ECF) repair is a failed operation leading to recurrence of the fistula, especially with IBD, fistula located in the small intestine, an interval of 36 weeks or longer between diagnosis and operation, and resection with stapled anastomosis (Brenner et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: A fistula is acquired in most cases. Clinical/History Height Weight Weight loss

BMI Diet history Temperature (Fever?)

I&O Pain, tenderness Malaise CT scan


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Fistulagram Serum Fe, Colonoscopy ferritin Endosonography Serum folate N balance Lab Work Alb, transthyretin H&H

RBP BUN, Creat Na, K, Cl Transferrin Ca, Mg

Common Drugs Used and Potential Side Effects • Antibiotics commonly are used. Metronidazole and ciprofloxacin are useful. • Infliximab has been used with some success for healing fistulas in IBD. • Octreotide (somatostatin analog) inhibits endocrine/ exocrine secretions and excessive GI motility. It is only used parenterally and can cause nausea, vomiting, abdominal pain, diarrhea, or flatulence.

INTERVENTION OBJECTIVES • Promote rest and healing, minimize drainage from fistula, and prevent organ failure from sepsis. • Monitor the type of dietary regimen according to the location of the fistula and surgical or medical treatment. Adjunctive steps following the operation usually include a gastrostomy and a catheter jejunostomy (Osborn and Fischer, 2009). • Replace fluid and electrolyte imbalances. • Decrease malnutrition and infections through aggressive nutritional support. Promote positive nitrogen balance. Additional surgery may be needed to drain infection.

FOOD AND NUTRITION • A jejunostomy may help a duodenal fistula. A higher protein intake than usual may be needed. Use of an elemental formula diet also may be beneficial for an extended period of time to support GI tract recovery. • Use CPN for jejunal fistulas. Monitor closely for hypertriglyceridemia. • Progress to a low-residue, soft or normal diet as tolerated.

SAMPLE NUTRITION CARE PROCESS STEPS

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Probiotic and prebiotic therapy may be useful.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Defined formula diets can help support spontaneous closure in approximately 4–6 weeks. If closure has not occurred, surgery is aided by better nutritional status. • Instruct the patient regarding the fiber content of foods. Discuss how much to include during periods of flare-up and how to gradually increase fiber to achieve the goal set individually for that person.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to this individual. • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Society of Colon and Rectal Surgeons http://www.fascrs.org/patients/conditions/anal_abscess_fistula/

Excessive Parenteral Nutrition

Assessment Data: High output small bowel fistula, elevated triglycerides (300 mg/dL), CPN for 10 days, 15 lb weight loss from Crohn’s disease and poor intake over past year. BMI 19.

Anal fissure http://www.gicare.com/diseases/Anal-fissure.aspx

Fistula http://www.nlm.nih.gov/medlineplus/ency/article/002365.htm

Nutrition Diagnoses (PES): Excessive intake from PN related to attempt to resolve high output small bowel fistula with CPN as evidenced by elevated triglycerides and use of CPN exceeding needs for 10 days.

INTESTINAL FISTULA—CITED REFERENCES

Interventions: Calculation of current needs for protein, kilocals, and lipids to lower TG level without compromising fistula repair. Monitoring and Evaluation: Weights, lab values (especially glucose and TG), gradual healing of fistula over 4–6 weeks without surgery, BMI improving slowly.

Brenner M, et al. Risk factors for recurrence after repair of enterocutaneous fistula. Arch Surg. 144:500, 2009. Laurent SR, et al. Laparoscopic sigmoidectomy for fistulized diverticulitis. Dis Colon Rectum. 48:148, 2005. Osborn C, Fischer JE. How I Do It: Gastrointestinal Cutaneous Fistulas [published online ahead of print 9 June 2009]. J Gastrointest Surg. 13:2068, 2009. Slater R. Nutritional management of enterocutaneous fistulas. Br J Nurs. 18:225, 2009. Visschers RG, et al. Development of hypertriglyceridemia in patients with enterocutaneous fistulas. Clin Nutr. 28:313, 2009.


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INTESTINAL LYMPHANGIECTASIA NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Intestinal lymphangiectasia (IL) is a rare protein-losing enteropathy (PLE). It occurs most often in children, with 11 years as the average age of onset. IL can also occur secondary to conditions such as Crohn’s disease, scleroderma, sclerosing mesenteritis, CD, lupus, lymphenteric fistula, constrictive pericarditis, or pancreatitis. IL is potentially fatal if not recognized and properly treated (McDonald and Bears, 2009). Increased intestinal lymphatic pressure with vessel dilatation occurs, discharging fluid into the bowel lumen. The fluid is then digested by intestinal enzymes and is reabsorbed. Massive fluid retention occurs from obstructed lymph vessels, especially in the abdomen and pleural cavities. While malabsorption and PLE occur, only marginal loss of protein occurs in most cases. The main clinical features of this disorder include edema, fat malabsorption, lymphopenia, and hypoalbuminemia. Nausea, vomiting, nonbloody diarrhea, and abdominal pain result. Long-range problems may include lymphoma, osteomalacia or osteoporosis. A low-fat diet associated with MCT supplementation is the cornerstone of medical management (Vignes and Bellanger, 2008). The need for dietary control appears to be permanent, because clinical and biochemical findings re-appear after low-fat diet withdrawal (Vignes and Bellanger, 2008).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Primary intestinal lymphangiectasia (PIL) is a rare disorder, generally diagnosed before 3 years of age; is it also called Waldman’s disease (Vignes and Bellanger, 2008). Three genes, FLT4 (VEGFR3), FOXC2, and SOX18, cause varying forms of primary lymphedema (Finegold et al, 2008). Clinical/History

Diarrhea Chylous ascites? Double-contrast radiographs of the small bowel Ultrasound or CT scans Jejunal biopsy

Height Weight BMI Weight loss, inability to gain weight Stunting? Diet history Fatigue Lab Work Abdominal pain Fecal concentraSteatorrhea tion of alphaPeripheral edema

1 antitrypsin (56 cc/d with diarrhea) Jejunal biopsy (dilated lymphatic lacteal vessels) Alb (decreased) Transthyretin Serum 25-OHvitamin D and fat-soluble vitamins (low?)

Trace metal defi- Serum Fe, ferritin ciency Transferrin Chol (normal (decreased) or low) TLC (LymphoTrig cytopenia) Na, K H&H

Hypogammaglobulinemia Gluc Ca (low) Mg BUN, Creat

INTERVENTION OBJECTIVES • Identify and correct the underlying cause (e.g., constrictive pericarditis). • Decrease symptoms and promote recovery. Minimize peripheral edema. • Decrease intake of long-chain fatty acids because they form chylomicrons and stimulate lymphatic flow into the gut. Use MCTs because they are more water-soluble and can be absorbed through the portal vein instead of the lymphatic system. • Meet all nutritional needs for age and sex. Monitor absorption of fat-soluble vitamins; ensure adequacy from dietary or supplemental sources.

FOOD AND NUTRITION • Reduce intake of long-chain fatty acids. A formula or lowfat diet using a high concentration of MCTs is useful. • Adequate protein and calories are needed, according to the individual’s needs. • Fat-soluble vitamins may be required in water-miscible form for adequate absorption. • A calcium supplement may also be needed.

SAMPLE NUTRITION CARE PROCESS STEPS Inappropriate Intake of Types of Fats Assessment Data: Peripheral edema, weight loss, diarrhea, fecal alpha-1 antitrypsin 60 cc/d, low albumin (3.0 g/dL) Nutrition Diagnoses (PES): Inappropriate intake of fatty acids (long-chain) related to intolerance of long-chain fatty acids and IL as evidenced by diarrhea, weight loss, altered labs (albumin, alpha-1 antitrypsin). Interventions: Food-Nutrient Delivery—reduce intake of longchain fatty acids and use MCTs instead. Education—teach diet principles. Counseling about the diet for managing the life-long condition. Monitoring and Evaluation: Improvements in edema, lab values, and diarrhea after following the diet and taking appropriate medication.


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Common Drugs Used and Potential Side Effects • Octreotide (Sandostatin) may be used. It is a potent inhibitor of growth hormone, glucagons, and insulin; it also suppresses gastrin, motilin, secretin, and pancreatic polypeptide. • Over-the-counter remedies (bulking agents, drugs to control diarrhea) may be useful.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Supplements of vitamins and calcium are generally prescribed.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of fat in digestion, along with the need for MCT oils in the daily diet. • Discuss fat-soluble vitamins and their sources in the diet. • To minimize peripheral edema, elevation of extremities above the head may be recommended to decrease cel-

lulitis and lymphangitis. In addition, use of a recliner or elastic support stockings is suggested. • It is not helpful to reduce salt intake or to use diuretics in this condition.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Intestinal Lymphangiectasia http://www.emedicine.com/med/topic1178.htm

Medscape http://emedicine.medscape.com/article/1086917-overview

Merck Manual http://www.merck.com/mmhe/sec09/ch125/ch125f.html

INTESTINAL LYMPHANGIECTASIA—CITED REFERENCES Finegold DN, et al. HGF and MET mutations in primary and secondary lymphedema. Lymphat Res Biol. 6:65, 2008. McDonald KQ, Bears CM. A preterm infant with intestinal lymphangiectasia: a diagnostic dilemma. Neonatal Netw. 28:29, 2009. Vignes S, Bellanger J. Primary intestinal lymphangiectasia (Waldmann’s disease). Orphanet J Rare Dis. 3:5, 2008.

INTESTINAL TRANSPLANTATION NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Intestinal transplantation (ITx) represents a difficult lifesaving intervention reserved for patients with irreversible intestinal failure (Varga et al, 2009). Intestinal failure leads to the inability to maintain protein energy, fluid, electrolyte, or micronutrient balance due to GI disease when on a normal diet. Transplantation is an effective therapy for the treatment of patients with end-stage intestine failure who cannot tolerate PN (Grant et al, 2005). The procedure should be considered before the development of PN failure (Matarese et al, 2007). PN-associated liver disease, recurrent catheter-related sepsis, and threatened loss of central venous access are the major reasons for transplantation. SBS, cancers, radiation enteritis, trauma, Crohn’s disease, or other major intestinal diseases may also warrant ITx. Transplantation of the small bowel restores quality of life for recipients who have functioning grafts. ITxs should be considered early in intestinal failure patients who develop liver injury to prevent irreversible liver disease that would mandate a simultaneous liver transplantation (Fryer, 2005). Medicare pays for ITx in patients who fail PN therapy in specific cases. Living-related donor transplantation is an option if a potential donor is available. The donor should have no history of liver disease or major intestinal pathology.

The carbohydrate and amino acid absorptive capacity of the transplanted intestine normalize within the first several months whereas fat absorption is impaired for several months. Morbidity and mortality following ITx are greater than that following liver or kidney transplantation, but longterm survival is improving. Infectious enteritis can occur in recipients after ITx; viral agents are the cause in most cases (Ziring et al, 2005). With newer immune-suppressive protocols, 1-year graft and patient survival rates have improved. Surgery and high-dose immunosuppression must be managed. Radiation to the small bowel before transplanting the organ, then administration of donor’s bone marrow stem cells may reduce organ rejection. A loop ileostomy is often created for future endoscopy. Patients with ITx will require regular expert follow-up care and careful attention. A serious complication of ITx is jejunal graft (JG) damage (Varga et al, 2009). Induction therapy, combined with advancements on surgical technique and clinical management, has improved patient and graft survival (Vianna and Mangus, 2009). An organized multidisciplinary approach is recommended for long-term follow-up. Early and progressive enteral feeding using a complex polymeric formula is safe and effective after successful transplantation, eventually followed by unrestricted oral diet (Matarese et al, 2007). This modality of treatment is an alternative to PN, especially for those patients who have a poor quality of life as a result of PN (Middleton, 2007).


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ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Transplantation is a surgical procedure for a variety of conditions, some of which may be genetic. Doppler ultrasonograHeight phy Dry weight, presLiver biopsy ent weight BMI Lab Work Diet history Alb, BP transthyretin I&O CRP Temperature Wireless capsule CBC count Coagulation endoscopy profile (CE) Human Colonoscopy leukocyte CT scan to antigen monitor for (HLA) status fistula or Ca, Mg obstruction Clinical/History

Na, K H&H Serum Fe, ferritin Serum folacin BUN, Creat Glomerular filtration rate (GFR) WBC, TLC Gluc Chol, Trig N balance Alk phos, phosphorus AST, ALT Bilirubin Serum pH and lactate

INTERVENTION OBJECTIVES • Timely nutrition assessment and intervention may improve outcomes. Recovery of normal motility and absorptive capacity are the goals after surgery. • Prevent infection and promote wound healing.

SAMPLE NUTRITION CARE PROCESS STEPS

• Replenish lost nutrient stores as malnutrition compromises posttransplantation survival. • Meet metabolic demands and support recovery. • Control complications. Diarrhea and high stomal output are common problems and can lead to nutrient deficits, especially electrolytes. • Supplement enteral feedings with MCTs for several months posttransplantation. • Supplement the diet with IV fats and fat-soluble vitamins (vitamin D, E, A, and K) until the intestinal lymphatics are reestablished.

FOOD AND NUTRITION • When GI function is re-established, as indicated by decreasing G-tube returns and increasing gas and enteric contents in the ileostomy, a diet can be initiated. Advance as tolerated to provide full nutritional support. Monitor fluid status and adjust as needed. • Daily intake of protein should be appropriate for age and sex; 1.5 g/kg while on steroids may be recommended. Calories should be calculated as 30–35 kcal/kg. • Control CHO intake and encourage use of whole grains, vegetables, and fruits in cases of hyperglycemia. • To avoid the development of chylous ascites, a no-fat or low-fat diet can be initially used. Gradually increase fat intake to 25–30% of total kilocal. • Daily intake of sodium should be 2–4 g until the drug regimen is reduced. Adjust potassium levels as needed. • Daily intake of calcium should be 1–1.5 times the DRI levels to offset poor absorption. Children especially need adequate calcium for growth. Daily intake of phosphorus should be equal to calcium intake. • Supplement diet with vitamin D, magnesium, and thiamin if needed. • Reduce gastric irritants as necessary if GI distress or reflux occurs. • The special diet may be discontinued when drug therapy is reduced to maintenance levels. Encourage exercise and a weight control plan thereafter.

Common Drugs Used and Potential Side Effects

Altered GI Function

• See Table 7-18.

Assessment Data: Recent ITx following failure to tolerate PN; hx Crohn’s disease; unintentional weight loss over past year.

Herbs, Botanicals, and Supplements

Nutrition Diagnoses (PES): Altered GI function related to intestinal surgery as evidenced by intolerance of oral, enteral and PN with poor nutrition quality of life. Interventions: Food and nutrient delivery—clear liquids, progressing slowly to enteral feedings that contain MCT. Progress gradually to oral diet. Educate about the transition period from enteral to oral diet. Counsel about potential problems, such as diarrhea, electrolyte depletion, vitamin and mineral deficiencies; teach about products or medications that may be needed. Monitoring and Evaluation: Tolerance of enteral feedings post surgery. Resolution of diarrhea, high stomal output, abnormal labs. Achievement of desirable body weight range.

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• Herbs and botanical supplements should not be used without discussing with the physician. • Grapefruit juice decreases drug metabolism in the gut (via P-450–CYP3A4 inhibition). One glass can affect medications up to 24 hours later. Avoid taking with cyclosporine and tacrolimus.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Indicate which foods are sources of protein, calcium, and other key nutrients in the diet.


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TABLE 7-18

Medications Used after Intestinal Transplantation

Education

Description

Antibiotics

Broad-spectrum intravenous antibiotics are administered for about 1 week after the transplant.

Antiviral prophylaxis

Ganciclovir and/or cytomegalovirus (CMV) immunoglobulin (CytoGam) may be used.

Corticosteroids (prednisone or Solu-Cortef)

Corticosteroids such as prednisone and Solu-Cortef are used for immunosuppression. Side effects include increased catabolism of proteins, negative nitrogen balance, hyperphagia, ulcers, decreased glucose tolerance, sodium retention, fluid retention, and impaired calcium absorption and osteoporosis. Cushing’s syndrome, obesity, muscle wasting, and increased gastric secretion may result. A higher protein intake and lower intake of simple CHOs may be needed.

Cyclosporine

Cyclosporine does not retain sodium as much as corticosteroids do. Intravenous doses are more effective than oral doses. Nausea, vomiting, and diarrhea are common side effects. Hyperlipidemia, hypertension, and hyperkalemia may also occur; decrease sodium and potassium as necessary. Elevated glucose and lipids may occur. The drug is also nephrotoxic; a controlled renal diet may be beneficial. Taking omega-3 fatty acids during cyclosporine therapy may reduce the toxic side effects (such as high blood pressure and kidney damage) associated with this medication in transplantation patients.

Immunosuppressants

Immunosuppressants such as muromonab (Orthoclone OKT3) and antithymocyte globulin (ATG) are less nephrotoxic than cyclosporine but can cause nausea, anorexia, diarrhea, and vomiting. Monitor carefully. Fever and stomatitis also may occur; alter diet as needed.

Induction Therapy

Monoclonal (alemtuzumab, basiliximab, daclizumab) or polyclonal (Thymoglobulin) antibody preparations are often administered intraoperatively or preoperatively.

Probiotics, Prebiotics

Although research is still preliminary, the use of probiotics and prebiotics may become common practice in the future.

Prostaglandin E1

Prostaglandin E1 is given to improve the small bowel microcirculation.

Tacrolimus (Prograf, FK506)

Tacrolimus suppresses T-cell immunity; it is 100 times more potent than cyclosporine, thus requiring smaller doses. Side effects include GI distress, nausea, vomiting, hyperkalemia, and hyperglycemia.

• If the patient does not drink milk or use dairy products, discuss other sources of calcium. • Alcohol should be avoided unless permitted by the doctor. • Discuss control of hyperglycemia when appropriate. Discuss long-term problems such as obesity and dyslipidemia. • Encourage moderation in diet; promote adequate exercise. • Financial constraints can be a burden. Home care has evolved, but many disciplines are needed to keep everything in order.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing graft–host rejection. • Prevent infections from foodborne illness; patients who have undergone transplantation may be prone to increased risk more than other individuals. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Intestinal Transplantation http://www.emedicine.com/ped/topic2845.htm

Intestinal Transplant Centers http://www.intestinaltransplant.org/centres.htm

Intestinal Transplant Registry http://www.intestinaltransplant.org/

INTESTINAL TRANSPLANTATION—CITED REFERENCES Fryer JP. Intestinal transplantation: an update. Curr Opin Gastroenterol. 21:162, 2005. Grant D, et al. 2003 Report of the Intestine Transplant Registry: a new era has dawned. Ann Surg. 241:607, 2005. Matarese LE, et al. Therapeutic efficacy of intestinal and multivisceral transplantation: survival and nutrition outcome. Nutr Clin Pract. 22:474, 2007. Middleton SJ. Is intestinal transplantation now an alternative to home parenteral nutrition? Proc Nutr Soc. 66:316, 2007. Varga J, et al. Development of jejunal graft damage during intestinal transplantation. Ann Transplant. 14:62, 2009. Vianna RM, Mangus RS. Present prospects and future perspectives of intestinal and multivisceral transplantation. Curr Opin Clin Nutr Metab Care. 12:281, 2009. Ziring D, et al. Infectious enteritis after intestinal transplantation: incidence, timing, and outcome. Transplantation. 79:702, 2005.


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Colon

DEFINITIONS AND BACKGROUND Irritable bowel syndrome (IBS) is a functional GI disorder affecting up to 3–15% of the general population in western countries (Camilleri and Andresen, 2009). The pathophysiology of IBS involves disturbances of the brain–gut axis (Camilleri and Andresen, 2009). Stimulated 5-HT3 receptors promote intestinal motility, secretion, and sensation. Approximately one in ten patients with IBS believe their IBS began with an infectious illness (Spiller and Garsed, 2009). Prospective studies have shown that 3–36% of enteric infections lead to persistent new IBS symptoms; bacterial enteritis, protozoan, and helminth infections are often followed by prolonged postinfective IBS (Spiller and Garsed, 2009). Rome III Diagnostic criteria for IBS include at least 3 months of continuous or recurrent symptoms of abdominal pain or discomfort relieved with defecation or associated with change in frequency of stool or changed consistency of stool. Individuals with IBS often have had a prolonged initial illness, a toxic infecting bacterial strain, history of smoking, mucosal markers of inflammation, female gender, depression and adverse life events in the preceding 3 months (Spiller and Garsed, 2009). Because 95% of the body’s serotonin is located in the GI tract, it is important to note that people with IBS have diminished receptor activity. There are several subgroups of IBS: alternating bowel habits (IBS-A), constipationpredominant IBS (IBS-C), and diarrhea-predominant IBS (IBS-D). Signs that IBS patients require medical attention include anemia, fever, persistent diarrhea, rectal bleeding, weight loss, and nocturnal symptoms. In addition, a family history of IBD, CD, or colorectal cancer requires further diagnostic work-up. Up to 65% of IBS patients attribute their symptoms to food allergies (Zar et al, 2005). However, this finding has not been confirmed (Brant et al, 2009). Some IBS sufferers may have a mild form of CD and should be tested for gluten

intolerance. Others may have lactose maldigestion. A food diary is useful to note symptoms and specific foods or practices that cause problems. Therapies focus on specific GI dysfunctions (e.g., constipation, diarrhea, pain), and medications should only be used when nonprescription remedies do not work or when symptoms are severe. In some IBS patients, there is H. pylori infection; appropriate antibiotics may relieve symptoms. Therapies focus on nerve–gut communication dysfunction and antibiotics. Probiotics are another important therapy. Symptoms may also be improved by diets supplemented with probiotics such as hydrolyzed guar gum (Hadley and Gaardner, 2005) or bifidobacteria. Where carbohydrate malabsorption (lactose, fructose, or sorbitol) occurs, restrict the offending sugar(s). Overall, there is a reduction in quality of life (Brant et al, 2009). The American Dietetic Association has recommended three MNT visits for patients who have IBS.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Genetic modeling has identified a genetic link for IBS in twin studies (Lembo et al, 2007). However, the heritable components are poorly understood (Camilleri and Andresen, 2009). Change in form of stool Height Belching, flatuWeight lence, heartWeight changes burn BMI Nausea Diet history Mucus in stool? Family history of Polycystic ovarian GI disorders syndrome? Recurrent Urgency for abdominal defecation pain or Lower GI x-rays discomfort Colonoscopy or Change in sigmoifrequency of doscopy stool Clinical/History

Lab Work tTG testing to rule out CD Hydrogen breath test for lactose tolerance CRP H&H Serum Fe, ferritin Alb, transthyretin Gluc Na, K Ca, Mg

INTERVENTION OBJECTIVES • Encourage regular eating patterns, regular bowel hygiene, adequate rest, and relaxation.


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SAMPLE NUTRITION CARE PROCESS STEPS Undesirable Food Choices Assessment: Diet history with analysis of fiber, caffeine, fluid, and CHOs; family history and medication/food allergies; bowel patterns. Nutrition Diagnosis (PES): Undesirable food choices related to excessive intake of colas and coffee as evidenced by abdominal pain each day, symptoms of IBS-D, and poor nutritional quality of life. Intervention: Educate about better fluid choices, probiotics, prebiotics, fiber, reduction in gas-forming foods. Monitoring and Evaluation: Dietary and fluid intake changes; changes in abdominal pain, bowel patterns, frequency of diarrhea. Improved enjoyment of meals and a variety of foods and beverages.

and tegaserod are all effective in the treatment of IBS (Ford et al, 2009). If constipation results, a lower dose may be needed (Krause et al, 2007). • Antidepressants, novel selective anticholinergics, alphaadrenergic agonists, opioid agents, cholecystokininantagonists, neurokinin-antagonists, somatostatin receptor agonists, corticotropin releasing factor antagonists, chloride channel activators, guanylate cyclase-c agonists, melatonin, atypical benzodiazepines, antibiotics, immune modulators are under study (Camilleri and Andresen, 2009). Many of these have mixed reviews at the present time. • Methylcellulose (Metamucil) and other bulking agents always must be taken with large amounts of water. Generally, 1 tablespoon is sufficient per day. Increased peristalsis occurs.

Herbs, Botanicals, and Supplements • Avoid constipation by increasing physical activity and consuming adequate fluids and fiber (American Dietetic Association, 2008). • Monitor for food intolerances to gluten in wheat, rye, barley; chocolate; lactose or milk products; caffeine; alcohol. Omit offending agents. • Individualize diet management to the patient’s symptoms. Alleviate pain, symptoms, and flatulence. Production of colonic gas, especially hydrogen, may be uncomfortable. • Improve nutritional quality of life.

FOOD AND NUTRITION • Fiber is marginally beneficial; insoluble fiber may worsen symptoms but soluble fiber may help to alleviate constipation (Heizer et al, 2009). In acute phases, a low-fiber diet may be better tolerated. As treatment progresses, use adequate but not excessive fiber and ensure adequate fluid intake (30–35 mL/kg). • Avoid high-fat foods, which may increase cholecystokinin release. Avoid high sugar intake, which increases osmolarity. • Liberal amounts of fruits and vegetables are useful. Omit gas-forming oligosaccharides (beans, barley, Brussels sprouts, cabbage, nuts, figs, and soybeans), if not tolerated. Limit or omit spicy foods if poorly tolerated. • A modified exclusion diet and stepwise reintroduction of foods or trials of eliminating classes of food may be useful (Heizer et al, 2009). Omit milk products if lactose is not tolerated; add calcium in other forms. • In patients with CD, omit gluten and supplement with Bcomplex vitamins if needed.

Common Drugs Used and Potential Side Effects • 5-HT is a key modulator of GI sensorimotor function and this has led to the development of 5-HT(3) antagonists and 5-HT(4) agonists; alosetron (Lotronex), cilansetron,

• Daily use of peppermint oil is effective in relieving IBS symptoms (Hadley and Gaardner, 2005; Heizer et al, 2009). • The usefulness of probiotics in the form of foods such as live-culture yogurt and buttermilk for IBS symptoms is not established (Heizer et al, 2009). Two double-blind, randomized, placebo-controlled studies identified that Bifidobacterium infantis provides relief from IBS (Brenner and Chey, 2009; Spiller, 2005). Yogurt and other cultured foods may not be as effective as specific probiotics with high concentrations of microbes, but they are good sources of nutrients. • To prevent intestinal gas from forming, try Beano and other products available on the market. • Twice-weekly Acupuncture/Moxabustion treatment improves average daily abdominal pain and discomfort (Anastasi et al, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Slowly increase dietary fiber by 2–3 g/d to prevent discomfort and to promote soft, painless stools. Large servings of bran may aggravate IBS; assess individually. • IBS does not harm the intestines and does not lead to cancer; it is unrelated to IBD. • Drink six to eight glasses of water or fluids per day. Avoid carbonated beverages, chewing gum, or eating quickly, which may promote gas production. • Regular times for bowel evacuation should be planned. • Ensure the patient has adequate food intake and is not afraid to eat because of potential pain. • A food diary may help to identify any food sensitivities. • Large meals can cause cramping and diarrhea; smaller meals or smaller portions eaten more often may help IBS symptoms. Meals that are low in fat and high in carbohydrates such as pasta, rice, whole-grain breads and cereals (except with CD), fruits, and vegetables may help. • Refer the patient for stress management. Patients with rapidly cycling symptoms may need further counseling and support (Tillisch et al, 2005). Cognitive behavioral therapy is beneficial.


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• Family members may need to flexible and help to create regularity in the home. Avoid disorganization, overscheduling, lack of planning. • Regular exercise is important, such as walking, swimming, or yoga. Adequate sleep is important as well.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort.

For More Information •

American College of Gastroenterology—IBS http://www.acg.gi.org/patients/ibsrelief/

E-Medicine Health http://www.emedicinehealth.com/irritable_bowel_syndrome/ article_em.htm

IBS Treatment Matrix http://www.acg.gi.org/patients/ibsrelief/treatmentmatrix/index.asp

International Foundation for Functional GI Disorders http://www.iffgd.org/

Living with IBS http://www.iamibs.org/

Mayo Clinic http://www.mayoclinic.com/health/irritable-bowel-syndrome/DS00106

National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/ddiseases/pubs/ibs_ez/ http://digestive.niddk.nih.gov/ddiseases/pubs/ibs_ez/IBS.pdf

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IRRITABLE BOWEL SYNDROME—CITED REFERENCES American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Anastasi JK, et al. Symptom management for irritable bowel syndrome: a pilot randomized controlled trial of acupuncture/moxibustion. Gastroenterol Nurs. 32:243, 2009. Brant LJ, et al. An evidence-based systematic review on the management of irritable bowel syndrome American College of Gastroenterology Task Force on IBS. Am J Gastroenterol. 104:1S, 2009. Brenner DM, Chey WD. Bifidobacterium infantis 35624: a novel probiotic for the treatment of irritable bowel syndrome. Rev Gastroenterol Disord. 9:7, 2009. Camilleri M, Andresen V. Current and novel therapeutic options for irritable bowel syndrome management [published online ahead of print 7 August 2009]. Dig Liver Dis. 41:854, 2009. Ford AC, et al. Efficacy of 5-HT3 antagonists and 5-HT4 agonists in irritable bowel syndrome: systematic review and meta-analysis. Am J Gastroenterol. 104:1831, 2009. Hadley SK, Gaardner SM. Treatment of irritable bowel syndrome. Am Fam Physician. 72:2501, 2005. Heizer WD, et al. The role of diet in symptoms of irritable bowel syndrome in adults: a narrative review. J Am Diet Assoc. 109:1204, 2009. Krause R, et al. A randomized, double-blind, placebo-controlled study to assess efficacy and safety of 0.5 mg and 1 mg alosetron in women with severe diarrhea-predominant IBS. Am J Gastroenterol. 102:1709, 2007. Lembo A, et al. Influence of genetics on irritable bowel syndrome, gastrooesophageal reflux and dyspepsia: a twin study. Aliment Pharmacol Ther. 25:11, 2007. Spiller RC. Probiotics: an ideal anti-inflammatory treatment for IBS? Gastroenterology. 128:783, 2005. Spiller R, Garsed K. Postinfectious irritable bowel syndrome. Gastroenterol. 136:1979, 2009. Tillisch K, et al. Characterization of the alternating bowel habit subtype in patients with irritable bowel syndrome. Am J Gastroenterol. 100:896, 2005. Zar S, et al. Food-specific serum IgG4 and IgE titers to common food antigens in irritable bowel syndrome. Am J Gastroenterol. 100:1550, 2005.

Web MD—IBS http://www.webmd.com/ibs/default.htm

LACTOSE MALDIGESTION NUTRITIONAL ACUITY RANKING: LEVEL 2–3 DEFINITIONS AND BACKGROUND Lactose is a disaccharide (glucose-1 galactose) found in milk. If lactase enzyme is missing, lactose passes into the colon, where it is fermented to gases and organic acids by colonic bacteria, resulting in bloating, cramping, nausea, or diarrhea. A limited proportion of the human adult population retains intestinal lactase-phlorizin hydrolase (LPH) activity during adulthood, the lactase persistence phenotype (Robayo-Torres and Nichols, 2007). Lactase persistence is an autosomal-dominant trait that is common in Europeanderived populations (Smith et al, 2009). A staggering 4000 million people cannot digest lactose properly (Campbell et al, 2005). As many as 75% of all African American, Jewish, Native American, and Mexican American adults and 90% of Asian American adults are lactose intolerant. A total of 95% of all adults have adult-type hypolactasia (ATH) and have difficulty digesting milk sugar (Robayo-Torres and Nichols, 2007). Table 7-19 describes the various types of this condition.

CD can lead to lactase deficiency (Ojetti et al, 2005). An increased prevalence of lactose intolerance is also seen in patients with IBS. In addition, fructose intolerance may be unrecognized, and testing should clarify which disaccharide TABLE 7-19

Types of Lactose Maldigestion

Type

Description

Incidence

Congenital, primary, or genetic

Rare, present at birth

Low incidence in children

Lactase “nonpersistence” or hypolactasia

Lactase decline, often to about 10% of neonatal values

Occurs after weaning; more common in adults

Secondary or acquired

From gastrointestinal disease, food allergy, antibiotics, or intestinal trauma

May occur in children after diarrhea or giardiasis. Common with HIV infection, inflammatory bowel disease.


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is poorly tolerated. Children with suspected lactose intolerance can be assessed clinically by dietary lactose elimination or by tests including noninvasive hydrogen breath testing or invasive intestinal biopsy determination of lactase (and other disaccharidase) concentrations. (Heyman and Committee on Nutrition, 2006). Lactose maldigesters can consume up to 1 cup (8 oz) of milk without experiencing symptoms; tolerance can be improved by consuming the milk with a meal, choosing yogurt or hard cheeses, or using products that aid in the digestion of lactose such as lactase supplements or lactosereduced milks (Byers and Savaiano, 2005). Symptoms caused by lactose maldigestion need not hinder ingestion of a diet rich in dairy products that supplies around 1500 mg calcium daily (i.e., 2 cups of milk, 1 cup of yogurt, and several ounces of cheese). Bloating, abdominal pain, diarrhea, and overall symptom severity are often tolerable. Pregnant women, children and teens who are lactose intolerant should be given appropriate counseling about intake of calcium from nonlactose sources. Individuals who are self-described as lactose intolerant may restrict dairy and calcium intake and are at greater risk of osteoporosis and bone fractures. The American Dietetic Association recommends at least three MNT visits for adults who have lactose maldigestion.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Congenital lactase deficiency (CLD) occurs because of an SNP upstream from the lactase (C-13910  T) gene (Ingram 2009). Clinical/History Height Weight BMI Weight changes Lactose challenge test Hydrogen breath test (3–5 hours)

Stool acidity test Mg Alk phos Lab Work Gluc H&H Alb, transthyretin Serum Fe, ferritin BUN, Creat  , K Na  Ca (better absorption can occur over time)

INTERVENTION OBJECTIVES • Manage pain and discomfort related to lactose ingestion that is caused by flatulence and bloating or diarrhea. Control lactose intake, which comprises 10% of the carbohydrate found in the American diet. • Regular consumption of milk by lactase-deficient persons may improve colonic tolerance. Check for actual tolerance by monitoring intake.

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Cho (Lactose) Intake Assessment: Food diary and records with analysis of grams of lactose consumed on average day, stool frequency, and GI complaint reports. Nutrition Diagnosis (PES): Excessive CHO (lactose) intake related to poor food choices as evidenced by frequent use of liquid dairy products, ice cream and milkshakes with resulting abdominal pain and diarrhea. Intervention: Counseling on lactose-restricted diet, use of LactAid and lactose-reduced products in meals and in cooking. Monitoring and Evaluation: Food records and reports of GI distress or diarrhea after diet alterations have been implemented consistently for at least 7 days.

• Offer calcium and riboflavin from other foods and sources besides lactose-containing dairy products.

FOOD AND NUTRITION • Most people can tolerate up to 6 g of lactose, which is found in 1⁄2 cup (4 oz) of fluid milk. If small amounts are gradually added over approximately 3 months, most adults can ultimately adapt to 12 g lactose, equal to one 8oz glass of regular milk. • Dairy foods contain approximately 1–8% lactose by weight (milk, 4–5%; yogurt, 4%; ice cream, 3–4%; milk chocolate, 8%; cottage cheese, 1–2%). Because symptoms are related to dose, consume no more than 8 oz of lactosecontaining milk at a time after other foods have been consumed to slow down transit time. See Table 7-20. • Provide lactase enzyme supplements (e.g., Lactaid, Lactrase, Dairy Ease) 30 minutes before the consumption of a lactose-containing product. Two capsules provide enough lactase to hydrolyze the lactose in an 8-oz glass of whole milk. Lactose-hydrolyzed milk is generally tolerated. Note that not all preparations are equally effective. • Persons on a lactose-free diet can use lactate, casein (curds), lactalbumin, and calcium. If the patient is highly sensitive, check labels of foods for fillers, whey protein, milk, whey solids, and milk solids; most people can tolerate small amounts in mashed potatoes, breads, and medications. Processed cheese or cheese foods may have nonfat dry milk solids; use in moderate amounts. • Fermented products (buttermilk, natural or aged cheese, yogurt with live and active cultures, cottage cheese, or sour cream) may be better tolerated than milk by many individuals. • Frozen yogurt has little or no lactase activity. It may be tolerated in small amounts. • For infants with the condition, try milk-free formulas; gradually introduce foods that contain milk or lactose to test for tolerance. Distinguish milk allergy (usually early in life) from lactose maldigestion (more often in adults). • Secondary lactase deficiency results from injury to the small intestine that occurs with severe diarrheal illness, CD, Crohn’s disease, or chemotherapy; this is more common in infancy.


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TABLE 7-20

Portion

Lactose (g)

Evaporated milk

1 cup

24

Sweetened condensed milk

1

20

Milk, reduced fat

1 cup

11–14

Acidophilus Milk

1 cup

11

⁄2 cup

Yogurt, whole milk

1 cup

10–12

Buttermilk

1 cup

10

Ice cream

1

6

Yogurt, plain, low fat

1 cup

5

Sour cream or light cream

1

4

Cottage cheese

1

⁄2 cup ⁄2 cup ⁄2 cup

3 creamed, 2 dry

Cheese, hard

1 oz

1–2

Swiss cheese

1 oz

1

Cream cheese

1 oz

1

Butter or margarine

1 tsp

Trace

Recipe Substitutes for Dairy Products • • • • • • • • •

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

Lactose and Substitutes in Common Foods

Food and Portion

1 cup whole milk  mix 1⁄2 cup water with 1⁄2 cup nondairy cream or use 1 cup soy or rice milk 1 cup skim milk  1⁄4 cup nondairy cream plus 3⁄4 cup water 1 cup evaporated milk  1 cup nondairy cream or soy milk 1 cup buttermilk  1⁄2 cup nondairy cream plus 1⁄2 cup water  1 tbsp lemon juice or vinegar 1 cup whipped cream  1 cup nondairy whipped topping 1 tbsp cream cheese  1 tbsp mayonnaise ⁄2 cup cottage cheese  1⁄2 cup tofu 1 tbsp butter  1 tbsp milk-free margarine or 1 tbsp vegetable oil 1 cup sour cream  1⁄4 cup cornstarch in 3⁄4 cup water plus 1⁄4 cup vinegar

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• Identify foods that are lactose free and foods that are lactose-free sources of calcium. • Reading labels is helpful. Store-bought cookies, cakes, bread, baked goods, cereals, instant potatoes, soups, margarine, lunch meat, salad dressings, pancakes, biscuits, nondairy creamers or whipped toppings, and candy may contain lactose. • The patient must read labels, looking for and avoiding “milk,” “lactose,” butter, cheese, cream, milk solids, powdered milk, and whey. • Home-cooked meals and lactose-free recipes are useful. Recipes are available for use of lactose-free formulas in products such as meat loaf. Advise that heating of milk does not change lactose. • If dairy products are eliminated, other dietary sources of calcium or calcium supplements need to be provided, especially for infants, children, teens (Heyman and Committee on Nutrition, 2006), and pregnant women. Calcium-fortified soy milk, broccoli, leafy greens, canned salmon, almonds, oranges, certain kinds of tofu and soy milk, and calcium-fortified breads and juices can be used. • Kosher foods are often acceptable if they are pareve (nonmilk, nonmeat). • Discuss how to use LactAid drops to allow the enzyme to hydrolyze the lactose. Five to 15 drops per quart of milk will reduce lactose by 70–99%. • Drink milk with meals rather than alone to decrease symptoms.

1

Common Drugs Used and Potential Side Effects

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort.

For More Information •

Dairy-Ease http://www.dairyease.com/benefits/

Lactose-Free Diet http://www.gicare.com/pated/edtgs05.htm

Lactose Intolerance http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance/

Lactose Intolerance Glossary http://www.medicinenet.com/lactose_intolerance/glossary.htm

Lactose Diet http://www.cpmc.org/advanced/pediatrics/patients/topics/lactosefree.html

Herbs, Botanicals, and Supplements

LactAid (McNeil Consumer Products) http://www.lactaid.com/

• Probiotics (such as lactobacilli and bifidobacteria) and prebiotics (nondigestible oligosaccharides) assist in alleviating lactose intolerance and improving calcium absorption (Doron and Gorbach, 2006). • Take calcium supplements containing calcium carbonate with meals because stomach acid enhances absorption. Calcium citrate can be taken with meals or on an empty stomach. Take calcium in doses of 500 mg several times a day rather than all at once. • Herbs and botanical supplements should not be used without discussing with the physician.

LactAid recipes http://lactaid.allrecipes.com/

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance_ ez/#food

• Many drugs contain lactose but seldom over 500 mg; most should be well tolerated. For example, some types of birth pills, as well as tablets for stomach acid and gas may contain lactose. • Antidiarrheal agents such as loperamide (Imodium A-D) help reduce symptoms of lactose intolerance.

LACTOSE MALDIGESTION—CITED REFERENCES Byers KG, Savaiano DA. The myth of increased lactose intolerance in African-Americans. J Am Coll Nutr. 24:569S, 2005. Campbell AK, et al. The molecular basis of lactose intolerance. Sci Prog. 88:157, 2005.


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Doron S, Gorbach SL. Probiotics: their role in the treatment and prevention of disease. Expert Rev Anti Infect Ther. 4:261, 2006. Heyman MB, Committee on Nutrition. Lactose intolerance in infants, children, and adolescents. Pediatrics. 118:1279, 2006. Ingram CJ. Lactose digestion and the evolutionary genetics of lactase persistence. Hum Genet. 124:579, 2009.

Ojetti V, et al. High prevalence of celiac disease in patients with lactose intolerance. Digestion. 71:106, 2005. Robayo-Torres CC, Nichols BL. Molecular differentiation of congenital lactase deficiency from adult-type hypolactasia. Nutr Rev. 65:95, 2007. Smith GD, et al. Lactase persistence-related genetic variant: population substructure and health outcomes. Eur J Hum Genet. 17:357, 2009.

MEGACOLON NUTRITIONAL ACUITY RANKING: LEVEL 3

Distended sigmoid colon

The ENS is the intrinsic segment of the GI tract that controls essential functions such as motility, secretion, and blood flow; it is organized into neurons and glial cells that are distributed throughout the entire length of the gut wall (Burns and Pachnis, 2009). Enteric nervous system stem cells (ENSSCs) provide potential tools to replenish absent ganglia in the congenital form of megacolon, Hirschsprung’s disease (Metzger et al, 2009). IBD is associated with a host of intestinal disease–related complications including toxic megacolon (Scherer, 2009). Subtotal colectomy with ileostomy remains the procedure of choice (Ausch et al, 2006; Gladman et al, 2005). Colectomy is complicated by considerable morbidity, while rates have improved over the past several decades (Teeuwen et al, 2009).

Aganglionic portion

ASSESSMENT, MONITORING, AND EVALUATION Rectum

Adapted from: Pillitteri, A. Maternal and Child Nursing, 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2003.

DEFINITIONS AND BACKGROUND Megacolon may come in three forms: acute (before age 1), chronic (after age 10), or toxic. Acquired megacolon is associated with chronic constipation. The enlarged bowel results from an abnormal colonic dilatation often reaching 8–10 cm in diameter. It may occur in elderly persons who have a long history of elimination problems created by laxative abuse or constipation. Persons with diabetes, hypothyroidism, scleroderma, spinal cord injury, Parkinson’s, multiple sclerosis, electrolyte imbalances, tumor, strictures, and other conditions may be affected. Worldwide, infection with Trypanosoma cruzi (Chagas disease) is the major cause of megacolon. Normal urges to defecate are affected by physical activity, neurological status, chemical/drug use, and bowel condition. Normal reflexes are needed for muscular and sphincter control. Family physicians must be alert for the presence of uncommon but serious megacolon (Biggs and Dery, 2006). Signs and symptoms of megacolon involve abdominal distention, flatus, absence of stool, smearing or bowel incontinence, nausea, anorexia, fatigue, and headache. Note that the colon provides reabsorption of water and electrolytes as well as elimination of waste and regulation of bacterial homeostasis; motility is crucial for these roles.

CLINICAL INDICATORS Genetic Markers: Hirschsprung’s disease is caused by a single gene mutation of the RET proto-oncogene on band 10q11.2. Megacolon can occur in multiple endocrine neoplasia type 2A (MEN 2A) or 2B (MEN 2B). Clinical/History Height Weight BMI Diet history BP I&O Stool pattern

Stool consistency H & H Serum Fe, Endoscopy Barium x-rays ferritin Abdominal girth Na, K, Cl Ca, Mg Lab Work Thyroid function BUN, Creat Stool guaiac Gluc

INTERVENTION OBJECTIVES • Prevent complications such as lung atelectasis from distention, sepsis, ulceration with hemorrhage or perforation, or sigmoid volvulus.


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SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Fluid Intake Assessment Data: Height, Weight, BMI normal. Hx chronic constipation and Parkinson’s disease. Recent identification of megacolon. Minimal intake of fluids without prompting. Signs of early dementia. Nutrition Diagnoses (PES): Inadequate fluid intake related to cognitive changes and forgetting to drink as evidenced by I & O records with chronic constipation and megacolon. Interventions: Increase fluid intake to meet estimated needs (30 mL/kg). Offer beverages every 2 hours. Educate staff and family about cueing to drink and offering beverages often. Review effects of laxatives, stool softeners, and other prescribed medications on constipation. Monitoring and Evaluation: Improvement in signs of chronic constipation; relief from megacolon. Improved fluid intake to meet estimated needs.

• Empty the bowel as needed, with osmotic laxatives, enemas, suppositories, cathartics, or digital disimpaction. • Normalize bowel function as much as possible. Evaluate bowel pattern by history and at present, including drug use and laxative abuse. Exclude underlying cause if possible, such as calcium channel antagonists, narcotics, anticholinergics. • Identify and correct any nutrient deficiencies, electrolyte imbalances, or protein-energy malnutrition. • Assure adequate hydration.

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• Suppositories and stool softeners may be used or may have been used excessively. Monitor specific medications accordingly and their side effects. • Anticholinergics, opiates, and antidepressants may increase or aggravate constipation. Limit use.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Many patients take natural herbal laxatives that contain cascara.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of exercise in maintaining normal bowel function. • Discuss the role of fluid and fiber in bowel regularity (American Dietetic Association, 2008). For example, drinking a cup of hot prune juice may be effective for some patients. • Include probiotic foods such as yogurt with live and active cultures, lactobacilli and bifidobacteria, and prebiotics (nondigestible oligosaccharides) for gut integrity.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information

FOOD AND NUTRITION • Use adequate fluid and fiber, pending status, and other conditions (such as heart failure). Prune juice added to hot cereal may help normalize bowel function. If raw fruits and vegetables are not tolerated at first, add over time. For some people, excessive bran will not be tolerated. • Avoid excesses of refined foods and concentrated sweets to the exclusion of desirable foods. • Fiber-rich TF may be needed for selected patients.

Common Drugs Used and Potential Side Effects • Osmotic agents, such as magnesium salts, sorbitol, or lactulose are often used; some may increase flatulence. • Stimulant laxatives (senna and bisacodyl) may decrease the ability of the colon to evacuate; they are not as helpful in this condition.

Acquired Megacolon http://www.emedicine.com/med/byname/megacolon-chronic.htm

NIH—Megacolon http://www.nlm.nih.gov/medlineplus/ency/article/000248.htm

MEGACOLON—CITED REFERENCES American Dietetic Association. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 108:1716, 2008. Ausch C, et al. Aetiology and surgical management of toxic megacolon. Colorectal Dis. 8:195, 2006. Biggs WS, Dery WH. Evaluation and treatment of constipation in infants and children. Am Fam Physician. 73:469, 2006. Burns AJ, Pachnis V. Development of the enteric nervous system: bringing together cells, signals and genes. Neurogastroenterol Motil. 21:100, 2009. Gladman MA, et al. Systematic review of surgical options for idiopathic megarectum and megacolon. Ann Surg. 241:562, 2005. Metzger M, et al. Enteric nervous system stem cells derived from human gut mucosa for the treatment of aganglionic gut disorders. Gastroenterology. 136:2214, 2009. Scherer JR. Inflammatory bowel disease: complications and extraintestinal manifestations. Drugs Today. 45:227, 2009. Teeuwen PH, et al. Colectomy in patients with acute colitis: a systematic review. J Gastrointest Surg. 13:676, 2009.


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OSTOMY: COLOSTOMY NUTRITIONAL ACUITY RANKING: LEVEL 2–3

Stoma

Adapted from: Neil O. Hardy. Wesport, CT. Stedman's Medical Dictionary, 27th ed. Baltimore: Lippincott Williams & Wilkins, 2000, p. 383.

DEFINITIONS AND BACKGROUND The colon functions primarily to absorb water and sodium and to excrete potassium and bicarbonate. A colostomy is an artificial outlet for intestinal wastes created surgically by bringing a portion of the colon through the abdominal wall, TABLE 7-21

resulting in a stoma. Colostomy can be permanent or temporary. It may be indicated for intestinal cancer, diverticulitis, perforated bowel, radiation enteritis, obstruction, and Hirschsprung’s disease. It may also be indicated for spinal cord–injured patients where bowel management (bowel care and defecation time) averages 6 hours/wk prior to stoma formation, but decreases to 1.5 hours/wk after a left colostomy, thus improving quality of life (Munck et al, 2009). Abdominoperineal resection, with iliac colostomy, remains a standard treatment (Portier et al, 2005). With proper patient selection, laparoscopic colorectal surgery can be performed. Video-assisted, double barreled wet colostomy is minimally invasive. Table 7-21 lists the common types of colostomies. Colostomy output is generally more formed than ileostomy output. Some colostomates can “irrigate,” using a procedure similar to an enema to clean stool directly out of the colon through the stoma. This requires special irrigation appliances: an irrigation bag and a connecting tube (or catheter), a stoma cone, and an irrigation sleeve. A special lubricant is sometimes used on the stoma in preparation for irrigation. Following irrigation, some colostomates can use a stoma cap, a one- or two-piece system that simply covers and protects the stoma. This procedure is usually done to avoid the need to wear an appliance.

ASSESSMENT, MONITORING, AND EVALUATION

Common Types of Colostomies

Colostomy Type

Description

Temporary Colostomy

Allows the lower portion of the colon to rest or heal. It may have one or two openings (if two, one will discharge only mucus).

Permanent Colostomy

Usually involves the loss of part of the colon, most commonly the rectum. The end of the remaining portion of the colon is brought out to the abdominal wall to form the stoma.

Sigmoid or Descending Colostomy

The most common type of ostomy surgery, in which the end of the descending or sigmoid colon is brought to the surface of the abdomen. It is usually located on the lower left side of the abdomen.

Transverse Colostomy

The surgical opening created in the transverse colon resulting in one or two openings. It is located in the upper abdomen, middle or right side.

Loop Colostomy

Usually created in the transverse colon. This is one stoma with two openings; one discharges stool, the second discharges mucus.

Ascending Colostomy

A relatively rare opening in the ascending portion of the colon. It is located on the right side of the abdomen.

Source: United Ostomy Association, Inc. What is ostomy? at http://www.uoa.org/ ostomy_main.htm, accessed March 31, 2005.

CLINICAL INDICATORS Genetic Markers: Colostomy is a surgical procedure, occasionally used for a congenital condition. Clinical/History Height Weight BMI Diet history I & O, hydration status Diarrhea or constipation

Renal stones? Lab Work H&H Serum Fe, ferritin Na, K Gluc

Alb, transthyretin Ca, Mg Chol, Trig Transferrin, TIBC Serum B12 Serum folate PT or INR

INTERVENTION OBJECTIVES • To avoid major problems of blockage, increased flatulence, and problems with certain foods, preoperative teaching and postoperative follow-up must include food selection guidance.


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SAMPLE NUTRITION CARE PROCESS STEPS Poor Nutritional Quality of Life—Ostomy Assessment: I & O records or food diary; weight fluctuations. Complaints of abdominal discomfort and unplanned ostomy output of large quantity. Nutrition Diagnosis (PES): Poor nutritional quality of life related to fear and frequent ostomy output as evidenced by weight fluctuations and reports of GI discomfort after meals.

Intervention: Educate about how to meet estimated nutritional needs using tolerated foods; how to track GI symptoms and food tolerances using a food diary.

• •

Monitoring and Evaluation: Improved I & O records; stabilized weight. Fewer or no GI distress following meals when foods poorly tolerated are omitted from the diet. Ostomy output more predictable and normal.

• Speed wound healing and recovery. • Correct weight loss or malnutrition from GI blood loss, anemia, protein malabsorption, steatorrhea. • Prevent watery or unscheduled bowel movements. Correct or prevent dehydration. • Individualize the diet: Eat regularly, avoid odor-causing foods, and monitor food preferences. Normalize nutritional quality of life as much as possible. • Avoid infection and skin irritants.

FOOD AND NUTRITION • Early oral feeding in the patients undergoing colorectostomy is feasible, safe, and associated with reduced postoperative discomfort; it can accelerate the return of bowel function and improve rehabilitation (Zhou et al, 2006). Most people can resume oral diet 2 days after surgery. • Progress from a liquid to a low-residue diet. To speed healing, the formula or diet should also be high in protein, energy, vitamins, and minerals. • Diet should provide normal or increased salt intake. One to two quarts of fluid, taken between meals, should be ingested daily. • Gradually introduce new foods; if done slowly, offending foods can be identified and obstruction can be controlled or prevented. Foods that may not be tolerated include: 1. Foods that may cause loose stools or diarrhea: apple juice, prune juice, dried beans, chocolate, green beans, raw fruits and raw vegetables, fried foods, highly spiced foods, broccoli, and leafy green vegetables. 2. Gas or odor-causing foods: alcohol (beer), beans, onions, cabbage, broccoli, cauliflower, Brussels sprouts, fish, eggs, asparagus, and garlic. Fresh parsley is a natural deodorizer. 3. Foods that cause urinary odor include asparagus and seafood. 4. Beets and red gelatin can cause abnormal stool coloration.

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5. Avoid high fiber foods: granola, bean sprouts, bamboo shoots, bran, whole-kernel corn, mushrooms, celery, nuts, pineapple, popcorn, coleslaw, apple skins, seeds, or coconut. 6. Foods most often avoided because of an ostomy include fresh fruits and vegetables such as cabbage, beans, onions, hot dogs, sausages and other meats with casings. Foods that thicken stool include applesauce, bananas, marshmallows, rice, pasta, peanut butter, tapioca, and yogurt. Progress to a high-fiber diet with short-fibered foods. If calcium oxalate stones develop after the colostomy, diet should provide a high-fluid intake. Restrict intake of oxalates from spinach, rhubarb, wild greens, coffee and tea, and chocolate. Signs of blockage include: almost constant spurt of highly watery stool, bloating, cramping, swelling around stoma, strong odor of stool, nausea, vomiting, and pain. Avoid eating solid food, and do not take any laxatives or stool softeners. Drink a hot, caffeinated beverage; try a hot bath; gently massage the abdomen; and apply a pouch that has a larger opening.

Common Drugs Used and Potential Side Effects • Probiotics and prebiotics may be useful for return of gut immunity. • Polyethylene glycol solution may be used as an alternative fluid regimen for colostomy irrigation. • Patients with electrolyte concerns should be carefully monitored if sodium phosphate preparations (Osmoprep, Visicol) are used for colonscopy preparation (Lichtenstein, 2009). • Prednisone: Restrict excessive sodium intake. Monitor nitrogen, calcium, and potassium losses when used over a long period of time. • Lomotil is a stool thickener and deodorizer; use plenty of fluids. • Bulk-forming agents such psyllium (Metamucil) may be useful. Increased peristalsis occurs.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Approximately 6 weeks are required to acclimate the bowel to new procedures of irrigation. Enemas are used to wash the bowel up to the ileocecal valve (with 1000 mL of tap water). Constipation can occur with dehydration; therefore, adequate intake of fluid and fiber is important. • Use of a commercial deodorant in the colostomy bag is preferred for eliminating highly flavored or nutrientdense foods.


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• Instruct the patient to eat slowly, chew foods well, and avoid swallowing air. • Irrigations should not be performed when there is vomiting or diarrhea. Working with an enterostomal therapist can be helpful for more suggestions. • Regular mealtimes should be encouraged. • Reassurance is needed, without misleading the patient. Some colostomies are permanent (Riansuwan et al, 2009). Quality of life may decrease after the procedure (Yau et al, 2009). • If a temporary colostomy is performed, a patient may be evaluated for a reversal of the colostomy where the remaining colon and rectum must be examined for normalcy.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort. • Proper ostomy care requires careful and constant hand washing. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Colostomy—Medicine Net http://www.medicinenet.com/colostomy_a_patients_perspective/ article.htm

Colostomy Guide http://www.cancer.org/docroot/CRI/content/CRI_2_6x_Colostomy.asp

Medline Plus http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/002942.htm

United Ostomy Association (UOA) http://www.uoa.org/ostomy_main.htm

OSTOMY: COLOSTOMY—CITED REFERENCES Lichtenstein G. Bowel preparations for colonoscopy: a review. Am J Health Syst Pharm. 66:27, 2009. Munck J, et al. Intestinal stoma in patients with spinal cord injury: a retrospective study of 23 patients. Hepatogasterenterology. 55:2125, 2009. Portier G, et al. Use of malone antegrade continence enema in patients with perineal colostomy after rectal resection. Dis Colon Rectum. 48:499, 2005. Riansuwan W, et al. Nonreversal of Hartmann’s procedure for diverticulitis: derivation of a scoring system to predict nonreversal. Dis Colon Rectum. 52:1400, 2009. Yau T, et al. Longitudinal assessment of quality of life in rectal cancer patients with or without stomas following primary resection. Dis Colon Rectum. 52:669, 2009. Zhou T, et al. Early removing gastrointestinal decompression and early oral feeding improve patients’ rehabilitation after colorectostomy. World J Gastroenterol. 2:2459, 2006.

OSTOMY: ILEOSTOMY NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND

Life ART image copyright © 2010 Lippincott Williams & Wilkins. All rights reserved.

Used to treat intractable cases of ulcerative disease, Crohn’s disease, polyposis, and colon cancer, an ileostomy is a surgical procedure (stoma/opening formation) that brings the ileum through the abdominal wall. It may be temporary or permanent. This procedure causes a decrease in fat, bile acid, and vitamin B12 absorption, as well as greater losses of sodium and potassium. Patients will be incontinent of gas and stool. Ideally, the ileocecal valve can be kept to decrease bacterial influx into the small intestine. Of these patients, 50–70% will have recurrent disease. Effective ostomy management is important and involves establishment of an effective system for managing altered dietary and fluid intake, maintaining fluid and electrolyte balance, and preventing food blockage (Doughty, 2005). Subtotal colectomy with ileostomy is a safe and effective treatment for patients requiring urgent surgery (Hyman et al, 2005). Interval ileal pouch–anal anastomosis reconstruction without a stoma after colectomy equals the more traditional protocol in terms of clinical outcome but yields lower hospital costs and probably a shorter length of hospital stay (Swenson et al, 2005). Table 7-22 describes the procedures for ileostomy.


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TABLE 7-22

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Ileostomy Procedures

Procedure

Description

Ileoanal Anastomosis

This is now the most common alternative to the conventional ileostomy. Technically, it is not an ostomy since there is no stoma. In this procedure, the colon and most of the rectum are surgically removed, and an internal pouch is formed out of the terminal portion of the ileum. An opening at the bottom of this pouch is attached to the anus such that the existing anal sphincter muscles can be used for continence. This procedure should only be performed on patients with ulcerative colitis or familial polyposis and who have not previously lost their rectum or anus. It is also called J-pouch, pull-thru, endorectal pullthrough, pelvic pouch, or a combination of these terms.

Continent Ileostomy

This surgical variation of the ileostomy is also called a Kock pouch. A reservoir pouch is created inside the abdomen with a portion of the terminal ileum. A valve is constructed in the pouch, and a stoma is brought through the abdominal wall. A catheter or tube is inserted into the pouch several times a day to drain feces from the reservoir. This procedure has generally been replaced in popularity by the ileoanal pouch. A modified version of this procedure called the Barnett continent ileal reservoir is performed at a limited number of facilities.

Source: United Ostomy Association, Inc. What is ostomy? at http://www.uoa.org/ostomy_main.htm, accessed March 31, 2005.

ASSESSMENT, MONITORING, AND EVALUATION

INTERVENTION OBJECTIVES

CLINICAL INDICATORS Genetic Markers: Ileostomy is a surgical procedure, occasionally used for a congenital condition. Clinical/History

Lab Work

Height Weight BMI Diet history Stool (occult blood) BP

H&H Serum Fe, ferritin BUN, Creat Na, K Alb, transthyretin

Transferrin TIBC Gluc WBC Ca, Mg Serum B12 Schilling test if needed Serum folate

• Modify the diet to counteract malabsorption of nutrients secondary to diarrhea, protein, and fluid losses, negative nitrogen balance from nutrient loss, and anorexia. • Correct any anemia caused by inadequate intake or blood losses. • Counteract weakness and muscle cramping from potassium losses. • Provide increased energy intake during periods of fever or infection. • Replenish calcium to reverse losses caused by steatorrhea and bone density loss if steroid therapy is used. • Prevent gallstones, renal oxalate stones, bacterial overgrowth, and fatty acid malabsorption.

FOOD AND NUTRITION

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Fluid Intake Assessment Data: I & O, weight changes, signs of dehydration, high output from ileostomy. Nutrition Diagnoses (PES): Inadequate fluid intake related to losses from ileostomy and insufficient intake as evidenced by I & O records (intake 1200 mL, output 1600 mL/d). Interventions: Food and nutrient delivery: Calculate needs, provide extra liquids with meals, offer a beverage every few hours. Educate: Discuss the need for extra fluids when ileostomal losses are increased, during febrile periods, when there is vomiting. Monitoring and Evaluation: I & O records, weight records, fewer signs of dehydration (poor skin turgor, sunken eyeballs, etc).

• Preoperatively: Fiber and lactose intolerances are common; alter diet accordingly. With strictures, avoid popcorn, nuts, seeds, mushrooms, celery, fruit skins, and vegetable skins. Have the patient chew thoroughly. • Postoperatively: Provide a high-energy, high-protein diet for wound healing that is low in excess insoluble fiber. Avoid the high-fiber foods suggested for preoperative care for about 4 weeks. Pectin in apples and oligosaccharides in oatmeal may be beneficial to add back first. Spinach or parsley are natural intestinal deodorizers, but beware of excesses of oxalate-rich foods. • The patient needs an adequate intake of protein (provided by low-fat sources such as lean meats and egg white), vitamin B12 (provided by liver, fish, and eggs), folacin, calcium, magnesium, iron, sodium, vitamin C, and potassium. • Diet should provide an adequate amount of fluids, especially in hot weather. Add salt if needed. • Apple juice has chemoprotective properties for human colon cells. Intake of apple juice results in bioavailable polyphenols in the gut lumen, which could contribute


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to reduced genotoxicity, enhanced antigenotoxicity and favorable modulation of GSTT2 gene expression (Veeriah et al, 2008). • Since obesity can cause more discomfort, a weight management plan may be useful.

• Eating before bedtime should be avoided to lessen discomfort. • More than half of patients operated with proctocolectomy will need surgical intervention within 20 years; the failure rate is more than 10% and complications must be addressed (Wasmuth et al, 2009).

Common Drugs Used and Potential Side Effects • Corticosteroids: With prednisone, restrict excessive sodium intake and monitor nitrogen and calcium losses. The corticosteroid budesonide (Entocort) may be administered to increase the absorptive capacity of the intestinal mucosa in patients with ileostomies (Ecker et al, 2005). Side effects may include increased appetite and weight gain, hypokalemia, and elevated CRP. • Lomotil is a stool thickener and deodorizer. Plenty of fluids should be used. • Probiotics and prebiotics may be useful to help with recovery of gut immunity. Research is underway for the use of a special form of Bacteroides ovatus (Hamady et al, 2008). • Psyllium (Metamucil) is used as a bulk-forming agent. Increased peristalsis will occur.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Use of fish oil may be beneficial during periods of inflammation.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain which foods are common sources of the needed nutrients in a diet or suggest supplementation with multivitamins and minerals. Encourage use of apple juice and other protective foods as tolerated. • Monitor individual tolerance to offending foods such as gas-forming or fried foods, highly seasoned foods, nuts, raisins, and pineapple. Foods that may cause rapid intestinal transit or discomfort may include dried fruits, prune juice, fresh strawberries or peaches, coconut, nuts, seeds, cabbage, celery, bamboo shoots, corn, and milk. • An enterostomal therapist may be of assistance. • Discuss replacement of fluid and sodium, especially during hot weather.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual who may be experiencing diarrhea and related discomfort. • Proper ostomy care requires careful and constant hand washing. • If home TF or PN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Continent Ileostomy http://www.medicinenet.com/caring_for_a_continent_ileostomy/ article.htm

Ileostomy http://digestive.niddk.nih.gov/ddiseases/pubs/ileostomy/

Ilesotomy Guide—American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_6x_Ileostomy.asp

Jackson Gastroenterology http://www.gicare.com/pated/ecdgs11.htm

Mayo Clinic—Ostomy http://www.mayoclinic.com/health/ostomy/SA00072

United Ostomy Association http://www.uoa.org/ostomy_facts_ileostomy.htm

OSTOMY: ILEOSTOMY—CITED REFERENCES Doughty D. Principles of ostomy management in the oncology patient. J Support Oncol. 3:59, 2005. Ecker KW, et al. Long-term treatment of high intestinal output syndrome with budesonide in patients with Crohn’s disease and ileostomy. Dis Colon Rectum. 48:237, 2005. Hamady ZZ, et al. Identification and use of the putative Bacteroides ovatus xylanase promoter for the inducible production of recombinant human proteins. Microbiology. 154:3165, 2008. Hyman NH, et al. Urgent subtotal colectomy for severe inflammatory bowel disease. Dis Colon Rectum. 48:70, 2005. Swenson BR, et al. Modified two-stage ileal pouch-anal anastomosis: equivalent outcomes with less resource utilization. Dis Colon Rectum. 48:256, 2005. Veeriah S, et al. Intervention with cloudy apple juice results in altered biological activities of ileostomy samples collected from individual volunteers. Eur J Nutr. 47:226, 2008. Wasmuth HH, et al. Long-term surgical load in patients with ileal pouch-anal anastomosis. Colorectal Dis. 11:711, 2009.

PERITONITIS NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND In peritonitis, inflammation of the peritoneal cavity due to infiltration of intestinal contents occurs. Contents from

such conditions as ruptured appendix, gastric or intestinal perforation such as in diverticulitis, trauma, fistula, anastomotic leaks, or failed peritoneal dialysis (PD) may initiate the problem.


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Bacterial peritonitis is a major cause of morbidity in pediatric PD patients and can lead to catheter removal, hospitalizations, peritoneal membrane dysfunction, and sepsis (Chand et al, 2009). Spontaneous bacterial peritonitis is also common in patients with cirrhosis and ascites because of bacterial translocation. The diagnostic evaluation of ascites involves an assessment of its cause by determining the serumascites albumin gradient and the exclusion spontaneous bacterial peritonitis (Hou and Sanyal, 2009). Peritonitis in liver transplant patients may suggest organ rejection (Macedo et al, 2005). Prophylactic antibiotics and omentectomy at catheter insertion are useful (Chand, 2009). Aggressive nutritional supplementation pre- and postoperatively is suggested (De Frietas et al, 2008). It is important to avoid refeeding syndrome.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Peritonitis is the result of infection and not genetic origins. Ileus Sepsis? Height X-rays Weight Paracentesis BMI (250 polyDiet history morphonuAbdominal pain, cleate cells) tenderness Laparoscopy Abdominal rigidity Lab Work (washboard appearance) H & H Serum Fe, Fever? ferritin BP WBC I&O Clinical/History

BUN, Creat Gluc Alb, transthyretin CRP Na, K Ca, Mg TLC

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INTERVENTION OBJECTIVES • Correct fluid/electrolyte imbalances when present. Vigorous IV rehydration is needed. • Provide bowel rest and recovery. PN may be better than NG feeding but further studies into dualenteral nutrition and PN are needed (De Frietas et al, 2008). • Improve nutritional status, especially if patient has been malnourished over a period of time or if there is anorexia or ileus. • Avoid high risk for refeeding syndrome (De Frietas et al, 2008).

FOOD AND NUTRITION • Patient generally is NPO with IV feedings for at least 24 hours. Progress as tolerated to a soft or general diet appropriate for the condition that caused the peritonitis originally. • Increase protein intake to correct catabolic state. Increase calories because basal energy expenditure is generally elevated by 10–17%.

Common Drugs Used and Potential Side Effects • Ciprofloxacin is effective in the treatment. Other antibiotics may be used for bacterial peritonitis. Monitor for specific side effects. • Probiotics may be useful; research continues in this area. • PPIs suppress gastric acid secretion, allowing bacterial colonization of the upper GI tract, this may predispose to bacterial overgrowth, translocation and peritonitis (Bajaj et al, 2009). Research is needed in this area.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Energy Intake Assessment Data: I & O records, weight, severe abdominal pain, intake 25% in past 24 hours, fever 102F. Nutrition Diagnoses (PES): Inadequate energy intake related to inability to eat orally and abdominal pain as evidenced by intake 25% in past day and fever demands about 21% higher energy needs than normal. Interventions: IV fluids with dextrose until able to eat orally. Monitor for readiness to eat again, based on drop in fever, return of bowel sounds, tolerance for soft or bland foods. Monitoring and Evaluation: Gradual return to oral diet with improved I & O records; weight returning to usual. No fever or signs of abdominal pain or peritonitis No signs of refeeding.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • With patients on CAPD, diet may need to be altered similar to the diet typical for renal patients. • Discuss diet appropriate for the illness of origin (such as diabetes, hypertension, toxemia, or renal disease).

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.


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For More Information •

Mayo Clinic http://www.mayoclinic.com/health/peritonitis/DS00990/ DSECTION%3Dcauses

NIH—Peritonitis http://www.nlm.nih.gov/medlineplus/ency/article/001335.htm

Peritonitis http://www.nlm.nih.gov/medlineplus/ency/article/001335.htm

Chand DH, et al. Multicenter study of effects of pediatric peritoneal dialysis practices on bacterial peritonitis [published online ahead of print 25 August 2009]. Pediatr Nephrol. 25:149, 2009. De Frietas D, et al. Nutritional management of patients undergoing surgery following diagnosis with encapsulating peritoneal sclerosis. Perit Dial Int. 28:271, 2008. Hou W, Sanyal AJ. Ascites: diagnosis and management. Med Clin North Am. 93:801, 2009. Macedo C, et al. Sclerosing peritonitis after intestinal transplantation in children. Pediatr Transplant. 9:187, 2005.

PERITONITIS—CITED REFERENCES Bajaj JS, et al. Association of proton pump inhibitor therapy with spontaneous bacterial peritonitis in cirrhotic patients with ascites. Am J Gastroenterol. 103;1130, 2009.

SHORT BOWEL SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND SBS is the predominant cause of intestinal failure, with a high degree of morbidity and mortality. Intestinal failure involves reduction of gut mass below the minimal amount needed for nutrient absorption. SBS involves surgical resection of a portion of the small bowel, compromising the absorptive surface and resulting in malabsorption (especially if more than 50% of the small intestine has been removed). Malnutrition from maldigestion, malabsorption diarrhea, and steatorrhea may result. A bowel resection that results in SBS may be due to Crohn’s disease, intestinal cancer, scleroderma, or fistula in adults; or it may be due to necrotizing enterocolitis, intestinal atresia, or mesentery artery occlusion in infants. If only 30% of the small intestine remains in an adult (or 30 cm in infants), the resulting malabsorption may be life threatening. Problems are significant when more than 70% of the bowel is resected, unless the terminal ileum and ileocecal valve remain. Every attempt should be made to keep the ileocecal valve to prevent contamination of the small intestine. See Table 7-23 regarding the implications of bowel resections. Normal bowel length is about 600 cm. SBS generally leaves less than 150 cm of small intestine. A total of 100 cm is necessary to completely absorb bile salts; 50–70 cm of jejunum–ileum maintains minimal intestinal autonomy. The minimal length of functional bowel needed for enteral feeding is over 100 cm in the absence of an intact colon and over 60 cm in continuity with the colon. Patients with SBS require long-term PN. After massive intestinal resection, the intestine undergoes adaptation, and nutritional autonomy may be obtained if the adaptive process is supported by both nutritive and nonnutritive factors (Weale et al, 2005). Length of small intestine remaining after resection is the best predictor of the final success in terminating PN. Home PN may cost between $400 a day; most insurance companies cover up to $1 million, about 10 years of reimbursement.

Aggressive nutritional intervention is necessary for resolution of nutritional deficits and recovery of health. Early oral feeding after colorectal surgery is safe. Bowel adaptation takes about 1 year. Assessment must include oral intake, stool and urine output, serum electrolytes and visceral proteins, and body weight (DiBaise et al, 2006). Diarrhea and high stomal output are common problems and can lead to dehydration; hypokalemia; deficiencies of calcium, magnesium, and zinc; carbohydrate and lactose malabsorption; protein malabsorption; renal oxalate stone formation; cholesterol biliary stones; gastric acid hypersecretion; vitamin B12 or iron deficiency; fat-soluble vitamin deficiency; and diarrhea. See Table 7-24 for malabsorption concerns in SBS. Patient education and motivation are key factors in successful weaning from PN, where possible (DiBaise et al, 2006).

TABLE 7-23

Implications of Bowel Resections

Loss of jejunum. Ileum undergoes hyperplasia; length and absorption per centimeter increases. Loss of ileum. This is more serious than loss of jejunum because vitamin B12 and bile salts will be reabsorbed poorly as a result. The ileocecal valve keeps colonic bacteria out of the small intestine and regulates chyme flow. Some colonic adaptation occurs during the next 2–5 years. Loss of colon. Overall, with removal of the colon versus the small intestine, fewer malabsorption problems occur. Loss of electrolyte and water-absorbing capacity occurs, as well as loss of salvage absorption of CHO and other nutrients. Most oxalate absorption occurs here. In short bowel syndrome (SBS), short-chain triglycerides have a precursor in pectin; oligosaccharides increase O2 uptake in the colon, thereby maintaining gut integrity. Early refeeding (i.e., free fatty acids, sugars, proteins) stimulates mucosal growth. Hyperphagia can increase enterocyte production. Adaptation requires adequate nutrition, intraluminal nutrients, and bile and pancreatic secretions. Enhancers of the adaptive process seem to include gastrin, glutamine, growth hormone, insulin, short-chain fatty acids, fats, some dietary fibers, cholecystokinin (CCK), glucagon, insulin-like growth factor I, neurotensin, and glucose.


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TABLE 7-24 Malabsorption Concerns in Short Bowel Syndrome Bacterial overgrowth, if ileocecal valve is absent Decreased bile acid concentration (with loss of ileum and bacterial overgrowth)

Barium followthrough (BaFT) examination Schilling test Serum B12

Serum amylase, lipase Serum copper Bile acid breath test

457

Lactose tolerance test Hydrogen breath test Fecal fat test

Decreased surface area and lessened fluid reabsorption Dumping syndrome from rapid transit and reduced bowel length Gastric acid oversecretion with resulting damage to duodenal cells and altered pH, thus affecting pancreatic enzyme and bile activity Maladaptive remaining small bowel, especially from original bowel disease, lactase deficiency Pancreatic enzyme activity loss from duodenum, with malnutrition

The use of trophic substances may increase the absorptive function of the remaining gut. Glucagon-like peptide 2 (GLP-2) has been shown to improve intestinal absorption in SBS patients; it reduces fecal weight and enables SBS patients to maintain their intestinal fluid and electrolyte absorption at lower oral intakes (Jeppesen et al, 2009). Current guidelines, however, suggest that the use of growth hormone, glutamine and GLP-2 should not be recommended in patients with short bowel syndrome (Van Gossum et al, 2009). Serial transverse enteroplasty (STEP) procedure is a safe way to lengthen the small bowel in patients with SBS (Ehrlich et al, 2007). Surgical bowel lengthening should be considered in any chronically PN-dependent patient when there is substantial bowel dilation, regardless of remnant bowel length (Thompson and Sudan, 2008). ITx may also restore quality of life by recovery of normal motility and absorptive capacity. While high-dose immunosuppression is a potential problem, advances in transplantation hold promise as an alternative to intestinal failure and chronic dependence on CPN.

ASSESSMENT, MONITORING, AND EVALUATION

INTERVENTION OBJECTIVES • Determine the location and amount of the intestine that was resected to predict likelihood of diarrhea, malabsorption, and malnutrition (see Table 7-24). Provide nutrient replacements, dependent on area of resection (proximal jejunum—calcium, iron, magnesium, protein, CHO, and fat; terminal ileum—bile acids and intrinsic factor-bound vitamin B12). • Manage post surgical phases. The first phase lasts 1–3 months, massive diarrhea and limited absorption; the second phase: 4–12 months where weight gain begins and absorption improves. In the last phase between 13 and 24 months, maximal adaptation occurs, with possible discontinuation of PN when fluid is 7 L daily and when energy intake is sufficient for desired weight goal. • Support hyperphagia, in which the amount of protein absorbed increases relative to the amount of remnant small bowel length. Try weaning off PN without trophic factors. If this is unsuccessful, a trophic factors should be attempted (Steiger et al, 2006). • Prevent and correct fluid and electrolyte imbalances and dehydration. Oral intake could aggravate already massive losses of fluid (3–10 L/d is common). Immediately postoperatively, NPO with IV fluid replacement is likely. Eventually switch to oral intake as tolerated. • Use remaining bowel surface and maximize efficacy. Prevent atrophy of small bowel mucosa, catheter sepsis, metabolic bone disease, and liver disease with long-term use of CPN. Carefully monitor for signs and symptoms of these problems and manage accordingly.

CLINICAL INDICATORS Genetic Markers: SBS is a surgical procedure. Clinical/History

Lab Work

Height Weight BMI Diet history Weight changes I&O Steatorrhea Stool output Dehydration? Urinary output DEXA bone density scan

H&H Serum Fe, ferritin Transferrin CRP, ESR D-xylose absorption Serum gastrin (increased) Ca, Mg 25-hydroxyvitamin D level

Alk phos Na (serum, urine, stool) K (serum, urine, stool) Fecal nitrogen GTT Gluc RBP N balance Serum oxalate Alb, transthyretin

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Parenteral Infusion Assessment Data: Calculations of energy needs showing PN infusion at a rate exceeding goal by 25%; hypophosphatemia, hypokalemia and signs of refeeding syndrome. Nutrition Diagnoses (PES): Excessive parenteral infusion (NI 2.4) related to order for CPN solution that exceeds estimated needs by 25% (200 kcal/d) as evidenced by signs of refeeding syndrome with hypophosphatemia and hypokalemia. Interventions: Reduction in CPN infusion to meet rather than exceed requirements Intervention code. Monitoring and Evaluation: Consistent monitoring of labs until resolution of refeeding syndrome; tolerance of CPN solution with no further complications.


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• Correct symptoms of deficiency and malabsorption, when possible, for vitamins B12, A, D, E, and K and for the minerals zinc, potassium, and magnesium. • Minimize weight loss (approximately 10 lb monthly until adaptation occurs). Maximize energy intake from fats and carbohydrates without worsening the diarrhea. • Omit lactose if not tolerated; provide adequate calcium replacements. • Decrease oxalate from the diet to reduce renal stone formation. Excess bile in the colon from decreased ileal absorption enhances absorption of free oxalate (normally only 10–15% is absorbed). • Control or prevent gallstone formation (increased risk of two to three times normal), anemia, PLE, peptic ulcer from increased gastric acid secretion, and liver disease (often from home CPN). Parenteral fish-oil lipid or oliveoil emulsions are now more available. • Allow remaining intestine to compensate over time by hypertrophy of villi and increased diameter. Home CPN is expensive but can be lifesaving for months or years. Transitional feedings may be needed over several months from PN to oral diet. For care of colostomy or ileostomy, see appropriate entries.

FOOD AND NUTRITION • First Postoperative Phase: IV nutrition or CPN may be appropriate immediately before and approximately 5 days after surgery to allow rest. Determine whether the patient has problems with bloating. The first phase involves extensive diarrhea greater than 2 L daily; advance CPN slowly to avoid refeeding syndrome. At the end of this time, if diarrhea continues to be greater than 2 L, CPN may be lifelong. • Second Postoperative Phase: Diarrhea is lessened and intestinal adaptation begins; CPN may be slowly reduced and polymeric TF started at a slow, continuous rate according to stomal output or stool output. Provide 40–60 kcal/kg and 1.2–1.5 g protein/kg. Providing patients with enteral nutrition, glutamine, dietary fiber, and r-hGH during bowel rehabilitation therapy allows weaning from CPN. If weight loss is greater than 1 kg/wk, CPN may need to be restarted. • Nocturnal enteral rehydration is an intervention using ORS through PEG tubes at night; this allows for earlier discontinuation of CPN and improved fluid absorption. • Third Postoperative Phase: Complete bowel adaptation begins as TF is tolerated and oral diet is slowly resumed (from 2 months to 1 year). Six small feedings that are high CHO and low fat may be tolerated (60% CHO, 20% protein, 20% fat, with a limit on MCT of 40 g/d). With no colon, the jejunostomy feeding may need to be 40–50% CHO, 20% protein, 30–40% fat. PN reductions can be made by either decreasing the days of PN infusion per week or decreasing the PN infusion volume equally across all days of the week. • Supplemental zinc, potassium, liquid magnesium, oral calcium (600–1000 mg), manganese, iron, vitamin C, selenium, B-complex vitamins (especially folic acid), and other nutrients may be needed. Determine needs based on site of resection and signs of malnutrition.

• Monitor for needs for vitamins A, E, and D; use watermiscible forms. Patients with SBS are depleted in dietderived carotenoids despite oral and IV multivitamin supplementation; reduction of PN lipid infusion may improve serum alpha-tocopherol concentrations (Luo et al, 2009). With antibiotic use, the patient will need extra vitamin K. • Lactose-restricted and oxalate-restricted diets may be needed for an extended period of time. Rhubarb, spinach, beets, cocoa and chocolate, sweet potatoes, strawberries, celery, and peanuts are high-oxalate foods. Nuts and nut butters, berries, Concord grapes, sweet potatoes and potatoes, and most vegetables have smaller amounts. • Omit alcoholic beverages and caffeine unless physician permits small quantities. • Taking fluids between instead of with meals may be helpful to reduce dumping. Restrict at first to 1500 mL; progress as tolerated. • With osmotic diarrhea, a reduction in simple carbohydrates and an increase in complex carbohydrates may be needed. Sorbitol, mannitol, and xylitol are usually poorly absorbed. • Restricted foods such as lactose may be attempted and added back to the diet if they are tolerated. Bowel adaptation occurs over time and may eventually lead the patient back to an unrestricted diet.

Common Drugs Used and Potential Side Effects (see Table 7-25) • Note: Most oral medications are poorly tolerated in this condition! Accelerated intestinal luminal transit time causes a reduction in absorption of certain antimicrobial agents, digoxin, hydrochlorothiazide, cyclosporine, cimetidine, mesalazine (5-aminosalicylic acid), oral contraceptives, and levothyroxine. • Dietary glutamine (GLN) or oral antibiotics (ABX) can blunt gut barrier dysfunction (Tian et al, 2009). Antibacterial drugs, antimotility drugs, antidiarrheal agents, H2 antagonists and PPIs, pancreatic enzymes, somatostatin analogs, antimicrobials, and trophic factors have been quite helpful in addition to nutritional therapy (Matarese and Steiger, 2006).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Probiotics and foods such as acidophilus or yogurt are useful aids in bowel adaptation phases. Not all probiotic bacteria have similar therapeutic effects. Research is available for probiotic supplementation for children with SBS (Wallace, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Importance of nutrition and supplementation must be discussed to prevent or correct malnutrition and


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TABLE 7-25

459

Medications Used in Short Bowel Syndrome

Medication

Description

Antibiotics

Tetracycline, Flagyl, Septra, or Cipro may be needed for bacterial overgrowth. Monitor hydrogen breath tests (especially with blind loop).

Antidiarrheals

Antidiarrheals such as Lomotil, Imodium, and codeine are useful. Liquid preparations often are better tolerated. If dehydration occurs, use oral rehydration therapy but not sports drinks, which do not have the adequate electrolyte replacements.

Bile salt replacements

Cholylsarcosine (CS) is a semisynthetic bile salt that may be useful in bile salt replacement therapy of short bowel syndrome (Furst et al, 2005).

Calcium supplements

Oral calcium supplements (OsCal or Tums four times daily) often are used to bind oxalate excesses and to decrease diarrhea. Do not take with a bulk-forming laxative or with an iron supplement. Increase water intake.

Cholestyramine

Cholestyramine may be used for choleraic diarrhea when less than 100 cm is resected and when the colon is in continuity; prevent excessive use. Take before meals. Nausea, vomiting, or constipation may occur.

Cimetidine or omeprazole

Cimetidine and omeprazole may be needed to decrease gastric hypersecretion; parenteral administration may be needed. Serum gastrin levels should be monitored. A dose two to three times higher than normal may be needed because of gastric hypersecretion; lack of sufficient time with intestinal mucosa leads to insufficient absorption. Vitamin B12 absorption decreases with use of these medications.

Clonidine

Clonidine can effectively reduce intestinal fluid and electrolyte losses and should be considered in patients with short bowel syndrome.

Growth hormone

Growth hormone increases water/sodium transport. It is useful in combination with glutamine and a modified diet, but results have been mixed.

Minerals

Liquid potassium and intravenous or intramuscular magnesium may be needed.

Pancreatic enzymes

Pancrelipase may improve fat and protein absorption after jejunal resection; results are variable.

Peptides

Glucagon-like peptide-2 (GLP-2) is an enteroendocrine peptide that is released in response to luminal nutrients; it seems to help support the adaptive response to resection (Martin et al, 2005).

Probiotics and prebiotics (synbiotics)

This type of therapy might be a potent modulator of intestinal flora and a promising strategy to treat short bowel patients with enterocolitis.

Vitamins

Vitamins that are chewable or in liquid form may be better tolerated. Parenteral vitamin B12 may be necessary. Add extra fat-soluble vitamins A, E, D, and K if deficiency occurs. Do not use vitamin C in excessively large quantities; some links with oxalate stones have been noted.

• • • •

malabsorption. After adaptation, significant energy intakes will be needed to maintain desired weight. Provide recipes or food-preparation tips to support the specific dietary regimen and to evaluate tolerances over time. Progression in diet is allowed when the small intestine adapts over several months. Use yogurt with live and active cultures. Discuss the need for free water. The use of home CPN is beneficial in many cases. Judicious use of home CPN in this setting requires careful clinical assessment on a patient-by-patient basis (Hoda et al, 2005). A supportive attitude from family and caregivers is essential. There are potential benefits of a multidisciplinary intestinal rehabilitation program. Interventions can help decrease incidence and economic impact of intestinal failure. Exercise, such as resistance training, can help regenerate lean body mass.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual.

• If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

E-medicine http://www.emedicine.com/ped/topic2088.htm

Short Bowel Syndrome http://digestive.niddk.nih.gov/ddiseases/pubs/shortbowel/

Short Bowel Syndrome—Pediatrics http://depts.washington.edu/growing/Assess/SBS.htm

SHORT BOWEL SYNDROME—CITED REFERENCES DiBaise JK, et al. Strategies for parenteral nutrition weaning in adult patients with short bowel syndrome. J Clin Gastroenterol. 40:S94, 2006. Ehrlich PF, et al. The 2 STEP: an approach to repeating a serial transverse enteroplasty. J Pediatr Surg. 42:819, 2007. Furst T, et al. Enteric-coated cholylsarcosine microgranules for the treatment of short bowel syndrome. J Pharm Pharmacol. 57:53, 2005. Hoda D, et al. Should patients with advanced, incurable cancers ever be sent home with total parenteral nutrition? A single institution’s 20-year experience. Cancer. 103:863, 2005. Jeppesen PB, et al. Short bowel patients treated for two years with glucagonlike Peptide 2: effects on intestinal morphology and absorption, renal function, bone and body composition, and muscle function. Gastroenterol Res Pract. 2009:616054, 2009. Luo M, et al. Prospective analysis of serum carotenoids, vitamin A, and tocopherols in adults with short bowel syndrome undergoing intestinal rehabilitation. Nutrition. 25:400, 2009.


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Martin GR, et al. Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome. Am J Physiol Gastrointest Liver Physiol. 288:431, 2005. Matarese L, Steiger E. Dietary and medical management of short bowel syndrome in adult patients. J Clin Gastroenterol. 40:S85S, 2006. Steiger E, et al. Indications and recommendations for the use of recombinant human growth hormone in adult short bowel syndrome patients dependent on parenteral nutrition. J Clin Gastroenterol. 40:S99S, 2006. Thompson J, Sudan D. Intestinal lengthening for short bowel syndrome. Adv Surg. 42:49, 2008.

Tian J, et al. Dietary glutamine and oral antibiotics each improve indexes of gut barrier function in rat short bowel syndrome. Am J Physiol Gastrointest Liver Physiol. 296:348, 2009. Van Gossum A, et al. ESPEN Guidelines on Parenteral Nutrition: gastroenterology. Clin Nutr. 28:415, 2009. Wallace B. Clinical use of probiotics in the pediatric population. Nutr Clin Pract. 24:50, 2009. Weale AR, et al. Intestinal adaptation after massive intestinal resection. Postgrad Med J. 81:178, 2005.

TROPICAL SPRUE NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Tropical sprue is an acquired disorder that presents with chronic diarrhea, anorexia, weight loss, megaloblastic anemia (folic acid deficiency), light-colored stools, diarrhea, weight loss, pallor, sore tongue (vitamin B12 deficiency), and easy bruising (vitamin K deficiency). Etiology is often bacterial, viral, or parasitic infection or toxins in spoiled food. Giardia intestinalis is a common culprit. Tropical sprue may occur after traveling to the Caribbean, southern India, and Southeast Asia. Tropical sprue causes progressive villus atrophy in the small intestine, similar to CD (“nontropical” sprue). Villi of the small intestinal mucosa become blunted, or obliterated. Treatment of tropical sprue includes folic acid and vitamin B12 replacement. However, even prolonged treatment fails to resolve malabsorption. While tropical sprue is less common than it was decades ago (Nath, 2005), sporadic tropical sprue is still an important cause of malabsorption in adults and in children in South Asia (Ramakrishna, 2007). Biomarker (13)C-sucrose breath test (SBT) to measure enterocyte sucrase activity can be used as a marker of small intestinal villus integrity and function (Ritchie et al, 2009). Enhanced magnification endoscopy can help identify patchy areas of partial mucosal atrophy, potentially reducing the need for blind biopsies (Lo et al, 2007).

ASSESSMENT, MONITORING, AND EVALUATION

Gas, indigestion Paleness Biopsy Enhanced magnification endoscopy (EME) Lab Work Gluc SBT

Na, K H & H, Serum Fe, ferritin (decreased) Alb, transthyretin (decreased) Serum B12 (decreased) Serum folate (decreased)

Ca (decreased) Mg PT or INR (altered)

INTERVENTION OBJECTIVES • Provide fluids and electrolytes. • Differentiate between tropical sprue and CD. Control diarrhea, which leads to malabsorption and malnutrition over time. • Improve or correct folic acid, vitamin B12, and vitamin K deficiencies. Treat tropical sprue with folate and vitamin B12 cures the macrocytic anemia and the accompanying glossitis. • Avoid fatty foods that can cause oily, foul-smelling stools.

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function Assessment Data: Diarrhea, fever, macrocytic anemia, biopsy showing flattened villi and diagnosis of tropical sprue.

CLINICAL INDICATORS Genetic Markers: An infectious cause is suspected in tropical sprue. Clinical/History Height Weight BMI

Diet history Weight loss? I & O; dehydration?

Malabsorption, especially for xylose Glossitis Cramps, nausea

Nutrition Diagnoses (PES): Abnormal GI function related to infectious process as evidenced by diarrhea, macrocytic anemia, and flattened villi on biopsy. Interventions: Provide folic acid and vitamin B12 in supplemental form along with antibiotic therapy; extra fluids, sodium and potassium as needed. Progress to low-fat diet. Monitoring and Evaluation: Improvement in macrocytic anemia; resolution of diarrhea.


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FOOD AND NUTRITION • Use a regular diet with supplements of vitamin B12 and folic acid. Good sources of folacin include liver, kidney, yeast, leafy greens, lean beef, and eggs. Good sources of vitamin B12 include meat, poultry, fish, dairy products, and eggs. • Avoid meals with fatty foods. • Diet should provide sufficient amounts of energy intake, protein, calcium, iron, and vitamins. • Extra fluid may be needed for dehydration. • No gluten restriction is needed.

Common Drugs Used and Potential Side Effects • Tetracycline may be used; do not take within 2 hours of a calcium-containing supplement or meal as calcium makes the drug less effective. • Vitamin supplements are required, especially for vitamin B12, folate, and vitamin K. Calcium may also be needed. Avoid excesses of any single nutrient for an extended time period. • Suggest use of probiotics such as yogurt with live and active cultures during antibiotic therapy. Intestinal flora modifiers (e.g., Lactobacillus acidophilus, Lactinex, Bacid) also help recolonize normal intestinal flora in people on antibiotics. A common order is three to four packages every day for 3 days in adults. They may be mixed with water for TFs.

Herbs, Botanicals, and Supplements

461

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain to the patient which foods are good sources of folic acid and vitamin B12. • Describe good sources of protein and calories from the diet. • Describe how to follow a low-fat diet and how to use MCT oil in cooking.

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

NIH—Tropical Sprue http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/000275.htm

Tropical Sprue http://www.intelihealth.com/IH/ihtIH/WSIHW000/9339/10902.html

TROPICAL SPRUE—CITED REFERENCES Lo A, et al. Classification of villous atrophy with enhanced magnification endoscopy in patients with celiac disease and tropical sprue. Gasdtrointest Endosc. 66:377, 2007. Nath SK. Tropical sprue. Curr Gastroenterol Rep. 7:343, 2005. Ramakrishna BS. Tropical malabsorption. Postgrad Med J. 82:779, 2007. Ritchie BK, et al. 13 C-sucrose breath test: novel use of a noninvasive biomarker of environmental gut health. Pediatrics. 124:620, 2009.

• Herbs and botanical supplements should not be used without discussing with the physician.

WHIPPLE’S DISEASE (INTESTINAL LIPODYSTROPHY) NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Whipple’s disease is a chronic systemic inflammatory disease caused by Tropheryma whipplei. The hallmark of Whipple’s disease is invasion of the intestinal mucosa with macrophages incompetent to degrade T. whipplei (Moos et al, 2010). This condition presents with weight loss, arthralgias, and diarrhea that involves infiltration of the small intestine with glycoprotein-laden macrophages in varying body tissues (Muller et al, 2005). Endocarditis and heart murmur are common. Infection may spread to the central nervous system, which may lead to loss of memory, confusion, or disturbed gait. Treatment is antibiotic therapy.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Decreased production of Interleukin (IL)-12, IL-2 and Interferon (IFN)-g accompanied by an increased secretion of IL-4 may predispose patients for an infection with T. whipplei (Deriban and Marth, 2006).


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Clinical/History Height Weight BMI Weight loss? Wasting? Diet history Fever I&O Malabsorption, cholestasis Gray to brown skin pigmentation

Lymphadenopa- CRP (elevated?) Acid-Schiff thy (PAS)-positive Confusion, foamy memory loss macrophages Edema? T whipplei DNA— Duodenal polymerase biopsy; villous chain reaction blunting (PCR) assays Skin biopsy H&H Lab Work (decreased) Serum Fe, Alk phos ferritin Na, K Transferrin Ca, Mg Alb (decreased)

• Provide adequate fluid intake to reduce fever and replenish tissues. • If edema is a problem, control excess sodium.

Common Drugs Used and Potential Side Effects • Antibiotic treatment is mandatory and leads to a rapid clinical improvement and remission in most patients: 2-week parenteral cephalosporins followed by long-term therapy with trimethoprim-sulfamethoxazole. Trimethoprim-sulfamethoxazole (Bactrim) combinations may have numerous side effects; monitor closely for anorexia, nausea, vomiting, and diarrhea.

Herbs, Botanicals, and Supplements INTERVENTION OBJECTIVES • Reduce fever and inflammatory processes. • Correct malnutrition and malabsorption. • Correct anemia, iron overloading, or hypoproteinemia when present. • Prevent or correct dehydration and electrolyte imbalances.

FOOD AND NUTRITION • Use a high-protein/high-calorie diet appropriate for the patient’s age and sex. • Ensure that the diet includes sufficient vitamins and minerals, especially for vitamin D and calcium, when steatorrhea is a problem. Vitamins A, B-complex, and K may also be needed.

• Use probiotic or prebiotic foods when possible to replenish “good” gut bacteria. • Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss inclusion of high-quality proteins in the diet. Frequent snacks may be beneficial if large meals are not tolerated. • Provide lists for nutrient-dense foods rich in specific and needed nutrients (e.g., iron, calcium, etc).

Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information SAMPLE NUTRITION CARE PROCESS STEPS

NIH—Medline http://www.nlm.nih.gov/medlineplus/ency/article/000209.htm

Weight Loss

Whipple’s Disease http://www.whipplesdisease.net/

Assessment Data: I & O, weight loss, BMI, fever; low albumin, elevated CRP

Whipple’s Disease Info http://www.whipplesdisease.info/

Nutrition Diagnoses (PES): Involuntary weight loss (NC-3.2) related to fever and infection as evidenced by BMI below usual range and inflammatory process with elevated CRP. Interventions: Offer frequent small meals and snacks with nutrient dense, calorie-rich foods. Educate about the role of nutrition in maintaining healthy immune system. Monitoring and Evaluation: Weight gain back to usual weight; no further fever or weight loss. Maintain adequate hydration.

WHIPPLE’S DISEASE—CITED REFERENCES Deriban G, Marth T. Current concepts of immunopathogenesis, diagnosis and therapy in Whipple’s disease. Curr Med Chem. 13:2921, 2006. Moos V. Impaired immune functions of monocytes and macrophages in Whipple’s disease [published online ahead of print 4 August 2009]. Gastroenterology. 138:210, 2010. Muller SA, et al. Deadly carousel or difficult interpretation of new diagnostic tools for Whipple’s disease: case report and review of the literature. Infection. 33:39, 2005.


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FECAL INCONTINENCE NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Fecal incontinence is the inability to control bowel movements, and stool may leak from the rectum unexpectedly. More than 5.5 million Americans have fecal incontinence, affecting both children and adults, especially seniors. Fecal incontinence is more common in women than in men (Novi and Mulvihill, 2005); see Table 7-26. Fecal incontinence affects up to 20% of community-dwelling adults and more than 50% of nursing home residents, and is one of the major risk factors for elderly persons in the nursing home (Leung and Rao, 2009). Bowel training helps some people relearn how to control their bowels. In some cases, it involves strengthening muscles; in others, it means training the bowels to empty at a specific time of day. Biofeedback and sacral nerve stimulation may be useful in refractory patients and should be considered before colostomy (Leung and Rao, 2009; Jarrett et al, 2005). Biofeedback helps strengthen and coordinate the muscles. Kegel exercises may be used to strengthen the muscles in the pelvic floor, including those involved in controlling stool. This condition is often correlated with the presence of stroke and diabetes, or use of certain psychoactive medications (Quander

TABLE 7-26

et al, 2005). Treatment depends on the cause and severity of fecal incontinence; it may include dietary changes, medication, bowel training, and/or surgery. Surgery may be needed if fecal incontinence occurs in severe cases where injury has taken place. In patients with functional bowel disorders not responding to maximal medical treatment, bowel lavage or biofeedback therapy, can nowadays be treated by sacral nerve neuromodulation (Govaert et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Clinical/History Height Weight

BMI Diet history I&O

BP History of diarrhea

Fecal Incontinence: Causes and Comments

Cause

Comments

Constipation

One of the most common causes of fecal incontinence, constipation causes large, hard stools to become lodged in the rectum. Watery stool can then leak out around the hardened stool. Constipation also causes the muscles of the rectum to stretch, which weakens the muscles so they cannot hold stool in the rectum long enough for a person to reach a bathroom. In children, early toilet training or some developmental disorders can cause or aggravate constipation. Consult the doctor for specific management techniques.

Damage to the anal sphincter muscles

Fecal incontinence can be caused by injury to one or both of the ring-like muscles at the end of the rectum called the anal internal and/or external sphincters. The sphincters keep stool inside. When damaged, the muscles are not strong enough to do their job, and stool can leak out. In women, the damage often happens when giving birth. The risk of injury is greatest if the doctor uses forceps to help deliver the baby or does an episiotomy, which is a cut in the vaginal area to prevent it from tearing during birth. Hemorrhoid surgery can damage the sphincters as well.

Damage to the nerves of the anal sphincter muscles or the rectum

Fecal incontinence can also be caused by damage to the nerves that control the anal sphincters or to the nerves that sense stool in the rectum. If the nerves that control the sphincters are injured, the muscle does not work properly, and incontinence can occur. If the sensory nerves are damaged, they do not sense that stool is in the rectum. The individual will not feel the need to use the bathroom until stool has leaked out. Nerve damage can be caused by childbirth, a long-term habit of straining to pass stool, stroke, and diseases that affect the nerves, such as diabetes and multiple sclerosis.

Loss of storage capacity in the rectum

Normally, the rectum stretches to hold stool until a person can get to a bathroom. But rectal surgery, radiation treatment, and inflammatory bowel disease can cause scarring that makes the walls of the rectum stiff and less elastic. The rectum then cannot stretch as much and cannot hold stool, and fecal incontinence results. Inflammatory bowel disease also can make rectal walls very irritated and thereby unable to contain stool.

Diarrhea

Diarrhea, or loose stool, is more difficult to control than solid stool that is formed. Even people who do not have fecal incontinence can have an accident when they have diarrhea.

Pelvic floor dysfunction

Abnormalities of the pelvic floor can lead to fecal incontinence. Examples of some abnormalities are decreased perception of rectal sensation, decreased anal canal pressures, decreased squeeze pressure of the anal canal, impaired anal sensation, a dropping down of the rectum (rectal prolapse), protrusion of the rectum through the vagina (rectocele), and/or generalized weakness and sagging of the pelvic floor. Often the cause of pelvic floor dysfunction is childbirth, and incontinence does not show up until the midforties or later (Bharucha et al, 2005).


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Constipation Anal manometry Anorectal ultrasonography Proctography Proctosigmoidos copy Anal electromyography tests for nerve damage

Lab Work H&H Serum Fe, ferritin BUN Transferrin, TIBC PT Alb, transthyretin

Stool (occult blood) Na, K Ca, Mg • • •

INTERVENTION OBJECTIVES • Timely assessment and intervention are needed to manage constipation and incontinence of stool. Maintain a food diary to determine when incontinence occurs and to identify changes that may be helpful. • Establish a bowel training regimen to develop a regular pattern of bowel movements; some people train themselves to have bowel movements at specific times during the day, such as after every meal. • Identify and treat underlying causes, such as diet- or medication-induced diarrhea, constipation, and fecal impaction (Leung and Rao, 2009). • Prepare for surgery if needed.

such as sausage, ham, or turkey; spicy foods; alcohol; dairy products such as milk, cheese, and ice cream; fruits such as apples, peaches, or pears; fatty and greasy foods; sweeteners, such as sorbitol, xylitol, mannitol, and fructose, which are found in diet drinks, sugarless gum and candy, chocolate, and fruit juices. Serve smaller meals more frequently. Since liquid helps move food through the digestive system, drink half an hour before or after meals. Foods that contain soluble, digestible fiber slow the emptying of the bowels. Bananas, rice, tapioca, bread, potatoes, applesauce, cheese, smooth peanut butter, yogurt, pasta, and oatmeal may be helpful. High-fiber foods will add bulk and make stool easier to control. Fiber is found in fruits, vegetables, and grains. 20–30 g of fiber a day is needed; add it slowly. Too much fiber all at once can cause bloating, gas, or even diarrhea. If fiber intake makes diarrhea worse, cut back to two servings each of fruits and vegetables and remove skins and seeds. Increase fluid intake when fiber intake is increased to prevent fecal obstruction.

Common Drugs Used and Potential Side Effects • If diarrhea is causing the incontinence, medication may help. Sometimes doctors recommend using bulk laxatives to help people develop a more regular bowel pattern. Antidiarrheal medicines, such as loperamide or diphenoxylate, may be used to slow down the bowel activity. • Use of probiotic or prebiotic therapy is under study for this condition.

FOOD AND NUTRITION • Daily intake of protein should be appropriate for age and sex. Calories should be calculated as 30–35 kcal/kg. • Foods that may make the problem worse are drinks containing caffeine, such as coffee, tea, and chocolate, which relax the internal anal sphincter muscle. Other foods that have been implicated are cured or smoked meats

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Physical Activity Assessment Data: I & O, constipation and fecal incontinence, bedridden with no transfer from bed to chair; no walking. Nutrition Diagnoses (PES): Inadequate physical activity related to nonambulatory status as evidenced by being bedridden for 5 months after hip replacement leading to fecal incontinence. Interventions: Ensure adequate fluid and fiber intake; prune juice once daily as tolerated. Coordinate with physical therapy to enhance strengthening exercises; with nursing to offer bowel training. Monitoring and Evaluation: Improvement in fecal continence; resident more compliant with bed exercises for strengthening lean body mass.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The key to a successful bowel management program rests in tailoring the type of enema, medication, and diet to the specific type of colon (Bischoff et al, 2009). • The skin around the anus is delicate and sensitive. Constipation and diarrhea or contact between skin and stool can cause pain or itching. To relieve discomfort, wash the area with water, but not soap, after a bowel movement; wash in the shower with lukewarm water or use a sitz bath. Premoistened, alcohol-free towelettes are a better choice than toilet paper. Let the area air dry after washing. Use a moisture-barrier cream. Wear loose clothing, absorbent pads and special undergarments (Leung and Rao, 2009). • Ensure that the patient adequately exercises, rests, and maintains regular bowel habits. • Indicate which foods are sources of fiber and other key nutrients in the diet. See Table 7-27.


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TABLE 7-27

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Fiber Content of Common Foods

Fruits

Amount

Figs Pear Raspberries Strawberries, raw Apple, large with skin Apple, medium Prunes, dried Orange Banana Tangerine Peach Peaches, canned Raisins

2 dried 1 pear 1/2 cup 1 cup, sliced 1 apple 1 apple 5 prunes 1 orange 1 banana 1 medium 1 medium 1/2 cup 1 miniature box (14 g)

Vegetables Peas, split, cooked Lentils, cooked Beans, kidney, canned Lima beans, cooked Black eyed peas Peas, green, canned Cauliflower Spinach, cooked Cabbage, raw Brussels sprouts Squash, acorn Carrots, raw Potatoes, boiled Zucchini, raw Broccoli, raw Celery, raw Lettuce, iceberg

1/2 cup 1/2 cup` 1/2 cup 1/2 cup 1/2 cup 1/2 cup 1 cup raw 1/2 cup 1 cup 1/2 cup 1 cup raw 1/2 cup 1/2 cup 1 cup 1/2 cup 1/2 cup 1 cup shredded

Grams of Fiber 4.6 4.0 4.0 3.8 3.7 3.3 3.0 3.1 2.8 1.9 1.8 1.3 0.6

8.1 7.8 4.5 4.5 4.0 3.5 2.5 2.2 2.0 2.0 2.1 1.8 1.6 1.4 1.3 1.0 0.8

Fruits

Amount

Grams of Fiber

Grains All Bran Raisin bran Shredded wheat Wheat bran flakes Rice, brown, cooked Total cereal Oatmeal, cooked Wheatena, cooked Oat bran muffin Bread, whole wheat Bread, whole grain (check label) Rye crisp wafer Crackers, graham Bread, white wheat

1/2 cup 1 cup 2 biscuits 3/4 cup 1 cup 3/4 cup 3/4 cup 1 packet One muffin 1 slice 1 slice

9.6 7.5 5.0 4.6 3.5 3.4 3.0 3.0 2.6 1.9 1.7–2

1 wafer 2 squares 1 slice

1.7 0.4 0.6

Other Nuts, mixed, dry roast Apple pie, sliced Chocolate cake, sliced Yellow cake, sliced

1 oz 1 slice 1 slice 1 slice

2.6 1.9 1.8 0.2

Source: U.S. Department of Agriculture Nutrient Database for Standard Reference, Release 14 http://www.nal.usda.gov/fnic/foodcomp/Data/SR14/sr14.html, accessed September 1, 2009.

Patient Education—Foodborne Illness

FECAL INCONTINENCE—CITED REFERENCES

• Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

Bharucha AE, et al. Relationship between symptoms and disordered continence mechanisms in women with idiopathic faecal incontinence. Gut. 54:546, 2005. Bischoff A, et al. Treatment of fecal incontinence with a comprehensive bowel management program. J Pediatr Surg. 44:1278, 2009. Govaert B, et al. Neuromodulation for functional bowel disorders. Best Pract Res Clin Gastrointest. 23:545, 2009. Jarrett ME, et al. Sacral nerve stimulation for fecal incontinence following surgery for rectal prolapse repair: a multicenter study. Dis Colon Rectum. 48:1243, 2005. Novi JM, Mulvihill BH. Fecal incontinence in women: a review of evaluation and management. Obstet Gynecol Surv. 60:261, 2005. Quander CR, et al. Prevalence of and factors associated with fecal incontinence in a large community study of older individuals. Am J Gastroenterol. 100:905, 2005.

For More Information •

Mayo Clinic http://www.mayoclinic.com/health/fecal-incontinence/DS00477

Medicine Net http://www.medicinenet.com/fecal_incontinence/article.htm

NIDDK—Fecal incontinence http://digestive.niddk.nih.gov/ddiseases/pubs/fecalincontinence/


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HEMORRHOIDS NUTRITIONAL ACUITY RANKING: LEVEL 1 stay, and earlier return to work (Chung et al, 2005). Transanal hemorrhoidal dearterialization is also a potential treatment option for second-degree and third-degree hemorrhoids (Giordano et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

Rectum

CLINICAL INDICATORS

Anal canal

Genetic Markers: Hemorrhoids are not likely to have a genetic origin. Clinical/History

Internal hemorrhoid

External hemorrhoid

Adapted from: Thomas H. McConnell, The Nature Of Disease Pathology for the Health Professions, Philadelphia: Lippincott Williams & Wilkins, 2007.

DEFINITIONS AND BACKGROUND Chronic constipation is believed to be the main cause of hemorrhoids. The disorder is common in Americans (50% of Americans older than 50 years of age will have suffered at least once, especially if obese). Causes include increased abdominal pressure secondary to straining during bowel movements, heavy lifting, childbirth, and benign prostatic hypertrophy. Internal hemorrhoids are normal anatomical structures and rarely are painful (they may only bleed). External hemorrhoids are usually from excessive diarrhea or from constipation; they are tender, painful, bluish, localized swellings of varicose veins at the anal margin. Bleeding, pain, soiling, and prolapse are the classic symptoms in hemorrhoid disease (Johannsson et al, 2005). Although some patients fear that rectal bleeding signifies colorectal cancer, most patients with the primary diagnosis of symptomatic hemorrhoids do not need further investigative procedures (Tang et al, 2005). Techniques that fix the cushions back in position can be performed in outpatients with reasonable success rates. Sclerotherapy—Used to treat varicose veins, in this procedure a chemical solution is injected into the vein, which causes the hemorrhoid to collapse. Surgery should be aimed at symptomatic hemorrhoids. Stapled hemorrhoidectomy is safe and effective for acute thrombosed hemorrhoids (Wong et al, 2009). Patients have reduced pain, shorter length of

Height Weight BMI Diet history I&O Anal itching Bright red blood on toilet tissue Pain during bowel movements

One or more hard tender lumps near the anus Anoscope or sigmoidoscopy History of diarrhea Constipation

BUN Transferrin, TIBC Alb, transthyretin Stool (occult blood) Na, K Ca, Mg

Lab Work H&H Serum Fe, ferritin

INTERVENTION OBJECTIVES • Provide comfort. Prevent prolapse and thrombosis. • Avoid constipation, infection, and anemia.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Fiber Intake Assessment Data: I & O and diet history revealing low fiber intake (10 g daily). Nutrition Diagnoses (PES): Inadequate fiber intake related to poor dietary intake as evidenced by recurrent hemorrhoids. Interventions: Food and Nutrient Delivery—provide high fiber foods and extra fluids. Education—high fiber diet and how to assure adequate hydration; increasing physical activity such as walking. Monitoring and Evaluation: Fewer complaints of hemorroids, straining during deification at stool, dry stool consistency.


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• Reduce possible irritation from excessive amounts of fiber. Avoid irritants, such as laxatives. • After surgery, reduce irritation while patient heals. Promote rapid healing. Prevent future recurrence.

FOOD AND NUTRITION • Diet should be low in fiber only when the patient is in pain. Otherwise, a high-fiber diet (25–35 g) should be used. • Fluids should be increased to 8–10 glasses daily. • After surgery, a low-fiber/soft diet should be used until full recovery occurs. Eventually, adequate fiber (25–35 g) should be taken. • Omit lactose and highly seasoned foods only if not tolerated by the individual.

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Ensure that the patient adequately exercises, rests, and maintains regular bowel habits. Limit the time sitting on the toilet. Avoid straining. • Teach the patient about the role of fiber in the diet. • Persistent or recurrent bleeding requires medical attention, especially to monitor vitamin K, iron, and B-complex vitamin levels and to prevent additional losses. • It is important to keep the anal skin area dry. • Over-the-counter products may aggravate an allergic response. • Warm sitz baths may help to reduce symptoms.

Patient Education—Foodborne Illness

Common Drugs Used and Potential Side Effects • Hemorrhoid creams with lidocaine, over-the-counter, can reduce pain. • Laxatives and enemas may have caused faulty bowel function. Avoid use unless prescribed by the doctor. • Troxerutin and carbazochrome are used as a combination therapy. Monitor for any untoward side effects. • Lubrication with glycerin suppositories may help to reduce symptoms. • Medicated suppositories such as Anusol HC (contains hydrocortisone) may help to decrease inflammation. Limit steroid-containing medications to less than 2 weeks of continuous use to avoid atrophy of anal tissues. • Psyllium laxatives (Metamucil) can help with constipation; long-term use alters electrolytes. Flatulence or steatorrhea may occur.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Comfrey, plantain, butcher’s broom, horse chestnut, and witch hazel have been recommended for this condition, but no clinical trials have proven efficacy.

• Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Ano-Rectal Algorithm http://www.uwgi.org/guidelines/ch_10/ch10.htm

Hemorrhoids http://digestive.niddk.nih.gov/ddiseases/pubs/hemorrhoids/

Web MD http://www.webmd.com/a-to-z-guides/hemorrhoids-topic-overview

HEMORRHOIDS—CITED REFERENCES Chung CC, et al. Stapled hemorrhoidopexy vs. harmonic scalpel hemorrhoidectomy: a randomized trial. Dis Colon Rectum. 48:1213, 2005. Giordano P, et al. Transanal hemorrhoidal dearterialization: a systematic review. Dis Colon Rectum. 52:1665, 2009. Johannsson HO, et al. Bowel habits in hemorrhoid patients and normal subjects. Am J Gastroenterol. 100:401, 2005. Tang T, et al. An approach to haemorrhoids. Colorectal Dis. 7:143, 2005. Wong JC, et al. Stapled technique for acute thrombosed hemorrhoids: a randomized, controlled trial with long-term results. Dis Colon Rectum. 51:397, 2009.

PROCTITIS NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Proctitis is inflammation of the lining of the rectal mucosa and may be acute or chronic. Proctitis may be a side effect of medical treatments such as radiation therapy or antibiotics. It may also be caused by UC, rectal injury, bacterial infection,

allergies, malfunction of the nerves in the rectum, Crohn’s disease, or sexually transmitted diseases. Proctitis is most common in UC patients at diagnosis, and younger patients are more likely than older patients to have extensive disease (Tarrant et al, 2008). For this form of proctitis, 5-aminosalicyclic acid (5-ASA) or corticosteroids may


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be applied directly to the area or taken in a pill form. Ileal pouch rectal anastomosis (IPRA) preserves bowel continuity and provides a good function (Kariv et al, 2009). There may also be a role for appendectomy in ulcerative proctitis (Bolin et al, 2009). Antibiotics are used for proctitis caused by bacterial infection. Lymphogranuloma venereum (LGV) L2b proctitis may cause proctitis in HIV-positive men who have sex with men (MSM); doxycycline is the drug of choice (White, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Clinical/History Height Weight BMI Diet history I&O BP Bowel habits Abdominal pain Rectal bleeding Mucus in stool Left-sided abdominal pain

Frequent or continuous urge to defecate Constipation Rectal fullness Proctoscopy Sigmoidoscopy Lab Work Stool (occult blood) HPV testing H&H Serum Fe, ferritin

Gluc BUN, Creat Transferrin, TIBC Alb, transthyretin CRP Na, K Ca, Mg Serum folate, vitamin B12

INTERVENTION OBJECTIVES • Manage symptoms and alleviate pain. Prepare for surgery if needed. • Reduce inflammation and promote healing. • Correct anemia from blood loss where present.

FOOD AND NUTRITION • Diet therapy depends on the cause of proctitis. Identify appropriate etiology and review entries in this text for dietary management. • Some patients find that avoidance of caffeine, red meat, dairy products, and artificial sweeteners can be beneficial. • Use of omega-3 fatty acids may be helpful to reduce inflammation.

Common Drugs Used and Potential Side Effects • Ulcerative proctitis patients with frequent relapses may need a longer duration of topical therapy. Prolonged oral mesalazine treatment period protects against the proximal spread of rectal inflammation (Pica et al, 2004). • 5-ASA or corticosteroids may be needed if IBD is the cause. Monitor for numerous side effects. • Antibiotics are the best treatment for proctitis caused by a specific bacterial infection. When proctitis is caused by use of an antibiotic that destroys normal intestinal bacteria, a doctor may prescribe metronidazole (Flagyl) or vancomycin (Vancocin), which should destroy the harmful bacteria.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Mineral (Iron) Intake Assessment Data: I & O, abdominal pain, mucus and blood in stool, constipation, poor oral intake, medical diagnosis of anemia, labs indicative of anemia (low H & H, ferritin, Fe).

• Teach the patient about the role of fiber in the diet. • It is important to keep the anal skin area dry. Over-thecounter products may aggravate an allergic response.

Nutrition Diagnoses (PES): Inadequate mineral (iron) intake related to blood loss and rectal bleeding in proctitis as evidenced by labs (low Fe, ferritin, H & H).

Patient Education—Foodborne Illness

Interventions: Food and Nutrient Delivery—enhance food choices with iron-rich food choices. Educate about food choices that are rich in iron; discuss heme and nonheme sources. Counseling about use of medications and dietary changes that may be needed with abdominal pain.

• Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the individual. • If home TF or CPN is needed, teach appropriate sanitation and food-handling procedures.

Monitoring and Evaluation: Improvement in serum labs, less abdominal pain, fewer incidents of rectal bleeding.

For More Information •

Ano-Rectal Algorithm http://www.uwgi.org/guidelines/ch_10/ch10.htm


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Mayo Clinic—Proctitis http://www.mayoclinic.com/health/proctitis/DS00705

Proctitis http://digestive.niddk.nih.gov/ddiseases/pubs/proctitis/

PROCTITIS—CITED REFERENCES Bolin TD, et al. Appendectomy as a Therapy for Ulcerative Proctitis [published online ahead of print 7 July 2009]. Am J Gastroenterol. 104:2476, 2009.

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Kariv Y, et al. Ileal pouch rectal anastomosis: a viable alternative to permanent ileostomy in Crohn’s proctocolitis patients. J Am Coll Surg. 208:390, 2009. Pica R, et al. Oral mesalazine (5-ASA) treatment may protect against proximal extension of mucosal inflammation in ulcerative proctitis. Inflamm Bowel Dis. 10:731, 2004. Tarrant KM, et al. Perianal disease predicts changes in Crohn’s disease phenotype-results of a population-based study of inflammatory bowel disease phenotype. Am J Gastroenterol. 103:3082, 2008. White JA. Manifestations and management of lymphogranuloma venereum. Curr Opin Infect Dis. 22:57, 2009.


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C

T

I

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N

Hepatic, Pancreatic, and Biliary Disorders

8

CHIEF ASSESSMENT FACTORS Clinical Factors

• • • • • • • • • • • • • • • • • • • • • • • •

Abnormal Liver MRI, Ultrasound, or Biopsy Abdominal or Radiating Pain Anorexia, Malaise, Fatigue Ascites, Large Abdominal Girth, Pot Belly Brownish spots or blemishes on the skin Darkened urine Depression or mood swings Diabetes, Hyperglycemia, Hypoglycemia Diarrhea, Steatorrhea Edema in feet or ankles Encephalopathy? Flushed facial appearance Gastrointestinal (GI) Bleeding Hepatomegaly or Shrunken Liver (in cirrhosis) Itchy skin Hypoglycemia Jaundice Light colored stools Malnutrition, Subjective Global Assessment (SGA) Score Offensive body odor Red, swollen or itchy eyes Unusual Weight Loss or Gain Varices Vomiting, Nausea

Laboratory Assessment A “liver panel” usually includes tests for alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, and alkaline phosphatase. Liver Function is best measured by the prothrombin time (PT), international normalized ratio (INR) and albumin (see below).

• •

Bilirubin (total or indirect) is released from destroyed red blood cells and passed on to the liver where it is excreted through bile. Bleeding/clotting times: PT, INR measure how long it takes blood to form a clot in seconds; a normal PT/INR indicates that a normal amount of blood-clotting protein is available.


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HEPATIC VEIN Returns blood from the liver to the heart.

LIVER Receives nutrients from the digestive tract and processes them for distribution throughout the body.

HEPATIC ARTERY Supplies oxygen-rich blood from the heart to the liver.

BILIARY SYSTEM Includes the gallbladder, which stores and secretes bile, and the bile ducts, which conduct bile from the liver to the gallbladder and from the gallbladder to the intestine.

• •

• • • • •

• •

• •

Blood product transfusions. Cholestasis tests: Serum alkaline phosphatase (Alk Phos), Gamma-glutamyltransferase (GGT). High alk phos level occurs when there is a blockage of flow in the biliary tract or a buildup of pressure in the liver, often from a gallstone. Family history of liver diseases. Glucose levels: poorly controlled diabetes can lead to fatty liver. Intake of medications, vitamins, herbs, drugs, and alcohol. Liver enzymes: ALT (SGPT), AST (SGOT). The AST level is not as helpful as the ALT level for checking the liver. Neutrophils: role in inflammation, formation of pus, and destruction of bacteria; check ANC regularly while on interferon treatment. Total white blood cell (WBC) count includes neutrophils plus the four other types (eosinophils, basophils, monocytes, and lymphocytes). Pancreatic enzyme levels. Serum proteins: PT, INR, albumin, globulin, mitochondrial antibodies, antinuclear and smooth muscle antibodies. A normal INR is 1.0. Low levels of total protein (TP) may indicate impaired liver function. Serum ammonia. Subjective global assessment (SGA:) evaluation of proteinenergy malnutrition (PEM) based on evidence of edema, ascites, muscle wasting, subcutaneous fat loss, decreased functional capacity, and GI symptoms of diarrhea, nausea, and vomiting.

PORTAL VEIN Carries nutrient-rich blood from the digestive tract to the liver. GI TRACT VEINS Transport absorbed nutrients to the portal vein.

• •

Specific markers: serum ferritin, ceruloplasmin, alphafetoprotein (tumor marker), alpha-1 antitrypsin. Thyroid tests: thyroid stimulating hormone (TSH) is produced by the pituitary gland in the brain and causes the thyroid gland to produce thyroid (T4 and T3). TSH may be high if using interferon treatments. Viral hepatitis tests (hepatitis A, B, and C serologies).

BACKGROUND: HEPATOBILIARY DISORDERS Nutrition and the liver are interrelated since everything is refined and detoxified by the liver. The liver is the largest organ in the body, and it performs many complex and essential functions (see Table 8-1). As the body’s internal chemical power plant, one cannot live without a liver. Mild elevations in liver chemistries such as ALT and AST can reveal serious underlying conditions, such as viral hepatitis, alcohol use, medication use, steatosis, fatty liver disease, nonalcoholic steatohepatitis (NASH), cirrhosis, or more chronic health conditions, such as diabetes, heart disease, or thyroid disease (Giboney, 2005). Serotonin is a mediator of several hepatic functions; in the diseased liver, it can promote hepatic fibrosis and steatohepatitis (Lesurtel et al, 2008). Jaundice is a yellowish discoloration of the skin, mucous membranes, and some body fluids from accumulation of bile or bilirubin. Jaundice may be classified as hemolytic (from excessive red blood cell destruction), hepatic (from an immature liver or from damage), or obstructive (from obstructed biliary ducts or gallstones). In neonatal jaundice, there is a somewhat normal pattern of hyperbilirubinemia that is generally not detrimental. In obstructive jaundice, no bile pigment


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TABLE 8-1

473

Liver, Gallbladder, and Pancreatic Functions

Liver The largest single organ of the body; it is the central biochemical organ of the body. Functionally, it: 1. Converts galactose and fructose to glucose; makes glycogen; degrades glycogen upon demand. 2. Converts proteins into glucose; synthesizes albumin, globulin, fibrinogen, prothrombin, and transferrin; removes nitrogenous wastes (ammonia); provides transamination; synthesizes purines and pyrimidines; forms amines by decarboxylation. 3. Synthesizes triglycerides; forms very low窶電ensity lipoproteins (VLDLs); oxidizes fatty acids for energy and ketones. 4. Synthesizes cholesterol from acetate; makes high-density lipoproteins (HDLs). 5. Stores vitamins A, D, E, and K and some vitamin B12 and C. 6. Hydroxylates vitamin D for renal activation; activates folic acid to tetrahydrofolic acid (THFA). 7. Stores minerals (e.g., iron, copper, zinc, magnesium). 8. Detoxifies drugs. 9. Produces bile. Gallbladder Stores bile, which helps counteract stomach acidity and aids in fat digestion through emulsification. Pancreas 1. Produces pancreatic juice when stimulated by secretin. Pancreatic juice contains bicarbonate, which helps neutralize acid chyme. 2. Secretes insulin and glucagon hormones. 3. Secretes metabolic/digestive enzymes involved in protein, carbohydrate, and fat metabolism. Pancreatic secretion has gastric, cephalic, and intestinal phases. The islets secrete insulin (b) and glucagon (a). The acini secrete lipase, amylase, trypsin, chymotrypsin, ribonuclease, and carboxypolypeptidase. The pancreas secretes enzymes (trypsin, lipase, and amylase) into the collecting duct as stimulated by cholecystokinin (also called pancreozymin), which is produced by the duodenum.

is present; stools become pale and clay colored, indicating fat maldigestion or malabsorption. Obstructive jaundice leads to bacterial translocation by disruption of the gut barrier, intestinal microecology, and impaired host immune defense. Anorexia is common in obstructive jaundice; biliary drainage improves appetite. Oral administration of an arginine, omega-3 fatty acids, glutamine, and an RNAsupplemented enteral diet for immunonutrition may be useful. Nonalcoholic fatty liver disease is accumulation of fat in the liver of people who drink little or no alcohol. It may have only symptoms of fatigue, or it may progress to hepatosteatosis (NASH) or liver failure. NASH may occur in obese individuals and may have an inflammatory origin. Oxidative stress contributes to hepatic cell damage when there is an excess of reactive species derived from oxygen (ROS) and nitrogen (RNS), or a defect of antioxidant molecules (Leung and Chan, 2009). This cell damage aggravates alcoholic liver disease, chronic viral hepatitis, autoimmune liver diseases and nonalcoholic steatohepatitis. Antioxidants in S-adenosylmethionine (SAMe), vitamin E, polyenylphosphatidylcholine, or silymarin have a protective effect on the liver and continue to be studied. Malnutrition is often a problem in liver diseases. Oral nutritional supplements and tube feeding (TF) can be used to supplement intake when needed. TF improves nutritional status and liver function, reduces the rate of complications, and prolongs survival in cirrhosis and in acute liver

failure (ALF). Long-term PN still promotes hepatobiliary dysfunction and steatosis and is used less often. Use herbs and alternative therapies with caution. Use of glycyrrhizin, phyllanthin, silibinin, milk thistle, and sho-saiko to show merit. However, some herbs are hepatotoxic and should be avoided; this includes comfrey, chaparral, germander, and Chinese herbal mixtures.

BACKGROUND: PANCREATIC AND GALLBLADDER DISORDERS In the United States, acute pancreatitis, chronic pancreatitis, and pancreatic cancer are the most common pancreatic disease states. Pancreatic cancer is responsible for nearly 30,000 deaths annually. Excessive consumption of alcohol is the major risk factor for pancreatic disease, and smoking causes pancreatic cancer (Lowenfels et al, 2005). To reduce the burden of pancreatic disease, focus on the control of three lifestyle factors: smoking, drinking, and obesity. Bile is the greenish-yellow fluid made of bile salts and waste products such as bile pigments. Bile flows through small bile ducts inside the liver, then into the common bile duct outside of the liver. Some flows directly to the duodenum, and the rest is stored in the gallbladder. After a meal, the gallbladder releases some bile into the small intestine to help digest fats. Gallbladder disease is also strongly associated with obesity.


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A For More Information •

Abnormal Liver Function Test Algorithm http://www.uwgi.org/guidelines/ch_09/ch09txt.htm

American Association for the Study of Liver Diseases http://www.aasld.org/

American Liver Foundation http://www.liverfoundation.org/

Centers for Disease Control and Prevention (CDC)—Fast Statistics http://www. cdc.gov/nchs/fastats/liverdis.htm

National Digestive Diseases Information Clearinghouse http://digestive.niddk.nih.gov/

B

CITED REFERENCES Giboney PT. Mildly elevated liver transaminase levels in the asymptomatic patient. Am Fam Physician. 1:1105, 2005. Lesurtel M, et al. Role of serotonin in the hepato-gastroIntestinal tract: an old molecule for new perspectives. Cell Mol Life Sci. 65:940, 2008. Leung PS, Chan YC. Role of oxidative stress in pancreatic inflammation. Antioxid Redox Signal. 11:135, 2009. Lowenfels AB, et al. The epidemiology and impact of pancreatic diseases in the United States. Curr Gastroenterol Rep. 7:90, 2005.

LIVER DISORDERS

ALCOHOLIC LIVER DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Alcohol is a hepatotoxin and is ulcerogenic, especially to the esophagus and other organs. Alcohol cannot be stored and is used preferentially over other energy fuels. Alcoholic liver disease (ALD) is a major cause of illness and death. ALD affects about 2 million people in the United States. Signs and symptoms of alcoholism include restlessness, agitation, spider angiomas on the face or back or belly, insomnia, anorexia, weight loss, GI cramping, malnutrition, delirium tremens, and hand tremors. In men, altered hair distribution and gynecomastia may occur. Understanding alcohol addiction is key to treating ALD, since abstinence leads to improvement in all forms of alcoholic liver damage (Lucey, 2009). Section 4 addresses alcohol addiction. Table 8-2 lists stages and effects of alcoholism. Given the benefit of drug treatment, it is important to identify patients at risk of early mortality from alcoholic hepatitis using tools such as the Maddrey Discriminant Function, the Model of End-Stage Liver Disease score, and the Glasgow Alcoholic Hepatitis score (Maher, 2007). Alcoholics may replace as much as one third of their daily energy requirements from alcohol. As a result, they are malnourished. Either they eat poorly or alcohol metabolism prevents them from properly absorbing, digesting, and using nutrients, particularly vitamin A (Plauth et al, 2006). Classic effects of malnutrition from alcoholism include Wernicke’s

encephalopathy, Korsakoff’s psychosis, muscle wasting, weight loss, and liver disease. Most tissues of the body contain enzymes capable of ethanol metabolism, but significant activity occurs only in

TABLE 8-2

Stages of Alcoholism-Related Effects

Stage

Condition

Effects

I.

Fatty liver (steatosis)

Reversible. Acetaldehyde promotes hepatic fat accumulation. Hepatomegaly, hypertriglyceridemia, hypoalbuminemia, cytochrome P-450 2E1 induction, free radical generation, lipid peroxidation, and increased transcription of proinflammatory mediators, including TNF-alpha, occur.

II.

Alcholic hepatitis

Fibrosis begins. Fever with tachycardia; liver enlargement is mild, and tenderness can occur.

III.

Cirrhosis

Not reversible. Diffuse necrosis and regeneration of fibrous tissue leading to loss of normal hepatic function.

IV.

Encephalopathy or Coma

May lead to death if not treated. Impaired mentation, altered neuromuscular function, and altered consciousness.


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the liver and stomach (Lieber, 2005). Alcohol dehydrogenase is made with zinc. Alcohol decreases absorption of fats, fat-soluble vitamins, thiamin, folic acid, vitamin B12, and zinc. Nicotine adenine dinucleotide (NADH) is significant in alcohol metabolism by reduction of pyruvate and promotion of steatosis. Adequate nutrition is critical and should be provided by TF if necessary (Maher, 2007). A prompt decline in serum bilirubin within 1 week indicates a favorable response to therapy; nonresponders have a 6-month mortality rate of 50% or higher (Maher, 2007). Plasma homocysteine levels are altered in actively drinking patients, causing brain atrophy and withdrawal seizures (Bleich et al, 2005). Methionine needs to be activated to S-adenosylmethionine (SAM); this metabolism is impaired in liver disease. Folate deficiency accentuates abnormal methionine metabolism, lipid oxidation, and liver injury (Halsted et al, 2002; Schalinske and Nieman, 2005). SAM, betaine, and folate decrease oxidative stress by upregulation of glutathione and interleukin-10 and downregulation of tumor necrosis factoralpha, TNF-a (Purohit et al, 2008). No benefit has been found in randomized, placebo-controlled clinical trials of colchicine, S-adenosylmethionine (SAMe), or phosphatidylcholine (Lucey, 2009). Betaine may attenuate ALD by increasing synthesis of SAM and glutathione, decreasing homocysteine (tHcy) levels (Song et al, 2008). More research is indicated. Alcohol-induced liver injury is an immunological response of the liver; neutrophils damage liver cells through cytotoxicity (Leevy and Elbeshbeshy, 2005). Men and women metabolize alcohol differently. It takes less time and lower doses of alcohol exposure to cause liver damage in females than in males. Community-dwelling heavy drinkers who are not in alcoholism treatment have dose-related gray matter volume losses (Cardenas et al, 2005). Treatment strategies for ALD include lifestyle changes for abstinence from alcohol consumption. Nutrition therapy and medications are also important. Serious alcoholic hepatitis has a mortality record of up to 50%. If necessary liver transplantation may be life-saving.

CAGE test (Cut down, Height Annoyed, Weight Guilty, Eye Body mass index opener) (BMI) Alcohol Use DisUsual body orders Identiweight fication Test (UBW) (AUDIT) Diet history Dual-energy Blood pressure x-ray absorp(BP) tiometry Intake and out(DEXA) put (I & O) bone scan Food intolerances, Lab Work taste Glucose aversions (increased or Anorexia, naudecreased) sea, vomiting, Glucose diarrhea tolerance test Scurvy— (sensitive and ecchymoses, reliable) hemorrhagic gingivitis, per- AST (increased) ALT (normal or ifollicular only mildly hemorrhages elevated) Leg edema, poor wound INR Bilirubin (often healing elevated) CT scan or ultrasound of Serum ammonia (may be abdomen elevated) Liver biopsy Blood urea Ascites (mild, nitrogen moderate, (BUN) or severe) (low?) Fatigue Clinical/History

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Albumin or transthyretin (low?) C-reactive protein (CRP) Triglycerides (increased?) Cholesterol (increased or decreased) WBC count Serum B12 and folate Plasma homocysteine (high?) Na (hyponatremia?) K Hemoglobin and hematocrit (decreased) Serum Fe, ferritin Transferrin Uric acid (UA, increased) Globulin Alk phos (mildly elevated) Mg (decreased) Ca Serum phosphorus (decreased)

ASSESSMENT, MONITORING, AND EVALUATION INTERVENTION CLINICAL INDICATORS Genetic Markers: The dopamine (DR2) receptor promotes effects of alcohol. People with a genetic deficit of beta-endorphin peptide are susceptible (Manzardo et al, 2005; Zalewska-Kaszubska and Czarnecka, 2005). The dopaminergic mesolimbic system activates the endogenous mu and delta opioid receptors; mu receptor polymorphisms may be associated with ethanol dependence ( Job et al, 2007). Polymorphisms in cytochrome P450 2E1 (CYP2E1), the major microsomal ethanol metabolizing enzyme, can alter detoxification of alcohol by glutathione-S-transferases M1 (GSTM1) and gamma-aminobutyric acid receptor gamma2 (Khan et al, 2009).

OBJECTIVES • Remove alcohol to allow the disabled liver to function more effectively while protecting it from metabolic stress. Avoid alcohol in miscellaneous products, such as vinegar, sauces, and cough syrup. • Improve health of liver so it can synthesize albumin and other serum proteins. Help liver tissue regenerate; replenish plasma proteins that are lost. Improve skeletal muscle synthesis. • Prevent hypoglycemia from blocked gluconeogenesis. Correct metabolic syndrome, hyperglycemia, hypertension, or hypertriglyceridemia. • Repair damage from fatty liver and diminished bile salt synthesis. • Repair neural damage from malnutrition and malabsorption.


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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Alcohol Intake Assessment Data: Dietary intake records; low protein and energy intake for age/gender. Intake of one fifth of vodka per day to the exclusion of most meals. Nutrition Diagnosis (PES): Excessive alcohol intake 25–30 g/d related to daily consumption above this level as evidenced by alcohol-induced liver injury, elevated LFTs and ascites. Intervention: Food and Nutrient Delivery: ND 1.1 General Healthful diet (avoid alcohol); ND 3.1.4 Modified food—increased calorie/protein intake. Education: E 1.3 Survival Information. Educate about nutrientdense foods and the role that alcohol plays in liver damage. E-1.1 Present concise and clear educational material with nutritional tips for patients with liver disease. Counseling: C 2.5 Social support—avoid social outings with alcohol present. Coordination of Care: RC 1.4 Referral to community agencies/ programs. RC-1.3 Refer to social worker for alcohol rehabilitation. C-2.9 Relapse prevention by explaining the pros of following diet and medications as recommended, as the importance of maintain sober. Monitoring and Evaluation: Track food intake through food diary or history. Coordinate care for rehabilitation program. Follow-up on intake of energy, protein and nutrients after omission of alcohol.

• Correct fluid and electrolyte imbalances, nutritional deficits such as iron deficiency anemia from chronic blood loss in varices, ulcers, and vomiting. • Be honest and direct in approach. Gently confront conflicting information when stated by the patient.

FOOD AND NUTRITION • Avoid alcohol to allow the liver to begin heal (DiCecco and Francisco-Ziller, 2006). • Malnourished alcoholics should consume a diet rich in carbohydrate and protein, preferentially via the oral or enteral route. Provide protein as 1.5 g/kg body weight if malnourished. Plan sufficient carbohydrates and fat to spare protein, but monitor for hyperglycemia or dyslipidemia. • In hypertensive patients, a Dietary Approaches to Stop Hypertension (DASH) diet may be planned that provides a sufficient mixture of nutrients without excessive kilocalories. All fasting or very low–calorie diets should be avoided. • Include a mix of fat from omega-3 (fish oils), omega-6 fatty acids, and medium-chain fatty acids. • Micronutrient deficiencies require supplementation. Supplement the diet with B-complex vitamins, but supplemental vitamins A and D may not be well tolerated. Oral diet should provide adequate amounts of vitamins C, E, and K, phosphorus, potassium, selenium, magnesium, zinc, and calcium.

• Provide small frequent meals to prevent hypoglycemia, resulting from limited glycogen storage. • Monitor iron intake to avoid excesses from diet or supplements, especially if there is the possibility of iron storage disease. • Make meals appealing to stimulate the appetite. • If TF is needed, avoid glutamine-enriched formulas which may increase ammonia levels.

Common Drugs Used and Potential Side Effects • Corticosteroids have become the standard of care in patients with severe alcoholic hepatitis (Lucey, 2009). Methylprednisolone improves the ability to produce albumin and to normalize PT and bilirubin levels. Side effects may include negative nitrogen balance, hypocalemia, or hyperglycemia. • Pharmacotherapy for alcoholism with naltrexone, acamprosate, topiramate, and baclofen is exciting (Lucey, 2009). Naltrexone is more effective in some individuals than in others (Rubio et al, 2005). • Disulfiram (Antabuse) is given with patient’s consent. It causes the patient to vomit after ingesting alcohol and can be dangerous. • Beta-blockers (propranolol, nadolol) or octreotide (Sandostatin) may be used to reduce portal hypertension when varices occur. • Insulin may be necessary; do not mix with alcohol. Alcohol intake may cause severe hypoglycemia in patients taking insulin (Pedersen-Bjergaard et al, 2005). Metformin should be avoided in patients with liver disease.

Herbs, Botanicals, and Supplements • Antioxidants are increasingly used. Agents involved in methionine metabolism such as SAM and betaine have shown efficacy in liver disease. Milk thistle (Silybum marianum) may have some therapeutic effect as well. Curcuma longa (turmeric) and Glycyrrhiza glabra (licorice) are being evaluated. Tea polyphenols, especially green tea, may alleviate liver damage (Zhang et al, 2005). • Herbs and botanical supplements should not be used without discussing with the physician. Chaparral is especially toxic to the liver and should be avoided; severe hepatitis or liver failure may result. Aloe vera should be avoided orally.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient on the sources of necessary nutrients in the diet and use of the prescribed multivitamins. Help patient in the planning and preparing of appetizing, nutrient-dense meals. • Explain that alcohol is metabolized readily by the liver but cannot be used for muscular activity or energy production. Chemical addiction is a disease; self-help programs and follow-up can reduce dependency. • General multivitamin–mineral supplementation may improve a poor appetite.


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• Obesity, diabetes, and hyperinsulinemia play a role in the development of hepatic steatosis; weight loss remains a critical part of protecting the liver against damage. • Identify sources of assistance for persons who need help with meal preparation or with access to meals.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Alcoholics Anonymous (AA) World Services http://www.alcoholics-anonymous.org/

Alcoholic Hepatitis http://www.emedicine.com/med/topic101.htm

International Society for Biomedical Research on Alcoholism http://www.isbra.com/

National Council on Alcoholism and Drug Dependence http://www.ncadd.org/

National Institute on Alcohol Abuse and Alcoholism (NIAAA) http://www.niaaa.nih.gov/

International Research Society on Alcoholism http://www.rsoa.org/

Substance Abuse and Mental Health Administration (DHHS) http://www.samhsa.gov/

ALCOHOLIC LIVER DISEASE—CITED REFERENCES Bleich S, et al. Evidence of increased homocysteine levels in alcoholism: the Franconian Alcoholism Research Studies (FARS). Alcohol Clin Exp Res. 29:334, 2005.

477

Cardenas VA, et al. Chronic active heavy drinking and family history of problem drinking modulate regional brain tissue volumes. Psychiatry Res. 138: 115, 2005. DiCecco SR, Francisco-Ziller N. Nutrition in alcoholic liver disease. Nutr Clin Pract. 21:245, 2006. Halsted CH, et al. Folate deficiency, methionine metabolism, and alcoholic liver disease. Alcohol. 27:169, 2002. Job MO, et al. Mu (mu) opioid receptor regulation of ethanol-induced dopamine response in the ventral striatum: evidence of genotype specific sexual dimorphic epistasis. Biol Psychiatry. 62:627, 2007. Khan AJ, et al. Polymorphism in cytochrome P450 2E1 and interaction with other genetic risk factors and susceptibility to alcoholic liver cirrhosis. Mutat Res. 664:55, 2009. Leevy CB, Elbeshbeshy HA. Immunology of alcoholic liver disease. Clin Liver Dis. 9:55, 2005. Lieber CS. Metabolism of alcohol. Clin Liver Dis. 9:1, 2005. Lucey MR. Management of alcoholic liver disease. Clin Liver Dis. 13:267, 2009. Maher JJ. Alcoholic steatohepatitis: management and prognosis. Curr Gastroenterol Rep. 9:39, 2007. Manzardo AM, et al. Developmental differences in childhood motor coordination predict adult alcohol dependence: proposed role for the cerebellum in alcoholism. Alcohol Clin Exp Res. 29:353, 2005. Pedersen-Bjergaard U, et al. Psychoactive drugs, alcohol, and severe hypoglycemia in insulin-treated diabetes: analysis of 141 cases. Am J Med. 118: 307, 2005. Plauth M, et al. ESPEN Guidelines on Enteral Nutrition: liver disease. Clin Nutr. 25:285, 2006. Purohit V, et al. Role of S-adenosylmethionine, folate, and betaine in the treatment of alcoholic liver disease: summary of a symposium. Am J Clin Nutr. 86:14, 2008. Rubio G, et al. Clinical predictors of response to naltrexone in alcoholic patients: who benefits most from treatment with naltrexone? Alcohol. 40: 227, 2005. Schalinske KL, Nieman KM. Disruption of methyl group metabolism by ethanol. Nutr Rev. 63:387, 2005. Song Z, et al. Inhibition of adiponectin production by homocysteine: a potential mechanism for alcoholic liver disease. Hepatology. 47:867, 2008. Zalewska-Kaszubska J, Czarnecka E. Deficit in beta-endorphin peptide and tendency to alcohol abuse. Peptides. 26:701, 2005. Zhang Y, et al. Effect of tea polyphenols on alcoholic liver injury. Zhonghua Gan Zang Bing Za Zhi. 13:125, 2005.

ASCITES AND CHYLOUS ASCITES NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Ascites is defined as a distended abdomen due to pathological fluid in the peritoneal cavity. The development of ascites indicates a pathological imbalance between the production and resorption of intraperitoneal fluid; appearance and composition vary based on the underlying pathophysiology (Rochling and Zetterman, 2009). Ascites develops in decompensated cirrhosis, cardiac failure, or renal insufficiency. Portal hypertensive gastropathy (PHG) causes upper gastrointestinal bleeding in advanced cases. Liver transplantation may be the only way to improve survival in refractory ascites (Sandhu and Sanyal, 2005). Although weight is not used for nutritional assessment here, it does help determine fluid balance. The goal of diuretic therapy in ascites is to promote weight loss of 1–3 kg/d. Nutrient depletion can occur if left untreated; fat, proteins, fat-soluble vitamins, and electrolytes may be lost. An oral diet devoid of long-chain triglycerides (LCTs) but that

includes medium-chain triglycerides (MCTs) may be used in mild cases. Management of ascites from decompensated liver disease focus on low-sodium diets and diuretics, supplemented by paracentesis or transvenous intrahepatic portosystemic shunts (Rochling and Zetterman, 2009). While paracentesis improves patient comfort and reduces intra-abdominal pressure and secondary renal dysfunction, it also carries risk for spontaneous bacterial peritonitis (SBP) or renal failure (Sargent, 2006). Bacterial contamination of ascites fluid leading to SBP is caused by bacterial translocation with subsequent bacteremia; proton pump inhibitors (PPIs) suppress gastric acid secretion, and possibly should be avoided in this population (Bajaj et al, 2009). Chylous ascites is a rare form of ascites, resulting from increased hydrostatic pressure and lymphatic blockade. Accumulation of LCT-dense chyle occurs in the peritoneum. Chyle leaks are a rare complication following abdominal surgery, trauma, cancer, or fistula. Although the incidence of chyle


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leak post surgery is low (1–4%), this complication can present significant challenges (Smoke and Delegge, 2008). Any source of large fluid volume losses, lymph vessel obstruction, or leakage may cause chylous effusions in the peritoneal cavities. Most chylous effusions heal spontaneously. Early introduction of enteral feeding may encourage chyle leaks (Malik et al, 2007), whereas total parenteral nutrition along with somatostatin can relieve the symptoms rapidly (Huang et al, 2004).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: No specific genetic causes are clear in cases of ascites. ALT AST Height Serum ascitesH & H (high in Weight albumin hemochroDry weight or gradient matosis) estimated dry (1.1 g/dL  Serum Fe, weight portal hyperferritin BMI tension) TIBC,% Diet history Alb (decreased) saturation BP Transthyretin Gluc I&O CRP Chol Temperature Na, K Trig Ascites, mild to Ca, Mg BUN, creatinine severe (Creat) Ultrasonography Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Reduce fluid retention, usually by diuretics. Mild ascites may present with fluid excess of 3–5 kg; moderate ascites may present with excess of 7–9 kg; and severe ascites may present with excess of 14–15 kg above usual weight. • Prevent electrolyte imbalances.

• Prevent further pain, fatigue, loss of lean body mass (LBM), and anorexia. • If possible, prevent hepatorenal syndrome, which can occur in patients with severe liver disease. If severe, it may require transplantation. Prepare for surgery, especially nutritionally (Hasse, 2006). • Individualize diet as needs change. • For chylous ascites, treat the underlying cause to decrease production of the chylous fluid. Malnutrition is a common result if left untreated; essential fatty acid deficiency must be avoided. Fluid and electrolyte replacement may be needed.

FOOD AND NUTRITION • Energy needs are often as high as 1.5 times normal, and protein needs are often 1.5 g/kg of body weight (Hasse and Matarese, 2008). Smaller, more frequent meals are often better tolerated. • If TF or central parenteral nutrition (CPN) is needed, use nutrient-dense formula but not glutamine-enriched formula; glutamine may increase ammonia production. While no high-quality data are available to prove that enteral nutrition is of benefit (Koretz, 2007), malnutrition should be addressed. • Ensure that intake of vitamins and minerals is adequate. Water-soluble forms of vitamins may be needed; zinc and magnesium may be needed since levels are often low after diuretic therapy (Hasse and Matarese, 2008). Monitor for signs of malnutrition. • Fluid restriction may be necessary (1–1.5 L/d), with two thirds with meals and one third for thirst/medicines. • Restrict patient’s intake of sodium to 2 g/d (Hasse and Matarese, 2008). • Often, patients take spironolactone (Aldactone) or have renal insufficiency, which may increase potassium retention. Diet should be altered in potassium if serum levels so indicate. Other diuretics may cause potassium losses. • For chylous ascites, a low-fat diet or enteral feeding is needed with MCTs as the preferred fat source; the addition of essential fatty acids (EFAs) will be needed. Adequate protein and calories are also needed since there may be significant losses. If oral diet fails, CPN may be needed (Assumpcao et al, 2008). Water-miscible forms of fat-soluble vitamins may be needed, along with extra fluid and electrolytes.

SAMPLE NUTRITION CARE PROCESS STEPS

Common Drugs Used and Potential Side Effects Excessive Sodium Intake-Ascites Assessment Data: Dietary intake records. Nutrition Diagnosis (PES): Excessive sodium intake related to presence of ascites and portal hypertension as evidenced by paracentesis of 7–8 kg over 24 hours. Intervention: Food and Nutrient Delivery—manage sodium intake. Educate about sodium sources and requirements. Counsel about preferred foods that are high in sodium and ways to alter intake that are acceptable; how to shop, dine out, travel. Monitoring and Evaluation: Track food intake through food diary. Follow-up on intake of sodium and alleviation of ascites.

• Diuretics are the most important treatment (Rosner et al, 2006). Furosemide (Lasix) is not very effective. Check whether the specific drug retains or spares potassium; spironolactone spares potassium. • Albumin replacement, while costly, may help to maintain oncotic pressure. • Somatostatin analogs have been demonstrated to be effective (Huang et al, 2004). • With bacterial peritonitis, antibiotic therapy is needed. Monitor for specific side effects. PPIs increase enteric bacterial colonization, overgrowth, and translocation (Campbell et al, 2008).


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Herbs, Botanicals, and Supplements

Chylous Ascites http://emedicine.medscape.com/article/185777-overview

• Herbs and botanical supplements should not be used without discussing with physician. • Milk thistle may have some therapeutic effects in liver disease, but no controlled trials have shown efficacy for ascites at this time.

Medicine Net http://www.medicinenet.com/ascites/article.htm

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient concerning good sources of key nutrients to include and which nutrients to limit. Instruct patient to follow high-energy, high-protein diet to prevent wasting. • Ensure that the patient follows a 2-g, low-sodium diet. Explain which foods have hidden sources of sodium, and share recipes if needed. • For chylous ascites, treatment is generally managed through a hospital stay.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Ascites http://www.nlm.nih.gov/medlineplus/ency/article/000286.htm

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ASCITES AND CHYLOUS ASCITES—CITED REFERENCES Assumpcao L, et al. Incidence and management of chyle leaks following pancreatic resection: a high volume single-center institutional experience. J Gastronintest Surg. 12:1915, 2008. Bajaj JS, et al. Association of proton pump inhibitor therapy with spontaneous bacterial peritonitis in cirrhotic patients with ascites. Am J Gastroenterol. 104:1130, 2009. Campbell MS, et al. Association between proton pump inhibitor use and spontaneous bacterial peritonitis. Dig Dis Sci. 53:394, 2008. Hasse J, Matarese L. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan L, Escott-Stump S, eds. Krause’s food nutrition and diet therapy. 12th ed. St Louis: Elsevier, 2008. Hasse JM. Examining the role of tube feeding after liver transplantation. Nutr Clin Pract. 21:299, 2006. Huang Q, et al. Chylous ascites: treated with total parenteral nutrition and somatostatin. World J Gastroenterol. 10:2588, 2004. Koretz RL. Do data support nutrition support? Part II. enteral artificial nutrition. J Am Diet Assoc. 107:1374, 2007. Malik HZ, et al. Chyle leakage and early enteral feeding following pancreatico-duodenectomy: management options. Dig Surg. 24:418, 2007. Rochling FA, Zetterman RK. Management of ascites. Drugs. 69:1739, 2009. Rosner MH, et al. Management of cirrhotic ascites: physiological basis of diuretic action. Eur J Intern Med. 17:8, 2006. Sandhu BS, Sanyal AJ. Management of ascites in cirrhosis. Clin Liver Dis. 9:715, 2005. Sargent S. The management and nursing care of cirrhotic ascites. Br J Nurs. 15:212, 2006. Smoke A, Delegge MH. Chyle leaks: consensus on management? Nutr Clin Pract. 23:529, 2008.

HEPATITIS NUTRITIONAL ACUITY RANKING: LEVEL 2 Nonviral hepatitis Dark area (necrotic area)

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Hepatitis is defined as liver inflammation resulting from alcohol use, toxic materials (carbon tetrachloride), or viral

infection (transmitted in food, liquids, or blood transfusions). There is also an autoimmune hepatitis and a NASH. Acute viral hepatitis is a widespread inflammation of the liver and is caused by hepatitis viruses A, B, C, D, or E. Hepatitis causes nausea, fever, liver tenderness and enlargement, jaundice, pale stools, and anorexia. The first stage of viral hepatitis is preicteric/prodromal (with flu-like symptoms); the second stage is icteric (with jaundice, dark urine, and light stools). The third stage is posticteric/convalescent. With chronic active hepatitis, inflamed liver cells continue for years, which is usually an autoimmune response. Metabolic diseases, such as Wilson’s disease, hemochromatosis, and alpha-1 antitrypsin deficiency, and use of some drugs, such as methyldopa, nitrofurantoin, papaverine, dantrolene, clometacine, and ticrynafen, can cause chronic hepatitis (Hasse and Matarese, 2008). American Indian and Alaska Native (AI/AN) people suffer disproportionately from infectious diseases including Hepatitis A virus (HAV) and Hepatitis B virus (HBV); childhood immunizations have reduced these disease disparities (Singleton et al, 2009). HAV, which is transmitted by fecal–oral route, comprises approximately 50% of hepatitis cases. HBV is considered a sexually transmitted disease; 20% of those affected develop


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TABLE 8-3

Hepatitis Symptoms, Transmission, and Treatment

Type

Incubation

Symptoms

Transmission

Treatment

Hepatitis A Infectious HAV

30 days

Flu-like illness, jaundice, nausea, fatigue, abdominal pain, anorexia, diarrhea, fever

Ingestion of items contaminated with infected feces, drinking water or ice contaminated with raw sewage, eating fruits, vegetables, or uncooked food contaminated during handling. Risk factors: overseas travel, anal sex, IV drug use, living in poor sanitation.

Immunoglobulin 2–3 months before or 2 weeks after exposure. Vaccine is available.

Hepatitis B Serum HBV

Can survive 7 days outside of the body

Flu-like illness, jaundice, nausea, fatigue, vomiting, fever, often no symptoms

Contact with contaminated body fluids, exposure to sharp instruments that contain contaminated blood, human bites, blood transfusion before 1975. Risk factors: IV drug use, multiple sex partners, travel or work in developing countries, transfusion before 1975.

Interferon alfa and lamivudine. HBV immunoglobulin (HBIG) within 14 days of exposure. There are safe and effective vaccines. Ribavirin is under study.

Hepatitis C HCV

Average 7–9 weeks; can live 28 weeks

Often no symptoms until liver damage occurs, flu-like illness, fatigue, nausea headaches, abdominal pain

Blood-to-blood contact, especially IV drug use and shared needles. Exposure to items with contaminated blood, such as needles (tattoo, body piercing, acupuncture), razors, nail files, toothbrushes, scissors, tampons. Sexually transmitted disease with rashes or sores. Blood transfusions before July 1992. At risk: IV drug use, had a blood transfusion or organ transplantation before July 1992, snorts cocaine. Widespread—affects 4 million people. Silent. Leading cause of cirrhosis in the United States.

Interferon or combination drug treatments. Liver transplantation for endstage. There are no vaccines. Treatment takes minimum of 1 year. Ribavirin is under study.

Hepatitis D HDV

Occurs only with HBV infection, cannot survive on own

Flu-like illness, jaundice, nausea, fatigue, vomiting, fever, often no symptoms

Sexual contact with HBV-infected person. Exposure to sharp instruments contaminated with HBV. At risk: IV drug use.

Interferon alpha for chronic cases. Vaccination against HBV provides protection against type D.

Hepatitis E HEV

2–9 weeks

Malaise, loss of appetite, abdominal pain, joint pain, fever

Fecal transmission, often through contaminated water. At risk: pregnant women, those who travel in developing countries.

No specific treatment.

some form of chronic liver disease. Table 8-3 provides symptoms and treatments for the many forms of hepatitis, including incomplete viral forms of Hepatitis D and E. Hepatitis E virus has been reported to result in chronic hepatitis in transplant patients. Hepatitis C virus (HCV) is a complex and challenging medical condition. Nearly 20% of Americans test positive for HCV. Many persons with HCV develop chronic disease; 25% of cases lead to cirrhosis, liver cancer, or liver failure that requires transplantation. Recently, the gene marker that predicts response to HCV therapy has been identified; this is significant because about half of cases respond poorly to treatment. Regular coffee consumption is associated with lower rates of disease progression (Freedman et al, 2009) and may actually reduce onset of hepatocellular cancer (Inouye et al, 2005). A deranged metabolic status and alcohol intake may trigger induction and progression of chronic HCV liver disease; variable intakes of carbohydrates, lipids, polyunsaturated fatty acids, iron, zinc, vitamin A, niacin, and alcohol are factors as are genotype, age, BMI, steatosis, and fibrosis (Loguercio et al, 2008). In the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) trial, insulin resistance, histologic

features of fatty liver disease, and weight change promoted poor outcomes; improvement in weight may modify disease progression (Everhart et al, 2009). HCV-related cirrhosis can lead to decompensation, end-stage liver failure, and death (Bruno et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: How the hepatitis virus DNA evolves and changes is of great interest to researchers. Since the identification of the hepatitis viruses over the past decades, the understanding of host innate and adaptive immune responses has increased significantly (Rehermann, 2009). Drug-induced liver injury may stem from concomitant hepatic diseases, age, and poor health status; polymorphisms of CYP liver enzymes,


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phenotyping and genotyping studies may also be needed (Tarantino et al, 2009).

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SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Bioactive Substance Intake

Clinical/History Height Weight BMI I&O Diet history Right upper abdominal pain Jaundice Temperature, fever Severe nausea, vomiting Dark urine Joint pain Lab Work IgM antibody for HAV Hepatitis B surface antibody (Anti-HBs or core antibody (Anti-HBc)

Hepatitis B e antigen (HBeAg) Hepatitis C Antibody (HCV Ab, anti-HCV) Hepatitis C viral load test (or PCR test) Bilirubin (increased) AST (increased) ALT Alk phos (increased) Chol Lactate dehydrogenase (LDH) (increased) Alb, transthyretin Globulin CRP

Absolute neutrophil count (ANC) BUN Serum ammonia Lipase Amylase (increased) PT or INR Gluc Transferrin (increased in acute stage) H & H, ferritin WBC GGT Na, K Ca, Mg

Assessment: Weight and diet history; abnormal liver tests. Intake 25% for past 3–4 weeks. Diet history reveals low intake of fruits, vegetables, whole grains, and coffee. Nutrition Diagnosis (PES): Inadequate bioactive substance intake related to loss of appetite as evidenced by low intake of nutrient-dense foods and coffee. Intervention: Food-Nutrient Delivery: high-protein, high-calorie diet in frequent small meals. Educate about the role of bioactive substances in protecting the liver; encourage use of coffee as tolerated. Monitoring and Evaluation: Evaluate diet history and weight. Assess for improvement in appetite and intake of foods rich in bioactive substances.

• Fat intake should be moderate to liberal, depending on tolerance. Cut back if diarrhea or other signs of malabsorption occur. • Supplement diet a multivitamin supplement with Bcomplex vitamins (especially thiamin, folate, and vitamin B12), vitamin K (to normalize bleeding tendency), vitamin C, and zinc for anorexia and to improve encephalopathy. Monitor for excesses of iron and vitamin A, which may not be well tolerated in a supplemental form. • Extra fluid should be encouraged, unless contraindicated. Encourage coffee intake (Freedman et al, 2009).

INTERVENTION OBJECTIVES • Promote liver regeneration and rest. Prevent further injury. • Prevent or correct weight loss, which often results from poor appetite, nausea, and vomiting. • Spare protein by providing a diet high in carbohydrates. • Force fluids to prevent dehydration, unless contraindicated. • Encourage intake of coffee and antioxidant foods. • Prevent the spread to others by hand washing and safe hygiene practices.

FOOD AND NUTRITION • For patients with all forms of hepatitis, provide a complete and balanced diet. If nutritional support is necessary, consider TF. Nocturnal feedings may be beneficial. • Use CPN only if necessary because of ileus or obstruction, and avoid products containing glutamine. • Progress to a diet of small, frequent feedings of regular or soft foods. • Diet should provide 30–35 kcal/kg body weight. Provide sufficient carbohydrate to replenish liver stores of glycogen; include 50–55% total energy as carbohydrate. • Intake of protein should be 1–1.2 g/kg body weight for acute hepatitis. Well-nourished or chronic active hepatitis patients may need levels that just meet dietary reference intake (DRI).

Common Drugs Used and Potential Side Effects • A combined HAV and HBV vaccine, Twinrix, is available in many parts of the world. Hepatitis B vaccine is found singly as Engerix-B, Recombivax, or Cornvax. Because of vaccinations, the incidence of HAV and HBV has declined, especially among children. • Two formulations of interferon (standard interferon (IFN) and pegylated IFN) can be used for sustained response to HBV and five nucleoside analogues (lamivudine, adefovir, entecavir, telbivudine, and tenofovir) for treatmentmaintained response (Buster et al, 2008). Interferon (Intron-A) can lead to dry mouth, stomatitis, nausea, vomiting, and calcium depletion. The oral antiviral entecavir (Baraclude) is more effective than lamivudine (Dienstag et al, 2007) or adefovir (Leung et al, 2009). • The gold standard for new patients with chronic HCV is the combination of pegylated interferon (Pegasys or PEG-Intron) and ribavirin (Copegus, Rebetol); individualizing dose and duration improves the sustained virologic response (Camma et al, 2005; Degertekin and Lok, 2009; McHutchison et al, 2009). There may be hemolytic side effects, depression, and weight or lipid changes. Etanercept as adjuvant therapy to interferon and ribavirin improves response and has decreased adverse effects (Zein et al, 2005). • Steroids may cause sodium retention, nitrogen depletion, or hyperglycemia.


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• Monitor for idiosyncratic drug-induced liver injury (DILI;) acute HCV may be present. DILI is caused by a single prescription medication in most cases and by multiple agents or dietary supplements in the remaining cases (Chalasani et al, 2008).

Herbs, Botanicals, and Supplements • Chaparral and kava kava are especially toxic to the liver and should be avoided. • Avoid excessive fat-soluble vitamin intake (vitamins A and D). Vitamin A toxicity is possible in compromised liver function; monitor all supplements carefully. Beta-carotene is much less toxic and may offer reasonable antioxidant protection. • Silybum marianum (milk thistle) has been shown to have clinical applications in the treatment of toxic hepatitis and viral hepatitis via its antioxidant properties. • Oregano, sage, peppermint, garden thyme, lemon balm, clove, allspice, and cinnamon as well as the Chinese medicinal herbs Cinnamomi cortex and Scutellariae radix contain very high concentrations of antioxidants. In a normal diet, intake of herbs contributes significantly to the total intake of plant antioxidants and can be an even better source of dietary antioxidants than other foods. • Herbs and botanical supplements should not be used without discussing with the physician. Carrot, schisandra, dandelion, Indian almond, and licorice have been recommended but need research.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Help patient make attractive, appetizing meals. Encourage frequent, small meals. • Educate patient about how to increase calorie, protein, and vitamin intakes. Discuss pros and cons of supplemental products. • Encourage coffee intake as well as intake of other antioxidant-rich foods. • Ensure patient abstains from alcohol and drugs that are hepatotoxic. DILI may occur with antibiotics, acetominophen, CNS agents, herbal or dietary supplements. • All children should receive Hepatitis B vaccinations. • The NIH recommends that all immigrants be screened and treated for HBV when they move to the United States to prevent liver failure or hepatic carcinoma (NIH, 2008). • In health care employment, follow standard precautions: handle needles and other sharps safely; report every needlestick on the job; get vaccinated against hepatitis B. • Consider the risks of HCV before getting a tattoo or body piercing; infection is possible if the tools have someone else’s blood on them, or if the artist or piercer does not follow practices such as washing hands and using disposable gloves.

Patient Education—Food Safety • HAV is usually spread by putting something in the mouth that is contaminated by the stool of another person with

hepatitis A. It is usually spread through household contact with an infected person, sharing utensils that are contaminated, eating or drinking contaminated food or water, touching a contaminated surface and then the mouth. • Teach safe personal hygiene in regard to hand washing and use of disinfectants, especially when traveling overseas. Boil water or drink bottled water in areas where there is a risk for HAV contamination. Eat cooked foods and fruits that you can peel and avoid eating vegetables or fruits that could have been washed with contaminated water, such as lettuce. Avoid eating raw or steamed shellfish, such as oysters, that live in contaminated waters. • Discuss other principles of food safety and personal hygiene. To protect against HCV, do not share items such as razors, toothbrushes, and other personal health items that might have had blood on them. Do not inject street drugs.

For More Information •

Centers for Disease Control and Prevention (CDC) Information http://www.cdc.gov/ncidod/diseases/hepatitis/

Department of Veterans Affairs http://www.hepatitis.va.gov/vahep?pagebasics-00–00

Hepatitis Information Network http://www.hepnet.com/

Hepatitis Information http://www.hepatitis.org

Hepatitis B Foundation http://www.hepb.org/

Hepatitis C Central http://www.hepatitis-central.com/

Hepatitis Foundation International http://www.hepatitisfoundation.org/

National HCV Prison Coalition http://www.hcvinprison.org/cms/index.php

NIDDK—Hepatitis http://digestive.niddk.nih.gov/ddiseases/pubs/viralhepatitis/

HEPATITIS—CITED REFERENCES Bruno S, et al. Predicting mortality risk in patients with compensated HCVinduced cirrhosis: a long-term prospective study. Am J Gastroenterol. 104:1147, 2009. Buster EH, et al. Peginterferon for the treatment of chronic hepatitis B in the era of nucleos(t)ide analogues. Best Pract Res Clin Gastroenterol. 22: 1093, 2008. Camma C, et al. Treatment of hepatitis C: critical appraisal of the evidence. Expert Opin Pharmacother. 6:399, 2005. Chalasani N, et al. Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States. Gastroenterology. 135:1924, 2008. Degertekin B, Lok AS. Update on viral hepatitis: 2008. Curr Opin Gastroenterol. 25:180, 2009. Dienstag JL, et al. Cross-study analysis of the relative efficacies of oral antiviral therapies for chronic hepatitis B infection in nucleoside-naive patients. Clin Drug Investig. 27:35, 2007. Everhart JE, et al. Weight-related effects on disease progression in the hepatitis C antiviral long-term treatment against cirrhosis trial. Gastroenterology. 137:549, 2009. Freedman ND, et al. Coffee intake is associated with lower rates of liver disease progression in chronic hepatitis C [published online ahead of print July 13, 2009]. Hepatology. 50:1360, 2009. Hasse J, Matarese L. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan L, Escott-Stump S, eds. Krause’s food nutrition and diet therapy. 12th ed. St Louis: Elsevier, 2008. Inouye M, et al. Influence of coffee drinking on subsequent risk of hepatocellular carcinoma: a prospective study in Japan. J Natl Cancer Inst. 97:293, 2005. Leung N, et al. Early hepatitis B virus DNA reduction in hepatitis B e antigen-positive patients with chronic hepatitis B: a randomized international study of entecavir versus adefovir. Hepatology. 49:72, 2009.


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Loguercio C, et al. The impact of diet on liver fibrosis and on response to interferon therapy in patients with HCV-related chronic hepatitis. 103: 3159, 2008. McHutchison JG, et al. Peginterferon alfa-2b or alfa-2a with ribavirin for treatment of hepatitis C infection. N Engl J Med. 361:580, 2009. NIH. NIH consensus development statement on management of hepatitis B. NIH Consensus Sci Statements. 25:1, 2008. Rehermann B. Hepatitis C virus versus innate and adaptive immune responses: a tale of coevolution and coexistence. J Clin Invest. 119:1745, 2009.

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Singleton R, et al. Impact of immunizations on the disease burden of American Indian and Alaska native children. Arch Pediatr Adolesc Med. 163:446, 2009. Tarantino G, et al. Drug-induced liver injury: is it somehow foreseeable? World J Gastroenterol. 15:2817, 2009. Zein NN, et al. Etanercept as an adjuvant to interferon and ribavirin in treatment-naive patients with chronic hepatitis C virus infection: a phase 2 randomized, double-blind, placebo-controlled study. J Hepatol. 42:315, 2005.

HEPATIC CIRRHOSIS NUTRITIONAL ACUITY RANKING: LEVEL 2–3 Fibrous septum

Regenerative nodules

Fatty cyst

Fibrous septa

Regenerative nodule

Necrotic area

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Cirrhosis is caused by chronic degeneration of the parenchymal liver cells and thickening of the surrounding tissue; the liver slowly deteriorates and malfunctions due to chronic injury. Alcoholism and hepatitis C are the most common causes; alcoholic cirrhosis is known as Laennec’s cirrhosis. Cirrhosis may also result from biliary stenosis, hepatitis B-D, obesity with nonalcoholic fatty liver disease (NAFLD), autoimmune hepatitis, prolonged exposure to toxic chemicals, and inherited diseases such as glycogen storage disease, cystic fibrosis, alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, or galactosemia. Malnutrition plays a significant role in the pathogenesis of liver injury and should be carefully managed. Cirrhosis is a disease of accelerated use of alternative fuel (such as fat) since liver stores of glycogen tend to be depleted after an overnight fast. About 50% of energy kilocalories should be consumed from carbohydrate to minimize use of fat stores or protein for energy. Glucose intolerance, insulin resistance, and higher circulating glucagon may cause early satiety, hypophagia, and depleted nutrient stores. There is a high incidence of muscle

wasting, weight loss, and malnutrition with cirrhosis. Table 8-4 list the related forms of malnutrition. Exercise and protein-rich nutrition at the early stage of liver cirrhosis can help to maintain or increase muscular volume (Kotoh et al, 2005). Nutritionally depleted patients need extra attention. Both enteral and parenteral nutritional support can improve the general nutrition condition; EN has fewer complications (Zhang et al, 2005). Cirrhosis related to CPN may be rapidly reversible after isolated intestinal transplantation (Fiel et al, 2009). Plasma aromatic amino acid (AAA) concentrations (phenylalanine, tyrosine, and tryptophan) tend to increase from rapid muscle proteolysis and decreased synthesis of proteins. Branched-chain amino acids (BCAAs) leucine, isoleucine, and valine are then imbalanced; the low BCAA to AAA ratio contributes to hepatic encephalopathy. When AAAs are high, BCAAs are more limited in cerebral uptake. A higher BCAA intake helps to improve cognitive status (Bianchi et al, 2005; Charlton, 2006). Long-term BCAA supplementation is associated with decreased frequency of hepatic failure and overall complication frequency, along with improved nutritional status (Charlton, 2006). Severe cirrhosis may lead to decreased serum lipids. Omega-3 fatty acids in enteral supplementation completely protect the liver; IV sources provide only partial protection (Alwayn et al, 2005). Liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. Participants who consume a diet high in protein are at a higher risk of hospitalization or death due to cirrhosis; those who report a diet high in carbohydrates are at a lower risk after adjusting for daily consumption of protein, carbohydrate, fat, tea or coffee, and alcohol, gender, race, age, educational attainment, U.S. geographical region, diabetes, and BMI ratio (Ioannou et al, 2009). Treatment will depend on the cause of cirrhosis and any related complications. Serum ammonia levels may be high. Fermentable fiber or lactulose may be used for management of cirrhosis. Antibiotic therapy works to prevent infections, including SBP in cirrhosis (Saab et al, 2009). Portal hypertension causes increased collateral flow, often with varices in parts of the GI tract. These veins become distended, may bleed, and cause pain. Esophageal varices are the most serious complication of cirrhosis. Splenorenal shunting with a trans-jugular intrahepatic portosystemic shunt


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TABLE 8-4

Causes of Malnutrition in Cirrhosis

Decreased Oral Intake • • • • • • • • •

Anorexia Ascites Altered mental status or encephalopathy Delayed gastric emptying Early satiety Inadequate diet or strict limits on protein, fluid and salt Medications causing GI distress or taste changes Nausea Restrictive diets or NPO for several days

Maldigestion and Malabsorption • • • • • • • • • • • • • • •

Accelerated intestinal transit Accelerated protein breakdown Anemia from impaired GI and liver function Bacterial overgrowth Biliary flow changes Choline depletion and betaine Decreased hepatic production and storage of nutrients Decreased fat absorption Diuresis, paracentesis, and micronutrient losses Increased rate of gluconeogenesis Increased urinary and fecal losses Lactulose use Pancreatic insufficiency Villi damaged by alcohol Vomiting

Adapted from Caly WR, et al. Different degrees of malnutrition and immunological alterations according to the aetiology of cirrhosis: a prospective and sequential study. Nutr J. 2:10, 2003. Stockslager JL, et al. Nutrition made incredibly easy. Baltimore: Lippincott Williams & Wilkins, 2003, p. 242.

(TIPS) is performed when the portal vein is obstructed. Portacaval blood flow is diverted from the liver by anastomosing the portal vein to the inferior vena cava. The shunt procedure is positive in most cases. Liver transplantation is needed when encephalopathy, ascites, or bleeding varices are uncontrollable.

Alb, transthyretin Height MELD score for (not valid in Weight severity (INR cirrhosis) BMI for clotting, ALT Weight loss? bilirubin, AST (increased) I&O creatinine) Bilirubin Diet history PT (prolonged); (increased) Bowel changes INR Alk phos Bleeding hemor- BUN (increased) rhoids Globulin WBC Confusion Somatomedin C Trig (increased) Loss of libido TP Chol (low?) Jaundice UA LDH Ascites Gluc (increased (increased) Spider-like or decreased) Copper, cerulo  blood vessels Na , K plasmin Ca, Mg on skin (increased) Transferrin Itching Folate H&H Fatigue GGT (decreased) BP (elevated?) Easy bruising or Serum ammonia (elevated?) bleeding CT scan Liver biopsy Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Slow the progression of scar tissue and support residual liver function. • Provide supportive treatment for ascites, edema, muscle wasting, weight loss, esophageal varices, and portal hypertension. • Monitor steatorrhea; offer suggestions for managing. • Correct nutritional deficiencies, which are common. Tube feed if needed.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Oral Food and Beverage Intake

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Autoimmune hepatitis is caused by the body’s immune system attacking liver cells and causing inflammation, damage, and cirrhosis; 70% of those with autoimmune hepatitis are female. A cirrhosisrisk score is being developed to assess host genetics and polymorphisms.

Assessment Data: Dietary intake records indicating poor appetite and intake of 50% at most meals; diagnosis of NASH; mild weight loss 5% in past 3 months; mild jaundice. Nutrition Diagnosis (PES): Inadequate oral food and beverage related to anorexia as evidenced by intake only about 50% and weight loss of  lb in past 3 months (5% UBW). Intervention: Food and Nutrient Delivery—offer smaller meals and snacks every few hours while awake; increase nutrient density and quality of foods chosen. Educate about the role of good nutrition in liver health and recovery. Assure no intake of alcohol. Monitoring and Evaluation: Improvement in appetite, reduced nausea or side effects of liver disease. Gradual return of usual weight.


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• Monitor closely for signs of hepatic encephalopathy such as drowsiness or confusion. • Provide adequate glucose for brain metabolism but beware of glucose intolerance, especially with alcoholic cirrhosis. • Prevent long-term bone disease, hyperkalemia or hypokalemia, hyponatremia, renal failure, and anemia. If hepatorenal failure occurs, hemodialysis may be necessary. • Avoid hepatic insults from alcohol, drugs, vitamins and herbal products. Consult the physician first.

FOOD AND NUTRITION • Increased energy is needed. Calculate energy at 50–75% above usual requirements if malabsorption is present or if repletion is needed. Use ideal or estimated dry weight. • Diet should provide 1–1.5 g of high-quality protein/kg body weight with adequate carbohydrates to spare protein. Meat has a high level of AAAs; vegetable proteins or casein may be better tolerated. • Fat is a preferred fuel in cirrhosis. Omega-3 fatty acids should be included (Alwayn et al, 2005). Malabsorption occurs from diminished lipase output; decrease LCTs in steatorrhea. Carefully monitor use of MCTs because they may cause diarrhea or acidosis. • Supplement diet with B-complex vitamins, vitamins C and K, zinc, and magnesium through foods or supplements. Monitor need for vitamins A and D; do not use excesses in liver disease. Liquid form may be needed for patients with esophageal varices. • TF can be used with cirrhosis or esophageal varices (Hasse and Matarese, 2008). PN is safe and improves mental state in patients with cirrhosis in whom enteral nutrition is insufficient or impossible (Plauth et al, 2009). Glutamine is not generally recommended in liver disease. • Avoid alcoholic beverages. • Control total carbohydrate intake with signs of hyperglycemia or with diabetes. • Low sodium intake (2–4 g) is recommended with ascites. • Decrease fluid if there is hyponatremia. • Enhance nutrient density of food choices if malnourished.

Common Drugs Used and Potential Side Effects • See Table 8-5.

Herbs, Botanicals, and Supplements • People with liver disease must be particularly careful because the liver processes almost everything consumed. Herbs and botanical supplements should not be used without discussing with the physician. Some herbal tea preparations may be harmful (such as Comfrey tea) and should be avoided. Chaparral is an herbal product that may contribute to severe hepatitis or liver failure (Stickel et al, 2005). Mistletoe, kava kava, European barberry, and germander should also be avoided.

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• Antioxidants, such as vitamin E and selenium, might help in treating cirrhosis. Supplements of vitamins A, C, E, selenium, methionine, and co-enzyme Q10 provide no specific benefit; fresh fruits, vegetables, and whole grains should be consumed instead. • Betaine (10 g twice daily) reduces elevated homocysteine levels and might be helpful in treating alcohol-induced cirrhosis. • Bupleurum (Bupleurum chinese) is a Chinese herb with anti-inflammatory properties that may lower risk of liver cancer in people with cirrhosis. • Licorice root (Glycyrrhiza glabra) contains glycyrrhizin. Stronger neominophagen C (SNMC) is a Japanese preparation that contains 0.2% glycyrrhizin, 0.1% cysteine, and 2% glyceine that has anti-inflammatory or cytoprotective drug. Do not take licorice with high blood pressure, pregnancy, steroid use, digoxin (Lanoxin), diuretics, or anticoagulants (warfarin/Coumadin). • Milk thistle (S. marianum) has been shown to have clinical applications in the treatment of cirrhosis through its antioxidative and anti-inflammatory effects. A total of 420 mg/d may protect the liver from damage caused by viruses, toxins, alcohol, and drugs such as acetaminophen, but milk thistle does not reduce mortality. • SAM (S-adenosylmethionine 1200–1600 mg/d) may be effective in alcoholic cirrhosis. People with liver disease have low levels of SAMe, and glutathione. Avoid use with prescription antidepressants. • Zinc deficiency has been implicated in the pathogenesis of liver diseases. Supplementation with zinc may have therapeutic benefits.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Diet may be an important and potentially modifiable determinant of liver disease (Ioannou et al, 2009). Higher CHO and lower protein intake may be a reasonable goal. • A better appetite at certain meals may be common; breakfast or another meal may be better tolerated. Some patients sleep late with a sleep reversal pattern. • Discuss use of nutrient-dense foods and higher intakes of vegetable and dairy sources of protein. • Dietary intake must be adjusted according to the changing status of the patient. Large meals increase portal pressure; recommend use of smaller meals throughout the day. • Avoid skipping meals. Discuss proper menu planning. • Avoid high doses of vitamins A and D, which may be toxic to the diseased liver. It is also not clear whether vitamin K supplementation is either safe or useful in cirrhosis. Vitamin E may be beneficial for its antioxidant properties; encourage dietary intake.

Patient Education—Foodborne Illness • Avoid raw shellfish, which may contain Vibrio vulnificus which is dangerous to people with cirrhosis.


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TABLE 8-5

Medications Used in Cirrhosis

Medication

Description

Antibiotics: tetracycline (Achromycin V), ampicillin (Polycillin), trimethoprimsulfamethoxazole (Bactrim, Septra)

Antibiotics kill the bacteria that cause infections, a common complication of cirrhosis. Possible side effects include nausea and vomiting, poor appetite, diarrhea, sore mouth or tongue, and increased sensitivity to sunlight (tetracycline).

Antiviral medications: interferon-alpha (Alferon N, Roferon-A, Intron A), ribavirin (Virazole), lamivudine (Epivir, Epivir-HBV), baraclude (Entecavir)

These may be used if viral hepatitis B or C is the cause of cirrhosis. Treatment usually lasts for 4 months. Ribavirin is an oral antiviral agent that is given twice a day. Lamivudine is used to treat hepatitis B infection. Sometimes lamivudine is combined with interferon. Side effects may include severe GI pain, feeling of fullness, nausea, tingling, burning, numbness, or pain in the hands, arms, feet, or legs.

Anti-inflammatory medications (corticosteroids): prednisone, azathioprine (Imuran)

Corticosteroids reduce liver inflammation and prevent the progression of cirrhosis. High doses given long term are associated with an increase in serious side effects. Lower doses of prednisone may be used when combined with azathioprine. Possible side effects include: hypertension, glucose intolerance, and bone thinning.

Antihypertensives (beta-blockers): atenolol (Tenormin), metoprolol (Lopressor), nadolol (Corgard), propranolol (Inderal), timolol (Blocadren)

Beta-blockers are used to reduce venous blood pressure in the abdomen (portal hypertension) to reduce the risk of esophageal variceal bleeding and other complications. Possible side effects associated with beta-blocker use include: drowsiness, dizziness, cold sensitivity, and sleep disorders.

Diuretics: “Loop” diuretics: bumetanide (Bumex), furosemide (Lasix); thiazide diuretics: hydrochlorothiazide (HydroDIURIL, Esidrix), chlorothiazide (Diuril); potassium-sparing diuretics: amiloride (Midamor), triamterene (Dyrenium)

Diuretics are used to treat the buildup of excess fluid in the body that occurs with cirrhosis (as well as other diseases). These drugs act on the kidneys to increase urine output, which reduces the amount of fluid in the bloodstream. This can help to reduce portal vein hypertension and help alleviate some of the symptoms of cirrhosis, such as fluid accumulation in the abdomen and legs. Possible side effects associated with diuretic use include: loss of appetite, nausea and vomiting, dizziness, headache, lethargy, and altered blood potassium level.

Insulin

If insulin is needed, monitor carefully for hypoglycemic episodes.

Laxatives: beta-galactosidofructose (lactulose [Cephulac] and kristalose [Chronulac])

In cirrhosis, laxatives such as beta-galactosidofructose (lactulose) can help to absorb or bind toxins, such as ammonia, in the intestine and remove them from the body. Possible side effects associated with laxative use include: diarrhea, abdominal cramping, flatulence and bloating, dehydration, and weakness. Take with food or milk.

Metal Chelating Agents: penicillamine (Cuprimine, Depen), trientine (Syprine), deferoxamine (Desferal)

Metal chelating agents draw toxic metals from the bloodstream so that the body can excrete them. Chelating agents are used to rid the body of excess copper in Wilson’s disease or excess iron in hemochromatosis. Both of these rare inherited diseases can produce liver damage resulting in cirrhosis. Possible side effects include: fever; joint pain; lesions on the face, neck, scalp, and/or trunk; rash, hives, or itching; swollen glands; sores or white spots on lips or in mouth; cyanosis; blurred vision; convulsions; wheezing or fast breathing; tachycardia; flushing of skin; nausea, vomiting or diarrhea; and blood in the urine.

Vitamin K: phytonadione (AquaMEPHYTON, Mephyton)

Bleeding abnormalities are common in cirrhosis. Vitamin K helps prevent excessive bleeding. Possible side effects include: flushing of the face and unusual taste.

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

CDC—Cirrhosis http://www.cdc.gov/nchs/fastats/liverdis.htm

Cirrhosis Diet http://digestive-system.emedtv.com/cirrhosis/cirrhosis-diet.html

Hepatic Foundation International http://www.hepfi.org/

Hep Net http://www.hepcnet.net/nutritionandcirhossis.html

Medicine Net—Cirrhosis http://www.medicinenet.com/cirrhosis/article.htm

Milk Thistle http://nccam.nih.gov/health/milkthistle/ataglance.htm

National Institutes of Health—Cirrhosis http://www.nlm.nih.gov/medlineplus/cirrhosis.html

University of Maryland http://www.umm.edu/altmed/articles/cirrhosis-000037.htm

Veterans Administration http://www.hepatitis.va.gov/vahep?pagediet-03–00

WebMD—Cirrhosis http://www.webmd.com/digestive-disorders/cirrhosis-liver

HEPATIC CIRRHOSIS—CITED REFERENCES Alwayn IP, et al. Omega-3 fatty acid supplementation prevents hepatic steatosis in a murine model of nonalcoholic fatty liver disease. Pediatr Res. 57:445, 2005. Bianchi G, et al. Update on branched-chain amino acid supplementation in liver diseases. Curr Opin Gastroenterol. 21:197, 2005. Charlton M. Branched-chain amino acid enriched supplements as therapy for liver disease. J Nutr. 136:295S, 2006. Fiel MI, et al. Rapid reversal of parenteral-nutrition-associated cirrhosis following isolated intestinal transplantation. J Gastrointest Surg. 13:1717, 2009. Hasse J, Matarese L. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan L, Escott-Stump S, eds. Krause’s food nutrition and diet therapy. 12th ed. St Louis: Elsevier, 2008. Ioannou GN, et al. Association between dietary nutrient composition and the incidence of cirrhosis or liver cancer in the United States population. Hepatology. 50:175, 2009. Kotoh K, et al. High relative fat-free mass is important for maintaining serum albumin levels in patients with compensated liver cirrhosis. World J Gastroenterol. 11:1356, 2005. Plauth M, et al. ESPEN Guidelines on Parenteral Nutrition: hepatology. Clin Nutr. 28:436, 2009. Saab S, et al. Oral antibiotic prophylaxis reduces spontaneous bacterial peritonitis occurrence and improves short-term survival in cirrhosis: a metaanalysis. Am J Gastroenterol. 104:993, 2009. Stickel F, et al. Herbal hepatotoxicity. J Hepatol. 43:901, 2005. Zhang K, et al. Early enteral and parenteral nutritional support in patients with cirrhotic portal hypertension after pericardial devascularization. Hepatobiliary Pancreat Dis Int. 4:55, 2005.


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HEPATIC FAILURE, ENCEPHALOPATHY, AND COMA NUTRITIONAL ACUITY RANKING: LEVEL 3–4

Coma

Jaundice

Spider nevi

Pectoral alopecia

Esophageal varices

Gynecomastia Liver damage

Splenomegaly

Distention of abdominal veins Ascites Palmar erythema

Testicular atrophy Altered hair distribution

Hemorrhagic tendency

Ankle edema

Asset provided by Anatomical Chart Co.

Bone marrow changes

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DEFINITIONS AND BACKGROUND Hepatic failure is common in critical illnesses. Acetaminophen overdose is the leading cause of the acute form. Hallmarks include coagulopathy, usually an INR of 1.5 or more, and encephalopathy. Typical nutrition assessment measures may not reflect the severity of malnutrition because ascites can mask loss of LBM. Blood levels of lactate appear to be good markers for predicting which patients can be managed medically and which need a transplantation (MacQuillan et al, 2005). If hepatorenal syndrome occurs, hemodialysis may be needed; creatinine is not useful here but glomerular filtration rate (GFR) is an important measure. Hepatic encephalopathy (HE) is a clinical complication caused by portosystemic venous shunting, with or without intrinsic liver disease (Munoz, 2008). HE can be precipitated by GI bleeding, abnormal electrolytes, renal failure, infection, diuretic therapy, use of sedatives or medications that affect the central nervous system, and constipation. HE is estimated to occur in 30–45% of patients with liver cirrhosis and in 10–50% of patients with portosystemic shunts (Eroglu and Byrne, 2009). Patients with HE present with the onset of mental status changes ranging from subtle psychologic abnormalities to profound coma (Munoz, 2008). See Table 8-6 for stages of HE. Acute forms may be reversible; chronic forms may worsen or lead to coma. Brain glutamine, a byproduct of ammonia detoxification, is elevated in HE (Rama Rao et al, 2005). Causes of hyperammonemia include GI bleed, muscle catabolism, infection, dehydration, noncompliance with lactulose/neomycin, and constipation. The basis of neurotoxicity from ammonia, gamma-aminobutyric acid (GABA), or other agents is not clear. Astrocytes are the most abundant cell type in the brain; they buffer extracellular K(), regulate neurotransmitter release, form the blood–brain barrier, release growth factors, and regulate the brain immune response (Gee and Keller, 2005). Acute exposure of the astrocytes to ammonia results in alkalinization, with calcium-dependent glutamate release and dysfunction (Rose et al, 2005). Encephalopathy is usually not caused by altered protein in the diet (Shawcross and Jalan, 2005). Protein restriction is only necessary in rare, refractory encephalopathy. Patients who have been given a portacaval

TABLE 8-6

shunt (TIPS) may benefit from mild protein restriction; nutritional status improves after the shunt. Decreased dopamine and BCAAs occur in HE; increased AAAs and serotonin also occur. Nevertheless, the use of BCAA solutions is not fully supported by the literature. Measuring nutritional status in HE can be a challenge. Subjective global assessment and other techniques are not very effective. Measuring handgrip strength may be useful in undernourished patients (Alvares da Silva and Reverbel da Silveira, 2005). Because oxidative stress is a possible trigger in the progression of chronic liver disease, antioxidants and omega-3 polyunsaturated fatty acids may be useful. In addition, because zinc improves taste and immune function, supplementation may improve neurological symptoms and nutrition (Grungrieff and Reinhold, 2005). Minimal hepatic encephalopathy (MHE) is the mild cognitive impairment commonly seen in patients who have cirrhosis, but it often goes undiagnosed (Stewart and Smith, 2007). It is important to identify signs and symptoms that require medical attention. Commonly associated disorders include energy production deficiencies (hypoglycemia), coagulation abnormalities, immune system dysfunctions, cerebral edema, or hepatic coma (Cochran and Losek, 2009). Treatment of HE involves correction of sepsis, gastrointestinal bleeding, and electrolyte imbalance (Sundaram and Shaikh, 2009). Lactulose may be used. Fischer’s ratio between BCAAs and AAAs correlates with the degree of HE; the lower Fischer’s ratio, the higher the grade of HE (Koivusalo et al, 2008). Some procedures, such as albumin dialysis, may be used; plasma levels of neuroactive amino acids, methionine, glutamine, glutamate, histidine, and taurine are lowered as a result (Koivusalo et al., 2008). Signs of impending coma include irritability, change in mentation; disorientation to time and place; asterixis or involuntary jerky movements of the hands; constructional apraxia (inability to draw simple diagrams;) difficulty with writing; ascites, edema; fetor hepaticus (sweet, musty odor of the breath); and GI or esophageal bleeding. Coma patients have increased intracranial pressure and brain edema with a poor prognosis without liver transplantation. Clearly, much more research is needed to resolve these life-threatening disorders.

Stages of Hepatic Encephalopathy—West Haven Classification

Grade 0

Minimal hepatic encephalopathy. Lack of detectable changes in personality or behavior. Minimal changes in memory, concentration, intellectual function, and coordination. Asterixis is absent.

Grade 1

Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be detected.

Grade 2

Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time.

Grade 3

Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, present but incomprehensible speech.

Grade 4

Coma with or without response to painful stimuli.

Adapted from: Emedicine. Accessed September 5, 2009, at http://www.emedicine.com/med/topic3185.htm.


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ASSESSMENT, MONITORING, AND EVALUATION

489

SAMPLE NUTRITION CARE PROCESS STEPS Underweight and Altered Nutritional Lab Values

CLINICAL INDICATORS Genetic Markers: HE is generally acquired.

Assessment Data: Dietary intake records; temporal wasting; low weight and BMI of 17; loss of LBM in arms and legs; ascites; confusion and signs of impending coma. Altered LFTs and albumin 2.1 g/dL. Nutrition Diagnoses (PES):

Electroencephalogram Height (EEG) Weight Handgrip Euvolemic (dry) strength weight Acute Physiology BMI and Chronic Diet history Health I&O Evaluation BP (APACHE II) Muscle stiffness score or rigidity Changes in menLab Work tation or Serum lactate personality levels Daytime sleepiBUN ness (decreased) Decreased Creatinine self-care (not valid?) Dysfunctional movements, Bilirubin (increased) agitation Flapping tremor Alk phos (increased) (positive AST (increased) Babinski Tumor necrosis reflex) factor Jaundice (elevated) Ascites ALT, GGT Early satiety? Ca, Mg Musty odor of H&H breath and (decreased) urine Clinical/History

Serum iron, ferritin Na, K Chol, Trig UA Ammonia Alb (decreased) Transthyretin Nitrogen (N) balance CRP PT or INR Transferrin Gluc (decreased) Actin-free Gc globulin (Af-Gc) Plasma isoleucine, leucine, valine Plasma tryptophan, phenylalanine, tyrosine Fischer’s ratio Serum insulin, epinephrine Thyroxine

NC 3.1 Underweight related to decreased appetite prior to admission as evidenced by 90% DBW, BMI 17. NC 2.2 Altered nutrition related lab value related to liver dysfunction as evidenced by elevated ALT, ALP, AST, NH3, albumin 2.7 g/dL. Interventions: Food and Nutrient Delivery: ND 1.2 Modify, distribution type or amount of food and nutrients within meals or specified time (recommend diet change to 2 g sodium, 60 g protein, and six small meals per day; focus on lower animal proteins) Education: E 1.1 Purpose of nutrition education Counseling: C 2.2 Goal setting(improve lab values with change) Coordination of Care: RC 1.1 Team meeting Monitoring and Evaluation: Track food intake (food diary or history); improvement in albumin or other lab values. Improvement in weight and BMI.

• Reduce circulating amines and lessen shunting of blood around the liver. Control hemorrhage and blood loss into the gut. • Correct anemia, zinc, and other deficiencies such as magnesium, thiamin, and folate (see Table 8-7). • Prevent progression to hepatic cancer and improve quality of life.

FOOD AND NUTRITION Follow Practice Parameters of the American College of Gastroenterology (Blei and Cordoba, 2009):

INTERVENTION OBJECTIVES • Treat specific causes and prevent multiple organ system failure. Stop any GI bleeding; offer life support if comatose. • Provide nutrition support to promote regeneration of liver tissue. Support respiratory, neurological, GI, circulatory systems while the liver regenerates. • Avoid skeletal muscle catabolism from inadequate oral intake, severely restricted diets or nothing by mouth (NPO) status. • Decrease ammonia and toxin production. Normalize serum amino acid patterns. • Avoid daytime or nocturnal fasting by using frequent meals and late evening snacks. • Prevent hypokalemia, sepsis, starvation, and acute crises.

• Acute encephalopathy: Withhold oral intake for 24–48 hours, and provide intravenous glucose until improvement is noted. Start TF if patient appears unable to eat after this period. Protein intake begins at a dose of 0.5 g/kg/d; progress to 1–1.5 g/kg/d. • Chronic encephalopathy: Focus protein intake on dairy products and vegetable-based diets. Consider oral BCAAs for individuals intolerant of all protein. • Problematic encephalopathy: Consider lactulose, neomycin, oral zinc, and surgical shunts. • With coma, use TF with 0.5–0.6 g protein/kg body weight; advance to 1–1.5 g/kg euvolemic weight. Higher intake of BCAAs and glutamine-enriched products are not usually beneficial. • Glucose is needed to reduce likelihood or presence of hypoglycemia. Start feeding slowly to prevent refeeding syndrome; then to progress to desired level of intake in the malnourished patient. It is prudent to start with


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TABLE 8-7 Nutrient Relationships in Hepatic Failure and Hepatic Encephalopathy Increased sodium and fluid

Edema; fluid retention

Decreased protein

Swollen belly (ascites) from decreased albumin production

Decreased protein and fat with malabsorption

Somnolence, euphoria, asterixis, coma

Decreased vitamin A

Increased respiratory infections

Decreased vitamins C and K

Hemorrhage; scurvy

Decreased magnesium, niacin, thiamin

Hallucinations, delirium, bei-beri, pellagra

Decreased B-complex vitamins, iron, and protein

Glossitis, anemias

Decreased thiamin

Amnesia, confabulation, Korsakoff’s psychosis

Decreased niacin

Memory loss

Decreased folacin

Degeneration of spinal cord

Decreased vitamin K

Muscle weakness

Decreased magnesium

Marked anxiety, hyperirritability, confusion, seizures, tremor

Decreased zinc

Poor taste acuity, impaired wound healing

• •

15–20 kcal/kg and progress as tolerated over several days. For the patient who is not comatose, diet should provide moderate-to-high levels of protein (Shawcross and Jalan, 2005). Protein restriction has been discontinued in most cases. Use enteral nutrition to correct protein–energy malnutrition. A calorie-dense product is desirable. A nasogastric tube placement may be better tolerated when there is ascites. To minimize muscle catabolism, diet should provide extra energy from carbohydrates and fats. Use 30 kcal/kg to maintain and 35 kcal/kg body weight to replete tissue; calculate needs using indirect calorimetry whenever possible. Fats should be 30–35% of kilocalories, using MCT if needed. When necessary, administer PN with 50% of energy as nonprotein kilocalories. Because PN does not use the gut, where bacteria may otherwise produce ammonia, parenteral protein is well tolerated and may be given as 1.0–1.5 g/kg. Parenteral solutions have risks of infection and metabolic complications. Ensure adequate intake of fluids and electrolytes as monitoring determines. Often, sodium is limited to aid diuresis. Restrict fluid only with dilutional hyponatremia (usually 1000–1500 mL). Vitamin–mineral supplements may be needed for niacin, thiamin, folate, phosphate, zinc, calcium, and magnesium. Monitor fat-soluble vitamin intake (vitamins A, D, E, and K) carefully and avoid excesses. Avoid copper and manganese at this time, and do not give iron supplements randomly.

• If oral diet is tolerated, use a bedtime snack to avoid hypoglycemia. Small meals and snacks throughout the day may increase intake; oral liquid supplements can be made readily available. Avoid severe restrictions of protein, sodium, fluid, fiber. Liquids are often better tolerated than bulky meals.

Common Drugs Used and Potential Side Effects • Drug-induced ALF accounts for approximately 20% of ALF in children and a higher percentage of ALF in adults; the most common cause of drug-induced ALF in children is acetaminophen (Murray et al, 2008). N-acetylcysteine is effective in ALF caused by acetaminophen overdose, with better results related to how soon it is given (Khashab et al, 2007). • For other treatments of HE, see Table 8-8.

Herbs, Botanicals, and Supplements • Healthy enterocytes can degrade peptides and amino acids and use ammonia via glutamate, glutamine, citrulline, and urea synthesis (Bergen and Wu, 2009). Probiotic, CO2-producing lactobacilli are useful for enhancing gut microbial metabolism in HE (Bergen and Wu, 2009; Bongaerts et al, 2005). Other treatments using prebiotics and probiotics are under study; see Table 8-9. • Avoid high doses of vitamins A and D, which may be toxic to the diseased liver. • Herbs and botanical supplements should not be used without discussing with physician. For example, chaparral use can lead to liver failure. Kava kava and many other products should also be avoided in this population. Silybum marianum (milk thistle) is not proven to have a therapeutic role in liver failure.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Hospitalization is usually required; discuss symptoms that require immediate medical attention. • Dietary intake must be adjusted according to the changing status of the patient. Large meals increase portal pressure; use smaller meals more frequently. • Milk and eggs tend to produce less ammonia than meats or poultry. • Discuss the importance of refraining from use of alcoholic beverages. • A better appetite at certain meals may be common. Identify if breakfast or another meal is best tolerated. Some patients sleep late and have a sleep reversal pattern. • Discuss proper menu planning. Avoid skipping meals.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.


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TABLE 8-8

491

Medications Used for Hepatic Encephalopathy

Medication

Description

Antibiotics: Neomycin

Orally administered antibiotics kill some of the bacteria present within the intestines that produce the dangerous toxins. Be careful not to miss doses. Adverse side effects are common.

Rifaximin

Rifaximin is a nonabsorbed antibiotic with a broad spectrum of activity against aerobic and anaerobic Gram-positive and Gram-negative organisms. It has a better safety and tolerability profile than that of lactulose and possibly neomycin.

Cholestyramine or ursodeoxycholic acid

For itching.

Dietary supplements

Vitamin D and calcium may be needed if osteopenia occurs. Fat-soluble excesses should be avoided since the liver is damaged.

Laxatives: Lactulose (Chronulac, Duphalac, Cholac Syrup, Constulose)

Lactulose is a synthetic sugar used to treat constipation. It is broken down in the colon into products that pull water out from the body and into the colon to soften stools. It also removes ammonia. One or two bowel movements a day are needed. Take lactulose with juice. It may cause abdominal bloating or gas. Be careful not to miss doses, but avoid excesses which can cause diarrhea.

Zinc sulfate or acetate

RNA oxidation and an increase of free intracellular zinc is a consequence of astrocyte swelling and ROS/RNOS production. RNA oxidation may impair postsynaptic protein synthesis, which is critically involved in learning and memory consolidation. Zinc supplementation is recommended.

Medications to avoid

Certain medications can increase the brainâ&#x20AC;&#x2122;s sensitivity to ammonia and other toxins and should not be taken: sedative drugs (Valium, Ativan, Xanax), pain medications (Darvocet, codeine, Vicodin, Percocet, Demerol), antinausea agents (Phenergan, Compazine), antihistamines (Benadryl)

TABLE 8-9

Prebiotics, Probiotics, and Healthy Foods Shopping Lista

Grains

Beans and Peas (canned/dried)

Oils

Whole grain breadsb (rye,c barley,c wheat,c oat,b buckwheatb) Pasta,b whole grainb Bulgur,b wheat berriesc Polenta, cornmeal Tortillas Flours,b whole grain (pastry)b Rice, brown Oats Wild rice Exotic grains (spelt, quinoa) Cereals, prepared whole grain Barley,b pearledc

Beans:b black, pinto, garbanzo, kidney lima, soy, small red, small white, cannellini, Black eyed peas, exotics Lentils:b black, red, brown, French Split peas (yellow, green) Edamame (soy beans)

Olive Canola or vegetable Peanut Sesame Walnut Exotic

Baking

Nuts and Seeds

Dairy and Cold Case

Flour, whole grain Jam or jelly Syrup Honey Sugar Baking soda/powder Tapioca Vanilla Yeast Chocolate Corn Starch Baking mixes Carob

Almondsb Cashews Coconuts, fresh Flaxseedb Hazelnuts Macadamias Peanuts Pecans Pine nuts Pistachios Poppy seeds Pumpkin seeds Sesame seeds Sunflower seeds Walnuts Tahini (ground sesame seeds) Nut butters from the above

Pesto Salsa Yogurtd Yogurt smoothiesd Kefird Cottage cheeseb (check for live cultures ord prebiotic inulin)b Skim Milk Acidophilus milkd Cheese Eggs Dips Spreads Tofue Miso (soy paste)e

(continued)


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TABLE 8-9 Prebiotics, Probiotics, and Healthy Foods Shopping Lista (continued) Beverages

Condiments

Meat, Poultry, Fish, Other

Coffee Tea Chocolate or cocoa Beere Winee Soymilk Nut milk Rice milk Kombucha (tea/live cultures)e

Vinegar (apple cider, balsamic, red wine, malt)e Horseradish Mustard Mayonnaise Catsup Worcestershiree Soy sauce/Tamarie Chutney Salsa Chile oil or sauce Wasabi

Chicken Turkey Beef Pork Lamb Fish Exotics: bison, ostrich, etc. Tofue Tempeh (soy beans)e Seitan (wheat gluten) Natto (fermented beans)e Soy turkey, soy lunchmeat, etc.

Fermented/Picklede

Snacks

Freezer Items

Deli

Pickled cucumbers Olives Pickled beets Kimchi (fermented cabbage) Sauerkraut

Popcorn Dips made from beans, vegetables Crackers with whole grain Chips, whole grain Snack barsb (check ingredients for whole grains,b inulin,b probioticsd)

Vegetables Fruits Waffles

Bean salads Grain salads Vegetable salads

Vegetables Artichokesc Asparagusc Avocados Bamboo shoots Beans, green or waxed Beans, lima (unshelled) Beets Bok choy Broccoli Broccoli rabe Brussel sprouts Burdockc Cabbage (red, green, Chinese) Cauliflower Carrots Celery Celery root Chestnuts Chicoryc Corn (in husks) Cucumbers Daikon radish Dandelion greensc Eggplant Endive Fennel Fiddleheads Garlicc

Ginger root Greens (spinachc, chard, leafy greens etc.) Horseradish Jerusalem artichokec Jicamac Kale Kohlrabi Leeksc Lettuce, iceberg Lettuce, leaf Lettuce (dandelion greensc, endive, watercress) Mushrooms Okra Onionsc Onions, dryc Onions, greenc Palm hearts Parsnips Peas (unshelled) Peppers, chili Peppers, bell Potatoes Potatoes, sweet, yams Pumpkin Radishes Rhubarb

Fruits Apples Apricots Asian pears Bananasc Berries (raspberry, blackberry, strawberry, gooseberry, elderberry, red currants, exotics) Cactus pears Cherries Coconut, fresh Cranberries Currants Dates Vegetables (continued) Rutabagas Salsifyc Seaweed, edible Shallotsc Snow peas Sprouts, bean, alfalfa, etc Squash, summer varieties Squash, winter varieties Taro Tomatillo Tomatoes Turnips Watercress

Herbs and Spices Yaconc Figs Gooseberries Grapefruit Grapes Guava Jujubee Kiwi Kumquat Lemon Lime Mango Melon, musk Nectarines Oranges Papaya Passion fruit Peaches Pears Persimmon Pineapple Plantain Plums, pluot, plumcot Pomegranate Pommelo Raisins Star fruit Quince Watermelon

Allspice Anise Basil Black Pepper Caraway Chili Cilantro Cinnamon Clove Coriander Cumin Dill Fennel Ginger Mace Marjoram Mint Nutmeg Oregano Parsley Rosemary Sage Savory Tarragon Thyme Turmeric Vanilla

NOTE—read labels: Strain. What probiotic is inside? Lactobacillus casei Shirota, Lactobacillus acidophilus, Bifidobacteriumlactis, Saccharomyces cereviase boullardii. CFU (Colony Forming Units). How many live microorganisms are in each serving? When does it expire? Packaging should ensure an effective level of live bacteria through the “best by” or expiration date. Suggested serving size. How much do I take? Health benefits. What can this product do for me? Proper storage conditions. Where do I keep it to ensure maximum survival of the probiotic? Corporate contact information. Who makes this product? Where to do I go for more information? From: International Scientific Association for Probiotics and Prebiotics, http://www.ISAPP.net. Adapted from: Gut Insight © 2009 Gut Insight: probiotics and prebiotics for digestive health and well-being by Jo Ann Tatum Hattner, MPH, RD, with Susan Anderes, MLIS. San Francisco: Hattner Nutrition, 2009. Used with permission. Other resources: U.S. Probiotics, http://www.usprobiotics.org/. a Seventy percent of the body’s immunity is in the gut. There are 300–1000 species of bacteria, 100 trillion in the gut (about 3 lb). Alcohol, smoking, stress, poor bowel hygiene, aging, intestinal infections, antibiotics, and a poor diet can affect intestinal microbiota. The normal levels of lactobacilli, bifidobacteria, and other “good bacteria” may be decreased. Imbalanced flora may lead to abnormal GI function, such as constipation, diarrhea, flares of inflammatory bowel disease or irritable bowel syndrome, other pancreatic or abdominal inflammations, allergic responses, and an impaired immune system. Choosing foods wisely can improve gut health. b Prebiotic potentials. c Prebiotic stars.* d Probiotics. e Fermented foods.


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For More Information •

Hepatic Encephalopathy http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm

Medline http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm

HEPATIC FAILURE, ENCEPHALOPATHY, AND COMA— CITED REFERENCES Alvares da Silva MR, Reverbel da Silveira T. Comparison between handgrip strength, subjective global assessment, and prognostic nutritional index in assessing malnutrition and predicting clinical outcome in cirrhotic outpatients. Nutrition. 21:113, 2005. Bergen WG, Wu G. Intestinal nitrogen recycling and utilization in health and disease. J Nutr. 139:821, 2009. Blei AT, Cordoba J. Practice Guidelines: Hepatic Encephalopathy. Accessed October 9, 2009, at http://www.nature.com/ajg/journal/v96/n7/abs/ ajg2001494a.html. Bongaerts G, et al. Effect of antibiotics, prebiotics and probiotics in treatment for hepatic encephalopathy. Med Hypotheses. 64:64, 2005. Cochran JB, Losek JD. Acute liver failure in children. Pediatr Emerg Care. 23:129, 2009. Eroglu Y, Byrne WJ. Hepatic encephalopathy. Emerg Med. 27:401, 2009.

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Gee JR, Keller JN. Astrocytes: regulation of brain homeostasis via apolipoprotein E. Int J Biochem Cell Biol. 37:1145, 2005. Grungrieff K, Reinhold D. Liver cirrhosis and “liver” diabetes mellitus are linked by zinc deficiency. Med Hypotheses. 64:316, 2005. Khashab M, et al. Epidemiology of acute liver failure. Curr Gastroenterol Rep. 9:66, 2007. Koivusalo AM, et al. Albumin dialysis has a favorable effect on amino acid profile in hepatic encephalopathy. Metab Brain Dis. 23:387, 2008. Macquillan GC, et al. Blood lactate but not serum phosphate levels can predict patient outcome in fulminant hepatic failure. Liver Transpl. 11: 1073, 2005. Munoz SJ. Hepatic encephalopathy. Med Clin Am. 92:795, 2008. Murray KF, et al. Drug-related hepatotoxicity and acute liver failure. J Pediatr Gastrointest Nutr. 48:395, 2008. Rama Rao KV, et al. Differential response of glutamine in cultured neurons and astrocytes. J Neurosci Res. 79:193, 2005. Rose C, et al. Acute insult of ammonia leads to calcium-dependent glutamate release from cultured astrocytes: an effect of pH. J Biol Chem. 280:20937, 2005. Shawcross D, Jalan R. Dispelling myths in the treatment of hepatic encephalopathy. Lancet. 365:431, 2005. Stewart CA, Smith GE. Minimal hepatic encephalopathy. Nat Clin Pract Gastroenterol Hepatol. 4:677, 2007. Sundaram V, Shaikh OS. Hepatic encephalopathy: pathophysiology and emerging therapies. Med Clin N Am. 93:819, 2009.

LIVER TRANSPLANTATION NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Liver transplantation (LT) is now a viable alternative for patients with end-stage hepatic failure due to cirrhosis, viral hepatitis, chronic active liver disease, alpha-1 antitrypsin deficiency, primary sclerosing cirrhosis, cholangiocarcinoma, hemochromatosis, autoimmune hepatitis, Budd–Chiari syndrome, hepatoma, primary biliary cirrhosis, or cystic fibrosis. Nutritional depletion occurs in this population before surgery. Muscle wasting, cachexia, and decreased fat stores are common. Supportive care for all patients with ALF includes adequate enteral nutrition, aggressive screening and treatment of infection, prophylactic broad-spectrum antibiotics, and antifungal agents (Hay, 2004). Patients are screened carefully for other underlying conditions; many will not be suitable for transplantation. Alcohol is a major contributor to cirrhosis and the need for transplantation. NASH, obesity, diabetes, and hyperinsulinism play a role in cirrhosis and the need for transplantation. Older age, higher BMI, diabetes and HTN are associated with poor outcomes (Malik et al, 2009). Symptoms and signs leading to the need for transplantation include ascites, jaundice, edema, CNS dysfunction, and cachexia. In living donor liver transplantation (LDLT), a

healthy, living person donates a portion of his or her liver to another person. Preoperative and early postoperative nutrition may speed recovery, lessen time in the intensive care unit, and promote fewer infections. Subjective global assessment (SGA) is often useful because lab work varies so much in liver disease. SGA includes physical signs and symptoms, dietary changes and intolerances, medical/surgical history, GI symptoms and complaints, history of weight loss, and functional capacity. Transthyretin may be a reliable test when the inflammatory process resolves. Patients with end-stage liver disease are prone to develop osteopenia and osteoporosis, and additional bone loss may occur with the use of immunosuppression agents after transplant. Bone loss occurs early after liver transplant and leads to postoperative fractures, especially with low bone mass. Calcium and vitamin D intake must be a priority. In general, enteral nutrition is effective in maintaining nutritional status after transplantation. Nutritional supplementation after LT quickly restores protein synthesis. PN may be needed (Plauth et al, 2009). Patients with LT regain a normal life within months of surgery but have a lifetime of immunosuppressive treatment. Intravenous fish oil lipid emulsion may be useful.


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INTERVENTION OBJECTIVES

CLINICAL INDICATORS Genetic Markers: Respiratory chain disorders may present with neonatal ALF, hepatic steatohepatitis, cholestasis, cirrhosis with chronic liver failure and the need for LT; molecular defects (mutations in nuclear genes such as SCO1, BCS1L, POLG, DGUOK, and MPV17 and the deletion or rearrangement of mitochondrial DNA) have been identified (Lee and Sokol, 2007). Methylmalonic acidemia with complete mutase deficiency (mut(0) type) is an inborn error of metabolism with high mortality and morbidity; LT may be a solution (Chen et al, 2009). Clinical/History Height Weight—usual Present weight BMI SGA with diet history Cachexia? Edema Nausea and vomiting I&O BP Ascites? Early satiety? Jaundice CNS dysfunction? DEXA

Serum Fe, ferritin Serum lactate Transferrin levels BUN, creatinine BUN, Creat Chol, Trig Alb, Carotenoids Transthyretin AST, ALT N balance GGT   Na , K Gluc CRP (elevated?) PT or INR Alk phos Bilirubin Amino acid profiles Serum ammonia Cerebrospinal fluid (CSF) Ca, Mg H&H Lab Work

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Intake From Enteral Nutrition Assessment Data: I & O records showing long periods without enteral infusion for testing, lab work and nursing shift changes. Dry weight beginning to drop below desired range. Nutrition Diagnosis (PES): Inadequate intake of enteral nutrition (NI-2.3) related to infusion being held for 3 hours daily as evidenced by intake at 70% of expected protein and kilocalories. Intervention: Food and Nutrient Delivery—recalculation of TF formula to provide appropriate protein and kilocalories over 21 versus 24 hours daily. Education of nursing staff about necessary change in the TF order; coordination of care. Monitoring and Evaluation: Track intake of enteral infusion; identify if weight is stable and labs are normal. Determine if current intake meets estimated needs; continue therapy. Evaluate every other day until discharge.

Pretransplantation • Correct malnutrition; lessen edema and ascites. • Treat hyponatremia and electrolyte imbalances, depending on medications and renal function. • Prevent or correct catabolic wasting of muscle mass from increased hormonal levels of insulin, glucagon, epinephrine, or cortisol. • Provide nutritional support in an appropriate mode of feeding to provide a normalized nitrogen balance and other normalized laboratory values. Consider nausea, vomiting, anorexia, diarrhea. • Correct fat malabsorption, with or without steatorrhea and diarrhea. • Normalize blood glucose levels and prevent hypoglycemia; diabetes is common. • Correct abnormal amino acid metabolism and neural accumulation of amino acids that are precursors for dopamine, serotonin, and norepinephrine. Normalize serum ammonia.

Posttransplantation • Promote normalized protein synthesis in the liver for albumin, globulins, clotting factors. Monitoring nutritional parameters will not be a simple process; many usual measurements are not useful markers of nutritional decline (Shahid et al, 2005). • Prevent or correct hyperglycemia, fasting hypoglycemia, and abnormal glucagon storage. Diabetes is a common complication from use of prednisone, cyclosporine, and tacrolimus. • Prevent hypophosphatemia and refeeding syndrome. • Support wound healing. • Prevent infection and rejection, the most common complications. Portal venous complications have been well documented and can lead to graft failure (Woo et al, 2007). • Manage long-term hypercholesterolemia, hypertension, obesity, osteopenia, or bone fractures. • The role of probiotics in LT is unclear (Jenkins et al, 2005).

FOOD AND NUTRITION Pretransplantation • Energy should be 35–45 kcal/kg dry weight for malnourished patients and 30–35 kcal/kg dry weight to maintain weight (Hasse, 2005). Use sufficient carbohydrate and fat to spare protein and meet energy needs. Monitor closely for hyperglycemia. • Protein needs will vary: 0.8–1.0 g/kg dry weight in compensated liver disease. Calculate 1.5–2.0 g/kg dry weight in decompensated liver disease and 0.6–1.0 g/kg dry weight for HE. • Modify for fluid, sodium, potassium, and other electrolytes depending on lab values and renal status. Restrict


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TABLE 8-10 Post–Liver or Pancreatic Transplant Nutrition Guidelines Nutrient

LIVER Short-Term

LIVER Long-Term

Pancreas Short-Term

Pancreas Long-Term

Calories

20–30% above normal or measure through indirect calorimetry; increase for weight gain

Maintenance: 30–35 kcal/kg depending on activity level

20–30% above normal or measure through indirect calorimetry; increase for weight gain

Maintenance: 30–35 kcal/kg depending on activity level

Protein

1.3–2 g/kg/d

1 g/kg/d

1.3–2 g/kg/d

1 g/kg/d

Carbohydrate

50–70% of calories

50–70% of calories; restrict simple sugars

45–55% of kcals; use CHO counting

45–55% of kcals; use CHO counting

Fat

30% of calories; up to 50% with severe hyperglycemia

30% of total calories; 10% saturated fats

25–35% of kcals, depending on lipid levels Up to 50% of calories with severe hyperglycemia

25–35% of total calories; 10% saturated fats

Calcium

800–1200 mg/d

1–1.5 g/d (consider the need for vitamin D supplements)

800–1200 mg/d

1000–1500 mg/d (consider the need for vitamin D supplements)

Sodium

2–4 g/d

3–4 g/d

2–4 g/d

3–4 g/d

Magnesium and phosphorus

Encourage intake of foods high in these nutrients

Encourage intake of foods high in these nutrients; supplement as needed

Encourage intake of foods high in these nutrients; supplement as needed

Encourage intake of foods high in these nutrients; supplement as needed

Potassium

Supplement or restrict based on serum levels

Supplement or restrict based on serum levels

Supplement or restrict based on serum levels

Supplement or restrict based on serum levels

Other vitamins and minerals

Multivitamin–mineral: supplement to DRI or RDA levels

Adequate vitamin D will be needed to prevent deficiency; multivitamin– mineral: supplement to DRI or RDA levels

Multivitamin–mineral: supplement to RDA levels

Multivitamin–mineral: supplement to RDA levels

Source: Hasse J, Matarese L. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan L, Escott-Stump S, eds. Krause’s food nutrition and diet therapy. 12th ed. St Louis: Elsevier, 2008.

sodium to 2- to 4-g and limit fluid to 1000- to 1500-mL with edema. • Use a low-volume TF if needed, diluting the concentration. Avoid glutamine-enriched solutions with elevated serum ammonia levels. Consider use of BCAA-enriched formulas. • Vitamins and minerals should be given at levels that meet but not exceed recommended daily allowances. Fat malabsorption is common; use water-miscible forms of vitamins A, D, E, and K with steatorrhea. B-complex vitamins may be depleted. Stores of calcium, magnesium, potassium, phosphorus, manganese, copper, and zinc are often low and should be repleted.

Post-transplantation • See Table 8-10.

Common Drugs Used and Potential Side Effects • See Table 8-11.

Herbs, Botanicals, and Supplements • Use of probiotics may be quite helpful in this population. A synbiotic composition in an enteral feeding, consisting of one lactic acid bacteria (LAB) and one fiber, greatly

reduces incidence of postoperative bacterial infections (Rayes et al, 2005). • Chaparral should be avoided after transplantation. Herbs and botanical supplements should not be used without discussing with physician. St. John’s wort interferes with the metabolism of cyclosporine and should not be used. • In one study, 50% of LT patients admitted to using vitamins after surgery, and 19% used herbal remedies combined with vitamins, mostly silymarin (Neff et al, 2004).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of diet in wound healing, graft retention, and improvement in health status. • Provide patient or family with recipes for no-added-salt and sugar-free foods as needed. • Obesity can occur unless energy intake is controlled over the long term. • Discuss sources of foods that contain calcium, magnesium, and other desirable nutrients. Individualize to patient preferences and needs. • Discuss the need for alcohol rehabilitation, family counseling, or other available services. Ethanol (ETOH) abuse affects such key nutrients as niacin, folate, vitamin B12, zinc, phosphorus, and magnesium.


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TABLE 8-11

Medications Used after Liver Transplantation

Medication

Description

Analgesics

Analgesics are used to reduce pain. Long-term use may affect such nutrients as vitamin C and folacin; monitor carefully for each specific medication.

Azathioprine (Imuran)

Azathioprine may cause anorexia, leukopenia, thrombocytopenia, oral and esophageal sores, macrocytic anemia, pancreatitis, vomiting, diarrhea, and altered taste acuity. Folate supplementation and other dietary modifications (liquid or soft diet, use of oral supplements, and flavor enhancements) may be needed. The drug works by lowering the number of T cells; it is often prescribed along with prednisone for conventional immunosuppression.

Corticosteroids (prednisone or Solu-Cortef)

Corticosteroids such as prednisone and Solu-Cortef are used for immunosuppression. Side effects include increased catabolism of proteins, negative nitrogen balance, hyperphagia, ulcers, decreased glucose tolerance, sodium retention, fluid retention, and impaired calcium absorption and osteoporosis. Cushing’s syndrome, obesity, muscle wasting, and increased gastric secretion may result. A higher protein intake and lower intake of carbohydrate and sodium may be needed.

Cyclosporine

Cyclosporine does not retain sodium as much as corticosteroids do. Intravenous doses are more effective than oral doses. Nausea, vomiting, and diarrhea are common side effects. Hyperlipidemia, hyperglycemia, and hyperkalemia may also occur; decrease fat intake as well as sodium and potassium if necessary. Magnesium may need to be replaced. The drug is also nephrotoxic; a controlled renal diet may be beneficial. Taking omega-3 fatty acids during cyclosporine therapy may reduce toxic side effects (such as high blood pressure and kidney damage) associated with this medication in transplantation patients. Avoid use with St. John’s wort.

Diuretics

Diuretics such as furosemide (Lasix) may cause hypokalemia. Aldactone actually spares potassium; monitor drug changes closely. In general, avoid use with fenugreek, yohimbe, and ginkgo.

Immunosuppressants

Immunosuppressants such as muromonab (Orthoclone OKT3) and antithymocyte globulin (ATG) are less nephrotoxic than cyclosporine but can cause nausea, anorexia, diarrhea, and vomiting. Monitor carefully. Fever and stomatitis also may occur; alter diet as needed.

Insulin

Insulin may be necessary during periods of hyperglycemia. Monitor for hypoglycemic symptoms during use.

Mycophenolate mofetil

Diarrhea is common. Extra fluids will be needed.

Muromonab (Orthoclone OKT3)

This drug can lead to nausea, vomiting, diarrhea, and anorexia, and meal adjustments may be needed.

Tacrolimus (Prograf, FK506)

Tacrolimus suppresses T-cell immunity; it is 100 times more potent than cyclosporine, thus requiring smaller doses. Side effects include GI distress, nausea, vomiting, hyperkalemia, and hyperglycemia; adjust diet accordingly by reducing carbohydrate or elevating potassium intake.

• Maintain a good diet and physical activity to support bone density.

USC Liver Transplant Guide http://www.surgery.usc.edu/divisions/hep/patientguide/

LIVER TRANSPLANTATION—CITED REFERENCES Patient Education—Foodborne Illness • Careful food handling and hand washing are important to prevent introduction of foodborne pathogens to the transplantation individual who may be experiencing graft–host rejection. • Prevent infections from foodborne illness; patients who have undergone transplantation may be prone to increased risk more than other individuals.

For More Information •

Medicine Net http://www.medicinenet.com/liver_transplant/article.htm

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)–Liver Transplant http://digestive.niddk.nih.gov/ddiseases/pubs/livertransplant/

United Network for Organ Sharing http://www.unos.org/

Chen PW, et al. Stabilization of blood methylmalonic acid level in methylmalonic acidemia after liver transplantation [published online ahead of print August 14, 2009]. Pediatr Transplant. 14:337, 2010. Hay JE. Acute liver failure. Curr Treat Options Gastroenterol. 7:459, 2004. Jenkins B, et al. Probiotics: a practical review of their role in specific clinical scenarios. Nutr Clin Pract. 20:262, 2005. Lee WS, Sokol RJ. Mitochondrial hepatopathies: advances in genetics and pathogenesis. Hepatology. 45:1555, 2007. Malik SM, et al. Outcome after liver transplantation for NASH cirrhosis. Am J Transplant. 9:782, 2009. Neff GW, et al. Consumption of dietary supplements in a liver transplant population. Liver Transpl. 10:881, 2004. Plauth M, et al. ESPEN Guidelines on Parenteral Nutrition: hepatology. Clin Nutr. 28:436, 2009. Rayes N, et al. Supply of pre- and probiotics reduces bacterial infection rates after liver transplantation—a randomized, double-blind trial. Am J Transplant. 5:125, 2005. Shahid M, et al. Nutritional markers in liver allograft recipients. Transplantation. 79:359, 2005. Woo DH, et al. Management of portal venous complications after liver transplantation. Tech Vasc Interv Radiol. 10:233, 2007.


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PANCREATITIS, ACUTE NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Acute pancreatitis is an inflammatory, clinical syndrome defined by a discrete episode of abdominal pain and elevations in serum enzyme levels (Gramlich and Taft, 2007). The exocrine pancreas secretes proteolytic, lipolytic, and amylolytic enzymes for nutrient digestion in the intestines. AP is initiated inside acinar cells by premature activation of digestive enzymes in the pancreas instead of the duodenum. Seventy-five percent to 85% of all pancreatic episodes are considered mild and self-limiting and do not require intervention with nutrition support (Gramlich and Taft, 2007). In the unfortunate 15–25% who need nutrition support, preventing multiple organ failure is important. AP is common in men between the ages of 35 and 45 years, primarily from alcohol abuse or secondarily from gallstones (cholelithiasis). It is often difficult to differentiate between pancreatitis and acute cholecystitis; the correct diagnosis is important because treatments are very different. Other causes of AP include end-stage renal disease, lupus, biliary tract disease, abdominal trauma, certain dyslipidemias (especially triglycerides 1000 mg/dL), AIDS, and pancreatic cancer. Symptoms of AP include sudden, severe abdominal pain, nausea, vomiting, and diarrhea. Complications include sepsis, acute renal failure, hypovolemia, circulatory shock, and pancreatic necrosis. Abdominal pain can be constant and disabling, causing some patients to become addicted to pain medications. About 25% of persons with AP go on to have chronic pancreatitis. Surgery for AP may include necrosectomy, pancreaticoduodenectomy, or sphincterotomy. Oxygen free radical–mediated tissue damage is well established in the pathogenesis of AP. Cytokines involved in the systemic inflammatory response in AP include lipid mediators (prostanoids, thromboxanes, and leukotrienes) generated from arachidonic acid. Reactive oxygen species mediate inflammatory cytokine expression and apoptosis of pancreatic acinar cells (Parks et al, 2009). Omega-3 fatty acids DHA and alpha-linolenic acid (ALA), suppress the expression of inflammatory cytokines (IL-1beta, IL-6) and inhibit the activation of transcription factor activator protein-1 in ceruleinstimulated pancreatic acinar cells (Parks et al, 2009). Heat shock proteins (HSPs) that inhabit almost all subcellular locations and cellular membranes play a major role in the protection of cells against stressful and injury-inciting stimuli, including acinar cell injury in AP (Dudeja et al, 2009). The role of the gut in maintaining immune system integrity is widely recognized. Therefore, nutrition support by the enteral route is preferred (Cao et al, 2008). Nasojejunal feeding tube and a low-molecular diet provide clear advantages compared to parenteral nutrition, such as fewer infectious complications, shorter length of hospital stay, lower cost, and less need for surgery (McClave et al, 2006; Meier and Beglinger, 2006; Petrov et al, 2008). Parenteral nutrition (PN) is used for short term when full nutritional requirements cannot be met enterally so that body composition is preserved (Chandrasegaram et al, 2005).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Evaluation for a susceptible genotype is important (Balog et al, 2005). This is true for pancreatic carcinoma more than pancreatitis per se. Clinical/History

Lab Work

Height Weight BMI (obese?) Diet history BP (low) Rapid heart rate Left upper quadrant abdominal pain Nausea, vomiting Temperature Chvostek’s sign Steatorrhea or oily stools Multiple Organ System Score (MOSS) CT scan showing interstitial pancreatic edema Magnetic resonance imaging (MRI)

CRP (used to measure severity in AP) Procalcitonin (elevated?) Lipase (110; more sensitive than amylase) Amylase (250) K (decreased) Na (decreased) PT or INR Bilirubin (elevated) Ca (decreased) Gluc (increased, 200) Chol (total decreased) LDL cholesterol (elevated?) Trig (increased)

Mg (decreased) LDH (700) ALT (elevated) AST (250) WBC (10,000 cells/mm3) Alb (low) Partial pressure of carbon dioxide (pCO2) (increased) Partial pressure of oxygen (pO2) (decreased) BUN H&H Serum folate Alk phos (increased) CT scan for necrosis Ultrasound Fecal fat study

SAMPLE NUTRITION CARE PROCESS STEPS Impaired Nutrient Utilization Assessment Data: Patient statement of not taking enzyme medication, reports of abdominal pain, diarrhea after eating, vomiting. Nutrition Diagnosis (PES): Impaired nutrient utilization related to pancreatic enzyme deficiency as evidenced by abdominal pain and steatorrhea and report of medication noncompliance. Intervention: Interventions would address the appropriate dose and frequency of medication intake. Monitoring and Evaluation: Plan would include asking patient time of next clinic visit. Evaluate change in steatorrhea and improvement in enzyme medication compliance.


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INTERVENTION OBJECTIVES • Reduce pain. Achieve pancreatic rest simultaneously with gut use. • Use enteral nutrition to reduce the systemic inflammatory response syndrome (Gramlich and Taft, 2007). Failure to use the GI tract in AP may exacerbate disease severity (McClave et al, 2006). • Avoid pancreatic irritants, especially alcohol and caffeine. Monitor for increased need for pancreatic enzymes with the use of TF. • Avoid overfeeding. • Correct fluid and electrolyte imbalances and malnutrition. Acid–base imbalance is common with nasogastric suctioning, fistula losses, renal failure, nausea, and vomiting. • Reduce fever; prevent shock and hypovolemia, hypermetabolism, sepsis, and compression of the stomach or colon. Avoid cardiovascular, pulmonary, hematological, renal, neurological, or metabolic complications with organ failure. Extensive necrosis and infection are associated with the development of organ failure (Garg et al, 2005). • Use CPN if abdominal pain is refractory. CPN use can promote positive nitrogen balance (Chandrasegaram et al, 2005).

FOOD AND NUTRITION • Postpyloric TF is often well tolerated (Niv et al, 2009). Products containing MCT are useful for TF, especially when there is steatorrhea. Omega-3 fatty acids are also helpful (Lasztity et al, 2005). Transition to jejunostomy can be considered when pain is refractory, using a standard formula and needle catheter jejunostomy. • Progress to a diet given in six daily feedings used with pancreatic enzymes for all meals and snacks.

TABLE 8-12

• Alcoholic beverages and nicotine are prohibited. Limit gastric stimulants, such as peppermint and black pepper, if not tolerated. • Diet should include adequate amounts of vitamin C, Bcomplex vitamins, and folic acid for water-soluble vitamin needs. Vitamin B12 deficiency can occur because intrinsic factor is prevented from binding with vitamin B12. Use fat-soluble vitamins in water-miscible form. • Antioxidants including selenium may be needed (Musil et al, 2005). Adequate calcium, magnesium, and zinc supplementation should also be provided.

Common Drugs Used and Potential Side Effects • Many drugs can trigger acute pancreatitis: furosemide (Lasix), azathioprine, dideoxyinosine, DDI (used for treating AIDS), 6-mercaptopurine, 6-MP (an immunosuppressant drug), angiotensin-converting enzyme (ACE) inhibitors, dapsone, acetaminophen, estrogens, methyldopa, nitrofurantoin, steroids, thiazides, cimetidine, erythromycin, salicylates, sulfonamides, and tetracyclines. • The most common cause of death in AP patients is infection with enteric bacteria, but there is no convincing evidence for routine administration of prophylactic antibiotics (Wittau et al, 2008). • See Table 8-12 for guidance on medications.

Herbs, Botanicals, and Supplements • Antioxidants have protective properties that can be beneficial. See Table 8-13. • Other herbs and botanical supplements should not be used without discussing with physician as many have hepatotoxic properties. • Probiotics have had mixed results; they may actually promote higher mortality in patients with AP (Besselink et al, 2008).

Medications Used in Pancreatitis

Medication

Description

Acute

Chronic

Antibiotics Bile salts

Antibiotics may be needed to manage necrosis and systemic complications.

X

X

Bile salts or water-miscible forms of fat-soluble vitamins may be needed.

X

X

Diuretics

Diuretics such as acetazolamide (Diamox) may be needed to control fluid retention. Nausea, vomiting, and diarrhea may result.

X

X

H2-receptor antagonists (cimetidine, ranitidine)

Cimetidine may deplete vitamin B12, especially among the elderly. Histamine H2-receptor antagonists or proton pump inhibitors can improve fat malabsorption and steatorrhea.

X

Insulin

Insulin may be necessary. Monitor for hypoglycemia during use.

X

X

Octreotide

Octreotide may have a beneficial role in the management of AP.

X

Opiates

Opiates may be prescribed for pain.

X

Painkillers

Pain control requires the use of morphine-like drugs (pethidine, morphine, and diamorphine), which have the risk of addiction, particularly if their use is not controlled.

X

Pancreatic enzymes

30,000 IU per meal may be needed to reduce steatorrhea to less than 20 g/d. Enteric coating is necessary to prevent destruction by enzymes. Take enteric-coated enzymes with cimetidine, food, or antacids. Capsules or tablets should be swallowed whole.

X

X


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TABLE 8-13 Antioxidants and Sourcesa Vitamins

Sources or Comments

See beta-carotene (below). Supplements are not recommended for general use.

Vitamin A as beta carotene protects vegetables and fruits from solar radiation damage. Vitamin C (ascorbic acid) is a reducing agent.

Vitamin E (alpha-tocopherol) protects lipid membranes. It also protects glutathione peroxidase (GPX-4). Some tocotrienol isomers also have antioxidant properties.

Citrus fruits (oranges, sweet limes, grapefruit, tangerines), green peppers, broccoli, black currants, strawberries, blueberries, raw cabbage. Destroyed by long-term storage or cooking. Wheat germ, nuts, seeds, whole grains, green leafy vegetables, vegetable oil, fish oil. GPX4 is the only molecule that efficiently reduces lipid hydroperoxides within the cell membranes.

Vitamin Cofactors and Minerals • • • • • •

Coenzyme Q10 Manganese Copper Zinc Iodide Selenium and Glutathione

Ubiquinol is made in the body and is poorly absorbed from the gut Part of the superoxide dismutase (SOD) enzyme in mitochondria Part of the superoxide dismutase (SOD) enzyme in the cytosol and extracellular fluid Part of the superoxide dismutase (SOD) enzyme in the cytosol and extracellular fluid Iodized salt and seafood Liver contains a large amount as part of detoxification system. Glutathione is made from amino acids, but diet does not control its production. Acetylcysteine is a sulfur-containing amino acid that may increase glutathione levels.

Carotenoid Terpenoids • •

Alpha-carotene Astaxanthin

Beta-carotene

• • • •

Canthaxanthin Lutein Lycopene Zeaxanthin

Less active than beta-carotene Found naturally in red algae and animals higher in the marine food chain. It is a red pigment familiarly recognized in crustacean shells and salmon flesh/roe. Butternut squash, carrots, orange bell peppers, pumpkins, broccoli, cantaloupe, peaches, apricots and sweet potatoes Edible mushrooms, crustaceans, fish such as carp. Spinach, red peppers. Destroyed by long-term storage or cooking. Ripe red tomatoes, tomato sauces, watermelon Yellow corn

Flavonoid Polyphenolics •

Flavones: • Apigenin • Luteolin • Tangeritin Flavonols: • Isorhamnetin • • •

Kaempferol Myricetin Proanthocyanidins, or condensed tannins

• Quercetin • Rutin Flavanones: • Eriodictyol • Hesperetin • Naringenin

Flavanols and their polymers: • Catechin, gallocatechin and gallate esters • Epicatechin, epigallocatechin • Theaflavin • Thearubigins Isoflavone phytoestrogens • Daidzein • Genistein • Glycitein

Tea, coffee, soy, fruit, olive oil, red wine, chocolate, cinnamon, oregano Parsley, celery, dandelion. Potent inhibitor of CYP2C9, which metabolizes drugs. Celery, thyme, green pepper, chamomile tea Tangerine and citrus peels. May help lower cholesterol or prevent Parkinson’s disease. The flavonols (kaempferol, quercetin, and myricetin) may reduce the risk of pancreatic cancer. Quercetin 3-O-methyltransferase uses S-adenosyl methionine and quercetin to produce S-adenosylhomocysteine and isorhamnetin. Tea, broccoli, grapefruit, brussel sprouts, applies Walnuts, grapes, berries, fruits, vegetables, herbs Sorghum bran, cocoa powder, and cinnamon are rich sources of procyanidins, found in many fruits and some vegetables Apples, onions, beans Citrus rinds, buckwheat, asparagus, cranberries. Rutin as ferulic acid can help lower cholesterol levels. From Yerba Santa plant; a glycoside found in rose hips Found in citrus fruits. Metabolizes to hesperidin. Grapefruit and citrus fruits. Metabolizes from naringin. Lowers blood lipids, has anticancer activity, inhibits CYP3A4 and CUP1A2 enzymes. Strawberries, green and black teas Cocoa, dark chocolate. Green tea. Improves blood flow. Black tea Formed during fermentation of tea leaves. Soy, peanuts, other members of the Fabaceae family Soybeans, tofu, textured vegetable protein Soybeans, tofu, textured vegetable protein Soy food products (continued)


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TABLE 8-13

Antioxidants and Sourcesa (continued)

Vitamins •

Stilbenoids: • Resveratrol • Pterostilbene Anthocyanidins • Cyanidin • • • • •

Delphinidin Malvidin Pelargonidin Peonidin Petunidin

Sources or Comments

Skins of dark-colored grapes, and concentrated in red wine Blueberries and grapes. Methoxylated analogue of resveratrol but not found in wine. May function like metformin to lower blood glucose; more research is needed. Grapes, bilberry, blackberry, blueberry, cherry, cranberry, elderberry, hawthorn, loganberry, acai berry and raspberry; apples, red cabbage, and plums. Blue-red grapes, pomegranate, cranberries. Red wine Ripe raspberries, blueberries, blackberries, plums, cranberries, pomegranates. Raw cranberries; blueberries, plums, grapes, cherries. Not found in frozen fruits; raw only. Chokeberries, muscadine grapes

Phenolic Acids and Their Esters • • •

Chicoric acid—a caffeic acid derivative Chlorogenic acid—produced from esterification of caffeic acid. Cinnamic acid and ferulic acid

• •

Ellagic acid Ellagitannins—hydrolyzable tannin polymer

• •

Gallic acid Gallotannins—hydrolyzable tannin polymer

• •

Rosmarinic acid Salicylic acid

Found only in Echinacea purpurea. High concentration in coffee (more concentrated in robusta than arabica beans), blueberries and tomatoes. Seeds of plants such as in brown rice, whole wheat and oats, as well as in coffee, apple, artichoke, peanut, orange and pineapple. Raspberry, strawberry. In ester form in red wine tannins. Formed when ellagic acid, a polyphenol monomer, esterifies and binds with the hydroxyl group of a polyol carbohydrate such as glucose Found in gallnuts, sumac, witch hazel, tea leaves, oak bark, and many other plants Formed when gallic acid, a polyphenol monomer, esterifies and binds with the hydroxyl group of a polyol carbohydrate such as glucose. High concentration in rosemary, oregano, lemon balm, sage, and marjoram. Found in most vegetables, fruits, and herbs; but most abundantly in the bark of willow trees (in aspirin).

Other Nonflavonoid Phenolics • • • • •

Curcumin Eugenol Flavoglycosides Flavonolignans—silymarin Xanthones—mangosteen and derivatives

Low bioavailability, because, much of it is excreted through glucuronidation. Chemopreventive. Oil of cloves. May be toxic if used in undiluted essential oils. Gingko Flavonolignans extracted from milk thistle. Mangostin may only be found in inedible shell

Other Organic Antioxidants • • • • •

Bilirubin, a breakdown product of blood Cannabidiol, THC and synthetic cannabinoids Citric acid Lignan—antioxidant and phytoestrogen N-Acetylcysteine—water soluble

Oxalic acid

Phytic acid (inositol, phytate)

R--Lipoic acid—fat and water soluble

Uric acid

Possibly a significant antioxidant Cannabidiol is protective against glutamate neurotoxicity; a potent cerebral antioxidant. Lemons, limes, other citrus fruits. Part of citric acid cycle, so found in all living things. Oats, flax seeds, pumpkin seeds, sesame seeds, rye, soybeans, broccoli, beans, and some berries. Augments glutathione reserves in the body to protect hepatocytes in the liver from acetaminophen toxicity. Precursor in the formation of the antioxidant glutathione in the body with antioxidant effects to reduce free radicals. Rhubarb, buckwheat, star fruit, black pepper, parsley, poppy seed, spinach, chard, beets, cocoa, chocolate, most nuts, berries, beans. Storage form of phosphorus in bran and seeds. Sesame seeds, pinto beans, Brazil nuts, peanuts, soybeans, linseed. Lipoic acid is found in almost all foods; slightly more in kidney, heart, liver, spinach, broccoli, and yeast extract. In humans, uric acid accounts for roughly half the antioxidant ability of plasma

Other Substances •

Melatonin, a hormone

Easily crosses the blood-brain barrier. Once oxidized, it cannot be reduced to its former state.

a

Antioxidants prevent or slow down oxidation where free radicals damage cells; they are often reducing agents. While supplements are available from many health food stores and nutraceutical companies, clinical trials have not found them to be useful and some may be harmful in elderly or vulnerable populations. See also, Table 1–23 and Table 2–2. Sources: 1. Antioxidants. Accessed September 15, 2009, at http://en.wikipedia.org/wiki/List_of_antioxidants_in_food. 2. Nothlings U, et al. Flavonols and pancreatic cancer risk. Am J Epid 166:924, 2007.


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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient to watch for signs and symptoms of diabetes, tetany, peritonitis, acute respiratory distress syndrome, and pleural effusion. These patients are best managed by a multidisciplinary team approach, especially in pediatrics (Stringer et al, 2005). • Discuss omission of alcohol and gas-forming foods. • Discuss tips for handling nausea and vomiting (e.g., dry meals, taking liquids a few hours before or after meals, use of ice chips, sipping beverages, asking physician about available antiemetics). • If home enteral nutrition is needed, teach appropriate management methods. • Teach use of a low-fat, high-protein, high-calorie oral diet when and if appropriate. • Discuss the use of foods rich in antioxidants.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Gastroenterological Association http://www.gastro.org/clinicalRes/brochures/pancreatitis.html

Childhood Pancreatitis http://www.aafp.org/afp/990501ap/2507.html

Medscape http://emedicine.medscape.com/article/775867-overview

Merck—Pancreatitis http://www.merck.com/mmhe/sec09/ch124/ch124b.html

PANCREATITIS, ACUTE—CITED REFERENCES Balog A, et al. Polymorphism of the TNF-alpha, HSP70–2, and CD14 genes increases susceptibility to severe acute pancreatitis. Pancreas. 30:46, 2005. Besselink MG, et al. Probiotic prophylaxis in predicted severe acute pancreatitis: a randomised, double-blind, placebo-controlled trial. Lancet. 371:651, 2008. Cao Y, et al. Meta-analysis of enteral nutrition versus total parenteral nutrition in patients with severe acute pancreatitis. Ann Nutr Metab. 53:268, 2008. Chandrasegaram MD, et al, The impact of parenteral nutrition on the body composition of patients with acute pancreatitis. J Parenter Enteral Nutr. 29:65, 2005. Dudeja V, et al. The role of heat shock proteins in gastrointestinal diseases. Gut. 58:1000, 2009. Garg PK, et al. Association of extent and infection of pancreatic necrosis with organ failure and death in acute necrotizing pancreatitis. Clin Gastroenterol Hepatol. 3:159, 2005. Gramlich L, TaftAK. Acute pancreatitis: practical considerations in nutrition support. Curr Gastroenterol Rep. 9:323, 2007. Lasztity N, et al. Effect of enterally administered n-3 polyunsaturated fatty acids in acute pancreatitis—a prospective randomized clinical trial. Clin Nutr. 24:198, 2005. McClave SA, et al. Nutrition support in acute pancreatitis: a systematic review of the literature. J Parenter Enteral Nutr. 30:143, 2006. Meier RF, Beglinger C. Nutrition in pancreatic diseases. Nutrition in pancreatic diseases. Best Pract Res Clin Gastroenterol. 20:507, 2006. Musil F, et al. Dynamics of antioxidants in patients with acute pancreatitis and in patients operated for colorectal cancer: a clinical study. Nutrition. 21:118, 2005. Niv E, et al. Post-pyloric feeding. World J Gastroenterol. 15:1281, 2009. Parks KS, et al. Inhibitory mechanism of omega-3 fatty acids in pancreatic inflammation and apoptosis. Ann N Y Acad Sci. 1171:421, 2009. Petrov MS, et al. Enteral nutrition and the risk of mortality and infectious complications in patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch Surg. 143:1111, 2008. Stringer MD, et al. Multidisciplinary management of surgical disorders of the pancreas in childhood. J Pediatr Gastroenterol Nutr. 40:363, 2005. Wittau M, et al. The weak evidence base for antibiotic prophylaxis in severe acute pancreatitis. Hepatogastroenterology. 55:2233, 2008. Xia Q, et al. Comparison of integrated Chinese and Western medicine with and without somatostatin supplement in the treatment of severe acute pancreatitis. World J Gastroenterol. 11:1073, 2005.

PANCREATITIS, CHRONIC NUTRITIONAL ACUITY RANKING: LEVEL 3 Pancreas

Pyloric sphincter

Accessory pancreatic duct Common bile duct Duodenal papilla

Duodenum Circular fold

Asset provided by Anatomical Chart Co.

501

Cell death and tissue damage Pancreatic duct


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DEFINITIONS AND BACKGROUND Chronic pancreatitis (CP) is an inflammatory disorder that results in permanent impairment of the pancreas. CP involves edema, fat necrosis, cellular exudate, fibrosis, and decreased enzymatic processes with abdominal pain, nausea, vomiting, and diarrhea. CP typically develops in people between the ages of 30 and 40, and can be caused by hereditary disorders of the pancreas, cystic fibrosis, hypercalcemia, excessive use of alcohol, hyperparathyroidism, hyperlipidemia, or lipase deficiency. The autoimmune forms of CP have been identified through elevated IgG4 levels. Approximately 5% of persons with acute pancreatitis go on to have CP. Very heavy alcohol consumption and smoking are independent risks for CP (Yaday et al, 2009). Chronic alcohol abuse is the cause in 70% of adult cases, proportional to the dose and duration of alcohol consumption. The factors determining which alcoholic will develop alcoholic CP involve genetic and dietary factors or pancreatic injury from trauma, gallstones, and viruses. There is a gradual decrease in antioxidant enzyme expression in the pancreatic cells in CP and many patients will progress to having diabetes or pancreatic cancer. Analysis of pancreatograms and textural changes of the parenchyma help diagnose CP (Kwon and Brugge, 2005). To avoid nutritional deterioration, screen early for fat malabsorption from decreased lipase levels. Steatorrhea occurs when fecal fat 7 g/dL is noted and over 90% of pancreatic enzyme secretion is lost. Weight loss is common, as is pain after intake of foods containing fat and protein. Jaundice, hypoalbuminemia, pancreatic pseudocysts or calcification, and splenic vein thrombosis may also occur. Abstinence from alcohol, dietary modifications, use of oral supplements, and pancreatic enzyme supplementation will suffice in most patients (Meier et al, 2006). Enteral nutrition may be necessary for those in whom weight loss continues. Long-term use of a jejunostomy feeding may be needed (Stanga et al, 2005). PN is very seldom needed and is not as beneficial. Oxidative stress occurs when there is an imbalance between generation of reactive oxygen species and inadequate antioxidant defense systems, causing cell damage either directly or through altering signaling pathways. Antioxidant supplementation relieves pain and reduces levels of oxidative stress (Bhardwaj et al, 2009; Verlaan et al, 2006). Patients may benefit from supplementation of vitamins A, C, E, selenium, and carotenoids. Episodes of inflammation and duct obstruction cause disabling pain (Gabbrielli et al, 2005). Some patients become dependent on pain medications. Supportive treatments, inhibition of gastric acid secretion, nerve blocks, reduction of oxidative stress, and endoscopic and surgical treatments are used. Surgery, such distal pancreatectomy, achieves pain relief and better quality of life. The first successful autoislet cell transplants in patients who have severe CP were performed recently by surgeons at the University of Arizona Medical Center. This procedure avoids surgically caused diabetes.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Tropical calcific pancreatitis (TCP) is an idiopathic pancreatitis prevalent in Asia; trypsin inhibitor (SPINK1) N34S variant partially explains the genetic susceptibility (Sundaresan et al, 2009). Clinical/History

Lab Work

Height Weight BMI Diet history SGA evaluation Alcohol intake Smoking history Left upper quadrant abdominal pain Vomiting Anorexia, nausea Steatorrhea Temperature (fever?) I&O Chvostekâ&#x20AC;&#x2122;s sign CT scan or MRI Endoscopic ultrasound Exploratory laparotomy Endoscopic retrograde cholangiopan creatography (ERCP) See Table 8-3 also

Bicarbonate levels (decreased; sensitivity 95) Secretin stimulation test IgG4 level, ESR, rheumatoid factor, ANA Thiobarbituric acid-reactive substances [TBARS] for oxidative stress Ferric-reducing ability of plasma [FRAP] for antioxidant status Fecal elastase (200 g/g) Sudan staining of feces Fecal fat test (24 hours on 100 g fat diet) CRP and WBC (elevated)

K, Na, Ca (decreased) Gluc (often increased) Lipase and Amylase (elevated?) Serum trypsinogen (low) Chol (LDL up, or total decreased) Trig (increased) Mg (decreased) LDH (700) AST (250) WBC (200) Bilirubin and Alk phos (increased) pCO2 (increased) and pO2 (decreased) Alb, transthyretin BUN H&H Serum folate

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Bioactive Substance Intake Assessment Data: Dietary intake records, Dx of CP with frequent abdominal pain. Nutrition Diagnosis (PES): Inadequate bioactive substance intake related to low intake of antioxidant-rich foods and beverages as evidenced by frequent bouts of abdominal pain with CP. Intervention: Food and Nutrient Deliveryâ&#x20AC;&#x201D;encourage intake of foods rich in antixoidants (see Tables 8-13 and 8-14). Monitoring and Evaluation: Track food intake (food diary or history) to assess increased intake of foods rich in antioxidants and fewer episodes of abdominal pain, hospitalization, and use of analgesics.


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TABLE 8-14

503

Oxygen Radical Absorbance Capacity (ORAC) Rating of Foodsa USDA Data on Foods with High ORAC Scores

Food

100 g Serving

Household Equivalent

Antioxidant capacity (TE) per 100 g

Other Common Unit

TE per Unit

Cinnamon, ground

100 g

14 Tbsp

264,543

1 Tbsp

19,110

Turmeric, ground

100 g

14 Tbsp

159,277

1 Tbsp

11,377

Sorghum, bran, black

100 g

1/3 cup

100,800

Cumin seed

100 g

14 Tbsp

76,800

— 1 Tbsp

— 5486

Parsley, dried flakes

100 g

4.7 cups

74,349

1/4 cup

3955

Basil, dried

100 g

4.7 cups

67,553

1/4 cup

3594

Curry powder

100 g

14 Tbsp

48,504

1 Tbsp

Dutched chocolate powder

100 g

1 cup

40,200

1/4 cup

3465 10,050

Sage, fresh

100 g

4.7 cups

32,004

1/4 cup

1702

Cloves, ground

100 g

14 Tbsp

31,446

1 Tbsp

2246

Mustard seed

100 g

8.75 Tbsp

29,257

1 Tbsp

3344

Pepper, black

100 g

14 Tsbp

27,618

1 Tbsp

1950

Marjoram

100 g

4.7 cups

27,297

1/4 cup

1452

Rice, brown

100 g

1/2 cup

24,287

Chili powder

100 g

14 Tbsp

23,636

1 Tbsp

Dark chocolate candy

100 g

3.5 oz

21,800

1 oz

6229

Oregano powder, dried

100 g

4.7 cups

20,019

1/4 cup

1065

Semi-sweet chocolate morsels

100 g

1/2 cup

18,053

1/4 cup

9027

— 1688

Pecans

100 g

7/8 cup

17,940

1/4 cup

5119

Paprika

100 g

14 Tbsp

17,919

1 Tbsp

1280

Tarragon, fresh

100 g

4.7 cups

15,542

1/4 cup

827

Ginger root, raw

100 g

1 cup

14,840

1/4 cup

3710

Elderberries, raw

100 g

1 cup

14,697

1/2 cup

7349

Peppermint, fresh

100 g

4.7 cups

13,978

1/4 cup

744

Oregano, fresh

100 g

4.7 cups

13,970

1/4 cup

743

Small Red Beans, dried

100 g

1/2 cup

13,727

Walnuts, English

100 g

7/8 cup

13,541

1/2 cup

3869

Wild blueberry

100 g

1 cup

13,427

1/2 cup

6713

Red kidney bean, dried

100 g

1/2 cup

13,259

Pinto beans

100 g

1/2 cup

11,864

Hazelnuts or filberts

100 g

3/4 cup

9645

Pears, dried

100 g

1/2 cup

9496

1/4 cup

— 4748

Blueberry, cultivated

100 g

1 cup

9019

1/2 cup

4510

Cranberry, whole

100 g

1 cup

8983

1/2 cup

4492

Pistachios

100 g

4 oz

7983

1 oz

1995

Artichoke hearts, cooked

100 g

1 cup

7904

1/2 cup

2635

Plums, black

100 g

11⁄3 medium

7581

Prunes

100 g

1/2 cup

7291

Lentils, raw

100 g

1/2 cup

7282

Milk chocolate candy

100 g

3.5 oz

7203

1 oz

— 2058

Dried apples (to 40% moisture)

100 g

1/2 cup

6681

Garlic powder

100 g

14 Tbsp

6665

1 Tbsp

Chocolate syrup

100 g

1/3 cup

6330

Baby food, fruit, peaches

100 g

3.5 oz

6257

Raspberries

100 g

2/3 cup

6058

476

(continued)


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TABLE 8-14

Oxygen Radical Absorbance Capacity (ORAC) Rating of Foodsa (continued) USDA Data on Foods with High ORAC Scores

Food

100 g Serving

Household Equivalent

Antioxidant capacity (TE) per 100 g

Other Common Unit

Strawberries

100 g

1 cup

5938

1/2 cup

Red Delicious apple

100 g

1 apple

5900

TE per Unit 2969 —

Blackberry, cultivated

100 g

3/4 cup

5775

Soybean seeds, raw, mature

100 g

1/2 cup

5764

Onion powder

100 g

14 Tbsp

5735

1 Tbsp

Granny Smith apple

100 g

1 apple

5381

Garlic, raw

100 g

21 cloves

5436

1 clove

Cilantro (coriander leaves), raw

100 g

4.7 cups

5141

410 — 259

Sweet cherries

100 g

10 cherries

4873

Baby food, fruit, apple and blueberry, Junior

100 g

3.5 oz

4822

Black plum

100 g

11⁄3 medium

4844

Russet potato

100 g

4 oz

4649

Almonds

100 g

3/4 cup

4454

1/4 cup

1485

Dill weed, fresh

100 g

4.7 cups

4392

1/2 cup

234

Black-eyed peas, cowpeas

100 g

1/2 cup

4343

Peaches, dried (40% moisture)

100 g

1/2 cup

4222

Black beans, dried

100 g

1/2 cup

4181

Plum

100 g

11⁄3 medium

4118

Gala apple

100 g

1 small

3903

Red table wine

100 g

3.5 oz

3873

Peanut butter, smooth, with salt

100 g

1/2 cup

3432

2 Tbsp

858

Currants, red, raw

100 g

2/3 cup

3387

1/3 cup

1694

Figs, dry

100 g

1/2 cup

3383

Peanuts, all types, raw

100 g

2/3 cup

3166

1/3 cup

1583 1519

Raisins, seedless

100 g

2/3 cup

3037

1/3 cup

Pear, raw

100 g

2/3 medium

2941

Blueberry juice

100 g

3.5 oz

2906

Lettuce, red leaf, raw

100 g

13⁄4 cup

2380

Concord grape juice

100 g

3.5 oz

2377

Cornflakes cereal, crumbs

100 g

1 cup

2359

1/2 cup

Pomegranate juice

100 g

3.5 oz

2341

Oats, quick, plain, dry

100 g

11⁄4 cup

2308

Ready to eat cereal, granola with raisins

100 g

3.5 oz

2294

1 oz

655

Red cabbage, raw

100 g

7/8 cup

2252

1/2 cup

643

Ready to eat cereal, toasted oatmeal squares

100 g

3.5 oz

2143

1 oz

612

Sweet potato, baked in skin

100 g

2/3 medium

2115

Chives, raw

100 g

4.7 cups

2094

1/2 cup

Prune juice, canned

100 g

3.5 oz

2036

Cashew nuts

100 g

4 oz

1948

1 oz

Orange, raw, navel

100 g

1 average

1819

Red grape juice

100 g

3.5 oz

1788

Radishes, raw

100 g

11 radishes

1736

3 radishes

473

Macdamia nuts

100 g

3/4 cup

1695

1/2 cup

565

— 1180

— 111 — 487 — —

(continued)


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TABLE 8-14

505

Oxygen Radical Absorbance Capacity (ORAC) Rating of Foodsa (continued) USDA Data on Foods with High ORAC Scores

Food

100 g Serving

Household Equivalent

Antioxidant capacity (TE) per 100 g

Other Common Unit

TE per Unit

Tangerines or mandarin oranges

100 g

1/3 cup

1620

Spinach, frozen

100 g

3/4 cup cooked

1515

Onions, red, raw

100 g

2/3 cup

1521

1/3 cup

Cranberry-grape juice

100 g

3.5 oz

1480

Butterhead lettuce, raw

100 g

13⁄4 cup

1423

Chocolate milk, fluid, commercial, low fat

100 g

3.5 oz

1263

8 oz

761 — — 2887

Grapes, red, raw

100 g

2/3 cup

1260

Tea, brewed green

100 g

3.5 oz

1253

Lemon juice, raw

100 g

3.5 oz

1225

1 oz

350

Onions, yellow, raw

100 g

2/3 cup

1220

1/3 cup

610

Olive oil, extra virgin

100 g

7 Tbsp

1150

1 Tbsp

164

Onions, raw

100 g

2/3 cup

1034

1/3 cup

517

Sweet pepper, orange

100 g

2/3 cup

984

1/3 cup

492

Mangos, raw

100 g

1 cup

982

1/2 cup

491

Sweet pepper, yellow

100 g

2/3 cup

964

1/3 cup

482

Romaine lettuce raw

100 g

13⁄4 cup

963

Eggplant, raw

100 g

7/8 cup

933

1/2 cup

266

Sweet pepper, green

100 g

2/3 cup

923

1/3 cup

462

Kiwi fruit, raw

100 g

1 kiwi

882

1/2 kiwi

441

Cranberry juice blend, red

100 g

3.5 oz

865

Lime juice, raw

100 g

3.5 oz

823

1 oz

White table wine

100 g

3.5 oz

392

— 235 —

a

Oxygen radical absorbance capacity (ORAC) is a method of measuring antioxidant capacities in biological samples. Values are expressed as the sum of the lipid soluble (e.g., carotenoid) and water-soluble (e.g., phenolic) antioxidant fractions (i.e., “total ORAC”) reported as in micromoles Trolox equivalents (TE) per 100 g sample. Foods rich in antioxidants have an ORAC rating of 1000 per 100 g. For household measurements: • 100 g  3.5 oz dry ingredients • 3 tsp  1 Tbsp. • 48 tsp  16 Tbsp  1 cup. • 1 Tbsp fresh herbs  1⁄2 teaspoon, dried, crushed • 1 oz  41⁄2 Tablespoons allspice, cinnamon, curry, paprika or dry mustard or 4 Tablespoons cloves or prepared mustard or 31⁄2 Tablespoons nutmeg or pepper or 3 Tablespoons sage, cream of tartar or cornstarch or 2 Tablespoons salt or any liquid • 1 pound  2 cups liquid or 4 cups flour or 10 eggs without shells or 4 cups grated cabbage, cranberries, coffee or chopped celery or 3 cups corn meal or 2 cups uncooked rice or 23⁄4 cups raisins or dried currants Sources: Nutrient Data Laboratory, Agriculture Research Service, U.S. Department of Agriculture, Oxygen radical absorbance capacity (ORAC) of Selected Foods—2007. Accessed September 15, 2009, at http://www.ars.usda.gov/SP2UserFiles/Place/12354500/Data/ORAC/ORAC07.pdf. Berry Health Fact Sheets. Accessed September 22, 2009, at http://berryhealth.fst.oregonstate.edu/health_healing/fact_sheets/index.htm. Natural antioxidants. Accessed September 15, 2009, at http://naturalantioxidants.org/.


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INTERVENTION OBJECTIVES • Decrease pain from oxidative stress. Abstain from alcohol and smoking. • Correct fluid and electrolyte imbalances and malnutrition; avoid overfeeding. Acid–base imbalance is common with nasogastric suctioning, fistula losses, renal failure, nausea, and vomiting. • Provide optimal nutrition support for weight gain as weight loss is common in the late course of CP (Stanga et al, 2005). • Alleviate steatorrhea; decrease number of stools per day if there is diarrhea. • Avoid or control complications (cardiovascular, pulmonary, hematological, renal, neurological, or metabolic); prevent multiple organ dysfunction. • With diabetes, it may be better to have glucose elevated slightly (200 mg/dL) than to allow prolonged hypoglycemia to occur. • If tube fed, monitor for abdominal pain or discomfort, and offer pain medication as needed. Administer pancreatic enzymes with meals or TF (Dominguez-Munoz et al, 2005; Stanga et al, 2005). CPN may be needed for resistant cases where pain does not subside.

FOOD AND NUTRITION • If tolerated, use a diet with low-to-moderate fat (0.7–1 g/kg) and high carbohydrates; calculate needs accordingly. Diet should be low in fiber with six small meals a day. Include adequate amounts of antioxidants (Tables 8-13 and 8-14), minerals (calcium, magnesium, selenium, and zinc), fat-soluble vitamins (A, D, E, and K) in watermiscible form, and water-soluble vitamins. • High-energy, standard feeding by enteral pump is desirable for those who need it. Estimate needs at 35 kcals/kg, 1–1.5 g protein per kilogram. Jejunal feeding is more beneficial than gastric placement. Needle catheter jejunostomy may be used safely (Stanga et al, 2005), but not with ascites. • Treat steatorrhea to minimize symptoms of the underlying disease and to promote weight retention or gain. MCTs and pancreatic replacement therapy combat maldigestion and malabsorption (Stanga et al, 2005). Monitor for hyperglycemia with a high-carbohydrate diet. • When CPN is needed (in about 1% of cases), estimate needs according to similar parameters as for oral diet. The benefits of BCAAs and glutamine are not clear. If intravenous lipids are used, do not use more than 1.5 g/kg for adults. Provide no more than 5 mg/kg/min of glucose. • Alcoholic beverages are absolutely prohibited.

Common Drugs Used and Potential Side Effects • See Table 8-12 for guidance on medications.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Antioxidant therapy with green tea polyphenols and gene therapy with superoxide dismutase can markedly attenuate disease (Dryden et al, 2005). • The combination of pre- and probiotics (synbiotics) have mixed results in this population. In the acute form of pancreatitis, probiotic use may actually increase mortality (Besselink et al, 2008).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient to watch for signs and symptoms of diabetes, tetany, peritonitis, acute respiratory distress syndrome, and pleural effusion. • Discuss omission of alcohol from the typical diet. • Discuss tips for handling nausea and vomiting (e.g., dry meals, taking liquids a few hours before or after meals, use of ice chips, sipping beverages, asking physician about available antiemetics, etc.). Dietary counseling has been found to be as effective as dietary supplementation for managing CP (Singh et al, 2008). Gas-forming foods may need to be omitted. Teach high-calorie, high-protein, lowfat diet rich in antioxidant foods with a frequent small meal pattern. • To prevent onset of pancreatic cancer, avoiding tobacco smoking.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Medline Plus http://www.nlm.nih.gov/medlineplus/ency/article/000221.htm

Merck Manual—Chronic Pancreatitis http://www.merck.com/mmpe/sec02/ch015/ ch015c.html#sec02-ch015-ch015c-901

PANCREATITIS, CHRONIC—CITED REFERENCES Besselink MG, et al. Probiotic prophylaxis in predicted severe acute pancreatitis: a randomised, double-blind, placebo-controlled trial. Lancet. 371: 651, 2008. Bhardwaj P, et al. A randomized controlled trial of antioxidant supplementation for pain relief in patients with chronic pancreatitis. Gastroenterology. 136:149, 2009. Dominguez-Munoz JE, et al. Effect of the administration schedule on the therapeutic efficacy of oral pancreatic enzyme supplements in patients with exocrine pancreatic insufficiency: a randomized, three-way crossover study. Aliment Pharmacol Ther. 21:993, 2005. Gabbrielli A, et al. Efficacy of main pancreatic-duct endoscopic drainage in patients with chronic pancreatitis, continuous pain, and dilated duct. Gastrointest Endosc. 61:576, 2005. Kwon RS, Brugge WR. New advances in pancreatic imaging. New advances in pancreatic imaging. Curr Opin Gastroenterol. 21:561, 2005. Meier R, et al. ESPEN Guidelines on Enteral Nutrition: pancreas. Clin Nutr. 25:275, 2006.


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Singh S, et al. Dietary counseling versus dietary supplements for malnutrition in chronic pancreatitis: a randomized controlled trial. Clin Gastroenterol Hepatol. 6:353, 2008. Stanga Z, et al. Effect of jejunal long-term feeding on chronic pancreatitis. J Parenter Enteral Nutr. 29:12, 2005. Sundaresan S, et al. Divergent roles of SPINK1 and PRSS2 variants in tropical calcific pancreatitis. Pancreatology. 9:145, 2009.

507

Verlaan M, et al. Assessment of oxidative stress in chronic pancreatitis patients. World J Gastroenterol. 12:5705, 2006. Yaday D, et al. Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis. Arch Int Med. 169:1035, 2009.

PANCREATIC INSUFFICIENCY NUTRITIONAL ACUITY RANKING: LEVEL 2–3 DEFINITIONS AND BACKGROUND Pancreatic insufficiency is caused by the inability of the exocrine pancreas to secrete digestive enzymes such as lipase. Cystic fibrosis (CF), type 1 (autoimmune) diabetes, Shwachman-Diamond Syndrome (SDS), pancreatic cancer, or pancreatitis will often lead to pancreatic insufficiency. Other disorders of the gastrointestinal tract, such as celiac disease, inflammatory bowel disease, Zollinger–Ellison syndrome or gastric resection can either mimic or cause pancreatic exocrine Insufficiency (Keller et al, 2009). Lipase is the key enzyme for breaking down triglycerides. Patients often have mild-to-moderate fat malabsorption. In CF, there may be recurrent problems with fatty acid abnormalities or pancreatitis (DeBoeck et al, 2005). Fecal elastase (FE) 1 levels indicate lipase activity; assessment should be used to verify pancreatic status (Cohen et al, 2005). A fecal fat or Steatocrit test may identify the problem. Stool trypsin tests or low levels of trypsinogen are used to determine whether sufficient amounts of this pancreatic enzyme are reaching the intestines to metabolize proteins. Because the overt clinical symptoms of pancreatic exocrine insufficiency are steatorrhea and maldigestion (Keller et al, 2009), oral pancreatic enzyme supplements should be properly administered to ensure adequate gastric mixing with the food. Nonendocrine pancreatic disease is a critical factor for development of diabetes; this “type 3c” affects over 8% of the general diabetic patient population (Hardt et al, 2008). There is a continuous interstitial matrix connection between the endocrine and exocrine pancreas; fibrosis and inflammation cause dysfunctional insulino-acinar-ductal-incretin gut hormone axis, resulting in pancreatic insufficiency and glucagon-like peptide deficiency and diabetes (Hayden et al, 2008). The delivery of sufficient enzyme concentrations into the duodenal lumen simultaneously with meals can reduce nutrient malabsorption, improve the symptoms of steatorrhea, and in some cases alleviate pain (Ferrone et al, 2007). The best duodenal pH permits optimal efficacy of these extracts and the buffered, enteric-coated enzymes are most useful (Brady et al, 2006; Pezzilli, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Diagnosis of chronic pancreatic insufficiency is difficult in early stages; eventually, genetic testing may prove to be helpful. Hereditary pancreatitis involves a cationic trypsingen gene (PRSS1) gene, where treatment involves attempting to inactivate that gene before it causes pancreatic insufficiency. CF patients will have the CFTR gene that is associated with pancreatic insufficiency. Clinical/History Height Weight BMI Weight loss? Malabsorption Steatorrhea Diet history I&O Pale, bulky stools

Abdominal bloating Stool weight CT scan or MRI ERCP Lab Work Amylase (increased) Lipase Trypsinogen

CRP Serum carotene FE 1 Ca, Mg Trig, Chol PT or INR Bicarbonate Gluc Na, K Alk phos H&H

INTERVENTION OBJECTIVES • Maintain or achieve BMI 19. • Correct fatty acid abnormalities, maldigestion, diarrhea, and steatorrhea. Prevent EFA deficiency. • Provide adequate energy intake while lowering intake of fats. • Provide fat-soluble vitamins A-D-E-K and zinc with malabsorption. Prevent overload of iron. • Attenuate intestinal inflammation (Pezzilli, 2009). Prevent or manage type 2 diabetes.


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SAMPLE NUTRITION CARE PROCESS STEPS Malnutrition Assessment Data: Dietary intake records; weight loss; streatorrhea; pale, bulky, foul stools.

• Lipase enzymes derived from microbial species show promise; plant-based enzymes, such as bromelain from pineapple, also serve as effective digestive aids in the breakdown of proteins (Roxas, 2008). • Herbs and botanical supplements should not be used without discussing with physician.

Nutrition Diagnosis (PES): Malnutrition related to inability to digest nutrients as evidenced by steatorrhea and unintentional weight loss. Intervention: Food and Nutrient Delivery—provide high kilocalories, high protein foods with low fat content. Include adequate pancreatic enzymes with every meal. Educate about the role of the pancreas in nutrient absorption. Counsel about ways to enjoy meals that are low fat while nutrient dense. Discuss the need for water-miscible forms of vitamins A, D E, and K if needed. Monitoring and Evaluation: Track food intake (food diary or history). Evaluate for signs of malnutrition. Review lab test results. Monitor for improvement in weight, decrease in steatorrhea and pale, bulky stools.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient in the role of the pancreas in digestion. • Discuss how pancreatic enzymes should be taken with meals or afterward for best results. • Discuss appropriate measures for recovery and control. • Share menu planning tips for a high protein, low fat diet and how to include desired nutrients.

Patient Education—Foodborne Illness

FOOD AND NUTRITION • Encourage high-calorie, high-protein intake to maintain body weight. Dose pancreatic enzyme replacement adequately to minimize fat malabsorption. • Use MCTs since they do not require lipase. They may be taken with simple sugars, jelly, jams and in mixed dishes. • Increase use of omega-3 fatty acids from tuna, mackerel, salmon, and other fatty fish, as well as flaxseed. Probiotics may be considered. • If diabetes is present, emphasize regular mealtimes and carbohydrate spacing to prevent hyperglycemia. • Use tender meats and low-fiber fruits and vegetables. • Alcoholic beverages are prohibited. • Tube feed in severe cases of malnutrition. Night feeding may be a reasonable option.

Common Drugs Used and Potential Side Effects • Pancreatic extract preparations contain pancreatin and pancrelipase; both contain principally amylase, protease, and lipase. Pancreatic enzymes (Cotazym, Creon) should be taken with food. Take enteric-coated tablets with cimetidine or antacids. Administration of lipase 25,000–40,000 units/meal is given by using pH-sensitive pancrelipase microspheres, along with dosage increases and compliance checks (Ferrone et al, 2007). • Fat-soluble vitamins should be taken in water-miscible form, with the pancreatic enzymes.

Herbs, Botanicals, and Supplements • New approaches may include the use of probiotics to reduce inflammation (Pezzilli, 2009).

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Cystic Fibrosis Foundation http://www.cff.org/

Food and Drug Administration (FDA) http://www.fda.gov/cder/drug/infopage/pancreatic_drugs/ default.htm

Lab tests on line http://www.labtestsonline.org/understanding/conditions/ pancreatic_insuf.html

National Pancreas Foundation http://www.pancreasfoundation.org/

Pancreas http://www.pancreas.org/

Recipes, Low fat http://www.pancreasfoundation.org/live/recipes.shtml

PANCREATIC INSUFFICIENCY—CITED REFERENCES Brady MS, et al. An enteric-coated high-buffered pancrelipase reduces steatorrhea in patients with cystic fibrosis: a prospective, randomized study. J Am Diet Assoc. 106:1181, 2006. Cohen JR, et al. Fecal elastase: pancreatic status verification and influence on nutritional status in children with cystic fibrosis. J Pediatr Gastroenterol Nutr. 40:438, 2005. DeBoeck K, et al. Pancreatitis among patients with cystic fibrosis: correlation with pancreatic status and genotype. Pediatrics. 115:e463, 2005. Ferrone M, et al. Pancreatic enzyme pharmacotherapy. Pharmacotherapy. 27:910, 2007. Hardt PD, et al. Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed? Diabetes Care. 31:165S, 2008. Hayden MR, et al. Attenuation of endocrine-exocrine pancreatic communication in type 2 diabetes: pancreatic extracellular matrix ultrastructural abnormalities. J Cardiometab Syndr. 3:234, 2008. Keller J, et al. Tests of pancreatic exocrine function—clinical significance in pancreatic and non-pancreatic disorders. Best Pract Res Clin Gastroenterol. 23:r425, 2009. Pezzilli R. Chronic pancreatitis: maldigestion, intestinal ecology and intestinal inflammation. World J Gastroenterol. 15:1673, 2009. Roxas M. The role of enzyme supplementation in digestive disorders. Altern Med Rev. 13:307, 2008.


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PANCREATIC TRANSPLANTATION NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Pancreatic islet cell transplantation is a treatment alternative for patients with type 1 diabetes who experience hypoglycemic unawareness despite maximal care (Onaca et al, 2007). Islet transplant can restore pancreatic endocrine function, endogenous insulin secretion, and insulin independence in more than 80% of patients, and recover the metabolism of glucose, protein, and lipids (Bertuzzi et al, 2006). It helps to decrease nephropathy, early or mild retinopathy, and neuropathy. Pancreas transplantation alone (PTA) involves transplanting a pancreas from a cadaver to a patient whose kidneys have not been damaged by diabetes. Simultaneous pancreas and kidney (SPK) transplantation involves kidney and pancreas being transplanted at the same time from a cadaver, often leading to freedom from both dialysis and insulin dependency. Pancreas after kidney (PAK) surgery is another option, as is islet cell or isolated beta-cell transplantation. Pancreatic islet cells are highly sensitive to hypoxia, which contributes to poor islet yield, inflammatory events, and cellular death during the early posttransplantation period (Lau et al, 2009). Pancreatic transplantation is major surgery, with risk of bleeding, infection, and reactions to anesthesia. Antirejection medicines, which have many side effects, have to be taken for a long time. Whole pancreas transplantation is associated with a significant risk of surgical and postoperative complications (Meloche, 2007). Islet cell transplantation has fewer side effects but does not yield an ideal level of glucose control. Persistent graft function results in improved glucose control and avoidance of hypoglycemic events (Onaca et al, 2007). Improved control of glycated HbA1c, reduced risk of recurrent hypoglycemia and of diabetic complications are benefits of islet cell transplantation, irrespective of the status of insulin independence (Bertuzzi et al, 2006).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Pancreatic transplantation is needed for type 1 diabetes, which has a genetic origin (American Diabetes Association, 2009). Clinical/History Height Weight, dry BMI Diet history Weight changes and goals

I&O BP Temperature Lab Work Gluc BUN, Creat

H&H Serum Fe Serum amylase Urinary amylase (only if bladder drained) Na, K Ca, Mg

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Oral Food and Beverage Intake Assessment Data: Dietary intake records pretransplantation indicate poor oral intake of both food and beverages; status posttransplant, 21 days on enteral nutrition; wishes to try some liquids and soft foods. Nutrition Diagnosis (PES): Inadequate oral food and beverage related to inability to be fed orally posttransplant as evidenced by 14 days on EN and now asking to attempt oral intake. Intervention: Food and Nutrient Delivery—offer one to two small items at mealtimes or every few hours while awake; gradually increase food intake as tolerated. Educate about the role of nutrition in liver health and recovery; discuss ways to progress orally and wean from enteral nutrition. Monitoring and Evaluation: Improved oral appetite. No nausea or unplanned side effects after surgery Gradual return of usual weight and tolerance of oral intake closer to desired level.

INTERVENTION OBJECTIVES • Preoperatively: Meet nutritional needs; improve visceral protein stores; maintain lean tissue. Nutritional management of candidates requires management of renal function, and treatment of obesity in advance as a BMI 27 kg/m2 may delay wound healing. • Postoperatively: Support graft survival. Promote wound healing. Improve or maintain nutritional status. • Long Term: Weaned off CPN within the first year to achieve optimal nutritional status. Prevent weight gain. Prevent complications such as gastroparesis, hypertension, hyperlipidemia, hyperglycemia, and osteoporosis. Attain near-normal blood glucose control and normal hemoglobin A1c levels without risks of severe hypoglycemia (Meloche, 2007).

FOOD AND NUTRITION • Preoperatively: Meet nutritional needs; improve visceral protein stores; maintain lean tissue. • Postoperatively: Control carbohydrates if there is diabetes or hyperglycemia. Manage diet carefully to prevent hypoglycemia in patients who take insulin.

Common Drugs Used and Potential Side Effects • See Table 8-15.


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TABLE 8-15 Medications Used after Pancreatic Transplantation Medication

Description

Analgesics

Analgesics are used to reduce pain. Long-term use may affect such nutrients as vitamin C and folacin; monitor carefully for each specific medication.

Azathioprine (Imuran)

Azathioprine may cause leukopenia, thrombocytopenia, oral and esophageal sores, macrocytic anemia, pancreatitis, vomiting, diarrhea, and other complex side effects. Folate supplementation and other dietary modifications (liquid or soft diet, use of oral supplements) may be needed. The drug works by lowering the number of T cells; it is often prescribed along with prednisone for conventional immunosuppression.

Corticosteroids (prednisone or Solu-Cortef)

Corticosteroids such as prednisone and Solu-Cortef are used for immunosuppression. Side effects include increased catabolism of proteins, negative nitrogen balance, hyperphagia, ulcers, decreased glucose tolerance, sodium retention, fluid retention, and impaired calcium absorption and osteoporosis. Cushing’s syndrome, obesity, muscle wasting, and increased gastric secretion may result. A higher protein intake and lower intake of carbohydrate and sodium may be needed.

Cyclosporine

Cyclosporine does not retain sodium as much as corticosteroids do. Intravenous doses are more effective than oral doses. Nausea, vomiting, and diarrhea are common side effects. Hyperlipidemia, hyperglycemia, and hyperkalemia may also occur; decrease fat intake as well as sodium and potassium if necessary. Magnesium may need to be replaced. The drug is also nephrotoxic; a controlled renal diet may be beneficial. Taking omega-3 fatty acids during cyclosporine therapy may reduce toxic side effects (such as high blood pressure and kidney damage) associated with this medication in transplantation patients (Tsipas and Morphake, 2003). Avoid use with St. John’s wort.

Diuretics

Diuretics such as furosemide (Lasix) may cause hypokalemia. Aldactone actually spares potassium; monitor drug changes closely. In general, avoid use with fenugreek, yohimbe, and ginkgo.

Immunosuppressants

Immunosuppressants such as muromonab (Orthoclone OKT3) and antithymocyte globulin (ATG) are less nephrotoxic than cyclosporine but can cause nausea, anorexia, diarrhea, and vomiting. Monitor carefully. Fever and stomatitis also may occur; alter diet as needed.

Insulin

Insulin may be necessary during periods of hyperglycemia. Monitor for hypoglycemic symptoms during use; teach patient self-management tips.

Pancreatic Enzymes

Pancreatic enzymes may be needed if pancreatitis occurs again after transplantation.

Tacrolimus (Prograf, FK506)

Tacrolimus suppresses T-cell immunity; it is 100 times more potent than cyclosporine, thus requiring smaller doses. Side effects include GI distress, nausea, vomiting, hyperkalemia, and hyperglycemia; adjust diet accordingly by controlling carbohydrate and enhancing potassium intake.

multidisciplinary team is required to maximize long-term quality of life.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • St. John’s wort interferes with the metabolism of cyclosporine and should not be used after transplantation.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Encourage activity to prevent excessive weight gain; 14–30 lb may be a common gain. • Discuss surgical stress. Encourage positive protein balance to promote anabolism and wound healing. • Over the long term, follow a low-cholesterol and low–saturated fatty acid dietary plan. • Sudden abdominal pain, fever, and increased amylase and glucose can occur and are signs of pancreatitis even after transplantation. Report these warning signs immediately to the physician. • Problems after transplantation include diabetic complications, bone loss, and failure of the pancreas graft. A

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

E-medicine http://emedicine.medscape.com/article/429408-overview

Insulin http://www.insulin-free.org/

Mayo Clinic—Pancreatic Transplant http://www.mayoclinic.com/health/pancreas-transplant/DA00047

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://diabetes.niddk.nih.gov/dm/pubs/pancreaticislet/

NIH—Genetics of Diabetes http://www.ncbi.nlm.nih.gov/bookshelf/ br.fcgi?bookdiabetes&partA987

University of Minnesota—Diabetes Institute http://www.diabetes.umn.edu/diabinst/video/index.html

USC Pancreatic Transplant Program http://www.pancreastransplant.org/


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PANCREATIC TRANSPLANTATION—CITED REFERENCES American Diabetes Association. Accessed September 19, 2009, at http:// www.diabetes.org/diabetes-research/summaries/exploring-the-geneticsof-type1-diabetes.jsp. Bertuzzi F, et al. Islet cell transplantation. Curr Mol Med. 6:369, 2006.

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Lau J, et al. Oxygenation of islets and its role in transplantation [published online ahead of print September 9, 2009]. Curr Opin Organ Transplant. 14:688, 2009. Meloche RM. Transplantation for the treatment of type 1 diabetes. World J Gastroenterol. 13:6347, 2007. Onaca N, et al. Pancreatic islet cell transplantation: update and new developments. Nutr Clin Pract. 22:485, 2007.

ZOLLINGER–ELLISON SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 3

Gallbladder

hypersecretion in ZES patients prevents death and favors long-term survival (Quatrini et al, 2005). Resection of localized gastrinomas often does not require extended surgical resection and is associated with excellent long-term outcomes (Mortellaro et al, 2009). Total gastrectomy is reserved for patients with extensive tumor involvement of the gastric wall or for patients with emergency bleeding.

Common hepatic duct Cystic duct Common bile duct Pyloric sphincter

ASSESSMENT, MONITORING, AND EVALUATION

Accessory pancreatic duct

Pancreas Pancreatic duct

Duodenal papilla Duodenum

Ulcers caused by Zollinger-Ellison syndrome

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Zollinger–Ellison syndrome (ZES) is a severe disease with ulceratogenic tumor (gastrinoma) of the delta-cells of the pancreatic islets of Langerhans; the cells produce gastrin. Almost every patient with ZES has marked gastric acid hypersecretion and ulcerations in the esophagus, stomach, duodenum, and jejunum. It is more common among 30- to 50-year-old men. ZES occurs in less than 1% of all patients with duodenal ulcers. Gastrinomas producing ZES are the most frequent symptomatic, malignant pancreatic endocrine tumors (Gibril and Jensen, 2005). They frequently are accompanied by secretory diarrhea. Interestingly, insulin production is often increased in the beta-cells. Of all cases, 60% occur in males; two thirds of cases are malignant. Widespread metastasis indicates a poor prognosis. Gastric carcinoid tumors in patients with longstanding ZES may be symptomatic and aggressive and may metastasize to the liver; they require long-term medical treatment. Curing gastrinoma or appropriately inhibiting gastric acid

CLINICAL INDICATORS Genetic Markers: The disease is more common in people who have an inherited condition called multiple endocrine neoplasia type 1 (MEN1). Evaluate for family history of hyperparathyroidism, nephrolithiasis, or gastrinoma. Clinical/History Height Weight BMI Weight loss? Diet history I&O Burning abdominal pain Nausea, vomiting Severe esophageal reflux

Heartburn Diarrhea or malabsorption BP Negative H pylori testing Upper GI endoscopy Somatostatin receptor scintigraphy (SRS) Gastrin radioimmunoassay CT Scan

Lab Work N balance Na Ca (usually increased) Alb H&H K (decreased) Mg BUN Serum insulin Serum gastrin Trig, Chol Gluc

INTERVENTION OBJECTIVES • Relieve stomach acid to lessen ulcer symptoms, usually with medications. Surgery may be needed to remove tumors.


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SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function

5-fluorouracil (Adrucil) or doxorubicin (Doxil) may be used. Monitor for side effects. • Octreotide or interferon may also be used.

Assessment Data: Dietary intake records, diarrhea, steatorrhea, weight loss, nausea and vomiting.

Herbs, Botanicals, and Supplements

Nutrition Diagnosis (PES): Abnormal GI function related to excessive gastrin production as evidenced by gastrinoma with weight loss, nausea & vomiting, diarrhea and steatorrhea.

• Herbs and botanical supplements should not be used without discussing with physician.

Intervention: Food and Nutrient Delivery—provide easily tolerated foods, low acid.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

Monitoring and Evaluation: Track food intake (food diary or history).

• Overcome malabsorption and lessen diarrhea. • Decrease problems with dysphagia and reflux. • Prevent complications such as esophageal stricture or abdominal perforation. • Manage or reduce cancer, which can occur in 25% of cases.

• Explain which modifications of fiber in the diet are appropriate. • Explain how malabsorption compromises nutritional status. Discuss limiting fat intake, as appropriate for the patient. • Lower acid foods may be better tolerated; discuss ways to adjust recipes or good choices.

Patient Education—Foodborne Illness

FOOD AND NUTRITION • Modify fiber, seasonings, and textures as necessary. Decrease intake of acidic foods if not tolerated (such as citrus juices, tomato products). • Alter feeding modality to TF such as jejunostomy placement as needed.

• If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

NIDDK http://digestive.niddk.nih.gov/ddiseases/pubs/zollinger/

Common Drugs Used and Potential Side Effects

ZOLLINGER–ELLISON SYNDROME—CITED REFERENCES

• PPIs are used for the treatment of acid-related disorders. Use of these medications can prevent the need for surgery (Hirschowitz et al, 2005). Take omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), or pantoprazole (Protonix) before meals. Iron and vitamin B12 levels may become depleted. Rabeprazole (Acifex) has been tested and has fewer side effects than some other PPIs (Baldwin and Keam, 2009). • Chemotherapy may be needed if surgery to remove the tumors is not feasible. Streptozotocin (Zanosar),

Baldwin CM, Keam SJ. Rabeprazole: a review of its use in the management of gastric acid-related diseases in adults. Drugs. 69:1373, 2009. Gibril F, Jensen JT. Advances in evaluation and management of gastrinoma in patients with Zollinger-Ellison syndrome. Curr Gastroenterol Rep. 7:114, 2005. Hirschowitz BI, et al. Clinical outcome using lansoprazole in acid hypersecretors with and without Zollinger-Ellison syndrome: a 13-year prospective study. Clin Gastroenterol Hepatol. 3:39, 2005. Mortellaro VE, et al. Long-term results of a selective surgical approach to management of Zollinger-Ellison syndrome in patients with MEN-1. Am Surg. 75:730, 2009. Quatrini M, et al. Follow-up study of patients with Zollinger-Ellison syndrome in the period 1966–2002: effects of surgical and medical treatments on long-term survival. J Clin Gastroenterol. 39:376, 2005.

BILIARY DISORDERS

BILIARY CIRRHOSIS NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Biliary cirrhosis, also called cholangiolitic hepatitis or obstructive jaundice, occurs in two to five cases per 100,000 worldwide. Symptoms include pruritus, jaundice, and portal

hypertension. Biliary atresia is the result of an inflammatory process that affects the intrahepatic and extrahepatic bile ducts, leading to fibrosis and obliteration of the biliary tract with development of biliary cirrhosis in infants (Tang et al, 2005).


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Primary biliary cirrhosis (PBC) is characterized by progressive destruction of intrahepatic bile ducts; it primarily affects middle-aged women. Autoimmune factors may trigger the disease in genetically susceptible hosts; genetic susceptibility is a predisposing factor. Environmental factors (infection, chemicals, smoking) may also be relevant. Environmental xenobioticsmay aggravate genetic weaknesses in mechanisms of immune regulation, and subsequent immunopathology (Gershwin and Mackay, 2008). PBC that is associated with other autoimmune diseases such as Sjogren’s syndrome, scleroderma, Raynaud’s phenomenon, or CREST syndrome is regarded as an organ-specific autoimmune disease. Osteoporosis is prevalent in this population (Guanabens et al, 2005) and celiac disease is also commonly found (Duggan and Duggan, 2005). Homocysteine has been proposed to be involved (Ebrahimkhani et al, 2005). In symptomatic patients, advanced age, elevated serum bilirubin levels, and decreased serum albumin levels lead to shortened survival. PBC slowly progresses and may lead to liver failure where transplantation is the only effective therapy.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: There is a role for HLA to determine PBC susceptibility (Invernizzi et al, 2008). Vitamin D receptor polymorphisms are also being studied. Transferrin Tissue transglutHeight Antimitochondraminase Weight ial antibodies (for celiac BMI (AMA) disease) Diet history Bilirubin Globulin Jaundice (increased) Gluc Portal hyperten- Alk phos Ca, Mg sion? (increased) Na, K Pruritus ALT/AST Chol Xanthomas Alb, (increased) Cholangiogtransthyretin Ceruloplasmin raphy PT (decreased) Liver biopsy Serum homocysteine Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Correct diarrhea, steatorrhea, malnutrition, and osteomalacia. Prevention of bone density loss is important, as vitamin D deficiency is common. • Limit or control symptoms. Prevent progression to endstage liver disease when possible. • Prevent or correct zinc and vitamin deficiencies.

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SAMPLE NUTRITION CARE PROCESS STEPS Altered Nutrition-Related Labs Assessment Data: Dx biliary cirrhosis with presence of AMA, elevated bilirubin and alk phos. Nutrition Diagnosis (PES): Altered nutrition-related labs related to biliary cirrhosis with cholestasis as evidenced by AMA, elevated bilirubin and alk phos levels. Intervention: Food and nutrient delivery—use antioxidant-rich foods, supplement with fat-soluble vitamins. Monitoring and Evaluation: Track lab values.

• Manage related disorders (such as Sjögren’s syndrome or celiac disease).

FOOD AND NUTRITION • Increase vitamin D and calcium intake to protect against osteopenia. Vitamin K may also play an important role in protection of bone health and may be supplemented (Plaza and Lamson, 2005). Use water-miscible sources of vitamins A, D, E, and K with steatorrhea. • Reduce cholesterol and saturated fats in hypercholesterolemia. • Ensure adequate intake of zinc from diet. • To lower elevated homocysteine levels, which seem to aggravate hepatic fibrogenesis, be sure the diet contains adequate amounts of folic acid and vitamins B6 and B12 (Ebrahimkhani et al, 2005). • If the patient also has celiac disease, omit gluten from the diet (e.g., wheat, rye, barley). Initiation of a gluten-free diet may help to resolve iron deficiency anemia, pruritus, and elevated serum liver biochemistries. • Control carbohydrate intake with hyperglycemia.

Common Drugs Used and Potential Side Effects • Prolonged administration of ursodeoxycholic acid (UDCA) in patients with PBC is associated with survival benefit and delay of LT. Ursodeoxycholic acid (UDCA) is the only currently known medication that can slow the disease progression. When UDCA is ineffective, cholestyramine is the treatment of choice; it decreases bile acids but can cause belching or constipation. • Budesonide is a glucocorticoid that may help when given with UDCA to improve liver status (Rautiainen et al, 2005). Weight gain and increased appetite often result. • Bezafibrate, a hypolipidemic drug, has been shown to benefit patients with PBC in some studies (Akbar et al, 2005).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • High doses of vitamin E (tocopherol) will elevate transaminases.


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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of bile salts in fat and fat-soluble vitamin absorption. If supplements are used, water-miscible forms may be needed. • Protection of bone mineral density will be important. Discuss the role of medications, calcium, and vitamin D on bone health (Plaza and Lamson, 2005).

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Mayo Clinic—Primary Biliary Cirrhosis http://www.mayoclinic.com/health/primary-biliary-cirrhosis/DS00604

Medicine Net http://www.medicinenet.com/primary_biliary_cirrhosis/article.htm

BILIARY CIRRHOSIS—CITED REFERENCES Akbar SM, et al. Therapeutic efficacy of decreased nitrite production by bezafibrate in patients with primary biliary cirrhosis. J Gastroenterol. 40:157, 2005. Duggan JM, Duggan AE. Systematic review: the liver in celiac disease. Aliment Pharmacol Ther. 21:515, 2005. Ebrahimkhani MR, et al. Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis. Life Sci. 76:2497, 2005. Gershwin ME, Mackay IR. The causes of primary biliary cirrhosis: convenient and inconvenient truths. Hepatology. 47:737, 2008. Guanabens N, et al. Severity of cholestasis and advanced histological stage but not menopausal status are the major risk factors for osteoporosis in primary biliary cirrhosis. J Hepatol. 42:573, 2005. Invernizzi P, et al. Human leukocyte antigen polymorphisms in Italian primary biliary cirrhosis: a multicenter study of 664 patients and 1992 healthy controls. Hepatology. 48:1906, 2008. Plaza SM, Lamson DW. Vitamin K2 in bone metabolism and osteoporosis. Altern Med Rev. 10:24, 2005. Rautiainen H, et al. Budesonide combined with UDCA to improve liver histology in primary biliary cirrhosis: a three-year randomized trial. Hepatology. 41:747, 2005. Tang ST, et al. Diagnosis and treatment of biliary atresia: a retrospective study. Hepatobiliary Pancreat Dis Int. 4:108, 2005.

CHOLESTASIS NUTRITIONAL ACUITY RANKING: LEVEL 2–3 DEFINITIONS AND BACKGROUND Cholestasis involves reduced bile flow in any liver disease with bilirubin over 2.0 mg/dL. Disturbance of the flow of bile leads to intracellular retention of biliary constituents. Hepatic causes of cholestasis include viral hepatitis, ALD, hemochromatosis, and autoimmune hepatitis. Biliary causes include primary sclerosing cholangitis (in which the intrahepatic and/or extrahepatic bile ducts undergo inflammation and fibrosis), choledocholithiasis, PBC, and biliary atresia. It can also occur with inflammatory bowel disease (Huang and Lichtenstein, 2005). Prolonged PN may be needed in the absence of GI tract stimulation. Cholestasis interferes with excretion of the bile salts required for emulsification and absorption of dietary fat. Reduced bile secretion impairs micelle formation, which is needed for digestion of fat by pancreatic enzymes. Vitamin and mineral deficiencies and alterations are common, especially if cholestasis is significant. Zinc, magnesium, and calcium may be deficient because they are albumin-bound and the liver is not working properly. Deficiency of fat-soluble vitamins A, D, E, and K may occur. Of particular concern is vitamin E, which circulates in the blood almost exclusively attached to the lipoprotein fractions. In chronic cholestasis with biliary obstruction, hyperlipidemia and accumulation of copper result, and manganese can accumulate in the brain; avoid overfeeding with copper

or manganese. Hepatic copper overload in CPN patients occurs through chronic cholestasis in CPN-associated liver disease regardless of duration (Blaszyck et al, 2005). Chronic CPN may induce fatty liver and inflammation, especially in patients with short bowel syndrome. Deficiency of choline in parenteral solutions has been proposed as the mechanism for liver disease. With CPN, cholestatic jaundice may occur from a lack of enteral nutrition and failure of biliary stimulation. In patients receiving home PN, prevalence of liver disease increases with duration. Signs and symptoms of cholestasis can include glossitis from B-complex vitamin deficiency, protein and iron deficiency, hemorrhagic tendencies due to vitamin C or K inadequacy, and flatulence. Patients with steatorrhea may benefit from a low-fat diet or from use of MCTs. Intrahepatic cholestatic syndromes cause a decrease in bile flow with no overt bile duct obstruction; bile constituents accumulate in the liver and blood. Ursodeoxycholic acid and adequate nutritional support are the usual treatments, with LT being performed in severe cases only (Huang and Lichtenstein, 2005). Depending on the cause (such as medication effects, postoperative jaundice, sepsis, CPN, or acalculous cholecystitis), treatment includes removal of offending drugs, supportive care, broad-spectrum antibiotic agents with drainage of infected fluids, CPN adjustment including cycling and limiting carbohydrates, and cholecystectomy.


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ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Because ATP-binding cassette (ABC) transporters are important for normal bile secretion, hereditary and acquired ABC transporter defects play a central role in the pathogenesis of cholestasis (Trauner et al, 2007). Clinical/History Height Weight BMI Diet history Ascites Edema I&O Jaundice Pale stools Fatty yellow deposits in skins Eas bleeding Small, spiderlike blood vessels visible on skin

Serum carotene (increased or decreased) Lab Work Bun, Creat H&H Chol, Trig Serum Fe (increased) Alb, PT (prolonged) transthyretin AST, ALT Globulin (increased) Amylase, lipase Bilirubin Serum (increased, manganese 2 mg/dL) Serum zinc Somatomedin C Na, K Alk phos Ca, Mg (increased) Gammaglutamyl transpeptidase (very high) Nausea Flatulence

INTERVENTION OBJECTIVES • Promote return of normal liver function and bile flow. • Treat fat malabsorption and deficiency of any additional nutrients. • Correct steatorrhea, GI bleeding, and copper overloading when present. • Prevent or correct for liver failure, osteomalacia, or osteoporosis. • Correct nutrient excesses (e.g., manganese). • Prepare for surgery when indicated.

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FOOD AND NUTRITION • In chronic cases, 10–20% added kilocalories may be needed. Infants need more kilocalories, and adults tend to use CHO poorly. In acute stages, use IV glucose to prevent hypoglycemia and protein catabolism. • In acute stages, infants will need 1.0–1.5 g/kg protein. Children, teens, and adults need 0.5–1.2 g protein/kg; highlight BCAAs sources. In chronic cases, use 3 g protein/d for infants and 1–1.5 g protein/kg in adults. • Supplement with vitamins and minerals, especially fat-soluble vitamins. Vitamin D and calcium will be needed if osteopenia is present. Zinc and selenium may be needed. • Small, frequent feedings and snacks may be better tolerated than large meals. • Use enteral nutrition (where possible), if CPN has caused cholestasis. If CPN is required, early use of cyclic CPN may be useful. Avoid excesses of copper (Blaszyck et al, 2005) in the solutions.

Common Drugs Used and Potential Side Effects • Ursodeoxycholic acid slows disease progression and should be used in relatively high doses as 20–30 mg/kg/d (Huang and Lichtenstein, 2005). • Treat pruritus with bile acid–binding exchange resins such as cholestyramine or colestipol (Huang and Lichtenstein, 2005). Use with a low-fat diet and increase fluids and fiber. Constipation, nausea, or vomiting may be a side effect. • Water-miscible forms of fat-soluble vitamins A, D, E, and K may be needed in cholestasis. Sample amounts of vitamin A may be given at 25,000–50,000 IU/d as Aquasol A; vitamin D may be given as 12,000–50,000 IU/d over a month; and vitamin E may be given as 10–25 IU/kg/d. Once nutrient stores are repleted and cholestasis is resolved, the supplementation can stop. • Medications known to cause cholestasis include estrogens and anabolic steroids, chlorpromazine, erythromycin, and oxypenicillins.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. Cholestatic liver injury may occur from some herbal remedies, such as greater celandine, glycyrrhizin, chaparral.

SAMPLE NUTRITION CARE PROCESS STEPS Excessive CPN Infusion Assessment Data: Intake records indicating CPN solution exceeding estimated kilocalories requirements. Nutrition Diagnosis (PES): Excessive CPN solution related to exceeding calculated needs as evidenced by cholestasis. Intervention: Food and Nutrient Delivery—change CPN solution to meet and not exceed kilocalories needs. Monitoring and Evaluation: Track CPN intake according to estimated needs; evaluate labs, weight, liver function.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of fat in normal metabolic processes; simplify explanation in correlation to absorption of fatsoluble vitamins and other nutrients affected by the liver. • Discuss ways to increase satiety from the diet with appetizing recipes. • Discuss use of over-the-counter (OTC) vitamin and mineral supplements, especially regarding possible toxicity if taken in large doses with liver disease.


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• LT works best in a well-nourished patient. Promote good tolerance and intake.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Characteristics of Liver Disease http://www.umm.edu/liver/common.htm

Merck Manual—Cholestasis http://www.merck.com/mmhe/sec10/ch135/ch135c.html

CHOLESTATIC LIVER DISEASE—CITED REFERENCES Blaszyck H, et al. Hepatic copper in patients receiving long-term total parenteral nutrition. J Clin Gastroenterol. 39:318, 2005. Huang CS, Lichtenstein DR. Treatment of biliary problems in inflammatory bowel disease. Curr Treat Options Gastroenterol. 8:117, 2005. Trauner M, et al. MDR3 (ABCB4) defects: a paradigm for the genetics of adult cholestatic syndromes. Semin Liver Dis. 27:77, 2007.

GALLBLADDER DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND The gallbladder, located under the liver, collects and stores bile, which is made up of bile salts, electrolytes, bilirubin, cholesterol, and other fats. Bile helps the small intestine digest fats and remove waste products, especially through bilirubin. It passes from the liver’s bile duct into the duodenum through the common bile duct. Bile contains 85–95% water; electrolytes (sodium, potassium, chloride, bicarbonate, calcium, magnesium); bile acids and bilirubin; lecithin, cholesterol and protein. Loss of bile can cause malabsorption and maldigestion of fat, electrolyte imbalances, and poor excretion of drugs or heavy metals. Cholelithiasis is defined as the presence of gallstones. In developed countries, at least 10% of white adults harbor cholesterol gallstones, especially after age 65. Women have twice the risk (Shaffer, 2005). There is also prevalence among persons who have hepatitis C, diabetes, obesity, pregnancy, use of estrogens, insulin, oral contraceptives, cholestyramine (Bini and McGready, 2005; Ko et al, 2005). The western diet that is high in kilocalories, fat, and refined carbohydrate is also a factor. Being Hispanic or Native American predisposes to gallbladder disease, as does sickle cell anemia and some other genetic traits. Gallstones are a hepatobiliary disorder due to biochemical imbalances in the gallbladder bile (Uppal et al, 2008). Some gallbladders can concentrate bile normally but cannot acidify it. The result is that calcium may be less soluble in bile and precipitates out. Increasing consumption of magnesium (Mg) appears to decrease the risk of symptomatic gallstones in men (Ko, 2008). Magnesium deficiency can cause dyslipidemia and insulin hypersecretion, which may facilitate gallstone formation (Tsai et al, 2008). Gallstones contain primarily cholesterol, bilirubin, and calcium salts, formed into either cholesterol or pigment stones. Symptoms include steady pain in the upper abdomen that increases rapidly and lasts from 30 minutes to several hours, pain in the back between the shoulder blades or under the right shoulder, nausea, vomiting, abdominal bloating, intolerance for fatty foods, belching, and indigestion. Gallstones also form if the gallbladder does not contract completely or often enough to empty bile; this can also

occur after eating too little, after periods of starvation, or fasting. Rapid weight loss or crash dieting is to be avoided. Preventive measures include a controlled weight loss rate, reduction of the length of overnight fast, inclusion of a small amount of fat in the diet, and eating foods rich in magnesium (nuts, vegetable protein, beans, and soy). Cholecystitis is inflammation of the gallbladder. Rather than a single clinical entity, cholecystitis is a class of related disease states with different causes, degrees of severity, clinical courses, and management strategies. Gallstones with low-grade inflammation, scarring, and thickening are common triggers. If the gallbladder is removed, fat absorption still occurs, but it is less efficient because bile is not as concentrated. Endoscopic stent placement in the gallbladder is effective for patients with gallbladder disease who are poor surgical candidates (Conway et al, 2005). However, surgery is needed for most cases. There are over 700,000 cholecystectomies performed annually in the United States alone (Shaffer, 2005). Laparoscopic cholecystectomy (LC) reduces the length of hospital stay and can be performed on patients who are morbidly obese (Simopoulos et al, 2005). Extracorporeal shock wave lithotripsy (ESWL) is also effective. Gallbladder cancer is not common but is more prevalent in women who have had gallstones for many years. Jaundice, pain above the stomach, lumps in the abdomen, and fever should be addressed. Gallbladder cancer is usually associated with late diagnosis, unsatisfactory treatment, and poor prognosis.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Alagille syndrome is a genetic disorder with mutations in the JAG1 and NOTCH2 genes where there are too few bile ducts to function properly;


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this occurs in one in 70,000 people. Activation of nuclear receptor liver X receptor (LXR) sensitizes mice to lithogenic diet-induced gallbladder cholesterol crystallization; studies are needed in humans (Uppal et al, 2008). Clinical/History Height Weight BMI Diet history Intolerance for fatty foods? WBC Jaundice Nausea, vomiting I&O Temperature CT scan or endoscopic ultrasound

Magnetic resonance cholangiography (MRC) Hepatobiliary iminodiacetic acid (HIDA) scan (cholescintigraphy) Endoscopic retrograde cholangiopan creatography (ERCP) Cholecochoscopy

Lab Work Mg (low?) Alk phos (ALP), elevated? Bilirubin (increased) AST, ALT (elevated?) Amylase, Lipase (increased?) Alb, transthyretin Chol Trig (elevated?) H&H Na, K Ca

INTERVENTION OBJECTIVES • Lose excess weight, if needed but avoid fasting for rapid weight loss, which can lead to gallstones. • Limit foods that cause pain or flatulence. • For the patient with cholelithiasis, overcome fat malabsorption caused by obstruction and prevent stagnation in a sluggish gallbladder. Decreased bile secretion, bile stasis, bacteria, hormones, or fungi may be a problem;

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Fat Intake Assessment Data: Dietary intake records indicating intake of fried foods at most every meal; dining at fast food restaurants six to seven times weekly; abdominal and back pain, nausea, vomiting for 3 days. Nutrition Diagnosis (PES): Excessive fat intake related to extensive use of fried foods and fast food choices as evidenced by diet history and signs of cholecystitis. Intervention: Food and Nutrient Delivery—offer lower fat meals; prep for surgery. Educate about the role of the gallbladder in fat metabolism. Counsel about postsurgical diet (low fat, frequent small meals perhaps better tolerated) and gradual return to a general diet that contains more nutrient-dense and lower fat options. Discuss the role of minerals such as magnesium in maintaining GB health. Monitoring and Evaluation: Track food intake (food diary or history). Evaluate for resolution of abdominal pain, nausea and vomiting after surgery; tolerance for diet and use of foods that are more nutrient-dense and lower in fat.

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bacterial overgrowth alters bile acids so that they can no longer emulsify fats. Prevent biliary obstruction, cancer, or pancreatitis. Provide fat-soluble vitamins (ADEK) with signs of steatorrhea. Include a high magnesium food source daily. Ascorbic acid affects the catabolism of cholesterol to bile acids and the development of gallbladder disease; supplement the diet if needed.

FOOD AND NUTRITION • In acute cholecystitis, NPO or a low-fat diet may be needed. Progress to a diet with fewer condiments and gas-forming vegetables, which cause distention, increased peristalsis, and irritation. • In chronic cholecystitis, use a fat/calorie-controlled diet to promote drainage of the gallbladder without excessive pain. Patient should consume adequate amounts of CHO, especially pectin, which binds excess bile acids. • In cholelithiasis, encourage a diet that is high fiber, low in calories (as needed). • Assure an adequate dietary intake of magnesium from nuts, bran, halibut, pollack, spinach, black or lima or white beans. • Fat-soluble vitamins A-D-E-K may need to in water-miscible form. • Increase dietary intake of sources of vitamin C such as citrus fruits and juices. Use supplemental forms if needed.

Common Drugs Used and Potential Side Effects • Ursodiol (Actigall, Urso) is made from bile acid help dissolve small cholesterol gallstones over months or years. Take with food or milk. Ursodiol can lead to metallic taste, abdominal pain, mild diarrhea, or vomiting. • The potent cholesterol absorption inhibitor ezetimibe reduces biliary cholesterol content and may be a promising strategy for preventing or treating cholesterol gallstones (Wang et al, 2008). • Ursodeoxycholic acid decreases cholesterol saturation of bile and gallstone incidence during weight loss and may help to prevent gallstone formation. Orlistat is another option. • Antibiotics may be used to counteract infection. Evaluate the need to take with food, milk or other liquids. • If analgesics (Demerol, meperidine) are used to relieve pain, side effects such as nausea, vomiting, constipation, and GI distress can occur. • Oral contraceptives and estrogens increase the risk of gallstones, especially after prolonged use. Orlistat has also been shown to cause gallstones for some patients. Thiazide diuretics have also been linked with gallstones (Leitzmann et al, 2005).

Herbs, Botanicals, and Supplements • Herbal medicine such as turmeric and oregon grape may reduce gallbladder inflammation and relieve liver congestion.


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• Herbs and botanical supplements should not be used without discussing with physician. Celandine, peppermint, couch grass, and goldenrod have been recommended for gallbladder disease, but no clinical trials have proven efficacy at this time.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • After a cholecystectomy, fat intake should be limited for several months to allow the liver to compensate for the gallbladder’s absence. Fats should be introduced gradually; excessive amounts at one meal should be avoided. Use more unrefined carbohydrates as well. • If diarrhea persists after surgery, try using antidiarrheal medications, such as loperamide (Imodium) and a highfiber diet for more bulk. • Avoid fasting and rapid weight loss schemes. • People who have had their gallbladders removed should have their cholesterol levels checked periodically. To prevent new gallstones from forming, maintain a healthy weight.

Patient Education—Foodborne Illness • If home TF is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American College of Surgeons—Cholecystectomy http://www.facs.org/public_info/operation/cholesys.pdf

Bile Duct Diseases http://www.nlm.nih.gov/medlineplus/bileductdiseases.html

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)—Gallstones http://digestive.niddk.nih.gov/ddiseases/pubs/gallstones/index.htm

GALLBLADDER DISEASE—CITED REFERENCES Bini EJ, McGready J. Prevalence of gallbladder disease among persons with hepatitis C virus infection in the United States. Hepatology. 41:1029, 2005. Conway JD, et al. Endoscopic stent insertion into the gallbladder for symptomatic gallbladder disease in patients with end-stage liver disease. Gastrointest Endosc. 61:32, 2005. Ko CW, et al. Incidence, natural history, and risk factors for biliary sludge and stones during pregnancy. Hepatology. 41:359, 2005. Ko CW. Magnesium: does a mineral prevent gallstones? Am J Gastroenterol. 103:383, 2008. Leitzmann MF, et al. Thiazide diuretics and the risk of gallbladder disease requiring surgery in women. Arch Intern Med. 165:567, 2005. Shaffer EA. Epidemiology and risk factors for gallstone disease: has the paradigm changed in the 21st century? Curr Gastroenterol Rep. 7:132, 2005. Simopoulos C, et al. Laparoscopic cholecystectomy in obese patients. Obes Surg. 15:243, 2005. Tsai CJ, et al. Long-term effect of magnesium consumption on the risk of symptomatic gallstone disease among men. Am J Gastroenterol. 103:375, 2008. Uppal H, et al. Activation of liver X receptor sensitizes mice to gallbladder cholesterol crystallization. Hepatology. 47:1331, 2008. Wang HH, et al. Effect of ezetimibe on the prevention and dissolution of cholesterol gallstones. Gastroenterology. 134:2101, 2008.


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CHIEF ASSESSMENT FACTORS Warning Signs of Type 1 Diabetes

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Drowsiness, Lethargy, Blurred Vision Extreme Thirst Frequent Urination Fruity, Sweet, Wine-Like Odor on Breath Glucose or Ketones in Urine Heavy, Labored Breathing Increased Appetite Sudden Weight Loss Stupor, Unconsciousness

Risk Factors for Type 2 Diabetes

• • • • • • • • • • •

Age 45 Years Ethnicity—African American, Hispanic American, Native American, Asian American, Pacific Islander Family History (Parents or Siblings with DM) Habitually Sedentary High-Density Lipoprotein Cholesterol Level 35 mg/dL and Triglyceride Level 250 mg/dL History of Gestational Diabetes Mellitus (GDM) or Women Delivering Babies Weighing 9 lb History of Impaired Fasting Glucose (IFG) or Impaired Glucose Tolerance (IGT) Hypertension (Blood Pressure 140/90 mm Hg) Obesity with Body Mass Index 25 kg/m2 Polycystic ovarian syndrome, other conditions associated with insulin resistance Vascular disease

Assessment in Diabetes

• •

Assessment for Mood Disorder Contraception; Reproductive and Sexual History • Current Treatment: Medications, Meal Plan, Results of Glucose Monitoring, Patients’ Use of Data • Eating Patterns, Nutritional Status, and Weight History; Growth and Development in Children and Adolescents • Exercise History • Family History of Diabetes and Other Endocrine Disorders • Frequency, Severity, and Cause of Acute Complications Such as Ketoacidosis and Hypoglycemia


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History and Treatment of Other Conditions, Including Endocrine and Eating Disorders Infections: Skin, Foot, Dental, and Genitourinary Tract (Prior and Current) Laboratory Tests, Symptoms and Special Examination Results Related to the Diagnosis of Diabetes Lifestyle, Cultural, Psychosocial, Educational, and Economic Factors That Influence the Management of Diabetes Other Medications That May Affect Blood Glucose Levels Previous Treatment Programs (Nutrition and Diabetes SelfManagement Education, Attitudes, and Health Beliefs) Prior HbA1c Records Risk Factors for Atherosclerosis: Smoking, Hypertension, Obesity, Dyslipidemia, and Family History Symptoms of Celiac Disease in Type 1 Diabetic Patients Symptoms and Treatment of Chronic Eye; Kidney; Nerve; Genitourinary (Including Sexual), Bladder, and Gastrointestinal Function; Heart; Peripheral Vascular; Foot; and Cerebrovascular Complications Associated with Diabetes Tobacco, Alcohol, and/or Controlled Substance Use

OVERVIEW OF DIABETES MELLITUS

LifeART image copyright © 2010. Lippincott Williams & Wilkins. All rights reserved.

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Diabetes affects 24 million Americans; 54 million are estimated to have prediabetes, and over 200,000 individuals die each year of related complications (CDC, 2009; CMS, 2009).

Assessment in Other Endocrine Conditions

• • • • • • • • • • •

• • • • •

Adult Changes in Size of Head, Hands, Feet Altered Consciousness; Numbness, Tingling, or Paresthesia Anorexia, Nausea, Abdominal Pain, Malabsorption, Gastroparesis Bone Pain Decreased Libido, Erectile Dysfunction Diagnosis of Thyroid Disease or Other Endocrine Disorder Dysuria Goiter; Exophthalmos; Intolerance to Heat or Cold Headache, Seizures, Syncope Hormone Imbalances (Excess or Deficiency) Hormone Therapy: Anabolic Hormones—Growth Hormones, Androgens, Sex Hormones; Catabolic Hormones—Stress Hormones (Causing Gluconeogenesis from Protein) Such as Catecholamines (Epinephrine, Norepinephrine), Glucocorticoids (Cortisone, Cortisol), or Glucagon Hyperglycemia, Hypoglycemia Postural Hypotension, Weakness Pruritus, Dryness of Skin or Hair Shortness of Breath, Hoarseness Weight Changes

Diabetes is divided into distinct types: type 1, type 2, gestational diabetes mellitus (GDM), and other types (see Table 9-1). Type 2 diabetes (T2DM), composing 90% of diabetes cases, is affected by both genetic and environmental factors. Types of diabetes affecting children and teens are listed in Table 9-2. Adiposity-associated inflammation and insulin resistance are strongly implicated in the development of T2DM as well as the metabolic syndrome (Shah et al, 2008). Activation of nuclear transcription factor-B has been linked with a variety of inflammatory diseases, including diabetes. Antioxidant spices, herbs, and omega-3 fatty acids help to suppress inflammatory pathways. Amino acids are also important; they support cell signaling, gene expression, and hormone synthesis. While physiological concentrations of amino acids and their metabolites (e.g., nitric oxide, polyamines, glutathione, taurine, thyroid hormones, and serotonin) are required, elevated levels of their products (e.g., ammonia, homocysteine, and asymmetric dimethylarginine) contribute to oxidative stress (Wu, 2009). Dietary supplementation with one or a mixture of arginine, cysteine, glutamine, leucine, proline, and tryptophan may be beneficial for ameliorating health problems including fetal growth restriction, neonatal morbidity and mortality, obesity, diabetes, cardiovascular disease (CVD), the metabolic syndrome, and infertility (Wu, 2009). Medical nutrition therapy (MNT) replaced the term “diet therapy” years ago. There is no single “diabetic” or “ADA” diet. The recommended diet is an individualized nutrition prescription, based on assessment findings and treatment


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TABLE 9-1

Etiologic Classification of Diabetes Mellitus

I. Type 1 diabetes (results from auto-immune beta-cell destruction, usually leading to absolute insulin deficiency). II. Type 2 diabetes (results from a relative deficiency or insulin resistance). III. Other specific types of diabetes due to other causes, for example, genetic defects in beta-cell function, genetic defects in insulin action, diseases of the exocrine pancreas (such as cystic fibrosis), or drug- or chemical-induced diabetes (such as in the treatment of AIDS or after organ transplantation). A. Genetic defects of beta-cell function: Maturity-onset diabetes of youth (MODY) B. Genetic defects in insulin action: Leprechaunism, Rabson–Mendenhall syndrome, Lipoatrophic diabetes C. Diseases of the exocrine pancreas: Pancreatitis, Trauma/ pancreatectomy, Neoplasia, Cystic fibrosis, Hemochromatosis, Fibrocalculous pancreatopathy D. Endocrinopathies: Acromegaly, Cushing’s syndrome, Glucagonoma, Pheochromocytoma, Hyperthyroidism, Somatostatinoma, Aldosteronoma E. Drug- or chemical-induced: Nicotinic acid, Glucocorticoids, Thyroid hormone, Beta-adrenergic agonists, Thiazides, Dilantin, Alpha-interferon F. Infections: Congenital rubella, Cytomegalovirus G. Other genetic syndromes sometimes associated with diabetes: Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome, Friedreich’s ataxia, Huntington’s chorea, Myotonic dystrophy, Porphyria, Prader-Willi syndrome IV. Gestational diabetes mellitus (GDM) is diabetes first diagnosed during pregnancy. Adapted from American Diabetes Association. Diagnosis and classification of diabetes mellitus. Web site accessed September 20, 2009, at http://care.diabetesjournals.org/ content/29/suppl_1/s43.full; American Diabetes Association. Standards of Medical Care in Diabetes–2009.

TABLE 9-2

Types of Diabetes in Children and Teens

Type 1 Diabetes (Immune-Mediated) • • • •

• • •

Usually not obese; often recent weight loss. Short duration of symptoms (thirst and frequent urination). Presence of ketones at diagnosis, with about 35% presenting with ketoacidosis. Often a honeymoon period after blood sugars are in control during which the need for insulin diminishes for awhile. Low dose of longacting insulin, such as glargine (Lantus), may prolong the honeymoon phase. Ultimate complete destruction of the insulin-producing cells needing exogenous insulin for survival. Ongoing risk of ketoacidosis. Only about 5% with a family history (in first- or second-degree relatives) of diabetes.

Type 2 Diabetes (Insulin-Resistant) • • • • • • • • • • • •

goals. MNT considers usual eating habits and other lifestyle factors. Strategic patient counseling should identify benefits of the plan, self-efficacy, obstacles, and lifestyle changes the patient is willing to make; these interventions will help reach desired outcomes. Using open-ended discussion and counseling encourages the client to assess and determine a realistic self-management plan. MNT should be offered in phases, according to patient comprehension and readiness. Screening for diabetes is outlined in Table 9-3. The nutrition care process include assessment, nutrition diagnosis, intervention, followed by monitoring and evaluation. Monitoring of blood glucose, medications, physical activity, education, behavior modification, and evaluation of cardiovascular and renal status are all relevant. In addition, prevention of complications is essential; see Table 9-4. A diabetes educator is defined as a health professional who has mastered the core knowledge and skills, communication, counseling, and education. The credentials of certified diabetes educators (CDE) designate professionals who have at least 1000 hours of direct diabetes teaching and who have successfully completed an examination. An advanced credential has been developed for registered dietitians (RDs), nurses, and pharmacists who have advanced degrees and meet experiential requirements; this credential is known as BC-ADM.

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Usually overweight at diagnosis; little or no weight loss. Usually have sugar in the urine but no ketones. As many as 30% will have some ketones in the urine at diagnosis. About 5% will have ketoacidosis at diagnosis. Often little or no thirst and minimal increased urination. Strong family history of diabetes. 45–80% have at least one parent with diabetes. Diabetes may span many generations of family members. 74–100% have a first- or second-degree relative with diabetes. Typically from African, Hispanic, Asian, or American Indian origin. Disorders likely to cause insulin resistance are common. About 90% of children with type 2 diabetes have dark shiny patches on the skin (acanthosis nigricans), which are most often found between the fingers and between the toes, on the back of the neck (dirty neck), and in axillary creases. Polycystic ovarian syndrome (PCOS).

Maturity-Onset Diabetes of the Young (MODY) • • • • • • • •

• •

Rare form of diabetes; several varieties exist. Early age of onset (ages 9–25 years) with autosomal dominant inheritability. Results from defects to insulin-producing cells caused by a genetic defect in the pancreatic beta-cell function. Symptoms run the gamut from mild elevation in blood sugar to a severe disturbance. MODY can occur in all ethnic groups. Gene abnormalities are rare and can only be identified through testing that is currently available only in research laboratories. Not usually obese. Environmental stressors, such as illness or puberty, may unmask the genetically limited insulin secretory reserve of patients with undiagnosed MODY. Unlike type 1 diabetes, MODY does not cause polyuria, thirst, or extreme hunger. The primary goal is euglycemia. Fasting insulin and C-peptide levels are usually normal or elevated slightly.

Sources: American Diabetes Association, Web site accessed September 20, 2009, at http://spectrum.diabetesjournals.org/content/18/4/249.full; Children with Diabetes Web site accessed September 20, 2009, at http://www.childrenwithdiabetes.com/ clinic/mody.htm


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TABLE 9-3

Evaluation for Diabetes

Screen for prediabetes and diabetes in high-risk, asymptomatic, undiagnosed adults and children. An oral glucose tolerance test (OGTT) may be considered in patients with impaired fasting glucose (IFG) to better define the risk of diabetes. Testing for diabetes should be considered in all individuals at age 45 years and above, particularly in those with a BMI of 25 kg/m2, and if normal, testing should be repeated at 3-year intervals. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss plus one of the following: 1. Symptoms of diabetes and a casual plasma glucose of 200 mg/dL. Casual is defined as any time of day without regard to time since last meal. 2. A fasting plasma glucose (FPG) test, a 2-hour OGTT (75-g glucose load), or both are appropriate. FPG 126 mg/dL. Fasting is defined as no caloric intake for at least 8 hours. 3. Two-hour plasma glucose of 200 mg/dL during an OGTT. The test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. American Diabetes Association. Standards of Medical Care in Diabetes–2009. Web site accessed September 22, 2009, at http://care.diabetesjournals.org/content/32/Supplement_1/S13.full

TABLE 9-4

Potential Complications of Diabetes

ACUTE Hyperglycemia

Symptoms include polyphagia, polydipsia, polyuria, dehydration, weight loss, weakness, muscle wasting, recurrent or persistent infections, hypovolemia, ketonemia, glycosuria, blurred or changed vision, fatigue, muscle cramps, and dry mouth. Blood glucose 250 mg/dL should be evaluated; monitor blood or urine ketones to check for diabetic ketoacidosis (DKA). Three forms of hyperglycemia may be noted in the hospitalized patient: (1) someone with a history of diagnosed diabetes; (2) previously unrecognized diabetes; (3) hospital-related fasting blood glucose of 126 mg/dL or random blood glucose of 200 mg/dL that reverts to normal after discharge.

DKA or nonketotic hyperosmolar state

The stress of illness, trauma, and/or surgery frequently aggravates glycemic control and may precipitate DKA or nonketotic hyperosmolar state. A vomiting illness accompanied by ketosis may indicate DKA, a life-threatening condition that requires immediate medical care to prevent complications and death (American Diabetes Association, 2009). Cerebral edema can occur. Early consultation with an endocrinologist is needed.

Hypoglycemia

Symptoms include shakiness, confusion, diplopia, irritability, hunger, weakness, headache, rapid and shallow breathing, numbness of mouth/lips/tongue, pulse normal or abnormal, convulsions, lack of coordination, dizziness, staggering gait, pallor, slurred speech, tingling, diaphoresis, nausea, sweating, tremors, and nightmares. Treat when blood glucose level is 70 mg/dL with 15 g of liquid or fat-free sources of glucose or carbohydrates (CHO); wait 15 minutes and retest, then treat with another 15 g of CHO if still 70 mg/dL. Evaluate blood glucose after 1 hour. Continue to monitor until next meal. Adding protein to carbohydrate does not affect the glycemic response and does not prevent subsequent hypoglycemia, but adding fat may retard and then prolong the acute glycemic response (American Diabetes Association, 2009). In rare, severe hypoglycemia (when the individual requires the assistance of another person and cannot be treated with oral carbohydrate), emergency glucagon kits may be used; these require a prescription and they can expire over time (American Diabetes Association, 2009).

Dawn phenomenon

The dawn phenomenon is the end result of a combination of natural body changes that occur during the sleep cycle. Between 3:00 a.m. and 8:00 a.m., the body naturally starts to increase the amounts of counter-regulatory hormones (growth hormone, cortisol, and catecholamines) which work against insulin’s action to drop blood sugars. These cause a blood sugar levels to rise in the morning.

Somogyi effect

“Rebound hyperglycemia” leads to high blood sugar levels in the morning preceded by an episode of asymptomatic hypoglycemia. When blood sugar drops too low in the middle of the night, the body counters by releasing hormones to raise the sugar levels. Too much insulin earlier or not enough of a bedtime snack may be the problem.

Acute illness or infection

Any condition leading to deterioration in glycemic control necessitates more frequent monitoring of blood glucose and urine or blood ketones (American Diabetes Association, 2009). Aggressive glycemic management with insulin is needed with severe acute illness (American Diabetes Association, 2009). The risk for DKA is higher during this time; test blood glucose, drink adequate amounts of fluid, ingest CHO (50 g CHO every 3–4 hours) if blood glucose levels are low, and adjust medications to keep glucose in desired range and to prevent starvation ketosis. Marked hyperglycemia requires temporary adjustment of the treatment program and, if accompanied by ketosis, frequent interaction with the diabetes care team (American Diabetes Association, 2009). Hospitalization may be needed. In a pediatric case, cerebral edema may occur; referral to a pediatric endocrinologist is important.

Vaccines

Annually provide an influenza vaccine to all diabetic patients 6 months of age; provide at least one lifetime pneumococcal vaccine for adults with diabetes (American Diabetes Association, 2009). Persons who have diabetes tend to be at higher than normal risk for bacterial forms of pneumonia.

Critical illness

In critically ill patients, blood glucose levels should be kept as close to 110 mg/dL (6.1 mol/L) as possible and generally 180 mg/dL (10 mol/L); intravenous insulin is usually needed (American Diabetes Association, 2009). Scheduled prandial insulin doses should be given in relation to meals and should be adjusted according to point-of-care glucose levels; traditional sliding-scale insulin regimens may be ineffective and are not useful (American Diabetes Association, 2009). (continued)


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TABLE 9-4

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Potential Complications of Diabetes (continued)

INTERMEDIATE Children with T1DM

Children’s growth and development may be impaired with diabetes; adequate protein and energy must be provided. Children may be picky eaters. Blood glucose goals are less strict. Target range for normal blood glucose (90–130 mg/dL before eating for 13–19 year olds; 90–180 mg/dL for 6–12 year olds; and 100–180 mg/dL for 0–5 year olds) may be altered according to the health care provider’s evaluation. Near-normalization of blood glucose levels is seldom attainable in children and adolescents after the honeymoon (remission) period (American Diabetes Association, 2009). The A1c goals also vary in children. Most children under 6 or 7 years of age have “hypoglycemic unawareness;” young children lack the cognitive capacity to recognize and respond to hypoglycemic symptoms (American Diabetes Association, 2009). Children with diabetes differ from adults in many ways, including insulin sensitivity related to sexual maturity, physical growth, ability to provide self-care, vulnerability to hypoglycemia, differing family dynamics, developmental stages, and physiological differences (American Diabetes Association, 2009). Work with the family and school to plan for emergencies such as low or high blood glucose levels.

Children with T2DM

Distinction between type 1 and type 2 diabetes in children can be difficult because autoantigens and ketosis may be present in a substantial number of patients (American Diabetes Association, 2009). Children with T2DM are usually overweight or obese and present with glycosuria with or without ketonuria, absent or mild polyuria and polydipsia, and little or no weight loss. Up to 33% have ketonuria at diagnosis; some may have ketoacidosis without any associated stress, illness, or infection.

Preconception

All women with diabetes and childbearing potential should be educated about the need for good glucose control before pregnancy, the need for family planning, and need for early treatment for diabetic retinopathy, nephropathy, neuropathy, and cardiovascular disease (American Diabetes Association, 2009). A1c levels should be normal or as close to normal as possible (1% above the upper limits of normal) in an individual before conception is attempted (American Diabetes Association, 2009).

Pregnancy and diabetes

Infant mortality rates are approximately twice as high for babies born to women with uncontrolled diabetes compared with babies born to women without diabetes. To reduce the risk of fetal malformations and maternal or fetal complications, pregnant women and women planning to become pregnant require excellent blood glucose control. These women need to be seen frequently by a multidisciplinary team. Specialized laboratory and diagnostic tests may be needed. Women with diabetes must be trained in selfmonitoring of blood glucose (SMBG). Nutrition recommendations for women with preexisting diabetes must be based on a thorough assessment. Monitoring blood glucose levels, blood or urine ketones, appetite, and weight gain is needed to develop an individualized nutrition prescription and to make adjustments to the meal plan. Plasma glucose should be maintained at 65–100 mg/dL before meals and in fasting; 110–135 mg/dL 1 hour after meals; and 120 mg/dL 2 hours after meals. Use an extra 300 kcal daily during the second and third trimester; 1 g/kg/d or an additional 25 g/d of protein; 175 g/d of CHO; 600 g folic acid. Added iron and calcium may also be required.

Gestational diabetes

See the entry later in this chapter.

Lactation

Extra protein, calcium, and folic acid will be needed. Monitoring of blood glucose is recommended, but hypoglycemia should be avoided. Breastfeeding lowers blood glucose and may require women to eat a CHO-containing snack either before or during breastfeeding. Extra 330–400 kcal meets the needs of most lactating mothers.

Older adults

Unexplained weight loss should be viewed as a symptom of a problem. Diabetes is an important health condition for the aging population; at least 20% of patients over the age of 65 years have diabetes. These patients tend to have higher rates of premature death, functional disability, and coexisting illnesses such as hypertension, heart disease, and stroke than those without diabetes (American Diabetes Association, 2009). New-onset diabetes in adults over the age of 50 may signal underlying pancreatic cancer, which should be investigated. Strict diets in long-term care are not warranted and may lead to dehydration and malnutrition; specialized diabetic diets are not required, and a balanced diet with consistent timing of CHO is to be recommended. Modify medications, rather than diet, as needed. Lower hypertension gradually; implement the DASH diet whenever possible. A multivitamin–mineral supplement may be beneficial for this population.

CHRONIC A1c levels

Achieve and maintain normal blood glucose (BG) and lipids. Intensive therapy (IT) helps reduce onset or progression of vascular problems. Maintain hemoglobin A1c levels 7% (A1c level of 7  BG 170). For evaluation, note that A1c of 5%  BG 100; 6%  BG 135; 7%  BG 170; 8%  BG 205; 9%  BG 240; 10%  BG 275; 11%  BG 310.

Microvascular

Retinopathy, ocular abnormalities, nephropathy, neuropathy (sensory or motor conditions, which may lead to ulceration or even limb amputation, orthostatic hypotension, intractable nausea and vomiting, and diabetic gastroenteropathy), diabetic cystopathy, and chronic diarrhea. (continued)


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TABLE 9-4

Potential Complications of Diabetes (continued)

CHRONIC Retinopathy

Retinopathy from diabetes accounts for 12,000–24,000 cases of blindness each year. Optimal glycemic and blood pressure control can substantially reduce the risk and progression of diabetic retinopathy (American Diabetes Association, 2009). In the presence of proliferative diabetic retinopathy (PDR) or severe nonproliferative diabetic retinopathy (NPDR), vigorous aerobic or resistance exercise may be contraindicated because of the risk of triggering vitreous hemorrhage or retinal detachment (American Diabetes Association, 2009). Pregnancy in T1DM may aggravate retinopathy; laser photocoagulation surgery can minimize this risk (American Diabetes Association, 2009).

Microalbuminuria and nephropathy

Early signs of nephropathy include hyperfiltration, renal hypertrophy, and microalbuminuria (loss of 30–300 g/mg creatinine in the urine). Protein losses at a rate of 300 g/mg creatinine may indicate advancement toward chronic kidney disease (CKD). To reduce the risk and/or slow the progression of nephropathy, optimize glucose and blood pressure control (American Diabetes Association, 2009). Nephropathy is preceded by microalbuminuria for several years; onset of end-stage renal disease is about 5 years after onset of microalbuminuria. For diabetic nephropathy, liberalize CHO intake and control insulin levels accordingly. Controlled protein intake will slow down progression of nephropathy. Adults need 0.8–1 g protein/kg daily (American Diabetes Association, 2009). Protein restriction is of benefit in slowing the progression of albuminuria, glomerular filtration rate (GFR) decline, and occurrence of end-stage renal disease (ESRD). Protein restriction should be considered in patients whose nephropathy seems to be progressing despite optimal glucose and blood pressure control and use of angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin receptor blockers (ARBs) (American Diabetes Association, 2009). Intensive diabetes management with the goal of achieving near normoglycemia has been shown to delay the onset of microalbuminuria (American Diabetes Association, 2009). Refer to a physician experienced in the care of diabetic renal disease when the estimated GFR has fallen to 60 mL/min or if difficulties occur in the management of hypertension or hyperkalemia (American Diabetes Association, 2009). ACE inhibitors are almost always prescribed to decrease progression. Phosphorus should be controlled at 8–12 mg/kg/d. Some people may need phosphate binders and calcium supplements.

End-stage renal disease

Diabetes is the leading cause of CKD, especially among blacks, Mexican Americans, and Native Americans. Diabetic nephropathy occurs in 20–40% of patients with diabetes and is the single leading cause of ESRD (American Diabetes Association, 2009). Creatinine and GFR should be assessed annually in this population. Microalbuminuria (30–299 mg/24 h) and macroalbuminuria (300 mg/24 h) should be carefully monitored (American Diabetes Association, 2009). While physical activity can acutely increase urinary protein excretion, there is no evidence that vigorous exercise increases the rate of progression of diabetic kidney disease (American Diabetes Association, 2009).

Autonomic neuropathy

About 70% of persons who have diabetes have some degree of neuropathy, including impaired sensation in the hands and feet, slowed digestion, or carpal tunnel syndrome. Autonomic neuropathy can decrease cardiac responsiveness to exercise, causing postural hypotension, impaired thermoregulation, impaired skin blood flow and sweating, impaired night vision, impaired thirst, risk of dehydration, and gastroparesis with unpredictable food delivery (American Diabetes Association, 2009). Neuropathy may be delayed with careful blood glucose management. Weight loss may be beneficial for obese persons.

Skin and joints

Decreased pain sensation in the extremities may increase risk of skin breakdown and infection and joint destruction; it may be best to encourage nonweight-bearing activities such as swimming, bicycling, or arm exercises (American Diabetes Association, 2009).

Genitourinary

Diabetic autonomic neuropathy is associated with recurrent genitourinary tract disturbances or bladder and/or sexual dysfunction.

Amputations

Lower extremity amputations are painful and disabling; prevention is desirable. Amputation and foot ulcers are the most common consequences of diabetic neuropathy and the major causes of morbidity and disability in people with diabetes (American Diabetes Association, 2009).

Cardiac neuropathy

Major clinical manifestations of cardiac neuropathy in diabetes include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, “brittle diabetes,” and hypoglycemic autonomic failure (American Diabetes Association, 2009). Evaluate cardiac status before starting an exercise program.

Gastrointestinal (GI) neuropathy

GI disturbances (esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control (American Diabetes Association, 2009). (continued)


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TABLE 9-4

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Potential Complications of Diabetes (continued)

Macrovascular CVD is a major cause of mortality and also a major contributor to morbidity in diabetics. T2DM is an independent risk factor for Coronary artery macrovascular disease (American Diabetes Association, 2009). Other risk factors include insulin resistance, hyperglycemia, hyper disease and arterial tension, dyslipidemia, and smoking. Smoking is related to the premature development of microvascular complications of diabetes vascular disease and may have a role in the development of T2DM (American Diabetes Association, 2009). Advise all patients not to smoke; include smoking cessation as a routine component of care (American Diabetes Association, 2009). Dyslipidemia

Lifestyle modification focusing on the reduction of saturated fat and cholesterol intake, weight loss (if indicated), and increased physical activity has been shown to improve the lipid profile in patients with diabetes (American Diabetes Association, 2009). Guidelines promote low-density lipoprotein (LDL) cholesterol levels of 100 mg/dL as optimal for all patients and lowering of triglyceride levels when 150 mg/dL. Statins may be helpful. Elevate high-density lipoprotein (HDL) to levels 50 mg/dL. If HDL is 50 mg/dL and LDL is between 100 and 129 mg/dL, a fibric acid derivative or niacin might be used. Niacin raises HDL but can significantly increase blood glucose at high doses (American Diabetes Association, 2009). Use aspirin therapy (75–162 mg/d) as a secondary prevention strategy in those with diabetes with a history of CVD (American Diabetes Association, 2009). Tailor nutrition interventions according to each patient’s age, type of diabetes, pharmacological treatment, lipid levels, and other medical conditions. Focus on the reduction of saturated fat, cholesterol, and trans fat intake (American Diabetes Association, 2009). Monitoring of homocysteine levels and related actions should be taken. Adequate insulin therapy often returns lipids to normal in T1DM. Elevated levels in T2DM require strict management; limit saturated fat to 7–10% of total calories. The rate of heart disease is about two to four times higher in adults who have diabetes; it is the leading cause of diabetes-related deaths. Since people with diabetes tend to have high triglyceride and low HDL levels, omega-3 fatty acids from DHA and EPA (fish and marine oils) can help.

Hypertension

Over 70% of adults with diabetes also have hypertension. Control of hypertension in diabetes has been linked to reduction in the progression of both microvascular and macrovascular disease. In T1DM, hypertension is often the result of underlying nephropathy, whereas in T2DM, it may be present as part of the metabolic syndrome (American Diabetes Association, 2009). Patients with systolic blood pressure 140 mm Hg or diastolic blood pressure 90 mm Hg should receive drug therapy in addition to lifestyle and behavioral therapy (American Diabetes Association, 2009). Blood pressure should be measured at every routine diabetes visit; patients with diabetes should be treated to reach a systolic blood pressure 130 mm Hg and a diastolic blood pressure 80 mm Hg (American Diabetes Association, 2009). In patients with T1DM with hypertension and any degree of albuminuria, ACE inhibitors have been shown to delay the progression of nephropathy. With T2DM, hypertension, and microalbuminuria, ACE inhibitors and ARBs have been shown to delay the progression to macroalbuminuria (American Diabetes Association, 2009). Modest weight loss is helpful. Prevent hypokalemia, which can blunt insulin release. Control glucose; limit alcohol and smoking; and add exercise. Use the DASH diet because it increases intake of calcium, magnesium, and potassium while lowering alcohol and excess weight.

Hypertension in pregnancy

Pregnancy-induced hypertension is two to four times more common in women with T1DM than in the general population. Screen for microalbuminemia as a strong predictor of pre-eclampsia. In pregnant patients with diabetes and chronic hypertension, blood pressure target goals are 110–129/65–79 mm Hg; avoid lower blood pressure because fetal growth may be impaired (American Diabetes Association, 2009). ACE inhibitors and ARBs are contraindicated during pregnancy (American Diabetes Association, 2009).

Stroke

Stroke risk is two to four times higher among persons with diabetes, and high blood pressure should be carefully controlled.

Catabolic illness

Catabolic illness (such as HIV infection, AIDS, or cancer) changes body compartments, with increased extracellular fluid and shrinkage of body fat and cell mass. Monitor unexplained weight losses carefully, especially 10% or more of usual weight. Standard tube feedings are usually well tolerated in persons with diabetes (50% CHO or lower); monitor fluid status, weight, plasma glucose and electrolytes, and acid–base balance. Overfeeding is to be avoided; start with 25–35 kcal/kg of body weight. Protein needs may be 1 g/kg up to 1.5 g/kg in stressed individuals, and pressure ulcers may require a higher level of protein and calories than normal for healing. Addition of insulin may be needed. Oral glucose-lowering medications need to be adjusted to achieve adequate control of glycemia.

Additional data from: American Diabetes Association, 2009; Centers for Disease Control and Prevention, 2009.


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TABLE 9-5

Key Concepts in Diabetes Management

Glucose Control • • • • • •

Improved glycemic control benefits people with either type 1 or type 2 diabetes. For every 1% reduction in results of A1c blood tests (e.g., from 8.0% to 7.0%), the risk of developing microvascular diabetic complications (eye, kidney, and nerve disease) drops by 40%. A1c is the primary target for glycemic control. More stringent glycemic goals (i.e., a usual A1c, 6%) may further reduce complications at the cost of increased risk of hypoglycemia. Less-intensive glycemic goals may be indicated in patients with severe or frequent hypoglycemia. Postprandial glucose may be targeted if A1c goals are not met despite reaching preprandial glucose goals. Goals should be individualized, and lower goals may be reasonable based on benefit–risk assessment. Certain populations (children, pregnant women, and elderly) require special considerations. See guidelines: Plasma Blood Glucose Goal

Values by Age (years)

Pre-prandial (mg/dL)

Bedtime/ Overnight

Toddlers and preschoolers age (0–6)

100–180

School age (7–12)

A1c

Rationale

110–200

8.5% (but 7.5%)

High risk and vulnerability to hypoglycemia

90–180

100–180

8%

Risks of hypoglycemia and relatively low risk of complications prior to puberty

Adolescents and young adults (13–19)

90–130

90–150

7%

Risk of severe hypoglycemia; developmental and psychological issues; a lower goal 7% is reasonable if achieved without excessive hypoglycemia

Adults (20)

90–130

7%

Peak post-prandial 180 mg/dL 1–2 hours after beginning of meal

Blood Pressure Control • Goal: blood pressure 130/80 mm Hg. • Restriction of sodium to 2400 mg/d assists in the control of hypertension. • Blood pressure control can reduce cardiovascular disease (heart disease and stroke) by approximately 33–50% and can reduce microvascular disease (eye, kidney, and nerve disease) by approximately 33%. • In general, for every 10-mm Hg reduction in systolic blood pressure, the risk for any complication related to diabetes is reduced by 12%. Control of Blood Lipids • •

Improved control of cholesterol or blood lipids (e.g., high-density lipoprotein [HDL], low-density lipoprotein [LDL], and triglycerides) can reduce cardiovascular complications by 20–50%. Goals: Total cholesterol minus HDL should be 130 mg/dL; LDL 100 mg/dL; Triglycerides150 mg/dL; HDL40 mg/dL in men, 50 mg/dL in women.

Preventive Care Practices for Eyes and Feet • •

Detecting and treating diabetic eye disease with laser therapy can reduce the development of severe vision loss by an estimated 50–60%. Comprehensive foot care programs can reduce amputation rates by 45–85%.

Preventive Care for Kidneys (Prerenal Failure) • • • •

Detecting and treating early diabetic kidney disease by lowering blood pressure can reduce the decline in kidney function by 30–70%. Angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are most effective in reducing the decline in kidney function. With protein intakes greater than 20% of energy intake, there is an association with increased albumin excretion rate. Once albuminuria is present, reduce protein to 0.8–1.0 g/kg/d with microalbuminuria and to 0.8 g/kg/d with macroalbuminuria. There may be a benefit to lowering phosphorus intake to 500–1000 mg/d. There is evidence for a benefit on renal function, glucose, lipids, and blood pressure from weight-maintaining diets.

Adapted from: National Diabetes Guidelines, Web site accessed September 20, 2009, at http://guidelines.gov/Compare/comparison.aspx?fileDIABETES_NUTRITION1.inc#t3general


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Collaborative, multidisciplinary teams are best suited to provide such care for people with chronic conditions such as diabetes and to empower patients’ performance of appropriate self-management (American Diabetes Association, 2009). MNT provided by RDs to patients with type 1 and T2DM has been shown to improve glycemic outcomes. Community-based education that incorporates Social Cognitive Theory and Stages of Change Theory, with three group sessions focused on meal planning with cooking demonstrations, is effective; the education successfully promotes use of herbs in place of salt, use of olive or canola oils, use of artificial sweeteners in baking, knowledge of diabetes and nutrition, and self-efficacy (Chapman-Novakofski and Karduck, 2005). Table 9-5 offers more tips for diabetes management. It is also important to address culturally specific eating habits. For example, a recent study in South Dakota found that a diet patterned after the historical hunter–gatherer type diet (with the 25% of energy supplied from protein), provided better blood glucose control and lower the circulating insulin levels in Northern Plains Indians with T2DM. The same may be true for other high-risk groups.

Diabetic Gourmet Magazine http://diabeticgourmet.com/dgarchiv2.shtml

Diabetes Research Institute Foundation http://www.drinet.org/

International Diabetes Federation http://www.idf.org

Joslin Diabetes Center, Boston, MA http://www.joslin.org/

Juvenile Diabetes Research Foundation International http://www.jdrf.org

Low Literacy Information http://www.learningaboutdiabetes.com

National Diabetes Education Program http://www.ndep.nih.gov/

National Guideline Clearinghouse – Diabetes http://guidelines.gov/summary/summary.aspx?doc_id 12816&nbr006618

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) http://www.diabetes.niddk.nih.gov/

Park Nicollet–International Diabetes Center http://www.Parknicollet.com/diabetes

School Guidelines http://www.ndep.nih.gov/diabetes/pubs/Youth_ NDEPSchoolGuide.pdf

For More Information

Taking Control of Your Diabetes http://www.tcoyd.org

American Association of Diabetes Educators http://www.aadenet.org/

American Diabetes Association http://www.diabetes.org/

American Diabetes Association Youth Zone http://www.diabetes.org/youthzone/youth-zone.jsp

Calorie and Nutrient Information http://www.calorieking.com

Canadian Diabetes Association http://www.diabetes.ca/

Centers for Disease Control and Prevention (CDC) Diabetes Public Health Resources http://www.cdc.gov/diabetes/index.htm

CDC Division of Diabetes http://www.cdc.gov/diabetes

Centers for Medicare and Medicaid Services Diabetes Guidelines http://www.cms.hhs.gov/DiabetesScreening/

Children with Diabetes http://www.childrenwithdiabetes.com

Diabetes Care and Dietetic Practice Group http://www.dce.org/

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CITED REFERENCES American Diabetes Association. Standards of Medical Care in Diabetes–2009. Web site accessed September 22, 2009, at http://care.diabetesjournals. org/content/32/Supplement_1/S13.full CDC (Centers for Disease Control and Prevention). National diabetes fact sheet. Web site accessed September 21, 2009, at http://www.cdc.gov/ diabetes/pubs/general.htm#impaired Chapman-Novakofski K, Karduck J. Improvement in knowledge, social cognitive theory variables, and movement through stages of change after a community-based diabetes education program. J Am Diet Assoc. 105:1613, 2005. CMS (Centers for Medicare and Medicaid Services). Diabetes Screening. Web site accessed September 20, 2009, at http://www.cms.hhs.gov/ DiabetesScreening/ Shah A, et al. Adipose inflammation, insulin resistance, and cardiovascular disease. JPEN J Parenter Enteral Nutr. 32:638, 2008. Wu G. Amino acids: metabolism, functions, and nutrition. Amino Acids. 37:1, 2009.


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DIABETES MELLITUS, COMPLICATIONS, AND RELATED CONDITIONS

TYPE 1 DIABETES MELLITUS NUTRITIONAL ACUITY RANKING: LEVEL 4 Microaneurysms

Microaneurysms and hemorrhage

Microaneurysms, hemorrhape, and exudates

Proliferative diabetic retinopathy

Glomerulosclerosis Cataracts

Necrotizing papillitis Coronary atherosclerosis Autonomic dysfunction (diarrhea)

Focal demyelination Occlusive atherosclerosis

Chronic ulcers

Dry gangrene

Calcium

Atheroma

Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND Type 1 diabetes mellitus (T1DM) is absolute insulin deficiency with total failure to produce insulin. Previously used terms include “type I,” “insulin-dependent diabetes mellitus (IDDM),” “juvenile,” “brittle,” or “ketosis-prone” diabetes. T1DM involves autoimmune destruction of the pancreatic beta-cells (the islets of Langerhans). Onset often follows viral infection such as mumps. It usually starts in children or young adults, affecting 10% of cases of diabetes; beta-cell damage is often more severe in patients diagnosed before puberty. Signs and symptoms of diabetes include polyuria (frequent urination, including frequent bedwetting in otherwise

trained children), polydipsia (excessive thirst), polyphagia (extreme hunger), weakness, fatigue, irritability, and sudden weight loss. A fasting plasma glucose (FPG) test or an oral glucose tolerance test (OGTT) can be used. FPG is the preferred method; level of 126 mg/dL or higher is considered to be diabetes. With the OGTT, blood glucose is measured after fasting and 2 hours after drinking a glucose beverage; results between 140 and 199 mg/dL indicate prediabetes, and a level of 200 mg/dL represents diabetes. Hemoglobin A1c (HbA1c) test is not recommended for diagnosis; finger-prick tests are also not valid. Serious complications begin earlier than previously thought. Glucose control really matters, as proven by the


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results of the Diabetes Control and Complications Trial (DCCT) and other trials. More than 65% of people with diabetes die from heart disease or stroke (American Diabetes Association, 2009). Diabetes is the chief cause of blindness, renal failure, and amputations and is a leading cause of birth defects. Intensive therapy to achieve near-normal glucose levels results in lower onset and progression of complications. Caution is needed to prevent hypoglycemia, especially in the very young (6-year old) and those with vision loss or kidney disease. Fasting blood glucose should be measured three to eight times daily when on a new insulin regimen; this may be tapered down when stable (American Dietetic Association, 2009). Protein and nutrient metabolism are affected by insulin availability. The long-term effects of diets high in protein and low in carbohydrate (CHO) are unknown at this time. Vitamin and mineral intakes are being studied for their various impacts on blood glucose levels. In addition, it is important to note that antioxidant foods and spices may be helpful in lowering blood glucose levels. Individuals using insulin should eat at consistent times synchronized with the time-action of the insulin preparation used, monitor their blood glucose levels, and determine their required insulin doses for the amount of food usually eaten. Intensified insulin therapy, including multiple daily injections, continuous subcutaneous insulin infusion with an insulin pump, and rapid-acting insulin, allows for more flexibility in the timing of meals and snacks, as well as in the amount of food eaten. Medical costs for patients with diabetes account for a significant percentage of all health care costs. National Standards for Diabetes Self-Management have been written to support a team approach to patient care; they include the RD as an essential team member. Ongoing nutrition self-management education includes assessment, care plans, treatment goals, desired outcomes, and monitoring metabolic parameters such as blood glucose, lipids, A1c, and related lab values. The use of evidence-based MNT can lead to effective lifestyle changes. Use of technology to track quarterly weight and lab values is an effective way to help patients with their self-management goals (Chima et al, 2005). Multidisciplinary team interventions are suggested to help improve patients’ A1c levels and to reduce complications, hospital readmissions, and hospital stays. The American Dietetic Association recommends a specific number of MNT visits to promote the desired outcome (see Table 9-6).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: The pathogenesis of most DM is multifactorial including both genetic and environmental factors. Interleukin, HLA-DR or HLA-DQ alleles, INS-23, and vitamin D receptor (VDR) gene polymorphisms may be associated with risk of developing T1DM. Much more research is needed to clarify how these present in various haplotypes or ethnic groups.

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Hormonal imbalance controls key proteins that regulate the folate-SAM-homocyteine pathways. Poor folate status has been associated with endothelial dysfunction in adolescents with type 1 diabetes (Wiltshire et al, 2008). The methylene-tetrahydrofolate reductase (MTHFR) AC genotype may confer protection against early nephropathy with lower homocysteine (tHcy) levels, whereas MTHFR 677 TT genotypes may have earlier onset of retinopathy (Wiltshire et al, 2008). High-density lipoprotein Height HbA1c (goal (HDL) Weight 7%) Low-density Weight:height Fasting blood lipoprotein percentiles glucose (FBG) (LDL) Body mass index (goal 90–130 Triglycerides (BMI) mg/dL) (Trig) Diet history OGTT results Urinary Waist circumUrine glucose ketones ference Blood urea Na, K Visual acuity nitrogen Ca, Mg Blood pressure (BUN) Serum (BP) Creatinine phosphorous Intake and out(Creat) (PO4) put (I & O) MicroalbuminThyroidAbsence of uria stimulating menstruation? C-reactive hormone Increased protein (TSH) hunger, thirst, (CRP) Serum D3 level urination Total Nausea, Cholesterol vomiting, (Chol) abdominal pain Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Individualize MNT as needed to achieve treatment goals, preferably provided by an RD familiar with the components of diabetes MNT (American Diabetes Association, 2009).

TABLE 9-6 Recommended Medical Nutrition Therapy Visits for Type 1 Diabetes Encounter

Length of Contact

Time between Encounters

1

60–90 minutes

2–4 weeks

2, 3

30–45 minutes

2–4 weeks

4, 5

30–45 minutes

6–12 months

6, 7, 8

30–45 minutes

As indicated by clinical data and/or changes in medication

Adapted from: National Guideline Clearinghouse. Nutrition practice guidelines for type 1 and type 2 diabetes mellitus. Web site accessed September 20, 2009 at http://guidelines.gov/summary/summary.aspx?doc_id12816&nbr006618


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SAMPLE NUTRITION CARE PROCESS STEPS Altered Nutrition Labs-Type 1 Diabetes Assessment Data: Blood glucose log and food history. Nutrition Diagnosis (PES): Altered nutrition-related lab values related to wrong dose of insulin as evidenced by blood glucose readings consistently 250 mg/dL before lunch. Intervention: Education and counseling to address appropriate timing of food and insulin dose; CHO counting. Monitoring and Evaluation: Ask patient to fax blood glucose logs for next 3 days.

• Address the metabolic abnormalities of glucose, lipids, and BP (Kulkarni, 2006). Meet the specific needs of the patient; modify drug therapy to enhance outcomes and quality of life. • Regularly evaluate food/nutrition history, physical exercise, activity patterns, excessive weight gain. • Develop food/meal planning with client; share plan with medical team so an insulin regimen can be integrated into the client’s usual lifestyle. In hospital settings, avoid use of restrictive diets. • Promote lifestyle changes according to client readiness, educational, and skill level. Early referral for lifestyle changes and advice yields the most benefit (Kulkarni, 2006). • Plan meal plan, exercise, and medication to achieve blood glucose and lipid goals. Minimize intake of trans fatty acids; saturated fat should be 7% of total calories (American Diabetes Association, 2009). • Prevent early onset of complications by controlling glucose, lipids, and BP. If there are complications, delay or prevent consequences. The DCCT intensive therapy group had substantially lower complication rates; fewer than 1% became blind, required kidney replacement, or had an amputation because of diabetes (DCCT Research Group, 2009). • Both the amount (grams) of carbohydrate as well as the type of carbohydrate in a food influence blood glucose level. Monitoring total grams of carbohydrate remains a key strategy in achieving glycemic control (American Diabetes Association, 2009). • Teach individuals how to use carbohydrate counting and how to adjust insulin doses based on planned carbohydrate intake. • Promote self-monitoring of blood glucose (SMBG) multiple times per day, and more often during illness.

FOOD AND NUTRITION • A meal plan based on the individual’s usual food intake should be used as the basis for integrating insulin therapy into the usual eating and exercise patterns (American Diabetes Association, 2009). • Choose a variety of heart-healthy foods, including an average of five servings of fruits and vegetables, six servings of grains (three whole grain), and two servings of low-fat dairy. Foods in the meat and fat groups do not directly affect blood glucose. • Discourage meal skipping.

• Determine appropriate energy intake for age. Pregnant and growing individuals should receive more: sedentary, 25 kcal/kg; normal, 30 kcal/kg; undernourished or active, 45–50 kcal/kg. Reassess as activity or life stage changes. • Monounsaturated fatty acids and carbohydrates combined should provide about 60–70% of daily energy intake; limit saturated fats to 10% of energy intake. Use a plan that includes CHO at 45–65% of total energy intake each day to prevent ketosis (American Diabetes Association, 2009). • Apply carbohydrate counting, dietary guidelines, or MyPyramid food guidance principles. Focus on carbohydrates more than total energy or source of carbohydrate. • Determine insulin to carbohydrate ratios for each individual. One CHO unit equals 15 g CHO (standard starch, fruit, sweet, or milk servings are based on 15 g CHO). • Provide consistent carbohydrate with each meal and snack with set doses of insulin. Each of the following portions is one carbohydrate choice (15 g CHO): • Grains, breads, cereals: 1 oz bread (1 slice bread, 1/4 large bagel, 6 tortilla); 1/2 cup cooked dried beans; 1/3 cup pasta or rice; 1 cup soup; 3/4 cup cold cereal; 1/2 cup cooked cereal. • Milk and yogurt: 1 cup milk; 2/3 cup unsweetened yogurt (6 oz) or sweetened with noncaloric sweetener. • Fruits: 1 small fresh fruit; 1/2 cup fruit; 1 cup melon or berries; 1/2 cup fruit juice; 1/4 cup dried fruit. • Sweets and snack foods: 3/4 oz snack food (pretzels, chips, 4–6 crackers); 1 oz sweet snack (two small sandwich cookies, five vanilla wafers); 1 tbsp sugar or honey; 1/2 cup ice cream. • Vegetables: 1/2 cup potato, peas, or corn; 3 cups raw vegetables; 11⁄2 cups cooked vegetables; small portions of nonstarchy vegetables. • Most women need about 3–4 carbohydrate choices (45–60 g CHO) at each meal; men generally need about 4–5 carbohydrate choices (60–75 g CHO) per meal. Active young women may need 2500 kcal, or about 75–90 g CHO/meal; an active young man who needs 3000 kcal/d may need 90–100 g CHO/meal. Use 1–2 carbohydrate choices (15–30 g CHO) for snacks; body size and activity level will determine the number of choices needed. • Include plenty of fiber from rice, beans, vegetables, barley, oat bran, fruits, and vegetables. Recommendations for fiber intake for people with diabetes are similar to the recommendations for the general public (DRI: 14 g/1000 kcal) and diets containing 44–50 g of fiber daily truly improve glycemia (American Dietetic Association, 2009) Whole grains are good sources of vitamin E, fiber, and magnesium. • To reduce the risk of nephropathy, protein intake should be limited to the recommended dietary allowance (American Diabetes Association, 2009). If there is microalbuminuria, a more controlled protein intake may be required. • Cut down or eliminate fried and creamed foods. Include omega-3 fatty acids (as from salmon, mackerel, tuna, walnuts, and canola oil) to control blood lipids and reduce inflammatory processes. A high–monounsaturated fat diet seems to have a favorable effect on lipoproteins in diabetes. • For minerals, assure adequacy of intake; routine supplementation is not advised. Replenish potassium and magnesium, if needed. Adequate calcium is important: 500 mg in 1–3 year olds, 800 mg in 4–8 year olds, 1300 mg


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• •

• •

in 9–18 year olds, and 1000 mg in adults should be attained daily. Sodium intake should be limited to 2400 mg daily or less. Routine supplementation with antioxidant vitamins E and C and beta-carotene is not advised because of lack of evidence of efficacy (American Diabetes Association, 2009). Folate is important in women of childbearing ages; acquire 400 g prepregnancy and 600 g during pregnancy. Vitamin D has been found to play an important role in auto-immune disorders. Encourage intake of vitamin-D fortified foods, but also encourage adequate time in the sun. If foods containing sucrose are chosen, they should be substituted for other carbohydrate foods. Sucrose intakes of 10–35% of total energy intake do not affect on glycemic or lipid responses negatively when substituted for isocaloric amounts of starch (American Dietetic Association, 2009). If adults with diabetes choose to use alcohol, intake should be limited to 1 drink/d or less for adult women and 2 drinks/d or less for adult men. One drink is defined as 12 oz beer, 5 oz wine, or 1.5 oz distilled spirits (American Diabetes Association, 2009). To avoid hypoglycemia, alcohol should be consumed with a carbohydratecontaining food. Abstain in pregnancy, pancreatitis, advanced neuropathy, extremely elevated triglycerides, or a history of alcohol abuse. Nonnutritive sweeteners are safe when consumed within the acceptable daily intake levels established by the Food and Drug Administration (FDA) (American Diabetes Association, 2009). The FDA has approved use of several sweeteners; see Table 9-7. Adequate carbohydrate replacement during and after exercise is important to prevent hypoglycemia. Decrease rapid-acting insulin doses during the physical activity; 30–50% less is reasonable. In critical illness, blood glucose management is a challenge. Enteral feeding is generally preferred but specialty formulas are not usually required. Regular blood glucose monitoring and insulin replacement may be needed. If parenteral nutrition is needed, use strict blood glucose control. Hyperglycemia reflects illness severity and results in deleterious consequences. Plan 30% of nutrient intake as fat, 50% as CHO, and 15–20% as protein unless other disease states require alternative plans.

Common Drugs Used and Potential Side Effects • Anti-CD3 mAbs may prolong beta cell function up to 2 years in patients with new onset Type 1 diabetes (T1DM) but studies are still ongoing (Herold et al, 2009). • Insulin/diet correlation is essential. Persons with T1DM are usually dependent on insulin for life. The primary potential effect is hypoglycemia. Sources of insulin must be noted because they affect the peak times and duration of effect, and some affect the speed of absorption. Human insulin is produced synthetically from Escherichia coli or yeast with identical amino acid sequence to the human insulin. See Table 9-8 for insulin onset, peak, and duration times. • Insulin pumps (continuous subcutaneous insulin infusion [CSII]) may be good to maintain glucose levels. If a pump is used, meal schedules are not as strict but should not be abused. With multiple daily insulin injections (MDI), test blood glucose before meals to determine

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insulin doses. Insulin pens available are convenient for insulin dosing. Insulin glargine (Lantus) is well tolerated in MDI regimens for pediatric patients with T1DM and may be more efficacious than NPH/Lente in those with elevated A1 c (White et al, 2009; Chase et al, 2008). • Insulin analogs match postprandial blood glucose excursions better than traditional insulin. Bolus analogs are used for more rapid onset to cover meal CHO and to correct hyperglycemia. Basal agents release at a more constant rate to cover between-meal glucose needs or the body’s basal insulin needs. Premixed insulins are discouraged except when patients are not able to be compliant with MDI. Adverse effects include the potential for hypoglycemia, especially when HbA1c is less than 7%. Analog insulins are less likely to lead to hypoglycemia, especially overnight hypoglycemia. Weight gain with use of insulin can be counteracted with attention to food intake and physical activity.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. There is still insufficient evidence to draw definitive conclusions about the efficacy of beans, peanuts, onion, Coccinia indica, aloe vera, Momordica charantia, and bitter gourd. • Adequate Vitamin D should be available, especially for bone health (Svoren et al, 2009). • See Table 9-9 for guidance on specific herbs and supplements in diabetes. The American Diabetes Association also has a book on herbs and supplements for diabetes care, available from the Web site.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The RD should assess food intake (focusing on carbohydrate), medication, metabolic control (glycemia, lipids, and BP), anthropometric measurements, and physical activity to serve as the basis for implementation of the nutrition prescription, goals, and intervention that are tailored for the individual (American Dietetic Association, 2009). • Diabetes self-management education (DSME) is an essential element of diabetes care, and national standards have been based on evidence. DSME helps patients optimize metabolic control, prevent and manage complications, and maximize quality of life in a cost-effective manner (American Diabetes Association, 2009). Learning can lead to behavioral changes (healthy eating, being active, taking medications, monitoring glucose, problem-solving) which may then lead to desired clinical and health outcomes. Overall, improved health status includes better quality of life, fewer days lost from school or work, fewer complications and health care costs. Weekly problem-based, self-management support interventions can yield health benefits (Tang et al, 2005), as can even a single session with a dietitian (Gaetke et al, 2006). • Teach patient about the importance of self-care, optimal functioning, the roles of carbohydrate intake and physical activity in maintaining metabolic control. Blood glucose testing is essential. Insulin injections must be given at planned, regular intervals for persons with T1DM.


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TABLE 9-7

Sugar and Sweetener Summary

The percentage of calories from carbohydrate (CHO) in the diet for diabetes will vary; it is individualized based on eating habits and glucose and lipid goals. Glycemic load (GL)

GL  glycemic index available CHO amount

Although various starches do have different glycemic responses, first priority should be given to the total amount of CHO consumed rather than the source of the CHO. If the use of glycemic index (GI) is proposed as a method of meal planning, the RD should advise on the conflicting evidence of effectiveness of this strategy. Studies comparing high versus low GI diets report mixed effects on A1C.

Sweets

Sugar equivalents (teapoons)

Soft drink, 12 oz (10 tsp) Chocolate bar, 1.5 oz (5.5 tsp) Froot-loop cereal, 1 cup (3.5 tsp) Sweet pickle, 1 oz (2.25 tsp) Catsup, 1 Tbsp (1 tsp) Barbequed chips, 1 oz. (1/2 tsp) Unsweetened cereal, 1 cup (1/3 tsp)

Nutritive Sweeteners Sugar (sucrose)

Sucrose  16 kcal/tsp (4 g CHO)

Sucrose is saccharose (C12H22O11). Sucrose is a disaccharide; that is, it is made up of two monosaccharides—glucose and fructose. It is one of the sweetest of sugars. Sucrose-containing foods should be substituted for other carbohydrate foods. Sucrose intakes of 10–35% of total energy intake do not have a negative effect on glycemic or lipid responses when substituted for isocaloric amounts of starch.

Corn syrup, molasses, dextrose, glucose, and maltose

Corn sugar (called glucose, or dextrose), milk sugar (lactose), and malt sugar (maltose).

If sucrose is taken as a standard of 1, the sweetness of glucose is 0.5–0.6, that of lactose is 0.27, and that of maltose is 0.6 There is no evidence that foods sweetened with these sweeteners have any significant advantage or disadvantage over foods sweetened with sucrose in decreasing total calories or CHO content of the diet or in improving overall diabetes control.

Fructose and honey

Fructose: 11 kcal/tsp (3 g CHO); fruit sugar; 1.1–2 times as sweet as sucrose.

Fructose, found in fruits and honey, is the sweetest. Although dietary fructose produces a smaller rise in plasma glucose than equal amounts of sucrose and most starches, it is not to replace more than 20% of calories in adults because of its potential adverse effects on lipids, especially triglycerides. There is no reason to recommend that people with diabetes avoid consumption of fruits and vegetables, in which fructose occurs naturally. In children, fructose works well as a substitute in baked goods because their lipids are not yet a problem and fructose has little impact on blood glucose levels.

Sugar alcohols

Sugar alcohols: 2 kcal/g (50% of kilocalories of other nutritive sweeteners such as sucrose) Sorbitol: 50% as sweet as sucrose Xylitol: 16 kcal/tsp (4 g CHO)

Sugar alcohols produce a lower postprandial glucose response than sucrose or glucose and have lower available energy. With foods containing sugar alcohols, subtraction of one half of sugar alcohol grams from total CHO grams is appropriate, particularly when using the CHO counting method for meal planning. There is no evidence that the amounts of sugar alcohol likely to be consumed will result in significant reduction in energy intake or long-term improvement in glycemia. The use of sugar alcohols appears to be safe. Excessive amounts of polyols may have a laxative effect. The calories and CHO content from all nutritive sweeteners must be accounted for in the meal plan and have the potential to affect blood glucose levels. (continued)


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TABLE 9-7 Sugar and Sweetener Summary (continued) Non-Nutritive Sweeteners Acesulfame potassium (Sunette®) Alitame Aspartame (Equal®, NutraSweet®) Neotame Saccharin (Sweet ‘N Low®) Sucralose (Splenda®)

Acesulfame: 200 times sweeter than sugar; heat stable Alitame is made from amino acids, 2000 times sweeter than sugar. Still awaiting FDA approval. Aspartame: 180 times sweeter than sugar; 4 kcal/tsp; contains phenylalanine and cannot be used in PKU. Equally contains aspartame, dextrose, and maltodextrin. Neotame: 6000 times sweeter than sugar; heat stable Saccharin: 300–400 times sweeter than sugar; heat stable; leaves a slightly bitter aftertaste Sucralose: 600 times sweeter than sugar; heat stable

The Food and Drug Administration has approved five nonnutritive sweeteners for use in the United States. All have undergone rigorous scrutiny and have been shown to be safe when consumed by the public, including people with diabetes and women who are pregnant. If persons with diabetes choose to consume products containing U.S. Food and Drug Administration (FDA)-approved non-nutritive sweeteners, at levels that do not exceed the acceptable daily intakes (ADIs), the RD should advise that some of these products may contain energy and carbohydrate from other sources that needs to be accounted for. Research on non-nutritive sweeteners reports no effect on changes in glycemic response.

For more information: International Food Information Council, Web site accessed September 22, 2009, at http://www.ific.org/publications/factsheets/lcsfs.cfm; American Diabetes Association, 2009; National Diabetes Evidence-based guidelines, Web site accessed September 20, 2009, at http://guidelines.gov/summary/summary.aspx? doc_id12816&nbr006618

• Identify potential or real obstacles; discuss options for resisting temptations, dining away from home, feeling deprived, time pressures, food offers from others, competing priorities, handling social events, family or social support, and food intolerances. • Encourage regular mealtimes and snacks. Children and teens in particular may need planned snacks. • A nondiet approach to diabetes management encourages regular eating according to actual hunger and making gradual changes for healthier eating. • Discuss visual assessment of portions. Practice with measuring cups, spoons, and scales. • Teach patient how to read labels and how to identify carbohydrates in processed foods.

• Empowerment is important; help patients to gain mastery over their affairs and to effect change (Funnell et al, 2005). Discuss emotional eating, such as from boredom, anger, frustration, loneliness, and depression; alternative choices should be designed from the client perspective. Research reports sustained improvements in A1 c at 12 months and longer with long-term followup encounters with an RD (American Dietetic Association, 2009). • Discuss the weight gain that occurs with intensive insulin therapy and improved glucose control. • Low-carbohydrate diets are not recommended for the management of diabetes (American Diabetes Association, 2009).

TABLE 9-8

Insulin Onset, Peaks, and Durationa

Insulin Type

Begins Working

Peaks at

Ends Working in

Low Occurs at

Humalog (Lispro)

15–20 minutes

30–90 minutes

3–4 hours

2–4 hours

Novolog (Aspart)

15–20 minutes

40–50 minutes

3–4 hours

2–4 hours

30–60 minutes

80–120 minutes

4–6 hours

3–7 hours

NPH

2–4 hours

6–10 hours

14–16 hours

6–12 hours

Lente

3–4 hours

6–12 hours

16–18 hours

7–14 hours

Ultralente

4–6 hours

10–16 hours

18–20 hours

12–24 hours

2–3 hours

Almost no peak; flat action throughout duration

18–26 hours

4–24 hours

Rapid, Bolus

Short-Acting Regular (Novolin R, Humulin R) Intermediate-Acting

Long-Acting Lantus (Glargine)

a

Insulin can be used after 1 month if stored at cooler than 86 C and out of direct sunlight or heat. Unopened bottles of insulin should be stored in a refrigerator; do not freeze insulin. Syringes may be prefilled and stored in a refrigerator for up to 3 weeks. Roll the syringes before use to mix the insulin. Adapted from: North Coast Medical Center, accessed September 22, 2009, at http://www.northcoastmed.com/insulin.htm; and Medscape, accessed September 22, 2009, at http://img.medscape.com/pi/emed/ckb/endocrinology/116364–138562-117853–118003.jpg


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TABLE 9-9

Herbs and Supplements in Diabetes Management

Aloe vera

Studies in Japan found that the phytosterols in aloe vera might play a role in lowering blood glucose levels. Further research is needed.

Alpha lipoic acid (thitoic acid)

Alpha lipoic acid (thioctic acid) may have some potential benefits. It is found in the mitochondria and seems to have antioxidant properties that protect vitamin C, vitamin E, and glutathione. Natural sources include red meat, yeast, potatoes, and spinach. Supplementation may provide protection against cataracts, neuropathy in diabetes, cardiovascular disease; research is needed.

Antioxidants

Antioxidants from food should include good sources of beta carotene, vitamins C and E, selenium and zinc.

Bilberry

Bilberry contains anthocyanosides that counteract cellular damage to the retina. Mild drowsiness and skin rashes have been noted.

Biotin

Biotin shows preliminary evidence of being useful for controlling blood glucose.

Bitter melon (Momordica charantia)

Bitter melon has traditionally been used as a remedy for lowering blood glucose.

Chromium

Chromium enhances use of insulin. Skin allergies, renal toxicity, and altered iron and zinc absorption can occur. There are no proven benefits if a patient is not deficient (American Diabetes Association, 2009).

Cinnamon

Doses of 1, 3, or 6 g capsules of cinnamon daily lowered blood glucose levels in individuals with diabetes.

Essential oils

Essential oils from cinnamon, cumin, and oregano may enhance insulin sensitivity. Studies are ongoing.

Evening primrose oil

Evening primrose oil may prevent or limit neuropathy due to gamma linoleic acid, an essential fatty acid. It may cause headache and gastrointestinal distress.

Fenugreek

Fenugreek may lower glucose, triglyceride and cholesterol levels due to its psyllium content. Note that it is part of the peanut family and may cause allergic reactions. Do not take with monoamine oxidase (MAO) inhibitors; it has the potential for drug interactions with other medications as well.

Gamma linolenic acid

Evening primrose oil may be useful for preventing neuropathy in diabetes.

Garlic

Garlic may lower blood glucose levels if used in large amounts; more studies are needed.

Gingko biloba

Gingko biloba may help control neuropathy by maintaining integrity of blood vessels and reducing stickiness of blood and clotting. It has some antioxidant properties. Avoid taking with warfarin, aspirin, and other anticoagulant drugs. Headache and interactions with other drugs can occur.

Ginseng, American

Ginseng (American) may lower blood glucose levels. Avoid with warfarin, aspirin, MAO inhibitors, caffeine, antipsychotics, insulin, and oral hypoglycemics because of fluctuations in blood glucose levels, bleeding, platelet functioning, blood pressure and heart rate. Avoid taking with steroids. Headache, insomnia, nausea, or menstrual difficulties can occur. Take with a meal.

Guar gum

Guar gum is a fiber that normalizes the moisture content of the stool, absorbs excess liquid in diarrhea, softens the stool in constipation, and decreases the amount of cholesterol and glucose absorbed from the stomach and intestines.

Gymnema sylvestre

Gymnema sylvestre is a hypoglycemic herb. It is highly potent and should be used only under doctor’s supervision because it may change insulin requirements.

Magnesium

Magnesium is needed for hundreds of biochemical reactions; it helps regulate blood sugar levels and blood pressure. Some studies suggest that low magnesium levels may worsen blood glucose control in type 2 diabetes. Magnesium supplementation may help with insulin resistance, but avoid high doses.

Turmeric

Turmeric, the rhizome of Curcuma, may decrease blood glucose levels.

Vanadum

Vanadium may lower glucose levels. It has been associated with cancer cell growth and can be toxic at therapeutic levels.

Vitamin B6

Some studies suggest that an adequate intake of vitamin B6 (pyrodoxine) can helo with both T1DM and T2DM,

Vitamin D

Supplementation of up to 2000 IU daily in infants were less likely to develop type 1 diabetes over the next 30 years in Finland. This vitamin has a strong, protective effect. Experts are now recommending supplementation at the upper end of the current recommendations (i.e., 1000 IU).

Zinc

Zinc is part of the production and storage of insulin in the body. Fresh oysters, ginger root, lamb, pecans, split peas, egg yolk, rye, beef liver, lima beans, almonds, walnuts, sardines, chicken, and buckwheat are sources from the diet. Zinc should not be used with immunosuppressants, tetracycline, ciprofloxacin, or levofloxacin because of potential antagonist effects.

• Discuss the risks for CVD and how to manage them (American Diabetes Association, 2009; American Dietetic Association, 2009). • Eating disorders often occur in young women with diabetes; refer for psychotherapy if needed. • A1 c is often unacceptably high in adolescents; there is a need to more fully assess and understand factors such as race/ethnicity, education, and socioeconomic status on treatment recommendations (Paris et al, 2009).

• For sick days: Patients may require more insulin when ill. Liquid diets should provide 200 g CHO in equally divided amounts at mealtime and snacks; liquids should not be sugar free. • For surgery: Blood glucose should be in good control; perioperative hyperglycemia can be managed with doses of short-acting insulin. Correct abnormalities before surgery when possible. • Discuss reasonable use of the glycemic index (see Table 9-10).


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TABLE 9-10 Glycemic Index and Glycemic Load Glycemic index (GI) is a measure of serum glucose response to a food relative to a reference food that contains equal amounts of carbohydrate. It does not refer directly to quantified food exchanges. Glycemic load  GI available carbohydrate amount. A mixed diet yields varying results on blood glucose levels. Choosing low-GI foods in place of conventional or high-GI foods has a small, clinically useful effect on medium-term glycemic control in patients with diabetes (Brand-Miller et al, 2003). Carbohydrate Choices Choose low-GI carbohydrates most often because they digest slower and will be less likely to elevate blood glucose. Each choice  15 g of carbohydrate. Choose desired number of carbohydrate choices per meal or as needed by the individual. Children and teens, as well as young adults and athletes, will need much more per meal than sedentary adults. Glycemic Index

Grain or Bean Choices

Fruit Choices

Vegetable Choices

Low (best choice)

Barley, 1/3 cup

Apple, orange, or pear

Corn, 1/2 cup

Beans (kidney, pinto, etc.), 1/2 cup cooked

Cherries, 12

Squash, acorn, 1 cup cooked

Grapes, 17

Peas, green or lentils, 1/2 cup cooked

Lima beans, 2/3 cup

Grapefruit, 1/2

Muesli, 1/4 cup Oat bran, 1/3 cup

Cantaloupe or berries (blueberries, raspberries, strawberries, etc.)  1 cup

11⁄2 cups cooked or 3 cups raw vegetables (asparagus, beets, broccoli, carrots, cucumbers, mushrooms, onions, peppers, tomatoes, zucchini, and others)

Baked beans, 1/4 cup

Banana, 1 small

Potato, small, “new,” 1/2 cup

Bran flakes, 1/2 cup

Canned fruit, drained, 1/2 cup

Sweet potato, 1/2 cup cooked

Bread, 100% whole wheat, 1 slice

Dried fruit, 1/4 cup

English muffin, whole wheat, 1/2

Raisins, 2 tbsp

Medium (choose less often)

Granola, low sugar, 1/4 cup Hamburger or hot dog bun, 1/2 Oatmeal, old fashioned, 1/2 cup

Watermelon, 11⁄4 cups Orange juice, 1/2 cup Apple juice, 1/2 cup Grape juice, 1/3 cup

Pasta, 1/3 cup cooked Raisin bran, 1/3 cup Rice, converted or wild, 1/3 cup cooked Special K, 3/4 cup Tortilla, 6

High (choose rarely)

Bagel, large, 1/4 bagel

Potato, small russet, 3 diameter

Bread, white, 1 slice

Potato, mashed, 1/2 cup

Cream of wheat, 1/2 cup cooked Cheerios, 3/4 cup Corn flakes, 3/4 cup Instant oatmeal, 1/2 cup cooked Pancake, 4

Rice Krispies, 3/4 cup Rice, white, 1/3 cup cooked Shredded wheat, 1/3 cup Waffle, 4

(continued)


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TABLE 9-10 Glycemic Index and Glycemic Load (continued) Glycemic Index

Combination Foods

Sweets/Snacks

Milk/Yogurt/Milk Substitutes

Low

Soup, cream, low fat, 1 cup

Ice cream, low fat, 1/2 cup

Milk, skim or low fat (1%), 1 cup

Chili, low fat, 1/2 cup

Pudding, sugar free, 1/2 cup Chocolate candy, 15 kisses or 1-oz bar

Yogurt, low fat, artificially sweetened, 1 cup

Burrito, bean, flour tortilla, 7 long  3 carb choices

Popcorn, microwave light, popped, 3 cups

Soy milk, low fat or nonfat, 1 cup

Cookie, 3 across, 1

Pasta dish, 1/2 cup

Muffin, small, 1/2

Yogurt, low fat, sweetened, with fruit, 1/3 cup

Pizza, thin crust, medium, 1 slice ( 2 carb choices)

Pretzel twists, mini, 15 pieces

Pizza, thick crust, medium, 1 slice ( 3 carb choices)

Doughnut, 3 , 1/2 doughnut

Medium

High

Brownie or cake, no frosting, 2 square Granola bar, 1 Potato or tortilla chips, 15 chips Syrup, 1 tbsp

Source: Brand-Miller et al, 2003.

• Aim for 30 min/d of physical activity to burn a minimum of 1500 kcal/wk (see Table 9-11).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Dietetic Association: Type 1 Diabetes Evidence-Based Guidelines for Practice http://www.eatright.org/cps/rde/ xchg/ada/hs.xsl/home_21231_ENU_HTML.htm

American Diabetes Association–T1DM http://www.diabetes.org/type-1-diabetes.jsp

Juvenile Diabetes Research Foundation http://www.jdrf.org/index.cfm?page_id101982

Mayo Clinic – T1DM http://www.mayoclinic.com/health/type-1-diabetes/DS00329

TABLE 9-11 American Diabetes Association General Guidelines for Regulating Exercise Metabolic control before exercise

Avoid exercise if ketosis is present. Use caution if glucose levels are 300 mg/dL without ketosis. Ingest added carbohydrate if glucose levels are 100 mg/dL.

Blood glucose monitoring before and after exercise

Identify when changes in insulin or carbohydrate are necessary.

Food intake

Consume added carbohydrate, as needed, to avoid hypoglycemia.

Learn the glycemic response to different exercise conditions.

Carbohydrate-based foods should be readily available during and after exercise.

Medline Plus http://www.nlm.nih.gov/medlineplus/ency/article/000305.htm

TYPE 1 DIABETES MELLITUS—CITED REFERENCES American Diabetes Association. Diabetes: heart disease and stroke. Accessed September 22, 2009, at http://www.diabetes.org/diabetes-heart-diseasestroke.jsp American Diabetes Association. Standards of Medical Care in Diabetes–2009. Web site accessed September 22, 2009, at http://care.diabetesjournals. org/content/32/Supplement_1/S13.full American Dietetic Association. Evidence analysis library: Type 1 and Type 2 Diabetes. Web site accessed September 22, 2009, at https://www.adaevidencelibrary.com/topic.cfm?cat3481 Chase HP, et al. Insulin glargine versus intermediate-acting insulin as the basal component of multiple daily injection regimens for adolescents with type 1 diabetes mellitus. J Pediatr. 153:547, 2008. Chima CS, et al. Use of technology to track program outcomes in a diabetes self-management program. J Am Diet Assoc. 105:1933, 2005. DCCT Research Group. Modern-day clinical course of type 1 diabetes mellitus after 30 years’ duration: the diabetes control and complications trial/epidemiology of diabetes interventions and complications and Pittsburgh epidemiology of diabetes complications experience (1983–2005). Arch Int Med. 169:1307, 2009. Funnell MM, et al. Implementing an empowerment-based diabetes self-management education program. Diabetes Educ. 31:53, 2005. Gaetke LM, et al. A single nutrition counseling session with a registered dietitian improves short-term clinical outcomes for rural Kentucky patients with chronic disease. J Am Diet Assoc. 06:109, 2006. Herold KC, et al. Treatment of patients with new onset Type 1 diabetes with a single course of anti-CD3 mAb Teplizumab preserves insulin production for up to 5 years. Clin Immunol. 132:166, 2009. Kulkarni K. Diets do not fail: the success of medical nutrition therapy in patients with diabetes. Endocr Pract. 12:121S, 2006. Paris CA, et al. Predictors of insulin regimens and impact on outcomes in youth with type 1 diabetes: the SEARCH for Diabetes in Youth study. J Pediatr. 155:183, 2009. Svoren B, et al. Significant Vitamin D Deficiency in Youth with Type 1 Diabetes Mellitus. J Pediatr. 154:132, 2009. Tang TS, et al. Developing a new generation of ongoing diabetes self-management support interventions: a preliminary report. Diabetes Educ. 31:91, 2005. Williams KT, Schalinske KL. New insights into the regulation of methyl group and homocysteine metabolism. J Nutr. 137:311–314, 2007. White NH, et al. Comparison of glycemic variability associated with insulin glargine and intermediate-acting insulin when used as the basal component of multiple daily injections for adolescents with type 1 diabetes. Diabetes Care. 32:387, 2009.


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ISLET CELL TRANSPLANTATION NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Some native pancreatic beta cell function persists even years after disease onset in most type 1 diabetic patients (Liu et al, 2009). However, the destruction of beta cells leads to permanent insulin dependence. Islet cell transplantation can lead to insulin independence with excellent metabolic control. Islet transplantation can require more than one donor pancreas to achieve insulin independence (Rickels et al, 2005). Transplants may be performed by a radiologist, who uses x rays and ultrasound to guide placement of a catheter through the upper abdomen and into the portal vein, where islets are slowly infused. If this is not feasible, a surgeon may perform the procedure under anesthesia. The acute posttransplantation phase lasts up to 2 months; the chronic phase starts after 2 months. Drugs are needed to prevent rejection. Islet cell programs try to avoid using large doses of glucocorticoids. Most protocols are designed to use tacrolimus and sirolimus so that high-dose glucocorticoids would not have to be used. During the acute period of care, there is the issue that patients are variably managed with insulin therapy to allow for recovery of the islets after they have been placed into their new and not totally adequate environment in the liver. Most centers treat patients for up to a month, and treating hypoglycemia during this time is a concern. Long-term complications may include hyperlipidemia. In T1DM, the release of many hormones, not only from betacells, but also from adipocytes (adipokines) is altered (Stadler et al, 2009). After successful pancreas–kidney transplantation (PKTx), T1DM patients can revert to a nondiabetic metabolism, but altered adipokines are still present after PKTx; adipokines include visfatin, retinol-binding protein-4 (RBP-4), adiponectin, and high-molecular-weight (HMW) adiponectin (Stadler et al, 2009). More research in this area is needed.

ASSESSMENT, MONITORING, AND EVALUATION

Alkaline phosphatase (Alk phos) Aspartate aminotransferase (AST) Alanine aminotransferase (ALT)

Bilirubin Na, K Hemoglobin and hematocrit (H & H) Serum Fe Serum folacin BUN, Creat Ca, Mg

White blood cell (WBC) count Total lymphocyte (TLC) count Glucose (Gluc) Chol, Trig CRP

INTERVENTION OBJECTIVES • Meet the specific needs of the patient; modify drug therapy to enhance outcomes and quality of life. • Prevent infection and promote healing. • Monitor for abnormal electrolyte levels. • Monitor CHO intolerance but make sure that diet provides enough CHO to spare proteins. Treatment goals should reflect those of the American Diabetes Association; adjust as new evidence suggests. • Alleviate rejection episodes. • Control infections, especially during the acute phase. Support protein intake to prevent additional infections. • Force fluids unless contraindicated, as in retention. Match fluid output. • Help patient adjust to a lifelong medical regimen during chronic phase. Improve survival rate by supporting immune response. • Correct or manage complications that occur. • Control weight gain in the first year after transplantation.

SAMPLE NUTRITION CARE PROCESS STEPS Poor Nutrition Quality of Life Assessment Data: Weight, labs, nutritional history prior to transplantation, statement of “not liking to eat any more because of the pain.”

CLINICAL INDICATORS Genetic Markers: Transplantation may occur for T1DM, where there is a genetic component. Clinical/History

BP Temperature

Height Dry weight, presLab Work ent weight Albumin (Alb), BMI transthyretin Diet history HbA1c I&O

Nitrogen (N) balance Glomerular filtration rate (GFR)

Nutrition Diagnosis (PES): Poor nutritional quality of life related to abdominal pain after meals as evidenced by weight changes, vacillating lab results and statements about not enjoying meals. Intervention: Food and Nutrient Delivery—gradual weaning from nutritional support back to oral diet, using small portions of favorite foods. Education—how the transplant would eventually allow life without insulin shots and more normal meal experiences. Monitoring and Evaluation: Tolerance after weaning from nutrition support to oral diet. Acceptance of several favorite foods, and trying new foods with assistance of family members.


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TABLE 9-12

Medications Used after Islet Cell Transplantation

Medication

Description

Cyclosporine

Cyclosporine does not cause retention of sodium as much as corticosteroids do. Intravenous doses are more effective than oral doses. Nausea, vomiting, and diarrhea are common side effects. Hyperlipidemia, hyperglycemia, and hyperkalemia may also occur; decrease fat intake as well as sodium and potassium if necessary. Magnesium may need to be replaced. The drug is also nephrotoxic; a controlled renal diet may be beneficial. Take omega-3 fatty acids to reduce toxic side effects such as high blood pressure and kidney damage. Avoid St. John’s wort.

Diuretics

Diuretics such as furosemide (Lasix) may cause hypokalemia. Aldactone actually spares potassium; monitor drug changes closely. In general, avoid use with fenugreek, yohimbe, and ginkgo.

Immunosuppressants

Immunosuppressants such as muromonab (Orthoclone OKT3) and antithymocyte globulin (ATG) are less nephrotoxic than cyclosporine but can cause nausea, anorexia, diarrhea, and vomiting. Monitor carefully. Fever and stomatitis also may occur; alter diet as needed.

Insulin

Insulin may be necessary during periods of hyperglycemia. Monitor for hypoglycemic symptoms during use; teach patient selfmanagement tips.

Pancreatic enzymes

Pancreatic enzymes may be needed if pancreatitis occurs after transplantation.

Tacrolimus (Prograf, FK506)

Tacrolimus suppresses T-cell immunity; it is 100 times more potent than cyclosporine, thus requiring smaller doses. Side effects include gastrointestinal distress, nausea, vomiting, hyperkalemia, and hyperglycemia; adjust diet accordingly by controlling carbohydrate and enhancing potassium intake.

Tetranectin

Tetranectin binds plasminogen and may have a role in regulating pericellular proteolysis and in the survival of islets in the liver after islet transplantation.

FOOD AND NUTRITION • Progress solids as quickly as possibly postoperatively. Monitor fluid status, and adjust as needed. • Daily intake of protein should be appropriate for age and sex; 1.5 g/kg while on steroids may be recommended. Energy needs should be calculated as 30–35 kcal/kg. • Daily intake of sodium should be 2–4 g until the drug regimen is reduced. Adjust potassium levels as needed. • Daily intake of calcium should be 1–1.5 times the daily requirements to offset poor absorption. Children especially need adequate calcium for growth. Daily intake of phosphorus should be equal to calcium intake. • Supplement diet with vitamin D, magnesium, and thiamin as needed. Adequate vitamin intake will be essential to maintain immunity and to support wound healing. • Control CHO intake with hyperglycemia (45–50% total kcal); encourage healthy food sources of carbohydrate. Transplantation patients are at risk of further glucose intolerance from multiple medications. • Plan fats at 25–35% of total kilocalories (encourage monounsaturated fats and omega-3 fatty acids). Low saturated fats and cholesterol may be needed. A controlled fat intake is recommended for prevention and treatment of hyperlipidemia. • Reduce gastric irritants as necessary if GI distress or reflux occurs. • Monitor electrolytes carefully; hyperkalemia is common with cyclosporine or tacrolimus. • Special diets may be discontinued when drug therapy is reduced to maintenance levels. Encourage exercise and a weight control plan thereafter.

Common Drugs Used and Potential Side Effects • Thymoglobulin is an antibody preparation to prevent organ transplant rejection. The START trial is underway

to determine whether Thymoglobulin treatment can halt the progression of newly diagnosed type 1 diabetes when given within 6 weeks of disease diagnosis. • See Table 9-12 for other drugs used for the transplant.

Herbs, Botanicals, and Supplements • Herbals should be discouraged after transplantation. Those who self-medicate with herbals are taking a chance that their use of a herb may interact with their immunosuppressive drugs and either cause higher or lower than desired drug levels of these agents. • Chaparral is an herbal product that may cause severe hepatitis or liver failure. St. John’s wort interferes with the metabolism of immunosuppressants and should not be used after transplantation. • See Table 9-9 for guidance on more specific herbs and supplements.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Indicate which foods are sources of key nutrients such as protein in the diet. If patient does not like milk, discuss how other sources of calcium may be used in the diet. • Alcohol should be avoided unless permitted by the doctor. • Patients should know when to seek medical attention. • Discuss problems with long-term obesity and hypercholesterolemia. • Encourage moderation in diet; promote adequate exercise.


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Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association–Islet Cell Transplantation http://www.diabetes.org/type-1-diabetes/islet-transplants.jsp

Immune Tolerance Network (ITN) http://www.immunetolerance.org

Insulin-Free http://www.insulin-free.org/

NIDDK–Islet Cell Transplantation http://diabetes.niddk.nih.gov/dm/pubs/pancreaticislet/

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PANCREAS OR ISLET CELL TRANSPLANTATION— CITED REFERENCES Hermann M, et al. In the search of potential human islet stem cells: is tetranectin showing us the way? Transplant Proc. 37:1322, 2005. Liu EH, et al. Pancreatic beta cell function persists in many patients with chronic type 1 diabetes, but is not dramatically improved by prolonged immunosuppression and euglycaemia from a beta cell allograft. Diabetologia. 52:1369, 2009. Rickels MR, et al. Beta-cell function following human islet transplantation for type 1 diabetes. Diabetes. 54:100, 2005. Stadler M, et al. Adipokines in type-1 diabetes after successful pancreas transplantation: Normal visfatin and retinol-binding-protein-4, but increased total adiponectin fasting concentrations. [published online ahead of print September 21, 2009] Clin Endocrinol (Oxf ). 72:763, 2010.

METABOLIC SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND The metabolic syndrome (MetS; insulin resistance syndrome or syndrome X) has simultaneous clustering of low levels of HDL cholesterol, hyperglycemia, high waist circumference, hypertension, and elevated triglycerides. Any three of the following five criteria constitute diagnosis of MetS (Grundy et al, 2005): • Elevated waist circumference: 40 or 102 cm in men; 35

or 88 cm in women. • Elevated triglycerides (TG) 150 mg/dL or drug treatment for elevated TG. • Reduced HDL cholesterol: 40 mg/dL in men and 50 mg/dL in women or drug treatment for low HDL cholesterol levels. • Elevated BP: 130 mm Hg systolic BP or 85 mm Hg diastolic BP or drug treatment for hypertension. • Elevated fasting glucose: 100 mg/dL or drug treatment for elevated glucose. It is associated with CVD and often leads to T2DM. This condition affects some young people but usually affects persons aged 55 years and older. More than 64 million Americans have MetS, roughly one in four adults and 40% of adults aged 40 years and older. Increased birthweight, excessive energy intake, physical inactivity, obesity, smoking, inflammation, and hypertension contribute to MetS. Individuals who are obese and insulin resistant are particularly prone to this syndrome. An “apple” shaped figure (high waist circumference) is riskier because fat cells located in the abdomen release fat into the blood more easily than fat cells found elsewhere. Serum adiponectin levels are associated with insulin sensitivity; they are decreased in T2D and obesity. Genetic and environmental factors contribute to risk (Gable et al, 2006). The initial insult in adipose inflammation and insulin resistance is perpetuated through chemokine secretion, adipose retention of macrophages, and elaboration of pro-inflammatory

adipocytokines (Shah et al, 2008). In women, depressive symptoms are associated with MetS, especially with elevated afternoon and evening cortisol (Muhtz et al, 2009). Clearly, more research is needed. Management of MetS should focus on lifestyle modifications, especially reduced caloric intake and increased physical activity (Deedwania and Volkova, 2005). Phytochemicals, MUFA, antioxidant foods, spices such as turmeric, cumin, and cinnamon have anti-inflammatory effects. Intake of whole milk, yogurt, calcium, and magnesium protect against MetS whereas intake of cheese, low-fat milk, and phosphorus do not (Beydoun et al, 2008; McKeown et al, 2009). Mild-to-moderate alcohol consumption is acceptable but binges and early onset of drinking are not acceptable.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Candidate genes associated with CVD represent potential risk factors for the MetS (Goulart et al, 2009). Chronic inflammation and IL1beta genetic variants may be a concern; genetic influences are more evident among subjects with low (n-3) PUFA intake (Shen et al, 2007). Clinical/History Height Weight Weight pattern history Central Obesity?

BMI Waist circumferDiet history ence (35 or Waist circumfer88 cm in ence (40

women) or 102 cm BP (130/85 in men) mm Hg)


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Sleep apnea? Depression?

LDL Chol (high?) Trig (150 Lab Work mg/dL) Mg Gluc (100 Na, K mg/dL) Serum insulin HbA1 c Serum uric acid HDL Chol (40 (elevated?) mg/dL for CRP (elevated) men, 50 mg/dL for women)

High fibrinogen or plasminogen activator inhibitor [ 1] in the blood? Prothrombin time (PT) International normalized ratio (INR)

INTERVENTION OBJECTIVES • Reduce the inflammatory state and insulin resistance caused by excessive adipose tissue. Improve body weight; lessen abdominal obesity in particular. A realistic goal for weight reduction should be 7–10% over 6–12 months (Bestermann et al, 2005). • Promote physical activity. Recommendations should include practical, regular, and moderated regimens of exercise, with a daily minimum of 30–60 minutes and equal balance between aerobic and strength training (Bestermann et al, 2005). • Achieve and maintain cholesterol, blood glucose, and BP at levels indicated by the American Heart Association, as follows (Grundy et al, 2005):

For Atherogenic Dyslipidemia • For elevated LDL cholesterol: Give priority to reduction of LDL cholesterol over other lipid parameters. Achieve LDL cholesterol goals based on patient’s risk category. LDL cholesterol goals for different risk categories are: • High risk: seek 70–100 mg/dL • Moderately high risk: seek 100–130 mg/dL • Moderate risk: seek 130 mg/dL • Lower risk: 160 mg/dL is acceptable

• If TG is 200 mg/dL, then goal for non-HDL cholesterol for each risk category is 30 mg/dL higher than for LDL cholesterol. If TG is 200 mg/dL after achieving LDL cholesterol goal, consider additional therapies to attain non-HDL cholesterol goal. • If HDL cholesterol is 40 mg/dL in men or 50 mg/dL in women, raise HDL cholesterol to extent possible with standard therapies for atherogenic dyslipidemia. Either lifestyle therapy can be intensified or drug therapy can be used for raising HDL cholesterol levels, depending on patient’s risk category.

For Elevated BP • Reduce BP to at least achieve BP of 140/90 mm Hg (or 130/80 mm Hg if diabetes is present). Reduce BP further to extent possible through lifestyle changes. • For BP 120/80 mm Hg: Initiate or maintain lifestyle modification via weight control, increased physical activity, alcohol moderation, sodium reduction, and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products in all patients with MetS. • For BP 140/90 mm Hg (or 130/80 mm Hg if diabetes is present), add BP medication as needed to achieve goal BP.

For Elevated Glucose • For IFG, delay progression to T2DM. Encourage weight reduction and increased physical activity. • In diabetes, for hemoglobin A1 c at or above 7.0%, lifestyle therapy and pharmacotherapy, if necessary, should be used. Modify other risk factors and behaviors (e.g., abdominal obesity, physical inactivity, elevated BP, or lipid abnormalities).

For Prothrombotic State • Reduce thrombotic and fibrinolytic risk factors. Lowdose aspirin therapy or prophylaxis is recommended.

For Proinflammatory State • There are no specific therapies beyond lifestyle changes. The antioxidants and omega-3 fatty acids may be helpful.

SAMPLE NUTRITION CARE PROCESS STEPS

FOOD AND NUTRITION Inappropriate Intake of Types of CHO—Metabolic Syndrome Assessment Data: Food intake records: high refined CHO and soft drink intake; high juice but minimal fruit intake; low dietary fiber intake. Nutrition Diagnosis (PES): Inappropriate intake of types of CHO related to knowledge deficit about MetS as evidenced by FBS of 140 mg/dL and triglycerides of 300 mg/dL. Intervention: Education about desirable CHO, whole grains, and fiber; shopping tips; dining out. Monitoring and Evaluation: Improved labs in 3–6 months; dietary records showing improvement in intake of whole grains, whole fruits, and vegetables.

• The general recommendations include low intake of saturated fats, trans fats, and cholesterol. Increase use of omega-3 PUFA intake (Shen et al, 2007) and MUFA (especially extra virgin olive oil). • Plan a Mediterranean-type diet using more fiber and starches, especially whole grains, raw fruits, and vegetables. A plant-based diet may be useful (Barnard et al, 2005). • The DASH diet contains 3–4 g sodium with good sources of potassium, calcium, and magnesium. Dairy products provide calcium, magnesium, and potassium. • Monitor blood glucose levels. Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with MetS more than a low fat diet (Al-Sarraj et al, 2010).


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• Encourage soy protein as a meat substitute several times a week; soy protein may help with weight reduction and dyslipidemia (Bestermann et al, 2005). • Ensure adequate intake of folate, vitamins B6, B12, C, and E, preferably from food. • Dark chocolate in small amounts regularly may help lower BP, improve cholesterol, and help with insulin sensitivity. • Spread out the energy load by eating smaller meals.

Common Drugs Used and Potential Side Effects • To lower lipids, a statin should be used initially unless contraindicated (Bestermann et al, 2005). Statins decrease biomarkers of inflammation and oxidative stress in a dose-related manner; atorvastatin 80 mg compared with a 10-mg dose is superior for decreasing oxidized LDL, hsCRP, matrix metalloproteinase-9, and NF-kB activity (Singh et al, 2008). • Glucose-lowering medications must be carefully prescribed and monitored. Metformin may be indicated (Orchard et al, 2005). • BP medications may be prescribed; monitor for necessary restrictions of sodium and/or higher need for potassium. An ACE inhibitor or an angiotensin receptor blocker is usually the first medicine (Bestermann et al, 2005). • Medications that diminish insulin resistance and directly alter lipoproteins are necessary; combination therapy is often required (Bestermann et al, 2005). • If patients with MetS have elevated fibrinogen and other coagulation factors leading to prothrombotic state, aspirin is used (Deedwania and Volkova, 2005). Low-dose aspirin is not generally a problem; taken with a meal or light snack to prevent potential for GI bleeding.

Herbs, Botanicals, and Supplements • Antioxidant supplements are not recommended, but intake of antioxidant-rich foods should be suggested (Czernichow et al, 2009). Thus far, trials with alpha tocopherol have been disappointing; further trials with gamma and alpha-tocopherols are warranted. Include phytochemicals, antioxidant foods, and spices such as turmeric, cumin, and cinnamon in the diet. See Tables 8-13 and 8-14. • Chromium picolinate (CrPic) enhances insulin action by lowering plasma membrane (PM) cholesterol (Horvath et al, 2008). Coenzyme Q10 may have some merit, but further research is needed. • High serum selenium concentrations have been associated with prevalence of higher FPG, LDL, TG, and glycosylated hemoglobin levels; further research is needed to determine its role in the development or the progression of MetS (Bleys et al, 2008). • Other herbs and botanical supplements should not be used without discussing with physician. See Table 9-9 for guidance on more specific herbs and supplements.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Widespread screening is recommended to slow the growth of this syndrome. Prevention should start in childhood

• •

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with healthy nutrition, daily physical activity, and annual measurement of weight, height, and BP beginning at 3 years of age (Bestermann, 2005). Discuss the role of nutrition (DASH or Mediterranean diet principles) in managing this syndrome. Obesity is a major contributor to the problem, so weight loss (even 10 lb) can help improve health status. A diet rich in antioxidants and DHA is beneficial. Finally, the 2005 Dietary Guidelines are consistent with lowering risk for MetS (Fogli-Cawley et al, 2007). Regular physical activity can help to lower elevated blood cholesterol levels and BP. Walking, or an exercise that is pleasant for the individual, is the one to select. Aerobic and strength training exercises are beneficial. Reduce sedentary activities, including television and computer time (Ford et al, 2005). Smoking cessation measures may be needed. Offer guidance on how not to gain weight after quitting. Limit consumption of alcoholic beverages, which can elevate triglycerides in large doses.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association–Metabolic Syndrome http://www.diabetes.org/diabetes-research/summaries/ ekelund-metabolic.jsp

American Heart Association http://www.americanheart.org/presenter.jhtml?identifier534

Mayo Clinic http://www.mayoclinic.com/health/metabolic%20syndrome/DS00522

METABOLIC SYNDROME—CITED REFERENCES Al-Sarraj T, et al. Metabolic syndrome prevalence, dietary intake, and cardiovascular risk profile among overweight and obese adults 18–50 years old from the United Arab Emirates. Metab Syndr Relat Disord. 8:39, 2010. Barnard ND, et al. The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity. Am J Med. 118:991, 2005. Bestermann G, et al. Addressing the global cardiovascular risk of hypertension, dyslipidemia, diabetes mellitus, and the metabolic syndrome in the southeastern United States, part II: treatment recommendations for management of the global cardiovascular risk of hypertension, dyslipidemia, diabetes mellitus, and the metabolic syndrome. Am J Med Sci. 329:292, 2005. Beydoun MA, et al. Ethnic differences in dairy and related nutrient consumption among US adults and their association with obesity, central obesity, and the metabolic syndrome. Am J Clin Nutr. 87:1914, 2008. Bleys J, et al. Serum selenium and serum lipids in US adults. Am J Clin Nutr. 88:416, 2008. Czernichow S, et al. Effects of long-term antioxidant supplementation and association of serum antioxidant concentrations with risk of metabolic syndrome in adults. Am J Clin Nutr. 90:329, 2009. Deedwania PC, Volkova N. Current treatment options for the metabolic syndrome. Curr Treat Options Cardiovasc Med. 7:61, 2005. Ellison RC, et al. Relation of the metabolic syndrome to calcified atherosclerotic plaque in the coronary arteries and aorta. Am J Cardiol. 95:1180, 2005. Fogli-Cawley JJ, et al. The 2005 Dietary Guidelines for Americans and risk of the metabolic syndrome. Am J Clin Nutr 86:1193, 2007. Ford ES, et al. Sedentary behavior, physical activity, and the metabolic syndrome among U.S. adults. Obes Res. 13:608, 2005. Gable DR, et al. Adiponectin and its gene variants as risk factors for insulin resistance, the metabolic syndrome and cardiovascular disease. Atherosclerosis. 188:231, 2006. Goulart AC, et al. Association of genetic variants with the metabolic syndrome in 20,806 white women: The Women’s Health Genome Study. Am Heart J. 158:257, 2009.


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Grundy S, et al. Diagnosis and management of the metabolic syndrome. Circulation. 112:105, 2005. Horvath EM, et al. Antidiabetogenic effects of chromium mitigate hyperinsulinemia-induced cellular insulin resistance via correction of plasma membrane cholesterol imbalance. Mol Endocrinol. 22:937, 2008. McKeown NM, et al. Dietary magnesium intake is related to metabolic syndrome in older Americans. Eur J Nutr. 47:210, 2009. Orchard TJ, et al. The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: the Diabetes Prevention Program randomized trial. Ann Intern Med. 142:611, 2005.

Shah A, et al. Adipose inflammation, insulin resistance, and cardiovascular disease. JPEN J Parenter Enteral Nutr. 32:638, 2008. Shen J, et al. Interleukin1beta genetic polymorphisms interact with polyunsaturated fatty acids to modulate risk of the metabolic syndrome. J Nutr. 137:1846, 2007. Singh U, et al. Comparison effect of atorvastatin (10 versus 80 mg) on biomarkers of inflammation and oxidative stress in subjects with metabolic syndrome. Am J Cardiol. 102:321, 2008. Talpur N, et al. Effects of a novel formulation of essential oils on glucoseinsulin metabolism in diabetic and hypertensive rats: a pilot study. Diabetes Obes Metab. 7:193, 2005.

PREDIABETES NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Prediabetes (impaired glucose tolerance, IGT) distinguishes those people who are at increased risk of developing diabetes. People with prediabetes have IFG or IGT, or both. More than 54 million Americans are affected with this combination of genes, obesity, and physical inactivity. People who have prediabetes may have a family history of heart disease and apple-shaped (intra-abdominal) obesity. Elevated triglycerides and low HDL cholesterol are risks for T2DM (Zacharova et al, 2005); adiposity-associated inflammation and insulin resistance are also implicated (Shah et al, 2008). NIH has also reported that smoking increases insulin resistance and prediabetes. Under recent criteria, a normal blood glucose level is 100 mg/dL. Table 9-13 shows the tests and classification for IGT and IFG. Most people with prediabetes go on to develop T2DM within 10 years unless they make lifestyle changes. Studies have evaluated various interventions among people with IGT and risks for developing diabetes. The Diabetes Prevention Program (DPP) was a large prevention study of people at high risk for diabetes (American Diabetes Association, 2006). Half of the participants had MetS at the beginning of the study; lifestyle intervention and metformin therapy reduced development of the syndrome in the remaining participants (Orchard et al, 2005). Lifestyle interventions include modest weight loss from a low-calorie, low-fat diet,

TABLE 9-13 Prediabetes Classifications and Tests Condition/Classification

Test Used and Diagnostic Values

Impaired glucose tolerance (IGT)

• Oral Glucose Tolerance Test (OGTT), 75 g of glucose • 2-hour plasma glucose  140–199 mg/dL • Fasting plasma glucose (FPG) after 8-hour fast • Fasting plasma glucose  100–125 mg/dL

Impaired fasting glucose (IFG)

and increased moderate-intensity physical activity (such as walking for 21⁄2 hours each week). People treated with an intensive lifestyle intervention reduce their risk of developing diabetes by half over 4 years, whereas people treated with metformin reduce their risk by only one third (American Diabetes Association, 2006). Metformin is most effective among younger, heavier people (those 25–40 years of age, 50–80 lb overweight) and less effective among older people and people with lower BMIs. In the STOP-NIDDM Trial, treatment of people with IGT with the drug acarbose reduced the risk of developing diabetes by 25% over 3 years. The benefits of weight loss and physical activity strongly suggest that lifestyle modification should be the first choice to prevent or delay diabetes (American Diabetes Association, 2009). The dietitian plays an important role in nutrition education and counseling for these behavioral changes.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Researchers are learning how to predict a person’s odds of getting diabetes; Caucasians with type 1 diabetes have genes called HLA-DR3 or HLA-DR4 (American Diabetes Association, 2009). The HLA-DR7 gene may put African Americans at risk, and the HLA-DR9 gene may put Japanese at risk. The MTHFR CT polymorphism has a significant association with diabetic neuropathy in Caucasians and in persons with T2DM (Zintzaras et al, 2007). More rigorous studies are needed to define the role of genotypes in diabetes complications and management. Clinical/History Height Weight

Waist circumference BMI Diet history

I&O BP (140/90?) Smoker? PCOS?


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Heart disease? Fasting glucose after 8 hours Hx gestational diabetes? (100–120 mg/dL?) High risk ethnic background? HbA1 c Sedentary Chol, HDL and LDL lifestyle? Family hx T2DM? profiles Trig Lab Work CRP

Alb, transthyretin Na, K H&H Serum Fe Serum folacin BUN, Creat Ca, Mg GFR

Gluc OGTT with 2 hours postprandial (140–199 mg/dL?)

543

SAMPLE NUTRITION CARE PROCESS STEPS Not Ready For Lifestyle Change Assessment Data: Blood glucose log and food history; BMI 29 at age 48; family Hx diabetes (T2DM); previous counseling on lifestyle changes to prevent diabetes. Recent random blood glucose 140 mg/dL. Nutrition Diagnosis (PES): Not ready for lifestyle change related to potential for diabetes as evidenced by BMI 29, family history of diabetes, statement of “not being interested in many changes at this time.” Intervention: Counseling about the importance of lifestyle changes to reduce likelihood of diabetes. Monitoring and Evaluation: Follow-up clinic visit indicating that client did make some lifestyle changes after considering the last counseling session; random blood glucose 100 mg/dL; weight loss of 5 lb in two months; increase in physical activity noted.

INTERVENTION OBJECTIVES • Increase the probability of reverting from IGT to normal glucose tolerance. Prevent further insulin resistance, hyperglycemia, or progression to diabetes. • Modest weight loss (5–10% of body weight) and modest physical activity (30 minutes daily) are the recommended goals (American Diabetes Association, 2006). Walking can be encouraged for most people. • Prevent or delay heart and kidney diseases, stroke, eye disease, and other undesirable conditions. • Design a program that includes elements from the successful DPP trial: Clearly defined weight loss and physical activity goals

A flexible maintenance program

Individual case managers or “lifestyle coaches”

Culturally appropriate materials and strategies

Intensive, ongoing intervention

Local and national network of training, feedback and clinical support

A core curriculum

Supervised exercise sessions at least twice weekly

Source: CDC, Web site accessed September 25, 2009, at http://www.cdc.gov/diabetes/ faq/prediabetes.htm.

FOOD AND NUTRITION • Control CHO intake (about 45–50% of total kilocalories) and limit excess added sugars. Encourage less processed carbohydrate and fiber food sources. Individualize according to lab work, BMI, and other risk reduction requirements. • Maintain protein at about 20% of total energy. • Plan fats at about 30–35% of total kcal (encourage monounsaturated fats and omega-3 fatty acids). Low saturated fats and cholesterol may be needed to prevent or treat hyperlipidemia.

• A moderate reduction in total energy intake is important. Modest weight loss of 5–7% of body weight may be recommended. • Sufficient intake of minerals such as magnesium may be protective against diabetes. Include more almonds, whole wheat, cooked spinach, baked potatoes, and other magnesium-rich foods. • Excesses of iron and selenium should be avoided; studies suggest that high intakes cause deposits in the internal organs, including the pancreas. • Include adequate intake of fiber. A low fat vegan diet has been found to improve glycemia and elevated lipids (Barnard et al, 2009). • Essential oils such as fenugreek, cinnamon, cumin, and oregano enhance insulin sensitivity (Talpur et al, 2005). Cinnamon may improve blood sugar and lipid levels (1/2 teaspoon daily). • When a tube feeding is needed, there is insufficient evidence to support the use of specialty products as compared with standard products at this time.

Common Drugs Used and Potential Side Effects • Acarbose treatment in IGT subjects decreases the risk of progression to diabetes by 36% (Delorme and Chiasson, 2005). • Metformin reduces risk of developing diabetes, especially among younger, heavier people such as those 25–40 years of age who are 50–80 lb overweight (Herman et al, 2005). It is less effective among older people and people who were not as overweight.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. See Table 9-9 for tips.


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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Community Health Workers (CHW) may be trained for peer counseling when administered through a Diabetes Care Center (Katula et al, 2010). Lifestyle weight (LW) loss intervention has a goal of 7% weight loss achieved through increases in physical activity (180 min/wk) and decreases in caloric intake (approximately 1500 kcal/d) with CHW-led group-mediated cognitive behavioral meetings that occur weekly for 6 months and monthly thereafter for 18 months (Katula et al, 2010). Monthly small-group education sessions for a year are recommended by the CDC. • Weight loss is a key goal (Davis et al, 2009; Norris et al, 2005). Discuss foods and meal patterns that will help to reduce risk factors for the individual client. • Look AHEAD (Action for Health in Diabetes) trial participants (overweight adults diagnosed with diabetes) exceed recommended intake of fat, saturated fats, and sodium, which may contribute to increasing their risk of CVD and other chronic diseases (Vitolins et al, 2009). Therefore, it is important to address total fat intake (type of fat) and to suggest increasing intake of antioxidantrich, high fiber foods. A vegan or vegetarian diet can be safely recommended (Barnard et al, 2009). • Promote 8 oz or more of low fat milk, an ounce a day of nuts, filtered coffee, 1/2 teaspoon of cinnamon, and plenty of nonstarchy vegetables. • Exercise seems to promote more reliable glycemic control compared with specific dietary protocols (Nield et al, 2007). Promote physical activity that matches client interest and ability. Discuss how to handle medication changes accordingly.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association–Prediabetes http://www.diabetes.org/diabetes-prevention/pre-diabetes.jsp

CDC – Prediabetes http://www.cdc.gov/diabetes/faq/prediabetes.htm

Mayo Clinic – Prediabetes http://www.mayoclinic.com/health/prediabetes/DS00624

NIDDK–Prediabetes and Insulin Resistance http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/

PREDIABETES—CITED REFERENCES American Diabetes Association. Genetics. Website accessed September 25, 2009, at http://www.diabetes.org/genetics.jsp. Barnard ND, et al. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am J Clin Nutr. 89:1588S, 2009. Davis N, et al. Nutritional strategies in type 2 diabetes mellitus. Mt Sinai J Med. 76:257, 2009. Delorme S, Chiasson JL. Acarbose in the prevention of cardiovascular disease in subjects with impaired glucose tolerance and type 2 diabetes mellitus. Curr Opin Pharmacol. 5:184, 2005. Herman WH, et al. Diabetes Prevention Program Research Group. The costeffectiveness of lifestyle modification or metformin in preventing type 2 diabetes in adults with impaired glucose tolerance. Ann Intern Med. 142:323, 2005. Katula JA, et al. Healthy Living Partnerships to Prevent Diabetes (HELP PD): Design and methods. [published online ahead of print September 13,2009] Contemp Clin Trials. 31:71, 2010. Nield L, et al. Dietary advice for treatment of type 2 diabetes mellitus in adults. Cochran Database Syst Rev. 2007 Jul 18; (3):CD004097. Norris SL, et al. Long-term effectiveness of weight loss interventions in adults with pre-diabetes. A review. Am J Prev Med. 28:126, 2005. Orchard TJ, et al. The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: the Diabetes Prevention Program randomized trial. Ann Intern Med. 142:61, 2005. Shah A, et al. Adipose inflammation, insulin resistance, and cardiovascular disease. JPEN J Parenter Enteral Nutr. 32:638, 2008. Talpur N, et al. Effects of a novel formulation of essential oils on glucoseinsulin metabolism in diabetic and hypertensive rats: a pilot study. Diabetes Obes Metab. 7:193, 2005. Vitolins MZ, et al. Action for Health in Diabetes (Look AHEAD) trial: baseline evaluation of selected nutrients and food group intake. J Am Diet Assoc. 109:1367, 2009. Zacharova J, et al. The common polymorphisms (single nucleotide polymorphism [SNP] 45 and SNP 276) of the adiponectin gene predict the conversion from impaired glucose tolerance to type 2 diabetes: the STOP-NIDDM trial. Diabetes. 54:893, 2005.

TYPE 2 DIABETES IN ADULTS NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND T2DM arises because of insulin resistance, when there is failure to use insulin properly combined with relative insulin deficiency. Increased and unrestrained hepatic glucose production as well as diminished glucose uptake and utilization results from insulin resistance occurring in the cells of the liver and other peripheral tissue, especially skeletal muscle. Previous names for T2DM include “non–insulindependent diabetes (NIDDM),” “adult-onset,” “type II,” “maturity-onset,” and “ketosis-resistant” diabetes. T2DM accounts for 90% of all forms of diabetes. A significant per-

centage (about one third) of individuals who have T2DM are unaware of their diagnosis. Because T2DM is progressive, most patients will have already lost at least 50% of betacell function at the time of diagnosis. The American Diabetes Association recommends diagnostic screening at 3-year intervals beginning at the age of 45, especially in individuals who have a BMI greater than 25 kg/m2 (overweight). Risk factors include genetics, obesity, age, history of gestational diabetes, sedentary lifestyle, and smoking. Smoking cessation, decreasing BMI, and decreasing BP are major modifiable risk factors that are also major determinants of acquiring T2DM (Smith et al, 2005).


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TABLE 9-14 Number of Medical Nutrition Therapy Visits Recommended for Type 2 Diabetes Encounter Number

Length of Contact

Time between Encounters

1

60–90 minutes

2–4 weeks

2, 3

30–45 minutes

2–4 weeks

4, 5

30–45 minutes

6–12 months

From: National Guideline Clearinghouse. Nutrition practice guidelines for type 1 and type 2 diabetes mellitus. Accessed August 1, 2009, at http://guidelines.gov/summary/ summary.aspx?doc_id12816&nbr006618&stringnutritionANDvisitsAND diabetes

For reducing BP, numerous clinical trials and experts support reduction of sodium intake; modest weight loss; increased physical activity; a low-fat diet that includes fruits, vegetables, and low-fat dairy products; and moderate alcohol intake. MNT from RDs in the treatment of T2DM improves glycemic outcomes with a decrease in A1 c of approximately 1–2%, depending on the duration of diabetes. Early referral for lifestyle changes and advice will yield the most benefit (Kulkarni, 2006). The body’s first defense against invading pathogens or tissue injury is the innate immune system; the cholinergic anti-inflammatory pathway is a neural mechanism that suppresses the innate inflammatory response such as excessive cytokine release in T2DM (Oke and Tracey, 2009). The use of antioxidant foods, spices and the Mediterranean diet has shown positive results as compared with a low fat diet (Esposito et al, 2009). Patients should be educated about the progressive nature of diabetes and the importance of glycemic control with appropriate food choices and physical activity in conjunction with antidiabetes medication (Kulkarni, 2006). Maintain focus on lifestyle strategies that will improve blood glucose, BP, and lipids. Diabetes self-management training (DSMT), consisting of a 4-hour class, followed by individual dietitian consults and monthly support meetings can lower A1 c at a very low cost. Weight management is especially helpful (Davis et al, 2009). Addition of a modest-cost, RD-led lifestyle case-management intervention to usual medical care does not increase health care costs and yields modest cost savings among obese patients with T2DM (Wolf et al, 2007). Weight loss significantly reduces diabetes costs; for every 1% weight lost, there is a 3.6% savings in total health costs and a 5.8% savings in diabetes care costs (Yu et al, 2007). The American Dietetic Association recommends four MNT visits initially, then one visit every 6–12 months Table 9-14). Referral to a dietitian within the first month after diagnosis is important.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: T2DM has a stronger genetic basis than type 1, but depends more on environmental fac-

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tors such as obesity and a western diet. From wholegenome studies, affected family members are studied; calpain 10 (CAPN10) and hepatocyte nuclear factor 4 alpha (HNF4A) have been identified. Common genetic variation near melatonin receptor MTNR1B contributes to raised plasma glucose and increased risk of type-2 diabetes among Indian Asians and European whites (Chambers et al, 2009). Variants of the FTO (affectionately called the FATSO) gene are identified an obesity risk allele; this gene is associated with increased risk of TDM. Numbness or burning senHeight sation in feet, Weight ankles, legs BMI Signs of Obesity? dehydration? Diet Smoking history history Waist circumferElectrocardioence gram (ECG) BP (increased?) before exerBlurred cise program vision? Erectile Lab Work dysfunction CRP Fatigue FPG Frequent, slow-healing HbA1c Blood or infections urinary Increased ketones appetite, Total Chol, LDL, thirst, HDL urination Clinical/History

Trig (often increased) BUN, Creat Na, K ALT, AST Lactate dehydrogenase (LDH) Alk phos Ca, Mg Microalbuminuria Plasminogen activator inhibitor type 1 Fasting insulin Fasting C-peptide levels

SAMPLE NUTRITION CARE PROCESS STEPS Self-Monitoring Deficit In T2DM Assessment Data: Blood glucose self-monitoring records, food diary worksheets and meal records, blood glucose levels (fasting, 2-hour postprandial and/or HbA1c levels). Nutrition Diagnosis (PES): Self-monitoring knowledge deficit related to lack of understanding how to record food and beverage intake as evidenced by incomplete food records at last two clinic visits and lab of HbA1c  8.5 mg/dL. Intervention: Teaching patient and family member(s) about use of simple blood glucose self-monitoring records (recording of timing, amount, blood glucose levels) and meal records. Monitoring and Evaluation: HbA1c levels (goal 7 mg/dL); other glucose labs, food diary and records, discussion about complications of using the records.


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INTERVENTION OBJECTIVES • Provide persons with diabetes initial basic nutrition messages and schedule time for MNT with an RD who has expertise in diabetes management. • Maintain as near-normal blood glucose levels as possible by balancing food intake with insulin (either endogenous or exogenous) or oral glucose-lowering medications and activity levels. Improvement with MNT, if successful, is usually seen within 6 weeks and up to a maximum of 6 months. Medication may be needed if blood glucose levels are not under control. • Maintain glycosylated A1c levels 7%, preprandial capillary plasma glucose levels between 90 and 130 mg/dL, and peak postprandial capillary plasma glucose levels 180 mg/dL. The target goal range for the patient may vary by age and underlying disorders. • Protect beta-cell function by controlling hyperglycemia. A1c tests should be done at least two times a year in patients who are meeting treatment goals and quarterly in patients whose therapy has changed or who are not meeting glycemic goals. • Achieve optimal serum lipid levels to reduce the risk for macrovascular disease. Dyslipidemia is a central component of insulin resistance in all ethnic groups. • Emphasis of MNT is on lifestyle strategies to reduce glycemia, dyslipidemia, and BP. Strategies should lead to reduced energy intake and increased energy expenditure through physical activity. The A to Z (Atkins to Zone Diet) weight loss diet analysis found that premenopausal overweight and obese women who followed the Atkins diet (lowest carbohydrate intake), lost more weight at 12 months than women assigned to follow the Zone diet (Gardner et al, 2007). Therefore, for some patients, a low-carbohydrate, high-protein, high-fat diet may be a feasible alternative recommendation for weight loss. • Maintain or improve overall health. The Dietary Guidelines for Americans and the MyPyramid food guide illustrate healthy nutritional guidelines and can be used by people with diabetes. • Encourage regular mealtimes. Maintain lifestyle changes through behavior modification, education, and problemsolving strategies. • Address individual needs according to culture, ethnicity, and lifestyle, while respecting willingness to change. For older adults, meet nutritional and psychosocial needs. For pregnant or lactating women, provide adequate energy and nutrients for optimal outcomes. Encourage therapeutic lifestyle changes (TLC), considering client’s readiness, skills, resources, and current needs. • Achieve BP levels that reduce risk for vascular disease and renal function decline. • Manage problems related to compulsive or binge eating. Patients often report deliberate omission of insulin or oral hypoglycemic agents (OHA) to lose weight. • Manage children with T2DM or maturity-onset diabetes of youth (MODY) differently than children who have T1DM; see appropriate entries. • Prevent and treat the acute and long-term complications of diabetes listed in Table 9-2.

FOOD AND NUTRITION • The dietitian should calculate CHO and fat requirements individually according to lipid and glucose levels. Assess dietary history, physical exercise, and activity patterns. • Include foods containing CHO from whole grains, fruits, vegetables, and low-fat milk. A vegan diet is also an effective consideration (Barnard et al, 2009; Turner-McGrievy et al, 2008). • Moderate weight loss in an obese patient (5–10% of starting weight) may reduce hyperglycemia, dyslipidemia, and hypertension. A moderate caloric restriction (250–500 calories less than average daily intake as calculated from a food history) and a nutritionally adequate meal plan should be recommended. Extremely low-calorie diets for adults should be performed only in a hospital setting. • In morbidly obese patients, bariatric surgery may be the only effective treatment. There are risks from surgery and anesthesia, but the benefits often outweigh the risks. • Space meals and spread nutrient intake, particularly carbohydrate, throughout the day. • Eating breakfast has beneficial effects on fasting lipid and postprandial insulin sensitivity. Avoid meal skipping. Individualize meal plan according to patient preferences. • Carbohydrate should be calculated between 45% and 65% of energy intake. Consistency is important. • Protein should be calculated at 15–20% of daily energy intake with normal renal function and control at 0.8– 1.0 g/kg with renal disease. Where weight loss is needed, use of a diet slightly higher in protein may help to enhance insulin sensitivity. • Fat should be 25–35% of energy intake (7–10% of kcal saturated fats, 10% polyunsaturated fats, and 10–15% monounsaturated fats). Limit intake of cholesterol to 200–300 mg/d. • Foods that benefit both the carbohydrate and lipid abnormalities should be consumed often. Recommendations are the same as for the general population concerning fiber: use more brown rice, beans, green leafy vegetables, oat bran, legumes, barley, produce with skins, apples, oranges, and other whole fruit and produce. • As part of a healthy lifestyle and to manage hypertension, teach the principles of the DASH diet; 2400 mg/d of sodium is recommended. • For most vitamins and minerals, ensure adequate dietary intakes. Higher levels of magnesium (Rumawas et al, 2006), chromium, and zinc are recommended. A multivitamin–mineral supplement may be used. Because altered vitamin D and calcium homeostasis may play a role in the development of T2DM, dual supplementation may prevent T2DM in high-risk populations (Tremblay and Gilbert, 2009; Pittas et al, 2007). Vitamin K as phylloquinone may also have a role in glucose management (Yoshida et al, 2008). • Discuss usefulness of artificial sweeteners and food diaries. • Discuss use of alcohol. Avoid hypoglycemia by consuming alcohol with food. Limit to 1 drink daily for women and two for men. Light-to-moderate amounts of alcohol do not increase triglyceride or BP levels. Indeed, moderate alcohol consumption has been associated with a decreased incidence of diabetes and heart disease; alcohol has been


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reported to increase insulin sensitivity and raise HDL cholesterol levels. Alcoholic beverages should be considered an addition to the regular food/meal plan. If consumed daily, calories from alcohol are calculated into the total energy intake. Abstain from alcohol in pregnancy, pancreatitis, advanced neuropathy, severe hypertriglyceridemia, and a history of alcohol abuse.

Common Drugs Used and Potential Side Effects (see Table 9-15) • T2DM is a progressive disease. Medications will need to be combined with lifestyle strategies. Insulin may be used in a combination with oral therapy or alone. If oral glucoselowering medications do not achieve normoglycemia, combined oral therapies (drugs from two or more classes) can be initiated. • If combination oral therapy does not work, insulin is needed. Insulin may also be needed for refractory hyperglycemia, diabetic ketoacidosis, stress, infection, or pregnancy.

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• Multiple drug therapy is generally required to achieve BP targets. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, diuretics, and calcium channel blockers may all be helpful. • Aspirin therapy (75–162 mg/d) is recommended to protect against cardiovascular events. • Overwhelming evidence suggests that the renin-angiotensin system (RAS) plays an important role in the pathogenesis of DM and its associated cardiovascular risks; RAS blockers may delay or prevent the onset (Braga and Leiter, 2009). • In individuals with diabetes over the age of 40 years and without overt CVD, statin therapy to achieve an LDL 100 mg/dL is recommended. For people with diabetes and overt CVD, an LDL cholesterol goal of 70 mg/dL is recommended. Lifestyle modifications focusing on reducing saturated fat and increasing physical activity are also important. • Antipsychotic agents contribute to the development of the metabolic syndrome and increase the risk for T2DM and heart disease. Monitor their use carefully.

TABLE 9-15 Medications Used for Type 2 Diabetes Combination therapy rather than monotherapy is typically used to achieve glucose control in patients who are not at glycemic goals. Classification

Medication

Route

The Way it Works

Time and Dose

Comments

Sulfonylureas

Glimepiride (Amaryl)

Oral

Increases insulin production.

One or two times a day

Never give to a patient who is fasting for any reason. Do not use with alcoholic beverages. May cause weight gain, nausea, diarrhea or heartburn. Check LFTs.

Glipizide (Glucotrol)

Long-acting.

Glipizide ER (Glucotrol XL) Glyburide (Diabeta, Micronase) Biguanides

Glucophage (Metformin) Glucophage XR

Oral

Lowers glucose from digestion; inhibits glucose release from the liver. Sensitizer.

Two to three times a day, XR once a day

Take with food. May cause diarrhea, flatulence, abdominal pain. Do not use with inflammatory bowel disease. Enhances weight loss.

Alpha-Glucosidase Inhibitors

Miglitol (Glyset)

Oral

Slows digestion, slows glucose production. Starch blocker that delays intestinal glucose absorption.

Take before each meal; swallow with first bite of food.

GI intolerance can occur. Exercise enhances effectiveness.

Thiazolidinediones

Rosiglitazone (Avandia)

Oral

Lowers glucose production; increases tissue glucose utilization, mostly in muscle.

Once daily with or without food

Liver damage is possible. Can lead to weight gain or heart failure.

Oral

Increases insulin production; short-acting.

5–30 minutes before meals

Offers better control of postprandial hyperglycemia and is associated with a lower risk of delayed hypoglycemic episodes.

Acrobose (Precose)

Pioglitazone (Actos) Meglitinides

Repaglinide (Prandin) Senaglinide (Starlix)

DPP-4 Inhibitors

Sitagliptin (Januvia)

Oral

Lowers glucose by blocking an enzyme

100 mg. Once a day

Incretin Mimetics

Exenatide (Byetta)

Injectable

Helps the pancreas make insulin, slows digestion

10 g. Inject within an hour of AM and PM meals

Anti-hyperglycemic

Amylin (Symlin)

Injectable

Controls postprandial blood glucose

15 g. Inject before major meals

Source: Diabetes Medications, NIDDK. Web site accessed September 22, 2009, at http://diabetes.niddk.nih.gov/dm/pubs/medicines_ez/

Acid or sour stomach, belching, diarrhea, dizziness, nervousness.


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• Medications such as steroids, beta-blockers, and diuretics may cause hyperglycemia in some patients. Supplements of Vitamin C may cause false-positive urinary glucose levels when given in large doses. • Melatonin may have a role. Carriers of the risk genotype exhibit increased expression of MTNR1B in islet cells; these individuals may be more sensitive to the actions of melatonin, leading to impaired insulin secretion. Blocking the inhibition of insulin secretion by melatonin may be a novel therapeutic avenue for T2DM. • Metformin improves insulin sensitivity in patients with IGT, but it does not reduce inflammatory biomarker levels (Pradhan et al, 2009). • Xenical (fat blocker) may help cut heart risk in patients with T2DM. The obese diabetic patient who is poorly controlled may benefit from weight-reducing agents, such as sibutramine or orlistat.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. See Table 9-9 for more details. • Vitamin D and calcium in combined supplementation may be beneficial in optimizing glucose metabolism (Pittas et al, 2007).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Medical nutrition intervention in patients with diabetes should address the metabolic abnormalities of glucose, lipids, and BP (Kulkarni, 2006). To meet the specific needs of the patient, adapt drug therapy to enhance outcomes and quality of life. • DSME is an essential element of diabetes care, and national standards have been based on evidence for its benefits. DSME helps patients optimize metabolic control, prevent and manage complications, and maximize quality of life in a cost-effective manner. Health care providers should refer newly diagnosed patients to a dietitian who should then regularly reassess patients over time for modification of medications and food intake patterns. • Emphasize the importance of regular mealtimes, use of medications, self-care and optimal functioning with instructions on how to handle illness, stress, exercise, label reading, use of sucrose or fructose and sugar alcohols. • Vegan diets increase intakes of carbohydrate, fiber, and several micronutrients even more than the American Diabetes Association recommended diet (Turner-McGrievy et al, 2008). It would be acceptable to promote a vegan lifestyle for diabetes management (Barnard et al, 2009). • Some restaurants offer foods lower in cholesterol, fat, and sodium, and higher in fiber. All restaurants offer low calorie sweeteners in the blue, yellow, or pink packets, and diet drinks. Many offer reduced-calorie salad dressings, low-fat or fat-free milk, and salt substitutes. Choose salads, fish, vegetables, baked or broiled food, and wholegrain breads.

• Clinical trials using antihyperglycemic medications to improve glycemic control have not demonstrated the anticipated cardiovascular benefits in patients with T2DM (Jenkins et al, 2008). • To improve glycemic control, assist with weight maintenance, and reduce risk of CVD, at least 150 min/wk of moderate-intensity aerobic physical activity (50–70% of maximum heart rate) is recommended or at least 90 min/wk of vigorous aerobic exercise (70% of maximum heart rate). Activity should be distributed over at least 3 d/wk, with no more than 2 consecutive days without physical activity. • While high-intensity exercise is beneficial, even in older adults, it should start gradually and increase to desired intensity and duration. Avoid high-intensity exercise and resistance training in persons with neuropathy, coronary heart disease, or retinopathy. In the absence of contraindications, people with T2DM should perform resistance exercise three times a week, targeting all major muscle groups and progressing to three sets of 8–10 repetitions. • Decrease sedentary behaviors, especially prolonged TV or computer time. • Identify potential or real obstacles. Discuss options for handling negative emotions, temptations, dining away from home, feeling deprived, time pressures, competing priorities, social events, family support, food refusal, and lack of support from friends. • Regular consumption of breakfast, self-weighing, and infrequent intake of fast foods are strategies that work well (Raynor et al, 2008). • Use culturally appropriate methods for teaching and guidance. For example, use of the Medicine Wheel in Plains Indians has shown more effective results than usual techniques (Kattelmann et al, 2009). • Encourage group support, behavior modification, and nutritional counseling for overweight. • Small changes lead to greater self-esteem. Sequential rather than simultaneous dietary changes work well for most people and can improve the sense of self-efficacy. • A comprehensive lifestyle self-management program using the Mediterranean low–saturated fat diet, stress management training, exercise, group support, and smoking cessation can reduce cardiovascular risk factors. • Dietitians have a distinct role in MNT versus DSME; but both education and counseling are more medically effective than either one alone (Daly et al, 2009). • A low-literacy tool can be useful in teaching key changes for those who need it. The goal is to achieve a sense of control over self-management of the diabetes. • Before any type of surgery, blood glucose should be maintained between 100 and 200 mg/dL. Perioperative hyperglycemia may be managed with doses of rapid-acting insulin. Correct abnormalities before surgery, when possible. • In noncritically ill hospitalized patients, premeal blood glucose should be kept as close to 90–130 mg/dL as possible, with a postprandial blood glucose 180 mg/dL; use insulin when necessary. • In critically ill hospitalized patients, blood glucose levels should be kept as close to 110 mg/dL as possible and generally 180 mg/dL. These patients will usually require intravenous insulin.


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Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association http://www.diabetes.org/food-nutrition-lifestyle/nutrition.jsp

American Diabetes Association–Medicare Policy and Benefits http://www.diabetes.org/for-health-professionals-and-scientists/recognition/dsmt-mntfaqs.jsp

American Diabetes Association–Type 2 Diabetes http://www.diabetes.org/type-2-diabetes.jsp

American Dietetic Association: Type 2 Diabetes Practice Guidelines http://www.eatright.org/cps/rde/xchg/ada/hs.xsl/index.html

Annals of Internal Medicine – Mediterranean Diet Implications for Patients http://www.annals.org/cgi/summary_pdf/151/5/306.pdf

Mayo Clinic – T2DM http://www.mayoclinic.com/health/type-2-diabetes/DS00585

Web MD – T2DM http://diabetes.webmd.com/guide/type-2-diabetes

TYPE 2 DIABETES IN ADULTS—CITED REFERENCES Barnard ND, et al. Vegetarian and vegan diets in type 2 diabetes management. Nutr Rev. 67:255, 2009. Braga MG, Leiter LA. Role of renin-angiotensin system blockade in patients with diabetes mellitus. Am J Cardiol. 104:835, 2009. Chambers JC, et al. Common genetic variation near melatonin receptor MTNR1B contributes to raised plasma glucose and increased risk of type-2 diabetes amongst Indian Asians and European whites. [published online ahead of print August 3,2009] Diabetes. 58:2703, 2009. Daly A, et al. Diabetes white paper: Defining the delivery of nutrition services in Medicare medical nutrition therapy vs Medicare diabetes selfmanagement training programs. J Am Diet Assoc. 109:528, 2009. Davis N, et al. Nutritional strategies in type 2 diabetes mellitus. Mt Sinai J Med. 76:257, 2009.

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Esposito K, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial. Ann Int Med. 151:306, 2009. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA, 297:969, 2007. Jenkins DJ, et al. Effect of a low-glycemic index or a high-cereal fiber diet on type 2 diabetes: a randomized trial. JAMA. 300:2742, 2008. Kattelmann KK, et al. The medicine wheel nutrition intervention: a diabetes education study with the Cheyenne River Sioux Tribe. J Am Diet Assoc. 109:1532, 2009. Kulkarni K. Diets do not fail: the success of medical nutrition therapy in patients with diabetes. Endocr Pract. 12:121S, 2006. Oke SL, Tracey KJ. The inflammatory reflex and the role of complementary and alternative medical therapies. Ann N Y Acad Sci. 1172:172, 2009. Pittas AG, et al. The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 92:2017, 2007. Pradhan AD, et al. Effects of initiating insulin and metformin on glycemic control and inflammatory biomarkers among patients with type 2 diabetes: the LANCET randomized trial. JAMA. 302:1186, 2009. Raynor HA, et al. Weight loss strategies associated with BMI in overweight adults with type 2 diabetes at entry into the Look AHEAD (Action for Health in Diabetes) trial. Diab Care. 31:1299, 2008. Rumawas ME, et al. Magnesium intake is related to improved insulin homeostasis in the Framingham offspring cohort. J Am Coll Nutr. 25:486, 2006. Tremblay A, Gilbert JA. Milk products, insulin resistance syndrome and type 2 diabetes. J Am Coll Nutr. 28:91S, 2009. Turner-McGrievy GM, et al. Changes in nutrient intake and dietary quality among participants with type 2 diabetes following a low-fat vegan diet or a conventional diabetes diet for 22 weeks. J Am Diet Assoc. 108:1636, 2008. Wolf AM, et al. Effects of lifestyle intervention on health care costs: Improving Control with Activity and Nutrition (ICAN). J Am Diet Assoc. 107:1365, 2007. Yoshida M, et al. Phylloquinone intake, insulin sensitivity, and glycemic status in men and women. Am J Clin Nutr, 88:210, 2008. Yu AP, et al. Short-term economic impact of body weight change among patients with type 2 diabetes treated with antidiabetic agents: analysis using claims, laboratory, and medical record data. Curr Med Res Opin. 23:2157, 2007.

TYPE 2 DIABETES IN CHILDREN AND TEENS NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND T2DM arises because of insulin resistance, when there is failure to use insulin properly combined with relative insulin deficiency. In children, obesity or puberty often unmasks T2DM in genetically susceptible individuals. For example, the emergence of T2DM presents a new challenge for pediatricians and other health care professionals; preventive efforts, early diagnosis, and collaborative care of the patient and family are essential. Breastfeeding, reduced television and sedentary lifestyles, healthy eating principles, family-based approaches, and screening are all important in managing this epidemic. Screening should be available for children whose BMI is greater than the 85th percentile at puberty or at age 10 plus any two of the following risk factors: family history, increased risk by ethnicity, or signs of insulin resistance such as polycystic ovary syndrome

(PCOS), hypertension, dyslipidemia, or acanthosis. Weight greater than 120% of ideal for height also warrants screening. In addition to obesity, family history of T2DM, and absence of GAD-65 antibodies, children with new-onset T2DM may be distinguished from those with T1DM by a combination of biochemical parameters of C-peptide, IGFBP-1, CO(2), and urine ketones (Katz et al, 2007). However, one third of the children with T2DM may have at least one detectable beta-cell autoantibody, classified as latent autoimmune diabetes in youth. Fasting blood glucose levels should be checked at least every 2 years in high-risk children. T2DM in childhood can lead to end-stage renal disease and mortality in middle age; long duration is more detrimental (Pavkov et al, 2006). There is an ongoing effort for diabetes prevention in trials specifically designed to address the adolescent population (Karam and McFarlane, 2009).


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ASSESSMENT, MONITORING, AND EVALUATION •

CLINICAL INDICATORS Genetic Markers: The presence of multiple risk alleles amounts to a significant difference in children who have diabetes (Kelliny et al, 2009). Genetic variations for glucokinase (GCK), GCK regulatory protein (GCKR), islet-specific glucose 6 phosphatase catalytic subunitrelated protein (G6PC2), and melatonin receptor type 1B (MTNR1B) are associated.

C-peptide, IGFBP-1, Height CO(2) Weight Beta-cell autoanBMI tibodies Diet history (anti-GAD, Waist circumferanti-IA-2, and ence anti-ICA)? BP (often Urine ketones increased) CRP Sleep-disordered Urinary microalbreathing? buminuria Plasminogen Lab Work activator inhibitor FPG type 1 HbA1c

Clinical/History

Total Chol, LDL (high?) HDL (usually low) Trig (often increased) BUN, Creat Na, K ALT, AST LDH Alk phos Ca, Mg Alb

• •

• •

• • •

INTERVENTION OBJECTIVES • Maintain as near-normal blood glucose levels as possible by balancing food intake with insulin (either endogenous

SAMPLE NUTRITION CARE PROCESS STEPS Altered Nutritional Labs – T2DM In Teenager Assessment Data: Blood glucose self-monitoring records, food diary worksheets and meal records, hour HbA1c levels 9 mg/dL, BMI 85% for age. Family Hx T2DM (both parents). BP normal but LDL cholesterol slightly elevated Nutrition Diagnosis (PES): Altered nutritional labs related to overweight, knowledge deficit about diabetes and self-monitoring difficulty as evidenced by HbA1c  8.5 mg/dL and LDL chol 130 mg/dL and statement that “I don’t really understand my diabetes very well.” Intervention: Teaching patient and family member(s) about use of simple blood glucose self-monitoring records (timing, blood glucose testing, role of HbA1c in evaluating past 3 months, meal records). Monitoring and Evaluation: HbA1c levels 7 mg/dL. Other labs WNL; food diary and glucose records showing improvement in outcomes of lab testing.

or exogenous) or oral glucose-lowering medications and activity levels. Try to maintain glycosylated A1c levels 7%. Target goal range for the patient may vary by age and underlying disorders: 6-year old, 7.5–8.5%; 6- to 12-year old, 8%; 13to 9-year old, 7.5%. Preprandial capillary plasma glucose levels should be kept between 90 and 130 mg/dL. Protect beta-cell function by controlling hyperglycemia. A1c tests should be done at least twice a year in patients who are meeting treatment goals and quarterly in patients who are not meeting glycemic goals. Achieve optimal serum lipid levels to reduce the risk for macrovascular disease. Emphasis of MNT is on lifestyle strategies to reduce hyperglycemica, dyslipidemia, and hypertension. Prevent and treat acute complications, short-term illnesses, and exercise-related problems, the long-term complications of renal disease, autonomic neuropathy, hypertension, and CVD. Maintain BP levels that reduce risk for vascular disease. Elevated BP has a major impact on renal function. Improve overall health through optimal nutrition and physical activity. Dietary Guidelines for Americans and the MyPyramid food guidance system illustrate nutritional guidelines and can be used by young people with diabetes. Encourage regular mealtimes. Maintain lifestyle changes through behavior modification, education, and problemsolving strategies. Working with the whole family is important. Promote family and individualized psychosocial counseling to handle depression and emotions. Address individual needs according to culture, ethnicity, and lifestyle, while respecting willingness to change. Encourage TLC, considering the child’s needs and family circumstances. Manage problems related to compulsive or binge eating. Patients often report deliberate omission of medication in order to lose weight.

FOOD AND NUTRITION • Calculate CHO and fat requirements individually according to age, serum lipid, and glucose levels. Assess dietary history, physical exercise, and activity patterns. Studies support the importance of carbohydrate from whole grains, fruits, vegetables, and low-fat milk. • Moderate weight loss (5–10% of starting weight) may reduce hyperglycemia, dyslipidemia, and hypertension. A moderate restriction of 250–500 calories less than average daily intake (as calculated from a food history) and a nutritionally adequate meal plan are recommended. • For teen boys over age 15, it may be useful to calculate caloric needs as 18 kcal/lb for usual activity and 16 kcal/lb if sedentary. Teen girls over age 15 have needs that are estimated the same as those for an adult. • Extremely low-calorie diets are not recommended for children or teens. In morbidly obese children, gastric bypass surgery should be the last option as malnutrition is a permanent side effect.


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• Spacing of meals (spreading carbohydrate throughout the day) and eating breakfast have beneficial effects on fasting lipid and postprandial insulin sensitivity. • Meal skipping should be discouraged. Individualize meal plan according to patient preferences. • Carbohydrate should be calculated as 45–65% of energy intake. Daily consistency is important. • Protein should be calculated at 15–20% of daily energy intake with normal renal function; control at 0.8–1.0 g/kg with presence of renal disease. • Fat should be 25–35% of energy intake, with 7–10% of kilocalories saturated fats, 10% polyunsaturated fats, and 10–15% monounsaturated fats. Limit intake of cholesterol to 200–300 mg/d. • Recommendations for fiber include rice, beans, vegetables, oat bran, legumes, barley, produce with skins, apples, oranges, other produce. Include 19–38 g/d, larger amounts for older children and teens. • As part of a healthy lifestyle and to manage hypertension, teach the principles of the DASH diet; 2400 mg/d of sodium is recommended. • For vitamins and minerals, ensure that patient has adequate dietary intakes. Higher levels of magnesium, chromium, and potassium are recommended when serum levels are low. There is no need for supplements of any singular nutrient; a pediatric multivitamin–mineral supplement may be used. • Include phytochemicals and antioxidants in the diet (see Table 8-14 in the pancreatic chapter). • Discuss use of artificial sweeteners, food diaries, menu options at school, fast food choices that are lower in total fat, benefits and goals for physical activity, and the need for adequate fluid intake.

Common Drugs Used and Potential Side Effects (see Table 9-15 also) • Oral agents may be used when blood glucose and other treatment goals are not met through diet and exercise alone. Glucophage should be the first oral agent used but not in children with known liver and kidney disease, low oxygen problems, or severe infections. Other oral agents such as a sulfonylurea or meglitinide can be added if control does not improve after 3–6 months. Thiazolidinediones probably should not be used in children. • Insulin therapy should be started in children with severely elevated blood sugar levels or children with intense thirst and frequent urination. There are a wide variety of insulin regimens that can be used, anywhere from bedtime alone to multiple daily injections. Once blood sugars are under control, glucophage can be added while decreasing insulin dosage. • Pharmacologic options for weight loss, including metformin, orlistat, and sibutramine have been studied (Miller and Silverstein, 2006). They should be used only under close medical supervision.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used in children and teens. There is insufficient evidence to draw

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definitive conclusions about the efficacy of individual herbs and supplements for diabetes, especially in children. However, inclusion of spices and seasonings in the diet would be acceptable. • See Table 9-9 for guidance on more specific herbs and supplements that the client may be using.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Health care providers are encouraged to refer newly diagnosed patients to a dietitian. The dietitian should regularly reassess children and teens for overall growth and health status. • Stress the importance of parental supervision and support. • Children often benefit from attending diabetes camps for youth and support groups for family counseling. DSME is helpful for SMBG, medication use, physical activity goals, and meal planning. • Emphasize the importance of regular mealtimes, proper use of medications, and balanced activity. Home blood glucose monitoring records and food/exercise records are important. • Emphasize the importance of self-care and optimal functioning for illness, stress, dining out, exercise. • Identify potential or real obstacles and discuss options for handling negative emotions, temptations, dining away from home, feeling deprived, time pressures, competing priorities, social events, family support, food refusal, and lack of support from friends. • Explain food and nutrition labeling as well as how to manage sucrose, fructose, and sugar alcohols in the diet. Reduce sugar-sweetened beverage intake as much as possible. • Encourage group support, behavior modification, and nutritional counseling for overweight. Small changes lead to greater self-esteem than continued failures. Sequential rather than simultaneous dietary changes work best and can improve self-efficacy. • Reduce stress where possible. BMI and stress are independent determinants of TNF-alpha (an inflammatory cytokine) and adipocytokine among Latino children (Dixon et al, 2009). • Suggest guidelines for physical activity: three to four times a week, exercise for 30–60 min/d. Aerobic exercise is protective against age-related increases in visceral adiposity (Kim and Lee, 2009).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Centers for Disease Control and Prevention (CDC) Diabetes Projects http://www.cdc.gov/diabetes/projects/cda2.htm

CDC Reference Documents http://www.cdc.gov/diabetes/projects/ref.htm

Children with Diabetes http://www.childrenwithdiabetes.com/d_0n_d00.htm

National Diabetes Education Program http://www.ndep.nih.gov/publications/PublicationDetail.aspx? PubId154


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TYPE 2 DIABETES IN CHILDREN AND TEENS— CITED REFERENCES Dixon D, et al. Stress and body mass index each contributes independently to tumor necrosis factor-alpha production in prepubescent Latino children. J Pediatr Nurs. 24:378, 2009. Karam JG, McFarlane SI. Prevention of type 2 DM: implications for adolescents and young adults. Pediatr Endocrinol Rev. 5:980S, 2009. Katz LE, et al. Fasting c-peptide and insulin-like growth factor-binding protein-1 levels help to distinguish childhood type 1 and type 2 diabetes at diagnosis. Pediatr Diabetes. 8:53, 2007.

Kelliny C, et al. Common Genetic Determinants of Glucose Homeostasis in Healthy Children: The European Youth Heart Study (EYHS). [published online ahead of print September 9, 2009] Diabetes. 58:2939, 2009. Kim Y, Lee S. Physical activity and abdominal obesity in youth. Appl Physiol Nutr Metab. 34:571, 2009. Miller JL, Silverstein JH. The treatment of type 2 diabetes mellitus in youth: which therapies? Treat Endocrinol. 5:201, 2006. Pavkov ME, et al. Effect of youth-onset type 2 diabetes mellitus on incidence of end-stage renal disease and mortality in young and middle-aged Pima Indians. JAMA. 296:421, 2006.

GESTATIONAL DIABETES NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND GDM involves glucose intolerance with first onset or recognition during pregnancy. It affects 14–25% of all pregnancies, increasing over the past decade (March of Dimes, 2009). Pregnancy itself is a metabolic stress test. During the first half of pregnancy, transfer of maternal glucose to the fetus occurs; during the second half of pregnancy, placental hormones outweigh glucose transfer and insulin requirements typically double. The placenta functions as a nutrient sensor, altering placental transport according to the maternal supply of nutrients. Placental transporters are regulated by hormones such as insulin. Insulin resistance occurs when gestational hormones such as human placental lactogen (HPL) interfere with insulin action. The accelerated fetal growth in women with diabetes is characterized by increased activity of placental and glucose transporters (Jansson and Powell, 2006). Cell signaling for insulin changes in GDM; women with diabetes or GDM may need one to two times more insulin than other pregnant women. All pregnant women should be assessed for risk of GDM at the first prenatal visit; most women are screened between 24 and 28 weeks of gestation. One or more of the following factors identifies women at risk for GDM: • Ethnicity: Hispanic American, African American, Asian, Pacific Islander, American Indian. • Family history of diabetes in a first-degree relative (parents or siblings). • Gestational diabetes or presence of a birth defect in a previous pregnancy. • History of pregnancy-induced hypertension, urinary tract infections, or hydramnios (extra amniotic fluid). • History of abnormal glucose tolerance. • Older maternal age (25-year old). • Prepregnancy overweight or obesity; BMI 29. • Previous birth of a large baby (9 lb). • Previous stillbirth or spontaneous miscarriage. Hyperglycemia in pregnancy poses many complications and risks for the infant such as macrosomia, neural tube defects, hypocalcemia, hypomagnesemia, hyperbilirubinemia, birth trauma, prematurity, or neonatal hypoglycemia. Daily SMBG is important; fasting glucose levels should not

exceed 105 mg/dL. Excellent blood glucose control with diet and, when necessary, insulin will result in improved perinatal outcome. HbA1c testing is not useful in GDM. Women with a prior history of GDM and obesity are at significant high risk of developing MetS (Vohr and Boney, 2009). There is a higher risk of hypertension, pre-eclampsia, urinary tract infections, cesarean section, and future diabetes. About half of women who have GDM will proceed to have T2DM later, especially women who are hypertensive. Nutrition recommendations should be based on a thorough nutrition assessment. Monitoring blood glucose levels, urine ketones, appetite, and weight gain guides the individualized nutrition prescription and meal plan. Adjustments should be made to the meal plan throughout pregnancy to ensure desired outcomes. See Table 9-16. In women who have had bariatric surgery, close nutritional evaluation will be needed. Deficiencies in iron, vitamin A, vitamin B12, vitamin K, folate, and calcium can result in both maternal anemia and fetal complications, such as congenital abnormalities, IUGR and failure to thrive (Guelinckx et al, 2009). Offspring of women with GDM are at increased risk for respiratory distress, macrosomia, jaundice, hypoglycemia, hyperinsulinemia, birth trauma, and developmental problems. Development of MetS in late adolescence and young adulthood is related to maternal glycemia in the third trimester, maternal obesity, neonatal macrosomia, and childhood obesity (Vohr and Boney, 2009). Although treatment of mild GDM does not significantly reduce the frequency of stillbirth, perinatal death, or several neonatal complications, it does reduce the risks of fetal overgrowth, shoulder dystocia, cesarean delivery, and hypertensive disorders (Landon et al, 2009). Family planning, early screening for fetal abnormalities, compliance, glycemic and BP control during pregnancy, and improved neonatal care can make a difference. After birth, rapid adaptation is necessary for infants to be able to maintain independent glucose homeostasis; this is compromised in infants who are small for gestational age (SGA), premature, or large for gestational age (Beardsall et al, 2008). Obesity, insulin resistance, and abnormal lipid metabolism bear ominous consequences for future generations (Vohr and Boney, 2009). For women who are offered treatment for mild GDM in addition to routine obstetric care,


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TABLE 9-16 Glucose Testing for Gestational Diabetes Mellitus (GDM) GDM often presents with hyperglycemia and glycosuria. Selective screening at 24–28 weeks of pregnancy is generally recommended, with a glucose challenge test and 1-hour assessment using either a 100-g or 75-g oral glucose load. Two or more of the venous plasma glucose concentrations must be met or exceeded for a positive diagnosis. The test should be done in the morning after an overnight fast. American Diabetes Association criteria for GDM are noted below: One-Step Approach Perform a diagnostic oral glucose tolerance test (OGTT) without prior plasma or serum glucose screening. The one-step approach may be cost effective in high-risk patients or populations. Two-Step Approach Perform an initial screening by measuring the plasma or serum glucose concentration 1 hour after a 50-g oral glucose load (glucose challenge test [GCT]), and perform a diagnostic OGTT on the subset of women exceeding the glucose threshold value on the GCT. When the two-step approach is used, a glucose threshold value 140 mg/dL (7.8 mol/L) identifies approximately 80% of women with GDM, and the yield is further increased to 90% by using a cutoff of 130 mg/dL (7.2 mol/L). Glucose Load

Glucose (mg/dL)

Glucose load, 100 g Fasting

95

1 hour

180

2 hours

155

3 hours

140

Sources: American Diabetes Association. Standards of Medical Care in Diabetes–2009.

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2-hour postFrequent prandial gluurinary tract Height cose (not infections? Pregravid weight above 120 Ultrasonography Pregravid BMI mg/dL) for fetal Pregravid waist Na, K growth circumference BUN Expected date of Lab Work Creat (often eleconfinement vated) Ketones, fasting (EDC) Alb, No. of risk factors H & H transthyretin Serum Gluc on for GDM Microalbuminawakening Current weight uria (95 mg/dL Goal weight Serum homocysor lower) Weight gain teine levels 1-hour postpattern Ca, Mg prandial gluDiet history TSH (altered?) cose (not BP OGTT above 140 Edema? CRP mg/dL) Periodontal disease? Clinical/History

INTERVENTION OBJECTIVES • Prevent complications, perinatal morbidity, and mortality by normalizing the levels of glycemia and other metabolites (i.e., lipids and amino acids) to the levels of nondiabetic pregnant individuals.

SAMPLE NUTRITION CARE PROCESS STEPS Inconsistent CHO Intake and Knowledge Deficit

additional charges are incurred but fewer babies experience serious perinatal complication or death (Moss et al, 2007). Nutritional intervention for GDM saves thousands of dollars per case. All women with GDM should receive nutritional counseling by an RD. MNT, initiated within 1 week of diagnosis and with a minimum of three nutrition visits, results in decreased hospital admissions and insulin use, improves likelihood of normal fetal and placental growth, and reduces risk of perinatal complications, especially when diagnosed and treated early (American Dietetic Association, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: GDM is associated with increased anti–human leukocyte antigen (HLA) class II antibodies in the maternal circulation (Steinborn, 2006). There may be some link between both autoimmune and nonautoimmune forms of diabetes and GDM.

Assessment Data: Blood glucose self-monitoring records, food diary worksheets and meal records, blood glucose levels (fasting, 2-hour postprandial). Nutrition Diagnoses (PES): (1) Inconsistent CHO intake (NI 5.8.4) related to lack of knowledge and confusion concerning gestational diabetic meal plan and CHO portion sizes as evidenced by postprandial blood sugars above and below desired ranges. (2) Food and nutrition-related knowledge deficit (NB 1.1) related to gestational diabetic meal plan as evidenced by patient reported confusion and lack of confidence in meal planning and reported diet recall indicating inconsistent carbohydrate intake. Interventions: E 2.2—review purpose of meal plan, CHO containing foods, portion sizes, CHO limits at meals/snacks. E 2.3, 2.5— provide advanced training in CHO counting, food label reading, menu planning, shopping tips. Monitoring and Evaluation: Improvements in blood glucose levels; food diary and meal records showing more consistent intake of CHO throughout the day and before bedtime. Monitor at routine clinic visits for HgbA1c and weight gain. Assess need for further education/counseling; patient verbalizes better understanding of a meal plan and agrees to continue following plan.


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• Optimize growth and development of the fetus. Desirable maternal weight gain will vary according to prepregnancy and current weight. Optimal weight gain is generally as follows: first trimester 0.5–1 kg (1–2 lb); second and third trimesters 0.2–0.5 kg/wk (0.5–1 lb/wk). Prevent weight loss. • Obese women should control weight gain carefully. Excessive weight gain may be a forerunner of the MetS in offspring (Pirkola et al, 2008). • Prevent infections and unexpected outcomes. Fetal glucose exposure and consequent fetal insulin secretion is normally tightly regulated by glucose delivery from the mother during pregnancy (Beardsall et al, 2008). The risk of spontaneous preterm birth increases with increasing levels of pregnancy glycemia. • Control BP. • Avoid incidents of starvation ketosis (where glucose is needed) and diabetic acidosis (where insulin and potassium are needed) by regular preprandial and postprandial SMBG. Ketosis is harmful to the baby. • Use insulin when necessary, based on measures of maternal glycemia with or without assessment of fetal growth. Insulin therapy is recommended when nutrition intervention fails to maintain fasting whole-blood glucose at desired levels. • Prevent hypoglycemic episodes, urinary tract infections, and candidiasis. • Promote healthy lifestyle changes for the mother that will last long after delivery. • Women with GDM should be encouraged to breastfeed. • Physical activity, especially after meals, can help to maintain blood glucose control. Contraindications to exercise may include pregnancy-induced hypertension, intrauterine growth retardation, preterm labor or history of preterm labor, incompetent cervix/cervical cerclage, and persistent second or third trimester bleeding (American Dietetic Association, 2009).

FOOD AND NUTRITION • Use a carbohydrate-controlled meal plan with adequate intake to keep weight gain appropriate while preventing glycemic shifts or ketonuria; manage for age and weight goals. Provide adequate energy and nutrients to meet the needs maternal blood glucose goals that have been established. The typical diet may include 30–35 kcal/kg; 20% protein, 40–45% CHO, and 35–40% fat. • Select CHO from whole grains, one fruit portion, or one milk portion at a time. Limit juices, sweets, or desserts. Sufficient CHO intake is needed, 175 g at minimum. Many women with GDM undereat out of fear of needing insulin; interval weight loss may indicate presence of fasting ketones. Insulin may be needed. • While a low glycemic index diet may be beneficial for some outcomes for both mother and child, results are inconclusive at this time (Tieu et al, 2008). • For obese women (BMI 30), a calorie limit 25 kcal/kg actual weight per day has been shown to reduce hyperglycemia and plasma triglycerides with no increase in ketonuria. For many women, this translates to an energy

• • •

• •

• •

intake around 1700–1800 kcal. Artificial sweeteners may be used, but not saccharin. Maintain an adequate intake of polyunsaturated fats; keep saturated fats to 10% of total fat or less. Most women require three meals and four to five snacks; snacks are eaten at least 2–3 hours between feedings and should contain carbohydrate. Smaller, more frequent meals and snacks will be beneficial because of insulin resistance. Work closely with a dietitian to establish the best pattern according to typical blood glucose levels. A snack before bedtime may be needed. DASH diet principles may be helpful if BP is elevated. Include regular use of antioxidant foods and spices such as cinnamon. Ensure intake of a prenatal vitamin–mineral supplement (especially containing 600 g folic acid, 30–60 mg iron, vitamin C, and adequate calcium). Include adequate chromium intake from diet (as in yeast breads). Tube feeding may be useful in patients who cannot be fed orally or with hyperemesis. CHO-controlled products are not necessarily required; monitor closely. After delivery, a review of glucose tolerance and postpartum nutrition is suggested at 6–12 weeks.

Common Drugs Used and Potential Side Effects • Investigators found no substantial maternal or neonatal outcome differences between use of glyburide or metformin compared with use of insulin in GDM (Nicholson et al, 2009). Insulin may be required to control blood glucose if diet and exercise do not help. Careful physician and self-monitoring is important. The insulin lispro is associated with fewer hypoglycemic events. • Use prenatal vitamin–mineral supplements as prescribed. Avoid large doses of vitamin C, which may show false-positive urinary glucose levels; more than 200 mg/d is not needed. • Low-dose estrogen–progesterone oral contraceptives may be used after GDM, if no medical contraindications exist. However, medications that worsen insulin resistance (e.g., glucocorticoids, nicotinic acid) should be avoided if possible.

Herbs, Botanicals, and Supplements • In general, pregnant women should not take any herbs and botanical products. They should discuss concurrent or previous use with their physician. • Supplements of 1,25-dihydroxyvitamin D3 may influence glucose metabolism in GDM by increasing insulin sensitivity. More research is needed on postpartum requirements. • Only limited evidence exists to support prenatal omega-3 supplementation; use caution for an unbalanced high DHA intake during the first two trimesters of pregnancy, that is, DHA without additional amino acid (AA) supplementation (Hadders-Algra, 2008).


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• Conflicting results have been found for specific nutrients. Zinc and selenium seem to be protective, whereas chromium does not; more research is needed for micronutrient recommendations to be made (American Dietetic Association, 2009).

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Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The RD should monitor and evaluate blood glucose, weight, food intake, physical activity, and pharmacological therapy (if indicated) in women with GDM at each visit; MNT results in improved maternal and neonatal outcomes (American Dietetic Association, 2009). • Communicate the importance of meal spacing, timing, adequacy, and consistency (i.e., patient should not skip meals). Instructions on what to eat and what to avoid will be important. Carrying a snack at all times is helpful (e.g., fruit, peanut butter, crackers). Follow current evidencebased guidelines. • Regular aerobic exercise, such as walking, is beneficial. Exercise after meals may help to control blood sugar, but do not exercise until short of breath. Upper body exercises are also beneficial. Avoid exercises while lying on back as this decreases blood flow when the weight of the fetus presses on the main artery. Avoid exercises that increase the risk of falling. • Encourage breastfeeding. • Babies born to women who have GDM may have low levels of lipids such as arachidonic acid and docosahexaenoic acid (DHA); further studies are needed (Bitsanis, 2006). • Encourage family planning to ensure optimal glucose regulation for all subsequent pregnancies. Women with a history of GDM are more likely to have recurrent diabetes if they are older, heavier and wait longer between pregnancies (e.g., 3 vs. 2 years) in many cases (Holmes et al, 2010). Recurrence of GDM is common, especially among non-Caucasian populations (Kim et al, 2007). • Counsel regarding risk for T2DM. Any degree of abnormal glucose homeostasis during pregnancy independently predicts an increased risk of glucose intolerance and CVD postpartum (Retnakaran, 2009). Elevated FBG, OGTT 2-hour blood glucose, and OGTT glucose A1c are strong and consistent predictors of subsequent T2DM (Golden et al, 2009). Long-term lifestyle modifications, maintenance of normal body weight, and physical activity should be discussed. • Discuss the potential impact of GDM on offspring, who are at increased risk of obesity, glucose intolerance, and diabetes in late adolescence or adulthood.

American Diabetes Association http://www.diabetes.org/gestational-diabetes.jsp

Baby Center – GDM http://www.babycenter.com/0_gestational-diabetes_2058.bc

Diabetes and Pregnancy http://www.otispregnancy.org/pdf/diabetes

NIDDK http://diabetes.niddk.nih.gov/dm/pubs/gestational/

GESTATIONAL DIABETES—CITED REFERENCES American Dietetic Association. Evidence Analysis Library, Gestational Diabetes. Web site accessed October 9, 2009, at http://www.adaevidencelibrary.com/topic.cfm?cat1399. Bitsanis D, et al. Gestational diabetes mellitus enhances arachidonic and docosahexaenoic acids in placental phospholipids. Lipids. 41:341, 2006. Golden SH, et al. Antepartum glucose tolerance test results as predictors of type 2 diabetes mellitus in women with a history of gestational diabetes mellitus: a systematic review. Gend Med. 6:109S, 2009. Guelinckx I, et al. Reproductive outcome after bariatric surgery: a critical review. Hum Reprod Update. 15:189, 2009. Hadders-Algra M. Prenatal long-chain polyunsaturated fatty acid status: the importance of a balanced intake of docosahexaenoic acid and arachidonic acid. J Perinatal Med. 36:101, 2008. Holmes HJ, et al. Prediction of Diabetes Recurrence in Women with Class A1 (Diet-Treated) Gestational Diabetes. [published online ahead of print October 5, 2009] Am J Perinatol. 27(1):47, 2010. Jansson T, Powell TL. IFPA 2005 Award in Placentology Lecture. Human placental transport in altered fetal growth: does the placenta function as a nutrient sensor?—a review. Placenta. 27:91S, 2006. Kim C, et al. Recurrence of gestational diabetes mellitus: a systematic review. Diabetes Care. 30:1314, 2007. Landon MB, et al. A multicenter, randomized trial of treatment for mild gestational diabetes. N Engl J Med. 361:1396, 2009. March of Dimes. Gestational diabetes. Web site accessed October 8, 2009, at http://www.marchofdimes.com/pnhec/188_1025.asp. Moss JR, et al. Costs and consequences of treatment for mild gestational diabetes mellitus—evaluation from the ACHOIS randomised trial. BMC Pregnancy Childbirth. 7:27, 2007. Nicholson W, et al. Benefits and risks of oral diabetes agents compared with insulin in women with gestational diabetes: a systematic review. Obstet Gynecol. 113:193, 2009. Pirkola J, et al. Maternal type 1 and gestational diabetes: postnatal differences in insulin secretion in offspring at preschool age. Pediatr Diabetes. 9:583, 2008. Retnakaran R. Glucose tolerance status in pregnancy: a window to the future risk of diabetes and cardiovascular disease in young women. [published online ahead of print August 1, 2009] Curr Diab Rev. 5:239. Steinborn A, et al. The presence of gestational diabetes is associated with increased detection of anti-HLA-class II antibodies in the maternal circulation. Am J Reprod Immunol. 56:124, 2006. Tieu J, et al. Dietary advice in pregnancy for preventing gestational diabetes mellitus. Cochrane Database Syst Rev. 2008;16(2):CD006674. Vohr BR, Boney CM. Gestational diabetes: the forerunner for the development of maternal and childhood obesity and metabolic syndrome? J Matern Fetal Neonatal Med. 21:149, 2009.


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PRE-ECLAMPSIA AND PREGNANCYINDUCED HYPERTENSION NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Pre-eclampsia is defined as the association of pregnancyinduced hypertension (PIH) and proteinuria of 300 mg/24 h or more after 20-weeks estation. It is more common in primigravidas and in patients with multiple gestation, T1DM, teenage mothers, family history of PIH, age over 40 years, or underlying vascular or renal disease. It affects 2–8% of pregnancies and is a severe complication, which may lead to fetal morbidity and mortality. Risks for the baby include poor growth and prematurity (Duley, 2009). Pre-eclampsia can lead to problems in the liver, kidneys, brain, and the clotting system (Duley, 2009). Maternal morbidity includes placental abruption, HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) or eclampsia; treatment consists of ending the pregnancy. Early sonogram is recommended; many women will have to have total bed rest. Severe pre-eclampsia that develops at 34 weeks of gestation is associated with high perinatal mortality and morbidity (Sibai and Barton, 2007). Women who are 37week pregnant are induced immediately. Criteria for mild pre-eclampsia include hypertension as defined at 140/90 to 159/109 mm Hg; proteinuria 300 mg/24 h; mild edema with weight gain 2 lb/wk or

SAMPLE NUTRITION CARE PROCESS STEPS Disordered Eating Pattern Assessment Data: Food records, weight records. Diet hx reveals intake of one large meal daily, mostly canned soup and sandwiches; no fruits and few vegetables. BP 170/90 average; abnormal lung function tests (LFTs). Nutrition Diagnosis (PES): Disordered eating pattern (NB 1.5) related to lack of knowledge concerning nutrition during pregnancy as evidenced by excessive prenatal weight gain, frequent meal skipping, increased BP, and diet lacking in vitamins and minerals and statement that “I can’t eat more than once a day because it isn’t good for the baby.” Intervention: ND 3.2.1—daily use of prenatal vitamin. Education and counseling about appropriate dietary intake and meal frequency during pregnancy; dangers of skipping meals; when to contact the doctor. E 1.2—priority modifications of diet include not skipping meals, ensure adequate calcium, folic acid, potassium and magnesium; control sodium intake. C 1.3—Health Belief Model of counseling used to motivate patient in making necessary dietary changes. Monitoring and Evaluation: Weight and prenatal growth charts; improved intake. Lab reports and BP records showing improvement in all aspects. Check urine protein and presence of edema. Successful outcome for infant and mother, even if hospitalization is required.

6 lb/month; and urine output 500 mL/24 h. Signs and symptoms include increased BP, proteinuria, facial edema, pretibial pitting edema, irritability, nausea and vomiting, nervousness, headache, altered states of consciousness, epigastric pain, and oliguria. Criteria for severe pre-eclampsia include: BP 160/110 mm Hg on two occasions with patient on bed rest; systolic BP rise 60 mm Hg over baseline; diastolic BP increase of 30 mm Hg over baseline; proteinuria 5 g/24 h or 3 or 4 on a urine dipstick; massive edema; and oliguria 400 mL/24 h. Symptoms include pulmonary edema, severe headaches, visual changes, right upper quadrant pain, elevated liver enzymes, and thrombocytopenia in addition to the symptoms listed for mild pre-eclampsia. In eclampsia, a seizure occurs. Eclamptic seizures and symptoms of the HELLP syndrome occur. In severe cases, there may also be hepatic rupture, pulmonary edema, acute renal failure, placental abruption, elevated creatinine, intrauterine growth restriction, cerebral hemorrhage, cortical blindness, and retinal detachment. Maternal mortality rate is 8–36%. Because plasma homocysteine is often increased, sufficient intakes of folic acid, vitamins B12 and B6 are recommended (Mignini et al, 2005). Studies have also shown the effectiveness of magnesium in eclampsia and pre-eclampsia (Guerrera et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Women with pre-eclampsia have higher levels of a peptide that increases BP in the pieces of tissue linking mother and fetus. BP (mild, 140/90 mm Height Hg; severe, Pregravid weight 160/110 Pregravid BMI mm Hg) Pregravid waist Decreased urine circumferoutput ence Confusion, EDC apprehension Current weight Shortness of Weight gain patbreath tern Right upper Diet history quadrant Edema in lower abdominal extremities pain Clinical/History

Dizziness Visual changes (blurring, double vision) Excessive nausea or vomiting Severe headaches Fever? Blood in urine? Lab Work GFR Alb, transthyretin (often low)


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Proteinuria (300 mg/d is mild; 500 mg/d is severe) H&H Serum Fe Chol, Trig (elevated?) Gluc Ca Mg Na, K Uric acid (elevated)

BUN Liver function Creat (may be tests elevated) (AST, ALT, Homocysteine LDH) CRP MicroalbuminPT, INR uria HELLP syndrome (decreased platelets, abnormal liver function tests)

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supplementation and magnesium sulfate for eclamptic seizures (Duley, 2009). Avoid excessive magnesium from supplements if this medication is being used. • Corticosteroids for lung maturity may be necessary. • During pregnancy, typical diuretics and cardiac drugs are not used. ACE inhibitors and ARBs are contraindicated. Calcium pump inhibitors are often a first line choice.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used in pregnancy. • Evening primrose has been suggested for this condition. Coenzyme Q10 and alpha-tocopherol are potent antioxidants. • See Table 9-9 for guidance on more specific herbs and supplements that the client may have used.

INTERVENTION NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

OBJECTIVES • Reduce maternal and neonatal mortality and morbidity. In pregnant patients with diabetes and chronic hypertension, BP target goals of 110–129/65–79 mm Hg are suggested. Avoid lower BP because fetal growth may be impaired. • Lessen edema when present. Correct any underlying malnutrition or micronutrient deficiencies. • Monitor any sudden weight gains (1 kg/wk) that are unexplained by food intake. • Prevent, if possible, chronic hypertension and MetS after delivery.

• Rest is essential during this time. Biofeedback, yoga, meditation, and other forms of stress reduction are often beneficial. • Meal skipping should be avoided at all costs. • Discuss adequate sources of calcium from the diet, especially if dairy products are not tolerated or preferred. • Good sources of potassium and magnesium include nuts, fruits and vegetables. The DASH diet is an excellent diet to continue, even after pregnancy.

Patient Education—Foodborne Illness

FOOD AND NUTRITION • Maintain diet as ordered for age and pregnancy stage (generally 300 kcal more than prepregnancy diet). Use extra fruits and vegetables and less sucrose. • Sources of magnesium include green leafy vegetables, nuts, legumes, and whole grains. • Supplement with prenatal vitamins. Include folic acid, calcium, other B-complex vitamins, protein, selenium, and potassium from diet. The role of vitamins C and E does not benefit women at risk for pre-eclampsia (Villar et al, 2009). Antioxidant supplements are also not recommended (Rumbold et al, 2008). • Sodium intake may need to be controlled to 2 g/d if edema is severe. Diuretics generally are not used. • There may be some merit for including a sufficient intake of omega-3 fatty acids from salmon, tuna, walnuts, and flaxseed oil.

Common Drugs Used and Potential Side Effects • The only interventions shown to prevent pre-eclampsia are antiplatelet agents, primarily low-dose aspirin, calcium

• If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Diabetes and Preeclampsia http://diabetes.healthcentersonline.com/womensdiabetes/ preeclampsia.cfm

Mayo Clinic http://www.mayoclinic.com/health/preeclampsia/DS00583

Pregnancy and Preeclampsia http://familydoctor.org/064.xml

PRE-ECLAMPSIA AND PIH—CITED REFERENCES Duley L. The global impact of pre-eclampsia and eclampsia. Semin Perinatol. 33:130, 2009. Guerrera MP, et al. Therapeutic uses of magnesium. Am Fam Physician. 80:157, 2009. Rumbold A, et al. Antioxidants for preventing pre-eclampsia. Cochrane Database Syst Rev. CD004227, 2008. Sibai BM, Barton JR. Expectant management of severe preeclampsia remote from term: patient selection, treatment, and delivery indications. Am J Obstet Gynecol. 196:514, 2007. Villar J, et al. World Health Organisation multicentre randomised trial of supplementation with vitamins C and E among pregnant women at high risk for pre-eclampsia in populations of low nutritional status from developing countries. BJOG. 116:8780, 2009.


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DIABETIC GASTROPARESIS NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Gastroparesis occurs in approximately 50% of all cases of diabetes (Aring et al, 2005), with delayed gastric emptying (DGE) in the absence of mechanical obstruction. Diabetic gastroparesis is the result of ongoing damage to the nerves that are responsible for peristalsis and normal motility. Foods digest abnormally slowly or peristalsis is diminished so that it is difficult to match insulin action to digestion and absorption of the meals. If food stays in the stomach too long, infection is possible. Also, the food can harden into a solid lump; these bezoars may cause pain, nausea, and blockages in the digestive tract. Hypoglycemia can occur if insulin is working and if food remains in the stomach too long. Later, insulin action is diminished and food finally digests, causing hyperglycemia. Problems occur more often in type 1 than in T2DM. Strict glycemic control is key. A gastrostomy is rarely indicated, but a jejunostomy may be helpful in maintaining nutrition. Prokinetic agents are the best treatment option; see Section 7 for more details on management of gastroparesis. Gastric electrical stimulation may be used to send out brief, lowenergy impulses to the stomach to decrease nausea and vomiting.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: T1DM has a genetic component, but gastroparesis would be individually acquired. Clinical/History Height Weight BMI I&O Diet history Early satiety DGE Diarrhea or constipation Vomiting undigested food Nausea Reflux or heartburn

Abdominal bloating or pain Upper endoscopy Barium x-ray Gastric emptying scintigraphy (GES) Gastric manometry Lab Work HbA1c H&H

Serum Fe Gastrin Gluc (fasting and 30 minutes after meals) Na, K Alb, transthyretin CRP Chol, Trig

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function Assessment Data: Blood glucose self-monitoring records, nausea, gastroesophageal reflux (GERD) and reflux with meals, abdominal discomfort. Irregular FBG levels from day to day. Nutrition Diagnosis (PES): Abnormal GI function related to gastroparesis as evidenced by nausea, GERD, and abdominal discomfort. Intervention: Meal records and food diary listing symptoms and frequency of discomfort. Blood glucose self-monitoring records. Discussion about use of prokinetic agents. Monitoring and Evaluation: Glucose records, food diary and records, discussion about GI symptoms.

INTERVENTION OBJECTIVES • Correct the fluctuating blood glucose levels through careful food and insulin management, frequent blood glucose checks and monitoring records. • For nausea and vomiting, restore volume and hydration and provide antiemetics generously. • Relieve symptoms (pain, diarrhea, constipation) and maintain adequate nutritional status. • Differentiate from ketoacidosis, which has similar symptoms of nausea and vomiting. • Prevent infection or bezoar formation from accumulation of indigestible solids.

FOOD AND NUTRITION • Monitor intake carefully; blood glucose fluctuations are common. Include 200–240 g CHO daily, spread throughout the day. Use two to three CHO servings per meal. Be consistent from day to day. • Soft-to-liquid diet may be useful to prevent delay in gastric emptying. Six small meals may be better tolerated than large meals. • Use a low-fat diet to improve digestion and to improve stomach emptying. Stay sitting after meals. • Decrease overall fiber intake from meals or supplements. Oranges, broccoli, green beans, berries, figs, and fresh apples may be difficult to digest. • For dry mouth, add extra fluids and moisten foods with broth or allowed sauces or gravies. • If nausea occurs, cold foods and low-odor choices may be better tolerated.


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• In severe problems, a percutaneous jejunostomy (PEJ) tube feeding may be indicated. It can be used temporarily if needed to correct malnutrition.

• See Table 9-9 for guidance on more specific herbs and supplements.

Common Drugs Used and Potential Side Effects • Prokinetics such as metoclopramide (Reglan) may be given 30 minutes before meals to increase gastric contractions and to relax pyloric sphincter. Dry mouth, sleepiness, diarrhea or nausea can be side effects. Emitasol is a nasal spray form of this medication. Metoclopramide prophylaxis to reduce gastric volumes before elective surgery is unnecessary unless the patient has a prolonged history of poor blood glucose control (Jellish et al, 2005). • Rapid-acting insulin should be injected with or after meals. Use SMBG to monitor delayed absorption and glucose changes. Insulin lispro (Humalog) is quite effective because it starts working shortly after injection. To control blood glucose, it may be necessary to take insulin more often, to take insulin after eating instead before, and to check blood glucose often after eating. • If a liquid diet is used, more insulin may be needed. Insulin pumps may be beneficial because insulin delivery rates can be programmed to the patient’s individual needs. • Because there is a reciprocal relationship between gastric emptying and ambient glucose concentrations, newer diabetes therapies that decelerate the rate of gastric emptying may be a beneficial tool (Samsom et al, 2009). • Antiemetics may be used for vomiting. Monitor for specific side effects. Zofran may cause constipation or headache. • Erythromycin improves stomach emptying by increasing the contractions that move food through the stomach. Side effects are nausea, vomiting, diarrhea, and abdominal cramps. • Dramamine (dimenhydrinate) is an antihistamine that helps prevent nausea and vomiting; slight-to-moderate drowsiness and thickening of bronchial secretions may occur. • Motilium (domperidome) is used to manage the upper GI problems; side effects may include headache.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss delayed digestion and absorption of food. • Discuss role of diet in maintaining weight and controlling discomfort. Emphasize nutrient-dense foods if intake has been poor. Blenderized foods or smoothies may be well tolerated. • Bezoar formation may occur after eating oranges, coconuts, green beans, apples, figs, potato skins, Brussels sprouts, broccoli, sauerkraut, corn, sauerkraut, and other high-fiber foods. • Discuss insulin management, as appropriate. Include information about SMBG and meal spacing. Advise the doctor if blood glucose levels are 200 mg/dL.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association http://www.diabetes.org/type-1-diabetes/Gastroparesis.jsp

Ask the Dietitian http://www.dietitian.com/drugnutr.html

Diabetic Gastroparesis http://digestive.niddk.nih.gov/ddiseases/pubs/gastroparesis/

Gastroparesis and Dysmotilities Association (GPDA) http://www.digestivedistress.com/main/page.php?page_id26

DIABETIC GASTROPARESIS—CITED REFERENCES Jellish WS, et al. Effect of metoclopramide on gastric fluid volumes in diabetic patients who have fasted before elective surgery. Anesthesiology. 102:904, 2005. Samsom M, et al. Diabetes mellitus and gastric emptying: questions and issues in clinical practice. Diab Metab Res Rev. 25:502, 2009. van der Voort IR, et al. Gastric electrical stimulation results in improved metabolic control in diabetic patients suffering from gastroparesis. Exp Clin Endocrinol Diabetes. 113:38, 2005.


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DIABETIC KETOACIDOSIS NUTRITIONAL ACUITY RANKING: LEVEL 3–4 Islets of Langerhans Food

β-cell destruction

Glucagon

Adipose tissue

Insulin deficiency

Glucose

Lack of insulin

Muscle

Lack of insulin

Liver

Increased production of glucose by liver

Ketone production from fatty acids and amino acids Fat breakdown

Protein breakdown

Amino acids

Polyphagia

Ketoacidosis

Hyperglycemia

Fatty acids Kidney

Diabetic coma

Ketonuria & Glycosuria

Polyuria

Adapted from: Thomas H. McConnell, The Nature of Disease Pathology for the Health Professions, Philadelphia: Lippincott Williams & Wilkins, 2007.

Low blood pressure or shock

Volume depletion

Loss of calories

Polydipsia

Polyphagia


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DEFINITIONS AND BACKGROUND Ketones in the urine mean that the body is burning fat to get energy because glucose is not available. The lack of insulin leads to gluconeogenesis in the liver, then glucose spills into the urine and causes an osmotic diuresis with dehydration. Free fatty acids are released from the adipose tissue and converted into acidic ketones (acetoacetate and -Hydroxybutyrate) by the liver. Large amounts of ketones in the serum and urine can be dangerous. Diabetic ketoacidosis (DKA) is classic metabolic acidosis, a medical emergency that accounts for more than 100,000 hospital admissions yearly in the United States. A patient with a low serum potassium level should be assumed to have a potentially life-threatening crisis. Causes of DKA include not getting enough insulin from missed injections; alkaline reserves depleted by too little insulin, flu or colds, fever, pregnancy, stress, trauma, or myocardial infarction; infection (leading cause); urinary tract infections and pneumonia. The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA. These metabolic derangements result from the combination of absolute or relative insulin deficiency and increased levels of the counterregulatory hormones of glucagon, catecholamines, cortisol, and growth hormone. Table 9-17 provides defining characteristics for DKA and hyperosmolar hyperglycemic state (HHS). DKA is seen primarily in patients with T1DM; a few type 1 diabetic patients presenting with DKA on initial diagnosis. In children, DKA is a leading cause of hospitalization and is a cause of cerebral edema, which may lead to death if untreated. DKA can also occur in T2DM, usually from urinary tract infections, trauma, stress, pregnancy, surgery, or myocardial infarction. Inflammatory processes may play a role. Both DKA and its treatment produce varying degrees of immunological stress (Jerath et al, 2005). All individuals with DKA should be tested for hyperthyroidism (Potenza et al, 2009). Use of standardized written guidelines have merit.

Beta-hydroxybutyrate levels Mild: blood pH K (low?) 7.25â&#x20AC;&#x201C;7.30; Urinary glucose, bicarbonate ketones, 15â&#x20AC;&#x201C;18 osmolality mol/L; alert T3, T4, TSH Moderate: pH levels 7.00â&#x20AC;&#x201C;7.25, CRP bicarbonate BUN (increased) 10â&#x20AC;&#x201C;15, mild Creat drowsiness Na (decreased) Severe: Cl (decreased) pH  7.00, HbA1c bicarbonate Amylase 10, stupor (increased) or coma WBC (elevated Gluc (250 with mg/dL) infections) HgbA1c Lab Work

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pCO2 (decreased) pO2 Uric acid (increased) AST (decreased) ALT, LDH, creatine kinase (CK) (increased) Phosphate (often decreased) Mg (often decreased) Chol (increased), Trig Ca

INTERVENTION OBJECTIVES â&#x20AC;˘ Correct the high blood glucose level by giving more insulin. Frequent blood glucose and ketone monitoring is necessary. Note that urine ketones lag behind serum ketones because it takes time to the empty the bladder, where they have accumulated and been stored. â&#x20AC;˘ Replace fluids and electrolytes lost through excessive urination and vomiting. â&#x20AC;˘ Promote return to wellness after poor health for several days. â&#x20AC;˘ Evaluate precipitating factors such as surgery, trauma, urinary tract infection, pneumonia, or influenza. â&#x20AC;˘ Monitor frequently to prevent recurrence of DKA. TABLE 9-17 Diagnostic Criteria for Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: There are no specific genes for DKA, but diabetes itself has a genetic component. Clinical/History Height Weight BMI Diet history Temperature I&O BP (often low)

Nausea and vomiting Hot or dry and flushed skin Diarrhea Fruity breath Intense thirst Profound dehydration

Dim vision Labored or rapid breathing (Kussmaul) Pruritus Polyuria Cramping Seizures or drowsiness

DKA Criteria

Mild

Moderate

Severe

HHS

Plasma glucose (mg/dL)

250

250

250

600

Arterial pH

7.25â&#x20AC;&#x201C;7.30

7.00â&#x20AC;&#x201C;7.24

7.00

7.30

Serum bicarbonate (mEq/L)

15â&#x20AC;&#x201C;18

10â&#x20AC;&#x201C;15

10

15

Urine ketones

Positive

Positive

Positive

Small

Serum ketones

Positive

Positive

Positive

Small

Effective serum osmolality (mOsm/kg)

Variable

Variable

Variable

320

Altered mental status

Alert

Alert/ drowsy

Stupor/ coma

Stupor/ coma

Adapted with permission from Kitabchi AE, et al. Hyperglycemic crises in diabetes. Diabetes Care. 27:S95, 2004.


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SAMPLE NUTRITION CARE PROCESS STEPS Self Monitoring Deficit Assessment Data: Admission to unit with DKA, random blood glucose levels 600, semi-comatose state, unable to eat orally. Nutrition Diagnosis (PES): Self monitoring deficit (NB-1.4) related to blood glucose monitoring and diabetes management as evidenced by DKA, BG  600, lethargy, nausea and vomiting past 2 days, and report by family that “he doesn’t test his sugars as he should.” Intervention: Food and nutrient delivery with IVs and tube feeding until semicomatose state resolves and glucose levels are below 200 consistently. Educate patient when possible about the dangers of not monitoring BG levels. Teach methods for simplifying records, tracking lab results, and self-monitoring of glucose and activity levels to match insulin therapy. Monitoring and Evaluation: Improved cognition and ability to resume an oral diet. Able to describe how to track glucose, lab results, physical activity, and insulin; defined own goals for reporting signs and symptoms to doctor when hyperglycemia persists. Able to state the signs of impending DKA and measures to take immediately.

• Prevent complications such as shock, arterial thrombosis, renal failure, or cerebral edema (CEDKA). CEDKA remains a significant problem with a high mortality rate (Lawrence et al, 2005). Young children are especially vulnerable and may slip into a coma. • For chronically high fasting glucose levels, adjust evening intermediate- or long-acting insulin doses or timing.

FOOD AND NUTRITION • If patient is comatose, intravenous insulin, electrolytes, and fluids are used. A nasogastric tube may be placed to prevent aspiration during feeding. If patient is alert and oriented, offer plenty of fluids orally. • As treatment progresses, a 5% glucose solution is usually given as glucosuria and hyperglycemia subside. If glucosuria and hyperglycemia do not decrease, try tea and salty broth. Later, fruit juices and liquids high in potassium may be given. • Resolution of DKA leads to the ability to tolerate oral nutrition and fluids, normalization of blood acidity (pH7.3), and absence of ketones in blood (1 mol/l). Once this has been achieved, insulin may be switched to the usual regimen.

• • • •

NPH and regular insulin after the resolution of DKA (Umpierrez et al, 2009). Dextrose in saline is given once plasma glucose decreases to avoid accidental hypoglycemia. Potassium, phosphate and magnesium levels may be low. Bicarbonate therapy is needed only rarely (Trachtenbarg, 2005). Intravenous antibiotic therapy will be needed where there is sepsis. Atypical antipsychotics, thiazide diuretics, and corticosteroids can lead to DKA if the patient is not carefully monitored.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • See Table 9-9 for guidance on more specific herbs and supplements.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain demand for more insulin during illness and infection. Use of a diabetes record may be useful if episodes of high blood glucose are frequent. • Never exercise when there are ketones present. • Because every episode of DKA implies breakdown in clinical communication, appropriate diabetes education should be reinforced. Education of patients and their social environment to promote frequent testing—especially during sick days—and to lower their glucose levels, as well as to recognize the early symptoms of hyperglycemia and DKA is of paramount importance in preventing the development of severe DKA (Weber et al, 2009). • When strict control through insulin is administered, weight gain is common. Insulin omission and reduction, which are eating disorder symptoms unique to diabetes mellitus, are associated with an increased risk of DKA. Attention to this disorder is important in overall treatment planning and management. • The biggest risk of insulin pump therapy is DKA since no long-acting insulin is used. Any interruption to insulin delivery or pump malfunctioning can cause DKA. To prevent this reaction, monitor blood glucose regularly. Insulin pump users also need to check often to see that insulin is still flowing through the tubing.

Patient Education—Foodborne Illness

Common Drugs Used and Potential Side Effects • Insulin and fluid are usually given intravenously to decrease blood glucose by 50–75 mg/dL/h. Guidelines may recommend a bolus (initial large dose) of insulin of 0.1 unit of insulin/kg of body weight if potassium level is higher than 3.3. Regular and glulisine insulin are equally effective during the acute treatment of DKA; a basal bolus regimen with glargine and glulisine is safer than

• If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Diabetes Association http://www.diabetes.org/type-1-diabetes/ketoacidosis.jsp

Merck manual – DKA http://www.merck.com/mmpe/sec12/ch158/ch158c.html

NIDDK–Diabetic Ketoacidosis http://diabetes.niddk.nih.gov/DM/pubs/dictionary/K-O.htm


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DIABETIC KETOACIDOSIS—CITED REFERENCES Jerath RS, et al. Complement activation in diabetic ketoacidosis and its treatment. Clin Immunol. 116:11, 2005. Lawrence SE, et al. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 146:688, 2005.

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Potenza M, et al. Excess thyroid hormone and carbohydrate metabolism. Endocrin Pract. 15:254, 2009. Trachtenbarg DE. Diabetic ketoacidosis. Am Fam Physician. 71:1705, 2005. Umpierrez GE, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 32:1164, 2009. Weber C, et al. Prevention of diabetic ketoacidosis and self-monitoring of ketone bodies: an overview. Curr Med Res Opin. 25:1197, 2009.

HYPEROSMOLAR HYPERGLYCEMIC STATE NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Diabetic HHS is a life-threatening emergency with marked elevation of blood glucose, hyperosmolarity, and minimal or no ketosis (Stoner, 2005). HHS is preventable if blood glucose is monitored regularly in order to correct elevating levels before problems occur. The condition occurs in patients older than age 70 years with T2DM and profound dehydration as precipitating factors. If recognized early, HHS can frequently be treated in the outpatient setting if the patient can take fluids. Table 9-18 provides diagnostic criteria. Sometimes DKA is the first time that diabetes is diagnosed. Identification and treatment of the underlying and precipitating causes of HHS are absolutely essential. Predisposing factors for this syndrome include long-term uncontrolled hyperglycemia, pancreatic disease, infections or sepsis, stroke, surgery, extensive burns, renal or CVD, corticosteroid use, diuretics, excessive total parenteral nutrition (TPN), dialysis. Underlying poor compliance with medications, infections, alcohol, or cocaine abuse are the most common causes. In children, corticosteroid use and gastroenteritis are common causes. The mortality rate is high at 10–20%. Areas of future research include prospective randomized studies to determine the pathophysiological mechanisms for the absence of ketosis in HHS and to investigate the reasons for elevated proinflammatory cytokines and cardiovascular risk factors (Kitabchi et al, 2008).

TABLE 9-18 Quick Sources of Glucose 4 oz grape, cranberry, or prune juice

19 g CHO

1 tbsp honey

17 g CHO

1/2 cup sweetened gelatin

17 g CHO

1 tbsp corn syrup, jam, jelly or glucose

15 g CHO

5 Lifesavers candies

15 g CHO

4 oz orange, apple, pineapple, grapefruit juice

12–15 g CHO

4 oz regular soft drink

13 g CHO

1 tbsp sugar, dissolved in water

13 g CHO

2 tablespoons raisins

10–15 g CHO

5–6 Lifesaver candies

10–15 g CHO

1 cup 2% or skim milk

12 g CHO

3–4 glucose tablets

4–5 g CHO each

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: HHS is acquired and not genetic, although T2DM has a genetic component. African Americans, Hispanics, and Native Americans have the highest rates. Clinical/History Height Weight BMI Diet history BP (hypotension?) I&O Profound dehydration (8–12 L) Fever or hypothermia? Excessive thirst and urination Dry, parched mouth Sunken eyes Dry skin with no sweating

Weakness, lethargy Leg cramps Sleepiness or confusion Rapid pulse and abnormal respirations Convulsions, grand mal seizures, or coma Lab Work Gluc (600 mg/dL) Na, K Bicarbonate 15 mEq/L

Serum osmolality (usually 320 mOsm) pH levels greater than 7.30 Mild or absent ketonemia Elevated serum urea nitrogen (BUN)-tocreatinine ratio Alb H&H PO4 Chol, Trig CRP

INTERVENTION OBJECTIVES • Correct dehydration, shock, and cardiac arrhythmias. • Reduce elevated blood glucose levels with isotonic saline, then hypotonic saline along with insulin. • Monitor fluid status and replace deficits, which may be 10–20% of total body weight. This may require up to 9 L in 48 hours (Stoner, 2005).


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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Alcohol Intake Assessment Data: Blood glucose self-monitoring records with FBG 650; recent heavy intake of alcohol; fever; profound dehydration and signs of HHS; admitted to Emergency Room from a wedding reception; lives with son and daughter-in-law. Nutrition Diagnosis (PES): Excessive alcohol intake related to lack of understanding about the impact of alcohol on diabetes as evidenced by confusion, profound dehydration, FBG 650, and fever after intake of four alcoholic beverages within 3 hours at a wedding reception. Intervention: Teaching patient and family members about dangers of large doses of alcohol mixed with diabetes medication, especially with aging. Counseling about how to include an occasional alcoholic beverage and ways to participate in social events without excessive intake.

cytokines; insulin therapy provides a strong anti-inflammatory effect (Stentz et al, 2004). • Potassium replacements may be needed. Monitor carefully. • Antibiotic therapy may be needed in cases of underlying infections. • Drugs that may precipitate HHS include diuretics, beta blockers, clozapine, olanzapine, H2 blockers, cocaine, alcohol.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • See Table 9-9 for guidance on more specific herbs and supplements.

Monitoring and Evaluation: Improved glucose labs, resolution of HHS, fever and dehydration.

• Prevent future crises by appropriate DSME and regular monitoring of blood glucose. • Prevent acute renal failure, which could result from prolonged hypovolemia.

FOOD AND NUTRITION • Offer fluid replacement, often 1 L/h until volume is restored; 9–12 L may be needed. • Patient is likely to nothing by mouth (NPO) during a crisis or perhaps tube fed during a comatose state. As appropriate, intake may be progressed gradually to a balanced diet, controlling calories as needed. • Correct electrolyte deficits. Potassium or magnesium may be needed. • The reported sodium level should be corrected when the patient’s glucose level is markedly elevated. In this circumstance, extracellular fluid (ECF) osmolality rises and exceeds that of intracellular fluid (ICF), since glucose penetrates cell membranes slowly in the absence of insulin, resulting in movement of water out of cells into the ECF (Merck Manual, 2009). Types of fluids administered will depend on the corrected serum sodium level, calculated using the following formula: measured sodium  [(serum glucose 100)/100) 1.6]. • A renal diet plan may be needed if renal failure is identified.

Common Drugs Used and Potential Side Effects • Insulin is needed to normalize blood glucose levels. Infusions will be needed until full rehydration is complete. DKA and HHS are associated with elevation of proinflammatory

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss, where possible, predisposing factors, how to avoid future incidents, and blood glucose monitoring. • CHO-controlled diets may be beneficial if patient can comprehend. Family intervention may be required. • Discuss possible neglect or abuse, if suspected. • Continuous management of the fluid, electrolyte, and glucose disturbances is necessary until resolved. • Provide diabetes teaching to prevent recurrence. Adjust insulin or oral hypoglycemic therapy on the basis of the insulin requirement once serum glucose level are stable. • Coordinate home visits from nursing or dietitian if needed to evaluate the inadequate access to water.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Diabetic Hyperosmolar Hyperglycemic State http://www.diabetes.org/type-2-diabetes/treatment-conditions/ hhns.jsp

E-medicine http://www.emedicine.com/emerg/topic264.htm

HYPEROSMOLAR HYPERGLYCEMIC STATE— CITED REFERENCES Kitabchi AE, et al. Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. J Clin Endocrinol Metab. 93:1541, 2008. Merck Manual. Hyperosmolar Hyperglycemic State. Web site accessed October 13, 2009, at http://www.merck.com/mmpe/sec12/ch158/ ch158d.html. Stentz FB, et al. Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. Diabetes. 53:2079, 2004. Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician. 71:1723, 2005.


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HYPOGLYCEMIA NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Hypoglycemia occurs primarily in patients with T1DM. Except in diabetic patients receiving insulin or sulfonylureas, hypoglycemia is a rare disorder. True low blood sugar (70 mg/100 dL or lower) releases hormones such as catecholamines, which produce hunger, trembling, headache, dizziness, weakness, and palpitations. Sources of bodily glucose are from dietary intake, glycogenolysis, and gluconeogenesis. The metabolism of glucose involves oxidation and storage as glycogen or fat. The body makes great effort to supply glucose for the CNS and red blood cells. Glycogenolysis is stimulated by secretion of glucagon from the alpha-cells of the pancreas; this is impaired in patients with T1DM. As different causes can stimulate hypoglycemia, treatments will differ accordingly. Skipped or insufficient meals, errors in insulin dosing, taking too much insulin, alcohol consumption, or extra physical exertion can lead to hypoglycemic episodes. Oxidative stress and zinc release contribute to neuronal death after hypoglycemia (Suh et al, 2008). Recurrent episodes of iatrogenic hypoglycemia induce a state of hypoglycemia unawareness and defective counterregulation, which defines hypoglycemia-associated autonomic failure (HAAF). It is essential to manage these episodes carefully. A prooxidant state is promoted in certain brain regions during hypoglycemia and after glucose reperfusion, which results from the activation of several oxidative stress pathways; subsequent cell death occurs in particular brain regions including the cerebral cortex, the striatum, and the hippocampus (Haces et al, 2010). Approaches to the prevention of hypoglycemia include glucose monitoring, patient education, meal planning, and medication adjustment. Adequate carbohydrate replacement during and after exercise seems to be an important measure to prevent hypoglycemia. Insulin dosage adjustment with a decrease from 20% to 30% is needed only for exercise duration over an hour (Grimm et al, 2004).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: A genetic deficiency in the p47(phox) subunit of NADPH oxidase may be relevant (Suh et al, 2008). Clinical/History Height Weight BMI

Diet history I&O Temperature BP Trembling

Headache Dizziness, weakness Palpitations Seizures or coma

Blood glucose and insulin regimen records Exercise history and habits Hypoglycemia unawareness? Type and duration of diabetes

Lab Work Serum Gluc (70 mg/dL) HbA1c Serum insulin Na, K Alb

CRP Chol, Trig Ca Mg OGTT results using 1 g glucose/kg

INTERVENTION OBJECTIVES • Normalize blood glucose levels. If the problem is recurrent, stabilize blood glucose levels through consistent mealtimes, CHO consistency, insulin dose adjustments, and blood glucose self-monitoring. For those individuals on insulin, appropriate insulin timing with food or use of CHO to insulin ratio are important factors to consider. • Minimize length of time between meals. • Prevent seizures and coma, with precipitating symptoms such as neuroglycopenia with confusion, light headaches, and aberrant behavior. • Determine frequency, symptoms of hypoglycemia, activity levels for the individual. • Delayed hypoglycemia after strenuous or prolonged exercise may occur up to 24 hours after exercise and is related to increased insulin sensitivity from exercise as well as

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Physical Activity Assessment Data: Blood glucose self-monitoring records, food diary worksheets and meal records, blood glucose levels (fasting, 2-hour postprandial and/or HbA1c levels). Recent exercise program including aerobic dancing for 1 hour thrice weekly. Low blood glucose levels and signs/symptoms of hypoglycemia twice weekly. Nutrition Diagnosis (PES): Excessive physical activity related to a new exercise regimen as evidenced by two bouts of blood glucose levels below 70 in past week. Intervention: Education of patient, exercise partner, and family member(s) about blood glucose self-monitoring records (timing, blood glucose levels before and after exercise), insulin dosing, and activity records. Counseling about timing of FBG testing, insulin reductions, and close monitoring before and after dance sessions. Monitoring and Evaluation: Glucose lab results within desirable range; no symptoms of hypoglycemia. Food diary and activity records showing effective self-management.


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repletion of glycogen stores. Plan appropriately by increasing carbohydrate, decreasing insulin for periods of activity, and increasing frequency of blood glucose monitoring. • Always recheck blood glucose 15–20 minutes after treatment to make sure that problem is resolved. Very low blood glucose levels (50 g/dL) may take 30 g CHO or more to resolve, especially after exercise.

FOOD AND NUTRITION • For insulin-induced hypoglycemia, use a normal diet with adequate CHO content. Consider a possible reduction of medication if the hypoglycemia is recurrent. • Have patient ingest fruit juice when needed or use candy for an immediate corrective measure. If there are symptoms of hypoglycemia (blood glucose 70 g/dL), carry quick sources of glucose (see Table 9-18). Fat is not as effective as CHO in normalizing blood glucose. • In most cases, mild hypoglycemia can be handled with use of readily available CHOs, including milk, fruit, and crackers. Balanced, regular mealtimes or frequent small snacks are also useful. • For hypoglycemia at night that is caused by excessive insulin or insufficient dinner meal or evening snack, adjust evening and bedtime doses of insulin. A slightly larger dinner or snack containing CHO may be needed.

Common Drugs Used and Potential Side Effects • Insulin and other glucose-lowering medications must be carefully prescribed and monitored. Careful use of sliding scales of insulin is the goal (Smith et al, 2005). Glycemic control to a lower glucose target range can be achieved using a computerized insulin dosing protocol with particular attention to timely measurement and adjustment of doses (Juneja et al, 2009). • Glucose tablets have 4–5 g CHO per tablet. Patients should receive instructions regarding quantity, when to use, and when not to use. Most people will need three to four tablets to treat low blood glucose levels. • If the individual passes out from hypoglycemia and uses insulin on a daily basis, it may be necessary to give a glucagon shot and call for emergency assistance. Glucagon can cause vomiting. Intravenous dextrose is administered by medical professionals.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. Clinical trials are lacking for this condition. • See Table 9-9 for guidance on more specific herbs and supplements.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Teach benefits of frequent blood glucose monitoring. Explain signs, symptoms, and treatment of hypoglycemia. • Review appropriate timing of meals, snacks, and medications. Promote regular mealtimes, meal spacing, and planned exercise. • Teach routine blood glucose before and after exercise. Discuss carrying a quick source of glucose. • Encourage patients to obtain and carry diabetes identification. • Discuss observations that require medical attention. Teach when to contact physician for medication adjustment. • Discuss use of alcoholic beverages and potential effects. Excess alcohol increases the risk of hypoglycemia. Alcohol is processed in the liver to acetaldehyde at a time when the liver cannot do gluconeogenesis because nicotinamide adenine dinucleotide (NAD) is depleted. The biggest risk occurs when a patient drinks alcohol without carbohydrates being available, such as 4 hours or longer after the last meal. One drink takes 1–1.5 hours to process in the liver. Women should stick to one alcoholic beverage a day; men should limit their intake to two per day; both should consume a CHO with their drinks. • In the elderly who are monitoring blood glucose levels closely, the benefits of intensive therapy in an effort to lower A1c must be weighed against the greater risk of unpredictable hypoglycemia (Alam et al, 2005).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Mayo Clinic http://www.mayoclinic.com/health/hypoglycemia/DS00198

NIDDK–Hypoglycemia in Diabetes http://diabetes.niddk.nih.gov/dm/pubs/hypoglycemia/

HYPOGLYCEMIA—CITED REFERENCES Alam T, et al. What is the proper use of hemoglobin A1c monitoring in the elderly? J Am Med Dir Assoc. 6:200, 2005. Grimm JJ, et al. A new table for prevention of hypoglycaemia during physical activity in type 1 diabetic patients. Diabetes Metab. 30:465, 2004. Haces ML, et al. Selective vulnerability of brain regions to oxidative stress in a non-coma model of insulin-induced hypoglycemia. [published online ahead of print October 7, 2009] Neuroscience. 165:28, 2010. Juneja R, et al. Computerized intensive insulin dosing can mitigate hypoglycemia and achieve tight glycemic control when glucose measurement is performed frequently and on time. Crit Care. 13:165, 2009. Smith WD, et al. Causes of hyperglycemia and hypoglycemia in adult inpatients. Am J Health Syst Pharm. 62:714, 2005. Suh SW, et al. Sequential release of nitric oxide, zinc, and superoxide in hypoglycemic neuronal death. J Cereb Blood Flow Metab. 28:1697, 2008.


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HYPERINSULINISM AND SPONTANEOUS HYPOGLYCEMIA NUTRITIONAL ACUITY RANKING: LEVEL 3–4 SEVERE, PERSISTENT HYPOGLYCEMIA

CONGENITAL HYPERINSULINISM EVALUATION Testing for CH-associated mutations in ABCC8, KCNJ11, GLUD1, GCK

CH-associated mutation in KCNJ11

One recessive mutation

Focal CH should be considered

CH-associated mutation in ABCC8

Two recessive mutations

Two recessive mutations

Sever diffuse CH: Near-total pancreatectomy

One recessive mutation

Focal CH should be considered

Dominant mutation

CH-associated mutation in GLUD1

CH-associated mutation in GCK

Dominant mutation

Dominant mutation

Mild diffuse CH: Drug therapy

Parent testing to confirm paternal inheritance

Localization of focal pancreatic lesion, e.g., by arterial stimulation venous sampling

Partial pancreatectomy

DEFINITIONS AND BACKGROUND Hyperinsulinism consists of insulin levels above 3 U/mL when glucose levels are below 50 mg/dL. Treatment depends on the cause and the severity of the hyperinsulinism. Congenital hyperinsulinism (CH) is familial hyperinsulism (FHI) with profound hypoglycemia because of excessive insulin secretion. CH can lead to developmental delay, mental retardation or death if untreated. CH occurs at an approximate frequency of 1/25,000 to 1/50,000 live births. New procedures spare healthy cells in the pancreas while allowing surgeons to remove abnormal tissue. Spontaneous hypoglycemia is an underlying symptom of some other diseases besides diabetes. Fasting and reactive hypoglycemias fall into the category of spontaneous forms. In fasting hypoglycemia, the body is not able to maintain adequate levels of sugar in the blood after a period without food in heavy drinkers who do not eat; people with islet cell tumors, viral hepatitis, cirrhosis, or liver cancer; and children with carbohydrate metabolic disorders. Hereditary

fructose intolerance, galactosemia, leucine sensitivity can cause this type of hypoglycemia. Reactive hypoglycemia describes recurrent episodes of hypoglycemia occurring 2–4 hours after a high CHO or glucose load. Etiologies include alimentary hypoglycemia (dumping syndrome following gastric surgery); hypothyroidism or other hormonal disorders; h. pylori-induced gastritis; or occult diabetes with an exaggerated hyperglycemia during a glucose tolerance test. Symptoms include weakness and agitation 2–4 hours after meals, perspiration, nervousness, and mental confusion. Diet remains the main treatment, although alpha-glucosidase inhibitors and some other drugs may be helpful. Brain glycogen supports energy metabolism when glucose supply from the blood is inadequate and its levels rebound to levels higher than normal after a single episode of moderate hypoglycemia (Oz et al, 2009). Glutamate serves important intracellular signaling functions; glutamate dehydrogenase (GDH) catalyzes the oxidative deamination of glutamate to alphaketoglutarate in brain, liver, kidney, and the pancreatic islets (Stanley, 2009).


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ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Individuals with congenital hyperinsulinism (CH) should be tested for gene mutations. Mutations in GLUD1, GCK, or HADHSC are response to drug therapy, but CHI associated with mutations in ABCC8 or KCNJ11 often requires pancreatectomy. Clinical/History Height Weight BMI Diet history Recent weight losses Craving for sweets BP Seizures, confusion Heart palpitation or fibrillation

Dizziness Lightheadness, tremors Headache Flushing Irritability Numb or cold extremities Lab Work Gluc Serum insulin Serum glucagon

Growth hormone levels Chol Trig Na, K Trig HgA1c Ca, Mg Acetone PO4 CRP

INTERVENTION OBJECTIVES • Reduce intake of concentrated CHO to a level that does not overstimulate the pancreas to secrete inappropriately large amounts of insulin, which may cause blood sugar to

SAMPLE NUTRITION CARE PROCESS STEPS Excessive CHO Intake Assessment Data: Recent bouts of low blood glucose, (50 mg/gL) without Hx of diabetes or insulinoma. Dumping syndrome 2–3 hours after meals with weakness, perspiration, heart palpitations, headache, and craving for sweets. Diet history reveals CHO intake averaging 250 g/d, especially between meals and before bedtime. Nutrition Diagnosis (PES): Excessive CHO intake related to high intake of sweets as evidenced by diet history. Intervention: Food and nutrient delivery—tracking of CHO intake at meals and snacks. Education—sources of CHO from each food group. Counseling—ways to decrease hunger; food diary for episodes of hypoglycemia; signs and symptoms and when to call the doctor; glycemic index and glycemic load of foods. Monitoring and Evaluation: Improvement through decreased episodes of hypoglycemia following meals and snacks with limitation of intake to 130–150 g daily.

drop. Limit total intake of carbohydrate to 130 g/d to reduce the severity of symptoms. • If required, ensure that patient loses weight gradually. • Reduce counterregulatory hormone responses to excessive insulin. • Exercise regularly and maintain consistency in meal times and daily routines.

FOOD AND NUTRITION • Diet should include frequent small meals, about every 3 hours. Eat a variety of foods, including meat, poultry, fish, or nonmeat sources of protein; whole grains; fruits and vegetables; dairy products. • Choose high-fiber foods and food with a moderate-to-low glycemic load. Avoid white rice, potatoes, corn. • Avoid or limit foods high in sugar, especially on an empty stomach; this includes sweetened beverages and dried fruits. • Avoid alcohol, caffeine. • Maintain protein intake at DRI levels; fat furnishes the remainder of calories. The traditional high protein, low CHO diet is not evidenced-based. • For the GLUD1 genetic form of HI, a low leucine diet and use of diazoside may be needed. Most of the other genetic forms will require surgery or just drug use.

Common Drugs Used and Potential Side Effects • Diazoside is needed for the GLUT1 form of HI. Diazoxide is believed to inhibit insulin secretion through opening KATP channels. Octreotide (a somatostatin analogue) or continuous dextrose is often used; but in KATP HI, drug therapy fails, and pancreatectomy is required. • Chemotherapy (e.g., streptozocin, fluorouracil) may be used for insulinomas. Monitor GI side effects and nephrotoxicity. • Alpha-glucosidase inhibitors may be where diabetes is identified. • Monitor all medications for their potential hypoglycemic effects.

Herbs, Botanicals, and Supplements • Products such as hemicelluose and pectin may help in dumping syndrome. • Herbs and botanical supplements should not be used without discussing with physician. • See Table 9-9 for guidance on more specific herbs and supplements.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain that alcohol blocks gluconeogenesis and should be avoided. • Ensure that patient keeps snacks available such as cheese and crackers. More frequent feedings are needed.


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• Avoid skipping meals; eat meals on time. Avoid any one meal that is unbalanced or especially high in carbohydrates. • Control caffeine intake and use of other stimulants, which may aggravate condition.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Congenital Hyperinsulinism http://www.chop.edu/service/congenital-hyperinsulinismcenter/home.html?id47690

Congenital Hyperinsulinism International http://www.congenitalhi.org/

NIDDK–Hypoglycemia (Nondiabetes) http://diabetes.niddk.nih.gov/dm/pubs/hypoglycemia/#nodiabetes

569

HYPERINSULINISM AND SPONTANEOUS HYPOGLYCEMIA—CITED REFERENCES Oz G, et al. Human brain glycogen metabolism during and after hypoglycemia. Diabetes 58:1978, 2009. Stanley GA. Regulation of glutamate metabolism and insulin secretion by GDH in hypoglycemic children. J Am Clin Nutr. 90:862S, 2009.

Other Endocrine Disorders Hormones can be separated into three categories: amines, these are simple molecules, proteins and peptides, which are made from chains of amino acids, and steroids, which are derived from cholesterol. Glands discharge hormones directly into the bloodstream, and they have feedback mechanisms that maintain a proper balance of hormones and prevent excess secretion. Endocrine disorders require varying levels of nutritional intervention. If medications are taken appropriately, many conditions can be readily managed. See Table 9-19.

TABLE 9-19 Other Endocrine Conditions There are many other disorders of endocrine function besides those affecting the pancreas that require some level of nutritional intervention. Listed below are essential hormones and functions of the endocrine glands. Gland

Hormones

Functions

Pancreas

Glucagon (from alpha-cells)

Alpha-cells in the pancreatic islets secrete the hormone glucagon in response to a low concentration of glucose in the blood.

Insulin (from beta-cells)

Beta-cells in the pancreatic islets secrete insulin in response to high blood glucose concentrations. See diabetes section.

Gastric mucosa

Gastrin

Stimulates production of hydrochloric acid and the enzyme pepsin, used in digestive processes.

Small intestinal mucosa

Secretin

Stimulates the pancreas to produce bicarbonate-rich fluid to neutralize stomach acid.

Cholecystokinin

Stimulates contraction of the gallbladder to release bile after a meal containing fat. Also stimulates the pancreas to secrete digestive enzymes.

Placenta

Human chorionic gonadotropin

Signals the mother’s ovaries to secrete hormones to maintain the uterine lining during pregnancy.

Hypothalamus

Gonadotropin-releasing hormone (GnRH) and other releasing hormones

Hunger and thirst; emotional and sexual responses of the limbic system; heart rate and blood pressure; circadian cycles; body temperature; bladder function; moods. Hypothalamus links the nervous system by synthesizing and secreting neurohormones that stimulate release of hormones from the anterior pituitary gland.

Pituitary (anterior)

Adrenocorticotropic hormone (ACTH)

Reacts with receptor sites in the cortex of the adrenal gland to stimulate the secretion of cortical hormones, particularly cortisol.

Human growth hormone (hGH or somatotropin hormone)

Growth of bones, muscles, and other organs by promoting protein synthesis; influences height.

Thyroid-stimulating hormone (TSH or thyrotropin)

Causes thyroid to secrete thyroid hormone.

Gonadotropins (folliclestimulating hormone [FSH]; luteinizing hormone [LH])

React with gonads to regulate growth and function of these organs. In females, FSH stimulates egg production; in males, it stimulates sperm production. In females, LH causes ovulation; in males, it causes the testes to secrete testosterone.

Prolactin (PRL)

Promotes development of glandular tissue in the female breast during pregnancy and stimulates milk production after the birth of the infant.

Oxytocin (OT)

Causes contraction of the smooth muscle in the wall of the uterus. It also stimulates the ejection of milk from the lactating breast.

Vasopressin (antidiuretic hormone [ADH])

ADH promotes the reabsorption of water by the kidney tubules; less water is lost as urine to conserve water for the body. Insufficient amounts of ADH cause excessive water loss in the urine.

Pituitary (posterior)

(continued)


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TABLE 9-19 Other Endocrine Conditions (continued) Gland

Hormones

Functions

Pineal gland

Melatonin (5-methoxy-N-acetyltryptamine)

Reproductive development and daily sleep–wake cycles; skin blanching. Derived from tryptophan. Production is stimulated by darkness and inhibited by light. Betablockers decrease release of melatonin.

Adrenal cortex

Adrenal medulla

Adrenal cortex has control of 28 hormones, all of which are steroids. Mineralocorticoids (such as aldosterone)

Aldosterone conserves sodium ions and water.

Glucocorticoids (such as cortisol)

Cortisol increases blood glucose levels.

Gonadocorticoids (sex hormones: androgens and estrogens)

Normal reproductive functioning.

Epinephrine (adrenalin) and norepinephrine (noradrenalin)

These two hormones are secreted in response to stimulation by the sympathetic nerve, particularly during stressful situations. They cause faster heartbeat and increased blood glucose levels. A lack of hormones from the adrenal medulla produces no significant effects. Hypersecretion, usually from a tumor, causes prolonged or continual sympathetic responses.

Thyroid

Thyroid hormones: thyroxine (95%) and triiodothyronine (5%)

Growth and development, metabolism. Thyroid hormones need iodine.

Calcitonin

Calcitonin is secreted by the parafollicular cells of the thyroid gland. This hormone opposes the action of the parathyroid glands by reducing the calcium level in the blood. If blood calcium becomes too high, calcitonin is secreted until calcium ion levels decrease to normal.

Thymus

Thymosin

Immunity; T cells; lymphocytes. Currently being studied for its possible role in AIDS and hepatitis.

Parathyroid glands

Parathyroid hormone (PTH)

Regulation of calcium and phosphorus; secreted in response to low blood calcium levels in order to increase those levels. PTH mobilizes calcium by increasing calcium resorption from bone and by raising calcium reabsorption in the proximal kidney tubule.

Gonads (testes and ovaries)

Androgens (testosterone)

Growth and development of the male reproductive structures; increased skeletal and muscular growth; enlargement of the larynx accompanied by voice changes; growth and distribution of body hair; increased male sexual drive.

Estrogen and progesterone

Development of the breasts; distribution of fat evidenced in the hips, legs, and breasts; maturation of reproductive organs such as the uterus and vagina. Progesterone causes the uterine lining to thicken in preparation for pregnancy. Together, progesterone and estrogens are responsible for the changes that occur in the uterus during the female menstrual cycle.

Sources: Surveillance, Epidemiology, and End Results. Endocrine glands and their functions. Accessed July 1, 2005, at http://training.seer.cancer.gov/module_anatomy/ unit6_3_endo_glnds.html and Cotterill S. The endocrine system (hormones). Accessed July 1, 2005, at http://www.cancerindex.org/medterm/medtm12.htm#function

For More Information on Other Endocrine Conditions

American Association of Clinical Endocrinologists http://www.aace.com/

Endocrine Society http://www.aace.com/

American Medical Association http://www.ama-assn.org/ama/pub/category/7157.html

The Hormone Foundation http://www.hormone.org/

National Institutes of Health–Endocrine Disorders http://www.niddk.nih.gov/health/endo/endo.htm


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HYPOPITUITARISM NUTRITIONAL ACUITY RANKING: LEVEL 1

Hypothalamus

Infundibulum (pituitary stalk) Anterior lobe

Hypothalamicohypophysial tract Posterior lobe

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Hypopituitarism is an underactive pituitary gland. A deficiency in production of pituitary hormones may be caused by tumor, trauma, radiation to the brain, stroke or aneurysm, or surgery. In hypopituitarism, there is a lack of one or more of these hormones and loss of function in the affected gland or organ. Table 9-20 lists symptoms of pituitary disorders. It may take years for an accurate diagnosis to be made. If all pituitary hormones are missing, this is panhypopituitarism; it is relatively rare. Adrenocorticotropic hormone (ACTH) stimulates the adrenal gland to release cortisol to maintain BP and blood glucose levels. If ACTH is missing, depression, fatigue, low BP, nausea and diarrhea, dizziness, pale skin, weakness, and weight loss are signs and symptoms. A shortage of cortisol can be life threatening. Arginine vasopression (AVP) was formerly known as antidiuretic hormone (ADH). AVP controls water loss by the kidneys. If AVP is deficient, severe thirst and excessive urination occur; diabetes insipidus may result. In rare instances, deficiency may occur after an event such as brain surgery. TABLE 9-20 Symptoms of a Pituitary Disorder Headaches

Short stature if during growth period

Depression

Cold intolerance

Mood/emotion swings

Weight loss

Abdominal pain, anorexia

Infertility in women

Loss of memory

Impotence in men

Loss of sleep

Cessation of or irregular menses

Sexual dysfunction

Lethargy, fatigue

Failure in lactation

Weakness

Low blood pressure

Loss of armpit, body, pubic or facial hair

Source: Pituitary Network Association. Available at http://www.pituitary.org/

Growth hormone (GH) regulates somatic growth, carbohydrate and lipid metabolism, and adipocyte functions. There is a complex interplay between GH and insulin signaling (Perrini et al, 2008). If GH is deficient in children, short stature (below 5 feet) can result. This condition causes 10% of all dwarfism. In adults, there is abnormal body composition, osteopenia, impaired quality of life, cardiac dysfunction, and an adverse lipid profile. Follicle-stimulating hormone (FSH) and Luteinizing hormone (LH) control sexual function and fertility in males and females. When gonadotropin (FSH, LH) deficiency occurs, men and women will lose interest in sex and can experience fatigue, weakness, loss of body hair, impotence in men, and loss of menstruation in women. Oxytocin stimulates the uterus to contract during labor and the breasts to release milk. Oxytocin mechanisms are necessary for successful pregnancies (Kubler et al, 2009). Pregnancy is uncommon when oxytocin levels are low. Prolactin stimulates female breast development and milk production. Prolactin deficiency is rare but can stop milk production in women. TSH stimulates the thyroid gland to release hormones that affect the bodyâ&#x20AC;&#x2122;s metabolism. When TSH is deficient, this can lead to an underactive thyroid (hypothyroidism). Cold intolerance, constipation, weight gain, and pale and waxy or dry skin can occur.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Transcription factors have an impact on target genes; different phenotypes result when the gene encoding the relevant transcription factor is mutated. Many genes are involved. Clinical/History

Lab Work

Height Weight BMI Diet history BP Brain scan Pituitary MRI Dual-energy x-ray absorptiometry (DEXA) scan

ACTH level Cortisol Serum estradiol Serum testosterone Serum IGF-1 Thyroxine (T4) (decreased?) Triiodothyronine (T3) FSH, LH, TSH (decreased?)

Protein-bound iodine (PBI) uptake (decreased?) Glucose Glucose tolerance test (GTT) Chol, Trig Homocysteine CRP Alb Complete blood count (CBC)


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Osmolarity Na, K Ca, Mg

Serum Gluc Uric acid

3. GH (somatotropin) requires no specific dietary interventions. It may help alleviate elevated triglycerides. Long-term GH replacement therapy in adults is safe for lifelong therapy in order to maintain the benefits. 4. Estrogen, progesterone, or testosterone replacement should be monitored for side effects related to heart disease and elevated lipids. 5. Cortisone may be needed during periods of stress or illness if ACTH is deficient.

H & H, serum ferritin Transferrin

INTERVENTION OBJECTIVES • • • •

Replenish missing hormones. Prevent dehydration, hypoglycemia, and related problems. Improve lean muscle mass stores. Monitor serum levels of cholesterol and triglycerides; prevent vascular complications.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

FOOD AND NUTRITION • Dietary alterations may be needed, such as higher or lower energy intake, until hormone levels are normalized. A modified fat, cholesterol, and carbohydrate intake may be needed. Ensure sufficient intake of protein. • Six small feedings may be better tolerated than larger meals. • Increase fluids unless contraindicated. • Ensure adequate intake of all vitamins and minerals. Calcium and vitamin D should be taken in sufficient amounts to prevent osteoporosis.

Common Drugs Used and Potential Side Effects Hormone replacement therapy may include any of all of the following: 1. Corticosteroids (hydrocortisone [Cortef], cortisol) are often used and can alter glucose, calcium, and phosphate tolerance. Potassium and folacin must be increased; sodium must be decreased. Monitor for signs of hyperglycemia. 2. Thyroid preparations (levothyroxine) may be needed.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Have patient avoid fasting and stress. • Discuss the need to use small, frequent meals instead of large meals. • Discuss the possibility of hyperglycemia and how to manage. • Hormone replacement is usually permanent, so doctor visits will be needed to check for diabetes and signs of osteoporosis.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Hormone Foundation–Pituitary Hormone http://www.hormone.org/public/pituitary.cfm

Mayo Clinic http://www.mayoclinic.com/health/hypopituitarism/DS00479

Medline Plus http://www.nlm.nih.gov/medlineplus/pituitarydisorders.html

SAMPLE NUTRITION CARE PROCESS STEPS

Pituitary Disorders Education and Support http://www.pituitarydisorder.net/

Unsafe Food Handling

The Pituitary Society http://www.pituitarysociety.org/

Assessment Data: On home tube feeding. Unsanitary habits noted during home visit. Nutrition Diagnosis (PES): Unsafe food handling related to preparation and administration of tube feeding as evidenced by observations during home visit. Intervention: Education on how to sanitize counters and maintain safe procedures while handling tubing and enteral product. Monitoring and Evaluation: No signs of diarrhea or GI distress from contaminated TF.

HYPOPITUITARISM—CITED REFERENCES Kubler K, et al. High-risk pregnancy management in women with hypopituitarism. J Perinatol. 29:89, 2009. Perrini S, et al. Metabolic implications of growth hormone therapy. J Endocrinol Invest. 31:79, 2008. Verhelst J, et al. Baseline characteristics and response to 2 years of growth hormone replacement of hypopituitary patients with growth hormone deficiency due to adult-onset craniopharyngioma in comparison to patients with non-functioning pituitary adenoma: data from KIMS. J Clin Endocrinol Metab. 90:4636, 2005.


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ACROMEGALY NUTRITIONAL ACUITY RANKING: LEVEL 1 with hypoadiponectinemia; studies suggest a link between adiponectin, visfatin, fat mass, and bone changes (Sucunza et al, 2009). Premature death may result if left untreated. Treatment may include surgical removal of the tumor, radiation therapy, or injection of a GH blocking drug. Somatostatin analogs have been key in medical therapy. Pegvisomant, a GHreceptor antagonist, competitively binds to the GH receptor, blocking IGF-I production and allowing for a better control of cardiac disorders and glucose metabolism (Vance and Lawes, 2005). Improved insulin sensitivity occurs after use from a reduction in overnight endogenous glucose production (Higham et al, 2009). Somatuline Depot (lanreotide) can be used for a long-term treatment in patients who have had an inadequate response to surgery and/or radiation.

Adapted from: Weber J RN, EdD and Kelley J RN, PhD. Health Assessment in Nursing, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

DEFINITIONS AND BACKGROUND Acromegaly is a hormonal disorder caused by overproduction of human GH by the pituitary gland. Incidence is rare, with 50–70 cases per million in the U.S. population. Diagnosis is made common about a decade after oversecretion of GH begins. If GH-producing tumors occur in puberty, the condition is called gigantism. Genetics and nutrition impact the height of most children; unusual, continuing growth in stature beyond the twenties should be evaluated. GH (somatotropin) affects the growth of almost all cells and tissues and has direct and indirect effects. Direct effects of excessive GH include hyperinsulinism, lipolysis, insulin resistance in peripheral tissues, ketogenesis, hyperglycemia, and sodium and water retention. In over 98% of cases, overproduction of GH is related to a benign pituitary tumor. In a few patients, acromegaly is caused by tumors of the pancreas, lungs, or adrenal glands. Symptoms and signs of acromegaly include enlarged extremities with disproportionate growth of nose, lips, brow, lower jaw, tongue, hands, and feet. Serious side effects include heart failure, colon polyps that become cancerous, and diabetes. Elevated insulin-like growth factor I (IGF-I) also occurs in acromegaly, resulting in greater protein synthesis, amino acid transportation, muscle and bone growth, DNA and RNA synthesis, and cell proliferation. High levels of GH and increased IGF-1 levels (three to ten times above normal) may be used to diagnose acromegaly. Hormone-secreting pituitary tumors account for about 30% of all pituitary tumors (Patil et al, 2009). Surgical removal of the pituitary gland provides a 50–70% chance of cure (Vance and Laws, 2005). Acromegaly is complicated by an increased incidence of diabetes mellitus caused by impaired insulin sensitivity and reduced betacell function (Higham et al, 2009). Bone and cartilage growth may lead to arthritis. Acromegalic patients present

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Most pituitary tumors are from a genetic mutation that is acquired and not present from birth. BUN Serum Creat Height (increased) Weight Urine sugar BMI Gluc, HbA1c Weight changes GTT Diet history Serum BP (increased) insulin I&O Ca Increased coarse Lab Work (decreased) body hair Phosphorus Coarse, leathery IGF-I levels (best (increased?) marker) skin Alb GH (>5 higher Excessive Na, K than normal) diaphoresis H&H and oily skin N balance Clinical/History

Skin tags Impaired vision Osteoarthritis, carpal tunnel syndrome Deepening voice Headaches Fluid retention

INTERVENTION OBJECTIVES • Control weight. • Prevent or control diabetes, hypertension, or heart disease when present. • Prevent osteoporosis with calcium balance, which is often negative. • Monitor for complications such as colon polyps, which may lead to cancer.


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SAMPLE NUTRITION CARE PROCESS STEPS Involuntary Weight Gain Assessment Data: Diagnosis of acromegaly with recent weight gain of 10 lb over 6 weeks; FBG 130 mg/dL.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

Nutrition Diagnosis (PES): Involuntary weight gain (NC-3.4) related to excessive GH and IGF-1 levels as evidenced by 10 lb weight gain in 6 weeks. Intervention: Education—importance of controlling CHO and energy intake to manage weight and prevent diabetes. Counseling—tips for identifying hidden CHO sources and controlling energy intake. Monitoring and Evaluation: Weight stabilized; HgbA1c, FBS and other available lab results. No additional signs of hyperglycemia and no further weight gain.

• Achieve the goal for GH levels as 1–2 g/L (Sheppard, 2005).

FOOD AND NUTRITION • An CHO-controlled diet may be needed if diabetes is present. • Extra fluid intake may be needed. • Control sodium and fluid intake if there is heart failure. • Offer sufficient intake of calcium and vitamin D; a multivitamin–mineral supplement may be useful.

Common Drugs Used and Potential Side Effects • Bromocriptine (Parlodel) can be taken orally to reduce GH secretion. Side effects include gastrointestinal upset, nausea, vomiting, light-headedness when standing, and nasal congestion. Take with food. • Octreotide (Sandostatin) injection is a synthetic form of somatostatin. Side effects include diarrhea, nausea, gallstones, and loose stools. • Insulin may be needed if diabetes is also present. Be wary of excess doses; hypoglycemia is a dangerous side effect. • Cardiac medications may be needed; monitor for specific side effects accordingly. Atorvastatin treatment is safe, well-tolerated, and effective (Mishra et al, 2005). • Pegvisomant is used to normalize circulating levels of IGF-I, the principal mediator of GH action. • Somatuline Depot delivers an injection subcutaneously instead of into the muscle; side effects include diarrhea, cholelithiasis, abdominal pain, nausea, injection site reactions, flatulence, arthralgia, and loose stools.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss body changes and altered self-image. Exercise can help to improve physical functioning and quality of life (Woodhouse et al, 2006). • Teach patient about control of diabetes or heart failure, where present. • After surgery, potential complications include cerebrospinal fluid leaks, meningitis, and damage to the surrounding normal pituitary tissue, requiring lifelong pituitary hormone replacement.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Acromegaly http://www.acromegaly.org/

NIDDK–Acromegaly http://www.niddk.nih.gov/health/endo/pubs/acro/acro.htm

Pituitary Network Association http://www.pituitary.com/

Skull Base Institute http://www.skullbaseinstitute.com/acromegaly_gigantism.htm

Treatment Guidelines http://www.aace.com/pub/pdf/guidelines/ AcromegalyGuidelines2004.pdf

ACROMEGALY—CITED REFERENCES Higham CE, et al. Pegvisomant improves insulin sensitivity and reduces overnight free fatty acid concentrations in patients with acromegaly. J Clin Endocrinol Metab. 94:2459, 2009. Mishra M, et al. The effect of atorvastatin on serum lipoproteins in acromegaly. Clin Endocrinol. 62:650, 2005. Patil CG, et al. Non-surgical management of hormone-secreting pituitary tumors. J Clin Neurosci. 16:985, 2009. Sheppard MC. GH and mortality in acromegaly. J Endocrinol Invest. 28:75S, 2005. Sucunza N, et al. A link between bone mineral density and serum adiponectin and visfatin levels in acromegaly. J Clin Endocrinol. 94:3889, 2009. Vance ML, Laws ER Jr. Role of medical therapy in the management of acromegaly. Neurosurgery. 56:877, 2005. Woodhouse LJ, et al. The influence of growth hormone status on physical impairments, functional limitations, and health-related quality of life in adults. Endocr Rev. 27:287, 2006.


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CUSHING’S SYNDROME NUTRITIONAL ACUITY RANKING: LEVEL 1–2 needed. After surgical removal of the adrenal glands, most symptoms of CS disappear. Psychological impairment can persist despite successful treatment (Iacabone et al, 2005).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Adapted from: Rubin E. Essential Pathology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2000.

DEFINITIONS AND BACKGROUND

Genetic Markers: Rarely, CS results from an inherited tendency to develop tumors of one or more endocrine glands. With multiple endocrine neoplasia type 1 (MEN1), hormone-secreting tumors of the parathyroid glands, pancreas, and pituitary develop and may lead to CS. Urinary Gluc (increased) Height Gluc (increased) Weight HbA1c BMI Ca, Mg Diet history Urinary Ca BP (increased) Lab Work Lipid profile, Edema Chol, Trig 24-hour urinary Buffalo hump K (decreased) free cortisol Moon face Na (increased) level (50– Easy bruising, Alb, N balance 100 g/d) slow healing CRP Dexamethasone Red or purple pCO2 suppression striae on (increased), test skin pO2 Weakened bones Late-night saliWBC, TLC vary cortisol Sore, aching (decreased) joints in hip, Corticotropinreleasing back, shoulhormone ders (CRH) stimuExcess facial lation test for hair in ACTH levels women (altered) Clinical/History

Cushing’s syndrome (CS) is a disease caused by an excess of cortisol. It can be caused by extrinsic and excessive hormonal stimulation of the adrenal cortex by tumor of the anterior pituitary gland, adrenal hyperplasia, or exogenous cortisol use. Differential diagnosis is not simple. No existing test is accurate when used alone; focused imaging, including computed tomography (CT), magnetic resonance imaging (MRI), and nuclear imaging modalities can provide the diagnosis (Lindsay and Nieman, 2005). Pituitary CS occurs after puberty with equal frequency in boys and girls. In adults, it has a greater frequency in women than men, with most diagnosed between ages 20 and 50 years. The total incidence is about 10–15 million people per year. It is a disorder characterized by virilism, upper body obesity with thin arms and legs, hyperglycemia, glucosuria, hypertension, red moon face, vertigo, emotional liability, buffalo hump, purple striae over obese areas, acne, female balding or hirsutism, blurry vision, and pitting ankle edema. In some cases, osteoporosis and severe depression are present. Chronic cortisol hypersecretion causes central obesity, hypertension, insulin resistance, dyslipidemia, and prothrombotic state, manifestations of a MetS. There is a complex interaction between CS and inflammation; raised levels of IL8 and OPG in CS patients, despite glucocorticoid excess, may represent an inflammatory and pro-atherogenic phenotype (Kristo et al, 2008). If left untreated, CS can be fatal. Diagnosis is not simple. Late-night salivary cortisol may be a useful test (Carroll et al, 2009). Treatments differ according to the cause: ACTH dependent (pituitary or ectopic) or independent (an adrenal tumor), or iatrogenic (from excessive steroid hormone use). If iatrogenic, depletion of steroid hormones will be needed. If pituitary, the gland may need to be removed. CS caused by ACTH production from solid tumors can result in life-threatening hypercortisolemia (Uecker and Janzow, 2005). Radiation, chemotherapy, or surgery may be

Decreased fertility in men CT MRI for tumors DEXA scan

INTERVENTION OBJECTIVES • Control elevated blood glucose or lipids; manage diabetes and CVD. • Promote weight loss if needed; decrease fat stores while increasing lean body mass. • Control or lower BP.


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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Sodium Intake Assessment Data: Long-term corticosteroid use for lupus; dietary history reveals high intake of sodium from snack foods, canned soups and vegetables, luncheon meats; buffalo hump, slightly elevated glucose and lipids. BMI 27. BP averaging 190/80. Feet and hands edematous. Nutrition Diagnosis (PES): Excessive sodium intake related to high intake of salted and processed foods as evidenced by diet history and requirement for corticosteroids. Intervention: Education about a desirable lowering of sodium from dietary sources. Counseling about sources of well-flavored snack foods, use of more fruits and raw vegetables, use of varied spices and seasonings; choices in the supermarket, at restaurants, while traveling. Monitoring and Evaluation: Evaluation of impact of lower sodium from diet on BP and edema. Improved intake of fruits, raw vegetables and nonprocessed meats. Improved quality of life.

• Prevent or control side effects of corticosteroid therapy: vertebral collapse, heart failure, bone demineralization, osteoporosis, and hypokalemia.

FOOD AND NUTRITION • Restrict sodium if steroids are used. • Use an energy-controlled diet, if needed. Calculate diet according to patient’s desirable body weight. • Control glucose levels when elevated; carbohydrate counting can be useful. • Ensure adequate intake of calcium and potassium. • Ensure adequate intake of protein if losses are excessive (e.g., 1 g protein/kg or more). • Use an anti-inflammatory diet rich in omega-3 fatty acids, herbs, spices and antioxidant foods; see Tables 8-13 and 8-14.

Common Drugs Used and Potential Side Effects • With glucocorticoid therapy, osteoporosis and hypercalciuria are common side effects. Withdrawal of these medications after autoimmune or cancer management may cause iatrogenic CS. Adrenal insufficiency or steroid

withdrawal symptoms may occur (Hopkins and Leinung, 2005). • Large doses of vitamin D may be necessary; do not use for extended periods without monitoring for toxicity.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Help patient control weight as needed. • Explain which foods are good sources of calcium in the diet. • Explain how to control elevated blood sugars and lipids through balanced dietary intake. • Manage symptoms of MetS through dietary changes and exercise.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Cushing’s Support and Research Foundation http://csrf.net/

Hormone Foundation http://www.hormone.org/Other/upload/ cushings-syndrome-billingual-032309.pdf

NIDDK–Cushing’s Syndrome http://www.niddk.nih.gov/health/endo/pubs/cushings/cushings.htm

CUSHING’S SYNDROME—CITED REFERENCES Carroll T, et al. Late-night salivary cortisol for the diagnosis of Cushing syndrome: a meta-analysis. Endocr Pract. 15:335, 2009. Hopkins RL, Leinung MC. Exogenous Cushing’s syndrome and glucocorticoid withdrawal. Endocrinol Metab Clin North Am. 34:371, 2005. Iacabone M, et al. Results and long-term follow-up after unilateral adrenalectomy for ACTH-independent hypercortisolism in a series of fifty patients. J Endocrinol Invest. 28:327, 2005. Kristo C, et al. Biochemical markers for cardiovascular risk following treatment in endogenous Cushing’s syndrome. J Endocrinol Invest. 31:400, 2008. Lindsay JR, Nieman LK. Differential diagnosis and imaging in Cushing’s syndrome. Endocrinol Metab Clin North Am. 34:403, 2005. Uecker JM, Janzow MT. A case of Cushing syndrome secondary to ectopic adrenocorticotropic hormone producing carcinoid of the duodenum. Am Surg. 71:445, 2005.


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PITUITARY GLAND (POSTERIOR)

DIABETES INSIPIDUS NUTRITIONAL ACUITY RANKING: LEVEL 3 Bloodstream REABSORPTION Water Sugar Salts

SECRETION Acids

Renal arteriole

Glomerulus Sugar, water, salts, urea/other wastes

FILTRATION

Bowman’s capsule

Renal tubule Sugar, water, salts, urea/other wastes

Urine

Renal Pelvis

Ureter

Bladder

Blood

Urethra

Filtrate Urine Urinary meatus

DEFINITIONS AND BACKGROUND Diabetes insipidus (DI) can be caused by defects in the posterior pituitary gland or from an insufficient renal response to AVP, formerly ADH. Distinction is essential for effective treatment (Makaryus and MacFarlane, 2006). DI may be primary (congenital) or secondary (acquired after trauma, surgery, tumor, or infection). Both forms of DI are marked by excessive thirst, copious urination, and dry skin. There is potential for dehydration and weakness. Urine output may be 5–10 L/24 h. Nephrogenic DI is characterized by the kidney’s inability to respond to AVP. The multiple and complex functions of the renal tubule in regulating water, electrolyte, and mineral homeostasis make it prone to numerous genetic abnormalities (Chadra and Alon, 2009). Nephrogenic DI requires careful monitoring of body chemistry and adequate hydration.

Urine expelled from body

Neurogenic (primary) DI is more common in males. Children with DI may be irritable or listless and may have problems with bedwetting, fever, vomiting, or diarrhea (Linshaw, 2007). Neurogenic DI responds to nasal administration of 1-deamino-8-D-arginine vasopressin (desmopressin acetate) (DDAVP), a vasopressin analogue. Dipsogenic DI is a very rare forms of DI from a defect in the thirst mechanism in the hypothalmus. Gestational DI (GDI) is also very rare. DI can complicate up to 1 in 30,000 pregnancies. If DI occurs with pre-eclampsia, the baby may have to be delivered early. DDAVP may be used (Ananthakrishnan, 2009). Sometimes, the exact cause of DI is unknown. Patients undergoing surgery for pituitary tumors present with DI (Dumont et al, 2005). In acquired forms, the kidneys’ ability to respond to AVP can be impaired by drugs such as lithium,


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or by chronic disorders including polycystic kidney disease, sickle cell disease, kidney failure, partial blockage of the ureters, and inherited genetic disorders.

ASSESSMENT, MONITORING, AND EVALUATION

• Avoid fluid overload and rapid fluctuations in sodium concentration, especially in persons who cannot control their fluid intake themselves (Toumba and Stanhope, 2006). • Check patient’s weight three times weekly to determine fluid retention and effectiveness of drug therapy. At home, have weights recorded daily. • Reduce excess workload for the kidney and prevent stone formation.

CLINICAL INDICATORS Genetic Markers: Abnormal posterior pituitary development is found in genetic forms of central DI. The exact genes are being studied. Glucose Bicarbonate Height Arginine Urinary specific Weight vasopressin gravity BMI (AVP) in (decreased) Diet history serum, urine Uric acid BP Urinary osmo(increased in Excessive thirst lality (may adults) and urination be 300 BUN I&O mOsm/kg) Creat Fever? Fluid deprivation Na (increased) Vomiting, test (neuroK (altered?) diarrhea in genic vs. Alb children nephrogenic Brain MRI forms) Clinical/History

Lab Work

INTERVENTION

FOOD AND NUTRITION • Adjust fluid, sodium, and potassium intakes according to the cause. • A low-sodium diet and diuretics may also be needed to minimize workload of the kidney. • Sometimes a controlled-protein diet is needed to protect renal function.

Common Drugs Used and Potential Side Effects • DDAVP may cause abdominal pain, headaches, gastrointestinal distress, and weakness. It is administered parenterally, by pill, or by nasal spray. Patients should drink fluids or water only when thirsty, but be aware that a low urine volume is a risk factor for kidney stone formation (Mehandru and Goldfarb, 2005). Hyponatremic hypervolemia leading to seizures is a rare but potentially lifethreatening side effect. • If diuretics such as thiazides or amiloride are used, monitor for side effects. Potassium may be needed if a supplement is not used.

Herbs, Botanicals, and Supplements

OBJECTIVES • Reduce urine osmolality and increase electrolyte-free water excretion. • Raise serum sodium concentration.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Fluid Intake Assessment Data: Polyuria, polydipsia; preference for cold beverages or ice. Signs of poor skin turgor and dehydration; pale urine. Diagnosis of nephrogenic DI. Nutrition Diagnosis (PES): Inadequate fluid intake related to losses from frequent urination and diagnosis of DI as evidenced by pale urine, urination 10 times daily and during the night. Intervention: Education about the importance of taking prescribed medication and increasing fluid intake because of Dx of DI. Counseling about sources of fluid from beverages and foods; discussion of signs of dehydration and when to contact the physician. Monitoring and Evaluation: Reports of improved hydration status. Consistent use of medication. No emergency visits to the doctor or emergency room. Improved quality of life.

• Herbs and botanical supplements should not be used without discussing with physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Fluid adjustments will be made according to the type of DI. Caution patients not to limit fluid intake in an effort to lessen urine output. • Cold or ice water may be preferred. • Select low-calorie beverages to prevent excessive weight gain. • Avoid stimulant/diuretic-type beverages (e.g., coffee, tea, alcohol).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Diabetes Insipidus Foundation, Inc. http://diabetesinsipidus.com

Nephrogenic Diabetes Insipidus Foundation http://www.ndif.org/


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DIABETES INSIPIDUS—CITED REFERENCES Ananthakrishnan S. Diabetes insipidus in pregnancy: etiology, evaluation, and management. Endocr Pract. 15:377, 2009. Chadra V, Alon US. Hereditary renal tubular disorders. Semin Nephrol. 29:399, 2009. Dumont AS, et al. Postoperative care following pituitary surgery. J Intensive Care Med. 20:127, 2005.

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Linshaw M. Back to basics: congenital nephrogenic diabetes insipidus. Pediatr Rev. 28:372, 2007. Makaryus AN, MacFarlane SI. Diabetes insipidus: diagnosis and treatment of a complex disease. Cleve Clin J Med. 73:65, 2006. Mehandru S, Goldfarb DS. Nephrolithiasis complicating treatment of diabetes insipidus. Urol Res. 33:244, 2005. Toumba M, Stanhope R. Morbidity and mortality associated with vasopressin analogue treatment. J Pediatr Endocrinol Metab. 19:197, 2006.

PITUITARY GLAND

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH) NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Syndrome of inappropriate antidiuretic hormone (SIADH) involves hyponatremia and hyperosmolarity of urine. Normal renal and adrenal functioning with abnormal elevation of plasma vasopressin occurs (inappropriate for serum osmolality). Hyponatremia and SIADH can occur among elderly long-term care patients with febrile illness (Arinzon et al, 2005). Other causes of SIADH are listed in Table 9-21. Hyponatremia is usually the first symptom of SIADH. In severe hyponatremia, convulsions or coma can occur. Other signs and symptoms include irritability, lethargy, seizures, and confusion. SIADH or cerebral salt-wasting syndrome (CSWS) can occur after pituitary surgery; differential diagnosis can be difficult. SIADH syndrome often requires sodium replacement or use of loop diuretics.

BUN (low, 10 mg/dL) Creat K

Ca, Mg Bicarbonate (normal)

Uric acid (may be low) GFR (increased)

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Sodium Intake Assessment Data: Serum Na levels low at 110 mol/L; elevated urinary osmolality. Nutrition Diagnosis (PES): Inadequate sodium intake related to salt wasting syndrome after pituitary surgery as evidenced by low serum Na (110) and high urinary mOsm. Intervention: Food-nutrient delivery – Add extra salt to meals; send extra salt packet with delivered meals. Monitoring and Evaluation: Normal serum Na and urinary osmolality at next lab visit.

ASSESSMENT, MONITORING, AND EVALUATION TABLE 9-21 Causes of Syndrome of Inappropriate Antidiuretic Hormone

CLINICAL INDICATORS Genetic Markers: SIADH is usually acquired and not genetic. Clinical/History Height Current weight Edema-free weight BMI Diet history I&O Temperature Edema

Irritability Lethargy, confusion Low urine volume Lab Work Serum Na 135 mol/L

Serum osmolality 280 mOsm/kg Serum AVP (elevated) Urine osmolality 500 mol/kg Urinary Na (elevated)

Acute leukemia Brain abscess, stroke or meningitis Drugs: chlorpropamide, cyclophosphamide, carbamazepine Gillain-Barre syndrome Head injury Lung cancer (especially small-cell lung cancer) Lymphoma Olfactory neuroblastoma Pancreatic cancer Pituitary surgery Pneumonia Prostate cancer Rocky Mountain spotted fever Sarcoidosis Temporal arteritis, polyarteritis nodosa


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INTERVENTION OBJECTIVES

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

• Treat the cause. • Restrict water intake. • Replace electrolytes as appropriate; usually intravenous saline is provided. • Normalize hormone secretion through drug therapy.

FOOD AND NUTRITION

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Provide counseling regarding water and fluid restrictions as ordered. • Discuss any underlying conditions that may have caused the syndrome; highlight needed dietary alterations.

• Restrict fluid intake, usually 1000–1200 mL/d. • Alter dietary sodium and potassium, as deemed appropriate for the condition. This will vary by patient condition and medications used. • When enteral feeding is needed, select a formula that is fluid restricted, such as those that are 2 kcal/mL. Monitor carefully for signs of dehydration. Check content of formula for sodium and potassium; select according to patient status and needs.

Patient Education—Foodborne Illness

Common Drugs Used and Potential Side Effects

SIADH—CITED REFERENCES

• Demeclocycline (Declomycin) may be used with side effects like those of tetracycline. Avoid taking with calcium or dairy products. • Conivaptan is a new agent available for use to antagonize the effects of vasopressin, especially in heart failure patients (Schwarz and Sanghi, 2006). • Hyponatremia as a result of SIADH is a relatively common serious side effect of the use of selective serotonin reuptake inhibitors (SSRIs) in (mostly elderly) adults (Vanhaesebrouk et al, 2005).

Arinzon Z, et al. Water and sodium disturbances predict prognosis of acute disease in long term cared frail elderly. Arch Gerontol Geriatr. 40:317, 2005. Casulari LA, et al. Differential diagnosis and treatment of hyponatremia following pituitary surgery. J Neurosurg Sci. 48:11, 2004. Goh KP. Management of hyponatremia. Am Fam Physician. 69:2387, 2004. Johnson AL, Criddle LM. Pass the salt: indications for and implications of using hypertonic saline. Crit Care Nurse. 24:36, 2004. Schwarz ER, Sanghi P. Conivaptan: a selective vasopressin antagonist for the treatment of heart failure. Expert Rev Cardiovasc Ther. 4:17, 2006. Vachharajani TJ, et al. Hyponatremia in critically ill patients. J Intensive Care Med. 18:3, 2003. Vanhaesebrouk P, et al. Phototherapy-mediated syndrome of inappropriate secretion of antidiuretic hormone in an in utero selective serotonin reuptake inhibitor-exposed newborn infant. Pediatrics. 115:508, 2005.

• If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

E-medicine http://www.emedicine.com/ped/topic2190.htm

National Library of Medicine–Dilutional Hyponatremia http://www.nlm.nih.gov/medlineplus/ency/article/000394.htm

OVARY

POLYCYSTIC OVARIAN DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Polycystic ovarian disease (PCOD; or polycystic ovarian syndrome [PCOS]) is an endocrine disorder characterized by hyperandrogenism, bilaterally enlarged polycystic ovaries, and insulin resistance. This syndrome affects about 6–10% of women of childbearing age (Barbieri, 2000). There is a lack of consensus between endocrinologists and gynecologists in the definition, diagnosis, and treatment of PCOD (Cussons et al, 2005). PCOD is currently considered as possibly the most frequent cause of female infertility; it is also closely associated with the MetS (Gleicher and Barad, 2006). Hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN syndrome) cause presentation of the insulin-

resistant syndrome PCOD (Barbieri, 2000). Insulin resistance and hyperandrogenism are caused by both genetic and environmental factors. Acanthosis nigricans is a dark, velvety patch of skin that indicates insulin resistance (Scalzo and McKittrick, 2000). Women of CaribbeanHispanic or African American descent seem to be more prone to this condition. Women with PCOD may have had a history of GDM. Many adolescents present with hirsutism and irregular menses. In PCOD, elevated LH to FSH ratio, hirsutism, acne, oily skin, male pattern baldness, menstrual irregularity, oligomenorrhea, and obesity can occur. Abnormally elevated levels of testosterone and LH disrupt the normal maturation process for ovulation. Immature cysts remain on the ovaries, giving the appearance of a “string of pearls.”


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Girls tested for anorexia nervosa (AN) may also have PCOD, with menstrual irregularities before weight loss and elevated LH and estrogen compared with individuals who have AN alone (Pinhas-Hamiel et al, 2006). In PCOD, biochemical abnormalities include hyperandrogenism, acyclic estrogen production, LH hypersecretion, decreased levels of steroid hormone–binding globulin (SHBG), and hyperinsulinemia (Mascitelli and Pezzetta, 2005). Infertility, hypertension, uterine cancer, diabetes, coronary heart disease, and endometrial carcinoma often follow (Legro, 2001).

ASSESSMENT, MONITORING, AND EVALUATION

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INTERVENTION OBJECTIVES • Lose weight or maintain a normal weight for height; obesity occurs in 50% of this population. • Prevent heart problems, stroke, and heart attack. Improve lipid profile. • Reduce serum androgens and improve menstrual regularity. • Decrease risk for endometrial cancer. • Alleviate glucose intolerance and insulin resistance. • Improve anxiety, moods, and quality of life.

FOOD AND NUTRITION CLINICAL INDICATORS Genetic Markers: Polymorphisms in the PPARGC1A, PPAR-delta and PPAR-gamma2 loci have been associated with PCOS. Clinical/History Height Weight BMI Diet history Weight gain pattern History (Hx) of GDM Irregular menses Amenorrhea Hirsutism Infertility Acne Male pattern baldness Acanthosis nigricans (dark, velvety patches on skin)

Vaginal ultrasound with enlarged ovaries Recurrent pregnancy loss? Lab Work Glucose CRP Chol, Trig (elevated?) Homocysteine Fasting serum insulin (elevated) C-peptide levels for insulin secretion

Serum estrogen Serum testosterone LH LH:FSH ratio (elevated) Plasminogen activator inhibitor-1 (PAI-1) (shows abnormal clotting) H&H Alb BUN, Creat ALT BP (elevated)

SAMPLE NUTRITION CARE PROCESS STEPS Food-Drug Interaction Assessment Data: Recent Dx of PCOD; wt at 110% of normal for height. Currently taking metformin but complaining of GI distress. Nutrition Diagnosis (PES): Food-drug interaction related to metformin use as evidenced by GI distress and use of the medication on an empty stomach.

• Offer a weight-control and exercise plan to meet weight goals. Loss of 5–10 lb may reduce symptoms. • Lower elevated blood glucose and lipids. Eat five to six small meals per day. • The DASH diet may be helpful to lower BP. Include lowfat dairy products and more fruits and vegetables. • Avoid low-fat, high-CHO diets, which promote extra insulin secretion (McKittrick, 2002). A diet of 30–40% fat, 45–50% complex CHOs, and 15–20% protein may be useful. • Include sufficient fiber (20–35 g/d). • Include sources of omega-3 fatty acids (fish, walnuts, and flaxseed). • Dietary or supplemental chromium should be included.

Common Drugs Used and Potential Side Effects • Symptoms may be managed by antiandrogen medication (e.g., birth control pills, spironolactone, flutamide, or finasteride). • Insulin-sensitizing drugs improve ovulation and hirsutism in PCOD (Azziz et al, 2001). Metformin (glucophage) allows for improved insulin sensitivity and reduced LH and testosterone. Metformin induces ovulation, has some marginal benefit in improving aspects of the MetS, improves objective measures of hirsutism, and seems to be effective in both obese and lean individuals (Lord and Wilkin, 2004). Do not use with heart failure, chronic obstructive pulmonary disease, or chronic kidney disease. Take with food; monitor for minor gastrointestinal side effects such as nausea, diarrhea, and flatulence. Hypoglycemia does not usually occur. • Rosiglitazone (Avandia) and pioglitazone (Actos) pose minimal risk of hepatotoxicity compared with older medications.

Intervention: Education about the need to eat before taking the prescription to evaliate if GI distress resolves.

Herbs, Botanicals, and Supplements

Monitoring and Evaluation: Follow-up about GI distress or other side effects while taking metformin. Evaluation of timing for food and medication use.

• Herbs and botanical supplements should not be used without discussing with physician. • Chromium picolinate (1000 g) may be useful as an insulin sensitizer in the treatment of PCOD (Lydic et al, 2006).


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For More Information

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Counsel about weight loss and nutrition. Regular mealtimes and snacks may help control cravings and overeating. • Encourage regular exercise and reduced sedentary lifestyle. • Explain relationship of insulin resistance and increased risk for T2DM. • Medical treatments may be needed to support reproduction. Some women will need in vitro fertilization (IVF) treatments.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food handling procedures.

E-medicine: PCOS http://www.emedicine.com/med/topic2173.htm

Polycystic Ovarian Syndrome Association, Inc. http://www.pcosupport.org

POLYCYSTIC OVARIAN DISEASE—CITED REFERENCES Cussons AJ, et al. Polycystic ovarian syndrome: marked differences between endocrinologists and gynaecologists in diagnosis and management. Clin Endocrinol. 62:289, 2005. Essah PA, Nestler JE. The metabolic syndrome in polycystic ovary syndrome. J Endocrinol Invest. 29:270, 2006. Gleicher N, Barad D. An evolutionary concept of polycystic ovarian disease: does evolution favor reproductive success over survival? Reprod Biomed Online. 12:587, 2006. Lydic ML, et al. Chromium picolinate improves insulin sensitivity in obese subjects with polycystic ovary syndrome. Fertil Steril. 86:243, 2006. Mascitelli L, Pezzetta F. Polycystic ovary syndrome. N Engl J Med. 352:2756, 2005. Pinhas-Hamiel O, et al. Clinical and laboratory characteristics of adolescents with both polycystic ovary disease and anorexia nervosa. Fertil Steril. 85:1849, 2006.

ADRENAL GLAND (CORTEX)

ADRENOCORTICAL INSUFFICIENCY AND ADDISON’S DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 1–2

Hyperpigmentation

Hypersecretion of melanocyte-stimulating hormone

Unchecked secretion of releasing hormones

Anterior pituitary

Lack of negative feedback to control pituitary hypersecretion

Proopiomelanocortin

Hypersecretion of adrenocorticotropin (ACTH)

Hypofunction of adrenal cortex, resulting in inadequate production of cortisol

Asset provided by Anatomical Chart Co.


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DEFINITIONS AND BACKGROUND In adrenocortical insufficiency, the adrenal cortex atrophies with loss of hormones (aldosterone, cortisol, and androgens). Primary adrenal insufficiency in the pediatric population (0–18 years) is most commonly attributed to congenital adrenal hyperplasia, which occurs in about 1 in 15,000 births, followed by Addison’s disease, with a likely autoimmune etiology (Perry et al, 2005). Secondary forms often result from tuberculosis, cancer, or surgery in which the adrenal glands are destroyed or damaged. Of patients with adrenocortical insufficiency, 33% also have diabetes. With T1DM, the expression of organ-specific autoantibodies is very high (Barker et al, 2005), and this suggests a need for careful screening in both of these conditions. Cortisol, a glucocorticoid, affects almost every organ and tissue in the body. Cortisol helps the body respond to stress. Among other tasks, cortisol helps to maintain BP and cardiac functioning, the immune system’s inflammatory response, the effects of insulin in breaking down sugar for energy through metabolism of macronutrients, and proper arousal and well-being. Aldosterone functions to conserve sodium and excrete potassium. When aldosterone is no longer secreted, the following events occur: excretion of sodium takes place, and the body’s store of water decreases, which leads to dehydration, hypotension, and decreased cardiac output. The heart becomes slower due to reduced workload. Increased serum potassium can lead to arrhythmias, arrest, and even death. Primary adrenal insufficiency causes abdominal pain, vomiting, weakness, fatigue, weight loss, dehydration, nausea, diarrhea, hyperpigmented (tan or bronze) skin, hypotension, low serum sodium, high serum potassium, and low corticosteroid levels. It may be temporary or may become a chronic insufficiency. Salt cravings can occur. Type I primary adrenal insufficiency (polyendocrine deficiency syndrome) occurs in children and exhibits underactive parathyroid glands, pernicious anemia, chronic Candida infections, chronic active hepatitis, and slow sexual development. Autoimmune thyroid diseases are often associated with T1DM and Addison’s disease, characterizing the autoimmune polyendocrine syndrome. Type II primary adrenal insufficiency (Schmidt’s syndrome) affects young adults and presents with underactive thyroid gland, slow sexual development, diabetes, vitiligo and changing skin pigmentation. In secondary adrenal insufficiency, which is much more common than the primary form, there is a lack of ACTH. Production of cortisol drops but not production of aldosterone. A temporary form of secondary adrenal insufficiency may occur when a person who has been receiving a glucocorticoid hormone such as prednisone for a long time abruptly stops or interrupts taking the medication. Glucocorticoid hormones, which are often used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, or ulcerative colitis, block the release of both CRH and ACTH. Normally, CRH instructs the pituitary gland to release ACTH. If CRH levels drop, the pituitary is not stimulated to release ACTH, and the adrenals then fail to secrete sufficient levels of cortisol. In secondary adrenal insufficiency, darkening of the skin does not occur, and GI symptoms are less common. Hypoglycemia, anxiety, nausea, and palpitations can occur.

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Addison’s disease is a strict insufficiency state of adrenal hormones, including cortisol and aldosterone. It affects about one in 100,000 people. Autoimmune Addison’s disease is caused by autoreactivity toward the adrenal cortex; T cells seem to be involved. An Addisonian crisis can be precipitated by acute infection, trauma, surgery, or excessive body salt loss. Patients with adrenal insufficiency, although on treatment, have a poor quality of life and an increased mortality (Debono et al, 2009). A normal lifespan is possible if daily medications are taken as prescribed. Delayed and sustained release oral formulations of hydrocortisone will match the more natural circadian rhythms of the body. Adrenalectomy may require steroid replacement therapy, a 2-g sodium diet, and control of carbohydrate to prevent hyperglycemia. Possibly, the addition of dehydroepiandrosterone (DHEA) to the treatment plan may lead to improved well-being and sexual function (Hahner and Allolio, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: Cytotoxic T lymphocyte antigen 4 (CTLA-4), protein tyrosine phosphatase nonreceptor type 22 (PTPN22), major histocompatibility complex class II transactivator (CIITA), and C-lectin type genes (CLEC16A) play a role in the primary form (Michels and Eisenbarth, 2009). Clinical/History Height Weight BMI Diet history BP (decreased) I&O Abdominal x-rays Skin changes

ACTH stimulation test Gluc BUN (increased)  K (increased) Cortisol N balance (decreased) Na (decreased) CRH stimulation  Ca (increased) test Cl2 (decreased) Alb WBC Mg (decreased) (increased) ACTH HbA1c (increased) Lab Work

INTERVENTION OBJECTIVES • Relieve symptoms of hormone deficiency by taking synthetic hormones (but not to excess). • Prevent hypoglycemia; avoid fasting. • Prevent weight loss. Improve appetite and strength. • Modify sodium according to drug therapy. Prevent hyponatremia, especially in warm weather when sodium losses from perspiration are higher than usual. • Prevent dehydration and shock. • Correct diarrhea, hyperkalemia, nausea, and improper medication administration. • If hyperglycemia or diabetes occurs, insulin may be needed.


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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Sodium Intake Assessment Data: Adrenal insufficiency with inadequate intake of medication replacement; recent labs showing elevated potassium and low serum sodium levels. Nutrition Diagnosis (PES): Inadequate sodium intake related to insufficient medication for Addison’s disease as evidenced by high serum potassium and low serum sodium and diet history revealing low sodium intake for the past week. Intervention: Educate about the importance of taking sufficient medication to maintain normal electrolyte levels and when to add salt to the diet. Monitoring and Evaluation: Review of serum electrolytes, quality of life, fewer episodes of Addisonian crisis, diet hx revealing controlled sodium intake as per medical advice.

FOOD AND NUTRITION • During an Addisonian crisis, low BP, low blood glucose, and high levels of potassium can be life threatening. Intravenous injections of hydrocortisone, saline, and dextrose are given by the medical team. • Use a high-protein, moderate-carbohydrate diet. Snacks may be needed. Control carbohydrate amount and frequency according to blood glucose and HgbA1c levels. • Ensure intake of sodium is adequate according to medications given. Monitor potassium levels and adjust diet if needed. • Force fluids (2–3 L) when allowed.

Common Drugs Used and Potential Side Effects • If aldosterone is missing, fludrocortisone (Florinef) is used as an oral, synthetic, sodium-retaining hormone. Be wary about overdosing, with potential side effects of hypertension and ankle edema. Postural hypotension can occur with a dose that is too low. Extra may be needed when exercising or in hot weather. • Long-acting synthetic glucocorticoids, such as oral dexamethasone or prednisone, are given for replacement. Side effects can include loss of calcium, decreased bone density, or risk of osteoporosis. To decrease gastric irritation, take hormones with milk or an antacid. • Signs of insufficient amounts of cortisol replacement include feeling weak and tired all the time, getting sick or vomiting, and anorexia. Weight loss can occur.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

• Help patient individualize diet according to symptoms. During illness or injury, the body normally makes up to 10 times more cortisol than usual. Be prepared to avoid a crisis with a prompt treatment. • Ensure patient does not skip meals. Instruct patient to carry cheese or cracker snack to prevent hypoglycemia. • Discuss simple meal preparation to lessen fatigue. • Discuss food sources of sodium and potassium according to the medical plan. • Use of Medic-Alert identification is recommended. Patients with this condition may need to carry a syringe prefilled with dexamethasone. • Pregnancy is possible, with carefully managed replacement medication. Evidence has accrued that fracture risk might be programmed during intrauterine life, mediated through pituitary-dependent endocrine systems such as insulin, growth hormone, and the HPA (hypothalamic-pituitary-adrenal) system (Cooper et al, 2009).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Adrenal Gland Disorders http://www.nlm.nih.gov/medlineplus/adrenalglanddisorders.html

JAMA – Patient Page for Adrenal Insufficiency http://jama.ama-assn.org/cgi/reprint/294/19/2528.pdf

National Adrenal Diseases Foundation http://www.medhelp.org/nadf/

National Institutes of Health http://www.cc.nih.gov/ccc/patient_education/pepubs/mngadrins.pdf

ADRENOCORTICAL INSUFFICIENCY AND ADDISON’S DISEASE—CITED REFERENCES Barker JM, et al. Autoantibody “subspecificity” in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups. Diabetes Care. 28:850, 2005. Cooper C, et al. Developmental origins of osteoporosis: the role of maternal nutrition. Adv Exp Med Biol. 646:31, 2009. Debono M, et al. Novel strategies for hydrocortisone replacement. Best Pract Res Clin Endocrinol Metab. 23:221, 2009. Hahner S, Allolio B. Therapeutic management of adrenal insufficiency. Best Pract Res Clin Endocrinol Metab. 23:167, 2009. Michels AW, Eisenbarth GS. Autoimmune polyendocrine syndrome type 1 (APS-1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS-2). J Intern Med. 265:530, 2009. Perry R, et al. Primary adrenal insufficiency in children: twenty years experience at the Sainte-Justine Hospital, Montreal. J Clin Endocrinol Metab. 90:3243, 2005.


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ADRENAL GLAND (CORTEX)

HYPERALDOSTERONISM NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND

ASSESSMENT, MONITORING, AND EVALUATION

Hyperaldosteronism is an increased production of aldosterone by the adrenal cortex. Aldosterone controls water and electrolyte balance by acting on mineralocorticoid receptors in the kidney and in the vascular system (Oberliethner, 2005). Hyperaldosteronism causes endothelial dysfunction regardless of high BP. Patients may be quite vulnerable to cardiac events, including stroke (Milliez et al, 2005). Primary aldosteronism (PA) is usually from an adenoma and involves hypertension, hypokalemia, and low plasma renin. Familial hyperaldosteronism type I (FH-I) represents about 1% of cases of primary hyperaldosteronism. It may be detected in asymptomatic individuals when screening the offspring of affected individuals, or patients may present in infancy with hypertension, weakness, and failure to thrive due to hypokalemia. It is inherited in an autosomal dominant manner. Conn’s syndrome is a benign tumor in one adrenal gland that can cause this condition. Urine 18-hydroxycortisol (18OHF) measurements are used to detect Conn’s syndrome with adrenal adenoma or glucocorticoid-suppressible hyperaldosteronism (Reynolds et al, 2005). Secondary forms of aldosteronism may occur after cancer, heart failure, hyperplasia, malignant hypertension, pregnancy, estrogen use, or cirrhosis. Aldosteronism is a diagnosis that should be considered in refractory hypertension. CT, MRI, and adrenal vein sampling (AVS) distinguish unilateral PA from the bilateral form; the unilateral form can be treated surgically, whereas bilateral PA is treated medically (Kempers et al, 2009).

CLINICAL INDICATORS Genetic Markers: Primary hyperaldosteronism may be the cause of essential hypertension in some people. Specific DNA mutations have emphasized the role of molecular genetics in this disorder (New et al, 2005). ECG with abnor- Aldosterone: renin ratio malities from Height low K levels Urine sodium Weight (altered) BMI Lab Work Urine 18Diet history hydroxycortiSodium load I&O sol (18-OHF) test (6 g BP (high) Na (altered) common) Fatigue K (low) Plasma Headache Urine potassium renin (low) Weakness, (altered) intermittent Plasma Ca aldosterone paralysis Mg (altered) (elevated) Numbness pCO2 (altered) Urinary Abdominal CT H&H aldosterone scan for adreSerum Fe (elevated) nal mass Clinical/History

INTERVENTION SAMPLE NUTRITION CARE PROCESS STEPS Excessive Sodium Intake Assessment Data: Hypertension (190/95); diet hx indicating daily use of high sodium foods and salty snacks. Nutrition Diagnosis (PES): Excessive sodium intake related to intake of high sodium foods and frequent salty snacks throughout the day as evidenced by dietary recall and food records estimated at about 8–9 g Na daily. Intervention: Food-nutrient delivery—limit dietary sources of sodium to 2–4 g sodium; monitor effects of medication. Educate about sources of sodium, potassium, and use of the DASH diet plan as appropriate. Counsel about ways to reduce sodium from foods and snacks; how to dine away from home; how to monitor for signs and symptoms requiring medical attention. Monitoring and Evaluation: Lower BP; normal serum labs, especially potassium. Diet history indicating great improvement in sodium regulation. Able to verbalize use of the DASH diet principles.

OBJECTIVES • • • •

Hydrate adequately. Alter diet as needed (sodium, potassium). Correct hypokalemia and hypertension. Prepare for surgery if a tumor is involved. Laparoscopic adrenalectomy (LA) is quite successful, after which BP returns to normal. If a tumor is not involved, medical treatment will be for life.

FOOD AND NUTRITION • Provide adequate fluid intake (unless contraindicated for other reasons). • A sodium-restricted diet may be needed. A high potassium intake and the DASH diet may be required, depending on the medical or surgical treatment used. • Small, frequent feedings may be needed.


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Common Drugs Used and Potential Side Effects • Antihypertensives may be used; monitor side effects specifically for the medications prescribed. Aldosterone antagonists have been available for many decades; spironolactone may be used alone or with ACE inhibitors or ARBs. • Eplerenone, a selective aldosterone antagonist, avoids the androgen and progesterone receptor–related adverse events that sometimes occur with spironolactone, such as breast tenderness, gynecomastia, sexual dysfunction, and menstrual irregularities (Pratt-Ubunama et al, 2005). • Digitalis may be used. Avoid herbal teas, high-fiber intakes, and excessive amounts of vitamin D. Include adequate amounts of potassium. Take the drug 30 minutes before meals.

• Have patient avoid fasting, skipping meals, and fad dieting. • Provide recipe suggestions. • Avoid consuming large amounts of real licorice, which can aggravate the condition.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Medline http://www.nlm.nih.gov/medlineplus/ency/article/000330.htm

Merck manual – Hyperaldosteronism http://www.merck.com/mmhe/sec13/ch164/ch164e.html

National Adrenal Foundation – Hyperaldosteronism http://www.nadf.us/diseases/hyperaldosteronism.htm

Herbs, Botanicals, and Supplements HYPERALDOSTERONISM—CITED REFERENCES • Herbs and botanical supplements should not be used without discussing with physician. • Products containing natural licorice should be avoided in this condition.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain altered sodium and potassium requirements. Teach principles of the DASH diet.

ADRENAL GLAND (MEDULLA)

PHEOCHROMOCYTOMA NUTRITIONAL ACUITY RANKING: LEVEL 1

Kempers MJ, et al. Systematic review: diagnostic procedures to differentiate unilateral from bilateral adrenal abnormality in primary aldosteronism. Ann Intern Med. 151:329, 2009. Milliez P, et al. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J Am Coll Cardiol. 45:1243, 2005. New MI, et al. Monogenic low renin hypertension. Trends Endocrinol Metab. 16:92, 2005. Oberleithner H. Aldosterone makes human endothelium stiff and vulnerable. Kidney Int. 67:1680, 2005. Pratt-Ubunama MN, et al. Aldosterone antagonism: an emerging strategy for effective blood pressure lowering. Curr Hypertens Rep. 7:186, 2005. Reynolds RM, et al. The utility of three different methods for measuring urinary 18-hydroxycortisol in the differential diagnosis of suspected primary hyperaldosteronism. Eur J Endocrinol. 152:903, 2005.


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DEFINITIONS AND BACKGROUND Pheochromocytoma (PHEO) is a rare tumor of the chromaffin cells most commonly arising from the adrenal medulla, resulting in increased secretion of epinephrine and norepinephrine. It is slightly more common in males. Hereditary PHEOs are typically intra-adrenal and bilateral, and patients typically present at a young age. PHEO may occur as a single tumor or as multiple growths. Symptoms and signs include very high BP, headache, excessive diaphoresis, and palpitations. Less-common symptoms are anxiety, chest pain, fatigue, weight loss, abdominal pain, and nervousness. About 10% of these tumors are malignant and can spread. Persons who have difficult-to-treat hypertension, have onset before age 35 or after age 60, or are taking four or more BP medicines may need to be tested for PHEO. BP often fluctuates up and down, daily testing is recommended. Diagnosis includes measurement of urinary catecholamines or their metabolites, vanillylmandelic acid and total metanephrines. The urinary metanephrines provide a highly sensitive clue to the presence of PHEO; see Table 9-22. Treatment usually involves surgical removal of the tumor. Before surgery, alpha-adrenergic blockers may be used. After surgery, about one quarter of patients will still suffer from hypertension and require lifelong management.

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endocrine neoplasia. Type IIB (MEN IIB) also leads to thyroid cancer and tumors of nerves in the lips, mouth, eyes and digestive tract. The NF1 neurofibromas may present with café-au-lait spots, an optic glioma, and PHEO. Clinical/History Height Weight BMI Diet history Increased appetite BP (very elevated) Orthostatic hypotension Headache Excessive diaphoresis, flushing Intolerance of heat

Heart palpitations Sleep disturbances CT scan, MRI Adrenal biopsy Metaiodobenzylguanidine (MIBG) scanning Lab Work (see Table 9-22) Urinary epinephrine and norepinephrine (increased)

Urinary metabolites (vanillylmandelic acid and metanephrines)* Gluc Na, K Alb CRP H&H Glucagon test (positive) T3, T4

*Testing may require dietary changes up to 3 days in advance.

ASSESSMENT, MONITORING, AND EVALUATION INTERVENTION CLINICAL INDICATORS Genetic Markers: PHEO may be transmitted as an autosomal dominant trait. At least five different gene mutations can cause PHEO. One type causes multiple

OBJECTIVES • Prepare for surgery to remove tumor. Patients with preoperative endocrinopathies present a challenge because the “endocrine axis” is complex (Kohl and Schwartz, 2009). If the tumor cannot be removed, lifelong medication will be needed.

TABLE 9-22 Catecholamines Catecholamine

Comments

Normal Urinary Value/24 h

Dopamine

A neurotransmitter (a chemical used to transmit impulses between nerve cells) found mainly in the brain. Metabolized by target tissues or by the liver to become inactive substances that appear in the urine—dopamine becomes homovanillic acid.

Dopamine

Epinephrine

Norepinephrine

A brain neurotransmitter, but is also a major hormone secreted from the adrenal medulla in response to low blood glucose, exercise, and various forms of stress where the brain stimulates release of the hormone. Epinephrine causes a breakdown of glycogen to glucose in liver and muscle, the release of fatty acids from adipose tissue, vasodilation of small arteries within muscle tissue, and increases in the rate and strength of the heartbeat. In the urine: epinephrine becomes metanephrine and VMA. The primary neurotransmitter in the sympathetic nervous system (controls the “fight or flight” reaction) and is also found in the brain. In the urine: norepinephrine becomes normetanephrine and vanillylmandelic acid (VMA).

Total

*For testing, a VMA-restricted diet may be required for lab results; omit chocolate, vanilla extract, and citrus. Source: Medline Plus. Catecholamines–urine. Accessed September 22, 2009, at http://www.nlm.nih.gov/medlineplus/ency/article/003613.htm

65–400 g Epinephrine 0.5–20 g Metanephrine: 24–96 g VMA: 2–7 mg*

Norepinephrine 15–80 g Normetanephrine: 75–375 g Total urine catecholamines: 14–110 g


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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Intake of Bioactive Substances Assessment Data: Hypertensive crisis following intake of caffeine and Chianti wine. Dx of PHEO; high levels of urinary epinephrine and norepinephrine, as well as vanillylmandelic acid and metanephrines. Diet history reveals recent intake of coffee, chocolate and Chianti wine at dinner meal, causing extreme heart palpitations and soaring BP. Nutrition Diagnosis (PES): Excessive intake of bioactive substances (caffeine, tyramine) related to coffee, chocolate and Chianti wine as evidenced by very high BP and diet history. Intervention: Education about foods to avoid, such as caffeine from food and beverages, tyramine-rich foods including beer, Chianti wine, processed meats, soy sauce, bananas, avocado. Monitoring and Evaluation: No further hypertensive crises related to food and beverage intake.

• Stabilize BP before surgery. Avoid overstimulation from even slight exercise, cold stress, or emotional upsets. • Correct nausea, vomiting, and anorexia. • Manage long-term hypertension. A severe BP level is any reading above 180/110 mm Hg. Prevent hypertensive crises, which could cause sudden blindness, kidney failure, seizures, acute respiratory distress, arrthymias or stroke. • Manage any complications such as heart attack or cardiomyopathy (Kassim et al, 2008).

• Phenoxybenzamine (or an alpha-1 adrenergic receptor antagonist such as prazosin) is needed to block alphaadrenergic activity. Diuretics should not be used. • Low doses of a beta-blocker such as propranolol are used to control BP and cardiac tachyarrhythmias but only after alpha blockade. Labetalol, an alpha- and beta-adrenergic blocker, has also been shown to be effective in the control of BP and symptoms of PHEO. • Avoid decongestants, amphetamines, MAO inhibitors (Nardil, Parnate). • High-dose MIBG may be used in the treatment of malignant PHEO but can have toxic side effects (Gonias et al, 2009). • If diabetes occurs, insulin may be needed.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss avoidance of caffeinated foods and beverages (e.g., coffee, tea, and chocolate). • Maintain a calm atmosphere for patient; prevent undue stress. • Exercise should be limited until condition is under control.

Patient Education—Foodborne Illness

FOOD AND NUTRITION • For urine testing, some doctors order a VMA diet where patient avoids bananas, caffeine from coffee or Pepsi/Coke, chocolate, tea, vanilla in foods, pineapple, alcoholic beverages, eggplant, plums, walnuts. While this was a common practice in the past, there is no strong evidence to support its use. • Increase fluids but avoid caffeinated beverages. Avoid tyramine-rich foods, especially if taking MAO inhibitors. • Six small feedings may be better tolerated than large meals. • Increase protein and calories if patient is having surgery. Postoperatively, provide adequate vitamins and minerals for wound healing. • Re-expansion of plasma volume may be accomplished by liberal salt or fluid intake with use of alpha-1 adrenergic receptor antagonists. • In recurrent cases, long-term drug therapy will be needed. Monitor for specific dietary changes and side effects.

Common Drugs Used and Potential Side Effects • Pharmacological treatment of catecholamine excess is mandatory.

• If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

Endocrine Web http://www.endocrineweb.com/pheo.html

Mayo Clinic http://www.mayoclinic.com/health/pheochromocytoma/DS00569

Medline http://www.nlm.nih.gov/medlineplus/ency/article/000340.htm

Merck Manual http://www.merck.com/mrkshared/mmanual/section2/ chapter9/9d.jsp

National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/ pheochromocytoma/patient

National Library of Medicine http://www.nlm.nih.gov/medlineplus/pheochromocytoma.html

Urology Health http://www.urologyhealth.org/adult/index.cfm?cat04&topic114

PHEOCHROMOCYTOMA—CITED REFERENCES Gonias S, et al. Phase II study of high-dose [131I]metaiodobenzylguanidine therapy for patients with metastatic pheochromocytoma and paraganglioma. J Clin Oncol. 27:4162, 2009. Kassim TA, et al. Catecholamine-induced cardiomyopathy. Endocr Pract. 14:1137, 2008. Kohl BA, Schwartz S. Surgery in the patient with endocrine dysfunction. Med Clin North Am. 93:1031, 2009.


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THYROID GLAND

HYPERTHYROIDISM NUTRITIONAL ACUITY RANKING: LEVEL 1

Overactive Thyroid Bulging eyes Face is thin from weight loss Swelling of neck (goiter)

Broken lines indicate normal size of thyroid.

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Hyperthyroidism results from oversecretion of the thyroid hormones, triiodothyronine (T3) or thyroxone (T4). These hormones affect every cell through controlling body temperature, heart rate, metabolism, and production of calcitonin. Thyroid hormone affects glucose homeostasis through increased hepatic glucose output, increased futile cycling of glucose degradation products between the skeletal muscle and the liver, decreased glycogen stores in the liver and skeletal muscle, altered oxidative and nonoxidative glucose metabolism, decreased active insulin output from the pancreas, and increased renal insulin clearance (Potenza et al, 2009). When the hypothalmus signals the pituitary gland to produce TSH, normally this is regulated to be just enough. See Table 9-23 for interpretation of lab results for thyroid disorders. The autoimmune thyroid diseases (AITD), Graves’ disease, and chronic lymphocytic thyroiditis (CLT) are among the most common endocrine diseases in childhood and adolescence (Brown, 2009). Usually in hyperthyroidism, the

TABLE 9-23 Thyroid Test Results TSH

T4

T3

Interpretation

High

Normal

Normal

Mild (subclinical) hypothyroidism

High

Low

Low or normal

Hypothyroidism

Low

Normal

Normal

Mild (subclinical) hyperthyroidism

Low

High or normal

High or normal

Hyperthyroidism

Low

Low or normal

Low or normal

Nonthyroidal illness; rare pituitary (secondary) hypothyroidism

Source: Lab Tests On Line, web site accessed October 25, 2009, at http://www.labtestsonline.org/understanding/analytes/t3/test.html

entire gland is overproducing thyroid hormone. Rarely, a single nodule is responsible for the excess hormone secretion. An elevated metabolic rate, tissue wasting, diaphoresis, tremor, tachycardia, goiter, heat intolerance, cold insensitivity, nervousness, increased appetite, exophthalmos, and loss of glycogen stores can occur. If left untreated, atrial fibrillation and osteoporosis can result. Autoimmune thyroiditis (AITD) may start out temporary, then lead to hyperthyroidism. The most common causes include Hashimoto’s thyroiditis, subacute granulomatous thyroiditis, or silent lymphocytic thyroiditis. The major environmental triggers of AITD include iodine, medications, infection, smoking, and possibly stress (Tomer and Huber, 2009). Specific digestive diseases (celiac disease or primary biliary cirrhosis) may be associated with autoimmune thyroid processes (Daher et al, 2009). Persons who have T1DM, mood disorders, psychosis, or Addison’s disease also seem to be at higher risk. Graves’ disease (diffuse toxic goiter) is the most common form; thyrotoxicosis is more severe. Clinical thyrotoxicosis in Graves’ disease patients is caused by thyrotropin receptor (TSHR)-stimulating autoantibodies (Schott et al, 2005). Most people who develop Graves’ ophthalmopathy have one or more of the following symptoms: dry and itchy eyes, a staring or bug-eyed look (exophthalmos), sensitivity to light, excessive tearing, a feeling of pressure around the eyes, difficulty closing the eyes completely, and peripheral double vision. Thyrotoxicosis can alter carbohydrate metabolism in a type 2 diabetic patient to such an extent that DKA develops if untreated (Potenza et al, 2009). Thyroid storm (thyroid crisis) is a potentially life-threatening condition that develops in a person with hyperthyroidism. The gland suddenly releases large amounts of thyroid hormone in a short period of time. Signs of thyroid storm include extreme irritability, high systolic BP, low diastolic BP, tachycardia, nausea, vomiting, diarrhea, high fever, confusion, and sleepiness. Shock, delirium, shortness of breath, fatigue, coma, heart failure, and death can result if not treated immediately. Emergency medical treatment is always needed. If thyroidectomy is needed, antithyroid agents and iodine are often given 4–6 weeks before surgery to minimize the risk of thyroid crisis. With thyroidectomy, the patient may require a high-calorie, high-protein diet preoperatively. Evaluate needs postoperatively with the doctor’s care plan.

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: In Graves’ disease a specific combination of polymorphisms for thyroglobulin and HLA-DR markedly increases the odds ratio for developing disease


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(Brown, 2009). Among the major AITD susceptibility genes that have been identified is the HLA-DR gene locus, as well as CTLA-4, CD40, PTPN22, thyroglobulin, and TSH receptor genes (Tomer and Huber, 2009). Clinical/History Height Weight BMI Rapid weight loss? Diet history Temperature BP I&O Nervousness, anxiety Tachycardia or palpitations Increased sensitivity to heat Difficulty sleeping Fine tremor of hands

More frequent bowel movements Fatigue, muscle weakness Changes in menstrual habits Protruding eyeballs? Excessive tearing from one or both eyes? Thyroid scan Goiter (enlarged thyroid gland) Lab Work T3 (increased) T4 (increased)

TSH (normal or low) Protein-bound iodine (PBI) Gluc (increased) Alb, transthyretin Ca Mg (decreased) Na, K H&H Serum ferritin Chol, Trig (decreased) BUN, Creat N balance Alk phos (increased)

INTERVENTION OBJECTIVES • Achieve a euthyroid state to avoid the effects of triiodothyronine (T3) on the heart and cardiovascular system: decreased systemic vascular resistance and increased resting heart rate, left ventricular contractility, blood volume, and cardiac output (Dahl et al, 2008). • Prevent or treat complications accompanying high metabolic rate, including bone demineralization. This seems to be a greater problem in older women than in adolescents (Poomthavorn et al, 2005). • Replenish glycogen stores. Replace lost weight (usually 10–20 lb). • Correct negative nitrogen balance. • Replace fluid losses from diarrhea, diaphoresis, and increased respirations. However, exophthalmos, caused by increased accumulation of extracellular fluid in the eyes, may require fluid and salt restriction. • Monitor or treat fat intolerance and steatorrhea.

FOOD AND NUTRITION • Use a high-calorie diet (start with 40 kcal/kg). The patient’s caloric needs may be increased by 50–60% in this condition (or 10–30% in mild cases). Ensure adequate intake of carbohydrates. • Provide protein in the range of 1–1.75 g/kg body weight. • Fluid intake should be 3–4 L/d, unless contraindicated by renal or cardiac problems.

SAMPLE NUTRITION CARE PROCESS STEPS Altered Nutrient Utilization Assessment Data: Elevated T3 and T4, low TSH and serum calcium; BMI 18 with weight loss of 15 lb in 6 months. Dx hyperthyroidism. Nutrition Diagnosis (PES): Altered nutrient utilization (NC-2.1) related to hyperthyroidism as evidenced by elevated T4 of 112 g/100 mL; T3 of g/100 mL; low TSH level at 0.10 U/L; low serum calcium levels; weight loss of 15 lb in less than 6 months. Interventions: Food and Nutrition Delivery: ND-1.3 provide information on high calorie diet to promote weight gain, ensure high carbohydrate intake, importance of 1 quart of milk daily or equivalent, caffeine to be avoided, be cautious of raw goitrogens ND-3.2.1 continue use of daily multivitamin. ND3.2.4 continue use of daily calcium supplement. Nutrition Education: E-1.1 Discuss importance of high calorie diet (40 kcal/kg/d) to promote weight gain consisting of following healthy eating habits and to discuss interaction of raw natural goitrogens with antithyroid drugs. Counseling: C-2.2 RD to work with patient to set goals of weight gain and taking antithyroid drug to be prescribed by MD. Coordination of Care: RC-1.3 Collaboration with MD and referral to endocrinologist, to speak with MD about weight gain of 1–2 lb per week and drug–food interactions. Monitoring and Evaluation: Prevent the thyroid from producing excess hormones with use of antithyroid drug, Tapazole. Follow a weight gain of 1–2 lb/wk till patient reaches normal body weight range of 125–130 lb. Daily use of multivitamin and calcium supplementation. Successful food recording in food diary. Patient can recite raw natural goitrogens to be avoid them in her diet. Patient eating frequent snacks. Patient successfully gained 1 lb in 2 weeks bringing her weigh to 116 lb, BMI now 19.3. Patient to visit endocrinologist in next week.

• Include 1 quart of milk or equivalent daily to supply adequate calcium, phosphorus, and vitamin D. • Exclude caffeine and stimulants from diet because they aggravate excitability and nervousness. • Supplement diet with vitamins A, C, and B-complex vitamins, especially thiamin, riboflavin, B6, and B12. A general multivitamin–mineral supplement may be beneficial; monitor for iodine content. • Be aware of iodine in any supplements used. Chronic iodine intakes greater than 500 g/L are associated with adverse effects (Zimmermann et al, 2005). • Raw natural goitrogens (cabbage, Brussels sprouts, kale, cauliflower, soybeans, peanuts) should not be used with antithyroid medications because these substances increase side effects of the drugs. Cooking reduces this effect.

Common Drugs Used and Potential Side Effects • The goal of drug therapy is to prevent the thyroid from producing excess hormones. Antithyroid drugs, also called thionamides, such as methimazole (Tapazole) and propylthiouracil (PTU), can cause nausea, vomiting,


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altered taste sensation, and gastrointestinal distress. They should be taken with food. Avoid use of natural goitrogens in raw form; cooked forms are not a problem. • Thionamides represent the treatment of choice in pregnant women, during lactation, in children and adolescents, and in preparation for radioiodine therapy or thyroidectomy (Bartelena et al, 2005). • Radioactive iodine may be used to damage or destroy some of the thyroid cells. It can cause a temporary burning sensation in the throat. Hydrochlorothiazide (HCTZ) may be used to improve radioiodine uptake in hyperthyroid patients; replace potassium. • Some drugs can affect the thyroid glands. Amiodarone is a potent antiarrhythmic drug that also possesses betablocking properties; a 100-mg tablet contains an amount of iodine that is 250 times the recommended daily iodine requirement. Amiodarone-induced thyrotoxicosis is a difficult condition to diagnose and treat; monitor carefully (Basaria and Cooper, 2005).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. Bugleweed, verbena, lemon balm and kelp have been recommended; no clinical trials prove efficacy. • Limit use of large quantities of iodine-rich seaweed such as kombu (Laminaria japonica).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Thyroid hormone affects adipokines and adipose tissue, predisposing the patient to ketosis (Potenza et al, 2009). Beware of hyperglycemia after carbohydrate-rich meals. • Encourage quiet, pleasant mealtimes.

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• Exclude use of alcohol, which may cause a hypoglycemic state. • Frequent snacks may be needed. To avoid obesity, adjust patient’s diet as condition corrects itself.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Thyroid Association http://www.thyroid.org/

Endocrine Web–Hyperthyroidism http://www.endocrineweb.com/hyper1.html

European Thyroid Society http://www.eurothyroid.com/

Latin American Thyroid Society http://www.lats.org/

National Graves Disease Foundation http://www.ngdf.org/

University of Maryland Medical Center http://www.umm.edu/endocrin/hypert.htm

HYPERTHYROIDISM—CITED REFERENCES Bartelena L, et al. An update on the pharmacological management of hyperthyroidism due to Graves’ disease. Expert Opin Pharmacother. 6:851, 2005. Basaria S, Cooper DS. Amiodarone and the thyroid. Am J Med. 118:706, 2005. Brown RS. Autoimmune thyroid disease: unlocking a complex puzzle. Curr Opin Pediatr. 21:523, 2009. Daher R, et al. Consequences of dysthyroidism on the digestive tract and viscera. World J Gastroenterol. 15:2834, 2009. Dahl P, et al. Thyrotoxic cardiac disease. Curr Heart Fail Rep. 5:170, 2008. Poomthavorn P, et al. Exogenous subclinical hyperthyroidism during adolescence: effect on peak bone mass. J Pediatr Endocrinol Metab. 18:463, 2005. Potenza M, et al. Excess thyroid hormone and carbohydrate metabolism. Endocrin Pract. 15:254, 2009. Schott M, et al. Thyrotropin receptor autoantibodies in Graves’ disease. Trends Endocrinol Metab. 16:243, 2005. Tomer Y, Huber A. The etiology of autoimmune thyroid disease: a story of genes and environment. J Autoimmun. 32:231, 2009. Zimmermann MB, et al. High thyroid volume in children with excess dietary iodine intakes. Am J Clin Nutr. 81:840, 2005.

THYROID GLAND

HYPOTHYROIDISM NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND

Asset provided by Anatomical Chart Co.

Hypothyroidism is caused by the underfunctioning of the thyroid gland. It can be classified as primary (thyroid failure), secondary (from pituitary TSH deficit), or tertiary (from hypothalamic deficiency of thyrotropin-releasing hormone) or result from peripheral resistance to the action of thyroid hormones. Primary hypothyroidism causes about 95% of all cases. The most common cause of thyroid gland failure is Hashimoto’s thyroiditis, which is inflammation caused by the patient’s own antibodies (as in pernicious anemia, lupus, rheumatoid arthritis, diabetes, or chronic hepatitis). The


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second major cause of thyroid gland failure is from various medical treatments that affect the thyroid gland (e.g., surgery, chronic medication use). Hypothyroidism affects up to 10% of adult women, usually middle-aged and older women. Women may experience menstrual irregularities or difficulty conceiving. Triiodothyronine (T3) and thyroxine (T4) are elevated during pregnancy and with oral contraceptive and estrogen use. Physicians must treat hypothyroidism to avoid long-term complications, such as depression, infertility, and CVD. Risk decreases if thyroid hormones are taken as directed. Congenital hypothyroidism (CH) or cretinism is rare; incidence is one in 4000 births. Screening for this type of hypothyroidism is now common (Lanting et al, 2005). Treatment involves replacement of thyroid hormones and iodine. Cretinism can occur in areas where soil content of iodine is low. Myxedema is a nonpitting edema that can occur in adults with hypothyroidism; hydrophilic mucopolysaccharide accumulates in the skin and muscles. In end-stage myxedema coma, untreated hypothyroidism leads to progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock, and even death. It occurs most often in older patients with underlying pulmonary and vascular disease. Signs and symptoms of hypothyroidism are listed in Table 9-24. Thyroid autoimmunity is common and may contribute to miscarriages as well as to hypothyroidism. Infants are totally dependent on T4 from the mother during the first trimester for normal neurological development (Smallridge et al, 2005). Hypothyroidism from autoimmune disease or suboptimal iodine intake occurs in 2.5% of pregnant women; postpartum thyroid dysfunction (PPTD) occurs in 5â&#x20AC;&#x201C;9% of women (Lazarus and Premawardhana, 2005). Because of the potential problems for mother and baby, screening, diagnosis, and treatment of thyroid problems among pregnant women is important. Endemic goiter is an enlargement of the thyroid gland with swelling in front of the neck, resulting from iodine deficiency due to inadequate dietary intake or drug effects. Over 3 billion people in the world are on iodine supplementation programs. Optimal level of iodine intake to prevent thyroid disease is in a relatively narrow range around the recommended daily iodine intake of 150 g. Subclinical hypothyroidism (SCH) is mild thyroid failure and is diagnosed when peripheral thyroid hormone levels are within normal reference laboratory range but serum TSH levels are mildly elevated (Fatourechi, 2009). Iodine, iron, selenium, and zinc deficiencies can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid Peroxidase; iron supplementation may improve the efficacy of iodine supplementation. Anemia is a major manifestation in hypothyroidism not only because of impaired hemoglobin synthesis, but also because of iron deficiency from increased iron loss with menorrhagia, impaired intestinal absorption of iron, folate deficiency due to impaired intestinal absorption of folic acid, and pernicious anemia with vitamin B12 deficiency. Selenium deficiency and disturbed thyroid hormone status may develop in phenylketonuria, cystic fibrosis, as well as from poor nutrition in children, elderly people, or sick patients. In parts of the world where iodine and selenium are both deficient, dual supplementation may be advisable.

TABLE 9-24

Symptoms of Hypothyroidism By Life Stage

Infants Constipation Cyanosis Developmental delay Hoarse cry Marked retardation of bone maturation Persistent jaundice Poor feeding Respiratory difficulty Somnolence Umbilical hernia Children Evidence of mental retardation Poor performance at school Retarded growth Stunting, short stature Adults Abnormal menstrual cycles Brittle nails Broad flat nose Coarse features with protruding tongue Coarse, dry hair Cold intolerance Dry, rough pale skin Decreased libido Delayed dentition Difficulty losing weight Easy fatigue Hair loss Hoarse, husky voice Impaired mental development Muscle cramps, frequent muscle aches Puffy hands and face Reduced conversion of carotene to vitamin A Short stature Weakness Weight gain Widely set eyes

Vitamin A deficiency (VAD) and the iodine deficiency disorders (IDD) affect 30% of the global population; these deficiencies often coexist in vulnerable groups (Zimmerman, 2007). Given alone, without iodine repletion, high-dose vitamin A supplementation in combined VAD and ID may reduce thyroid hyperstimulation and reduce risk for goiter (Zimmerman, 2007). More research on vitamin and mineral therapies will be beneficial.


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ASSESSMENT, MONITORING, AND EVALUATION

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SAMPLE NUTRITION CARE PROCESS STEPS Overweight (NC-3.3) Assessment Data: Low serum levels of T4 and T3 with increased TSH. Unplanned weight gain of 30 lb in past 2 years. Recent Dx of hypothyroidism and initiation of synthroid. BMI 30.

CLINICAL INDICATORS

Nutrition Diagnosis (PES): Overweight (NC-3.3) as related to excess food and nutrition related knowledge deficit and hypothyroidism as evidenced by reports of overconsumption of high fat/calorie dense food and beverages, BMI 30, waist circumference 40 inches, and a fat mass of 51.7%.

Genetic Markers: Mutations in the DUOX2, PAX8, SLC5A5, TG, TPO, TSHB, and TSHR genes cause congenital hypothyroidism. Clinical/History Ca (see Table 9-24) Mg (increased) Height H&H Weight (decreased) BMI Serum ferritin Diet history Chol, Trig Temperature (increased) BP Gluc Goiter? Alk phos Thyroid scan (decreased) Serum copper Lab Work (decreased) T4 (decreased) Na and K T3 (decreased) (decreased) TSH (elevated) Serum folic acid Urinary iodine and vitamin concentration B12 (low) (UIC)

Creatine phosphokinase (CPK) GFR (decreased?) Thyrotropin Somatomedin C (increased) Uric acid (increased) Carotenoids (increased) Thyroglobulin (useful measure after introducing iodized salt) Serum vitamin D3

Interventions: Nutrition prescription (ND-1) of a weight control/ exercise plan with promotion of a diet including 30–40% fat, 45–50% complex carbohydrates, and 15–20% protein with a goal of cutting out 250–500 calories a day resulting in a 0.5–1 lb weight loss each week. Recommend adequate intake of fluid and foods high in fiber. Support use of Synthroid 25 g once daily. Initial/Brief nutrition education (E-1) to begin instruction on following a weight control/exercise plan with a diet including 30–40% fat, 45–50% complex carbohydrates, and 15–20% protein with a goal of cutting out 250–500 calories a day and provide basic nutrition related educational information on natural goitrogens, fiber, fluids, use of iodized salt, and physical activity. Monitoring and Evaluation: Follow up in 1 month to repeat a TSH and free T4 to reassess thyroid function status; repeat TSH and free T4 and adjust dose of Synthroid accordingly. Evaluate progress in weight loss and healthy eating habits. Schedule a counseling session for in-depth nutrition related knowledge regarding weight loss as well as hypothyroidism.

INTERVENTION OBJECTIVES • Control weight gain that results from a 15–40% slower metabolic rate, especially in the untreated patient. Measure weight frequently to detect fluid losses or retention. • Correct underlying causes, such as inadequate intake of iodine or congenital deficiency. Hormone replacement will be given. • Correct vitamin B12, folic acid, or iron deficiency anemias when present. • Because vitamin D3 has implications in autoimmune disorders, assure an adequate diet and supplementary source as needed. • Improve energy levels; reduce fatigue. • Improve cardiac, neurological, and renal functioning. • Screen for thyroid problems in pregnant or postpartum women; assure hormone replacement as needed.

• • •

poorly absorbed. Since T3 is an important hormone needed for vitamin A metabolism, serum levels may be low in this population. Include good sources of carotenoids such as lycopene. Ensure an adequate supply of antioxidant and fiber-rich foods as well as fluids. For pregnant women or children, make sure that adequate amounts of iodine are consumed. Natural goitrogens in cabbage, turnips, rapeseeds, peanuts, cassava, cauliflower, broccoli, and soybeans may block uptake of iodine by body cells; they are inactivated by heating and cooking. Achieve optimal iodine intakes from iodized salt (in the range of 150–250 g/d for adults) to minimize thyroid dysfunction (Zimmerman, 2009). Zinc, copper, and tyrosine are needed. Ensure adequate iodine status during parenteral nutrition, particularly in preterm infants (Zimmerman, 2009).

Common Drugs Used and Potential Side Effects FOOD AND NUTRITION • Use an energy-controlled diet adjusted for age, sex, and height. • A multivitamin–mineral supplement formula may be beneficial, especially to replace nutrients that have been

• Thyroid hormones (liotrix, sodium levothyroxine, or Synthroid) are used. Use caution with use of soy protein products since they can decrease effectiveness of the hormones. Thyroid hormones elevate glucose and decrease cholesterol; monitor persons who have diabetes carefully. Monitor


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for weight changes and fluid shifts. If rapid weight loss, sweating, or other symptoms of hyperthyroidism occur, the doctor should be contacted for immediate follow-up. • Lithium treatment for bipolar disorder has been associated with the development of goiter. Monitor patients closely.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Avoid kelp tablets and “thyroid support” supplements. Gentian, walnut, mustard, radish, and St. John’s wort have been recommended, but no clinical trials have proven efficacy. • Curcumin and vitamins A, B12, D3, and E may be beneficial; longer human studies are needed. • If large quantities of iodine-rich seaweed such as kombu (Laminaria japonica) are consumed, use should be monitored in patients who take thyroid replacement hormones.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss goitrogens in cabbage and Brassica vegetables, turnips, rapeseeds, peanuts, cassava, and soybeans; they are inactivated by heating and cooking. • Encourage use of iodized salt, as permitted. Avoid selfmedication with iodine supplements. • Encourage adequate fluid intake. • Women who are considering pregnancy may want to be screened to rule out thyroid problems. If their iodine intake is low, or if they live in an area without use of iodized salt, they may need an iodine supplement prescribed from their physician. A normal urinary iodine level would be 150–249 g/L. • In many developing countries, children are at high risk of iodine deficiency, VAD, and iron deficiency anemia. Select the proper supplements.

• Because subclinical hypothyroidism is common in individuals who have chronic kidney disease, close monitoring of GFR is recommended (Chonchol et al, 2008). • Exposure to large doses of metals such as lead, molybdenum, or arsenic may reduce thyroid function, with adverse effects on development, behavior, metabolism and reproduction (Meeker et al, 2009).

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Thyroid Association http://www.thyroid.org/

Endocrine Web http://www.endocrineweb.com/hypo1.html

Mayo Clinic http://www.mayoclinic.com/health/hypothyroidism/ DS00353/DSECTIONsymptoms

Synthroid Information http://www.synthroid.com/

HYPOTHYROIDISM—CITED REFERENCES Chonchol M, et al. Prevalence of subclinical hypothyroidism in patients with chronic kidney disease. Clin J Am Soc Nephrol. 3:1296, 2008. Fatourechi V. Subclinical hypothyroidism: an update for primary care physicians. Mayo Clinic Proc. 84:65, 2009. Lanting CI, et al. Clinical effectiveness and cost-effectiveness of the use of the thyroxine/thyroxine-binding globulin ratio to detect congenital hypothyroidism of thyroidal and central origin in a neonatal screening program. Pediatrics. 116:168, 2005. Lazarus JH, Premawardhana LD. Screening for thyroid disease in pregnancy. J Clin Pathol. 58:449, 2005. Meeker JD, et al. Multiple metals predict prolactin and thyrotropin (TSH) levels in men. Environ Res. 109:869, 2009. Smallridge RC, et al. Thyroid function inside and outside of pregnancy: what do we know and what don’t we know? Thyroid. 15:54, 2005. Zimmerman MB. Interactions of vitamin A and iodine deficiencies: effects on the pituitary-thyroid axis. Int J Vitam Nutr Res. 77:236, 2007. Zimmerman MB. Iodine deficiency. Endrocr Rev. 30:376, 2009.

PARATHYROID GLANDS The parathyroid glands have an overall regulatory role with action as a thermostat in the systemic calcium homeostasis to ensure tight regulation of serum calcium concentrations and appropriate skeletal mineralization. Parathyroid hormone (PTH) affects calcium, phosphorus, and vitamin D metabolism by removing calcium from bone to raise serum levels; it promotes hydroxylation of vitamin D to its active form. Calcitonin, in contrast to PTH, decreases serum calcium levels; it is secreted by the thyroid gland. The body secretes PTH in response to hypocalcemia or hypomagnesemia; the hormone then stimulates osteoclasts to increase bone resorption. PTH also stimulates adenyl cyclase to increase renal tubular calcium resorption and phosphate excretion. PTH works with vitamin D to regulate

total body calcium by activating conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, the active form that stimulates calcium and phosphate absorption from the GI tract. Calcitonin, in contrast to PTH, decreases serum calcium levels and is secreted by the thyroid gland. Fibroblast growth factor-23 (FGF23) is a hormone that regulates mineral and vitamin D metabolism (Juppner, 2009). Research on the effects of various genes and hormones in bone homeostasis is on-going.

PARATHYROID GLANDS—CITED REFERENCE Juppner H. Novel regulators of phosphate homeostasis and bone metabolism. Ther Apher Dial. 11:3S, 2007.


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HYPOPARATHYROIDISM AND HYPOCALCEMIA NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Hypoparathyroidism results from a deficiency of PTH from biologically ineffective hormones, damage or accidental removal of the glands, or impaired skeletal or renal response. In the hereditary form, parathyroid glands are either absent or not functioning properly; symptoms appear before age 10. Other causes include magnesium deficiency or neonatal immaturity. If untreated, hypoparathyroidismretardation-dysmorphism (HRD) may result. Cancellous bone in hypoparathyroidism is abnormal, suggesting that PTH is required to maintain normal trabecular structure (Rubin et al, 2010). Hypoparathyroidism with hypocalcemia is one of the most common results of damage to parathyroid glands during surgery; in fact, it may be diagnosed during a workup for hypocalcemia. Vitamin D levels may also be deficient. Intraoperative PTH levels are used widely during parathyroidectomy as an indicator of parathyroid gland function; vitamin D supplementation after surgery may be given to anticipate decreased parathyroid gland function and to avoid symptomatic hypocalcemia (Quiros et al, 2005). Hypoparathyroidism is a chronic condition that requires lifelong treatment with large doses of calcium and vitamin D supplements. Episodes of tetany are treated with calcium given intravenously to provide quick relief of symptoms. Controlled release of physiological concentrations of PTH can be achieved using a surgically implantable controlledrelease delivery system (Anthony et al, 2005).

ASSESSMENT, MONITORING, AND EVALUATION

CLINICAL INDICATORS Genetic Markers: There is a hypoparathyroidism-deafness-renal (HDR) dysplasia syndrome which is an autosomal dominant disorder caused by mutations of the GATA3 gene (Ali et al, 2007). Seizures Muscle cramps Height and tetany Weight Tingling of the BMI lips or fingers Diet history Hair loss, dry skin Weakness, Dental hypoplafatigue sia Hyperreflexia Chronic Chvostek’s sign cutaneous positive (with moniliasis tapping of Abnormal heart facial muscles) rhythms on Irritability or ECG psychosis Clinical/History

Lab Work PTH (low) Ca (serum levels 2.5–3 mg/dL) Urinary Ca (altered) Serum phosphorus (high) Mg (may be low) Na, K

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Mineral Intake Assessment Data: Abnormal labs with low PTH, serum calcium 2.4 mg/dL, high serum phosphorus; positive for Chvostek’s sign and tetany with muscle cramps and abnormal ECG. Diet history indicates no dairy intake for past several years. Medical diagnosis of hypoparathyroidism after thyroid surgery. Nutrition Diagnosis (PES): Inadequate mineral (calcium) intake related to nutritional intake low in calcium and hypoparathyroidism as evidenced by low PTH, low serum calcium (2.4), high serum phosphorus, and signs of tetany. Intervention: Food and nutrient delivery—provide foods rich in calcium (nondairy if necessary) and provide a calcium supplement calculated for body size and age. Educate about the role of calcium in alleviating signs of tetany and abnormal labs. Counsel about nondairy sources of calcium and tips for increasing intake throughout the day. Monitoring and Evaluation: Resolution of low serum calcium and PTH, high phosphorus. No signs of tetany, muscle cramps, irritability. Improvement in dry skin or hair loss. Normal ECG.

INTERVENTION OBJECTIVES • Normalize serum and urinary levels of calcium, phosphorus, and vitamin D. • Prevent long-term complications such as cataracts, pernicious anemia, Parkinson’s disease, and bone disease. • Prevent mental retardation or malformed teeth in affected children. • Decrease symptoms of tetany and improve overall health status.

FOOD AND NUTRITION • Use a high-calcium diet with dairy products, nuts, salmon, peanut butter, broccoli, and other green leafy vegetables. If tolerated, lactose should be included in the diet for better absorption of calcium. • Oral supplements high in calcium should be used, such as calcium carbonate. • Reduce excess use of meats, phytates (whole grains), and oxalic acid (spinach, chard, and rhubarb) if the diet contains large amounts. • Intake of vitamin D and protein should be adequate, at least meeting recommended levels.

Common Drugs Used and Potential Side Effects • Calcium lactate (8–12 g) may be used. Ergocalciferol (Calciferol) is a vitamin D analog that is used with calcium


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supplements in this condition. Calcitriol (Rocaltrol) also may be useful. • Diuretics sometimes are given to prevent too much calcium from being lost through the urine, which is a problem that can lead to kidney stones. Taking diuretics also reduces the amount of calcium and vitamin D supplements needed. • Overuse of steroids may cause hypocalcemia.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Indicate which foods are good sources of calcium, phosphorus, and vitamin D. • Indicate which foods are sources of phytates and avoided, if dietary intake is a concern. • Discuss role of sunlight exposure in vitamin D formation and how it relates to individual needs.

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information •

American Society for Bone and Mineral Research http://www.asbmr.org/

Hypoparathyroidism Association http://www.hypoparathyroidism.org/

Medline http://www.nlm.nih.gov/medlineplus/ency/article/000385.htm

National Institutes of Health–Osteoporosis and Related Bone Diseases http://www.osteo.org/

HYPOPARATHYROIDISM AND HYPOCALCEMIA— CITED REFERENCES Ali A, et al. Functional characterization of GATA3 mutations causing the hypoparathyroidism-deafness-renal (HDR) dysplasia syndrome: insight into mechanisms of DNA binding by the GATA3 transcription factor. Hum Mol Genet. 16:265, 2007. Anthony T, et al. Development of a parathyroid hormone-controlled release system as a potential surgical treatment for hypoparathyroidism. J Pediatr Surg. 40:81, 2005. Quiros RM, et al. Intraoperative parathyroid hormone levels in thyroid surgery are predictive of postoperative hypoparathyroidism and need for vitamin D supplementation. Am J Surg. 189:306, 2005. Rubin MR, et al. Three dimensional cancellous bone structure in hypoparathyroidism. [published online ahead of print September 25, 2009] Bone. 46:190, 2010.

HYPERPARATHYROIDISM AND HYPERCALCEMIA NUTRITIONAL ACUITY RANKING: LEVEL 2 Emotional disorders

Parathyroid adenoma or hyperplasia Muscle atrophy Hypercalcemia Osteitis fibrosa cystica Peptic ulcer Pancreatitis Kidney stones Nephrocalcinosis

Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND Primary hyperparathyroidism (pHPT) results from parathyroid adenoma in up to 80% of cases, hyperplasia of the

parathyroid glands in 10–20% of cases, or cancer. Double parathyroid adenomas occur in 2–15% of pHPT cases (Abboud et al, 2005). pHPT has been associated with premature death in CVDs and should, therefore, be quickly managed (Nilsson et al, 2005). Secondary hyperparathyroidism (sHPT) occurs in renal failure or even after renal transplantation. Calcitriol deficiency and phosphorus retention are involved in the pathogenesis. Parathyroid gland hyperplasia develops in azotemic patients, producing hypercalcemia and hyperphosphatemia. Secondary hyperparathyroidism in chronic kidney disease is stimulated by dietary phosphate loading and ameliorated by dietary phosphate restriction (Martin et al, 2005). The disorder is complex in that not enough phosphate is cleared from the body; phosphate is released from bone and Vitamin D is not produced. Thereafter, absorption of calcium in the gut is low and serum levels of calcium are lowered. In children with renal failure, growth can be impaired. Postmenopausal women after Roux-en-Y gastric bypass may show evidence of secondary hyperparathyroidism with elevated bone resorption. There is an effect of early breast tumors on calcium homeostasis; subclinical hyperparathyroidism may increase the risk for breast cancer (Martin et al, 2010). Age-induced increased PTH plasma levels have been associated with cognitive decline and dementia. Increased PTH levels may become a biological marker of both dementia and osteoporosis (Braverman et al, 2009).


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Parathyroidectomy can induce long-lasting improvement in regulation of BP, left ventricular diastolic function, and other signs of myocardial ischemia, with improved life expectancy (Nilsson et al, 2005). A minimally invasive procedure is available. After surgery, mild cognitive changes seem to improve, especially for depression and anxiety (Walker et al, 2009).

ASSESSMENT, MONITORING, AND EVALUATION

Genetic Markers: Peroxisome proliferator-activated receptor gamma PPARgamma2 has a dominant role in controlling osteoblast differentiation and numerous gene–gene interactions suggests there is a “master” regulatory process (Shockley et al, 2009). Familial multiple endocrine neoplasia type 1 and familial tumoral calcinosis account for 2% of pHPT cases. In the second form, altered GALNT3 is usually present. More studies are needed on the effects of genes on calcium and bone homeostasis.

Height Weight BMI Diet history BP Weakness, fatigue Constipation Growth delay or rickets in children Anorexia, weight loss Increased thirst Dehydration Itchy skin Back pain

Bone and joint pain Bone x-rays showing fractures or reabsorption X-rays, ultrasound, or Sestamibi scan of parathyroids Lab Work PTH (60 pg/mL) Serum Ca (11 mg/dL)

SAMPLE NUTRITION CARE PROCESS STEPS Excessive Mineral Intake Assessment Data: Abnormal nutritional labs with PTH 65 pg/mL; serum Ca 12.5 mg/dL; urinary Ca levels elevated; elevated serum phosphorus; diagnosis of hyperparathyroidism related to early renal failure without dialysis. Signs of weakness and anorexia. Poor intake because of nausea. Unplanned weight loss of 2 lb recently. Nutrition Diagnosis (PES): Excessive phosphorus intake related to inability of kidneys to metabolize vitamin D3 in renal failure as evidenced by abnormal labs (PTH 65 pg/mL; serum Ca 12.5 mg/dL; urinary Ca levels elevated; serum phosphorus 6, anorexia and weight loss.

CLINICAL INDICATORS

Clinical/History

597

Urinary Ca (elevated) Serum phosphorus (high?) Calcium-phosphorus product (Ca P)* Albumincorrected calcium level (Ca corr) FGF23 assessment, as available Mg, Na, K Alb, BUN, Creatinine H & H, serum ferritin Gluc

*Calcium phosphate product (Ca Pi) is a clinically relevant tool to estimate the cardiovascular risk of patients with renal failure.

INTERVENTION

Intervention: Food-Nutrient Delivery—provide a low-phosphorus diet. Educate about foods to avoid and which to include (see Table 9-25). Counsel about dining away from home, packing a lunch, or other relevant guidelines, how to take Sevelamer and Sensipar according to doctor’s orders. Monitoring and Evaluation: Improvement in serum and urinary labs related to calcium, PTH and phosphorus. Resolution of symptoms including weight loss, nausea, anorexia. Able to state foods to avoid when PTH is elevated and when to contact the physician.

• Alleviate constipation, anorexia, weight loss, and weakness. • Avoid clinical consequences such as renal osteodystrophy, hyperphosphatemia, cardiovascular calcification, extraskeletal calcification, endocrine disturbances, neurobehavioral changes, compromised immune system, altered erythropoiesis, renal stones, and sleep disturbances. • Prevent rickets and growth delay in children (Sabbagh et al, 2005). • Prepare for surgery if parathyroidectomy is necessary.

FOOD AND NUTRITION • Use a low-calcium diet with fewer dairy products, nuts, salmon, peanut butter, and green leafy vegetables. • Extra fluid is useful to correct or prevent dehydration, which can elevate serum calcium levels. • Limit phosphorus-containing foods if hyperphosphatemia is present. See Table 9-25. Use alternatives such as nondairy creamer, sorbet, jams and jellies, white rice, noodles with margarine, cream cheese, whipped cream, popcorn, pretzels, gingerale or Kool-aid if extra calories are needed. • Dietary protein 0.8 g/kg for a balanced intake of protein in adults.

OBJECTIVES Common Drugs Used and Potential Side Effects • Lower elevated serum calcium and urinary calcium levels. Maintain calcium levels between 8.4 and 9.5 mg/dL. • Normalize serum phosphate; keep phosphorus between 3.5 and 5.5 mg/dL and calcium phosphorus product below 55 mg/dL.

• Vitamin D therapy sends a signal to the parathyroid gland to slow down the making of PTH. This helps to prevent many of the unwanted complications of hyperparathyroidism.


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TABLE 9-25

Phosphorus Facts

Normal PO4 levels in plasma: 2.5–4.5 mg/dL Total body PO4 content: 500–700 g (85% in bone) Dietary Reference Intake: 700 mg Typical U.S. dietary intake: 1200 mg GI absorption—Mainly passive, through Na/Pi transporter; enhanced by vitamin D Kidney is major regulator—mediated by brush border Na/Pi transporter; PTH increases excretion and Vitamin D decreases excretion Phosphorus-Rich Foods Dairy Products

Sevelamer (Renagel) lowers serum phosphorus and PTH levels without inducing hypercalcemia. Sevelamer binds drugs such as furosemide, cyclosporine, and tacrolimus, making them less effective. The timing of administration should allow several hours between these medicines. Standard protocols are recommended for use of phosphate binders. • Once-yearly intramuscular cholecalciferol injections (600,000 IU) have been used to correct vitamin D deficiency; controlled trials are needed to determine the effect on PTH levels over time. • Some antacids may contain high levels of calcium; monitor carefully. • Bisphosphonates may be needed to decrease risks for osteoporosis.

Milk Cheese Yogurt Ice cream Pudding and custard Dried beans and lentils Kidney, lima, pinto Soy beans

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Conjugated linoleic acid (CLA) reduces prostaglandin E2 synthesis, which is required for PTH release. More research is needed.

Split peas Black-eyed peas

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT

Nuts and seeds Almonds Cashews Sunflower seeds Peanuts and Peanut Butter Meats Liver Organ meats Sweetbreads Smelt, sardines, herring Miscellaneous

• Discuss foods that are sources of calcium, phosphorus, and vitamin D. Indicate food sources of phytates and oxalates, if intake is a concern. • Discuss role of sunlight exposure in vitamin D formation and how it relates to individual needs. • Drink plenty of liquids. • In renal patients, focused counseling may help to clarify misunderstanding of simple dietary facts. • The doctor should monitor Ca and P monthly and PTH quarterly after stabilization. • Exercise and smoking cessation may be needed.

Beer Bran, bran flakes, wheat germ Chocolate Colas

Patient Education—Foodborne Illness • If home tube feeding is needed, teach appropriate sanitation and food-handling procedures.

For More Information • Treatment with active vitamin D from analogs can increase VDR expression, inhibit growth of parathyroid tumors, and reduce PTH levels (Akerstrom et al, 2005). Zemplar (paricalcitol) and Hectorol (doxercalciferol) are examples of vitamin D analogs. These products are especially useful for dialysis patients. • Cinacalcet (Sensipar) has been approved to treat sHPT in renal patients and parathyroid cancer. It also appears to effectively treat pHPT. Cinacalcet normalizes serum calcium with only modest increases in PTH (Sajid-Crockett et al, 2008). • Phosphate-binding agents that do not contain calcium offer therapeutic alternatives for managing renal osteodystrophy.

American Society for Bone and Mineral Research http://www.asbmr.org/

Endocrine Web http://www.endocrineweb.com/hyperpara.html

National Institutes of Health–Osteoporosis and Related Bone Diseases http://www.osteo.org/

NIDDK http://endocrine.niddk.nih.gov/pubs/hyper/hyper.htm

HYPERPARATHYROIDISM AND HYPERCALCEMIA— CITED REFERENCES Abboud B, et al. Existence and anatomic distribution of double parathyroid adenoma. Laryngoscope. 115:1128, 2005.


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Braverman ER, et al. Age-related increases in parathyroid hormone may be antecedent to both osteoporosis and dementia. BMC Endocr Disord. 9:21, 2009. Martin DR, et al. Acute regulation of parathyroid hormone by dietary phosphate. Am J Physiol Endocrinol Metab. 289:E729, 2005. Martin E, et al. Serum calcium levels are elevated among women with untreated postmenopausal breast cancer. [published online ahead of print October 24, 2009] Cancer Causes Controls. 21:251, 2010. Nilsson IL, et al. Maintained normalization of cardiovascular dysfunction 5 years after parathyroidectomy in primary hyperparathyroidism. Surgery. 137:632, 2005.

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Sabbagh Y, et al. Hypophosphatemia leads to rickets by impairing caspasemediated apoptosis of hypertrophic chondrocytes. Proc Natl Acad Sci U S A. 102:9637, 2005. Sajid-Crockett S, et al. Cinacalcet for the treatment of primary hyperparathyroidism. Metabolism. 57:517, 2008. Shockley KR, et al. PPARgamma2 nuclear receptor controls multiple regulatory pathways of osteoblast differentiation from marrow mesenchymal stem cells. J Cell Biochem. 106:232, 2009. Walker MD, et al. Neuropsychological features in primary hyperparathyroidism: a prospective study. J Clin Endocrinol Metab. 94:1951, 2009.


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CHIEF ASSESSMENT FACTORS

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Anorexia, Nausea, Vomiting, Diarrhea—Frequency, Length of Time Blood Pressure, Either Elevated or Very Low Levels Body Mass Index (BMI) Using Height and Weight Frame Size—Small, Medium, Large Goal Weight and Current Percentage of Goal Weight Healthy Body Weight Range History of Usual Body Weight, Present Weight, Recent Weight Changes,% Usual Body Weight Laboratory Values—Glucose, Albumin/Transthyretin, Hemoglobin and Hematocrit (H & H), Lipids, C-Reactive Protein (CRP) Medical History—Disordered Eating; Cancer or Other Conditions or Disease States; Menstrual or Reproductive Problems in Women; Smoking and Alcohol Histories Physical Activity Level Sleep Apnea, Altered Lung Function; Sleep Disorder Triceps Skinfold (TSF) Measurements; Arm Muscle Circumference (AMC) Measurements—Comparing Individual Against Own Values Over Time Waist Circumference


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TYPES OF MALNUTRITION The malnourished state arises from a combination of inflammation and a disturbed nutrient balance in either undernutrition or overnutrition (Soeters and Schols, 2009). Malnutrition is defined by the American Society of Parenteral and Enteral Nutrition (ASPEN) as any derangement in the normal nutrition status. Undernutrition may be primary—from insufficient intake— or secondary—from impaired utilization; see Table 10-1. Malnutrition originates not only from an imbalance of calories but also from psychological, economic, physical, and social factors. Health problems, alcoholism, depression, restricted diets, and mobility problems may play a part. Undernutrition contributes to half of the world’s mortality in children, particularly in India and sub-Saharan Africa. Nutrition Day, which originated in Europe, is now recognized in the United States. The intent is to identify the type and percentages of malnourished patients in hospitals and nursing homes in order to clarify their impact on health outcomes. Overnutrition is caused by excessive calorie intake and/ or inadequate activity; see Table 10-2. The thrifty genotype

TABLE 10-1 •

• •

• • •

• •

developed when food was scarce; now, an environment where food is plentiful contributes to the dilemma (Bouchard, 2007). The study of extreme human obesity caused by single gene defects has provided a glimpse into the long-term regulation of body weight through a disrupted hypothalamic leptin-melanocortin system and extremely heterogeneous factors (Ranadive and Vaisse, 2008). In addition to the change in environment, thirst, hunger, and high calorie beverage intake have changed in the past few decades. The intake of energy-yielding beverages seems to be related to pleasure-oriented, hedonic factors rather than hunger or thirst (McKiernan et al, 2008). Pavlovian cues for rewards become endowed with incentive salience, guiding “wanting” to a learned reward (Tindell et al, 2009). Thus, the hedonic appetite has displaced genuine hunger in the current environment of plenty, perhaps in relation to conditioned stimuli. For example, salted food may be an addictive substance that stimulates the opiate and dopamine receptors in the brain’s reward and pleasure center; both salted food and opiate withdrawal stimulate the appetite, increase calorie consumption, and augment the incidence of overeating, becoming overweight, and becoming obese (Cocores and Gold, 2009).

Concerns with Undernutrition

The lack of adequate macronutrients or selected micronutrients (zinc, selenium, iron, and the antioxidant vitamins) can lead to clinically significant immune deficiency (Cunningham-Rundles et al, 2005). Iron deficiency alters myelination, monoamine neurotransmitter synthesis, and hippocampal energy metabolism in the neonatal period (Georgleff, 2007). Zinc deficiency alters autonomic nervous system regulation and hippocampal and cerebellar development (Georgleff, 2007). Inflammation and oxidative stress fuel each other. Cachexia includes distinct metabolic changes that are the result of an acute-phase response (APR) mounted by the host, including increased muscle proteolysis, increased fat lipolysis, and increased hepatic production of acute-phase proteins such as C-reactive protein and fibrinogen (Gullett et al, 2009). Children who are undernourished may not reach their potential in many aspects of development. Stunting represents growth failure resulting from poor nutrition and health during the pre- and postnatal periods (Milman et al, 2005). Intrauterine and early neonatal life is a period during which environmental and nutritional influences may produce chronic and frequent infections, long-term effects, and disease risk in adulthood (Buckley et al, 2005). The effect of any nutrient deficiency or overabundance on brain development will be governed by the principle of timing, dose, and duration (Georgleff, 2007). Bourre (2006) reported on nutritional requirements for the brain. The use of glucose by nervous tissue requires thiamin. Vitamins B6 and B12 are directly involved in the synthesis of some neurotransmitters. Supplementation with cobalamin improves cerebral and cognitive functions in the frontal lobe. Alphatocopherol is actively uptaken by the brain and is directly involved in the protection of nervous membranes. Vitamin K is also involved in nervous tissue biochemistry. Iron deficiency anemia is associated with apathy, depression, and fatigue. Iodine deficiency during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Long-chain polyunsaturated fatty acids are important for synaptogenesis, membrane function, and, potentially, myelination (Georgleff, 2007). The rise in autism, learning problems, cognitive decline with age, Alzheimer’s, Parkinson’s Disease, and the SIDS epidemic has a common link: dietary deficit in omega-3 brain-foods from fish and seafood (Saugstad, 2008). Undernutrition in adult women tends to be associated with high levels of undernutrition in children, reflecting overall food/nutrient insecurity (Nube, 2005). Prenatal exposure to famine can lead to low birth weight and cardiovascular disease in adulthood (Painter et al, 2005). A woman with a low body mass index (BMI) may have difficulty becoming pregnant; preconceptional undernutrition shortens gestation in those women who do become pregnant (Rayco-Solon et al, 2005). Recent weight loss appears to be the most important single indicator of nutritional status. Nutritional risk with muscle mass depletion increases lengths of stay in hospitals (Kyle et al, 2005). Undernutrition is associated with increased resting energy expenditure (REE; kcal/kg/d). Reduced respiratory quotient (RQ) and protein synthesis (g/kg/d) occur in patients with coexistent disease; refeeding normalizes this process (Winter et al, 2005). Involuntary weight loss can be categorized into one of three primary etiologies (Thomas, 2007): Starvation results in a loss of body fat and non-fat mass due to inadequate intake of protein and energy. Sarcopenia involves a reduction in muscle mass and strength occurring with normal aging, associated with a reduction in motor unit number and atrophy of muscle fibers; this leads to diminished strength and exercise capacity. Cachexia is severe wasting that accompanies disease states such as cancer or immunodeficiency disease. Malnutrition in pediatric hospitals ranges from 15–30% of patients, with an impact on growth, morbidity, and mortality; nutrition-support interventions can help (Agostoni et al, 2005). If a person has a BMI below 18, there is an increased risk for nutrition-related complications such as infections, poor wound healing, and pressure ulcer development. (continued)


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TABLE 10-1 Concerns with Undernutrition (continued) • •

Approximately 25–50% of hospital patients have been found to be malnourished. Only 50% of malnourished patients are identified by the medical and nursing staff (Kruizenga et al, 2005). Over half of older adults have protein–energy malnutrition at admission or acquire nutritional deficits while hospitalized (Pepersack, 2005). Malnutrition may come from the “11 Ds”: disease, drinking alcohol, drugs, deficits (sensory), desertion/isolation, dementia, delirium, depression, destitution, despair, and dysphagia. Cognitive function is particularly sensitive to glucose and insulin availability. Older individuals often have dementia, falls, mobility disorders, malnutrition, end-of-life issues, pressure ulcers, and urinary incontinence to consider. Nutritional screening and assessment must become routine. Subjective Global Assessment and the Mini Nutritional Assessment tools are used to detect patients who need preventive nutritional measures (Kyle et al, 2005). The short nutritional assessment questionnaire (SNAQ) is simple and may be used to screen for appetite changes—another important factor leading to undernutrition and its consequences (Wilson et al, 2005). Outcome monitoring and evaluation should include weight change, use of supplemental drinks and snacks between meals, use of tube feeding or parenteral nutrition, number of consultations by the hospital dietitian, and decreased length of hospital stay (Kruizenga et al, 2005).

REFERENCES Agostoni C, et al. The need for nutrition support teams in pediatric units: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr. 41:8, 2005. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 10:377, 2006. Buckley AJ, et al. Nutritional programming of adult disease. Cell Tissue Res. 322:73, 2005. Cunningham-Rundles S, et al. Mechanisms of nutrient modulation of the immune response. J Allergy Clin Immunol. 115:1119, 2005. Georgleff MK. Nutrition and the developing brain: nutrient priorities and measurement. Am J Clin Nutr. 85:214S, 2007. Gullett N, et al. Cancer-induced cachexia: a guide for the oncologist. J Soc Integr Oncol. 7:155, 2009. Kruizenga HM, et al. Effectiveness and cost-effectiveness of early screening and treatment of malnourished patients. Am J Clin Nutr. 82:1082, 2005. Kyle UG, et al. Hospital length of stay and nutritional status. Curr Opin Clin Nutr Metab Care. 8:397, 2005. Milman A, et al. Differential improvement among countries in child stunting is associated with long-term development and specific interventions. J Nutr. 135:1415, 2005. Nube M. Relationships between undernutrition prevalence among children and adult women at national and subnational level. Eur J Clin Nutr. 59:1112, 2005. Painter RC, et al. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reprod Toxicol. 20:345, 2005. Pepersack T