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Musculo-Skeletal and Collagen Disorders




• • • • • • • • • • • • • • •

Actual Height, Measured Annually for Height Loss Arthritis—Warning Signs and Symptoms 2 Weeks: Early Morning Stiffness; Swelling in One or More Joints; Redness and Warmth in a Joint; Unexplained Weight Loss, Fever, or Weakness Combined with Joint Pain Bone Density Assessment Bone-Wasting Medications Contractures Easy Fatigue Edema Extremity Weakness Inflammation of Joints Movement Problems, Stiffness Pain in Muscles, Joints, Bones, Spine Psoriasis Unsteady Gait and Propensity to Fall Weight Loss, Anorexia, Depression, Insomnia Vitamin D3 status (serum 25-OHD)

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TABLE 11-1

Autoimmune Rheumatic Disordersa

Blood and blood vessels

Lupus Polyarteritis nodosa


Temporal arteritis and Polymyalgia rheumatica


Digestive tract and mouth


Scleroderma Sjögren’s syndrome

Eyes Bronchusassociated lymphoid tissue

Sjögren’s syndrome Uveitis

Heart Axillary lymph nodes

Lupus Rheumatic fever Scleroderma

Spleen Intestine

Ankylosing spondylitis


Ankylosing spondylitis Lupus

Peyer’s patches


Inguinal lymph nodes

Rheumatoid arthritis Kidneys

Gout Lupus


Lungs Bone marrow

Lupus Rheumatoid arthritis Scleroderma



Nerves and brain



Lupus Scleroderma


Adapted from: Porth CM. Pathophysiology: Concepts of altered health states, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 1998.

Some rheumatic diseases involve connective tissues and others may be caused by autoimmune disorders, where the body attacks its own healthy cells and tissues. See Table 11-1. Rheumatic disorders include osteoarthritis (OA), rheumatoid arthritis (RA), juvenile RA, bursitis, tendonitis, infectious arthritis, spondyloarthropathies, polymyositis, psoriatic arthritis, systemic lupus erythematosus, scleroderma, polymyalgia rheumatica, polyarthritis nodosa, giant cell arteritis, gout, and fibromyalgia. Typically, treatment of these disorders includes a rheumatologist who specializes in the treatment of disorders that affect joints, soft tissue, bones and connective tissues. Arthritis represents a group of more than 100 different rheumatic diseases that cause stiffness, pain, swelling in the joints, muscles, ligaments, tendons or bones. Over 15% (40 million) of Americans have some form of arthritis. Spondylosis is OA of the spine. Infectious arthritis is caused by bacterial invasion spread from nearby joints following chickenpox, rubella, or mumps. Autoimmune disorders, Crohn’s disease, and psoriasis may cause seronegative arthritis. Mixed connective tissue disease shows features of RA, cutaneous systemic sclerosis, inflammatory myopathies and Raynaud’s syndrome. Mast cells and basophils are involved in several inflammatory and immune events and are known to produce a broad spectrum of cytokines (Rasheed et al, 2009). The activation of nuclear transcription factor-B is linked with arthritis, osteoporosis, and psoriasis. The cytokine tumor necrosis factor

When the immune system does not work right, the immune cells can mistake the body’s own cells as invaders and attack them; these are called autoimmune diseases. In this table a sample list of body systems affected by autoimmune rheumatic disorders. Adapted from: National Institutes of Health (NIH). NIH Publication No. 02–4858. Available at

alpha (TNF) plays a key role in chronic inflammatory and rheumatic diseases. Early recognition and treatment of these disorders are important. RA, juvenile idiopathic arthritis, the seronegative spondyloarthropathies, and lupus may have skeletal pathology (Walsh et al, 2005) and an inflammatory atherosclerosis. A multidisciplinary, multipronged approach is best. Physical and occupational therapies are beneficial for maintaining as much independence as possible in these conditions. Most rheumatic conditions are managed by use of nonsteroidal anti-inflammatory drugs (NSAIDs) and TNF antagonists. Etanercept, infliximab, and adalimumab significantly reduce symptoms and improve both functionality and quality of life (Braun et al, 2006; Nash and Florin, 2005). Fortunately, research is on-going for the autoimmune diseases. Gene profiling is helpful, especially in pediatrics (Jarvis, 2005). Osteoimmunology is a new branch of medical science, and anti-inflammatory therapies promise new treatments.

Role of Inflammation and Fatty Acids Excessive and inappropriate inflammation contributes to acute and chronic human diseases. It is characterized by the production of inflammatory cytokines, arachidonic

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MEMBRANE PHOSPHOLIPIDS Phospholipase A2 Indomethacin Arachidonic acid

COX-2 Inhibitors








Prostaglandin G2



Prostaglandin H2

Leukotriene A4


Thromboxane A2 synthase PGI2



Leukotriene E4

Leukotrien B4


acid-derived eicosanoids (prostaglandins, thromboxanes, leukotrienes, and other oxidized derivatives), other inflammatory agents (e.g., reactive oxygen species), and adhesion molecules (Calder, 2006). Three major types of omega-3 fatty acids are ingested in foods: alpha linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). The body converts ALA to EPA and DHA, which are readily used by the body. Omega-3 fatty acids help reduce inflammation, while omega-6 fatty acids tend to promote inflammation. The precursor ALA does not appear to exert anti-inflammatory effects at achievable intakes (Calder, 2006). A balance between omega-3 and omega-6 fatty acids in the diet is needed. The proper balance helps maintain and even improve health; one to four times more omega-6 fatty acids than omega-3 fatty acids is desirable, yet people who follow a Western diet consume a higher percentage of omega-6 fatty acids than they should. Long-chain omega-3 polyunsaturated fatty acids (PUFAs) act by replacing arachidonic acid as an eicosanoid substrate, inhibiting arachidonic acid metabolism; by altering the expression of inflammatory genes through effects on transcription factor activation; and by leading to anti-inflammatory mediators known as resolvins (Calder, 2006).

Role of Phytochemicals and Total Diet Phytochemicals known for their ability to protect tissue also appear to block the activity of an enzyme that triggers inflammation in joints. See Table 11-2.

Complementary and Alternative Medicine (CAM) Therapies Controlled scientific studies of many patients can prove that a particular treatment is beneficial or that an apparent improvement is incidental. The important consideration is that treatment should do no harm. Some studies have been done in alternative therapies, particularly diet in the treatment of arthritis, but none have shown any real long-term benefit. Patients often do benefit from complementary therapies, either because the treatment truly works or because of psychological (placebo) effects. While there is evidence of benefit for vitamin C, vitamin D, and nutraceuticals such as glucosamine, chondroitin, S -adenosylmethionine, ginger, and avocado/soybean unsaponifiables (McAlindon, 2006), specific diets and herbal or botanical products should only be used with medical consultation. While the best nutrition-based strategy for promoting optimal health and reducing the risk of chronic disease is to wisely choose a wide variety of foods, additional nutrients from supplements can help some people meet their nutrition needs (American Dietetic Association, 2009). Physicians reported familiarity with acupuncture (80%), yoga (74%), and Tai-Chi (72%) yet almost all of their patients use CAM therapies (Mak et al, 2009). It is logical, then, that dietetics practitioners must keep up to date on the efficacy, safety, and the regulatory issues in order to provide the best advice.

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TABLE 11-2

Phytochemicals and Dietary Factors Affecting Rheumatic Disorders


Foods or Ingredients


Cruciferous vegetables: broccoli, cauliflower, cabbage, bok choy


Boost phase 2 enzymes

Dairy products, low fat

To be identified; vitamin D?

Protective factors against gout (Choi, 2005).

Fruits: pomegranate, cranberry

Anthocyanins, tannins; ellagic acid; resverarol; quercetin; vitamins A, C; selenium

Potent anti-inflammatory activity (Rasheed et al, 2009).

Long-chain polyunsaturated fatty acids


Replace arachidonic acid as an eicosanoid substrate, inhibiting arachidonic acid metabolism. Alter expression of inflammatory genes through effects on transcription factor activation, leading to anti-inflammatory mediators termed resolvins (Calder, 2006).

Mediterranean diet

Resveratrol, olive oil, lower intake of red meat

Protects against severity of rheumatoid arthritis (Choi, 2005).


Turmeric (curcumin) Red pepper (capsaicin) Cloves (eugenol) Ginger (gingerol) Cumin, anise, and fennel (anethol) Basil, rosemary (ursolic acid) Garlic (diallyl sulfide, ajoene, S-allylmercaptocysteine)

Interrupts pathway for transcription factor-B (Aggarwal and Shishodia, 2004).

Vitamin D

Hormone affects over 2000 genes

Needed for healthy immune system, gene expression, strong bones.

Total protein and purine-rich vegetables


Do not tend to promote gout (Choi, 2005).

Vitamin E, beta-carotene, and retinol.


Have NOT been shown to halt the progression of rheumatic disorders

Red meats, seafood, beer, and liquor


Tend to promote symptoms of gout, inflammatory polyarthritis, or rheumatoid arthritis (Choi, 2005).

Sources: Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappa B activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 1030:434, 2004.

RHEUMATIC DISORDERS—CITED REFERENCES Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappa B activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 1030:434, 2004. American Dietetic Association. Position of the American Dietetic Association: Nutrient supplementation. J Am Diet Assoc. 109;2073, 2009. Braun J, et al. First update of the international ASAS consensus statement for the use of anti-TNF agents in patients with ankylosing spondylitis. Ann Rheum Dis. 65:316, 2006. Calder PC. Omega-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr. 83:1505S, 2006. Choi HK. Dietary risk factors for rheumatic diseases. Curr Opin Rheumatol. 17:141, 2005.

Jarvis JN. Gene expression profiling in pediatric rheumatic disease: what have we learned? What can we learn? Curr Opin Rheumatol. 17:606, 2005. Mak JC, et al. Perceptions and attitudes of rehabilitation medicine physicians on complementary and alternative medicine in Australia. Intern Med J. 39:164, 2009. McAlindon TE. Nutraceuticals: do they work and when should we use them? Baillieres Best Pract Res Clin Rheumatol. 20:99, 2006. Nash PT, Florin TH. Tumour necrosis factor inhibitors. Med J Aust. 183:205, 2005. Rasheed Z, et al. Polyphenol-rich pomegranate fruit extract (POMx) suppresses PMACI-induced expression of pro-inflammatory cytokines by inhibiting the activation of MAP Kinases and NF-kappaB in human KU812 cells. J Inflamm (Lond). 6:1, 2009. Walsh NC, et al. Rheumatic diseases: the effects of inflammation on bone. Immunol Rev. 208:228, 2005.

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Pectoral girdle (4)

Clavicle (2) Scapula (2)

Humerus (2)

Cranium (8) Skull and Auditory ossicles (6) associated bones (29) Face (14) Hyoid (1)

Sternum (1) Thoracic cage (25) Ribs (24)

Upper limb (60) Ulna (2) Radius (2)

Vertebrae (24) Sacrum (1) Vertebral column (26) Coccyx (1)

Carpals (16) Metacarpals (10) Phalanges (28) Hip bone coxa (2)

Pelvic girdle (2)

Femur (2) Patella (2) Tibia (2) Fibula (2) Lower limb (60)

Tarsals (14) Metatarsals (16) Phalanges (28)

Adapted from: Moore KL, Agur AMR. Essential Clinical Anatomy, 2nd ed. Baltimore. Lippincott Williams & Wilkins

Bones are living, growing, and changing parts of the body. The human skeletal system consists of bones, cartilage, ligaments, and tendons and accounts for about 20% of the body weight. Osteoblasts are bone-forming cells, osteoclasts resorb or break down bone, and osteocytes are mature bone cells. The osteoblast is an endocrine cell type. There is a reciprocal regulation of bone and energy metabolism by leptin and osteocalcin. Leptin inhibits insulin secretion by beta cells while osteocalcin favors it (Hinoi et al, 2009). Leptin deficiency leads to increased osteoblast activity and increased bone mass. Expression of the Esp gene, exclusive to osteoblasts, regulates glucose homeostasis and adiposity through controlling osteoblastic secretion of osteocalcin (Wolf, 2008). Osteocalcin deficiency leads to decreased insulin and adiponectin secretion, insulin resistance, higher serum glucose levels, and increased adiposity (Wolf, 2008). This recently understood concept has implications for diabetes and the metabolic syndrome.

There are 206 bones in the adult skeleton. The two types of bone tissue (compact and spongy) differ in density. Bone strength is derived from quantity (density and size) and quality (structure, consistency, and turnover). Bone mass is dependent upon individual genetic background. Adequate nutrient intake is needed from birth to achieve maximal bone mass and to prevent osteoporosis later in life. The trace elements, calcium and phosphorus, are involved in skeletal growth. Parathyroid hormone (PTH) regulates calcium and bone homeostasis; it is expressed in the placenta, regulates the placental expression of genes involved in calcium and other solute transfer, and may directly stimulate placental calcium transfer (Simmonds et al, 2010). Magnesium and fluoride are matrix constituents while zinc, copper and manganese are components of enzymatic systems involved in matrix turnover. A sufficient protein intake, along with adequate calcium, supports stronger

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TABLE 11-3 Recommendations for Prevention of Osteoporosis Get the recommended amounts of calcium and vitamin D3 for age and sex; use supplements when diets are inadequate. Maintain a healthy weight and be physically active 30 minutes a day for adults and 60 minutes a day for children, including weight-bearing activities to improve strength and balance. Minimize the risk of falls by removing items that might cause tripping, improving lighting, and encouraging regular exercise and vision tests to improve balance and coordination. Risks for patients of all ages should be evaluated by health care professionals. Obtain bone density tests for women over the age of 65 and for any man or woman who suffers even a minor fracture after the age of 50. “Red flags” for someone is at risk include a history of multiple fractures, those who take certain medications, and those who have a disease that can lead to bone loss. A BMD test is used to detect osteoporosis before fractures occur, predict chances of future fractures, or determine rate of bone loss and monitor the effects of treatment. The DEXA scan is most common. • •

Normal BMD: within 1 standard deviation (SD) of a “young normal” adult. Low bone mass (osteopenia): BMD is between 1 and 2.5 SD below that of a “young normal” adult. • Osteoporosis: BMD is 2.5 SD or more below that of a “young normal” adult.

bone density; this fact contradicts past suggestions that highprotein diets deplete bone strength. Changes in bone turnover markers may become accurate predictors of fracture risk. Assessing risk factors for low bone mass is important in monitoring the etiology of fracture in older individuals (Kelsey et al, 2006). In general, women’s bone health has been studied more extensively than that of men. Studies on the predictors of fractures in men are needed, such as bone architecture, morphology, biochemical markers of bone turnover, and hormonal levels (Szulc et al, 2005). Vitamins are important. Vitamin D3 plays a role in calcium metabolism. Vitamins C and K are cofactors of key enzymes for skeletal metabolism. Another indicator of bone health is heart health. There are similar pathophysiological mechanisms underlying cardiovascular disease (such as dyslipidemia, oxidative stress, inflammation, hyperhomocysteinemia, hypertension, and diabetes) and low bone mineral density (BMD). Sufficient folic acid, vitamins B6 and B12 can help improve bone health by lowering elevated homocysteine levels. Antioxidant nutrients, including vitamins A and C and selenium, play a role in bone health. While calcium is widely recognized for bone health, other minerals are equally important. Iron promotes production of collagen in bone structure; 18 mg is most protective for women but balance is also critical as too much iron may throw off calcium balance. Finally, silicon in the form of choline-stabilized orthosilicic acid is the bioavailable form that enhances calcium and vitamin D3 in bone health. Omega-3 fatty acids such as EPA help increase levels of calcium in the body, deposit calcium in the bones, and improve bone strength. People who are deficient in EFAs EPA and gamma linolenic acid (GLA) are more prone to bone loss.

Former U.S. Surgeon General Richard H. Carmona (2005) warned in a landmark report that, by 2020, half of all American citizens older than 50 would be at risk for fractures from osteoporosis and low bone mass if immediate action is delayed by individuals at risk, doctors, health systems, or policymakers. At least 10 million Americans over the age of 50 have osteoporosis, another 34 million are at risk for developing osteoporosis, and roughly 1.5 million people have suffered a bone fracture related to osteoporosis. About 20% of senior citizens who suffer a hip fracture die within a year of fracture; another 20% of individuals with a hip fracture end up in a nursing home. Hip fractures account for 300,000 hospitalizations each year. See Table 11-3 for recommendations to prevent osteoporosis.

For More Information •

American Academy of Orthopaedic Surgeons

American Academy of Physical Medicine and Rehabilitation

American Autoimmune-Related Diseases Association (AARDA)

American College of Rheumatology

American Osteopathic Association

American Pain Foundation

American Society for Bone and Mineral Research

Arthritis Foundation

Autoimmunity Resources

CAM Therapy Resources

CDC—Calcium for Bone Health

Clinical Trials Research Trials

Drug List

Journal of Immunology

National Institute of Arthritis and Musculoskeletal and Skin Disorders

Quack Watch for Unproven Remedies

Rheumatic Diseases Internet Journal

BONE DISORDERS—CITED REFERENCES Hinoi E, et al. An osteoblast-dependent mechanism contributes to the leptin regulation of insulin secretion. Ann N Y Acad Sci. 1173:20S, 2009. Kelsey JL, et al. Risk factors for fracture of the shafts of the tibia and fibula in older individuals. Osteoporos Int. 17:143, 2006. Simmonds CS, et al. Parathyroid hormone regulates fetal-placental mineral homeostasis [published online ahead of print September 23, 2009]. J Bone Miner Res. 25:594, 2010. Szulc P, et al. Bone mineral density predicts osteoporotic fractures in elderly men: the MINOS study. Osteoporos Int. 16:1184, 2005. Wolf G. Energy regulation by the skeleton. Nutr Rev. 66:229, 2008.

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the presence of autoantibodies against specific antigens shared by the colon and other extra-colonic tissues, increased intestinal permeability, osteoporosis and osteomalacia secondary to IBD (Rodriguez-Reyna et al, 2009). Elevated tumor necrosis factor alpha (TNF) is believed to be one of the causes of inflammation and bone destruction (Braun et al, 2006); therefore, anti-TNF therapy is effective (Barkham et al, 2005). Exercise to strengthen muscles that tend to cause pain on stooping or bending may be useful to relieve lower back pain. Attention to good posture will reduce some types of pain. Surgery may be needed to replace a joint or to relieve pain.




Genetic Markers: Genetic marker HLA-B27 can be detected in these individuals. Clinical/History


Carol Mattson Porth, Pathophysiology Concepts of Altered Health States, 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2005.

DEFINITIONS AND BACKGROUND Among the 100 different rheumatic diseases that affect the joints and muscles is a group of five called spondyloarthropathies. These include ankylosing spondylitis, reactive arthritis (Reiter’s syndrome), psoriatic arthritis or spondylitis, spondylitis of inflammatory bowel disease, and undifferentiated spondyloarthropathy. Spondylitis is inflammation of the joints linking the vertebrae (a fused spine is not uncommon). Spondylitis affects about 300,000 Americans and is more common in Caucasians than in African Americans. The condition is most common in men aged 16–35 years and may run in families. In ankylosing spondylitis, inflammation of connective tissue recedes but leaves hardened and damaged joints that fuse together the bones of the spinal column. The sacroiliac joints generally are affected first. Symptoms and signs include chronic lower back pain, early morning stiffness in the lower back where the lower spine is joined to pelvis, vague chest pains, tender heels, weight loss, anemia, anorexia, slight fever, recurring iritis or reddened eyes, valvular heart disease. Pain may occasionally start in the knees and shoulders. There is a strong link between the bowel and the osteo-articular system, notably with the HLA-B27 gene where there are symptoms such as abnormal antigen presentation,

Height Weight Body mass index (BMI) Weight changes Anorexia Fever? Lower back pain Pain in knees or shoulders Iritis or reddened eyes X-rays Lab Work HLA-B27 gene test (positive in 90%)

Erythrocyte sedimentation rate (ESR) (high) C-reactive protein (CRP) Ca, Mg Na, K Alkaline phosphatase (Alk phos) Blood urea nitrogen (BUN) Creatinine (Creat) Phosphorus (P)

Hemoglobin and hematocrit (H & H) Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Serum folate and B12 Homocysteine levels Vitamin D3 status (serum 25-OHD)

INTERVENTION OBJECTIVES • Reduce pain, inflammation, and disease activity; support improved functioning and ability to work or to maintain quality of life. • Correct anorexia, nausea, poor intake or weight loss, anemia, or fever where present.

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SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment: Loss of 15 lb this past 6 months, much pain and inflammation with ankylosing spondylitis, taking numerous medicines that cause GI distress and anorexia.

• Etanercept (Enbrel), an anti-TNF therapy, may improve mobility and quality of life (Braun et al, 2006; Davis et al, 2005; Temel et al, 2005). Infliximab (Remicade), another monoclonal antibody, also targets TNF and provides clinical improvement. Upper respiratory infections, psoriatic rashes, and allergic reactions can occur.

Nutrition Diagnosis (PES): Unintentional weight loss (NC-1.4) related to pain, inflammatory processes, and GI distress and evidenced by 15-lb unplanned weight loss in past 6 months.

Herbs, Botanicals, and Supplements

Interventions: Food and Nutrient Delivery: ND 1.2 Alter diet as tolerated. ND 32.3 and 32.4 Initiate vitamin and mineral supplementation.

• Herbs and botanical supplements should not be used without discussing with physician. Ginger, corn, pineapple, and pigweed have been recommended; no clinical trials prove efficacy.

Education: E-1.2 Discuss ways to increase energy and nutrient density in food choices. Counseling: C 2.2 Agree to goal of consuming only nutrient-dense foods for the coming month until next visit. C-2.3 Keep a food diary for one month. Monitoring and Evaluation: Review food diary after 1 month. Monitor weight for resolution of weight loss; goal is gain of 1–2 lb weekly.

• Improve ability to participate in physical activities of choice to maintain lean body mass.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Exercise is crucial, especially swimming, to relieve back pain. • Patient should practice deep breathing exercises for pain relief. Stretching and strengthening exercises also are important. • Patient will likely find that sleeping on a hard bed, supine, is most helpful. • Discuss role of energy intake for weight control.

Patient Education—Food Safety

FOOD AND NUTRITION • A normal diet is useful. Support gradual weight loss, if needed, to normalize weight. Some patients claim relief while using a vegetarian diet with less red meat. • Preferred foods should be offered to stimulate appetite. • Increase intake of foods rich in antioxidants such as vitamins E and C, selenium, and fish oils for rich sources of omega-3 fatty acids. Sufficient calcium and vitamin D are also important. • Include phytochemicals derived from spices 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) (Aggarwal and Shishodia, 2004).

Common Drugs Used and Potential Side Effects • Sulfasalazine, methotrexate, azathioprine, cyclosporine, leflunomide, and tumor necrosis factor-alpha blocking agents can be considered as first-line therapy but there are possible harmful effects on intestinal integrity, permeability, and even on gut inflammation (RodriguezReyna et al, 2009).

If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Ankylosing Spondylitis International Federation

National Ankylosing Spondylitis Society (NASS)–United Kingdom

Spondylitis Association of America

ANKYLOSING SPONDYLITIS—CITED REFERENCES Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappa B activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 1030:434, 2004. Barkham N, et al. The unmet need for anti-tumour necrosis factor (anti-TNF) therapy in ankylosing spondylitis. Rheumatology (Oxford). 44:1277, 2005. Braun J, et al. First update of the International ASAS Consensus Statement for the use of anti-TNF agents in patients with ankylosing spondylitis. Ann Rheum Dis. 65:316, 2006. Davis JC, et al. Reductions in health-related quality of life in patients with ankylosing spondylitis and improvements with etanercept therapy. Arthritis Rheum. 53:494, 2005. Rodriguez-Reyna TS, et al. Rheumatic manifestations of inflammatory bowel disease. World J Gastroenterol. 15:5517, 2009. Temel M, et al. A major subset of patients with ankylosing spondylitis followed up in tertiary clinical care require anti-tumour necrosis factor alpha biological treatments according to the current guidelines. Ann Rheum Dis. 64:1383, 2005.

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GOUT NUTRITIONAL ACUITY RANKING: LEVEL 2 TABLE 11-4 Acquired Causes of Hyperuricemia Cause


Increased urate production Nutritional

Excess ethanol or fructose intake


Myeloproliferative and lymphoproliferative disorders, polycythemia


Ethanol, cytotoxic drugs, vitamin B12 (treatment of pernicious anemia)


Obesity, psoriasis, hypertriglyceridemia

Decreased renal excretion of urate Drugs

Ethanol, cyclosporine (Sandimmune), thiazides, furosemide (Lasix) and other loop diuretics, ethambutol (Myambutol), pyrazinamide, aspirin(low-dose), levodopa (Larodopa), nicotinic acid (Nicolar)


Hypertension, polycystic kidney disease, chronic renal failure (any etiology)


Dehydration, lactic acidosis, ketosis, hypothyroidism, hyperparathyroidism


Obesity, sarcoidosis, toxemia of pregnancy

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

DEFINITIONS AND BACKGROUND Uric acid is the end product of purine metabolism. Because humans have lost hepatic uricase activity, this leads to uniquely high serum uric acid concentrations when compared with other mammals. About 70% of daily urate disposal occurs via the kidneys; in 5–25% of the human population, impaired renal excretion leads to hyperuricemia. Gout is a disorder of sudden and recurring attacks of painful arthritis with inflamed joints (usually the big toe, ankle, knees, and feet). Hyperuricemia promotes deposition of monosodium urate crystals in the joints and tendons. Gout affects more than 1% of adults in the United States and is the most common form of inflammatory arthritis among men (Saag and Choi, 2006). The disease tends to affect men between the ages of 30 and 50 years and is often hereditary. Risks include genetic factors; high intake of seafood and red meats (Choi et al, 2005; Johnson et al, 2005) as well as beer and fructose (Doherty, 2009). Higher intakes of coffee, low-fat dairy products, and vitamin C are associated with lower risk (Doherty, 2009). See Table 11-4 for other etiologies of hyperuricemia. Gout prevalence increases in direct association with age, metabolic syndrome, hypertension, and use of thiazide diuretics (Saag and Choi, 2006). There is increased incidence in postmenopausal women, with polyarticular onset, hand involvement, and development of tophi (Ene-Stroescu and Gorbien, 2005). Tophi are hard lumps of urate crystals that are deposited under the skin around the joints and may be permanent. Acute attacks may be triggered by surgery, sudden and severe illness, fasting, chemotherapy, or joint injury. Acute gout most commonly affects the first metatarsal joint of the foot, but other joints may also be involved. The joint swells, and skin turns warm, red, purplish, and shiny. Severe pain usually occurs, more so at night. Gout progresses from asymptomatic hyperuricemia to acute gouty arthritis, intercritical gout (intervals between acute attacks), and finally to chronic tophaceous gout. Tophi

Adapted from: Harris M, et al. Gout and hyperuricemia. Am Fam Physician. 59:925, 1999.

may develop if the condition goes untreated. Although attacks of gout can subside in a few days, repeated attacks can cause permanent joint damage, and the disease often results in substantial disability and frequent medical care. Treatment includes the pain-relieving NSAIDs and, for more serious outbreaks, corticosteroids. Most patients with gout eventually require long-term treatment with medications that lower blood uric acid levels. Patients with asymptomatic hyperuricemia should lower their urate levels by changes in diet or lifestyle.

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS Genetic Markers: About 10% of people with hyperuricemia develop gout. Genetic variants within the transporter gene, SLC2A9 (GLUT9), affect both fructose and uric acid transport. Other renal urate transporters have been identified, including URAT1. Clinical/History Height Weight BMI

Obesity Urate crystals Swollen, painful in urine big toe Use of thiazide (podagra) diuretics? Arthritis

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Tophus, Birefringent Ca, Mg suspected or crystals in the Na, K proven synovial fluid Albumin (Alb) Asymmetrical BUN Creat swelling (increased) Glucose (Gluc) within a joint Cholesterol AST, ALT on X-ray (Chol) Vitamin D3 staTriglycerides tus (serum Lab Work (increased?) 25-OHD) CRP Uric acid (increased)

• • •

• • •

cauliflower, and spinach yield a protective effect (Choi, 2005). Develop a weight loss plan if needed. Avoid excessive intake of seafood such as anchovies, sardines, caviar, and herring. Reduce intake of beef, pork, duck, bacon, turkey, and ham. Ensure a high-fluid intake, especially water and skim milk. Nonfat milk, low-fat yogurt, dairy products, fruits such as cherries, and high intakes of vegetable protein may reduce serum urate (Schlesinger, 2005). Use of 4 cups of coffee per day should be recommended (Choi and Curhan, 2007). Exclude alcoholic beverages (Schlesinger, 2005) and fructose or sugar-sweetened soft drinks (Choi et al, 2008). Use antioxidant-rich foods such as pomegranate, raspberries, and strawberries.

INTERVENTION OBJECTIVES • Lower bodily stores of uric acid crystal deposits to prevent the inflammatory processes and structural alterations. Increase excretion of urates and force fluid intake to prevent uric acid kidney stones. • Data from NHANES III show a remarkably high prevalence of the metabolic syndrome among individuals with gout, along with an increased risk of myocardial infarction and cardiovascular mortality (Hak and Choi, 2008). Encourage lifestyle changes including reduction in energy intake, weight, alcohol intake, red meat intake. • Promote gradual weight loss. In the obese, controlled weight management has the potential to lower serum urate (Schlesinger, 2005). • Correct any existing dyslipidemia and prevent complications such as renal disease, hypertension, and stroke.

FOOD AND NUTRITION • A low-fat, high-carbohydrate (CHO) diet increases excretion of urates. Vegetables such as peas, mushrooms,

Common Drugs Used and Potential Side Effects • Uricosuric drugs: Probenecid (Benemid) and sulfinpyrazone (Anturane) block renal absorption of urates. Serum uric acid levels should be kept below 360 mol/L (6 mg/dL). Use adequate fluid. Anorexia, nausea, vomiting, and sore gums may result. • The medication febuxostat (Uloric) shows promise. • Xanthine oxidase inhibitors: Allopurinol (Aloprim) blocks uric acid formation. Adequate intake of fluid is needed. Mild gastrointestinal (GI) upset, taste changes, or diarrhea can occur; take after meals. Febuxostat is even more effective than allopurinol; side effects are transient (Schumacher, 2005). • During more serious outbreaks, NSAIDs, colchicine (Colcrys), and corticosteroids (prednione) may be prescribed for short-term use. • Medications that can increase uric acid levels include hydrochlorothiazide (a diuretic) and some transplantation medications (cyclosporine and tacrolimus). Monitor for signs of gout.

Herbs, Botanicals, and Supplements SAMPLE NUTRITION DIAGNOSES Excessive Alcohol Intake Assessment Data: Diet history and food records, medication history, alcohol and fluid intake. Nutrition Diagnosis (PES): Excessive alcohol intake related to consuming large amounts of alcohol (36 oz whiskey daily) as evidenced by recent painful flare of gout with hyperuricemia. Intervention: Food-nutrient delivery—Decrease alcohol intake (ND 3.3). Education: Discuss role of proteins, alcohol, diet, fluid intake, and medications in managing gout. Counseling: Motivational interviewing and goal setting with patient (C 2.1, 2.2) to implement recommended lifestyle modifications into daily plan. Monitoring and Evaluation: Evaluation of alcohol intake records; improvement in symptoms of gout. Monitor need for additional education/counseling. Evaluate for decrease in uric acid levels and lower frequency of gouty attacks.

• Herbs and botanical supplements should not be used without discussing with physician. • Celery, avocado, turmeric, cat’s claw, chiso, and devil’s claw have been recommended; there are no clinical trials that prove efficacy. • Vitamin C shows some effectiveness; 1000 mg may be beneficial in preventing gouty attacks (Gao et al, 2008).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The inflammatory response may be suppressed by omega3 fatty acids from fish oils and from walnuts, flaxseed, and cherries. Use these foods several times a week. • Alcohol, beef, sardines, anchovies, and pork may precipitate a gouty attack (Choi et al, 2005). Otherwise, there is little need for a traditional “low purine” diet (Hayman and Marcason, 2009).

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• Weight loss may be helpful, but avoid fasting. Instruct patient to lose weight gradually. • Discuss the importance of adequate fluid ingestion. Recommend coffee intake (Choi and Curhan, 2007). Avoid sugar-sweetened soft drinks and fructose, but diet soft drinks are acceptable (Choi et al, 2008; Hak and Choi, 2008). • Aim to drink at least a half gallon of water and skim milk daily.

Patient Education—Food Safety If enteral or parenteral nutrition is needed, sanitation and handwashing are essential.

For More Information •

American College of Rheumatology


Diet for Gout

Mayo Clinic—Gout


GOUT—CITED REFERENCES Choi HK. Dietary risk factors for rheumatic diseases. Curr Opin Rheumatol. 17:141, 2005. Choi HK, et al. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 52:283, 2005. Choi HK, Curhan G. Coffee, tea, and caffeine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 57:816, 2007. Choi JW, et al. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 59:1109, 2008. Doherty M. New insights into the epidemiology of gout. Rheumatology. 48:2S, 2009. Ene-Stroescu D, Gorbien MJ. Gouty arthritis. A primer on late-onset gout. Geriatrics. 60:24, 2005. Gao X, et al. Vitamin C intake and serum uric acid concentration in men. J Rheumatol. 35:1853, 2008. Hak AE, Choi HW. Lifestyle and gout. Curr Opin Rheumatol. 20:179, 2008. Hayman S, Marcason W. Gout: is a purine-restricted diet still recommended? J Am Diet Assoc. 109:1652, 2009. Johnson RJ, et al. Uric acid, evolution and primitive cultures. Semin Nephrol. 25:3, 2005. Saag KG, Choi H. Epidemiology, risk factors, and lifestyle modifications for gout. Arthritis Res Ther. 8:2S, 2006. Schlesinger N. Dietary factors and hyperuricaemia. Curr Pharm Des. 11:4133, 2005. Schumacher HR Jr. Febuxostat: a non-purine, selective inhibitor of xanthine oxidase for the management of hyperuricaemia in patients with gout. Expert Opin Invest Drugs. 14:893, 2005.

IMMOBILIZATION NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Extended periods of immobilization, for various reasons, may be nutritionally depleting. Patients with orthopedic injuries may lose 15–20 lb from stress, immobilization, trauma, and bed rest. Prolonged immobilization and nonuse of lower and upper limb muscles may cause atrophy. Nitrogen depletion can be extensive. A large nitrogen loss and high protein oxidation can be related to extensive injury and elevated energy expenditure. Unloading of weight-bearing bones induced by immobilization has significant impacts on calcium and bone metabolism. Immobilization hypercalcemia involves nausea, vomiting, abdominal cramps, constipation, headache, and lethargy. Persons with physical disabilities frequently are nonambulatory and have bone loss due to immobility. Prevention of osteoporosis and related fractures in this population includes calcium and vitamin D supplementation and risk-based screening. With careful attention to functional capacity enhancements, bone mass can be restored (Rittweger et al, 2005). In older individuals, sarcopenia is the result of excessive loss of muscle mass and strength, loss of mobility, neuromuscular impairment, and balance failure. Falls and fractures can lead to immobilization, which induces more loss of muscle mass. One final group at risk for the consequences of immobilization are those individuals who are in intensive care units (ICU) for a prolonged period. There is a need for physical therapy, as possible, to avoid a long recovery.

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS Genetic Markers: Immobilization is usually from injury or other nongenetic causes, but may be a side effect of certain diseases with a genetic origin, such as spina bifida. Dual-energy x-ray absorpHeight or arm tiometry length/knee (DEXA) length Decreased range Weight of motion? BMI Contractures; Weight changes stiff joints? Triceps skinfold Blood clots (TSF) Pressure ulcers Midarm muscle Constipation circumference Indigestion, (MAMC) anorexia? Midarm Depression? circumference Change in qual(MAC) ity of life? Clinical/History

Lab Work H&H Alb Transthyretin, retinolbinding protein (RBP) CRP Nitrogen (N) balance Ca (increased?) Parathormone (PTH)

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Alk phos Urinary Ca Mg (high?) Red blood cell Vitamin D3 (RBC) count status (serum 25-OHD)

BUN, Creat Na, K

intake of phosphorus during the first few weeks may be useful. • Diet should provide a high-fluid intake. • Intake of vitamin C and zinc should be adequate to protect against skin breakdown. • Diet should provide adequate amounts of fiber to prevent constipation. Avoid overuse of fiber in cases where there is impaction.

INTERVENTION OBJECTIVES • Correct negative nitrogen balance from increased losses (perhaps up to 2–3 g of nitrogen per day) to prevent pressure ulcers and infections. Moderate exercise is beneficial in altering the inflammatory milieu associated with immobility, and in improving muscle strength and physical function (Truong et al, 2009). • Correct anorexia, indigestion, constipation. • Prevent deossification and osteoporosis of bones. Prevent hypercalcemia from low serum levels of albumin, which normally binds calcium. • Prevent kidney and bladder stones, urinary tract infections. • Provide adequate fluid intake to aid excretion of nutrients. • Prevent constipation, impactions, and obstruction. • Prevent anemias that result from inadequate nitrogen balance. • Prevent venous thrombosis (McManus et al, 2009). • Improve or sustain a positive quality of life.

Common Drugs Used and Potential Side Effects • Medications may be used to treat underlying conditions; they may have side effects that contribute to nutrient losses. • Take pain medications as directed to maintain relief of pain, rather than only taking then when you feel very badly. • Immobilization-induced hypercalcemia affects bone metabolism in Parkinson’s disease; this inhibits secretion of PTH, which in turn suppresses 1,25-dihydroxyvitamin D production (Sato et al, 2005). These abnormalities may be corrected by the suppression of bone resorption with bisphosphonate; supplementations of calcium and vitamin D should be avoided in these patients (Sato et al, 2005).

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


FOOD AND NUTRITION • Diet should provide adequate intake of high–biological value proteins to correct nitrogen balance. An intake of 1.2 g protein/kg body weight is often recommended. Provide adequate energy to spare protein; use sufficient carbohydrates and fats, including 1–2% total kilocalories as essential fatty acids (EFAs). • Encourage adequate intake of calcium since a high-protein diet raises the body’s calcium requirements. Increased

SAMPLE NUTRITION DIAGNOSES Physical Inactivity Assessment Data: Diet history, food records, medication history, fluid intake. New paraplegia following motorcycle accident. Nutrition Diagnosis (PES): Physical inactivity (NB 2.1) related to paraplegia as evidenced by inability to walk voluntarily after motorcycle accident. Intervention: Food-nutrient delivery—Offer food preferences to maintain desired intake; monitor calcium and protein intake in particular. Education: Discuss importance of physical therapy and nutrition in maintaining as much lean body mass as possible. Monitoring and Evaluation: Evaluate ability to tolerate sufficient physical therapy to maintain adequate skin integrity, muscle mass, and urinary tract function; ability to achieve desirable nitrogen and calcium balance.

• Explain that calcium and nutrient intakes will have to be monitored for patients who will be tube fed or on a liquid diet for extended periods of time. • Explain the need for adequate fiber and fluid (2–3 L) to prevent constipation, urinary tract infections, and so on. Early ambulation is the best treatment possible. • Because prolonged bed rest in the ICU affects the development of ICU-acquired weakness, early mobility requires a reduction in heavy sedation and bed rest (Truong et al, 2009). Identify strengths and limitations, and alternate rest periods with activity. Do range of motion exercises every day. • Monitor and report to a physician any symptoms such as pain and fatigue upon movement, new numbness in legs or arms, loss of motor strength, increased weakness, loss of bowel or bladder control, increased pain on movement.

Patient Education—Food Safety If enteral or parenteral nutrition is needed, sanitation and handwashing are essential.

For More Information •

Family Care Research Program—Immobility and Movement immobility.htm

Rehab Classworks

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IMMOBILIZATION—CITED REFERENCES McManus RA, et al. Thromboembolism. Clin Evid (Online). 2009;pii: 0208. Rittweger J, et al. Reconstruction of the anterior cruciate ligament with a patellatendon-bone graft may lead to a permanent loss of bone mineral content due to decreased patellar tendon stiffness. Med Hypotheses. 64:1166, 2005.


Sato Y, et al. Abnormal bone and calcium metabolism in immobilized Parkinson’s disease patients. Mov Disord. 20:1598, 2005. Truong AD, et al. Bench-to-bedside review: mobilizing patients in the intensive care unit–from pathophysiology to clinical trials. Crit Care. 13:216, 2009.


Lungs Heart

Kidney Joints Blood

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Lupus is an autoimmune disorder that involves areas of inflammation of the joints, tendons, other connective tissues, and skin. A pathologic CD4T cell subset with impaired extracellular signal-regulated kinase (ERK) pathway signaling, DNA hypomethylation, and consequent aberrant gene expression contributes to disease pathogenesis (Gorelik and Richardson, 2010). There are four types of lupus: neonatal, discoid, systemic, and drug induced. The systemic form (SLE) is the most common. One to two million people have lupus, especially Latino, African American, and Native American women, with onset in the late teens to thirties. For most people, lupus is a mild disease affecting only a few organs; for some, it may cause serious and even life-threatening problems. Because lupus has symptoms that mimic other disorders, careful diagnosis is important. Lupus may show symptoms similar to those of celiac disease. Infections can bring on a lupus flare, increasing the risk of even more infections. Other environmental factors that may trigger the disease include antibiotics (especially sulfa and penicillin), other drugs, and exposure to phthalate in toys, plastics, and beauty products. Active lupus contributes to coronary heart disease (CHD) risk (Haque et al, 2010). Premature cardiovascular disease in SLE patients is a consequence of inflammation. Type I interferons stimulate the cascade of atherosclerotic development, starting with endothelial damage and abnormal vascular repair (Von Feldt, 2008). SLE is characterized by autoantibodies to nuclear antigens and immune complex deposition in organs such as the kidney (Gorelik and Richardson, 2010). Lupus nephritis is the term for this form of kidney disease that occurs. About a third of patients with lupus will develop it, requiring medical evaluation and nutritional management. A cure for lupus is not yet possible, but treatments allow a more normal life. The use of methotrexate can reduce the dependency on steroids, which is desirable (Fortin et al, 2008). Antioxidant interventions have been studied extensively and show promise. Finally, supplementation with fish oil may reduce symptomatic disease activity.

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SAMPLE NUTRITION CARE PROCESS STEPS Drug–Nutrient Interaction Assessment Data: Weight and medical histories; medications; altered lab values for calcium, potassium. Complaints of swollen ankles and fluid retention.

CLINICAL INDICATORS Genetic Markers: Persons with close family members who have lupus have a 10 times greater frequency than the general population. Alleles in the TYK2 gene have been associated with SLE as well as multiple sclerosis. Achy joints (arthralgia) Height Swollen and Weight painful joints BMI (nonerosive BP arthritis) I&O Protein or Fever over 100F cellular Seizures and casts in urine cognitive Swollen ankles dysfunction Dry eyes Butterfly rash Easy bruising across cheeks and nose Lab Work Skin rashes, LE prep red raised ESR or CRP patches (elevated?) Photosensitivity Painless mouth Complement protein test or nose ulcers (C3, C4, Pale or purple CH50, fingers from CH100) cold or stress INR, abnormal (Raynaud’s blood clotting syndrome) Positive antiUnusual hair nuclear loss antibody Pleuritis or test (ANA) pericarditis Fatigue, prolonged Clinical/History

Antibodies to doublestranded DNA Serum copper (increased) Total protein (decreased) WBC (decreased) Gluc (increased) Low platelet count H & H, serum ferritin (decreased) Transferrin Chol (increased) BUN, Creat Specific gravity, urine (decreased) Alb, transthyretin Transferrin Ca, Mg Na, K Vitamin D3 status (serum 25-OHD)

INTERVENTION OBJECTIVES • Counteract steroid therapy; replenish potassium and nutrient reserves. • Reduce fever and replace nutrient losses and weight loss. • Control disease manifestations. • Manage cardiac effects. Accelerated atherosclerosis and premature CHD are recognized complications (Haque et al, 2010). Pericarditis is also common, with shortness of breath and chest pain. • Rule out gluten intolerance.

Nutrition Diagnosis (PES): Drug–nutrient interaction related to prolonged use of corticosteroids for lupus as evidenced by osteopenia, low serum calcium and potassium, negative nitrogen balance and sodium-fluid retention. Intervention: Food-nutrient delivery—Alter dietary intake to increase protein-rich foods, sources of potassium and calcium; decrease sodium intake. Education about the importance of managing specific nutrients while taking steroid medications (i.e., protein, calcium, potassium) and decreasing sodium-rich foods. Counseling about how to apply the DASH diet principles, which may be helpful. Monitoring and Evaluation: Fewer complaints of swollen ankles and fluid retention; improved lab values related to calcium, potassium, and nitrogen balance studies.

• Prevent or manage infections, such as urinary tract infections, shingles, respiratory infections such as colds, yeast infections, salmonella and herpes.

FOOD AND NUTRITION • Diet should be adequate in protein and energy during fever. • When renal disease is present, diet should be adjusted. Check lab values regularly. • Alter diet, if needed, to lower blood pressure (BP) levels or excess weight. Mildly restrict sodium intake and monitor for potassium and phosphorus changes. • Dietary nutrients may modify clinical course of disease. Vitamin C intake may prevent the occurrence of active disease; use a multivitamin–mineral supplement. • Anemia is often present. Vitamin B12, dietary fiber, iron, calcium, and folate may be low in the diets of lupus patients. However, avoid excessive doses of supplements; use DRI levels. • Use a nutrient-rich diet that includes nuts, fish and fish oils, olive oil, fruits, vegetables, and whole grains that are rich in phytochemicals, omega-3 fatty acids, and antioxidants. Include phytochemicals derived from spices (see Table 11-2). • If gluten intolerance is present, provide a gluten-free nutrition plan.

Common Drugs Used and Potential Side Effects • Benlysta (belimumab), is a new drug developed specifically for people with systemic lupus. Many other drugs are in clinical trials.

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• Steroid therapy may cause sodium retention, hyperglycemia, potassium and calcium depletion, and negative nitrogen balance. Side effects include weight gain, a round face, acne, easy bruising, fractures or osteoporosis, hypertension, cataracts, hyperglycemia or onset of diabetes, increased risk of infection, and stomach ulcers. Fish oil supplements may allow gradual reduction in use of steroids. • Methotrexate (Rheumatrex) confers an advantage in participants with moderately active lupus by lowering daily prednisone dose and slightly decreasing lupus disease activity (Fortin et al 2008). • Corticosteroid and cytotoxic drugs affect the immune system over time, making the individual prone to more infections. Immunosuppressive agents such as azathioprine (Imuran) and cyclophosphamide (Cytoxan) or methotrexate are used to control the overactive immune system but they have GI side effects. • NSAIDs and acetaminophen may be useful. • Sunscreens are needed to protect against the sun’s harmful rays; there are no systemic side effects. • Antimalarials, such as chloroquine (Aralen) or hydroxychloroquine (Plaquenil), may be used for skin and joint symptoms of lupus. Side effects are rare and consist of occasional diarrhea or rashes. Chloroquine can affect the eyes. Hydroxychloroquine may cause anorexia, nausea, abdominal cramps, and diarrhea.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Coumestrol, a natural phytoestrogen, may relieve some symptoms. • Use of indoles, conjugated linolenic acid (CLA), and vitamins C, E, and D may be beneficial.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Ensure patient has an adequate intake of fluids during febrile periods. • Explain which foods are sources of sodium and potassium in the diet.


• Adequate rest is needed during flare-ups. • Cortisone creams may be needed for persistent skin rashes. Sunblock should be used outdoors. • Discuss how to manage diet for elevated blood glucose; insulin may be needed. Carbohydrate counting may be useful. • Regular doctor visits and lab tests are important, especially blood and urine testing. • Dietary strategies for the prevention of obesity, osteoporosis, and dyslipidemia deserve attention. Weight loss plans may be needed.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Lupus Alliance of America

Lupus Canada

Lupus Foundation of America

Lupus Library

Lupus Organizations

SLE Foundation, Inc.

LUPUS—CITED REFERENCES Fortin PR, et al. Steroid-sparing effects of methotrexate in systemic lupus erythematosus: a double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 59:1796, 2008. Gorelik G, Richardson B. Key role of ERK pathway signaling in lupus [published online ahead of print December 7, 2009]. Autoimmunity. 37:322, 2010. Haque S, et al. Risk Factors for Clinical Coronary Heart Disease in Systemic Lupus Erythematosus: The Lupus and Atherosclerosis Evaluation of Risk (LASER) Study [published online ahead of print December 1, 2009]. J Rheumatol. 37:322, 2010. Tam LS, et al. Effects of vitamins C and E on oxidative stress markers and endothelial function in patients with systemic lupus erythematosus: a double blind, placebo controlled pilot study. J Rheumatol. 32:275, 2005. Von Feldt JM. Premature atherosclerotic cardiovascular disease and systemic lupus erythematosus from bedside to bench. Bull NYU Hosp Jt Dis. 66:184, 2008.

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MUSCULAR DYSTROPHY NUTRITIONAL ACUITY RANKING: LEVEL 2 Gene therapy, gene silencing, and cell therapy are potential therapies for MD patients. Some evidence exists supporting supplementation with creatine monohydrate to improve muscle strength (Davidson and Truby, 2009). Creatinine as a marker of renal function has limited value in DMD because of reduced muscle mass. There is potential value of cystatin C as a biomarker for monitoring renal function (Violett et al, 2009). The prognosis of MD varies according to type and progression. Some cases may be mild and very slowly progressive, with a normal lifespan. Other cases may have more marked progression of muscle weakness, functional disability, and loss of ambulation. Life expectancy often depends on the degree of progression and late respiratory deficit. In DMD, death often occurs in the late teens or early twenties. Rehabilitation, orthopedic, respiratory, cardiovascular, gastroenterology, nutrition, pain issues, as well as general surgical and emergency-room considerations are essential to address (Bushby et al, 2010).

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS DEFINITIONS AND BACKGROUND Actually a group of nine disorders, muscular dystrophy (MD) involves a hereditary condition with progressive degenerative changes in the muscle fibers, leading to weakness and atrophy. Most of the disorders are described in Table 11-5. Muscular biopsy is required for the definitive diagnosis of the specific congenital type. BMI should be used with caution for the evaluation of the nutritional status of patients with Duchenne MD (DMD); assessment of the compartmental distribution of muscle and fat are more sensitive. Extremely elevated serum creatine kinase (CK) levels may indicate muscle disease. In the late stages, fat and connective tissue may replace muscle fibers. Patients with MD may be prone to nutrient deficiency due to mobility limitations or oropharyngeal weakness (Motlagh et al, 2005). Micronutrient requirements are yet to be determined but, as a result of corticosteroid treatment, vitamin D and calcium should be supplemented (Davidson and Truby, 2009). Many patients demonstrate inadequate nutrient intake of protein, energy, vitamins (especially E), and minerals (calcium, selenium, and magnesium), and significant correlations exist between measures of strength and copper and water-soluble vitamins (Motlagh et al, 2005). Delayed growth, short stature, muscle wasting, and increased fat mass are characteristics that impact on nutritional status and energy requirements (Davidson and Truby, 2009). There may be loss of muscle mass, wasting, which may be hard to see because some types of MD cause a build-up of fat and connective tissue that makes the muscle appear larger (pseudohypertrophy).

Genetic Markers: Dystrophinopathies are due to a genetic defect of the protein dystrophin. Genetic counseling is advised when there is a family history of MD. Note that DMD can be detected by genetic studies performed during pregnancy. Eyelid drooping (ptosis) Height Dysphagia? Weight Drooling BMI (use only Chewing with other difficulty? parameters) Hand-to-mouth MAC, MAMC, coordination TSF ElectromyograMuscle weakness phy (EMG) Apparent lack of Electrocardiocoordination graphy (ECG) Progressive DEXA crippling Scoliosis? Lab Work Contractures of Muscle biopsy the muscles Creatine phosaround the phokinase joints (CPK), Clubfoot or increased? clawhand? Lactate dehydroHypotonia genase Loss of mobility Clinical/History

(LDH), increased Cystatin C Myoglobinurine/serum Creat (often decreased) Aldolase, AST (altered) BUN N balance Alb, transthyretin CRP H & H, serum ferritin Serum P Gluc AST, ALT Ca, Mg Na, K Vitamin D3 status (serum 25-OHD)

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TABLE 11-5 Types of Muscular Dystrophy and Nutritional Implications Type of MD


Nutritional Implications

Becker muscular dystrophy (BMD)

Very similar to DMD (see below), but onset is later (adolescence or adulthood). BMD patients live longer.

Weakness makes it difficult for selffeeding.

Congenital muscular dystrophy (CMD)

Caused by genetic mutations affecting some of the proteins necessary for muscles and some proteins related to the eyes and/or brain. Onset is at or near time of birth. Indicators include generalized muscle weakness with possible joint stiffness or looseness. Depending on the type, CMD may involve spinal curvature, respiratory insufficiency, mental retardation or learning disabilities, eye defects, and seizures.

Weakness makes it difficult for selffeeding.

Distal muscular dystrophy (DD)

DD is caused by a mutation in any of at least seven genes that affect proteins necessary to the function of muscles; it is usually passed on as an autosomal dominant or autosomal recessive trait. DD (Miyoshi form) first shows signs between ages 40 and 60 years, with weakness and muscle wasting of the hands, forearms, and lower legs; it progresses slowly.

Weakness and muscle wasting of the hands and forearms make selffeeding difficult.

Duchenne muscular dystrophy (DMD)

DMD primarily affects young boys, who inherit the disease through their mothers (X-linked recessive). Also called pseudohypertrophic. Caused by absence of dystrophin, a protein that helps keep muscle cells intact. DMD is the most severe form of dystrophinopathy. Aggressive forms appear in age 2–3, with frequent falls, difficulty in getting up from sitting or lying position. Generalized weakness and muscle wasting affect hip, thigh, shoulder, and trunk muscles first; large calf muscles. Weakness in lower leg muscles, resulting in difficulty running and jumping; waddling gait; mild mental retardation or scoliosis, in some cases. Survival is rare after the late twenties.

Facial muscles are involved; patient cannot suck, close lips, bite, chew, or swallow. DMD eventually affects all voluntary muscles, the heart, and lung muscles.

Emery-Dreyfus muscular dystrophy (EDMD)

EDMD is caused by gene mutations that produce emerin, lamin A, or lamin C, which are proteins in the membrane that surrounds the nucleus of each muscle cell. Onset in childhood, usually by age 10. Weakness and wasting of shoulder, upper arm, and shin muscles and joint deformities are common. Disease usually progresses slowly. Frequent cardiac complications are common, and a pacemaker may be needed.

Self-feeding becomes difficult.

Fascioscapulohumeral muscular dystrophy (FSHMD)

FSHMD (also called Landouzy-Dejerine) begins in childhood to early adulthood, with facial muscle weakness and weakness and wasting of the shoulders and upper arms. Caused by a missing piece of DNA on chromosome 4, it progresses slowly with some periods of rapid deterioration. Usually evident by age 20, it may span many decades. Inheritance is autosomal dominant, which means it can be passed on by either parent. It is considered to be the most common form.

Self-feeding becomes difficult; loss of skeletal muscle occurs. Abdominal muscles are affected.

Limb-girdle muscular dystrophy (LGMD)

LGMD is caused by a mutation in any of at least 15 different genes that affect proteins necessary for muscle function. LGMD has an onset in late childhood to middle age. Weakness and wasting affects shoulder and pelvic girdles first. Progression is slow, with cardiopulmonary complications often occurring in later stages of the disease. It is inherited as an autosomal recessive, autosomal dominant trait.

Self-feeding becomes difficult.

Myotonic dystrophy (MyD)

MyD (Steinert’s disease) has onset anywhere from birth to middle age. Congenital myotonic form is more severe. Generalized weakness and muscle wasting affect the face, feet, hands, and neck first. Delayed relaxation of muscles after contraction. Progression is slow, sometimes spanning 50–60 years. Inheritance is autosomal dominant; there is a repeated section of DNA on either chromosome 19 or chromosome 3. Individuals with MyD have long faces and drooping eyelids; men have frontal baldness.

Progression is slow. Often complicated by diabetes. Prone to nutritional deficiencies from associated dysmotility of the entire GI. Handgrip is significantly lower; knee extension is higher compared to other dystrophies (Motlagh et al, 2005).

Oculopharyngeal muscular dystrophy (OPMD)

OPMD has onset in early adulthood to middle age. It affects muscles of eyelids (causing droopy eyelids) and throat. It progresses slowly, with swallowing problems common. Inheritance is autosomal dominant, and onset is usually in the fourth or fifth decade. The gene that is defective in OPMD is called the poly(A) binding protein2 gene; extra amino acids in the protein made from the defective PABP2 gene cause the protein to clump together in the muscle cell nuclei, interfering with cell function. OPMD can be diagnosed with a DNA test.

Swallowing difficulty is common. Tube feeding should be considered before wasting occurs.

From the Muscular Dystrophy Association, accessed November 16, 2009, at

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Type of CMD


Inheritance Pattern

Merosin-deficient CMD

Lack of merosin (laminin 2) or other defect leading to merosin deficiency

Chromosome 6 gene Other genes

Ullrich CMD

Abnormalities in collagen 6

Chromosome 2 or 21 genes, recessive or dominant

Bethlem myopathy

Abnormalities in collagen 6

Chromosome 2 or 21 genes, dominant

Integrin-deficient CMD

Lack of integrin alpha 7

Chromosome 12 gene, recessive

Fukuyama CMD (FCMD)

Lack of fukutin

Chromosome 9 gene, recessive

Muscle-eye-brain disease (MEB)

Lack of POMGnT1, fukutin or fukutin-related protein

Chromosome 1, 9, or 19 genes, recessive

Walker–Warburg syndrome (WWS)

Lack of POMT1, POMT2, fukutin or fukutin related protein

Chromosome 9, 14, or 19 genes, recessive

CMD with rigid spine syndrome

Lack of selenoprotein N1

Chromosome 1 gene, recessive

INTERVENTION OBJECTIVES • Encourage patient to lead a relatively active life; exercise programs can help prevent contractures. • Prevent obesity, from inactivity; obesity complicates physical therapy. • Encourage activities other than eating to prevent dependency on food as a source of pleasure. • Malnutrition is a serious threat, especially with respiratory muscle weakness. Monitor nutritional intake and deficits

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function—Constipation Assessment Data: Weight and physical activity histories. Medical history, medications and lab values. Complaints of chronic constipation and GI discomfort. Diet hx showing low fiber and intake of 4 cups of fluid per day to avoid the need to urinate. Nutrition Diagnosis (PES): Abnormal GI function related to constipation and physical inactivity as evidenced by infrequent evacuation, hard stools, and GI discomfort. Intervention: Food and Nutrient Delivery—Increase fluid and fiber sources from tolerated foods such as whole grain cereals, fresh fruits, and vegetables. Educate about the desirable foods and fluid intake. Counsel about the importance of daily range of motion and physical exercises. Coordinate care with other disciplines according to needs, including PT, OT, nursing, medical team. Monitoring and Evaluation: Alleviation of constipation. No further complaints of GI discomfort related to infrequent stooling pattern.

on a regular basis. Prevent aspiration pneumonia or nasal regurgitation. Use a multidisciplinary approach, especially for feeding difficulties such as texture modification and supplemental feeding (Davidson and Truby, 2009). • Avoid constipation because fecal impaction is frequent. • Prevent osteoporosis and fractures, which can occur in this population. • Manage long-term consequences, such as cardiomyopathy or respiratory failure.

FOOD AND NUTRITION • Work with the MyPyramid food guidance system as a basic guide. Check patient’s BMI and adjust intake accordingly. Use a low-energy diet if necessary to control or lessen obesity. Some patients’ requirements may be 30% lower than normal (Munn et al, 2005). • Use foods that are easy to chew and swallow for DMD, such as pureed or blenderized foods. Tube feed only if necessary. • Provide adequate fiber (prune juice, bran and other whole grains, fruits, and vegetables) if constipation becomes a problem. • Ensure adequate intake of fluid to prevent fecal impaction, dehydration, and related effects. • Adequate sodium chloride is important (Yoshida et al, 2006). Manage carefully if there are cardiac side effects or problems with BP.

Common Drugs Used and Potential Side Effects • The myotonia (delayed relaxation of a muscle after a strong contraction) may be treated with medications

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such as phenytoin or quinine. Side effects can include folic acid depletion. • Early introduction of steroids can exacerbate weight gain in a population already susceptible to obesity (Davidson and Truby, 2009). • It may be useful to try beta2-adrenergic agonists, which can increase muscle mass. Albuterol may be needed for some individuals prior to exercise and strength training.

Patient Education—Food Safety

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. Approximately 50% of children are on herbal preparations, 30% of adolescents take herbal medications, and 70% of adults use some aspect of complementary medicine (Buehler, 2007). • Green tea extract may improve muscle health by reducing or delaying necrosis by an antioxidant mechanism (Dorchies et al, 2006). • Traditional Chinese medicine has been advocated for treatment of types of MD, but studies are needed to identify active ingredients. • Supplementation with creatine monohydrate may improve muscle strength (Davidson and Truby, 2009).


Provide low-calorie snack tips for patients who are obese. Help patient modify food textures to meet needs. Discuss problems related to inactivity or weight gain. Discuss the importance of adequate fluid intake. Discuss methods to prevent aspiration and pneumonia. Comprehensive management strategies can improve function, quality of life, and longevity (Bushby et al, 2010). Work with the occupational therapist and other therapists to maintain optimal levels of function.


If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Facioscapulohumeral Dystrophy (FSHD) Society

Muscular Dystrophy Association (MDA)

Muscular Dystrophy Association of Canada

Muscular Dystrophy Family Foundation

National Institute—MD

Neuromuscular Disorders in the MDA Foundation

Parent Project for Muscular Dystrophy Research

Rare Muscular Dystrophy types

MUSCULAR DYSTROPHY—CITED REFERENCES Buehler BA. Complementary and alternative medicine (CAM) in genetics. Am J Med Genet A. 143:2889, 2007. Bushby K, et al. Diagnosis and management of Duchenne muscular dystrophy, part 2: implementation of multidisciplinary care [published online ahead of print November 27, 2009]. Lancet Neurol. 9:177, 2010. Davidson ZE, Truby H. A review of nutrition in Duchenne muscular dystrophy. J Hum Nutr Diet. 22:383, 2009. Dorchies OM, et al. Green tea extract and its major polyphenol (-)-epigallocatechin gallate improve muscle function in a mouse model for Duchenne muscular dystrophy. Am J Physiol Cell Physiol. 290:C616, 2006. Motlagh B, et al. Nutritional inadequacy in adults with muscular dystrophy. Muscle Nerve. 31:713, 2005. Munn MW. Estimate of daily calorie needs for a neuromuscular disease patient receiving noninvasive ventilation. Am J Phys Med Rehabil. 84:639, 2005. Violett L, et al. Utility of cystatin C to monitor renal function in Duchenne muscular dystrophy. Muscle Nerve. 40:438, 2009. Yoshida M, et al. Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy. Am J Physiol Regul Integr Comp Physiol. 290:R449, 2006.

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Adapted from: William J. Koopman, Larry W. Moreland, Arthritis and Allied Conditions A Textbook of Rheumatology, 15th ed. Philadelphia: Lippincott Williams & Wilkins, 2005.

DEFINITIONS AND BACKGROUND Myofascial pain syndromes are a group of disorders characterized by achy pain and stiffness in soft tissues, including muscles, tendons, and ligaments. In the United States, fibromyalgia (FM) is estimated to occur in 2% of adults (Mease, 2005). Diagnosis is difficult, and the etiology is not clear. Corticotropin-releasing hormone (CRH) and substance P (SP) are found in increased levels in the cerebral spinal fluid (CSF) of FM patients, and increased interleukin (IL)-6 and IL8 are found in the serum where they release proinflammatory and neurosensitizing molecules (Lucas et al, 2006). FM, or “fibrositis,” is a central sensitivity syndrome with abnormalities in the peripheral, central, sympathetic nervous systems, and the hypothalomo–pitutary–adrenal axis stress response system (Mease, 2005). Etiology theories abound, including inadequate sleep, physical or psychological trauma, or exposure to viruses such as hepatitis B or C, or HIV infection. Serotonin and dopamine levels may be lower than normal. Insulin-like growth factor-1 (IGF-1) levels may also be low; they are a surrogate marker for low growth hormone secretion during stage 3 and 4 of sleep, when tissue repair occurs (Rosenzweig and Thomas, 2009). FM causes widespread pain and stiffness either throughout the body or localized along the spine. Persistent symptoms may be disruptive but are not life threatening. Symptoms include sleep disturbance, depression, fatigue, headaches, irritable bowel syndrome, numbness in the hands and feet, and mood disorders. Acupuncture may offer relief (Martin et al, 2006). Polymyalgia rheumatica (PMR) affects people over age 70 years, usually women. It causes aching, severe muscle stiffness, and pain. Symptoms start suddenly and may affect several areas in the neck, shoulders, hips, and/or thighs. It

usually goes away with treatment but may reoccur. Symptoms include mild joint stiffness and swelling, face pain, anemia, extreme fatigue, unintentional weight loss, and anorexia. The cause of PMR is not known but may be related to aging. Diagnosis is difficult. Many people with PMR also have giant-cell arteritis with double vision, severe headaches, or vision loss. Low-dose corticosteroids may be needed for up to a year (Hernandez-Rodriguez et al, 2009). Treatment of myofascial pain disorders may include exercise, medications such as glucocorticoids and NSAIDs, a healthy diet rich in antioxidants, and adequate rest. Massage and cognitive behavioral therapy (CBT) are helpful (Mease, 2005). After a warm-water swimming program, a significant decrease in IL-8, IFNgamma, and CRP has been noted (Ortega et al, 2009). Use of a phyochemical-rich diet results in a decrease in joint stiffness and pain as well as an improvement in self-reported quality of life. Plant foods are rich natural sources of antioxidants (quercetin, myristin, and kaempherol) in addition to fiber and other nutrients. A vegan diet often shows highly increased serum levels of betaand alpha-carotenes, lycopene, lutein, and vitamins C and E. Rapid-paced discovery is taking place in genetics, patient assessment, new therapeutic targets, and novel methods of treatment delivery (Williams and Clauw, 2009). The best multidisciplinary team includes a rheumatologist, physical therapist, exercise therapist, dietitian, and massage therapist (Lemstra and Olszynski, 2005).


CLINICAL INDICATORS Genetic Markers: A multigenic or genome-wide approach may be needed to alter individualized pain therapy according to the patient’s genotype. For example, DRD2 polymorphisms decrease the functioning of the dopaminergic reward system; this could cause an individual to require more pain medicine. Research is ongoing to determine whether individuals with FM have the genetic tendency toward lower pain thresholds. Clinical/History Height Weight BMI Tender areas, back pain Headache Depression, mood disorders

Morning FM-pain in stiffness shoulders, Fatigue, sleep pelvis, and disturbances hips (pain in Fibromyalgia 11/18 trigger Impact points) Questionnaire Carpal tunnel (FIQ) syndrome (in PMR)

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Trig, Chol Alb, CRP or ESR transthyretin (may be high) BUN, Creat Plasma adrenoCa, Mg medullin Na, K (high in Gluc PMR) Lab Work

Alk phos Vitamin D3 status (serum 25-OHD)

INTERVENTION OBJECTIVES • Relieve pain. Acupuncture, massage, cognitive-behavior therapy (CBT) and varied exercises may be recommended (Assefi et al, 2005; Rosenzweig and Thomas, 2009). • Lose weight, if obese. • Correct underlying problems such as hypertension. • Support lifestyle changes, including stress reduction, relaxation techniques, and exercise. • Prevent blindness in PMR when there is giant-cell arteritis.

FOOD AND NUTRITION • Use a balanced diet. The MyPyramid food guidance system is another useful tool for planning a healthy diet. Include phytochemicals; dietary quercetin should be encouraged (Lucas et al, 2006). Table 11-2 is also a useful reference. • A vegan diet may be beneficial with berries, fruits, vegetables, roots, nuts, germinated seeds, and sprouts. • A weight loss plan may be needed.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Intake of Bioactive Substances Assessment Data: Weight and physical activity histories. Medical history, medications and lab values. Much pain; diagnosed FM. Diet hx and 3-day food record shows intake of 2 fruits and vegetables daily. No food allergies. Nutrition Diagnosis (PES): Inadequate intake of bioactive substances related to low intake of fruits and vegetables as evidenced by diet history and intake records. Intervention: Food and Nutrient Delivery—Provision of more spices, fruits, vegetables and juices. Education about the role of antioxidants, spices, and phytochemicals in reducing inflammation and the possibility of lessening pain symptoms. Counseling about menus, recipes and cooking tips for including more bioactive ingredients. Encourage intake of fish oils, walnuts, fatty fish such as salmon for omega-3 fatty acids. Monitoring and Evaluation: Diet Hx showing improved intake of spices (such as turmeric, cumin, cinnamon), cocoa and coffee, fruits including berries and apples and pomegranates, vegetables such as broccoli and cabbage on a daily and weekly basis. Fewer complaints of overt pain.


• Increased intake of omega-3 fatty acids may help to reduce inflammation and relieve pain in some individuals. Increase intake of fatty fish, walnuts, and flaxseed.

Common Drugs Used and Potential Side Effects • Medications that decrease pain and improve sleep may be prescribed. Low doses of tricyclic antidepressants (amitriptyline, Elavil; cyclobenzaprine, Flexeril) and the serotonin-3 receptor antagonist tropisetron may be helpful (Lucas et al, 2006; Rosenzweig and Thomas, 2009). Opioids, NSAIDs, sedatives, muscle relaxants, and antiepileptics have been used to treat FMS (Mease, 2005). • Pregabalin (Lyrica) and duloxetine (Cymbalta) are used in FMS. Milnacipran (Savella) is a dual norepinephrine and serotonin reuptake inhibitor that has been shown to be safe (Arnold et al, 2009; Mease et al, 2009). • Opioids are not recommended for FM (Rosenzweig and Thomas, 2009). • For PMR, a trial of low-dose corticosteroids is given, usually in the form of 10–15 mg of prednisone (Deltasone, Orasone) per day. Side effects may include sleeplessness, weight gain, loss of nitrogen and calcium, cataracts, thinning of the skin, easy bruising. NSAIDS, such as ibuprofen (Advil, Motrin) and naproxen (Naprosyn, Aleve), are ineffective in the treatment of PMR.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. CAM is popular for musculoskeletal conditions. Some CAM modalities show significant promise, such as acupuncture (Martin et al, 2006). Excellent resources are available on the Internet from the National Center for Complementary and Alternative Medicine ( • Magnesium; sulfur compounds such as SAMe, dimethylsulfoxide (DMSO), taurine, glucosamine, and chondroitin sulfate; and reduced GSH may have clinical applications in the treatment of FMS; controlled trials are needed.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Aerobic exercise, patient education and CBT are quite effective. Daily exercise will be important for strengthening weak muscles. Exercise adherence can help reduce the need for pain medications (Lemstra and Olszynski, 2005). • Discuss weight management, as needed. • Discuss the role of omega-3 fatty acids in reduction of inflammation.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

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For More Information •

American Fibromyalgia Syndrome Association, Inc.

Fibromyalgia Network

Mayo Clinic

Myositis Association

National Fibromyalgia Partnership, Inc.

National Institute of Arthritis and Musculoskeletal and Skin Diseases

Polymyalgia Rheumatica conditions/polymyalgiarheumatica.asp

Polymyalgia Rheumatica and Giant Cell Arteritis

MYOFASCIAL PAIN SYNDROMES—CITED REFERENCES Assefi NP, et al. A randomized clinical trial of acupuncture compared with sham acupuncture in fibromyalgia. Ann Intern Med. 143:10, 2005.

Arnold LM, et al. Efficacy of duloxetine in patients with fibromyalgia: pooled analysis of 4 placebo-controlled clinical trials. Prim Care Companion J Clin Psychiatry. 11:237, 2009. Hernandez-Rodriguez J, et al. Treatment of Polymyalgia Rheumatica. Arch Intern Med. 169:1839, 2009. Lemstra M, Olszynski WP. The effectiveness of multidisciplinary rehabilitation in the treatment of fibromyalgia: a randomized controlled trial. Clin J Pain. 21:166, 2005. Lucas HJ, et al. Fibromyalgia—new concepts of pathogenesis and treatment. Int J Immunopathol Pharmacol. 19:5, 2006. Martin DP, et al. Improvement in fibromyalgia symptoms with acupuncture: results of a randomized controlled trial. Mayo Clin Proc. 81:749, 2006. Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. J Rheumatol. 75:6S, 2005. Mease PJ, et al. The efficacy and safety of milnacipran for treatment of fibromyalgia. a randomized, double-blind, placebo-controlled trial. J Rheumatol. 36:398, 2009. Ortega E, et al. Exercise in fibromyalgia and related inflammatory disorders: known effects and unknown chances. Exerc Immunol Rev. 15:42, 2009. Rosenzweig TM, Thomas TM. An update on fibromyalgia syndrome: the multimodal therapeutic approach. Am J Lifestyle Med. 10:226, 2009. Williams DA, Clauw DJ. Understanding fibromyalgia: lessons from the broader pain research community. J Pain. 10:777, 2009.


Bone Cartilage

Degeneration of cartilage

Loss of Cartilage

Cartilage particles

Bony outgrowth

Adapted from: Cohen BJ. Medical Terminology, 4th ed. Philadelphia. Lippincott Williams & Wilkins 2003.

DEFINITIONS AND BACKGROUND OA may be primary (in older individuals) or may follow an injury or disease involving the articular surfaces of synovial joints. The joint may lose its normal shape and bone spurs may grow on the edges of the joint. OA is a common health problem in populations over age 40 years, and it is a leading cause of pain and disability. OA mostly affects cartilage where the surface layer breaks down and wears away. The hands, knees, hips, and spine are most commonly affected.

Over 40 million Americans report that they have arthritis and many indicate that it limits their daily activities. High serum concentrations of tumor necrosis factor are associated with lower physical function and more pain, stiffness, and physical disability. Over a third of adults with arthritis experience limitations in their ability to work. Treatments for OA combine nonpharmacological modalities, pharmacological agents, and surgical procedures. Exercise, weight control, rest, and relief from stress on joints, nondrug pain relief, and various types of complementary

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medical techniques may be useful. Continuous passive motion (CPM), massage, and heat treatments may be used. Surgery is reserved for those persons for whom other treatments have been unsuccessful. Weight loss is a primary treatment for OA for individuals who are obese. Obesity is a significant risk factor for and contributor to increased morbidity and mortality from chronic diseases, including OA (Pi-Sunyer, 2009). Overweight causes strain on joints and should be managed early by health professionals (Gasbarrini and Piscaglia, 2005). An average weight loss of 5% in overweight and obese older patients brings an 18% gain in overall function (Messier et al, 2005), and a 10% weight loss improves function by 28% (Christensen et al, 2005). While vitamins A, C, and E have major roles in modulating oxidative stress, immune responses, and cell differentiation, controlled trials found that these vitamins do not halt progression of OA (Choi, 2005). Vitamins D and K play a protective role (Bergink et al, 2009; Oka et al, 2009). Diets rich in omega-3 fatty acids may reduce joint stiffness and pain, increase grip strength, and enhance walking pace. Pomegranate fruit extracts can block interleukin-1 (IL-1 ) enzymes that contribute to cartilage destruction and OA. Finally, cadgerin-11 is a protein that contributes to joint destruction and a related fabric has been developed for cartilage replacement.


CLINICAL INDICATORS Genetic Markers: OA is the breakdown and inflammation of joint cartilage, usually brought on by aging and repetitive joint usage. OA and cardiovascular disease share age and obesity as risk factors, but may also be linked by pathogenic mechanisms involving metabolic abnormalities and systemic inflammation (Puenpatom and Victor, 2009). Clinical/History Height Weight BMI Obesity? Pain, swelling of joints (arthralgia) Synovial joint stiffness Crunching sound of bone against bone

X-rays; DEXA OA Index Lab Work Antistreptolysin titer (ASO) Antirheumatoid factor BUN, Creat Sedimentation rate CRP

Gluc Alk phos Uric acid Ca, Mg Na, K Serum folate and B12 Vitamin D3 status (serum 25-OHD)


SAMPLE NUTRITION CARE PROCESS STEPS Overweight Assessment Data: Weight and physical activity histories; symptoms diary; medical history, medications, and lab values. Nutrition Diagnosis (PES): Overweight with joint pain related to eating double portions at lunch and dinner meals as evidenced by diet history and BMI of 29. Intervention: Food and Nutrient Delivery—Offer choices of lower fat and low energy foods and snacks. Educate about the role of excess weight and joint pain. Counsel and offer weight management tips, tips for dining out or snacking. Coordinate care with referral to physical therapy for exercises to reduce pain and stiffness in affected joints. Monitoring and Evaluation: Weight changes, food intake records, symptoms diary.

INTERVENTION OBJECTIVES • Control pain and improve joint function. If joint replacement is necessary, prepare for surgery accordingly. • Maintain a normal body weight. If needed, weight loss may be beneficial to lessen pressure on weight-bearing joints. • Maintain an active lifestyle as much as possible. • Encourage patient (especially if older) to consume adequate amounts of vitamins D and K, protein and calcium from a healthy, nutrient-dense, antioxidant-rich diet. • Maintain integrity of cartilage in affected joints. Omega3 fatty acids may reduce the activity of enzymes that destroy cartilage. Include fish oils and certain plant seed oils that impact immune and inflammatory responses as precursors of eicosanoids.

FOOD AND NUTRITION • Use a calorie-controlled diet if obesity is present. Use of a meal replacement may help to promote weight loss. • The inflammatory response may be suppressed by an increase in omega-3 fatty acids, as found in fatty fish (mackerel, herring, and salmon) and from walnuts and flaxseed. Use these foods several times a week. • Calcium is found in dark green, leafy vegetables, such as kale and broccoli; canned sardines and salmon with bones; fortified orange juice; milk and dairy products, such as cheese and yogurt; fortified bread, tofu or soy milk. • Vitamin C is needed for healthy collagen and cartilage. Good sources include citrus fruits, bell peppers, tomatoes, watermelon, strawberries, and kiwifruit. • Low dietary vitamin D intake increases the risk of progression of knee OA, particularly in subjects with low baseline BMD (Bergink et al, 2009). Include vitamin D from sardines, herring, fish-liver oil; butter and cream; egg yolks; liver; fortified cow’s milk and dairy

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products, such as cheese and yogurt; and fortified cereals. • Vitamin K may be found in leafy greens such as kale, Swiss chard, broccoli, spinach, raw parsley. It is also found in small amounts in olive, soybean or canola oils and in mayonnaise. • Boron may help OA. Sources include apples, legumes, leafy vegetables, carrots, pears, grapes, and some drinking water. • Include plenty of phytochemicals. Pomegranates and cranberries are especially protective because of the ellagic acid. See Table 11-2.

Common Drugs Used and Potential Side Effects • Because of GI risks (including ulcer complications) and cardiovascular risks, including hypertension and thrombotic events associated with NSAIDs, acetaminophen is the first choice anti-inflammatory agent (Berenbaum, 2008). Table 11-6 gives more details on medicines used for OA. Evaluate risks as well as benefits for all drug therapies.

TABLE 11-6 Medications Commonly Used for Osteoarthritis Medication


Side Effects

Anti-inflammatory drugs, nonsteroidal (NSAIDs)

Indomethacin (Indocin), aspirin piroxicam (Feldene), naproxen (Naprosyn), nabumetone (Relafen) and Ibuprofen (Advil, Motrin) may be recommended.

Nausea, GI distress, anorexia, flatulence, or vomiting can occur. Take with food. Prolonged use may cause GI bleeding or ulcers. Indomethacin may also cause renal failure, or diarrhea; naprosen may cause heartburn or increased risk of cardiovascular disease.

COX-2 Inhibitors

Cyclooxygenases are needed for the synthesis of prostaglandins. The COX-2 enzyme mediates inflammation and pain.

These agents may promote increased risk of heart attack and stroke. Rofecoxib (Vioxx) and valdecoxib (Bectra) were removed from the market in 2004 and 2005.

Celecoxib (Celebrex) is the only FDA-approved drug at this time. Misoprostol (Cytotec)

Misoprostol reduces stomach acid if NSAIDs are used.

Abdominal cramps may occur.

Frankincense (Boswellia frereana)

Interestingly, this herb may lessen arthritic pain. Epi-lupeol is the principal constituent of B. frereana. B. frereana prevents collagen degradation, and inhibits the production of proinflammatory mediators (Blain et al, 2010).

Fewer side effects than glucosamine and chondroitin.

Glucosamine sulfate and chondroitin

Glucosamine reduces cartilage damage and decreases pain associated with osteoarthritis. Taken with chondroitin, it may help relieve symptoms of osteoarthritis. Some pills do not contain sufficient levels to be effective; check brand with to select the best choice.

Glucosamine can increase blood glucose levels andaggravate shellfish allergy because it is made from these shells. Chondroitin may alter blood clotting activity in a manner similar to that of aspirin.

Hyaluronic acid substitutes (viscosupplements)

These injections are designed to replace a normal component of the knee joint involved in joint lubrication and nutrition.

A series of injections are required. When used with methotrexate, the benefits may be greater (Homma et al, 2009).

Omega-3 fatty acids

Supplementation causes a decrease in both degradative and inflammatory aspects of chondrocyte metabolism.

May increase effects of blood-thinning drugs and herbs.


Corticosteroids may cause sodium retention; calcium, nitrogen, and potassium depletion; truncal obesity; and hyperglycemia.

Corticosteroids may have a short-term effect in osteoarthritis (Bellamy et al, 2005). Injections are required.

Topical pain relievers (Zostrix, Icy Hot, Therapeutic Mineral Ice, Aspercreme, and Ben Gay)

Creams and rubs stimulate nerve endings to relieve pain; deplete the amount of neurotransmitter (substance P) that sends pain messages to the brain; and block prostaglandins that cause pain and inflammation.

No internal side effects.

Tramadol (Ultram)

Pain reliever that is prescribed when over-the-counter medications do not provide relief.

Potentially addictive.

REFERENCES Arthritis drug guide, available at Web site accessed December 6, 2009, at http:// Bellamy N, et al. Intraarticular corticosteroid for treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2:CD005328, 2005. Blain EJ, et al. Boswellia frereana (frankincense) suppresses cytokine-induced matrix metalloproteinase expression and production of pro-inflammatory molecules in articular cartilage [published online ahead of print November 26, 2009]. Phytother Res. 24:905, 2010. Cranney A, et al. Effectiveness and safety of vitamin D in relation to bone health. Evid Rep Technol Assess. 158:1, 2007. Homma A, et al. Novel hyaluronic acid-methotrexate conjugates for osteoarthritis treatment. Bioorg Med Chem. 17:4647, 2009. National Institite of Arthritis and Musculoskeletal and Skin Disorders. Web site accessed December 13, 2009, at default.asp#4

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TABLE 11-7 Side Effects of Herbs Commonly Used for Arthritis Bromelain

May increase effects of blood-thinning drugs and tetracycline antibiotics.


Might counteract immunosuppressant drugs, such as glucocorticoids, taken for lupus and rheumatoid arthritis; might increase side effects of methotrexate.

Evening primrose oil

Can counteract the effects of anticonvulsant drugs.

Folic acid

Interferes with methotrexate.

Gamma linoleic acid (GLA)

May increase effects of blood-thinning drugs and herbs.


Can increase effects of blood-thinning drugs and herbs


Can increase nonsteroidal anti-inflammatory drug (NSAID) side effects and effects of blood-thinning drugs and herbs.


May increase effects of blood-thinning drugs and herbs.


May increase effects of blood-thinning drugs, estrogens, and glucocorticoids; should not be used by those with diabetes; may interact with monoamine oxidase (MAO) inhibitors.


Can increase effects of alcohol, sedatives, and tranquilizers.


May interact with blood pressure medications.

S-adenosylmethionine (SAMe)

SAMe may rebuild eroded joint cartilage. Enteric coating is needed because of gastrointestinal (GI) side effects.

Soy and avocado extracts

Antioxidant effects in reducing the symptoms of osteoarthritis; avoid excessive use in patients with hormonal cancers.

St. John’s wort

May enhance effects of narcotics, alcohol, and antidepressants; increases risk of sunburn; interferes with iron absorption.


May enhance effects of sedatives and tranquilizers.

Vitamin E

Gamma-tocopherol may worsen osteoarthritis; alpha-tocopherol is better.


Can interfere with glucocorticoids and other immunosuppressive drugs.

Note: Herbs and botanical supplements should not be used without discussing with physician. Excerpted from The Arthritis Foundation’s guide to alternative therapies, Web site accessed December 6, 2009, at

Herbs, Botanicals, and Supplements • Boswellia frereana (frankincense) suppresses cytokineinduced matrix metalloproteinase expression and production of pro-inflammatory molecules; studies are on-going (Blain et al, 2010). • Glucosamine sulfate combined with omega-3 fatty acids may reduce OA symptoms, including morning stiffness and pain in hips and knees (Gruenwald et al, 2009). Undenatured type II collagen (UC-II) may be more effective in the treatment of OA than glucosamine and chondroitin (Crowley et al, 2009). • Green tea’s anti-inflammatory properties and ginger may aid in pain relief. • Table 11-7 provides a description of some side effects of products often used for OA.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Physical and occupational therapies, diet, and exercise play an extremely important role. Long-term exercise and dietary weight loss are most effective. Acupuncture may be used to relieve pain. • Because OA allows muscles around the joints to become weak, exercise and stretching should be suggested to maintain flexibility. Repetitive, high-impact movements are not recommended whereas Tai Chi helps balance and protects bones. Exercises include a series for strengthening, aerobic, agility, and range of motion. Long-term

• • •

weight training, walking programs, swimming, and flexibility exercises are helpful. Encourage patient to avoid fad diets for “arthritis cure.” Ensure that the patient’s diet is balanced and includes all nutrients. A weight-loss plan may be needed. To alleviate stress on the joints, pharmacological and behavioral techniques with self-monitoring, should be included (Berkel et al, 2005). Pain initiates and exacerbates sleep disturbance; therefore, improving the sleep of OA patients helps to reduce the pain (Vitello et al, 2009). Transcutaneous electrical nerve stimulation (TENS) directs mild electric pulses to nerve endings that lie beneath the skin in the painful area; it block messages to the brain and by modifies pain perception. CBT is also useful. Focus on abilities and strengths rather than on disabilities and weaknesses.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Arthritis Foundation

Arthritis Resource Center at Healingwell


Johns Hopkins Arthritis Center

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OSTEOARTHRITIS AND DEGENERATIVE JOINT DISEASE—CITED REFERENCES Berenbaum F. New horizons and perspectives in the treatment of osteoarthritis. Arthritis Res Ther. 10:S1, 2008. Bergink AP, et al. Vitamin D status, bone mineral density, and the development of radiographic osteoarthritis of the knee: The Rotterdam Study. J Clin Rheumatol. 15:230, 2009. Berkel LA, et al. Behavioral interventions for obesity. J Am Diet Assoc. 105:35S, 2005. Blain EJ, et al. Boswellia frereana (frankincense) suppresses cytokineinduced matrix metalloproteinase expression and production of proinflammatory molecules in articular cartilage [published online ahead of print November 26, 2009]. Phytother Res. 24:905, 2010. Choi HK. Dietary risk factors for rheumatic diseases. Curr Opin Rheumatol. 17:141, 2005. Christensen R, et al. Weight loss: the treatment of choice for knee osteoarthritis? A randomized trial. Osteoarthritis Cartilage. 13:20, 2005. Crowley DC, et al. Safety and efficacy of undenatured type II collagen in the treatment of osteoarthritis of the knee: a clinical trial. Int J Med Sci. 6:312, 2009.

Gasbarrini A, Piscaglia AC. A natural diet versus modern Western diets? A new approach to prevent “well-being syndromes.” Dig Dis Sci. 50:1, 2005. Gruenwald J, et al. Effect of glucosamine sulfate with or without omega-3 fatty acids in patients with osteoarthritis [published online ahead of print September 4, 2009]. Adv Ther. 26:858, 2009. Messier SP, et al. Weight loss reduces knee-joint loads in overweight and obese older adults with knee osteoarthritis. Arthritis Rheum. 52:2026, 2005. Oka H, et al. Association of low dietary vitamin K intake with radiographic knee osteoarthritis in the Japanese elderly population: dietary survey in a population-based cohort of the ROAD study. J Orthop Sci. 14:687, 2009. Pi-Sunyer X. The medical risks of obesity. Postgrad Med. 121:21, 2009. Puenpatom RA, Victor TW. Increased prevalence of metabolic syndrome in individuals with osteoarthritis: an analysis of NHANES III data. Postgrad Med. 121:9, 2009. Vitello MV, et al. Cognitive behavioral therapy for insomnia improves sleep and decreases pain in older adults with co-morbid insomnia and osteoarthritis. J Clin Sleep Med. 5:355, 2009.

OSTEOMYELITIS NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND Acute osteomyelitis may be caused by localized infection of the long bones or injury to bone and surrounding soft tissue. Staphylococcus aureus is implicated in most patients with acute osteomyelitis; S. epidermidis, S. aureus, Pseudomonas aeruginosa, Serratia marcescens, and Escherichia coli may be found in the chronic form. When a bone is infected, the bone marrow swells and compresses against the rigid outer wall of bone, and blood vessels may be compressed or die; abscesses may form. Osteomyelitis and inflammatory arthritis affect many children (Pruthi and Thapa, 2009). Some diseases predispose patients to osteomyelitis, including diabetes mellitus, sickle cell disease, acquired immunodeficiency virus (AIDS), intravenous drug abuse, alcoholism, chronic steroid use, immunosuppression, and chronic joint disease. Use of prosthetic orthopedic devices and recent orthopedic surgery or open fracture may also place a patient at risk for osteomyelitis. Patients with diabetes mellitus with poor glucose control may experience infections of the lower extremities, from superficial cellulitis to deep soft tissue infections and osteomyelitis. Because osteomyelitis is prevalent after diabetic foot ulcers, careful treatment is crucial to avoid amputation (Schinabeck and Johnson, 2005). Prompt treatment is important. If not treated properly, the condition may become chronic with a poor prognosis. Treatment generally involves evaluation, staging, determination of etiology, antimicrobial therapy, and debridement or stabilization of bone. In children, serious musculoskeletal infections include osteomyelitis, septic arthritis, pyomyositis, and necrotizing fasciitis (Frank et al, 2005).


CLINICAL INDICATORS Genetic Markers: Deficiency of the interleukin-1receptor antagonist (DIRA) promotes neonatal osteomyelitis, an autosomal recessive autoinflammatory disease caused by mutations in IL1RN (Aksentijevich et al, 2009). Clinical/History Height Weight BMI Intake and output (I & O) BP Bone pain Sudden, acute pain in joints near the infection Fever, chills Tachycardia, diaphoresis Nausea Dehydration, electrolyte imbalance

Local swelling, redness Contractures in affected extremities Magnetic resonance imaging (MRI) Bone densitometry or x-rays Pressure ulcers or lesions with a sinus tract? Lab Work CRP and ESR (increased)

White blood cell (WBC) count (increased) Gluc Alb, transthyretin BUN, Creat Alk phos AST, ALT Ca, Mg Na, K Vitamin D3 status (serum 25OHD)

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SAMPLE NUTRITION CARE PROCESS STEPS Underweight Assessment Data: Weight and physical activity histories. Medical history, medications, and lab values. Nutrition Diagnosis (PES): Underweight related to poor nutrition quality of life and inadequate oral intake as evidenced by insufficient pain medicine before meals and BMI of 18. Intervention: Food and nutrient delivery—offer nutrient and energy-dense favorite foods. Educate about the benefits of gaining weight to tolerate medical therapies more effectively, to gain energy, and to improve nutritional quality of life. Coordinate timing of medicines with meals to assure that pain medicine is given 20–30 minutes before meals.

for at least 4–6 weeks if needed. Vancomycin or amphotericin B may be used; monitor for side effects related to timing and meals. • Analgesics may be used for pain. GI distress is a common side effect.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • It is reasonable to include phytochemical-rich foods each day. See Table 11-2.


Monitoring and Evaluation: Weight gain in 3–6 months; improved timing of meals with pain medicine to decrease anorexia at mealtime.

INTERVENTION OBJECTIVES • Characterize and treat the infection. Prevent further infection, dehydration, and other complications. • Promote recovery and healing of any skin lesions or pressure ulcers. • Correct defective blood flow to allow nutrients and oxygen to reach all tissues. • Control serum glucose and alleviate hyperglycemia with insulin if needed. • Correct anorexia, poor intake, weight loss, nausea and vomiting where present.

FOOD AND NUTRITION • Encourage adequate fluid intake. • Maintain a normal to high intake of calories, protein, zinc, vitamin A, and vitamin C in particular. A multivitamin–mineral supplement may be needed. • With diabetes, control carbohydrate to promote more effective healing.

Common Drugs Used and Potential Side Effects • For optimal results, antibiotic therapy must be started early, with antimicrobial agents administered parenterally


• Discuss role of nutrition in wound healing, immunity, and other conditions related to this disorder. • Discuss signs that may indicate reversal of status or recovery, such as increased fever, elevated glucose levels, additional infections, more redness in affected areas. • Promote use of nutrient-dense foods that are rich in antioxidants, phytochemicals, protein, zinc and vitamins.

Patient Education—Food Safety • If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used. Infection control is extremely important to avoid additional microbial contamination.

For More Information •

Cleveland Clinic—Osteomyelitis hic_osteomyelitis.aspx

Mayo Clinic—Osteomyelitis

National Institutes of Health–Osteomyelitis

OSTEOMYELITIS—CITED REFERENCES Aksentijevich I, et al. An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist. N Engl J Med. 360:2426, 2009. Frank G, et al. Musculoskeletal infections in children. Pediatr Clin North Am. 52:1083, 2005. Pruthi S, Thapa MM. Infectious and inflammatory disorders. Radiol Clin North Am. 47:911, 2009. Schinabeck MK, Johnson JL. Osteomyelitis in diabetic foot ulcers. Prompt diagnosis can avert amputation. Postgrad Med. 118:11, 2005.

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CLINICAL INDICATORS Genetic Markers: The vitamin D receptor (VDR) is responsible for the expression of over 900 genes, or about 3% of the human genome.

Adapted from: Yochum TR and Rowe LJ. Yochum and Rowe’s Essentials of Skeletal Radiology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.


Lab Work

Height Weight BMI Bone pain, aches Softened, deformed bones Muscular weakness, listlessness Numbness of arms, feet Easy bone fractures Bone densitometry, DEXA Bone biopsy

Serum P (decreased) Serum Ca (decreased) Urinary Ca Vitamin D3 (serum 25OHD): normal 30 ng/mL; low between 15 and 30 ng/mL; very low at less than 15 ng/mL

PTH Mg Na, K Serum phos Alk phos (increased) Alb, transthyretin CRP BUN, Creat

DEFINITIONS AND BACKGROUND Osteomalacia, adult rickets, causes softening and demineralization of the bone from insufficient vitamin D. Osteomalacia may occur in conjunction with bone loss and hip fractures. It more commonly results from intestinal malabsorption as from Crohn’s disease, colon resection, cystic fibrosis, celiac disease, or chronic use of anticonvulsants. It is also seen in kidney failure, liver disease, and some types of cancer. Severe vitamin D deficiency leads to secondary hyperparathyroidism, increased bone turnover and losses. Derangements in serum phosphate level result in osteomalacia (Saito and Fukumoto, 2009). Matrix extracellular phosphoglycoprotein (MEPE) inhibits mineralization; altered expression is associated with oncogenic osteomalacia and hypophosphatemic rickets (Boskey et al, 2010). In addition, deficient actions of fibroblast growth factor, FGF23, result in hypophosphatemic osteomalacia; FGF23 works as a hormone (Saito and Fukumoto, 2009). Osteomalacia often occurs in older people, in darkskinned individuals who live in northern latitudes, and in those who have limited sunlight exposure. Vitamin D is produced in response to sun exposure, so the process works faster in pale individuals. Sun exposure of about 15 minutes without sunscreen a few times a week is needed. Darker skinned individuals may need to take supplements.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin D Intake Assessment Data: Weight, physical activity histories, medical history, medication use, lab values. Limited sunlight exposure; works indoors in a sedentary job. Complains of bone pain. Low serum vitamin D3 at 17. Diet Hx shows limited to no intake from milk and milk products, dislike of fish, no use of multivitamin supplements. Nutrition Diagnosis (PES): Inadequate vitamin D intake related to limited sunlight exposure, indoor job, and diet low in vitamin–D rich foods as evidenced by low serum vitamin D levels. Intervention: Food-nutrient delivery—Encourage intake of more fortified dairy products, fish; use daily supplement containing the active form of vitamin D (cholecalciferol) in dose as prescribed by physician. Educate about the need to get sunlight exposure (20 minutes without sunscreen) several times weekly. Counsel about ways to use vitamin–D rich foods in menu planning and recipes that are acceptable to patient and/or family members. Monitoring and Evaluation: Serum levels of 25-hydroxyvitamin D (25-OHD) at more desirable level after 2–3 months. Patient statement of acceptance of foods rich in vitamin D, such as cream soups and casseroles made with milk. No further signs of osteomalacia.

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INTERVENTION OBJECTIVES • Provide correct amount of calcium, phosphorus, and vitamin D3. Include other nutrients that support bone health; meet DRI levels. See Table 11-8. • Prevent or reverse, if possible, bone density loss resulting from calcium loss in the bone matrix. • Prevent heart disease and stroke, which may be consequences of severe vitamin D deficiency.

FOOD AND NUTRITION • Diets should be high in calcium; adults will need 1200–1500 mg. If patient is lactose intolerant, try Lactaid


or other forms of lactose-free milk, broccoli, greens, and other sources of calcium. • Vitamin D is administered at high levels. Dietary sources include fish (particularly salmon, tuna, and mackerel) and fish liver oils. Small amounts are found in egg yolk and beef liver. • Potassium, magnesium, vitamins C and K and other potentially important nutrients should be highlighted.

Common Drugs Used and Potential Side Effects • Monitor treatment with calcium salts to prevent hypercalcemia; use with plenty of liquids. Avoid taking with iron supplements or bulk-forming laxatives. High-calcium diets may reduce zinc absorption and balance and may, therefore, increase zinc intake.

TABLE 11-8 Nutrients and Bone Health Nutrient



Moderate drinking (1–2 glasses of wine daily) is associated with increased trochanteric bone mineral density (BMD), but higher intakes may be associated with lower BMD. Heavy alcohol consumption may be linked to tobacco use, poor dietary habits, and poor bone health.

B-complex vitamins

Folic acid and vitamins B6 and B12 help to lower homocysteine when elevated.


Some role but not clearly defined.


Over 300 mg/d of caffeine can negatively impact the vitamin D receptor gene (VDR), and the Site Testing Osteoporosis Prevention and Intervention Trial (STOP-IT) found that greater amounts of caffeine affect BMD negatively (Rapuri et al, 2007). Limit intake to three cups of coffee daily and five servings of caffeinated soft drinks or tea; be sure to include adequate amounts of calcium.

Calcium and vitamin D

Dietary supplementation with calcium (1200 mg or more) and vitamin D (800–1000 IU) supports strong bone matrix, moderately reduces bone loss, and reduces the incidence of fractures. Vitamin D may actually be more important than calcium.


Copper is integral to the process of cross-linking of collagen and elastin molecules, and may have other roles in bone cells as well. Copper is found in meat, poultry, shellfish, organ meats; chocolate; nuts; cereal grains; dried legumes and dried fruits.

Dietary Fiber

A high intake of dietary fiber may interfere with calcium absorption; this may impact vegans, who consume 50 or more grams of fiber per day.


Iron is important for collagen maturation, and has other roles in osteoblasts and osteoclasts. Iron is found in organ meats, such as liver, kidney, heart; seafood; lean meat, poultry; dried beans; egg yolks; dried fruits; dark molasses; whole-grain and enriched breads or cereals.


Low intakes of magnesium contribute to bone loss. More than 50% of the total magnesium in the body is found in the bone, mostly in bone fluids. Magnesium is found in seeds, nuts; legumes; milled cereal grains; dark-green leafy vegetables such as spinach, broccoli, turnip greens, dark lettuces; milk.


Manganese is necessary for the formation of bone matrix and is found in whole grains, nuts, legumes, tea, instant coffee, fruits, and vegetables.


Meat, poultry, fish, eggs; cereals, grains; legumes; milk and dairy products, nuts.


70–100 g/d provides more bone building. Avoid larger doses, which can lead to excessive urinary calcium losses.


There may be a role for silicon in stimulation of collagen synthesis and osteoblast differentiation. Intake of biologically active silicon, orthosilicic acid, enhances bone density and may help to preserve bone mass (Devine et al, 2005).


Excesses can increase calcium excretion. Avoid using salt at the table, and limit total intake to 2400 mg/d.


Soy seems to be protective against fractures. Isoflavones increase bone density; use dietary sources.

Vitamin A

Too much retinal (not derived from the carotenoids found in plant sources) may contribute to hip fractures, especially in postmenopausal Caucasian women. Preformed vitamin A is found in liver, milk fat, fortified skim milk, eggs.

Vitamin C

Part of collagen, which supports healthy bone structure. Tissues saturate at 200 mg, therefore large doses are wasted.

Vitamin K

Supports osteocalcin for bone strength, reduces urinary calcium excretion, and modifies bone matrix proteins. A low intake of this fat-soluble vitamin increases the risk for bone fracture. Supplement with 120 g if needed. Vitamin K is found in dark-green leafy vegetables, dairy products, meat, and eggs.


The enzymes in osteoblasts require zinc in order to synthesize collagen. Zinc is found in animal products such as meat, fish, poultry; fortified and whole-grain cereals; milk and milk products; shellfish; liver. Zinc is also found in dry beans; nuts.

REFERENCES Devine A, et al. Protein consumption is an important predictor of lower limb bone mass in elderly women. Am J Clin Nutr. 81:1423, 2005.

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• Anticonvulsant therapy, tranquilizers, sedatives, muscle relaxants, and oral diabetic agents may deplete vitamin D. Phosphate binders with aluminum may precipitate osteomalacia; calcium carbonate may be useful, but do not take it with whole grains, bran, high-oxalate foods, or iron tablets.

• A spoonful of cod liver oil contains about 1300 IU of vitamin D; an 8-oz glass of fortified milk contains about 100 IU. • Vegetarians who avoid dairy products may be at risk for calcium and vitamin D depletion; discuss alternative sources from diet or from necessary supplementation.

Herbs, Botanicals, and Supplements

Patient Education—Food Safety

• Herbs and botanical supplements should not be used without discussing with physician. • Many doctors believe that between 1000–2000 IU of vitamin D per day may be needed to maintain adequate serum levels of this hormone. The upper limit for vitamin D is 10,000 IU per day.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Explain which foods are good sources of vitamin D. Encourage use of cholecalciferol (vitamin D3) and not vitamin D2. • Encourage patient to spend time in the sun for skin synthesis of vitamin D; 15–20 minutes may be needed, after which use a sunscreen to avoid sunburn.

If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Mayo Clinic—Osteomalacia

Medline—Osteomalacia 000376.htm#Definition

OSTEOMALACIA—CITED REFERENCES Boskey AL, et al. MEPE’s Diverse Effects on Mineralization [published online ahead of print December 9, 2009]. Calcif Tissue Int. 86:42, 2010. Rapuri PB, et al. Caffeine decreases vitamin D receptor protein expression and 1,25(OH)2D3 stimulated alkaline phosphatase activity in human osteoblast cells. J Steroid Biochem Mol Biol. 103:368, 2007. Saito T, Fukumoto S. Fibroblast Growth Factor 23 (FGF23) and Disorders of Phosphate Metabolism. [published online ahead of print October 7, 2009] Int J Pediatr Endocrinol. 2009:496514.



5'3" 5'0" 4'9"




10-year postmenopause

15-year postmenopause Height loss 1.5"

25 -year postmenopause Height loss 3.5"

Adapted from: Smeltzer SC, Bare BG. Textbook of Medical-Surgical Nursing, 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2000.

Osteopenia is a decrease in the amount of calcium and phosphorus in the bones. It is identified by a decrease in bone density, which is evident through a DEXA scan. It can occur in premature infants or in adults as a result of longterm inflammatory bowel disease, especially Crohn’s disease, or from low BMI. Plasma 25-hydroxyvitamin D (25-OHD) is the most sensitive indicator of BMD and clinical vitamin D3 status. Osteoporosis is the most common bone disease in humans; it is characterized by low bone mass, structural deterioration, and decreased bone strength in an estimated 10 million Americans (NOF, 2009). The aging population is highly affected. Seven percent of non-Hispanic white and Asian men aged 50 and older are estimated to have osteoporosis, and 35% are estimated to have low bone mass. Men are especially vulnerable when they have renal failure, smoke, or take medications on a regular basis, such as anticonvulsants, corticosteroids, or barbiturates. The World Health Organization (2009) defines osteoporosis as a BMD value that is 2.5 standard deviations or more below the mean of a young adult of the same sex. The lower the BMD, the greater the fracture risk. Osteoporosis can be a silent disease until a fragility fracture occurs at the hip and proximal humerus, when significant physical disability can result.

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TABLE 11-9 Risk Factors for Osteoporosis Factors That Cannot Be Changed Advanced age

History of fracture in a first-degree relative

Caucasians (e.g., Northern European and Asian)

Low body mass index (BMI) and low muscle mass Personal history of fracture after age 50 years

Female gender Family history of osteoporosis Factors That Might Be Altered Anorexia nervosa

Hypogonadism, as from low estrogen levels or anorexia nervosa

Current smoking

Lifetime diet low in calcium (poor diet, excess fiber)

Depression, past or current

Low testosterone levels in men


Low vitamin D intake or sunlight exposure

Estrogen deficiency (premature menopause, amenorrhea)

Use of chemotherapy, tamoxifen, glucocorticoids, lithium, and some anticonvulsants

Excessive use of alcohol

Total parenteral nutrition, long-term use

Sedentary lifestyle or extended bed rest (immobilization)

Homocysteine, elevated plasma levels Hypertension Conditions or Diseases That May Lead to Osteoporosis AIDS/HIV


Liver disease, severe

Primary biliary cirrhosis


Gaucher’s disease

Lymphoma or leukemia

Rheumatoid arthritis

Ankylosing spondylitis


Malabsorption syndromes

Spinal cord transection

Celiac disease




Chronic obstructive pulmonary disease


Multiple myeloma


Congenital porphyria


Multiple sclerosis

Thyrotoxicosis Tropical sprue

Cushing’s syndrome

Idiopathic scoliosis


Diabetes, type 1

Inflammatory bowel disease

Pernicious anemia

Women can lose up to 20% of their bone mass in the 5–7 years following menopause; 50% of will experience an osteoporotic fracture at some point in time. About 20% of postmenopausal white women in the United States have osteoporosis and 1.5 million fractures occur annually, especially of the hip and spine. Falls are associated with a high risk of frailty fractures (Schwartz et al, 2005). Spinal or vertebral fractures may lead to loss of height, severe back pain, and spinal deformities such as kyphosis or stooped posture. Hip fractures require hospitalization and major surgery; they impair the ability to walk and may cause disability or death. By 2050, the annual number of hip fractures is expected to triple (World Health Organization, 2009). Awareness and management of risk factors is important for preventing osteoporosis and the related disability. Both genetic and lifestyle factors play a role. A family history of hip fracture carries a twofold increased risk of fracture among descendants; genetic factors play a major role in BMD and in osteoporosis risk (Ferrari, 2008). Yet BMD is just one of many contributors to bone strength and fracture risk reduction. Dairy, fruit, and vegetable intakes have

emerged as an important modifiable protective factor for bone health (Tucker, 2009). Women may lose bone during lactation if their diets are low in calcium and other nutrients. Magnesium, potassium, vitamin C, vitamin K, several B vitamins, and carotenoids are important (Tucker, 2009); see Table 11-8. In the skeleton, interleukin-1 protein causes an increase in the number and activity of osteoclastic cells—the cells that break down bone tissue. Depression and elevated plasma homocysteine levels are also associated with osteoporosis. See Table 11-9 for the full list of risk factors for osteoporosis. Physical activity has different effects depending on its intensity, frequency, and duration, and the age at which it is started, with greater effects in adolescence and as a result of weight-bearing exercise. In addition, diet contributes significantly. Building strong bones during childhood and adolescence can be the best defense against developing osteoporosis later. By about age of 20, most women have acquired 98% of total bone mass. Acquisition of a high peak bone mass (reaching genetic potential) by 30 years of age helps reduce bone losses later in life.

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Markers of bone turnover can be used to predict the rate of bone loss in post-menopausal women and can also be used to assess the risk of fractures (Eastell and Hannon, 2008). Markers of bone formation include serum bone alkaline phosphatase, total osteocalcin and the procollagen type I N-terminal propeptide assay (Eastell and Hannon, 2008). Serotonin can serve as a marker for low bone mass. Circulating levels of the neurotransmitter serotonin are inversely associated with bone mass in women; this may have implications when using SSRIs. Bone formation is inhibited by serotonin in the gut. Inactivation of the leptin receptor in serotonergic neurons identifies a molecular basis for the common regulation of bone and energy metabolisms (Yadav et al, 2009). A drug that stops the gut from synthesizing serotonin may be able to reverse severe bone loss and prevent osteoporosis. Measurements of the urinary excretion of N- and Cterminal cross-linked telopeptides and of serum C-terminal cross-linked telopeptides are sensitive and specific for bone resorption (Eastell and Hannon, 2008). These measures are as important as measurement of BMD.


SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake Assessment Data: Food records, DEXA scan showing two deviations below normal. Weight and physical activity histories. Medical history, medications, and lab values. Nutrition Diagnosis (PES): Inadequate intake of vitamin D (NI5.9.1.3) related to poor diet, no food sources, and no use of supplements as evidenced by very low BMD on DEXA. Intervention: Food and Nutrient Delivery: ND 1.3—add calcium containing beverages and foods, vitamin–D rich foods, adequate protein. ND—Supplement use for Vitamin D. Education: E 2.2—Educate patient concerning calcium and vitamin D food and beverage sources to meet needs along with supplement, sunlight exposure 10–30 min/d, protein needs, increased physical activity. Counseling: Good sources of vitamin D from diet and supplements, meal planning and shopping tips, dining out guide, referral to Meals-on-Wheels or other social agencies as appropriate, appropriate role for sunshine exposure. Monitoring and Evaluation: Improvements in dietary and supplemental intake of vitamin D as shown in food records, lab values. DEXA scan report showing no further decline, and a slight improvement in risk level. No fractures.

CLINICAL INDICATORS Genetic Markers: Genes coding for the LDL-receptor related protein 5 (LRP5), estrogen receptor alpha (ESR1), and osteoprotegerin, OPG (TNFRSf11b) are known to pose a risk for osteoporosis (Ferrari, 2008). In a large-scale study, single nucleotide polymorphisms (SNPs) from nine gene loci (ESR1, LRP4, ITGA1, LRP5, SOST, SPP1, TNFRSF11A, TNFRSF11B, and TNFSF11) were associated with BMD, but not always in a predictable manner (Richards et al, 2009). Mg Na, K Height Vitamin D3 Weight status (serum BMI 25-OHD) Back pain Alb BP CRP Bone densitomePTH (useful in try, DEXA some patients) Serum P Lab Work (decreased Ca with Urinary Ca hyperparathy(24 hours) roidism) Clinical/History

TSH Total testosterone in men Serum homocysteine Serum folate and vitamin B12

INTERVENTION OBJECTIVES • Preserve height, support independence, and improve functional status. Prevent fractures (Tussing and Chapman-Novakofski, 2005).

• Optimize bone health: choose a balanced diet rich in calcium and vitamin D; use weight-bearing and resistance-training exercises. Follow a healthy lifestyle with no smoking. • Decrease precipitating factors, such as use of anticonvulsants or corticosteroids, lactase deficiency, low intake of fruits and vegetables and dairy, calcium malabsorption, sedentary lifestyle, and low BMI. Provide adequate time for evaluating improvement (6–9 months at least). • Assure adequate intake of protein. Rather than having a negative effect on bone, protein intake appears to benefit bone status, particularly in older adults (Tucker, 2009). • Intake of magnesium, potassium, fruit, and vegetables is positively associated with bone health and total bone mass.

FOOD AND NUTRITION • Advise all patients to consume adequate amounts of calcium ( 1200 mg/d, including supplements if necessary) and vitamin D. Women after menopause or over age 65 years will need 1500 mg calcium daily. To fulfill the requirement, 1 quart of milk daily can be consumed. If fluid milk is not consumed, dry skim milk powder can be added to many foods. Aged cheeses and yogurt are sources as well. • Calcium supplements can be used if dairy products are not tolerated; calcium absorption averages approximately 30–40% from most sources See Table 11-10. Space the supplements throughout the day; take no more than 500–600 mg two or more times daily with meals. Use with vitamin D and magnesium. • For vitamin D, choose fortified milk, cod liver oil, egg yolks, and fatty fish. Supplements may be needed. Do not exceed 10,000 IU/d.

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TABLE 11-10


Tips on Calcium Supplementsa


Source of Calcium (mg)

No. of Tablets/Day to Provide About 900–1000 mg Calcium Per Tablet

Caltrate 600

Carbonate (600 mg)


Os-Cal 500

Carbonate from oyster shell (500 mg)


Os-Cal 500  Vitamin D

Carbonate from oyster shell (500 mg)


Posture (600 mg)

Phosphate (600 mg)


Posture–Vitamin D

Phosphate (600 mg)



Citrate (200 mg)


Citracal  Vitamin D

Citrate (315 mg)


Citracal Liquitab

Citrate (500 mg)


Tums 500 mg

Carbonate from limestone (500 mg)


Tums E-X

Carbonate from limestone (300 mg)


Tums Ultra

Carbonate from shell (400 mg)


Calcet  Vitamin D

Carbonate, lactate, gluconate (300 mg)



Carbonate, gluconate, lactate (175 mg)



Excesses of calcium supplements can cause hypercalcemia; monitor intakes carefully and take no more than 500–600 mg two or more times daily with meals. Avoid taking with iron supplements. Use extra water with supplements. Excess vitamin D can cause vitamin D calcinosis. Rates of calcium absorption vary, and dietary sources are the best absorbed; calcium maleate is also well absorbed. Elemental calcium varies in different supplements, as follows: 1. Calcium carbonate (Tums, Roxane, Os-Cal, Calciday, Oyst-Cal, Oystercal, Caltrate) contains 40%. Calcium carbonate temporarily decreases gastric acidity, which is needed for calcium absorption. Tricalcium phosphate provides 39%. 2. Calcium chloride contains 36%. 3. Bone meal or Dolomite contains 33% but should be avoided as it also contains lead. 4. Calcium acetate (Phos-Ex, PhosLo) contains 25%. 5. Calcium citrate (Citracal) contains 21%. 6. Calcium lactate contains 13%. 7. Calcium gluconate contains 9%. Updated from: Shils M, et al, eds. Modern nutrition in health and disease. Baltimore: Lippincott Williams & Wilkins, 1999.

• Extra protein may be needed (Devine et al, 2005; Tucker, 2009). • For sufficient intake of vitamin B12, include dairy products, meat, poultry, fish, and fortified cereals. • Isoflavones may also be beneficial; use two to three servings of soy foods daily. • If patient is obese, use a nutrient-rich, calorie-controlled diet that provides adequate protein, vitamins, calcium, and other minerals. Adequate manganese, vitamins C and K, potassium, and magnesium should be consumed to meet at least the DRI levels. Include fruits and vegetables that contribute to bone health. • Assure that folic acid and vitamins B6 and B12 are adequate, especially if serum homocysteine levels are elevated. • Sodium must be controlled. Keep sodium within desired limits while increasing potassium and magnesium. • Beware of excesses of wheat bran because phytates may increase calcium excretion. • Caffeine from coffee does not seem to be a problem if calcium (as from milk) is consumed in adequate amounts. However, cola drinks should be limited (Tucker, 2009). • Moderate alcohol intake shows positive effects on bone, particularly in older women (Tucker, 2009).

Common Drugs Used and Potential Side Effects • Adequate calcium is crucial; supplementation in bioavailable forms is necessary in individuals who do not

• •

achieve recommended intake from dietary sources (see Table 11-11). Side effects may include abdominal pain, anorexia, constipation, vomiting, nausea or dry mouth. Oral doses of vitamin D3 in the range of 1800 to 4000 IU per day may be needed to take serum levels up to 75 to 110 nmol/L (Bischoff-Ferrari et al, 2010). Oral alendronic acid is the reference drug for menopausal women with osteopenia. It may be used with parathormone as well, but this has a 2-year limit (Black et al, 2005). See Table 11-12 for more guidance. The once monthly injections of risedronate (150 g) are beneficial for those for which daily or weekly dosing is a challenge (Rackoff, 2009). Bone markers can be used to monitor the efficacy of antiresorptive therapy such as hormone-replacement therapy, raloxifene and bisphosphonates (Eastell and Hannon, 2008). SSRIs have been associated with lower BMD and increased rates of bone loss, as well as increased rates of fracture (Haney et al, 2010). Their use should be closely monitored.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Cabbage, pigweed, dandelion, avocado, and parsley have been recommended, but have not shown efficacy.

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TABLE 11-11

Medications Commonly Used for Management of Osteoporosisa

Medication Comments



Bisphosphonates: risedronate (Actonel); alendronate (Fosamax)

Effective agents for reducing vertebral and nonvertebral fracture risk. Alendronate is approved for the treatment of osteoporosis in men. Alendronate and risedronate are approved for use by men and women with glucocorticoidinduced osteoporosis. Zoledronic acid is under study. Bisphosphonates inhibit atherogenesis.

Risedronate may cause dysphagia, esophageal ulcer, and stomach ulcer. Take on an empty stomach 30 minutes before meals; sit upright. Take additional vitamin D and calcium. Headache, gastrointestinal (GI) distress, diarrhea, nausea, constipation, and rash may occur, although rarely. Alendronate may cause metallic taste, nausea, diarrhea, and decreased potassium and magnesium. Avoid in severe renal disease, pregnancy, or breastfeeding. Nausea, heartburn, irritation or pain of the esophagus, anorexia, vomiting, dysphagia, sensation of fullness, and constipation or diarrhea may occur.

Calcitonin-salmon (Miacalcin)

Bone loss is reduced, and bone mass increases, although not in the hip. A modest increase in bone mass occurs.

200 IU/d, the recommended regimen, reduces vertebral fracture risk by 33% in women with low bone mass. Calcitonin makes calcium more available to bones. It is given as an injection or nasal spray; it may cause allergic reactions and flushing of the face and hands, urinary frequency, anorexia, nausea, constipation, or skin rash.

Calcitriol (1,25-dihydroxyvitamin D)

Active form of vitamin D hormone that increases GI absorption of calcium from the gut, kidney reabsorption of calcium, stimulates bone resorption, decreases PTH production, and stimulates skeletal osteoblasts/osteoclasts. Larger doses than the DRI for vitamin D may be needed; 700–800 IU may be beneficial along with 500–1200 mg calcium (Cranney et al, 2007).

Anorexia, abdominal cramping, headache, lethargy, nausea, weight loss, and weakness may result from larger doses.

Ibandronate (Boniva)

Ibandronate is used to treat or prevent osteoporosis in women after menopause; it may increase bone mass by slowing loss of bone.

Should not be taken if hypocalcemia is a problem.

PTH (teriparatide; Forteo)

PTH is the only anabolic osteoporosis agent available for clinical use to lower vertebral fracture incidence by triggering formation of new bone.

Use only in ambulatory patients.

Raloxifene (Evista)

Significantly reduces vertebral fracture risk but not nonvertebral fracture risk.

Protects against thin, weak bones and fractures; also lowers serum cholesterol by 7% and low-density lipoprotein (LDL) by 11%. It may trigger menopausal symptoms, including hot flashes, but is less likely to have an estrogen-like increase in cancer risk.

Sodium fluoride

The slow-release form may increase bone formation and decrease the risk of fractures.

In patients with mild-to-moderate osteoporosis, long-term supplements with fluoride plus calcium result in lower rates of vertebral fracture than supplementation with calcium alone. Intake of fluoride in drinking water at 1 ppm does not appear to be associated with increased risk of hip fracture. Side effects may include abdominal pain, diarrhea, nausea, vomiting.


Statins, agents that reduce atherogenesis, stimulate bone formation.

Cardiovascular disease and low bone mineral density have some common etiologies.


The FDA approves calcitonin, alendronate, raloxifene, and risedronate for the treatment of postmenopausal osteoporosis; alendronate, risedronate, and raloxifene are approved for the prevention of the disease. Current pharmacological options for osteoporosis prevention and/or treatment are bisphosphonates (alendronate and risedronate), calcitonin, estrogens and/or hormone therapy, parathyroid hormone (PTH 1–34), and raloxifene. Source: National Osteoporosis Foundation Web site accessed December 14, 2009, at:

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Prevention is the best medicine. Encourage patient to stand upright, rather than sit or recline, as often as feasible. Measures to decrease fall frequency and to slow down the rapid life pace of healthy people with low bone mass should prevent some fractures (Kelsey et al, 2005).

• Change a sedentary lifestyle. Regular resistance and highimpact exercise, contributes to development of high peak bone mass and may reduce the risk of falls in older individuals (Moayyeri, 2008). Aerobic and strengthening exercises are helpful as well. • Walking or running is beneficial. However, excessive weight-bearing exercise can cause amenorrhea in premenopausal women when a low-calorie diet is consumed.

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TABLE 11-12

Features of Rheumatic Arthritis

Tender, warm, swollen joints


• When steroids are used, check on bone density changes; there is a high incidence of osteoporosis. • Note that improvements in BMD may take up to 3 years to note improvement (Compston, 2009).

Symmetrical pattern of affected joints Joint inflammation often affecting the wrist and finger joints closest to the hand

Patient Education—Food Safety

Joint inflammation sometimes affecting other joints, including the neck, shoulders, elbows, hips, knees, ankles, and feet

If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

Fatigue, occasional fevers, a general sense of not feeling well Pain and stiffness lasting for more than 30 minutes in the morning or after a long rest Symptoms that last for many years Variability of symptoms among people with the disease Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases. Available at

• An educational osteoporosis prevention program with hands-on activities can increase self-efficacy (Tussing and Chapman-Novakofski, 2005). Explain that calcium absorption declines with age and that adequate calcium and vitamin D are important throughout life. The overall benefit of healthful eating must be strongly emphasized. Consider calcium and vitamin D supplementation in the elderly. • Describe importance of the use of milk, cheeses, yogurt, broccoli, kale and other greens, and soybeans. Provide recipes and shopping tips. • Decrease the use of tobacco. Use only moderate amounts of alcohol. • Caffeine poses a minimal risk unless it replaces calciumcontaining beverages; BMD is not affected by caffeine if at least 1 glass of milk is consumed daily. • Encourage adequate exposure to sunlight (10–30 min/d). Avoid sunburn and overexposure, with its risks of skin cancer. • Remind all teenagers that osteoporosis is “kid stuff;” maintenance of weight-bearing activity is important during the growing years. Intake of carbonated beverages instead of milk is a big concern. • Some mineral waters are excellent sources of calcium; bioavailability is good. • Avoid long-term use of high doses of retinol from fortified foods or supplements. • Persons with previous fractures are at risk and should be monitored carefully for osteoporosis. The National Osteoporosis Foundation supports an Awareness and Prevention Month in May of each year.

For More Information •

Clinical Guidelines–Osteoporosis

National Osteoporosis Foundation


OSTEOPENIA AND OSTEOPOROSIS—CITED REFERENCES Bischoff-Ferrari H, et al. Benefit-risk assessment of vitamin D supplementation [published online ahead of print December 3, 2009]. Osteoporos Int. 21:1121, 2010. Black DM, et al. One year of alendronate after one year of parathyroid hormone (1–84) for osteoporosis. N Engl J Med. 353:555, 2005. Compston J. Monitoring osteoporosis treatment. Baillieres Best Pract Res Clin Rheumatol. 23:781, 2009. Eastell R, Hannon RA. Biomarkers of bone health and osteoporosis risk. Proc Nutr Soc. 67:157, 2008. Ferrari S. Human genetics of osteoporosis. Baillieres Best Pract Res Clin Endocrinol Metab. 22:723, 2008. Haney EM, et al. Effects of selective serotonin reuptake inhibitors on bone health in adults: time for recommendations about screening, prevention and management? Bone. 46:13, 2010. Kelsey JL, et al. Reducing the risk for distal forearm fracture: preserve bone mass, slow down, and don’t fall! Osteoporos Int. 16:681, 2005. Moayyeri A. The association between physical activity and osteoporotic fractures: a review of the evidence and implications for future research. Ann Epidemiol. 18:827, 2008. NOF. National Osteoporosis Foundation. Accessed December 14, 2009, at Rackoff P. Efficacy and safety of risedronate 150 mg once a month in the treatment of postmenopausal osteoporosis. Clin Interv Aging. 4:207, 2009. Richards JB, et al. Collaborative meta-analysis: associations of 150 candidate genes with osteoporosis and osteoporotic fracture. Ann Intern Med. 151: 528, 2009. Schwartz AF, et al. Increased falling as a risk factor for fracture among older women: the study of osteoporotic fractures. Am J Epidemiol. 161:180, 2005. Tucker KL. Osteoporosis prevention and nutrition. Curr Osteoporos Rep. 7:111, 2009. Tussing L, Chapman-Novakofski K. Osteoporosis prevention education: behavior theories and calcium intake. J Am Diet Assoc. 105:92, 2005. World Health Organization. Prevention and management of osteoporosis. Accessed December 14, 2009 at TRS_921.pdf. Yadav VK, et al. A serotonin-dependent mechanism explains the leptin regulation of bone mass, appetite, and energy expenditure. Cell. 138:976, 2009.

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PAGET’S DISEASE (OSTEITIS DEFORMANS) NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND Paget’s disease of the bone (PDB) is a disorder of skeletal remodeling, where areas on bone grow abnormally, enlarging and becoming soft. It is of unknown etiology, with excessive bone destruction and repairing. Of all persons older than 50 years of age, 3% have an isolated lesion; actual clinical disease is much less common. PDB is the second most common bone disease in the world. A systematic laboratory screening including serum alkaline phosphatase of an older subject complaining of bone pain, articular pain, or back pain is a strategy to improve the diagnosis of PDB (Varenna et al, 2009). The disease tends to run in families. Genetic analysis indicates that 40% of patients with Paget’s disease have an affected first-degree relative. Approximately 3 million Americans have the disease; it rarely occurs before age 40. Juvenile Paget’s disease is very debilitating. Osteoclasts are larger than normal and increased in size (Deftos, 2005). Juvenile Paget’s disease usually presents in infancy or childhood and results in progressive deformity, growth retardation, and deafness. The disease is higher in frequency in people who are aged 65 or older. There is a slight male predominance. Prognosis is good in mild cases. Sarcoma can also be found in this population (Mankin and Hornicek, 2005). There has been a decline in incidence of this complication but where it does occur, prognosis is still poor (Mangham et al, 2009).


Genetic Markers: There seem to be strong ties to European ancestry in Paget’s disease, including Australia and New Zealand. A majority of cases harbor germline mutations in the SQSTM1, Sequestosome1 gene (Merchant et al, 2009).

Height Weight BMI Deep “bone pain” Joint pain, neck pain Skull enlargement Hearing loss

Headaches Tickening of long bones Bowing of limbs Reduced height Spontaneous fractures X-rays (denser, expanded bones) Bone scans

Alb, transthyretin CRP Transferrin Serum P

H&H Serum B12 Radiolabeled bisphosphonate

INTERVENTION OBJECTIVES • Prevent complications, especially related to the nervous system (e.g., fractures, spinal stenosis, paraplegia, cardiac failure, and deafness). • Prevent side effects of drug therapy. • Promote full recovery when possible. • Differentiate from other conditions with bone lesions. • Alleviate anemia and other complications.

FOOD AND NUTRITION • Adequate protein is important, with adequate calories to spare protein. • Adequate levels of calcium and vitamins C and D may be needed. • To correct anemia, monitor serum levels of iron and vitamin B12 to determine need for an altered diet.

Common Drugs Used and Potential Side Effects • Drugs that inhibit bone resorption—bisphosphonates (etidronate, pamidronate, clodronate, or alendronate)—



PTH (abnormal) Ca, Mg Na, K

Lab Work Alk phos (increased) Urinary Ca (altered) Vitamin D3 status (serum 25-OHD) Uric acid (UA), elevated?

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal Nutritional Labs Assessment Data: Weight and physical activity histories. Medical history, medications, abnormal lab values for alk phos, uric acid, serum vitamin D3, and PTH. Nutrition Diagnosis (PES): Abnormal nutritional labs related to metabolic changes from Paget’s disease as evidenced by increased alk phos, altered urinary calcium, abnormal PTH, elevated uric acid levels, diagnosis of anemia, and bone pain. Intervention: Treatment with bisphosphonates to alter serum and urinary labs; careful monitoring for side effects affecting intake and appetite. Food-nutrient delivery—Correct iron-deficiency anemia from poor intake and disease process. Monitoring and Evaluation: Improvement in serum lab values; resolution of anemia; decreased bone pain.

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• •

may be used to slow the progression. Bisphosphonates are pyrophosphate analogs that bind to bone at active sites of remodeling. The bisphosphonate zoledronic acid (Zometa), given in a single injection, yields a rapid and long-lasting improvement in bone health (Reid et al, 2005). The nitrogen-containing BPs pamidronate (Aredia) and zoledronic acid (Zometa) are capable of causing bisphosphonate-associated osteonecrosis of the jaw (Grewal and Fayans, 2008). Risedronate (Actonel) can cause dysphagia, esophageal ulcer, and stomach ulcer. Take on an empty stomach 30 minutes before meals; consume additional vitamin D and calcium. Headache, diarrhea, nausea, constipation, and rash may occur, although they are rare. Osteoprotegerin may be used in managing the juvenile form of Paget’s disease (Cundy et al, 2005). Thyrocalcitonin or synthetic calcitonin may be used to decrease passage of calcium from bones to bloodstream. Methods of administration include a nasal spray. Monitor for nausea or vomiting. Analgesics may be needed for pain.


vitamins, iron, protein, and vitamin D. Monitor carefully, if supplements are used, in addition to dietary guidance. • Discuss side effects for the specific drugs ordered.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

National Association for the Relief of Paget’s Disease

National Institute of Arthritis and Musculoskeletal and Skin Diseases

National Institutes of Health Osteoporosis and Related Bones Diseases

Paget’s Disease

Paget Foundation

PAGET’S DISEASE—CITED REFERENCES Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Unusual bone diseases may be associated with use of Chinese herbs.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss appropriate dietary alterations for patient’s condition, individualized for the current condition and status. Include good food sources of calcium, B-complex

Cundy T, et al. Recombinant osteoprotegerin for juvenile Paget’s disease. N Engl J Med. 353:918, 2005. Deftos LJ. Treatment of Paget’s disease—taming the wild osteoclast. N Engl J Med. 353:872, 2005. Grewal VS, Fayans EP. Bisphosphonate-associated osteonecrosis: a clinician’s reference to patient management. Todays FDA. 20:38, 2008. Mangham DC, et al. Sarcoma arising in Paget’s disease of bone: declining incidence and increasing age at presentation. Bone. 44:431, 2009. Mankin HJ, Hornicek FJ. Paget’s sarcoma: a historical and outcome review. Clin Orthop Relat Res. 438:97, 2005. Merchant A, et al. Somatic mutations in SQSTM1 detected in affected tissues from patients with sporadic Paget’s disease of bone. J Bone Miner Res. 24:484, 2009. Reid IR, et al. Comparison of a single infusion of zoledronic acid with risedronate for Paget’s disease. N Engl J Med. 353:898, 2005. Varenna M, et al. Demographic and clinical features related to a symptomatic onset of Paget’s disease of bone [published online ahead of print December 1, 2009]. J Rheumatol. 37:155, 2010.

POLYARTERITIS NODOSA NUTRITIONAL ACUITY RANKING: LEVEL 1–2 DEFINITIONS AND BACKGROUND Polyarteritis nodosa (PAN) is characterized by necrotizing inflammation of medium- or small-sized arteries without glomerulonephritis or vasculitis in arterioles, capillaries, or venules (Colmegna and Maldonado-Cocco, 2005). Viral infections such as hepatitis B may trigger it. In PAN, arteries become inflamed in several organs, causing damage in brain, heart, liver, GI tract, or renal tissues. Renal involvement develops and is accompanied by hyper-

tension in half of patients. PAN also commonly involves the gut (abdominal angina, hemorrhage, perforation), heart (myocarditis, myocardial infarction), or eye (scleritis); rupture of renal or mesenteric microaneurysms can also occur. PAN is two to three times more common in men and usually develops between ages 40 and 50 years. Rarely, it occurs after a Hepatitis-B vaccination. It is fatal if not treated. Treatment includes use of prednisone, plasmapheresis to remove immune complexes, and antiviral therapy (lamivudine) for the hepatitis B infection.

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CLINICAL INDICATORS Genetic Markers: Medium-sized artery vasculitides that occur in childhood manifest mostly as PAN, with high morbidity and mortality rates (Dillon et al, 2009). PAN is likely to have a genetic connection; MEFV is one gene under study. Myalgias, weakness Height Neuropathy Weight Hematuria BMI Fatigue Weight loss 4 kg Rash, nodules or since onset of Raynaud’s illness disease Hematuria Biopsy of Edema medium Chest pain vessels Tachycardia Shortness of Lab Work breath ESR (elevated) Fever? Abdominal pain CRP Glucose BP (elevated) Clinical/History

• Reduce edema, anorexia, hypertension, and other effects of the disorder.

Hepatitis B antigen or antibody in serum Ca, Mg Na, K Alb, transthyretin BUN, Creat (elevated but not from dehydration) Transferrin H&H Vitamin D3 status (serum 25-OHD)

INTERVENTION OBJECTIVES • Treat as soon as possible to decrease heart and renal damage. • Improve appetite and intake. • Prevent weight loss. • Increase calorie intake when there is fever.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Oral Food and Beverage Intake Assessment Data: Weight and physical activity histories. Medical history, medications, and lab values. Nutrition Diagnosis (PES): Inadequate oral food and beverage intake related to anorexia, fever and abdominal pain as evidenced by weight loss of 3 kg in 8 weeks. Intervention: Food-Nutrient delivery—Offer preferred foods, enhanced with energy kilocalories from milk powder, fats, etc. Educate about how to manage nausea; suggest small, frequent meals throughout the day and liquids separate from meals. Coordinate care with nursing, medical teams if medications are needed. Monitoring and Evaluation: Resolution of weight loss; no further losses. Improvement in nausea and abdominal pain.

• A high-energy intake may be beneficial in case of weight loss. • A normal to high protein intake generally is required. • Fluid or sodium intake may be limited with hypertension, kidney disease, or edema or with use of steroids. • Include phytochemicals derived from spices 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, and ajoene); and pomegranate (ellagic acid) (Aggarwal and Shishodia, 2004).

Common Drugs Used and Potential Side Effects • Steroids such as prednisone may be used for 2 weeks. Side effects of long-term use include negative nitrogen and potassium balances; decreased calcium and zinc levels; CHO intolerance; and excessive sodium retention. With weight gain, a calorie-controlled diet may be useful. • Pain relievers may be needed; monitor individually for side effects such as GI distress. • Immunosuppressive cyclophosphamide may be used; long-term effects can reduce the ability to fight infections. Corticosteroids plus cyclophosphamide is the standard of care, in particular for patients with more severe disease, in whom this combination prolongs survival (Colmegna and Maldonado-Cocco, 2005). • Infliximab may be used as an alternative agent for the treatment of patients with PAN refractory to conventional therapy (Al-Bishri et al, 2005).

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss alternate dietary guidelines as appropriate for medications and side effects of the disease. • Discuss sources of nutrients as appropriate for the ordered diet. Provide guidance on enhancing nutrient and energy density from meals and snacks. • With abdominal pain and GI bleeding, PAN occasionally is mistaken for inflammatory bowel disease. Be certain to see a trained specialist as needed.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

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For More Information •

Johns Hopkins Vasculitis Center

Polyarteritis Nodosa Foundation

Polyarteritis Nodosa

Vasculitis Foundation


POLYARTERITIS NODOSA—CITED REFERENCES Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappa B activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 1030:434, 2004. Al-Bishri J, et al. Refractory polyarteritis nodosa successfully treated with infliximab. J Rheumatol. 32:1371, 2005. Colmegna I, Maldonado-Cocco JA. Polyarteritis nodosa revisited. Polyarteritis nodosa revisited. Curr Rheumatol Rep. 7:288, 2005. Dillon MJ, et al. Medium-size-vessel vasculitis [published online ahead of print November 28, 2009]. Pediatr Nephrol. 25:1641, 2010.

RHABDOMYOLYSIS NURITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Rhabdomyolysis (RML) is a clinical and biochemical syndrome resulting from skeletal muscle injury with release of myoglobin into the plasma and breakdown of muscle fibers with release into the circulation. Some of these changes are toxic to the kidney, often resulting in kidney damage or acute renal failure. A disturbance in myocyte calcium homeostasis takes place. RML may occur in infants, toddlers, and adolescents who have inherited enzyme deficiencies of carbohydrate or lipid metabolism, DMD, or malignant hyperthermia. RML may also occur from extensive muscle damage as from a crushing injury, major burn, electrical shock, toxins, bacterial infections, excessive exercise (Olpin, 2005), seizures, alcoholism, overdose of cocaine, or use of drugs such as cholesterol-reducing statins. The most common causes of RML in adults include crush injury, overexertion, alcohol abuse, use of certain medicines, and toxic substances. Postoperative RML in bariatric surgery occurs with prolonged muscle compression; potential consequences may lead to death (de Menezes Ettinger et al, 2005). Muscle pain caused by RML may involve specific symptoms of groups of muscles or may be generalized throughout the body. Muscles in the calves and the lower back are commonly affected but each patient is different. Early complications of RML include severe hyperkalemia with cardiac arrhythmia and arrest. The most serious late complication is acute renal failure. RML can be defined with CK values exceeding 10–25 times the upper limit of normal irrespective of renal function (Linares et al, 2009). Management of suspected drug-induced myopathy should include immediate discontinuation of the offending agent and supportive care (Mor et al, 2009).

inherited myopathies. Elevated CK levels have been found with a high-density SNP genotype in a p.Trp3X allele; this mutation is associated with a mild Becker phenotype of MD (Flanigan et al, 2009). Weakness of the affected Height muscles Weight Muscle stiffness BMI or aching Weight gain (myalgia) (uninSeizures tentional) Joint pain I&O Fatigue Tea-colored Abnormally urine dark colored Temperature urine from BP (elevated) excretion of Exposure to toxic myoglobin substances or chronic alcoLab Work hol use Creatine phosUse of medicaphokinase tions such as (CPK) (very statins high) Muscle tenderness Clinical/History

Serum myoglobin test (positive) Urinary casts or hemoglobin Ca, Mg Na K (may be high from muscle breakdown) Alb, transthyretin CRP BUN Creat Transferrin H&H UA (elevated) Vitamin D3 status (serum 25-OHD)



CLINICAL INDICATORS Genetic Markers: RML may occur in infants, toddlers, and adolescents who have inherited enzyme deficiencies of carbohydrate or lipid metabolism or who have

• Preserve renal function. • Eliminate myoglobin out of the kidneys with early and aggressive hydration. Medicines may also be needed to make the urine more alkaline. • Treat kidney failure or hyperkalemia if needed.

FOOD AND NUTRITION • Hydration needs with muscle necrosis may approximate the massive fluid volume needs of a severely burned patient.

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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Physical Activity Assessment Data: Weight and physical activity histories. Medical history with diagnosis of RML. Nutrition Diagnosis (PES): Excessive physical activity related to 2-hour workouts twice daily as evidenced by complaints of weakness, muscle stiffness and tenderness, and very high CPK levels.

discussing with physician. There are 17 dietary supplements that have been associated with direct renal injury, CAM-induced immune-mediated nephrotoxicity, nephrolithiasis, RML with acute renal injury, and hepatorenal syndrome (Gabardi et al, 2007). • Even brief exposure to atorvastatin causes a marked decrease in blood coenzyme Q10 concentration, with commonly reported adverse effects of exercise intolerance, myalgia, and myoglobinuria.

Intervention: Education about a more desirable level of physical activity to lessen strain on muscles. Counseling about nutrition for athletics and maintenance of other healthy habits, including adequate rest and sleep. Physical activity logs. Monitoring and Evaluation: Improvement in muscle stuffness and tenderness; CPK levels returning to a normal range. Physical activity logs showing workouts no longer than 30 minutes twice daily.

• Special dietary advice is required if there is renal disease or the need for dialysis. • It is important to offer advice according to the medical condition that preceded RML. Avoidance of fasting, feeding with a high-carbohydrate and low-fat diet, and intravenous drip infusion soon after every onset of RML may be needed for children (Korematsu et al, 2009).

Common Drugs Used and Potential Side Effects • Statins block the enzyme in the liver that is responsible for making cholesterol, hydroxy-methylglutaryl-coenzyme A reductase (HMG-CoA reductase). • Despite the withdrawal of cerivastatin because of fatal RML, the risk of this complication with other statins is extremely low (Waters, 2005). Options for managing statin myopathy include statin switching, particularly to fluvastatin or low-dose rosuvastatin; nondaily dosing regimens; nonstatin alternatives, such as ezetimibe and bile acid-binding resins; and coenzyme Q10 supplementation (Joy and Hegele, 2009). • Diuretic therapy may be needed if there is hypertension. • If there is hyperkalemia, calcium chloride or calcium gluconate may be used.

Herbs, Botanicals, and Supplements • Health care practitioners must take an active role in identifying patients who are using CAM and provide appropriate patient education (Gabardi et al, 2007). Herbs and botanical supplements should not be used without

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss alternate dietary guidelines as appropriate for medications and side effects of the disease. • Discuss how to use diet and exercise to manage high serum cholesterol if this information has not been given before. Reinforce what the patient has been doing well. • After damage to any muscles, extra fluid is needed to dilute urine and to eliminate myoglobin. Among soldiers, RML occurs in 25% of those who are injured (Carter et al, 2005).

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •



RHABDOMYOLYSIS—CITED REFERENCES Carter R III, et al. Epidemiology of hospitalizations and deaths from heat illness in soldiers. Med Sci Sports Exerc. 37:1338, 2005. de Menezes Ettinger JE, et al. Prevention of rhabdomyolysis in bariatric surgery. Obes Surg. 15:874, 2005. Flanigan KM, et al. DMD Trp3X nonsense mutation associated with a founder effect in North American families with mild Becker muscular dystrophy. Neuromuscul Disord. 19:743, 2009. Gabardi S, et al. A review of dietary supplement-induced renal dysfunction. Clin J Am Soc Nephrol. 2:757, 2007. Joy TR, Hegele RA. Narrative review: statin-related myopathy. Ann Intern Med. 150:858, 2009. Korematsu S, et al. Novel mutation of early, perinatal-onset, myopathic-type very-long-chain acyl-CoA dehydrogenase deficiency. Pediatr Neurol. 41:151, 2009. Linares LA, et al. The modern spectrum of rhabdomyolysis: drug toxicity revealed by creatine kinase screening. Curr Drug Saf. 4:181, 2009. Mor A, et al. Drug-induced myopathies. Bull NYU Hosp Jt Dis. 67:358, 2009. Olpin SE. Fatty acid oxidation defects as a cause of neuromyopathic disease in infants and adults. Clin Lab. 51:289, 2005. Waters DD. Safety of high-dose atorvastatin therapy. Am J Cardiol. 96:69, 2005.

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Adaprted from: Strickland JW, Graham TJ. Master Techniques in Orthopeadic Surgery: The Hand, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2005.

TABLE 11-13

RA is a chronic polyarthritis mainly affecting the smaller peripheral joints and is accompanied by general ill health. Crippling deformities can occur. Of all cases, 75% are women. Most patients are between ages 20 and 40, and RA affects over 1.3 million Americans. To diagnose RA, symptoms must have been present for at least 6 weeks; see Table 11-12. The cause of RA is increased inflammatory cytokine production, such as from mast cells, interleukin-6, tumor necrosis factor alpha (TNF), and acute-phase proteins. Inflammation of synovial tissues is the dominant manifestation. Antibodies against IgG and collagen are noted. Hand involvement and knees or ankles/feet are involved in most. Table 11-13 provides a list of the variant forms of RA. Some studies show an improvement in RA symptoms over the short term with a diet high in omega-3s or fish oil supplements. Omega-3 fatty acids reduce tenderness in joints, decrease morning stiffness, and reduce the amount

Variant Forms of Rheumatic Arthritis (RA)



Nutritional Implications

Juvenile RA (JRA)

JRA causes joint inflammation and stiffness for more than 6 weeks in a child 16 years of age or less. It is classified into three types, depending on symptoms, number of joints involved, and presence or absence of antibodies in the blood. Pauciarticular JRA is most common and affects mainly the knees. The polyarticular form affects 30% of children with JRA. Stills disease is the systemic form; it tests negative for the usual antibodies, may affect internal organs, may become chronic in adulthood and affects 20% of children with JRA. Both genetic factors and environmental factors, such as a virus, can trigger JRA. Because JRA often affects knees, limping can occur. Salicylates, gold salts, or glucocorticoids may be used.

Children suffering from JCA may have reduced serum levels of beta-carotene, retinol, and zinc.

Sjögren’s syndrome

Dry eyes and dry mouth occur as a result of insufficient production of lacrimal and salivary secretions. Artificial tears and glucocorticoids may be needed. Sjögren’s syndrome is relatively common and affects 4 million Americans, mostly women. It is most often related to RA, lupus, scleroderma, or polymyositis. Debilitating pain and fatigue can occur. Sensitivity to sunlight is common; sunscreen is helpful.

Plan meals and use artificial saliva for easier swallowing. Chewing sugar-free gum can stimulate saliva production if any is available. Gel-based saliva substitutes are useful. Sip water often, and avoid caffeinated drinks, which can be dehydrating. Drink water during meals to help with swallowing. Mouth infections are common; use good oral hygiene. With dry mouth or dysphagia, there is a risk for aspiration pneumonia. Weight loss and digestive problems are common.

Felty’s syndrome

Felty’s syndrome only affects about 1% of RA patients. This is a triad of RA, granulocytopenia, and splenomegaly. Painful, stiff, and swollen joints occur. Infections, leg ulcers, burning eyes, and anemia also can complicate the condition. Sometimes, splenectomy is indicated; drug therapy may be helpful to others.

Fever, weight loss, and brown pigmentation may occur. If immunosuppressive drugs are used, monitor for side effects.

Rheumatoid vasculitis

Rheumatoid vasculitis can be life threatening and usually occurs in patients with severe deforming arthritis and a high titer of rheumatoid factor. A majority have a strong human leukocyte antigen relationship. Vasculitic lesions include rheumatoid nodules, small nail fold infarcts, and purpura. Fatigue, weight loss, fever, organ ischemia, CNS infarctions, myocardial infarction, and peripheral neuropathy can occur.

Corticosteroids are the usual treatment. D-penicillamine and prednisone generally are used.

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of medication needed; they also downregulate T-cell proliferation. People with RA who eat 4 oz of fish every day have less morning stiffness, swollen joints, and all-around pain. Fish oil and aspirin are blood thinners, and they should not be taken together for a long time. Supplements of GLA, as from borage oil, may reduce generation of mediators of inflammation and attenuate symptoms but may cause potentially harmful increases in serum arachidonic acid unless EPA is also used. GLA increases prostaglandin E levels, which increase cyclic adenosine monophosphate (cAMP) levels which, in turn, suppress TNF synthesis. Epidemiological studies suggest that the antioxidant potential of dietary carotenoids may protect against the oxidative damage that can result in inflammation (Pattison et al, 2005). Proper antioxidant nutrients provide defense against increased oxidant stress. Supplementation of folate and vitamin B12 is needed in patients treated with methotrexate to reduce side effects and to offset elevated plasma homocysteine. Complications of RA may include osteoporosis and chronic anemia. Calcium and vitamin D reduce the bone loss in patients who take steroids. An iron supplement may prevent anemia, and serum ferritin levels may be low. Patients benefit from a basic dietary supplement. Higher intakes of meat and total protein and lower intakes of fruit, vegetables, and vitamin C are associated with an increased risk of RA (Choi, 2005). However, dietary factors such as fruit, coffee, long-chain fatty acids, olive oil, vitamins A, E, C, and D, zinc, selenium, and iron need to be studied over a longer time period (Pedersen et al, 2005). Rheumatoid cachexia, loss of muscle mass and strength and increase in fat mass, is very common in patients with RA and persists even after joint inflammation improves (Roubenoff, 2009). Cardiovascular disease is a concern. Body composition studies are as important as BMI and other traditional assessment measures (Elkan et al, 2009).

ESR (increases with inflammation) ANA Rheumatoid factor (RF) Antistreptococcal antibody titer Immunoglobulins (may be elevated in Sjögren’s)

Ceruloplasmin (may be increased) H&H Serum ferritin Serum B12 Transferrin Serum folate, RBC folate Serum copper

Alb, transthyretin Gluc BUN Ca, Mg Na, K Vitamin D3 status (serum 25-OHD)

INTERVENTION OBJECTIVES • Preserve a high level of physical and social functioning to promote good quality of life; reduce the effects of pain and swelling. • Maintain satisfactory nutritional status; malnutrition and loss of lean body mass are common in this condition. Monitor weight changes. • Simplify meal preparation. • Support the immune system. Consume foods rich in antioxidants, such as carotenoids (Pattison et al, 2005), vitamin E, selenium, and vitamin D. A vegetarian diet may have significant benefits. • Promote adequate growth in children who have RA; stunting can occur from glucocorticoids. • Promote return of fat-free body mass and improvement in muscle strength. • Restrict sodium intake, if needed.



Drug–Nutrient Interaction Assessment Data: Weight and physical activity histories. Medical history, medications and lab values. DEXA scan results.

CLINICAL INDICATORS Genetic Markers: B cell, cytokine and inflammation response, and antigen presentation pathways are associated with RA; this confirms the known biological mechanisms for auto-immunity (Ballard et al, 2009). Clinical/History Height Weight BMI Temperature

Pain and stiffness 30 minutes in the morning or after a long rest Food allergies

Lab Work RBC CRP LE prep Creat (may be decreased)

Nutrition Diagnosis (PES): Food-Medication interaction (NC-2.3) related to corticosteroid use secondary to diagnosis of RA as evidence by abnormal Ca level 8.4, DEXA scan at 80% of desirable range for age, perimenopausal status, low calcium and vitamin D intake from diet history. Intervention: Food-Nutrient Delivery—include extra calcium-rich foods. Education about use of steroid therapy and its impact on nutritional status. Counseling about good sources of calcium and vitamin D from diet and supplements, meal planning and shopping tips, dining out guide, referral to Meals-on-Wheels or other social agencies as appropriate. Coordinate care with nursing and physician to administer calcium and vitamin D supplements at different time than corticosteroids to help increase absorption. Monitoring and Evaluation: Improvements in dietary and supplemental intake of vitamin D and calcium as shown in food records, lab values, and DEXA scan report.

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• Modify patient’s diet if hyperlipidemia is present or if there is elevated homocysteine. • Avoid or correct constipation. •

FOOD AND NUTRITION • Use a high-protein and high-calorie diet if patient is malnourished. Cachexia is common (Marcora et al, 2005). • A diet that lessens inflammation is useful; olive oil should be used often because it contains oleocanthal, a natural anti-inflammatory agent. • Eating fatty fish, such as salmon, sardines, mackerel, herring, and tuna, two times per week is suggested. In addition to fatty fish, other good sources of omega-3s include flaxseed, walnuts, soy, canola oils. Try to acquire 3–6 g of omega-3 fatty acids per day for 4 months. • An uncooked vegan diet may be useful, with berries, fruits, vegetables, roots, nuts, and seeds; see Table 11-2. There is improvement in RA when eating a lactovegetarian, vegan, or Mediterranean diet (Skoldstam et al, 2005). • Adequate fluid, fiber, vitamins, and minerals are important. Use foods high in beta-carotene, lutein lycopene, TABLE 11-14

• • • •


selenium, vitamins C and E; choose nutrient-dense foods. Antioxidants such as beta-cryptoxanthin (as from one glass of freshly squeezed orange juice daily) can reduce the risk of developing RA (Pattison et al, 2005). Increase vitamin D intakes to decrease the incidence and severity of RA. Provide adequate intake of calcium, magnesium, B-complex vitamins, potassium, and zinc. Increase folic acid if methotrexate is used; enhance diet or encourage folic acid supplements. Provide meals that are easy to tolerate when the drugs being used cause gastric irritation. Avoid acidic or highly spiced foods if needed. With dysphagia, tube feed or use soft/thick, pureed foods as needed. Identify and eliminate any food allergens. Individualize the diet accordingly.

Common Drugs Used and Potential Side Effects • With biologic therapies, such as TNF inhibitors, many patients with RA have seen significant improvement in symptoms, function, and quality of life (Barton et al, 2009). See Table 11-14.

Medications Used in Rheumatoid Arthritis



Side Effects


Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs)

Analgesics relieve pain; NSAIDs relieve pain and reduce inflammation.

Upset stomach, peptic ulcer, bleeding, renal failure. Use of NSAIDs may increase rate of miscarriage for pregnant women.

For all traditional NSAIDs: avoid drinking alcohol or using blood thinners; avoid if there is sensitivity or allergy to aspirin or similar drugs, kidney or liver disease, heart disease, high blood pressure, asthma, or peptic ulcers.

Usually no side effects when taken as directed.

Not to be taken with alcohol or with other products containing acetaminophen. Not to be used for more than 10 days unless directed by a physician.


Aspirin: buffered, plain

Aspirin is used to reduce pain, swelling, and inflammation, allowing patients to move more easily and carry out normal activities. It is generally part of early and ongoing therapy.

Upset stomach; tendency to bruise easily; ulcers, pain, or discomfort; diarrhea; headache; heartburn or indigestion; nausea or vomiting.

Doctor monitoring is needed. Not used for children in whom Reye’s syndrome is a risk, but otherwise useful in lessening inflammation.

Traditional NSAIDs: ibuprofen, ketoprofen, naproxen

NSAIDs help relieve pain within hours of administration in dosages available over the counter (available for all three medications). They relieve pain and inflammation in dosages available in prescription form (ibuprofen and ketoprofen). It may take several days to reduce inflammation.

For all traditional NSAIDs: abdominal or stomach cramps, pain, or discomfort; diarrhea; dizziness; drowsiness or light-headedness; headache; heartburn or indigestion; peptic ulcers; nausea or vomiting; possible kidney and liver damage (rare).

For all traditional NSAIDs: avoid drinking alcohol or using blood thinners; avoid if there is sensitivity or allergy to aspirin or similar drugs, kidney or liver disease, heart disease, high blood pressure, asthma, or peptic ulcers.

Cyclo-oxygenase (COX)-2 inhibitor NSAIDs: celecoxib, valdecoxib

COX-2 inhibitors, such as traditional NSAIDs, block COX-2, an enzyme in the body that stimulates an inflammatory response. Unlike traditional NSAIDs, however, they do not block the action of COX-1, an enzyme that protects the stomach lining. Vioxx was withdrawn by FDA.

Stomach irritation, ulceration, and bleeding may occur. Caution is advisable for patients with a history of bleeding or ulcers, decreased renal function, hepatic disease, hypertension, or asthma.

Doctor monitoring for possible allergic responses to valdecoxib and celecoxib is important.


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TABLE 11-14

Medications Used in Rheumatoid Arthritis (continued)



Side Effects



These are steroids given by mouth or injection. They are used to relieve inflammation and reduce swelling, redness, itching, and allergic reactions.

Increased appetite, indigestion, nervousness, or restlessness.

For all corticosteroids, advise the doctor if there is presence of the following: fungal infection, history of tuberculosis, underactive thyroid, herpes simplex of the eye, high blood pressure, osteoporosis, or stomach ulcer.

Methylprednisolone, prednisone

These steroids are available in a pill form or as an injection into a joint. Improvements are seen up to 24 hours after administration. There is potential for serious side effects, especially at high doses. They are used for severe flares or when the disease does not respond to NSAIDs and disease-modifying antirheumatic drugs.

Osteoporosis, mood changes, fragile skin, easy bruising, fluid retention, weight gain, muscle weakness, onset or worsening of diabetes, cataracts, increased risk of infection, and hypertension.

Doctor monitoring for continued effectiveness of medication and for side effects is needed.

Disease-modifying antirheumatic drugs (DMARDs)

These are common arthritis medications. They relieve painful, swollen joints and slow joint damage, and several DMARDs may be used over the disease course. They take a few weeks or months to have an effect and may produce significant improvements for many patients. Exactly how they work is still unknown.

Side effects vary with each medicine. DMARDs may increase risk of infection, hair loss, and kidney or liver damage.

Doctor monitoring allows the risk of toxicities to be weighed against the potential benefits of individual medications.


This drug was first used in higher doses in cancer chemotherapy and organ transplantation. It is used in patients who have not responded to other drugs and in combination therapy.

Cough or hoarseness, fever or chills, loss of appetite, lower back or side pain, nausea or vomiting, painful or difficult urination, unusual tiredness or weakness.

Avoid with allopurinol or kidney or liver disease. May decrease immunity; contact doctor immediately with chills, fever, or a cough. Regular blood and liver function tests are needed.


This medication was first used in organ transplantation to prevent rejection. It is used in patients who have not responded to other drugs.

Bleeding, tender, or enlarged gums; high blood pressure; increase in hair growth; kidney problems; trembling and shaking of hands.

Avoid with sensitivity to castor oil (if receiving the drug by injection), liver or kidney disease, active infection, or high blood pressure. Using this drug may make you more susceptible to infection and certain cancers. Do not take live vaccines while on this drug. Avoid St. John’s wort and echinacea.


It may take several months to notice the benefits of this drug, which include reducing the signs and symptoms of rheumatoid arthritis.

Diarrhea, eye problems (rare), headache, loss of appetite, nausea or vomiting, and stomach cramps or pain.

Doctor monitoring is important, particularly with an allergy to any antimalarial drug or a retinal abnormality.

Gold sodium thiomalate (Ridaura)

This was one of the first DMARDs used to treat rheumatoid arthritis.

Redness or soreness of tongue; swelling or bleeding gums; skin rash or itching; ulcers or sores on lips, mouth, or throat; irritation on tongue. Monitor joint pain 1 or 2 days after injection.

Avoid with lupus, skin rash, kidney disease, or colitis. Periodic urine and blood tests are needed to check for side effects.


This drug reduces signs and symptoms and slows structural damage to joints caused by arthritis.

Bloody or cloudy urine; congestion in chest; cough; diarrhea; difficult, burning, or painful urination or breathing; fever; hair loss; headache; heartburn; loss of appetite; nausea and/or vomiting; skin rash; stomach pain; sneezing; and sore throat.

Doctor must monitor for the following: active infection, liver disease, known immune deficiency, renal insufficiency, or underlying malignancy. Regular blood tests, including liver function tests, are needed. Leflunomide must not be taken during pregnancy; it may cause birth defects in humans. (continued)

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TABLE 11-14


Medications Used in Rheumatoid Arthritis (continued)



Side Effects


Methotrexate (Rheumatrex)

This drug can be taken by mouth or by injection and results in rapid improvement (it usually takes 3–6 weeks to begin working). It is very effective, especially in combination with infliximab or etanercept. It produces more favorable long-term responses compared with DMARDs such as sulfasalazine, gold sodium thiomalate, hydroxychloroquine and may be used in pediatrics.

Abdominal discomfort, chest pain, chills, nausea, mouth sores, painful urination, sore throat, and unusual tiredness or weakness.

Doctor monitoring is important, particularly with an abnormal blood count, liver or lung disease, alcoholism, immune system deficiency, or active infection. Methotrexate must not be taken during pregnancy because it may cause birth defects in humans. Avoid Echinacea. Extra folic acid is needed.


This drug suppresses the immune system.

Abdominal pain, aching joints, diarrhea, headache, sensitivity to sunlight, loss of appetite, nausea or vomiting, and skin rash.

Doctor monitoring is important, particularly with allergy to sulfa drugs or aspirin or with a kidney, liver, or blood disease.

Biological response modifiers

These drugs selectively block cytokines, which play a role in inflammation. Long-term efficacy and safety are uncertain.

Increased risk of infection, especially tuberculosis. Increased risk of pneumonia, and listeriosis (a foodborne illness caused by the bacterium Listeria monocytogenes).

Avoid eating undercooked foods (including unpasteurized cheeses, cold cuts, and hot dogs) to reduce listeriosis while taking biological response modifiers.

Tumor necrosis factor inhibitors: etanercept (Enbrel), golimumab (Simponi), infliximab (Remicade), and adalimumab (Humira)

Highly effective for treating patients with an inadequate response to DMARDs. Often prescribed in combination with methotrexate. Etanercept requires subcutaneous injections twice weekly. Infliximab is taken intravenously (IV) during a 2-hour procedure, along with methotrexate. Adalimumab requires injections every 2 weeks.

Etanercept: pain or burning in throat, redness, itching, pain, and/or swelling at injection site, runny or stuffy nose. Infliximab: abdominal pain, cough, dizziness, fainting, headache, muscle pain, runny nose, shortness of breath, sore throat, vomiting, wheezing. Adalimumab: redness, rash, swelling, itching, bruising, sinus infection, headache, nausea. Golimumab: respiratory infection, sore throat and nasal congestion.

Doctor monitoring is important, particularly with active infection, exposure to tuberculosis, or a central nervous system disorder. Evaluation for tuberculosis is necessary before treatment begins.

Interleukin-1 inhibitor: anakinra (Kineret)

This medication requires daily injections. Long-term efficacy and safety are uncertain.

Redness, swelling, bruising, or pain at the site of injection; headache; upset stomach; diarrhea; runny nose; and stomach pain.

Doctor monitoring is required.

Selective Costimulation Modulator: Abatacept

Abatacept is given intravenously in a 30-minute infusion. It may be given alone or with DMARDs.

Cough, dizziness, headache, infections, sore throat.

Doctor monitoring is needed.

CD20 Antibody: Rituximab

This medication is for people whose rheumatoid arthritis has not responded to other biologic agents. It is given by two IV infusions 2 weeks apart. It is given with methotrexate.

Abdominal pain, chills/shivering, fever, headache, infection, itching.

Doctor monitoring is needed.

Other medications

Pilocarpine hydrochloride (Salagen) and cevimeline (Evoxac).

Available to treat dry mouth associated with Sjögren’s syndrome. They simulate the salivary glands.

Adapted from: National Institutes of Health. Health topics. Accessed December 19, 2009 at

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Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. Some people have tried acupuncture and other alternatives to traditional medicine, but it is important not to neglect regular health care or treatment of serious symptoms. Female patients tend to use alternative treatments for RA more than males; psychosocial intervention may be beneficial. • With borage oil, concomitant NSAID use may undermine the effects. Borage oil is contraindicated in pregnancy given the teratogenic and labor-inducing effects of prostaglandin E agonists. • St. John’s wort and echinacea should not be used with cyclosporine or methotrexate.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

American Autoimmune Related Diseases Association

American College of Rheumatology

Arthritis Foundation

Felty Syndrome

Information on Rheumatoid Arthritis

Juvenile Rheumatoid Arthritis

National Institute of Dental and Craniofacial Research–Sjögren’s Syndrome Opportunities_Sorted_By/ConceptClearance/CurrentCC/ SjogrenSynd.htm

National Sjögren’s Syndrome Association

Rheumatoid Vasculitis

Sjögren’s Syndrome Foundation—Food Tips

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Adoption of a Mediterranean diet confers health benefits in this population because of greater consumption of fruits and vegetables, lower consumption of animal products, and use of olive oil, which modulates immune function (Wahle et al, 2005). Inclusion of omega-3 fatty acids is also important (Berbert et al, 2005); herring, salmon, sardines, tuna, and mackerel are good dietary sources. • No evidence exists to prove that foods from the nightshade family (potatoes, tomatoes, eggplant, and sweet and hot peppers) should be excluded. • Encourage nutrient-dense foods. If intake is poor, a vitamin–mineral supplement may be needed. Dietary quinones, phenolics, vitamins, amino acids, isoprenoids, and other compounds in functional foods have become very popular (Losso and Bawadi, 2005). • Instruct patient about simplified planning and preparation tips. Sandwiches, prepared meals, precut fruits and vegetables are easy to use. Cook double portions and freeze leftovers for another day. • Discourage quackery and substitute sound health practices. • Carbohydrate intolerance occurs because of chronic inflammation and use of steroids; planning must reflect individual needs. • A support group may be helpful for coping. • Physical therapy and exercise are beneficial for most patients. Strengthening exercises may help improve patient’s ability to walk and may decrease joint pain and fatigue. Dynamic exercise is beneficial in RA (Hurkmans et al, 2009). • Check on bone density; there is a high incidence of osteoporosis when steroids are used.

RHEUMATOID ARTHRITIS—CITED REFERENCES Ballard DH, et al. A pathway analysis applied to Genetic Analysis Workshop 16 genome-wide rheumatoid arthritis data. BMC Proc. 15;3:91, 2009. Barton JL. Patient preferences and satisfaction in the treatment of rheumatoid arthritis with biologic therapy. Patient Prefer Adherence. 3: 335, 2009. Berbert AA, et al. Supplementation of fish oil and olive oil in patients with rheumatoid arthritis. Nutrition. 21:131, 2005. Choi HK. Dietary risk factors for rheumatic diseases. Curr Opin Rheumatol. 17:141, 2005. Elkan AC, et al. Rheumatoid cachexia, central obesity and malnutrition in patients with low-active rheumatoid arthritis: feasibility of anthropometry, Mini Nutritional Assessment and body composition techniques. Eur J Nutr. 48:315, 2009. Hurkmans E, et al. Dynamic exercise programs (aerobic capacity and/or muscle strength training) in patients with rheumatoid arthritis. Cochrane Database Syst Rev. 2009;(4):CD006853. Losso JN, Bawadi HA. Hypoxia inducible factor pathways as targets for functional foods. J Agric Food Chem. 53:3751, 2005. Marcora S, et al. Dietary treatment of rheumatoid cachexia with betahydroxy-beta-methylbutyrate, glutamine and arginine: a randomised controlled trial. Clin Nutr. 24:442, 2005. Pattison DJ, et al. Dietary beta-cryptoxanthin and inflammatory polyarthritis: results from a population-based prospective study. Am J Clin Nutr. 82:451, 2005. Pedersen M, et al. Diet and risk of rheumatoid arthritis in a prospective cohort. J Rheumatol. 32:1249, 2005. Roubenoff R. Rheumatoid cachexia: a complication of rheumatoid arthritis moves into the 21st century. Arthritis Res Ther. 11:108, 2009. Wahle KW, et al. Olive oil and modulation of cell signaling in disease prevention. Lipids. 39:1223, 2005.

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RUPTURED DISC NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Determining the cause of back pain is complicated as it is often multifactorial; anatomical abnormalities are common in the spine and may not necessarily translate into clinical symptoms (Sheehan et al, 2010). A slipped or ruptured disc is called a cervical radiculopathy, herniated intervertebral disc, lumbar radiculopathy, or prolapsed intervertebral disc. In this condition, slipping or prolapse of a cervical or lumbar disc occurs, with neck, shoulder, or low back pain accordingly. Degenerating changes in the disks begin around 30 years of age. Overweight and obesity increase the risk of low back pain and the need for medical attention (Shiri et al, 2010). With lumbar radiculopathy, ambulation may be painful, and limping can occur. Muscular weakness, severe back pain that radiates to buttocks or legs and feet, pain that worsens with coughing or laughing, tingling or numbness in legs or feet, and muscle contractions or spasms may also result. With cervical radiculopathy, neck pain in back and sides is deep; pain may radiate to shoulders, upper arms, or forearms and worsens with coughing or laughing. Spasm of neck muscles and pain that worsens at night may occur. A laminectomy surgically removes the lamina of a vertebra. Percutaneous automated discectomy (PAD) surgery can be performed in some cases; this surgery breaks up the disc and removes fragments. There is no convincing medical evidence to support routine use of lumbar fusion, but it may be useful in patients with associated spinal deformity, instability, or associated chronic low-back pain (Resnick et al, 2005). Surgery for radiculopathy with herniated lumbar disc and symptomatic spinal stenosis is associated with short-term benefits compared to nonsurgical therapy, though benefits diminish with long-term follow-up in some trials (Chou et al, 2009).


CLINICAL INDICATORS Genetic Markers: This condition is acquired and not genetic. Clinical/History

Myelography Discography Spinal or neck x-rays Nerve conduction velocity test

Height Weight BMI I&O BP Constipation Edema Lab Work MRI or computed tomography H & H Ca, Mg (CT) scan

Na, K Alb, transthyretin BUN, Creat Alk phos Gluc Vitamin D3 status (serum 25-OHD)

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function Assessment Data: Weight and physical activity histories. Medical history and medications. Nutrition Diagnosis (PES): Abnormal GI function related to constipation and infrequent stooling pattern as evidenced by GI distress and evacuation every 3–4 days. Intervention: Food-nutrient delivery—Assure intake of adequate fluid and fiber at all meals. Education—Discuss tips for alleviating constipation through use of specific foods rich in fiber (fruits, vegetables, whole grains, beans and legumes). Coordinate care— Work with nursing and physicians to determine if any medications that cause constipation can be changed, or if some type of laxative can be added. Monitoring and Evaluation: Improvement in bowel habits; alleviation of constipation.

INTERVENTION OBJECTIVES • Maintain adequate rest and activity levels, as assigned by physician. • Prevent weight gain from decreased activity. • Encourage adequate hydration. • Prevent constipation and straining. • Assist with feeding, if patient is in traction. • Relieve pain and promote healing.

FOOD AND NUTRITION • A regular diet generally is sufficient. For some, a strict energy-controlled diet may be beneficial to promote weight loss. • Increased fluid and fiber intake can be helpful to reduce constipation. Fresh fruits and vegetables, dried beans, legumes, whole grains, bran, and other foods may be needed.

Common Drugs Used and Potential Side Effects • Anti-inflammatory drugs may be used. NSAIDs are used for long-term pain control, but narcotics may be given if the pain does not respond. Nausea, GI distress, and anorexia may result. Follow directions regarding when to take (e.g., before or after meals). • Analgesics may be helpful to relieve pain. Chronic use of aspirin may cause GI bleeding. • Muscle relaxants may be ordered. GI distress or nausea can occur.

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

For More Information •

Herniated Disk

Lumbar Radiculopathy pulposus

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Instruct patient regarding effective methods of relieving constipation. • Discuss role of nutrition and exercise in health maintenance. Weight loss may be needed. • After surgery, the role of nutrition in wound healing should be discussed.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

RUPTURED INTERVERTEBRAL DISC—CITED REFERENCES Chou R, et al, Surgery for low back pain: a review of the evidence for an American Pain Society Clinical Practice Guideline. Spine. 34:1094, 2009. Resnick DK, et al. Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 8: lumbar fusion for disc herniation and radiculopathy. J Neurosurg Spine. 2:673, 2005. Sheehan NJ. Magnetic resonance imaging for low back pain: indications and limitations. Ann Rheum Dis. 69:7, 2010. Shiri R, et al. The Association Between Obesity and Low Back Pain: A Meta-Analysis [published online ahead of print 2009]. Am J Epidemiol. 171:135, 2010.


Adapted from: Goodheart HP, MD. Goodheart’s Photoguide of Common Skin Disorders, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

DEFINITIONS AND BACKGROUND Scleroderma is a chronic disease characterized by fibrosis and autoantibodies. Approximately 2% of the population in Europe and North America suffers from disorders such as scleroderma (Chen and von Mikecz, 2005). Genetic, immunological, hormonal, and environmental factors are considered to be triggers (Molina and Shoenfeld, 2005). The diffuse form affects a large area of the skin and several organs; it is also called systemic sclerosis (SSc). In SSc, pathological deposition of fibrous connective tissue in the skin and visceral organs occurs. Fibrosis involves an increase of hydroxylysine aldehyde collagen cross-linkages as well as an increase in inflammatory cytokines (Brinckmann et al,

2005). The GI tract is affected, and Raynaud’s syndrome (ischemia of fingers) is common. The limited form of scleroderma affects the skin and sometimes the lungs. The CREST syndrome (limited cutaneous sclerosis) is less severe than SSc and causes less internal organ damage. Calcium deposits, Raynaud’s phenomenon, esophageal dysfunction, skin damage on fingers, and telangiectasia form the acronym for CREST. As the disease progresses, large areas of the skin or just the fingers (sclerodactyly) may be affected. Skin on the face tightens and causes a mask-like appearance. Spider veins (telangiectasia) occur on the fingers, chest, face, lips, or tongue. Calcium deposits can occur on the fingers or other bony areas; sores or contractures may result from the scarring. Scarring of the esophagus may be especially detrimental, causing blockage or even cancer. Lungs can be affected, leading to shortness of breath with exercise. Neurological involvement consists of epilepsy, central nervous system vasculitis, peripheral neuropathy, vascular malformations, headache, and neuroimaging abnormalities; ocular manifestations include uveitis, xerophthalmia, glaucoma, and papilledema (Zulian et al, 2005). SSc is characterized by vasculopathy, inflammation, vasospasm, microvascular involvement is common; an increased prevalence of distal peripheral artery disease in the digits has been found (Hetterna et al, 2008). Scleroderma renal crisis (SRC) occurs in 5–10% of SSc patients, who may present with an abrupt onset of hypertension, acute renal failure, headaches, fevers, malaise, hypertensive retinopathy, encephalopathy, and pulmonary edema (Denton et al, 2009). Multiple organ system dysfunction may occur. Pulmonary hypertension, heart failure, and respiratory failure cause serious morbidity and mortality. There is no known cure, and SSc can be fatal.

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There seems to be an increased prevalence of celiac disease in patients with scleroderma (Rosato et al, 2009). Both disorders require careful management. Current therapies for scleroderma target the immune system, with the goal of reducing inflammation, ischemic injury to the involved organs, and secondary tissue injury and fibrosis (Henness and Wigley, 2007).


CLINICAL INDICATORS Genetic Markers: Genetic factors contribute to disease susceptibility; transforming growth factor-ss is a cytokine that contributes to fibroblast activation, collagen overproduction, and pathological tissue fibrosis (Varga, 2008). T-cell polarization is implicated in the lung disease of SSc (Boin et al, 2008). Gluc Prothrombin Height time (PT) Weight Alb, transthyretin BMI CRP I&O GFR Weight loss BUN, Creat Fever? Lab Work Homocysteine BP Ca, Mg ANA (high) Thickening, Na, K RF (high) swelling of Alk phos LDL Cholesterol the ends of Vitamin D3 (elevated) the fingers status (serum Trig (may be Dysphagia 25-OHD) low) Heartburn Fecal fat test, Anti-tTG Fibrosis of hydrogen antibody salivary and breath Serum folate lacrimal test for malH&H glands absorption Abdominal pain, Serum B12 flatulence Clinical/History

Nausea, vomiting Diarrhea, constipation Skinfold measurements

SAMPLE NUTRITION CARE PROCESS STEPS Difficulty Swallowing Assessment Data: Weight, medical history, medications. Low salivation and difficulty swallowing. Nutrition Diagnosis (PES): Difficulty swallowing related to low saliva production as evidenced by fibrosis, inability to swallow solids. Intervention: Food-Nutrient Delivery—Alteration in food choices to liquefy meals and make them easier to swallow. Educate about the use of saliva substitutes, more fluids, altered food choices as needed. Counseling about when to request changes, such as tube feeding. Monitoring and Evaluation: Improvement in swallowing and tolerance for meals. No weight loss.


INTERVENTION OBJECTIVES • Prevent or correct protein-energy malnutrition and nutrient deficiencies. • Correct xerostomia where present; decreased saliva, dysphagia, and difficulty in chewing will result. • Monitor dysphagia with esophageal involvement; alter method of feeding as needed. • Counteract vitamin B12 and fat maldigestion and absorption, which may be common. • Monitor hypomotility and gastroparesis; alter fiber intake as appropriate. For many patients, nutritional support and relief of symptoms remain the primary management goals. • Improve quality of life and reduce fatigue; allow return to work or maintenance of energy levels.

FOOD AND NUTRITION • Diets high in energy (30–40 kcal/kg) and adequate to high in protein are often necessary. A soft diet with moistened foods and extra fluids is useful. Add fiber if constipation is a problem (such as adding crushed bran to hot cereal). • Small, frequent feedings may be needed. Tube feed if patient is dysphagic or has obstruction. • Use parenteral nutrition if GI tract is highly affected, with intractable diarrhea and severe malabsorption. • If there is celiac sensitivity, omit gluten from the diet. • Reduce lactose if intolerance occurs. Extra calcium may be needed if lactose is not tolerated orally. • Give supplements of fat- and water-soluble vitamins. • With hypertension and multiple organ system dysfunction, reduced sodium or fluid restriction may be needed.

Common Drugs Used and Potential Side Effects • Topical or systemic corticosteroids, vitamin D analogs (calcitriol and calcipotriol), photochemotherapy, laser therapy, antimalarials, phenytoin, D-penicillamine, and colchicine all have varying degrees of success. Topical tacrolimus cream is an immunosuppressive antibiotic. • Interstitial lung disease can be treated with cyclophosphamide, vascular disease of the lungs and digits with endothelin receptor antagonists, and general symptoms with phosphodiesterase inhibitor sildenafil or prostacyclins (Henness and Wigley, 2007). • Early, aggressive treatment with angiotensin-converting enzyme inhibitors helps with a renal crisis (Denton et al, 2009). • Anti-inflammatory agents, such as steroids, are often used in SSc. Monitor for nitrogen and calcium losses, altered electrolyte levels, and elevated glucose levels. Correct diet accordingly. • Antihypertensives usually are needed; monitor BP results. Potassium supplements may or may not be required; determine need according to medication selected. • Trental (pentoxifylline) is used for Raynaud’s syndrome to improve circulation. Anorexia or GI distress may result.

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Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • For Raynaud’s disease, evening primrose, gingko, mustard, garlic, borage, and red pepper have been suggested, but there are no clinical trials that prove effectiveness. • CAM is frequently used to treat stress-related disorders such as scleroderma; some merit can be noted (Hui et al, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Artificial saliva (Xero-Lube) or lemon glycerine may be useful. • Chew sugarless gum. • If eating orally, adequate chewing time will be required. • Consume adequate fluids. Choose moist foods or foods with sauces/gravies. • For heartburn, keep head elevated after meals; decrease or limit intake of chocolate, caffeine, fatty foods, alcohol, citrus, and tomatoes. • Physical therapy and exercise may help maintain muscle strength but cannot totally prevent joints from locking into stiffened positions.

Patient Education—Food Safety If enteral or parenteral nutrition is used, careful sanitation and handling techniques must be taught and used.

For More Information •

Scleroderma Foundation

Scleroderma Research Foundation

SCLERODERMA—CITED REFERENCES Boin F, et al. T cell polarization identifies distinct clinical phenotypes in scleroderma lung disease. Arthritis Rheum. 58:1165, 2008. Brinckmann J, et al. Interleukin 4 and prolonged hypoxia induce a higher gene expression of lysyl hydroxylase 2 and an altered cross-link pattern: important pathogenetic steps in early and late stage of systemic scleroderma? Matrix Biol. 24:459, 2005. Chen M, von Mikecz A. Xenobiotic-induced recruitment of autoantigens to nuclear proteasomes suggests a role for altered antigen processing in scleroderma. Ann N Y Acad Sci. 1051:382, 2005. Denton CP, et al. Renal complications and scleroderma renal crisis. Rheumatology (Oxford). 48:32S, 2009. Henness S, Wigley FM. Current drug therapy for scleroderma and secondary Raynaud’s phenomenon: evidence-based review. Curr Opin Rheumatol. 19:611, 2007. Hetterna ME, et al. Macrovascular disease and atherosclerosis in SSc. Rheumatology (Oxford). 47:578, 2008. Hui KK, et al. Scleroderma, stress and CAM Utilization. Evid Based Complement Alternat Med. 6:503, 2009. Molina V, Shoenfeld Y. Infection, vaccines and other environmental triggers of autoimmunity. Autoimmunity. 38:235, 2005. Rosato E, et al. High incidence of celiac disease in patients with systemic sclerosis. J Rheumatol. 36:965, 2009. Varga J. Systemic sclerosis: an update. Bull NYU Hosp Jt Dis. 66:198, 2008. Zulian F, et al. Localized scleroderma in childhood is not just a skin disease. Localized scleroderma in childhood is not just a skin disease. Arthritis Rheum. 52:2873, 2005.

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Hematology: Anemias and Blood Disorders




• • • • • • • • • • • • • • • •

Anorexia Beefy, Red Tongue or Magenta Tongue; Other Signs of Nutrient Deficiencies Blood Type Bruising Concurrent Asthma, Cancer, Cerebrovascular Disease, Hemorrhage, Myocardial Infarction, Renal Disease Dietary Habits: Use of Heme and Nonheme Iron, Vitamin and Mineral Deficiencies, Protein Intake, Vegan Lifestyle Exposure to Lead Paint, Other Toxins Family History of Allergies, Anemias, Cancer, Immune Disorders, and Leukemias Fatigue History of Alcohol and Nicotine Use Infections, Sepsis Lymphadenopathy Medication Use (Prescriptions, Over-the-Counter) and Use of Herbal or Botanical Medications Occupational or Environmental Exposure to Toxic Substances Previous Blood Disorder, Bleeding Tendencies, Blood Transfusion, or Exposure to Radiation Surgery, Especially Gastric, Hepatic, or Renal

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GENERAL INFORMATION ABOUT ANEMIAS Blood contains plasma and cells. Plasma is clear and yellow and makes up 55% of blood. It contains proteins, nutrients, hormones, and electrolytes. White cells, red blood cells (RBCs), and platelets make up the remaining 45% of blood. The white cells fight infection, platelets are necessary for blood clotting, and RBCs carry oxygen throughout the body. Hepcidin, the main iron regulatory hormone, is made primarily in hepatocytes in response to liver iron levels, inflammation, hypoxia, and anemia (Munoz et al, 2009). Erythropoietin is the hormone that stimulates RBC production. The erythrocyte life span is 120 days, after which the cells are destroyed by the spleen. Anemias are a set of hematological disorders with a reduced number of RBCs, reduced amount of hemoglobin (Hgb), or reduced number of volume-packed RBCs (hematocrit [Hct]). Excessive bleeding, decreased RBC production, and increased RBC destruction may lead to anemias. The main consequences of these disorders include hypoxia and decreased oxygen-carrying capacity. Overall, anemias affect over 3.4 million people in the United States. Chronic disease and iron deficiency are the most common causes. Other causes of anemias include peptic ulcers, inflammation, infection, cancers, gastritis, liver

disease, renal disease, hypothyroidism, history of blood transfusions, blood coagulation disorders, and poor diet. Generally, Hgb, serum iron, TIBC or UIBC, and serum ferritin will establish iron status. In conditions due to blood cell production or cancers, other tests or procedures are needed to determine the cause for abnormal iron levels. These may include a complete blood count (CBC) with differential, zinc protoporphyrin (ZPP) immunological tests, hormone tests, reticulocyte count, C-reactive protein (CRP), sedimentation rate (SED rate), B12 or folate levels, genetic testing, tissue biopsy, MRI, ultrasound, bone marrow aspiration, blood smears, urine or fecal sampling, scopes (endoscope or colonoscopy), and tests associated with specific diseases or conditions that can have anemia or iron overload. Anemias can be encountered with generalized or specific nutritional deficiencies (Table 12-1). The nutritional anemias are caused by deficits, but not all anemias require nutritional intervention. Use caution when evaluating single laboratory results; most anemias have a specific profile. For example, iron and copper participate in one-electron exchange reactions; the same property that makes them essential also generates free radicals that can be seriously deleterious to cells (Arredondo and Nunez, 2005). Table 12-2 provides some key definitions that are used to describe anemias.

Anemia ( Hb and Hct)

MCV, RDW, Retic


Retic or (N) RDW (N) Iron deficiency anemia ( RDW) Thalassemia trait Lead poisoning Chronic disease Sideroblastic anemia

Retic, RDW Thalassemia syndromes (SB thalassemia, Hb H disease) Hb C disorders Hb E disorders

Review of smear Further Diagnostic Test

Iron studies Hb electrophoresis Lead level


Retic or (N) RDW (N) Chronic disease Transient erythroblastopenia of childhood Acute inflammation Acute hemorrhage Malignancy

Retic, RDW Immune hemolysis RBC membrane disorder (HS, He) RBC enzyme defects (G6PD, PK deficiency) Microangiopathic hemolysis (HUS, TTP, DIC) Sickle-cell anemia

Review of smear


Retic or (N) RDW (N) Folate deficiency B12 deficiency Bone marrow failure (aplastic anemia, Fanconi anemia, DBA) Myelodysplastic syndrome Hypothyroidism Drug-induced (anticonvulsants)

Retic, RDW Active hemolysis with brisk reticulocytosis

Review of smear

Further Diagnostic Test

Further Diagnostic Test

Other diseases (infection, renal, liver, metabolic) Coombs test Osmotic fragility Enzyme assays (G6PD, PK) Hb electrophoresis

Folate, B12 level Thyroid function test Bone marrow aspirate and biopsy Evaluate hemolysis

Red cell distribution width (RDW), a measure of heterogeneity in the size of circulating erythrocytes, is associated with some chronic diseases and predicts mortality.

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TABLE 12-1 Nutritional Factors in Blood Formation

TABLE 12-3 Iron Tests



Reflects the level of functional iron. Low levels can indicate iron-deficiency anemia or ACD. Hemoglobin values help determine if anemia is present and if a blood donation can be done

Serum ferritin

Measures the amount of iron in storage. One ferritin molecule can hold as many as 4500 iron atoms. Ferritin can be elevated when a person has an infection or inflammatory condition

Serum iron (Fe)

Free or unbound iron in serum. Ideal range is 40–180 g/dL. Measurement is best done fasting because serum iron is sensitive to foods or supplements recently consumed, time of day, and menstruation


Iron-binding and transport protein that can bind to and transport two molecules of iron. Transferrin carries iron through the bloodstream to the bone marrow, the liver, and ferritin. Transferrin is no longer measured directly by most physicians, instead TIBC is used


Demonstrates the iron-binding ability of transferrin. Serum iron divided by TIBC  100% provides the transferrin-iron saturation percentage (Tsat%), which is also called iron saturation. Normally, Tsat% is 25–35%. Higher numbers are suggestive of iron loading. Lower numbers are suggestive of irondeficiency anemia

Iron Vitamin C Vitamin E Folic acid Vitamin B6 Vitamin B12 Vitamin K Copper Riboflavin (minute amounts)

Inadequate intakes of many nutrients are now known to contribute to several chronic diseases. Folic acid and vitamin B12 are among the key nutrients involved. Vitamin B12 deficiency, iron or folate deficiency, chronic gastrointestinal (GI) bleeding, and myelodysplastic syndrome are causes of anemia in the elderly. Anemias are more common in the hospitalized elderly than among those who live independently. Iron is an essential micronutrient as it is required for adequate erythropoietic function, oxidative metabolism, and cellular immune responses (Munoz et al, 2009). Yet it is one of the most frequently lacking nutrients in both developing and developed countries. Iron-deficiency anemia (IDA) affects about 25% of infants worldwide. Adults, especially menstruating women, are also susceptible. Laboratory tests provide evidence of iron depletion in the body, or reflect iron-deficient red cell production; the appropriate combination of these laboratory tests help establish a correct

From: Iron Overload Disease Association, irontests.pdf, accessed December 21, 2009.

diagnosis of ID status and anemia (Munoz et al, 2009). Table 12-3 lists some relevant tests and Table 12-4 lists common signs and symptoms of anemias. Up to 10% of young women in developed countries are iron deficient. The problem is not easily resolved by adopting

TABLE 12-2 Definitions TABLE 12-4 General Signs and Symptoms of Anemia Acute anemia

Precipitous drop in the RBC population due to hemolysis or acute hemorrhage


Reduction in the number of circulating RBCs, the amount of hemoglobin, or the volume of packed RBCs (Hct)

Chronic anemia

Anemia that lasts 2 months or longer


Blood condition in which there is a low level of hemoglobin and color


Blood that is excessively pigmented

Microcytic anemia

Usually caused by or resulting in iron deficiency; RBCs are small in size

Macrocytic anemia

Folic acid or vitamin B12 insufficiency; RBCs are larger than usual

Megaloblastic anemia

Anemias in which there are large, nucleated abnormal RBCs that are irregular in shape, from pernicious anemia or use of certain immunosuppressive or antitumor drugs

Normocytic anemias

Inhibition of marrow by infection or chronic disease; RBCs are of usual size


Blood with a normal color and level of hemoglobin

• • • • • • • • • • • • • • • • • •

Anorexia Ascites Bowel irregularity Chest pain, palpitations Coldness of extremities Dizziness, especially postural Dyspnea, especially exercise intolerance Decreased libido or impotence Decreased urine output Difficulty sleeping or concentrating Fatigue, weakness, irritability Headache Mental status changes Pale conjunctiva Tachycardia Thirst Tinnitus Vertigo, syncope

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Total Iron Binding Capacity (TIBC)

Serum Ferritin

Serum Iron


Transferrin Iron Saturation Percentage

Comparing Disorders of Iron


Iron Deficiency Anemia Sideroblastic Anemia Thalassemia Porphyria Cutanea Tarda (PCT)


Anemia of Chronic Disease (ACD) OR NORMAL


African Siderosis (AS) Vitamin B12 Deficiency (pernicious anemia) OR NORMAL OR NORMAL OR NORMAL OR NORMAL OR NORMAL

an iron-rich diet because absorption varies greatly. Although the absorption of dietary iron (1–2 mg/d) is regulated tightly, it is balanced with losses (Munoz et al, 2009). Dietary heme iron is important and more readily absorbed than nonheme iron derived from vegetables and grains. Most heme is absorbed in the proximal intestine. Inherited Hgb disorders, such as sickle cell anemia and thalassemia, can be attributed to the effects of natural selection. In environments in which malaria was common, carriers were protected and survived to have more children.

For More Information •

National Anemia Action Center

National Heart, Lung, and Blood Institute Information Center

CITED REFERENCES Arredondo M, Nunez MT. Iron and copper metabolism. Mol Aspects Med. 26:313, 2005. Munoz M et al. An update on iron physiology. World J Gastroenterol. 15:4617, 2009.


ANEMIA OF CHRONIC DISEASE NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Anemia of chronic disease (ACD) is the condition of impaired iron utilization where functional iron (Hgb) is low, but tissue iron (such as in storage) is normal or high. ACD is known as anemia of inflammation (AI). Low Hgb,

low total iron-binding capacity (TIBC), and low transferrin with elevated ferritin are identified. ACD is the second most common type of anemia after anemia of iron deficiency; it results in increased morbidity and mortality of the underlying disease (Agarwal and Prchl, 2009). ACD is seen in a wide range of chronic autoimmune, cancerous or leukemic,

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inflammatory, and infectious disease conditions. In rheumatoid arthritis, ACD and iron-deficiency anemia coexist, resulting from GI bleeding due to the use of many drugs. ACD is also found in approximately 50% of patients with lupus (Giannouli et al, 2006). In aging and heart failure, chronic anemia is common. Hepcidin is the iron regulatory peptide that is synthesized in the liver to suppress iron absorption and utilization. Synthesis is suppressed by anemia, hypoxia, and erythropoiesis, and induced by inflammatory cytokines such as interleukin-6 (Matsumoto et al, 2009). ACD is characterized by macrophage iron retention induced by cytokines and hepcidin. Excess hepcidin causes proteolysis of the cellular iron exporter, ferroportin, trapping iron in macrophages, and iron-absorbing enterocytes (Ganz and Nemeth, 2009). Because circulating hepcidin levels affect iron traffic, its determination may aid to differentiate between ACD and iron-deficiency anemia to select an appropriate therapy (Theurl et al, 2009). Hgb improvement is an independent predictor of quality of life improvement in anemic patients, yet supplementation with iron for those with ACD can be harmful and even result in death. Levels of erythropoietin are reduced in ACD. The genetically engineered form (epoetin) can correct anemia caused by cancer in about 50–60% of patients and may improve survival in HIV infection. Epoetin can eliminate the need for transfusions but is very expensive. Successful treatment of the underlying disease improves ACD, but if not possible, treatment with erythropoietic agents (ESAs), supplemented with iron if necessary, is helpful in many cases (Agarwal and Prchl, 2009). ESAs are safe and may forestall some of the target-organ damage (Nurko, 2006).


SAMPLE NUTRITION CARE PROCESS STEPS Abnormal Nutritional Laboratory Values Assessment Data: Weight, BMI normal. Hgb is low at 10; ferritin is normal. GI bleeding and pain. Nutrition Diagnoses (PES): Abnormal nutritional laboratory values related to chronic anemia and high doses of medications for lupus as evidenced by low Hgb, normal serum ferritin, and GI bleeding. Interventions: Food-nutrient delivery—encourage nutrient-dense foods and frequent snacks; avoid fasting. Education about low-calorie, nutrient-dense foods and timing with medications. Counseling about timing of medications with food to reduce GI bleeding. Coordinate care with medical and nursing teams to review medications and determine which, if any, could be changed to reduce impact on GI tract. Monitoring and Evaluation: No additional GI bleeding or distress. Resolution or improvement of anemia. Hgb closer to normal.


Prevent infections or sepsis. Reduce fever and excessive inflammation. Lessen bleeding tendencies and hemorrhages. Ensure adequate periods of rest. Simplify meal planning if needed. • Prepare for bone marrow transplantation, if needed. • Prevent further complications and decline in organ functioning.

ASSESSMENT, MONITORING, AND EVALUATION FOOD AND NUTRITION CLINICAL INDICATORS Genetic Markers: Modifications of hepcidin gene expression suggest a key role for hepcidin in iron homeostasis. HAMP is the gene that encodes hepcidin. Hgb and Hct (H & H) Height (high) Weight Lab Work Serum ferritin Body mass index (high) Complete blood (BMI) Serum Fe count (CBC) Diet history Glucose (Gluc) RBC count Intake and Transferrin Serum hepcidin output (low) level (I & O) Albumin (Alb) Blood pressure Total ironC-reactive binding (BP) protein capacity Fatigue and (CRP) (TIBC) (low) weakness Clinical/History

Headache, irritability

• Provide a balanced diet that is easily prepared, with six small feedings. • Provide extra fluid unless contraindicated. • If steroids are used, limiting sodium intake may be needed. • Correct iron overload where present.

Common Drugs Used and Potential Side Effects • Genetically engineered erythropoietin (epoetin) is often used; given weekly, it can improve quality of life and levels of energy. • Avoid iron supplements in this condition; they can be harmful and even result in death. • Corticosteroids may be used. Watch side effects of chronic use such as elevated serum sodium levels, decreased potassium and calcium levels, and negative nitrogen balance. Hyperglycemia may occur; alter diet accordingly. • Antibiotics may be required when infections are present. Monitor for GI distress and other effects.

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Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Alpha tocopherol and N-acetylcysteine have been recommended, but more controlled studies are needed.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss needs of the patient, which are specific for signs, symptoms, and side effects of any medications. • Discuss nutritious meal planning. If patient has diabetes, heart failure, or cirrhosis, counsel specifically for those issues. • Correcting anemia in heart failure patients improves quality of life and exercise capacity in both men and women (Fox and Jorde, 2005). Once improvement is noted, activity levels can be increased. • Counsel about reduction of iron overload if present. For example, iron-fortified cereals and oral supplements containing iron should be avoided. Increase grains, fruits, vegetables, cheese, and dairy foods; use fewer heme iron sources.

• Being female is often independently associated with lower Hgb, so assess using sex-specific laboratory values (Fox and Jorde, 2005).

Patient Education—Food Safety If tube feeding or central parenteral nutrition (CPN) is needed, careful handwashing procedures should be followed.

For More Information •

Anemia of Chronic Disease

ANEMIA OF CHRONIC DISEASE—CITED REFERENCES Agarwal N, Prchl JT. Anemia of chronic disease (anemia of inflammation). Acta Haematol. 122:103, 2009. Fox MT, Jorde UP. Anemia, chronic heart failure, and the impact of male vs. female gender. Congest Heart Fail. 11:129, 2005. Ganz T, Nemeth E. Iron sequestration and anemia of inflammation. Semin Hematol. 46:387, 2009. Giannouli S, et al. Anemia in systemic lupus erythematosus: from pathophysiology to clinical assessment. Ann Rheum Dis. 65:144, 2006. Matsumoto M, et al. Iron regulatory hormone hepcidin decreases in chronic heart failure patients with anemia. Circ J. 2009 Dec 18. [Epub ahead of print] Nurko S. Anemia in chronic kidney disease: causes, diagnosis, treatment. Cleve Clin J Med. 73:289, 2006. Theurl I, et al. Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications. Blood. 113:5277, 2009.

ANEMIAS IN NEONATES NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Anemia of prematurity (AOP) is a normocytic, normochromic anemia that presents with very low Hgb and low erythropoietin level. Inadequate RBC production may occur, and the average life span of these cells is about 35–50 days (compared with 120 days for adults). Three causes of AOP include inadequate RBC production, shortened RBC life span, or blood loss. AOP is very common among those born prematurely, where prevalence may be as high as 50% in those born before 32 weeks of gestation. It is also especially common in those born with weight below 1500 g (Haiden et al, 2006). Hemolytic disease of the newborn (erythroblastosis fetalis) is a condition in which RBCs are broken down or destroyed more rapidly than normal, causing hyperbilirubinemia, anemia, or death; hemolytic disease of the newborn may occur in Rh-positive babies born to Rh-negative mothers (Merck Manual, 2009). Critically ill, extremely premature infants develop anemia because of intensive laboratory blood testing and undergo multiple RBC transfusions in the early weeks of life (Widness et al, 2005). Poor weight gain, apnea and tachypnea, lethargy, tachycardia, and pallor are symptoms. Reducing anemia in infants may be a preventive measure to lower disease burden from infectious disease in this

vulnerable population (Levy et al, 2005). Nutritional deficiencies of vitamin E, vitamin B12, and folate exaggerate the degree of anemia. Vitamin E supplementation, however, when given to preterm infants, does not reduce the severity of this anemia. Administration of vitamin B12 and folate with erythropoietin and iron may enhance erythropoietin-induced erythropoiesis more than erythropoietin alone (Haiden et al, 2006). When detected early in pregnancy, iron-deficiency anemia is associated with a greater risk of preterm delivery (Scholl, 2005). However, it is important not to overdo iron intake. High levels of Hgb, Hct, and ferritin are associated with an increased risk of fetal growth restriction, preterm delivery, and preeclampsia (Scholl, 2005). Diamond-Blackfan anemia (DBA) (erythrogenesis imperfecta or congenital hypoplastic anemia) is a rare blood disorder characterized by deficiency of RBCs at birth. Other symptoms including slow growth, abnormal weakness, fatigue, pallor, characteristic facial abnormalities, protruding shoulder blades, abnormal shortening of the neck due to fusion of cervical vertebrae, hand deformities, and congenital heart defects. DBA may be inherited as either an autosomal dominant or recessive genetic trait, where the body’s bone marrow produces little or no RBCs. A genetic error on chromosome

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19 is associated with about 25% of cases, and there is a family history of the disorder in 10–20% of cases. DBA affects approximately 600–700 million people worldwide but can be difficult to identify. The symptoms may also vary greatly, from very mild to severe and life threatening. DBA is usually diagnosed within the first 2 years of life, sometimes even at birth, on the basis of symptoms. The diagnosis of this anemia might not be recognized right away, however, because it is rare. The first line of treatment for DBA is prednisone. About 70% of children with DBA will respond to this lifelong treatment, where the medication stimulates the production of more RBCs. If steroids do not work, the next treatment is blood transfusions. Regular blood transfusions will provide RBCs but can lead to iron overloading. Normally, the body uses iron when making new RBCs, but since the person with DBA is not making many cells, the iron builds up. The person then needs to take medication that takes the excess iron out of the body. The only cure available for DBA is bone marrow transplantation. Stemcell transplantation with human leukocyte antigen (HLA)matched stem cells has been used for DBA (Kuliev et al, 2005).


SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin-Mineral Intake Assessment Data: Low birth weight (1450 g), poor suck. Lab work shows low Hgb and serum B12; diagnosis of anemia. Pallor, listlessness, and tachycardia. Nutrition Diagnoses (PES): Inadequate vitamin and mineral intake related to poor suck and low birth weight as evidenced by lab work with low Hgb and serum B12. Inadequate weight gain. Interventions: Nutrient delivery—specialized infant formula with added calories and administration of vitamin B12, folate, erythropoietin and iron. Monitoring and Evaluation: Improvement in heart rate, growth, and pallor. Resolution of anemia.

• Prevent further complications. • Support growth.



Common Drugs Used and Potential Side Effects

Genetic Markers: Anemia in a newborn may be caused by a genetic condition such as congenital hypoplastic anemia. In DBA, a genetic alteration on chromosome 19 has been noted. Clinical/History Height Weight BMI Diet history Slow growth in child (low height– weight percentiles) BP Weakness

Fatigue and pallor I&O Lab Work CBC RBC count H&H (2 standard deviations below mean for age)

• Provide an appropriate formula that is easily prepared, with small feedings given frequently. • Provide extra fluid unless contraindicated.

Serum Fe and ferritin Gluc Alb CRP Serum folic acid and B12 K, Na Calcium

• If corticosteroids are used, watch side effects of chronic use such as elevated serum sodium levels, decreased potassium and calcium levels, and negative nitrogen balance. Hyperglycemia may occur; alter diet accordingly. Besides diabetes, glaucoma, bone weakening, and high blood pressure can occur, and the medication may suddenly stop working for that person at any point in time. • Antibiotics may be required when infections are present. Monitor for gastrointestinal distress and other side effects.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT INTERVENTION OBJECTIVES • Provide improved oxygenation for tissues. • Prevent infections or sepsis. Reduce fevers or excessive inflammation. • Control hyperglycemia or other side effects of treatments.

• Discuss needs of the patient, which are specific for signs and symptoms and for side effects of any medications. • Discuss nutritious meal planning. • If patient has diabetes, counsel specifically for nutritional management. • Activity levels must be restricted to avoid accidents or falls that could promote bleeding. • Referral to the Women, Infants, and Children (WIC) Program can be beneficial. WIC programs are helpful in

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improving Hgb concentration among young children (Altucher et al, 2005). Age-specific values should be used to assess progress: Age-Specific Values for Hemoglobin and Hematocrit Age

Hb (g/dL)

Hct (%)

28-week gestation



32-week gestation






1–3 days



2 weeks



Source: Merck Manual,, accessed December 22, 2009.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

Anemia of Prematurity

Diamond Blackfan Anemia

Perinatal Anemia

ANEMIAS IN NEONATES—CITED REFERENCES Altucher K, et al. Predictors of improvement in hemoglobin concentration among toddlers enrolled in the Massachusetts WIC Program. J Am Diet Assoc. 105:716, 2005. Haiden N, et al. A randomized, controlled trial of the effects of adding vitamin B12 and folate to erythropoietin for the treatment of anemia of prematurity. Pediatrics. 118:180, 2006. Kuliev A, et al. Preimplantation genetics: improving access to stem cell therapy. Ann N Y Acad Sci. 1054:223, 2005. Levy A, et al. Anemia as a risk factor for infectious diseases in infants and toddlers: results from a prospective study. Eur J Epidemiol. 20:277, 2005. Merck Manual. Web site accessed December 22, 2009, mmhe/sec23/ch264/ch264q.html Scholl TO. Iron status during pregnancy: setting the stage for mother and infant. Am J Clin Nutr. 81:1218S, 2005. Widness JA, et al. Reduction in red blood cell transfusions among preterm infants: results of a randomized trial with an in-line blood gas and chemistry monitor. Pediatrics. 115:1299, 2005.

ANEMIA OF RENAL DISEASES NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Anemia of renal disease occurs in both acute and chronic renal disease. This type of anemia is often normochromic, normocytic, and sometimes microcytic. When the kidneys become diseased, scar tissue forms and prevents the cells that make erythropoietin from functioning. The buildup of uremic toxins and decreased erythropoietin production adversely affects erythropoiesis. The accumulation of toxic metabolites, which are normally excreted by the kidneys, shortens the life span of circulating RBCs. Management is complicated by a vicious circle of cardiorenal anemia syndrome in which CKD, heart failure, and anemia exacerbate each other (Besarab et al, 2009). There is an inverse relationship between blood urea nitrogen (BUN) levels and RBC life span, but there is also diminished renal production of erythropoietin. If no cause for anemia other than chronic kidney disease is detected on the basis of the workup and the serum creatinine is 2 mg/dL, anemia is most likely due to erythropoietin deficiency; measurement of serum erythropoietin levels is not needed. Anemia usually starts during the third stage of renal disease, when glomerular filtration rate (GFR) is below 60 cc/minute but before dialysis has started. Short daily hemodialysis and daily home nocturnal hemodialysis can control blood pressure and manage anemia in this population (Pierratos, 2005). Correction of anemia appears to improve cardiac function and quality of life without a greater risk for adverse events (Besarab et al, 2009).


CLINICAL INDICATORS Genetic Markers: In disorders such as type-2 diabetes, chronic kidney disease is common. Anemia may be present and cause fatigue and difficulty with daily activities such as climbing stairs. Clinical/History

Lab Work


Transferrin saturation Height CBC and RBC (serum iron Weight count  100  BMI Serum Fe TIBC) Diet history Hgb (may be 20%? BP 12 g/dL) b Reticulocyte I&O Hct (often hemoglobin Weakness 33%) content Fatigue and Serum ferritin: (CHr) pallor (100 absolute Serum soluble Dizziness deficiency; transferrin Difficulty overload receptor concentrating 800 ng/dL (sTfR)— Shortness of TIBC elevated? breath

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Gluc Test for occult Alb blood CRP Blood urea Serum folic acid nitrogen and B12 (BUN)

Creatinine (Creat) •


The best indicator for iron availability for erythropoiesis. Half-life of reticulocytes is 1 day; it represents immediate availability of bone marrow iron. b

INTERVENTION OBJECTIVES • Prevent infections or sepsis. Reduce fever and excessive inflammation. • Prevent further complications such as heart failure. Fluid may accumulate and build up in the lungs and liver. • Support growth in children. • Improve energy level and decrease fatigue, irritability, and infections.

FOOD AND NUTRITION • Provide a balanced diet that is easily prepared, with small feedings given frequently. • Provide extra fluid unless contraindicated. • Provide sufficient foods rich in iron and B-vitamins, as appropriate (depending on laboratory values, current status, predialysis, or dialysis).

Common Drugs Used and Potential Side Effects • Iron therapy is effective in 30–50% of patients with CKD. A serum ferritin concentration of 100–500 ng/mL is the target during oral and IV iron therapy for predialysis and

• •


peritoneal dialysis patients. IV administration and a target serum ferritin concentration of 200–500 ng/mL is recommended for hemodialysis patients (Besarab et al, 2009; Grabe, 2007). Erythropoietin Stimulating Agents (ESAs) are given when Hgb falls below 10 g/dL. Epoetin (EPO) is used when oral iron therapy fails (Nurko, 2006). This can be given every week, or every 2 weeks, or monthly. The two formulations of EPO, epoetin alpha (ProCrit) and darbepoetin (Aranesp, DPO), are effective. Longer half-life of darbepoetin alpha permits administration on a oncemonthly basis in patients with CKD and anemia (Grabe, 2007). A recent addition is methoxypolyethylene glycolepoetin beta (Mircera) that has a longer half-life and can be given every 2 weeks. Iron deficiency and inflammation are possible causes of inadequate response to ESAs (Grabe, 2007). In the ironreplete patient with an inadequate response to epoetin, the following conditions should be evaluated and treated, if reversible: infection or inflammation (AIDS, lupus); chronic blood loss; aluminum toxicity; hemoglobinopathies (thalassemias, sickle cell anemia); folate or vitamin B12 deficiency; multiple myeloma; malnutrition; or hemolysis. Ferric gluconate maintains Hgb and allows lower epoetin doses in anemic hemodialysis patients with low TSAT and ferritin levels up to 1200 ng/mL (Kapoian et al, 2008). Parenteral iron is reserved for dialysis patients or those who are intolerant of oral iron. Iron dextran (In-FeD, Dexferrum), sodium ferric gluconate (Ferrlecit), and iron sucrose (Venofer) are available. Ferumoxytol is a new IV iron preparation for CKD (Schwenk, 2010). Iron dextran may cause serious allergic reactions. Vitamin C helps increase absorption. Dairy and antacids decrease absorption. Docusate helps alleviate constipation. Iron supplements can darken stools.

Herbs, Botanicals, and Supplements SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake Assessment Data: CKD with low erythropoietin production; Hgb 12 and Hct 33% with EPO. Serum folic acid and vitamin B12 levels remain low. Physical signs of vitamin deficiency. Nutrition Diagnoses (PES): Inadequate vitamin intake related to poor oral intake as evidenced by diet history, recent anorexia, low serum levels of B12 and folate, and minimal use of prescribed water-soluble vitamins. Interventions: Food-Nutrient Delivery—In addition to EPO and iron, use vitamin B12 and folic acid supplements. Educate about the need to use the supplements daily and to retest lab work every 3–6 months. Counseling about good food sources of folic acid and vitamin B12. Monitoring and Evaluation: Lab work showing normal B12 and folic acid levels. Fewer complaints of fatigue; no physical signs of vitamin deficiency.

• Herbs and botanical supplements should not be used without discussing with the physician. Because the use of CAM is increasing among children and adults with chronic illnesses, efforts should be made to identify those therapies that are beneficial, harmless, and cheap for possible integration with conventional therapy (Oshikoya et al, 2008). Adverse side effects are possible.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss needs of the patient that are specific for signs and symptoms and side effects of any medications. • Discuss simplified, but nutritious, meal planning. • If patient has diabetes, heart failure, or cirrhosis, counsel specifically for nutritional management. • Activity levels must be restricted to avoid accidents or falls that could promote bleeding.

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• People who take EPO shots should have regular tests to monitor their Hgb. If it climbs above 12 g/dL, their doctor should prescribe a lower dose of EPO.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

American Association of Kidney Patients

National Institute of Diabetes and Digestive and Kidney Diseases–Anemia

National Kidney Foundation – Anemia

ANEMIA OF RENAL DISEASES—CITED REFERENCES Besarab A, et al. Iron metabolism, iron deficiency, thrombocytosis, and the cardiorenal anemia syndrome. Oncologist. 14:22S, 2009. Grabe DW. Update on clinical practice recommendations and new therapeutic modalities for treating anemia in patients with chronic kidney disease. Am J Health Syst Pharm. 64:8, 2007. Kapoian T, et al. Ferric gluconate reduces epoetin requirements in hemodialysis patients with elevated ferritin. J Am Soc Nephrol. 19:372, 2008. Nurko S. Anemia in chronic kidney disease: causes, diagnosis, treatment. Cleve Clin J Med. 73:289, 2006. Oshikoya KA, et al. Use of complementary and alternative medicines for children with chronic health conditions in Lagos, Nigeria. BMC Complement Altern Med.8:66, 2008. Pierratos A. New approaches to hemodialysis. Annu Rev Med. 55:179, 2005. Schwenk MH. Ferumoxytol: a new intravenous iron preparation for the treatment of iron deficiency anemia in patients with chronic kidney disease. Pharmacotherapy. 30:70, 2010.

APLASTIC ANEMIA AND FANCONI’S ANEMIA NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Aplastic anemia is a rare bone marrow disorder with normocytic, normochromic anemia in which normal marrow is replaced with fat. Aplastic anemia, myelodysplastic syndromes, and paroxysmal nocturnal hemoglobinuria (PNH) occur when the bone marrow stops making healthy bloodforming stem cells that produce RBCs, white blood cells, and platelets. Telomeres, repeat sequences at the ends of chromosomes, are protective chromosomal structures that shorten with every cell cycle; aplastic anemia is associated with inherited mutations in telomere repair or protection genes (Calado, 2009). In about 50% of cases, the cause may be inherited or due to autoimmunity. In other cases, exposure to toxic agents (e.g., radiation, heavy metals, inorganic arsenic) or use of drugs (e.g., phenylbutazone, chloramphenicol, anticonvulsants) may be the cause. Use of interferon-gamma (IFN- ) may be responsible for certain aspects of the pathology seen in bone marrow failure syndromes, including aplastic anemia (Zeng et al, 2006). Signs and symptoms are listed in Table 125. Treatment includes blood transfusion, preventive antibiotics, careful handwashing, hormone therapy, immunosuppressive therapy, and medications to enhance bone marrow cell production. Severe aplastic anemia (SAA) is life threatening and can be treated with bone marrow transplantation, immunosuppressive therapy, and high-dose cyclophosphamide (Brodsky et al, 2009). Resolution of iron overload (such as serum ferritin 1000 ng/mL) should be addressed before transplant because it may lead to lethal infections (Storey et al, 2009). Fanconi’s anemia (FA) is a rare, genetic disorder characterized by multiple congenital anomalies, progressive bone marrow failure, and an increased prevalence of leukemia or liver cancer (Fagerlie and Bagby, 2006). FA is characterized

by delayed bone marrow failure with progression to aplastic anemia. It may be apparent at birth or between ages 2 and 15 and is characterized by deficiency of all bone marrow elements including RBCs, white blood cells, and platelets (pancytopenia). FA is associated with cardiac, kidney, or skeletal abnormalities as well as vitiligo or patchy, brown discolorations (pigmentation changes) of the skin. There are TABLE 12-5 Signs and Symptoms of Aplastic or Fanconi’s Anemias Blood in stool Bronzing of skin (café au lait spots) Dizziness Headache, irritability Hemorrhagic diathesis (gums, nose, GI tract, urinary tract, vagina) Hemosiderosis with resulting cirrhosis, diabetes, heart failure Increasing fatigue and weakness Increasing or persistent infections Irritability Missing or horseshoe kidney (FA) Missing or misshapen thumbs (FA) Nausea Oral thrush or lesions Petechiae, ecchymosis Scoliosis Skeletal anomalies of spine, hips, ribs (FA) Slow thought processes, headache Small head, low birth weight (FA) Tachycardia, tachypnea, dyspnea Waxlike pallor

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several different subtypes, each of which results from abnormal mutations of different genes. Prognosis is poor among those individuals with low blood counts. Treatment of FA involves transfusions, bone marrow transplantation, or gene therapy. FA patients do not tolerate radiation well and are prone to cancers, even after transplantation. Currently, life span is not long; many children do not survive to adulthood.




Prevent infections or sepsis. Reduce fevers. Reduce bleeding tendencies and hemorrhages. Ensure adequate periods of rest. Prepare for splenectomy or bone marrow transplantation. Prevent further complications, where possible, and decline in cardiovascular and hepatic functions.

FOOD AND NUTRITION CLINICAL INDICATORS Genetic Markers: In Caucasians, genetic variations in IFNG may be found. Mutations TERC and TERT genes are also seen in aplastic anemia. The FANCM or FNACJ gene mutations are responsible for some forms of Fanconi’s anemia. Clinical/History

Lab Work

Height Weight BMI Diet history BP GI problems See Table 12-5 also Bone marrow biopsy Ultrasound Hand x-ray or CT scan

RBC count (decreased) Prothombin time (PT) Serum Fe Gluc Granulocytes (decreased) Transferrin H&H Platelets (decreased)

White blood cell (WBC) count (1500) Alb, transthyretin CRP Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Bilirubin

SAMPLE NUTRITION CARE PROCESS STEPS Self-Feeding Difficulty Assessment Data: Low BMI, medical hx with diagnosis of Fanconi’s anemia, misshapen thumbs with difficulty holding utensils. Nutrition Diagnoses (PES): Self-feeding difficulty (NB-2.6) related to hand deformity as evidenced by low BMI and difficulty consuming enough at mealtimes. Interventions: Food-nutrient delivery—add extra kilocalories to foods and recipes, such as extra fats and carbohydrates. Include extra protein-rich foods as tolerated between meals. Serve finger foods and beverages that can be taken through a straw (milkshake, eggnog). Educate parents about changes in menus and foods for greater intake of nutrient and energydense foods. Counsel for ways to enhance self-feeding with use of adaptive feeding equipment. Monitoring and Evaluation: Improvement in BMI over time and better intake from nutrient and energy-dense foods. Enhanced skills using adaptive feeding tools.

• Replenish nutrient stores. • Provide a balanced diet that is easily prepared, with six small feedings. • Provide extra fluid unless contraindicated (35 cc/kg or more). • If patient has mouth lesions, avoid excesses of hot or cold foods, spicy or acidic foods, or foods with rough textures. • If steroids are used, limit sodium intake.

Common Drugs Used and Potential Side Effects • Growth factors (erythropoietin, G-CSF, and GM-CSF) may help to improve blood counts. • Corticosteroids may be used. Side effects of chronic use include elevated serum glucose and sodium levels, decreased potassium and calcium levels, and negative nitrogen balance. • High-dose cyclophosphamide is highly effective therapy for SAA, but large randomized controlled trials are necessary to compare with either bone marrow transplantation or use of antithymocyte globulin and cyclosporine (Brodsky et al, 2009). • Antibiotics may be required for infections; monitor for GI distress and other side effects. • Aspirin should be avoided because it may aggravate blood losses. Other drugs that may aggravate the condition include chloramphenicol, phenylbutazone, sulfa drugs, and ibuprofen. Each of these has specific GI side effects that should be monitored (see index for more information). • A list of drugs that can cause acquired aplastic anemia is found at anemia/medic.htm#medication_causes_list

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss needs of the patient, which are specific for signs and symptoms and for side effects of any medications. • Discuss simplified, but nutritious, meal planning.

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• If patient has diabetes, heart failure, or cirrhosis, counsel specifically to those issues for nutritional management. • Activity levels must be restricted to avoid accidents or falls that could promote bleeding. • Genetic counseling is advised for parents who wish to have more children.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

America’s Blood Centers

Aplastic Anemia and MDS International Foundation, Inc.


Fanconi’s Anemia

Medline—Fanconi’s Syndrome

Fanconi Canada

APLASTIC ANEMIA AND FANCONI’S ANEMIA—CITED REFERENCES Brodsky RA, et al. High dose cyclophosphamide for severe aplastic anemia: long-term follow-up. Blood. 2009 Dec 16. [Epub ahead of print] Calado RT. Telomeres and marrow failure. Hematology Am Soc Hematol Educ Program. 1:338, 2009. Fagerlie SR, Bagby GC. Immune defects in Fanconi anemia. Crit Rev Immunol. 26:81, 2006. Storey JA, et al. The transplant iron score as a predictor of stem cell transplant survival. J Hematol Oncol. 2:44, 2009. Zeng W, et al. Interferon-gamma–induced gene expression in CD34 cells. Identification of pathologic cytokine-specific signature profiles. Blood. 107:167, 2006.

COPPER DEFICIENCY ANEMIA NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Copper has a role in the production of Hgb (the main component of RBCs), myelin (the substance that surrounds nerve fibers), elastin, collagen (a key component of bones and connective tissue), and melanin (a dark pigment that colors the hair and skin). It is required for the function of over 30 proteins, including superoxide dismutase, ceruloplasmin, lysyl oxidase, cytochrome c oxidase, tyrosinase, and dopamine beta-hydroxylase (Arredondo and Nunez, 2005). One third of the total body pool of copper is found in skeletal muscle; one third is found in brain and liver; the final third is found in bone and other tissues. Copper is also found in trace amounts in all tissues in the body and is excreted primarily in the bile. Copper is needed in minute amounts for the formation of Hgb. The metabolism of copper and iron are closely related. Systemic copper deficiency generates cellular iron deficiency, which results in diminished work capacity, reduced intellectual capacity, diminished growth, alterations in bone mineralization, and diminished immune response (Arredondo and Nunez, 2005). Copper deficiency also results in reduced activity of white blood cells and reduced thymus hormone production, thus resulting in increased infection rates. Marginal deficits of this element can contribute to the development and progression of a number of disease states including cardiovascular disease and diabetes (Li et al, 2005; Urui-Adams and Keen, 2005). Homocysteine thiolactone accumulates when homocysteine is high; it inhibits lysyl oxidase, which depends on copper to catalyze cross-linking of collagen and elastin in arteries and bone. A copper deficiency should, therefore, be avoided. Betaine, copper, folate,

pyridoxine, and vitamin B12 have proven to be beneficial in lowering serum homocysteine levels. Overall, supplementation with 3–6 mg of copper per day can improve copper status in otherwise healthy individuals; increased intake could reduce the risk of atherosclerosis by promoting improved fibrinolytic capacity (Bugel et al, 2005). Copper, along with zinc and iron, is an essential metal for normal central nervous system development and function. Imbalances can result in neuronal death (apoptosis), which may contribute to Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and Huntington’s disease. Imbalances can also result in neuron deaths in traumatic brain and spinal cord injury, stroke, and seizures (Levenson, 2005). People with poor intake of protein or whose diets are very high in milk may become deficient in copper or iron. Infants fed on all cow’s milk diet without copper supplements may develop copper deficiency. Acquired copper deficiency may be a delayed complication of gastric surgery. Zinc supplementation (150 mg/d) or vitamin C (1500 mg or more) will reduce copper absorption and increase the potential for anemia. Other conditions that can lead to copper deficiency include burns, pancreatic or liver disease, kidney disease, diarrhea, and prematurity. Bicytopenia (anemia and neutropenia) with normal platelet count is a feature of hematological disorders caused by copper deficiency; abnormalities improve within a few months after copper supplementation therapy (Nagano et al, 2005). Ceruloplasmin (Cp) is a copper-containing plasma protein with an important role in iron homeostasis; levels are low when copper intake is deficient. Hospitalized patients should be evaluated carefully. Although enteral feedings contain adequate concentrations

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of trace elements, problems with bioavailability may occur, and patients receiving long-term enteral feeding should be monitored to avoid anemia and leukopenia (Ito et al, 2005; Oliver et al, 2005). Copper supplementation is essential in parenteral nutrition to prevent an adverse effect of deficiency; requirements in CPN amount to 0.3 mg/d in adults and 20 g/kg body wt/d in infants or children (Shike, 2009). Nutritional deficiencies that can occur in otherwise asymptomatic normally growing children are often overlooked (Suskind, 2009). If present, they have a significant impact on the health of the child. Another area for careful review is bariatric surgery. Serum copper levels should be monitored in patients with a neurologic syndrome, who have undergone gastric bypass surgery (Naismith et al, 2009; Griffith et al, 2009).

TABLE 12-6


Symptoms of Copper Insufficiency and Anemia

Anorexia Bone fractures Cardiovascular disease, increased serum cholesterol levels Diarrhea Dermatitis or loss of pigmentation of skin, pallor Edema Fatigue Growth retardation Hair loss Irregular heart rhythms Labored respiration, decreased oxygen delivery Nerve conduction problems


Neurological and immunological abnormalities in newborns if mothers are deficient (Urui-Adams and Keen, 2005). Myeloneuropathy and myelopathy Poor collagen formation, decreased wound healing Reduced red blood cell function


Reduced thyroid function Shortened red cell life span

Genetic Markers: Copper anemias are acquired. Clinical/History Height Weight BMI Diet history BP See Table 12-6 Lab Work CBC Serum copper (low)

Ceruloplasmin (low) H&H Serum Fe Serum ferritin (increased) Macrocytic, hypochromic anemia Platelets (normal) Erythropoietin levels (elevated)

Serum zinc (Zn) (often elevated) Homocysteine Alb, transthyretin CRP Retinol-binding protein (RBP)


Skeletal defects from bone demineralization Skin sores Weakness

INTERVENTION OBJECTIVES • Correct copper deficiency and documented anemias. • Instruct patient regarding good sources of protein, iron, and copper to prevent recurrences. • Monitor use of zinc in supplements, diet, and enteral or parenteral sources to avoid overdosing and related copper depletion.

Inadequate Mineral Intake Assessment Data: Nutritional laboratories showing low-serum copper and Cp with high-serum zinc. Previous bariatric surgery (1 year) with recent medical visit. Other laboratories are normal. Diet hx reveals low intake of copper from foods. Nutrition Diagnoses (PES): Inadequate mineral intake of copper related to significant decrease in total food consumed each day for past year post-gastric bypass surgery as evidenced by lowserum Cu and Cp levels and regular use of Zn supplements. Interventions: Education about ways to enhance copper from meals and snacks. Decrease use of single-Zn supplements and use a multivitamin-mineral supplement that contains copper. Monitoring and Evaluation: Improved serum Cu and Cp levels after 3 months; better intake of copper-rich foods. Serum Zn within normal range.

FOOD AND NUTRITION • Good sources of copper include oysters, liver, nuts, dried legumes, and raisins. A typical diet provides about 2- to 3-mg copper/d, about half of which is absorbed. A supplement of 3- to 6-mg copper may be useful in adults. • Protein should be at least 1 g/kg for adults; iron intake should be adequate for age and sex. • Monitor use of multivitamin-mineral supplements to avoid large doses of zinc. Ascorbic acid can act as a pro-oxidant in the presence of metals such as iron or copper; large doses are not recommended. • Monitor tube-fed patients to ensure that they are receiving sufficient amounts of copper (Ito et al, 2005; Oliver et al, 2005).

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TABLE 12-7 Food Sources of Copper Blackstrap molasses Black pepper Chicken Chocolate (unsweetened or semisweet baker’s chocolate and cocoa) Enriched cereals (bran flakes, raisin bran, shredded wheat) Fruits (such as cherries, dried fruits, bananas, grapes)

• Patients at risk for copper deficiency should be counseled on how to avoid this condition. For example, patients with muscular dystrophy may not consume adequate amounts, and muscle strength can diminish as a result (Motlagh et al, 2005). • Discuss foods that are good sources of protein, iron, and copper; see Table 12-7. • Be aware that some denture creams contain a high amount of zinc that could be a concern (Spain et al, 2009).

Legumes (such as soybeans, lentils, navy beans, and peanuts) Nuts and nut butters (cashews, filberts, macadamia nuts, pecans, almonds, and pistachios) Organ meats (beef liver, kidneys, and heart) Potatoes

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

Seafood (oysters, squid, lobster, mussels, crab, and clams)

For More Information

Seeds (pumpkin)

Merck Manual chapter4/4j.jsp

Northwestern University – Copper Fact Sheet copper.html

Tea Vegetables (avocado, mushrooms, potatoes, sweet potatoes, tomatoes) Whole grains

Common Drugs Used and Potential Side Effects • Cupric sulfate is one brand of injectable copper supplement. Copper gluconate is given orally. Beware of excesses, which can be indicated by black or bloody vomit, bloody urine, diarrhea, heartburn, loss of appetite, lower back pain, metallic taste, nausea (severe or continuing), pain or burning while urinating, vomiting, yellow eyes or skin, dizziness or fainting, severe headache, or even coma. • Do not refrigerate this supplement. Discard when outdated. • Avoid taking copper supplements with nonsteroidal antiinflammatory drugs (NSAIDs), birth control pills, allopurinol, estrogen hormones, or cimetidine.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Have patient avoid fad diets. Monitor vegetarian (nonheme iron) diets carefully. • Zinc in large doses may deplete copper levels; discuss use of mineral supplements. (Rowan and Lewis, 2005).

COPPER DEFICIENCY ANEMIA—CITED REFERENCES Arredondo M, Nunez MT. Iron and copper metabolism. Mol Aspects Med. 26:313, 2005. Bugel S, et al. Effect of copper supplementation on indices of copper status and certain CVD risk markers in young healthy women. Br J Nutr. 94:231, 2005. Griffith DP, et al. Acquired copper deficiency: a potentially serious and preventable complication following gastric bypass surgery. Obesity (Silver Spring). 17:827, 2009. Ito Y, et al. Latent copper deficiency in patients receiving low-copper enteral nutrition for a prolonged period. J Parenter Enteral Nutr. 29:360, 2005. Levenson CW. Trace metal regulation of neuronal apoptosis: from genes to behavior. Physiol Behav. 86:399, 2005. Li Y, et al. Marginal dietary copper restriction induces cardiomyopathy in rats. J Nutr. 135:2130, 2005. Motlagh B, et al. Nutritional inadequacy in adults with muscular dystrophy. Muscle Nerve. 31:713, 2005. Nagano T, et al. Clinical features of hematological disorders caused by copper deficiency during long-term enteral nutrition. Intern Med. 44:554, 2005. Naismith RT, et al. Acute and bilateral blindness due to optic neuropathy associated with copper deficiency. Arch Neurol. 66:1025, 2009. Oliver A, et al. Trace element concentrations in patients on home enteral feeding: two cases of severe copper deficiency. Ann Clin Biochem. 42:136, 2005. Rowin J, Lewis SL. Copper deficiency myeloneuropathy and pancytopenia secondary to overuse of zinc supplementation. J Neurol Neurosurg Psychiatry. 76:750, 2005. Shike M. Copper in parenteral nutrition. Gastroenterology. 137:13S, 2009. Spain RI, et al. When metals compete: a case of copper-deficiency myeloneuropathy and anemia. Nat Clin Pract Neurol. 5:106, 2009. Suskind DL. Nutritional deficiencies during normal growth. Pediatr Clin North Am. 56:1035, 2009. Urui-Adams JY, Keen CL. Copper, oxidative stress, and human health. Mol Aspects Med. 26:268, 2005.

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O Tetrahydrofolic acid H N












O N5, N10-methylenetetrahydrofolic















Three steps for metabolism of dietary folic acid to the bioavailable form.

DEFINITIONS AND BACKGROUND Folic acid is composed of a pterin ring connected to paminobenzoic acid (PABA). Humans do not generate folate because they cannot synthesize PABA. The amino acid histidine is metabolized to glutamic acid. Formiminoglutamic acid (FIGLU) is an intermediary in this reaction, and tetrahydrofolic acid is the coenzyme that converts it to glutamic acid. Under normal conditions, sufficient intake of dietary histidine can prevent anemia. When dietary intake of histidine is diminished or urinary excretion is greatly increased, anemia results. Folate deficiency depletes histidine through increased urinary excretion. Folic acid is needed for the synthesis of DNA and maturation of RBCs. Deficiency of folate can lead to many clinical abnormalities, including macrocytic anemia, cardiovascular diseases, birth defects, and carcinogenesis (including colorectal cancer). Folic acid-deficiency anemia generally is caused by inadequate diet, intestinal malabsorption, alcoholism, or pregnancy (Table 12-8). Folic acid deficiency yields a hyperchromic, macrocytic, megaloblastic anemia. Because similar hematological changes occur with vitamin B12 deficiency, it is important to check the serum levels of vitamin B12 along with folate tests. Folate is best

measured by RBC folate because serum levels are misleading and reflect more recent intake. Homocysteine elevation is a risk factor for vascular and thrombotic disease. Genetic and acquired influences have been evaluated. While neural tube defects result from maternal

Folic acid anemic cells are hypochromic and macrocytic. Adapted from: Anderson’s Atlas of Hematology; Anderson, Shauna C., PhD. Copyright 2003, Wolters Kluwer Health/Lippincott Williams & Wilkins.

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TABLE 12-8 Folic Acid

Conditions and Medications That Deplete


which has been linked with the risk of arterial disease, dementia, and Alzheimer’s disease (Malouf et al, 2008). Decreasing or low levels of folic acid may also be associated with depression in older adults.

Alcoholism Blind-loop syndrome Burns


Cancers Celiac disease Crohn’s disease


Dialysis Elevated homocysteine levels Hemolytic anemias Hepatitis Infection Inflammatory diseases Malabsorption Megacolon Pregnancy and lactation Smoking Stress Surgery Medications that interact with folic acid: •

• •

Antiepileptic drugs (AED): phenytoin, carbamazepine, primidone, valproic acid, phenobarbital, and lamotrigine impair folate absorption and increase the metabolism of circulating folate Capecitabine: Folinic acid (5-formyltetrahydrofolate) may increase the toxicity of Capecitabine Dihydrofolate reductase inhibitors (DHFRI): DHFIs block the conversion of folic acid to its active forms, and lower plasma and red blood cell folate levels. DHFIs include aminopterin, methotrexate, sulfasalazine, pyrimethamine, triamterene, and trimethoprim. Administer leucovorin at the same time Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs inhibit some folate dependent enzymes. NSAIDs include ibuprofen, naproxen, indomethacin, and sulindac Cholestyramine, Colestipol, Cycloserine, Isotretinoin, oral contraceptives, Methylprednisolone, pancreatic enzymes, Pentamidine, Sulfasalazine either decrease folic acid absorption or increase excretion Smoking and alcohol: reduced serum folate levels may occur

folate insufficiency in the periconceptual period, there are also inborn errors of folate metabolism that aggravate the problem. DNA methylation occurs by transfer of a methyl group from S-adenosylmethionine (SAM) to cytosine (Abdolmaleky et al, 2004). SAM serves as a methyl group donor in important functions such as changing norepinephrine to epinephrine, chromatin remodeling, RNA inhibition and modification, and DNA rearrangement (Abdolmaleky et al, 2004). Prenatal intakes of folic acid, vitamin B12, choline, and betaine influence the degree of DNA methylation (Waterland and Jirtle, 2004). Methylation affects adult susceptibility to asthma, cancer, autism, bipolar disease, Alzheimer’s disease, stroke, and schizophrenia. Folate deficiency can result in congenital neural tube defects and megaloblastic anemia; inadequacy is associated with high blood levels of the amino acid homocysteine,

Genetic Markers: Congenital folate malabsorption, methylenetetrahydrofolate reductase (MTHFR) deficiency, and formiminotransferase deficiency are genetic defects. MTHFR deficiency causes neurological problems even without megaloblastic anemia. MTHFR polymorphisms on chromosome 1 affect 10% of the world’s population, especially Caucasians. Varied DNA methylation patterns influence the biological response to food components and vice versa (Milner, 2006). Serum Fe (increased) Height RBC folate Mean cell Weight (140 ng/ volume BMI mL) – best (MCV) Diet history Serum folate Leukopenia, BP (3 ng/mL) WBC I&O MTHFR alleles? Urinary Weight loss Mild formiminoAnorexia, malhyperhomoglutamic acid nutrition cystinemia (FIGLU) after Smooth and (15–25 histidine load sore red mmol/L) Serologic tongue Moderate hypertesting for Diarrhea homocystineparietal cell Fatigue, lethargy mia (26–50 and intrinsic Poor wound mmol/L) factor (IF) healing Low RBC antibodies Coldness of H&H (vs. Schilling extremities CBC (macrocytic test) History of cells) alcohol Transferrin abuse? Serum B12 Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Increase folate in diet and supplemental folic acid to alleviate anemia. • Improve diet to provide nutrients needed to make RBCs: folate and other B-complex vitamins, iron, and protein. Instruct patient to correct faulty diet habits if relevant. • Check for malabsorption syndromes (celiac disease, blind-loop syndrome, congenital or acquired megacolon, Crohn’s disease) and correct these as far as possible through use of medications and other treatments. • Monitor serum folic acid status regularly.

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Folic Acid


5 Formyl THF



Mg Tryptophan


5,10 Methylene THF








Creatinine ADP + Pi

SAHH Homocysteine







Guanidoacetate Creatine

B12 Dopa









Adenosine ADA


P5P Inosine



NE Taurine




Cystathionine Cysteine O2 Sulfinic Acid


MAO B VMA Sulfate




Glutamic Acid + _-Sulfinylpyruvic Acid H2O SulfIte



P5P Cysteine

Glutamic acid + ATP


ADP + Pi _-Glutamylcysteine GSH Synthetase Glutathione

Pyruvic Acid

Folic acid-B12 pathway, showing the many substances that could be impacted by deficiency or genetic alterations.

FOOD AND NUTRITION • Provide a diet that is high in folate, protein, copper, iron, and vitamins C and B12.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake and Food- and Nutrition–Related Knowledge Deficit Assessment Data: Hx of MTHFR (CT) allele and spina bifida in two infants. Diet Hx shows poor intake of folate from diet and no use of supplemental sources. Dislikes fruits and vegetables. Nutrition Diagnoses (PES): Inadequate vitamin intake of folate (NI related to lack of folic acid food sources in daily diet as evidenced by headache, fatigue, decreased serum and RBC folate, and giving birth to two infants with spina bifida in the past 5 years. Food and nutrition-related knowledge deficit (NB 1.1) related to lack of prior exposure and interest in accurate nutrition-related information as evidenced by daily intake lacking sources of folate, especially from fruits and vegetables. Interventions: ND 3.2.1,—multivitamin/mineral supplement, folic acid supplement of additional 400 mcg/d. E 1.2—priority modifications to diet including addition of food sources rich in folic acid, basic information concerning food pyramid, and balanced meal planning. Monitoring and Evaluation: One month follow-up visit acceptance of supplements, dietary recall for daily use of folic acid sources, and efficacy of personal meal planning for meeting basic nutrition needs/food pyramid servings.

• Folic acid is distributed widely in green leafy vegetables, citrus fruits, and animal products. Ingestion of one fresh fruit or vegetable provides sufficient folic acid for most people. Other sources include fish, legumes (dried beans and peas), whole grains, leafy dark green vegetables, broccoli, citrus juices, berries, and meats. • Food manufacturers in the United States have fortified grains with folic acid since 1998. These fortified foods include most enriched breads, flours, corn meal, rice, noodles, macaroni, and other grain products. • Diets that provide bland, liquid, or soft foods may be needed for patients with a sore mouth; six to eight small meals may be helpful.

Common Drugs Used and Potential Side Effects • Supplements of folic acid (Folvite) are better than diet alone to alleviate the anemia. Folate deficiency is generally treated with 800–1000 g of folic acid daily. Leucovorin is an active reduced form. • Be aware of the interdependence between vitamin B12 and folic acid, especially in older individuals. Vitamin B12 helps methylate folic acid so that it can travel into cells. The transport form is 5-methyltetrahydrofolate. Because B12 deficiency can produce anemia similar to folate deficiency, there is a risk that folate supplementation can delay the diagnosis of B12 deficiency, which can lead to irreversible neurological damage (Malouf, 2009). • 5-methyltetrahydrofolate is an option for supplementation and fortification without masking the anemia of vitamin B12 deficiency (Pentieva et al, 2004). Metafolin is a

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registered trademark of Merck; Deplin is one brand, containing 7.5 mg of L-methylfolate.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Vitamin C promotes absorption of folate from foods. See Table 12-9 for a list of folate sources. • Pregnant women should receive appropriate counseling; 30% may have a folate deficiency. Daily needs increase by approximately 200 g over the adult requirements of 400 g. Folate protects against neural tube defects in the first trimester. TABLE 12-9

Folic Acid Sources


• Women who have a folic acid allele in the MTHFR gene may need to use a special brand of supplement, such as Neevo ( during pregnancy. • Large intakes of folic acid (1 mg/d) can cure the anemia but may mask a correlated vitamin B12 anemia; monitor carefully. 5-methyl THFA enters cells via a diverse range of folate transporters where it may be demethylated to THFA, the active form. Because vitamin B12 is required in this conversion, its absence traps folic acid in its inactive form as 5-methyl THFA. • In seniors with low vitamin B12 status, high-serum folate is associated with anemia and cognitive impairment but when not vitamin B12 status was normal; however, highserum folate was associated with protection against cognitive impairment (Morris et al, 2009). • Attractive meals may help appetite. Fad and restrictive diets should be avoided. • Alcoholic beverages interfere with folate metabolism and absorption. • Food folates are oxidized easily and destroyed by lengthy cooking; advise patients accordingly.

Patient Education—Food Safety Folic Acid (g)

If tube feeding or CPN is needed, careful handwashing procedures should be followed.

Breakfast cereals fortified with 100% of the DV


Beef liver, cooked, braised, 3 ounces


For More Information

Black-eyed peas, immature, cooked, boiled, half cup


Spinach, frozen, cooked, boiled, half cup



Folic Acid Supplements

March of Dimes–Folic Acid Deficiency

Great Northern beans, boiled, half cup


Asparagus, cooked, four spears


Broccoli, cooked, half cup


Rice, white, long-grain, parboiled, enriched, cooked, half cup


Vegetarian baked beans, canned, one cup


Spinach, raw, one cup


Green peas, frozen, boiled, half cup


Broccoli, chopped, frozen, cooked, half cup


Egg noodles, cooked, enriched, half cup


Avocado, raw, all varieties, sliced, half cup sliced


Peanuts, all types, dry roasted, 1 ounce


Lettuce, Romaine, shredded, half cup


Wheat germ, crude, two tablespoons


Tomato Juice, canned, 6 ounces


Orange juice, chilled, includes concentrate, three-fourth cup


Derived from: NIH Fact Sheet,, accessed December 27, 2009.

FOLIC ACID DEFICIENCY ANEMIA—CITED REFERENCES Abdolmaleky AB, et al. Methylomics in psychiatry: modulation of gene-environment interactions may be through DNA methylation. Am J Med Genet B Neuropsychiatr Genet. 127:51, 2004. Malouf R, et al. Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people. Cochrane Database Syst Rev. 4:CD004514, 2008. Milner JA. Diet and cancer: facts and controversies. Nutr Cancer. 56:216, 2006. Morris MS, et al. Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification. Am J Clin Nutr. 85:193, 2007. Ng TP, et al. Folate, vitamin B12, homocysteine, and depressive symptoms in a population sample of older Chinese adults. J Am Geriatr Soc. 57:871, 2009. Pentieva K, et al. The short-term bioavailabilities of [6S]-5-methyltetrahydrofolate and folic acid are equivalent in men. J Nutr. 134:580, 2004. Waterland RA, Jirtle RL. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Nutrition. 20:63, 2004.

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HEMOLYTIC ANEMIAS NUTRITIONAL ACUITY RANKING: LEVELS 2–3 DEFINITIONS AND BACKGROUND In hemolytic anemia, RBCs have an abnormal membrane, which results in hemolysis. RBCs are destroyed faster than they can be produced in bone marrow. In severe cases in infancy, encephalomalacia can result. The incidence of all types of hemolytic anemias is 4 in 100,000 persons in the United States. Treatment may involve splenectomy or steroid use. Most are not affected specifically by vitamin E. Types of hemolytic anemias include Hgb-SC disease, hemolytic anemia due to glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary elliptocytosis, hereditary spherocytosis, idiopathic autoimmune hemolytic anemia, nonimmune hemolytic anemia caused by chemical agents, and secondary immune hemolytic anemia. This text covers aplastic anemia, sickle cell anemia, and thalassemia. Table 12-10 describes some of these types of anemias.

Dizziness Edema Pallor Nosebleeds, bleeding gums Dark urine Jaundice, splenomegaly Puffy eyelids Weakness, confusion Chills

Fatigue, intolerance for exercise Heart murmur Lab Work RBC (low) Hgb (low) Reticulocyte count (increased) Serum alphatocopherol levels

Hgb in urine Hemosiderin in urine TIBC Bilirubin (elevated) Transferrin Gluc AST (increased) Blood test for G6PD CRP


• Prevent further complications. • Correct anemia or deficits of nutrients, such as vitamin E.

CLINICAL INDICATORS Genetic Markers: Some types of hemolytic anemia have genetic links. Clinical/History Height Weight

TABLE 12-10

BMI Diet history Growth percentile


BP Tachycardia Shortness of breath

FOOD AND NUTRITION • Provide diet as usual for age and sex. • Avoid excesses of iron. • Ensure adequate intake of vitamin E and zinc, which may become deficient. Good sources of vitamin E include wheat germ, almonds, sunflower seeds, sunflower or safflower oil, peanut butter, peanuts, corn oil, spinach, broccoli, and

Types of Hemolytic Anemia



Acquired autoimmune hemolytic anemia

A rare autoimmune disorder characterized by the premature destruction of RBCs. Normally, RBCs have a life span of 120 days before the spleen removes them, but in this condition, RBCs are destroyed prematurely. Bone marrow production of new cells can no longer compensate. This anemia occurs in individuals who previously had a normal RBC system. Patients with autoimmune hemolytic anemia usually are associated with thrombosis

Familial hemolytic jaundice (spherocytic anemia)

A hereditary anemia in which RBCs are shaped like spheres rather than their normal, donut-like shape. Jaundice and anemia occur from destruction of the abnormal cells by the spleen. Surgical removal of the spleen usually is indicated. There is no permanent cure

Glucose-6-phosphate dehydrogenase (G6PD) deficiency anemia

This anemia is seen in about 10% of African–American males in the United States and is also common in persons from the Mediterranean area or Asia. The severity differs among different populations. In the most common form in the African–American population, the deficiency is mild, and the hemolysis affects primarily older RBCs. In Caucasians, G6PD deficiency tends to be more serious because even young red blood cells are affected. It affects millions of people worldwide, especially in malaria-prone areas

Hereditary nonspherocytic hemolytic anemia

A group of rare genetic blood disorders characterized by defective RBCs (erythrocytes) that are not abnormally “sphere shaped” (spherocytes). Membranes of RBCs, abnormal metabolism of a chemical contained in hemoglobin (porphyrin), and deficiencies in certain enzymes such as G6PD or pyruvate kinase are thought to be the cause of these disorders

Vitamin E–sensitive hemolytic anemia

This condition may occur in infants who receive polyunsaturated fatty acids (PUFAs) without adequate vitamin E. Children with cystic fibrosis should be screened for vitamin E–deficient hemolytic anemia

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SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment Data: BMI 20, recent weight loss 10#. GI distress and pallor noted. Diagnosis of hemolytic anemia with splenectomy planned. Nutrition Diagnoses (PES): Unintentional weight loss related to GI distress and loss of appetite as evidenced by recent weight loss of 10# in 6 weeks.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Flavonoid preparations, marketed for a variety of effects and generally safe, should be evaluated carefully because there have been reports of toxic flavonoid–drug interactions, hemolytic anemia, and other problems (Galati and O’Brien, 2004).

Interventions: Prepare for splenectomy; use nutrient-dense and energy-rich foods as tolerated, such as milkshakes or eggnogs with or between meals. Educate patient about ways to enhance food intake while not feeling well. Monitoring and Evaluation: Postoperative evaluations; return of appetite and improved intake. No further weight loss; eventual weight regained.

soybean oil. Good sources of zinc include oysters, beef shank, crab, pork, chicken, lobster, baked beans, cashews, and yogurt.

Common Drugs Used and Potential Side Effects • For hemolytic anemia that is sensitive to vitamin E deficiency, water-soluble vitamin E (alpha-tocopherol) is likely to be given daily. Avoid taking with an iron supplement, which could interfere with utilization. • Persons with G6PD deficiency need to avoid exposing themselves to certain medicines such as aspirin (acetylsalicylic acid), certain antibiotics used to treat infections, fava beans, and mothballs. • Medicines can improve autoimmune hemolytic anemia (AIHA). Where prednisone is used, monitor for side effects. Monoclonal antibody therapy such as rituximab is used in difficult cases; it appears to be a safe and effective option (Hoffman, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • For hemolytic anemia that is sensitive to vitamin E deficiency, discuss, in layman’s terms, the role of vitamin E in lipid oxidation and utilization. Discuss sources of polyunsaturated fatty acids (PUFAs) and why excesses should be controlled. Discuss sources of vitamin E in the diet; natural sources are more bioavailable than synthetic sources. • Discuss exercise tolerance and ability to eat sufficient amounts of food as related to fatigue.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

American Autoimmune Related Diseases Association, Inc.


NIH – Hemolytic Anemias

HEMOLYTIC ANEMIAS—CITED REFERENCES Galati G and O’Brien PJ. Potential toxicity of flavonoids and other dietary phenolics: significance for their chemopreventive and anticancer properties. ree Radic Biol Med. 37:287, 2004. Hoffman PC. Immune hemolytic anemia–selected topics. Hematology Am Soc Hematol Educ Program. 80–86, 2009.

IRON-DEFICIENCY ANEMIA NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Hgb transports oxygen to the tissues and carbon dioxide back to the lungs where it is exhaled. Hgb levels are influenced by sex, age, altitude, and smoking. In the adult male and the elderly, iron deficiency is usually caused by chronic blood loss. In children and women, low intake of iron may be a problem. The nutrient most commonly deficient in the world is iron. Iron deficiency affects two billion people, mostly in developing countries (Lynch, 2005).

IDA results from inadequate intake, impaired erythropoiesis or absorption of iron, blood loss, or demands from closely repeated pregnancies (Table 12-11). Serious systemic consequences include impaired cognitive function, koilonychia, and impaired exercise tolerance. Hct is the measure of RBCs in a given volume of blood, packed by centrifuge. Transferrin is the carrier protein that picks up iron from the intestines. Absorption of iron occurs in the ferrous form; storage is in the liver, spleen, and bone marrow. See Table 12-12 for

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TABLE 12-11

Stages of Iron Deficiency

Stages of Iron Deficiency


Stage 1 Depletion of iron stores

Stainable bone marrow iron Total iron binding capacity Serum ferritin concentration

Stage 2 Early functional iron deficiency

Diagnostic Range

Transferrin saturation Free erythrocyte protoporphyrin Serum transferrin receptor

Stage 3 Iron deficiency anemia

TABLE 12-13

Hemoglobin concentration Mean cell volume

Absent 400 g/dL 12 g/L 20 g/L  low Hb or Hct indicates iron deficiency 16% 70 g/dL erythrocyte 8.5 mg/L 12 g/dL 80 fL

Adapted from: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2002), Iron, p. 302 Food and Nutrition Board (FNB), Institute of Medicine (IOM).

content of iron in various body sources. Approximately 90% of the body’s store of iron is reused. Diet replaces iron lost through sweat, feces, and urine. The duodenum (upper small intestine) is where iron is best absorbed. Damage or surgery of the duodenum can greatly inhibit total iron absorption, thus leading to greater risk of deficiency. Table 12-13 describes factors that can modify iron absorption. IDA is the final stage of a long period of deprivation. Serum ferritin (storage form) is the most useful test to differentiate IDA from ACD. Iron deficiency is relatively common in toddlers, adolescent girls, and women of childbearing age. Ingestion of cow’s milk causes occult intestinal blood loss in young infants. The Hgb content of reticulocytes (young RBCs) is a good indicator of iron deficiency and IDA in children. Risk of iron deficiency may be underestimated in highrisk populations. Postpartum anemia is associated with breathlessness, tiredness, palpitations, and maternal infections, and blood transfusions and iron supplementation have been used in the treatment of IDA. Erythropoietin may be useful. TABLE 12-12

Normal Iron Distribution in the Body


Men (mg iron/kg BW)

Women (mg iron/kg BW)









Functional hemoglobin



Functional myoglobin








Transport protein: transferrin


Based on data from: Insel P, Turner R, Ross D. Nutrition. Sudbury, MA: Jones & Bartlett Publishers, 2001.


Factors That Modify Iron Absorption



Physical state (bioavailability)

Heme  Fe2  Fe3

High gastric Ph

Hemigastrectomy, vagotomy, pernicious anemia, histamine H2-receptor blockers, calcium-based antacids

Disruption of intestinal structure

Crohn’s disease, celiac disease (nontropical sprue)


Phylates, tannins, soil clay, laundry starch, iron overload


Cobalt, lead, strontium


Ascorbate, citrate, amino acids, iron deficiency

From: Information Center for Sickle Cell and Thalassemic Disorders. Iron deficiency. Available at

Celiac disease may be present in children and is associated with IDA (Goel et al, 2005). In persistent IDA, screening for celiac disease (anti-tissue transglutaminase antibodies), autoimmune gastritis (gastric, anti-parietal, or anti-IF antibodies), and Helicobacter pylori (IgG antibodies and urease breath test) is recommended (Hershko and Ronson, 2009). Because menstruation increases iron losses each month, women of childbearing age tend to become iron deficient. When there is not enough Hgb, free erythrocyte protoporphyrin (FEP) accumulates. Athletes are also at risk for iron deficiency. Recreational athletes should be screened for iron deficiency using serum ferritin, serum transferrin receptor, and Hgb (Sinclair and Hinton, 2005). As many as 25% of children and 20% of those seen in mental health clinics have pica, which is characterized by persistent and compulsive cravings to eat nonfood items. Pica can occur in pregnant women, in autism, and in persons with brain injuries. Pica is seen in about half of patients with iron deficiency; it is a consequence of iron deficiency and is relieved by iron supplementation. Exposure to lead also has a significant effect on Hgb and Hct levels. Serum levels above 50 mcg/dL are a problem. Lead poisoning reduces Hgb production, causes iron deficiency, and elevates FEP as the precursor. Poor intake of vitamins A, B12, C, and E, folic acid, and riboflavin is also linked to the development and control of IDA. Multiple micronutrient (MMN) supplementation during pregnancy reduces the risk of low birth weight, small-for-gestational age, and anemia; MMN supplementation improves CD4 counts and HIV-related morbidity and mortality in adults (Allen et al, 2009). When Hgb levels are seriously low, the heart is particularly vulnerable. Anemia in heart failure patients is associated with reduced exercise tolerance, increased heart failure hospitalizations, and increased all-cause mortality (Stamos and Silver, 2009). Whole-blood transfusion or IV iron may be needed. Iron fortification of food is also a cost-effective method for reducing the prevalence of nutritional iron deficiency. In populations where young children are routinely fed cooked rice daily, fortifying it with iron helps improve iron status (Beinner et al, 2010).

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CLINICAL INDICATORS Genetic Markers: Mutations in a type-II serine protease, matriptase-2/TMPRSS6, are associated with severe iron deficiency caused by inappropriately high levels of hepcidin expression; hemojuvelin is a cell surface protein that regulates hepcidin expression (Lee, 2009). Flatulence, vague Weight abdominal BMI pains Diet history Anorexia BP Diarrhea I&O Glossitis, Pallor stomatitis Brittle, spoonAnkle edema shaped Tingling in fingernails extremities (koilonychia) Palpitations Stool examinaAlopecia tion for occult Lab Work blood Impaired cogni- Ferritin (decreased tive function stores in liver, Blue sclerae spleen, bone Impaired marrow; exercise levels are tolerance 20 g/L) Weakness, Serum iron fatigue (low) Vertigo H & H (Hgb is Headache, more irritability sensitive) Heartburn Dysphagia Clinical/History

Mean cell Hgb (MCH) (decreased) Mean cell Hct (MCHC) (decreased) CBC (every 3–6 months after initial) Transferrin (increased) MCV (80) RBC (small, microcytic, hypochromic) WBC/ differential (increased) TIBC (increased 350 g/dL) Reticulocyte count Serum copper Cholesterol (Chol) Test for H. pylori

SAMPLE NUTRITION CARE PROCESS STEPS Harmful Beliefs About Food Assessment Data: Diet hx indicates pica during this pregnancy. Mom states that “the starch is good for my baby.” Eats starch after each meal. Twenty-weeks pregnant; age 19. Low H & H. Nutrition Diagnoses (PES): Harmful beliefs/attitudes (NB-1.2) about food or nutrition-related topics. Interventions: Initial/Brief nutrition education (N.I.2.2) to provide basic nutrition-related educational about food and foods rich in iron; reasons to discontinue eating starch and to begin taking a prenatal vitamin. Counseling—work with client to set goals for a healthier pregnancy. Monitoring and Evaluation: Improvement in H & H. Discontinuation of pica. Positive pregnancy outcome.

• Alleviate cause of the anemia and associated anorexia. • Provide adequate oral iron to replace losses or deficits, especially heme sources of protein (liver, beef, oysters, lamb, pork, ham, tuna, shellfish, fish, and poultry). • Provide an acid medium to favor better absorption. Enhancers include gastric juice and ascorbic acid. Food sources of vitamin C should be included daily. • Monitor and correct pica, including geophagia (clay eating), amylophagia (starch eating), ice eating, or any lead exposure. • Avoid or correct constipation. • Screen for IDA or sports anemia in athletes (Sinclair and Hinton, 2005). • Reduce iron inhibitors, such as excessive fiber (as in whole grains), phytic acid (as in spinach, bran, legumes, and soy products), tannins in tea, and polyphenols in coffee or red wine. In many developing countries, cereal and legume-based diets contain low amounts of bioavailable iron, which may increase the risk of iron deficiency (Zimmermann et al, 2005).

FOOD AND NUTRITION • If IDA is related to inadequate iron in diet, usually adding three portions of lean red meat (heme iron sources) per week, along with all other essential vitamins and minerals, will correct the anemia. The average mixed diet contains approximately 6 mg of iron per 1000 kcal. Iron absorption increases as stores become depleted. Good sources of iron include liver, dried beans, egg yolks, kidney, lean beef, dark meat of chicken, salmon, tuna, dried fruits, enriched whole-grain cereals, molasses, and oysters. • Heme iron is found readily in beef, pork, and lamb; consume with fruit or fruit juice. Heme iron is absorbed well, regardless of other foods in the diet. • Nonheme iron absorption is greatly affected by other foods. Absorption of nonheme iron is best in the presence of foods rich in vitamin C or with heme-containing sources. Increase intake of vitamin C (oranges, grapefruit, tomatoes, broccoli, cabbage, baked potatoes, strawberries, cantaloupe, and green peppers), especially with an iron supplement. • Detect pica and discuss with patient. Pica substance may displace other important foods, leading to nutrient malnutrition. The ingested substance may also be toxic. • Tea, coffee, wheat brans, and soy products tend to inhibit absorption of nonheme iron. Monitor use carefully; avoid excesses.

Common Drugs Used and Potential Side Effects (Table 12-14) • If anemia is caused by an increased demand for iron such as a growth spurt (toddlers, adolescents) or pregnancy, oral supplementation may be necessary: inorganic

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TABLE 12-14


Medications to Correct Iron-Deficiency Anemia



Ferrous salts (Feosol, Fer-In-Sol, Mol-Iron) or tablets (Feostat, Fergon, Feosol)

Prolonged-release ferrous sulfate (Slow Fe) improves iron absorption with fewer side effects than standard ferrous sulfate pills. Other forms include ferrous fumarate (Femiron, Feostat, Fumerin, Hemocyte, Ircon) and ferrous gluconate (Fergon, Ferralet, Simron). These may cause gastric irritation and constipation.

Enteric-coated or sustained-release iron

More expensive and often carry the iron past maximal absorption site in the upper intestine.

Heme iron (Proferrin Forte)

This is a medical food that contains heme iron plus folic acid. It is absorbed regardless of achlorhydria, and has fewer GI side effects than IV or ferrous iron sources. It can be taken with or without meals.

Parenteral or IV iron

Can be administered by injection or infusion. This therapy is reserved for cases of trauma where blood loss is life threatening and is not used for insufficiency due to inadequate dietary iron intake. Imferon can be given intramuscularly, if oral iron is not tolerated; pain and skin discoloration may result.

• •

iron in ferrous form (50–200 mg/d for adults; 6 mg/kg for children) combined with increased consumption of heme-rich sources of iron. This is best absorbed on an empty stomach, but with food if there are GI side effects. Iron pills should be taken 2 hours before or after other medications. Iron can inhibit the effectiveness of thyroid medications, antibiotics, and some antidepressant drugs. Once ingested, it is imperative that the stomach contains acid to dissolve the iron salt; if taking antacids or H2 blockers such as cimetidine (Tagamet), the iron salt will not dissolve. The amount of elemental iron contained in iron pills will vary. A 325-mg supplement is probably made of ferrous fumarate or gluconate, with only 100 mg of elemental iron per pill. Heme iron supplements (such as Proferrin) can be taken with meals, unlike ionic iron preparations, which must be taken on an empty stomach between meals. However, individuals with allergies to beef, milk, or other dairy products should not be given Proferrin. It takes 4–30 days to note improvements after iron therapy, especially in Hgb levels. Hgb should rise 0.1–0.2 g/dL/ day after the fifth day of treatment; then should rise 2.0 g/dL/week for 3 weeks. Iron therapy should be continued for at least 2 months after the Hgb has returned to normal to replenish the iron stores. Iron stores are replaced after 1–3 months of treatment. Increased supplementation in normal individuals can cause additional, unnecessary iron to go into storage, reflected by ferritin elevation. Aspirin or corticosteroids can cause GI bleeding or peptic ulceration. Vitamin C and nutrient levels may be decreased. Some medications, including antacids, can reduce iron absorption. Iron tablets may also reduce the effectiveness of other drugs, including the antibiotics tetracycline, penicillamine, and ciprofloxacin and the anti-Parkinson’s drugs methyldopa, levodopa, and carbidopa. Wait 2 hours between doses of these drugs and iron supplements.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Hgb is made from protein, iron, and copper. RBCs are made from vitamin B12, folacin, and amino acids. Explain which foods are good sources of iron, protein, vitamin C, and related nutrients. • Temporary changes in stool color (green or tarry and black) are common with supplements; this is not cause for alarm. To avoid side effects of supplements, take them with meals or milk; food iron has fewer side effects. • Foods and substances that can interfere with the absorption of iron include calcium, tannins, which are found in coffee, tea, grapes, red wine, purple or red rice, and bran fiber or chocolate. Avoid excesses of oxalates, alkalis, and antacids; discuss sources. Iron supplementation is best taken 2 hours after consuming these substances. • The average American diet contains 10–20 mg of iron daily, roughly 10% of which is absorbed. Avoid overdosing with iron supplements. The body can only synthesize 5–10 mg of Hgb per day, and excesses may work against the immune system. • Local or systemic infections interfere with iron absorption and transport. • In children under age 2, limit milk intake to no more than 500 mL/d for better iron status. • Explain nonfood pica—clay, starch, plaster, paint chips— and the relationship with nutrition. In food pica in which singular foods are eaten instead of balanced meals, the foods chosen are often crunchy or brittle. Excessive consumption of lettuce, ice, celery, snack chips, and chocolate has been noted; after iron supplementation, cravings often subside. • Iron deficiency may be partly induced by plant-based diets containing low levels of poorly bioavailable iron (Kesa and Oldewage-Theron, 2005). Young people who follow a vegan diet should have their iron status monitored closely. • Use culturally appropriate nutrition counseling. In some cultures, boys may be fed iron-rich foods preferentially over girls; counseling should be designed to improve intake by girls (Shell-Duncan and McDade, 2005).

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

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For More Information •


Iron Deficiency Anemia for Kids

Mayo Clinic

National Institutes of Health–Iron Deficiency Anemia

University of Maryland

IRON DEFICIENCY ANEMIA—CITED REFERENCES Allen LH, et al. Provision of multiple rather than two or fewer micronutrients more effectively improves growth and other outcomes in micronutrient-deficient children and adults. J Nutr. 139:1022, 2009. Beinner MA, et al. Iron-fortified rice is as efficacious as supplemental iron drops in infants and young children. J Nutr. 140:49, 2010.

Goel NK, et al. Cardiomyopathy associated with celiac disease. Mayo Clin Proc. 80:674, 2005. Hershko C, Ronson A. Iron deficiency, Helicobacter infection and gastritis. Acta Haematol. 122:97, 2009. Kesa H, Oldewage-Theron W. Anthropometric indications and nutritional intake of women in the Vaal Triangle, South Africa. Public Health. 119:294, 2005. Lee P. Role of matriptase-2 (TMPRSS6) in iron metabolism. Acta Haematol. 122:87, 2009. Lynch SR. The impact of iron fortification on nutritional anaemia. Best Pract Res Clin Haematol. 18:333, 2005. Shell-Duncan B, McDade T. Cultural and environmental barriers to adequate iron intake among northern Kenyan schoolchildren. Food Nutr Bull. 26:39, 2005. Sinclair LM, Hinton PS. Prevalence of iron deficiency with and without anemia in recreationally active men and women. J Am Diet Assoc. 105:975, 2005. Stamos TD, Silver MA. Management of anemia in heart failure. Curr Opin Cardiol. 2009 Dec 5. [Epub ahead of print] Zimmermann MB, et al. Iron deficiency due to consumption of a habitual diet low in bioavailable iron: a longitudinal cohort study in Moroccan children. Am J Clin Nutr. 81:115, 2005.


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

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DEFINITIONS AND BACKGROUND Gastrointestinal infestation by parasitic worms that feed on blood (hookworm) or on nutrients (tapeworm) may occur, especially in tropical or subtropical areas. Intestinal parasites that affect nutrition in particular include soil-transmitted helminths, Giardia duodenalis, Entamoeba histolytica, other parasites such as the coccidia, Schistosoma sp., and malarial parasites. Iron deficiency is found to be correlated with these parasites in tropical countries (Shell-Duncan and McDade, 2005). The neglected infections of poverty are parasitic, bacterial, and viral infections that disproportionately affect impoverished populations in the United States; these include Chagas disease, cysticercosis, congenital cytomegalovirus (CMV), toxocariasis, toxoplasmosis, and trichomoniasis (CDC, 2009). Toxoplasmosis is considered to be the third leading cause of death attributed to foodborne illness in the United States (CDC, 2009). Malaria is a bloodborne, parasitic infection transmitted by mosquitoes. It kills more than 1 million people annually, especially in Africa. Pregnant women, children, and immunocompromised individuals have the highest rates of morbidity and mortality (Schantz-Dunn and Nour, 2009). More than 1000 cases of malaria are reported to the Centers for Disease Control and Prevention each year in the United States. Travelers or immigrants present with fever, chills, nausea, vomiting, headache, abdominal pain, severe anemia, and acute renal failure (Vicas et al, 2005). Risks for miscarriage, intrauterine demise, premature delivery, low birth-weight neonates, neonatal death, severe anemia, and maternal death are high among pregnant women with malaria (Schantz-Dunn and Nour, 2009). Between 150 and 300 children die each hour from malaria (Breman, 2009). For those who survive, neurologic impairment, anemia, hypoglycemia, and low birth weight imperil normal development and survival (Breman, 2009). Malaria can be prevented with appropriate drugs, bednets treated with insecticide, and effective educational outreach. Resistance of Plasmodium falciparum to drugs and Anopheles mosquitoes to insecticides has stimulated discovery and development of artemisinin-based combination treatments (ACTs) and other drugs, long-lasting insecticide-treated bednets (with synthetic pyrethroids) and a search for nontoxic, long-lasting, affordable insecticides for indoor residual spraying (Breman, 2009). A malaria vaccine is under development (Greenwood, 2008).


Genetic Markers: Congenital CMV is passed from mother to infant during pregnancy.

Height Weight

BMI Diet history BP

Lab Work Hgb (often 5 g/dL) Hct Serum Fe Ferritin Serum B12

TIBC Alb Serum folic acid CRP Transferrin Gluc Serum Cu Serum Zn

INTERVENTION OBJECTIVES • Correct anemia from blood losses; eliminate parasitic infestation. • Prevent GI tract perforation or obstruction, when likely to exist. • Improve nutritional status and appetite. Parasitic infections affect the intake of food, subsequent digestion and absorption, metabolism, and nutrient storage and cause subtle micronutrient deficiency, such as vitamin A deficiency. • Prevent low birth weight and other adverse effects in pregnant or postpartum women and their infants.

FOOD AND NUTRITION • A diet high in protein, B-complex vitamins, and iron may be appropriate. Provide adequate energy to meet individual’s needs for anabolism where needed. • Foods rich in heme iron and vitamins C and A should be included in meals served or planned. Iron inhibitors should be excluded from diet as far as possible until recovery is complete. • Include plenty of other nutrient-dense foods, such as good sources of zinc and other micronutrients (Table 12-15).

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function Assessment Data: Weight loss, GI distress, Hgb 5, temperature averaging 101 degrees F. Dx of parasitic infection Giardia from drinking water at a campsite. Nutrition Diagnoses (PES): Abnormal GI function related to parasitic infection of Giardia as evidenced by fever, low Hgb 5, GI distress, and weight loss.



Abdominal discomfort Nausea, vomiting Fever Irritability Pica?


I&O Fatigue

Interventions: Food–Nutrient delivery—offer tolerated foods and beverages. Suggest use of a multivitamin-mineral supplement. Educate about risks of drinking potentially contaminated water from various sources. Monitoring and Evaluation: Improvement in Hgb level; return of lost weight. Resolution of Giardia.

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TABLE 12-15

Micronutrient Deficiencies in Parasitic Anemias such as Malaria


Deficiency Effects

Vitamin A

Increased susceptibility to malarial anemia, altered iron metabolism, deficit of retinol for synthesis of acute phase reactants

Vitamin C

Impaired T-lymphocyte response, delayed cutaneous hypersensitivity, impaired complement function, reduced phagocytic function

Vitamin E

Impaired T-lymphocyte response, altered B-cell function and impaired humoral response, delayed cutaneous hypersensitivity, impaired cytokine function or production, reduced phagocytic function; deficiency can contribute to oxidant damage to erythrocytes, leading to hemolysis, but deficiency can make the parasite more vulnerable to oxidation generated with some antimalarial drugs


Decreased iron absorption, increased erythrocyte fragility, depressed erythropoiesis; deficiency may protect against malaria by diminished parasite multiplication and growth


Impaired erythropoiesis; deficiency may protect against malaria through impaired parasite metabolism


Involvement in acute phase response to infection


Impaired erythropoiesis, decreased T-lymphocyte response, altered B-cell function and impaired humoral response, delayed cutaneous hypersensitivity, impaired cytokine function or production, reduced phagocytic function; deficiency and associated microcytosis may reduce malaria parasite multiplication. Avoid excesses.


Unknown role


Impaired immune function including decreased T-lymphocyte response, altered B-cell function and impaired humoral response, delayed cutaneous hypersensitivity, impaired cytokine function or production, reduced phagocytic function; can contribute to increased parasitemia

From: Nussenblatt V, Semba, RD. Micronutrient malnutrition and the pathogenesis of malarial anemia. Acta Trop. 82:321, 2002; and Scrimshaw NS, Sangiovanni JP. Synergism of nutrition, infection, and immunity: an overview. Am J Clin Nutr. 66:464S, 1997.

Common Drugs Used and Potential Side Effects • Artemisinin combination therapy replaces ineffective chloroquine and sulphadoxine pyrimethamine for firstline treatment of malaria and for the provision of longlasting, insecticide treated bednets (Greenwood, 2008). • If needed, oral or parenteral iron may be given to correct anemia more rapidly. Beware of excessive use of oral supplements because of their potential side effects with iron overloading; monitor all sources (including iron-enriched foods).

Patient Education—Food Safety • Avoid eating raw fish or meats. • Washing vegetables thoroughly before eating them and cooking meat to recommended temperatures to avoid toxoplasmosis (CDC, 2009). • If tube feeding or CPN is needed, careful handwashing procedures should be followed. • To prevent the spread of CMV, do not share food, drinks, or eating utensils with young children. Wash hands with soap and water after touching diapers or saliva.

For More Information

Herbs, Botanicals, and Supplements

Parasites of the Intestinal Tract

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

Parasitic Disorders

World Health Organization–Malaria

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss ways to prevent further parasitic infestations, as with small children playing in soil. Pregnant women must be particularly careful, especially in developing countries where malaria, hookworm, and other parasites are common. • Discuss ways to prepare foods high in necessary nutrients and methods to increase bioavailability (e.g., combining orange juice at breakfast with an iron-fortified cereal, etc.). In vulnerable populations, use fortified beverages to correct micronutrient deficiency. • In areas of malaria transmission, anemia is apparent from the first few months of life, and there is a great need to target interventions at pregnant women and infants, which are the groups at highest risk. Food-fortification programs can be very beneficial.

PARASITIC ANEMIA AND MALARIA—CITED REFERENCES Breman JG. Eradicating malaria. Sci Prog. 92(Pt 1):1, 2009. CDC. Web site accessed December 27,2009, at dpd/. Greenwood B. Progress in malaria control in endemic areas. Travel Med Infect Dis. 6:173, 2008. Schantz-Dunn J, Nour NM. Malaria and pregnancy: a global health perspective. Rev Obstet Gynecol. 2:186, 2009. Shell-Duncan B, McDade T. Cultural and environmental barriers to adequate iron intake among northern Kenyan schoolchildren. Food Nutr Bulletin. 26:39, 2005. Vicas AE, et al. Imported malaria at an inner-city hospital in the United States. Am J Med Sci. 329:6, 2005.

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MEGALOBLASTIC ANEMIAS: PERNICIOUS OR VITAMIN B12 DEFICIENCY NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND Megaloblastic anemias affect the nervous system if left untreated. Deficiency of folate and vitamin B12 changes in the concentrations of metabolites, such as methylmalonic acid and homocysteine. Pernicious anemia (PA) is a macrocytic anemia caused by a vitamin B12 deficiency and intrinsic factor (IF). PA is thought to be an autoimmune disorder and is often found with other disorders such as thyroid or diabetes. The antiparietal cell antibodies test measures the presence of antibodies against gastric parietal cells. Long-standing Helicobacter pylori infection probably plays a role with the irreversible destruction of the gastric body mucosa (Lahner and Annibale, 2009). The three forms of PA are congenital PA, juvenile PA, and adult-onset PA. The forms are based on the age at onset and the precise nature of the defect causing impaired vitamin B12 utilization (e.g., absence of IF). PA affects 1–2% of older individuals. Defective RBC production occurs, caused by a lack of IF of the stomach. IF helps vitamin B12 produce RBCs. IF is present in gastric juice and binds to B12. Once bound, IF changes and becomes less susceptible to digestion; this protects B12 and allows its absorption from gastric juice. When IF is not available, B12 cannot be properly absorbed. Vitamin B12 deficiency and achlorhydria have a detrimental effect on bone strength. Having PA increases the risk for hip fracture, even after treatment (Merryman et al, 2009). Vitamin B12-deficiency anemia may take 5–6 years to appear; this megaloblastic anemia is a reversible form of ineffective hematopoiesis. There may be almost 800,000 older adults in the United States who have undiagnosed and untreated vitamin B12 deficiency. It is often masked by high folate intakes. Hidden blood loss, gastric atrophy, and poor dietary intake should be addressed (Table 12-16). The Schilling test is no longer used. Serologic testing for parietal cell and IF antibodies are used instead. With normal absorption, the ileum absorbs more vitamin B12 than the body needs and excretes excess into the urine. With impaired

TABLE 12-16

absorption, however, little or no vitamin B12 is excreted into the urine. Low serum levels cannot identify all cases of vitamin B12 deficiency; serum methylmalonic acid level may also be needed. Holotranscobalamin (holoTC), when compared with the other markers of vitamin B12 deficiency, shows promise for diagnosing early vitamin B12 deficiency (Hvas and Nexo, 2005). Adequate selenium intake plays an important role in maintaining vitamin B12 adequacy. Glutathione forms a complex called glutathionylcobalamin, which could protect against diseases related to vitamin B12 depletion. Areas of research include intermittent vitamin B12 supplement dosing and better measurements of the bioavailability of vitamin B12 from fermented vegetarian foods and algae. Vegetarians are at risk for vitamin B12 deficiency (Allen, 2008). Vitamin B12 anemia is corrected by the use of oral cyanocobalamin.

ASSESSMENT, MONITORING, AND EVALUATION CLINICAL INDICATORS Genetic Markers: Human leukocyte antigen-DR genotypes suggest a role for genetic susceptibility in PA (Lahner and Annibale, 2009). In congenital PA, IF is missing. Nearly all people with PA test positive for antiparietal cell antibodies. Clinical/History Height Weight BMI Diet history Weight loss?

Postural hypotension? Fatigue Flatulence, nausea, and vomiting

Diarrhea Constipation Anorexia Tachycardia, cardiomegaly Achlorhydria

Risks and Causes of Pernicious Anemia or Vitamin B12–Deficiency Anemia

Pernicious Anemia

Vitamin B12–Deficiency Anemia

High risk:

High risk:

Family history of pernicious anemia; African, Scandinavian, or Northern European descent; autoimmune endocrine disorders

Vegans; elderly; persons with intestinal malabsorption or gastric atrophy or hypochlorhydria; stomach removal surgery; drug use (colchicine, neomycin); metabolic disorders (homocystinuria methylmalonic aciduria); breastfed infants of vitamin B1–deficient mothers; poor diet in infancy or pregnancy



Autoimmune endocrine diseases such as type 1 diabetes, hypoparathyroidism, Addison’s disease, hypopituitarism, testicular dysfunction, Graves’ disease, chronic thyroiditis, myasthenia gravis, secondary amenorrhea, vitiligo, gastric surgery, anorexia nervosa, or bulimia nervosa

Poor intake of extrinsic factor (vitamin B12). Chronic alcoholism. Helicobacter pylori infection with diminished production of intrinsic factor. Hidden blood loss. Fish tapeworm. Reduced intestinal absorption, as with celiac disease or Crohn’s disease

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Glossitis with beefy, red tongue Lemon yellow or waxy skin Numbness or tingling in hands and feet Impaired sense of smell

MCV, MCHC, MCH (increased) Macrocytic/ nucleated cells Reticulocyte count (low) Hct (low) Lactate dehydrogenase (LDH) (increased) Lab Work CBC (altered platelets and Parietal cell and WBC count) IF antibodies Gastrin RBCs (increased) Serum B12

TIBC Urinary methylmalonic acid Serum folate Serum homocysteine (elevated?) Holotranscobalamin (holoTC) Bilirubin Transferrin

INTERVENTION OBJECTIVES • Alleviate the etiology of anemia, where possible. • Provide foods that will not hurt a sore mouth. Glossitis decreases the desire to eat. • Correct patient’s anorexia. • Prevent neurological defects if treatment is delayed or insufficient; depression, psychosis, and mania can appear. • Where present, correct PA; prevent progression to gastric cancer. PA requires vitamin B12 injections. • Prevent or correct hyperhomocysteinemia.

FOOD AND NUTRITION • Diet should make liberal use of high biological value (HBV) proteins. Good sources of vitamin B12 include liver,

SAMPLE NUTRITION CARE PROCESS STEPS Abnormal Nutrition Laboratories Assessment Data: PA with low serum vitamin B12, Hgb, and Hct; elderly resident in long-term care facility. Nutrition Diagnoses (PES): Altered nutrition-related laboratories related to resident’s body inability to produce IF and to absorb cobalamin as evidence by abnormal vitamin B12 200 pg/mL, Hgb 12 gm/dL, and Hct 37%. Interventions: Food and nutrient delivery—provide resident with foods/beverages with vitamin C such as orange juice, citrus fruits, and melon to be consumed at every meal to aid with iron absorption. Resident will eat two scrambled eggs at breakfast to increase vitamin B12. Coordinate care with nursing and medical staff to administer vitamin B12 shots and support with adequate dietary intake. Monitoring and Evaluation: Monitor monthly laboratories; goal vitamin B12 200 pg/mL, Hgb 12, and Hct 38%.

other meats, fish, poultry, eggs, milk, cheese, yogurt, fortified products such as cereals, and soy milk. The daily average intake is 2–30 mg. • Supplement diet with iron, vitamin C, folic acid and other B vitamins, copper, and selenium. • If patient has a sore mouth, use a soft or liquid diet with fewer spicy or acidic foods.

Common Drugs Used and Potential Side Effects • Vitamin B12 deficiency is effectively treated with oral vitamin B12 supplementation. Crystamine or Rubramin PC is cyanocobalamin in drug form for vitamin B12 deficiency. • For PA, vitamin B12 injections are given weekly until remission, after which six to eight injections yearly will suffice. For some, vitamin B12 supplements may be as effective as injections; high doses, such as 1000 g, are needed daily for about 18 months. • Trinsicon contains vitamin B12, ferrous fumarate, vitamin C, folacin, and IF. It is less effective when taken with dairy products. • Some medications that conflict with vitamin B12 absorption include chloramphenicol, proton pump inhibitors, histamine 2 inhibitors, and metformin.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • True vegan diets do not contain vitamin B12; it is found only in animal foods. Include eggs, meat, fish, shellfish, cheese, milk, milk products, or use B12 fortified soy products. Some fad diets may also be low in vitamins and protein; monitor intake carefully. • PA develops after total gastrectomy unless vitamin B12 is administered. The problem may also occur in patients with partial gastrectomy or gastric bypass. Lifelong vitamin B12 replacement or injections are necessary. • Avoid fatigue; plan simple meals and snacks. • Megaloblastic B12 anemia may occur in elderly; careful food choices are essential. • Breastfed infants of vitamin B12–deficient mothers are at risk for severe developmental abnormalities, growth failure, and anemia. Counseling for lactating women is important.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

Medline–Pernicious Anemia

Pernicious Anemia

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Vitamin B12 Deficiency Anemia



Hvas AM, Nexo E. Holotranscobalamin—a first choice assay for diagnosing early vitamin B deficiency? J Intern Med. 257:289, 2005. Lahner E, Annibale B. Pernicious anemia: new insights from a gastroenterological point of view. World J Gastroenterol. 15:5121, 2009. Merryman NA, et al. Hip fracture risk in patients with a diagnosis of pernicious anemia. Gastroenterology. 2009 Dec 16. [Epub ahead of print]

Allen LH. Causes of vitamin B12 and folate deficiency. Food Nutr Bull. 29:20S, 2008.

SIDEROBLASTIC ANEMIA NUTRITIONAL ACUITY RANKING: LEVEL 1 X-linked sideroblastic anemia (delta-aminolevulinate synthase deficiency) is vitamin B6 responsive that responds to high pyridoxine doses (Clayton, 2006). Pyridoxal phosphate is the cofactor for over 100 enzyme-catalyzed reactions in the body. Vitamin B6 is the main vitamin for processing amino acids and is also needed to make melatonin, serotonin, and dopamine.


CLINICAL INDICATORS Genetic Markers: Mutations in the mitochondrial carrier family gene SLC25A38 cause nonsyndromic autosomal recessive congenital sideroblastic anemia (Petkau, 2009). The enzyme directly relevant to sideroblastic anemia is ALAS-2 or ALAS-e on the X chromosome. However, most sideroblastic anemias are acquired. Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND Sideroblastic anemias are a group of blood disorders characterized by an impaired ability of the bone marrow to produce normal RBCs. Inherited sideroblastic anemia comprises several rare anemias due to heterogeneous genetic lesions, all characterized by the presence of ringed sideroblasts in the bone marrow (Camaschella, 2009). Abnormal RBCs called sideroblasts are found in the blood of people with these anemias. This anemia is a microcytic, hypochromic anemia similar to that caused by iron deficiency, except that serum iron is normal or elevated. The iron inside RBCs is inadequately used to make Hgb, despite adequate or increased amounts of iron. Therapy comprises application of antioxidants, vitamins, iron, bone marrowstimulating factors, or substitution of cells (Finsterer, 2007). The disease X-linked sideroblastic anemia with ataxia is due to a mutation in the protein transporter that is thought to transfer iron clusters from the mitochondrion to the cytoplasm (Napier et al, 2005). Another name for the congenital type of anemia is hereditary iron-loading anemia.

Clinical/History Height Weight BMI Diet history BP I&O Alcohol or drug toxicity? Fatigue

Dizziness Decreased tolerance for exercise Lab Work Serum B6 levels Hgb (low at 4–10 g/dL) RBC

Transferrin saturation (often elevated) Serum folic acid Serum homocysteine WBC Serum Fe, ferritin Serum Cu

INTERVENTION OBJECTIVES • Identify causes and solutions. • Remove any precipitating factors, such as specific drugs or alcohol use. • Correct problems, such as suppression of bone marrow, iron loading, and anemia.

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busulfan, penicillamine, and cycloserine can cause abnormal vitamin B6 metabolism. Monitor for gastrointestinal side effects.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake Assessment Data: Diagnosis of sideroblastic anemia, pyridoxineresponsive. BMI normal. Complaints of fatigue and poor exercise tolerance. Diet indicates intake of B6-rich foods to be infrequent. Lab work with high transferrin saturation, Hgb of 6, and low serum B6 levels.

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

Nutrition Diagnoses (PES): Inadequate vitamin intake (B6) related to X-linked genetic defect and low dietary intake as evidenced by diet and medical histories.


Interventions: Trial of 100- to 200-mg pyridoxine by mouth. Counseling about foods rich in vitamin B6. Monitoring and Evaluation: Improvement in symptoms (less fatigue and better exercise tolerance). Lab work showing improvement in serum B6 and Hgb, and lower transferrin saturation levels.

FOOD AND NUTRITION • A diet high in vitamin B6 may be beneficial with medication. Potatoes, bananas, raisin bran cereal, lentils, liver, turkey, and tuna are good sources of vitamin B6. • Protein and carbohydrate (CHO) intake should be adequate, and energy should also be adequate to spare protein. Folic acid and copper may also be needed. • Alcohol intake should be severely limited. • Balanced meals and snacks, as necessary, may be helpful.

• Discuss adequate sources of all needed nutrients such as vitamin B6, especially if deficiency caused the anemia. • Discuss attractive menu planning and balancing of meals because appetite and intake may be poor chronically. Discuss snacks and frequency.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

Genetics Home Reference


Medline Plus: Anemia

Common Drugs Used and Potential Side Effects SIDEROBLASTIC ANEMIA—CITED REFERENCES • Vitamin B6 may be ordered; age-dependent doses are specified. The National Academy of Sciences performed an analysis of vitamin B6 studies. It is usually safe at intakes of up to 100 mg/d in adults, but neurological side effects can sometimes occur at or above that level. Vitamin B6 toxicity damages sensory nerves, leading to numbness in the hands and feet as well as difficulty walking. • Chloramphenicol may cause drug-induced bone marrow suppression, resulting in sideroblastic anemia. Isoniazid,

Camaschella C. Hereditary sideroblastic anemias: pathophysiology, diagnosis, and treatment. Semin Hematol. 46:371, 2009. Clayton PT. B6-responsive disorders: a model of vitamin dependency. J Inherit Metab Dis. 29:317, 2006. Finsterer J. Hematological manifestations of primary mitochondrial disorders. Acta Haematol. 118:88, 2007. Napier I, et al. Iron trafficking in the mitochondrion: novel pathways revealed by disease. Blood. 105:1844, 2005. Petkau TL. Same pathway, different gene: a second gene in the heme biosynthesis pathway causes inherited sideroblastic anemia. Clin Genet. 2009 Nov 11. [Epub ahead of print]

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SICKLE CELL ANEMIA NUTRITIONAL ACUITY RANKING: LEVEL 1 Biconcave erythrocyte HbS tetramers +O2 Reversibly sickled erythrocyte

–O2 Deoxy-HbS polymer

Retinopathy, blindness LUNG: • Pneumonia • Infarcts • Acute chest syndrome

Atrophic spleen Iron overload • Heart • Liver

Repeated cycles of deoxygenation

Pigment gallstones Irreversibly sickled erythrocyte K+, H2O


Adherence to endothelium Rearrangement of membrane phospholipids

Thrombosis of small blood vessels

KIDNEY: • Concentrating ability • Infarcts Avascular necrosis of femoral head


Skin ulcers

Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND Sickle cell disease (SCD) is the most common genetic disorder of the blood. SCD involves anemia that is hereditary and hemolytic. Cells in SCD are crescent shaped and become rigid; they lodge themselves in the capillaries of the peripheral-blood system outside the heart. The sickling of RBCs occurs when partially or totally deoxygenated Hgb molecules distort their normal disk shape, producing stiff, sticky, sickle-shaped cells that obstruct small blood vessels; this causes vaso-occlusion as well as deprivation of oxygen to body tissues (Edwards et al, 2005). Everyone with SCD has chronic hemolytic anemia, vasculopathy, vaso-occlusive disease, acute and chronic organ damage, and shortened life span (Steinberg, 2008). SCD has several forms including sickle cell anemia, sickle cell Hgb C disease, and sickle cell thalassemia disease. It is usually detected within the first year of life. Routine use of daily antibiotics until 5 years of age, immunization of children with pneumococcal vaccine, annual influenza vaccination after 6 months of age, and meningococcal vaccination after 2 years of age are important preventive measures (Mehta et al, 2006). The largest population in the world with sickle cell anemia is in Africa. While this condition most commonly

affects blacks of African descent, it is also found in people of Middle Eastern, East Indian, and Mediterranean origin. About 100,000 Americans have SCD (1 in every 400–500 African–Americans). Carrier frequency varies, with high rates associated with zones of high malaria incidence. Carriers are often protected against malaria. Patients with SCD are at risk for delayed growth and sexual maturation; acute and chronic pulmonary dysfunction; stroke; aseptic necrosis of the hip, shoulders, or both; sickle cell retinopathy; dermal ulcers; and severe chronic pain (Edwards et al, 2005). The homozygous state (SS) is associated with complications and a reduced life expectancy. Chronic anemia, pallor, and jaundice result because sickled cells do not last as long as normal blood cells. Bone marrow functions at six times the normal rate. Because there are fewer cells, the blood is thinner or anemic. When RBCs are destroyed, bilirubin is released into the blood and turns the whites of the eyes to a shade of yellow. Inadequate dietary intakes of folate are common, whereas vitamin B12 intakes are usually adequate. Low RBC folate levels may occur. Serum total homocysteine (tHcy) levels may be elevated in this population; greater intakes than normal of folate may be needed. Elevated tHcy levels contribute to

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thrombosis, a frequent event in this population. Children with sickle cell anemia have lower vitamin B6 concentrations. Infants and children who have SCD are at risk for nutritional deficiencies and loss of body mass during acute illness. Suboptimal vitamin A intake is common, with more frequent hospitalizations and poor growth. Low serum vitamin D status is highly prevalent in children with SCD; vitamin D status is associated with season and dietary intake. Prepubertal children with SCD may have zinc deficiency and may benefit from zinc supplementation. There is an underlying defect in lipid metabolism associated with SCD, manifested during the fasting state; this abnormality in lipid homeostasis has the potential to alter RBC membrane fluidity and function in SCD patients (Buchowski et al, 2007). Individuals with SCD have reduced levels of EPA and DHA in red cells, platelets, and mononuclear cells due to peroxidation from compromised antioxidant competence (Ren et al, 2008). Because dietary omega-3 fatty acids reduce prothrombotic activity, include omega-3 fatty acids in diet and in supplemental form. Cellular and tissue damage is caused by hypoxia, oxidant damage, inflammation, abnormal intracellular interactions, and reduced nitric oxide bioavailability (Steinberg, 2008). Young children with SCD are at a very high risk of stroke, with microvascular occlusion and painful episodes (Adams, 2007). Aggressive antibiotic therapy and transfusions can save lives. Transfusion is indicated for symptomatic anemia and specifically to prevent stroke, during acute stroke, and for acute chest syndrome (Roseff, 2009). Although life saving, transfusion therapy has resulted in the majority of sickle cell anemia patients being at risk for iron overloading and hemosiderosis-induced organ damage (Vichinsky et al, 2005). Iron overload has become easier to manage with the introduction of an oral iron chelator (Adams, 2007). Acute chest syndrome, triggered by infections and fat clots in the lungs, is the leading cause of death in sickle cell anemia. Treatment includes hydroxyurea therapy to decrease the frequency of painful episodes and hematopoietic cell transplantation (Mehta et al, 2006). Bone marrow transplantation requires a perfect match from a sibling. Because patients with SCD have problems with surgery, including prolonged bleeding, vitamin K should be given preoperatively (Raffini et al, 2006). Use of transcranial Doppler ultrasonography helps identify asymptomatic, at-risk children who should be considered for chronic blood transfusions (Mehta et al, 2006). Studies of gene expression are bringing new solutions. Human progenitor cell (from bone marrow, peripheral blood stem cells, or umbilical blood) transplant can cure the disease and is used for patients with severe disease for whom conventional therapy may not be effective (Roseff, 2009).


CLINICAL INDICATORS Genetic Markers: Sickle cell anemia is an autosomal recessive disease caused by a mutation in the hemoglobin

beta gene (HBB) found on chromosome 11p15.5. Genetic studies have identified regions on chromosome 6q23 and BCL11 A on chromosome 2p16 that account for 20–50% of the common variation in fetal Hgb levels in patients with sickle cell anemia (Thein et al, 2009). SNPs have also been found in KCNK6 (Sebastiani et al, 2009). Serum creatinine Height CBC, WBC N balance Weight Sickle cell test Alb BMI Hgb (often low) CRP Diet history Hct Cholesterol BP Serum Fe Triglycerides I&O (increased (Trig) Chronic anemia, from (decreased) pallor hemolysis) MCV Jaundice RBP Serum ferritin Bone pain (decreased) Partial pressure Abdominal Bilirubin of oxygen pain tHcy (often (pO2) Breathlessness elevated) Partial pressure Lower leg Transferrin of carbon ulcers saturation dioxide Casts or blood in Serum folic acid (pCO2) urine and B12 Uric acid Excessive thirst Serum and (increased) urinary zinc CT scan or MRI PT and INR Clinical/History

Lab Work

INTERVENTION OBJECTIVES • Supplement diet with missing nutrients. Correct any malnutrition. • Reduce oxygen debt and hemolytic crises. • Reduce painful cramps, liver dysfunction, cholelithiasis, jaundice, and hepatitis. • Lessen likelihood of pressure ulcers, infections, and renal failure. Infections may include pneumonia, cholecystitis, osteomyelitis, or urinary tract infections.

SAMPLE NUTRITION CARE PROCESS STEPS Involuntary Weight Loss Assessment Data: Weight pattern, percent desirable body weight, diet history, problems with meal planning or shopping, financial challenges. Nutrition Diagnosis (PES): Involuntary weight loss related to sick cell anemia with inadequate caloric intake as evidenced by 10% loss of usual body weight in the last 2 months. Intervention: Nutrition counseling, encouraging energy-dense foods and favorites. Coordination of care with referral to social service agencies for help with meal preparation and delivery. Monitoring and Evaluation: Weight records, improvements in appetite and intake.

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TABLE 12-17 Equation to Predict Energy Needs in Adolescents with Sickle Cell Disease Basal energy requirements are higher in adolescents with sickle cell anemia than in healthy control subjects (Buchowski et al, 2002) Males: REE (kcal/d) 1305  18.6  weight (kg) 55.7. hemoglobin (g/dL)

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • A phytomedicine, Niprisan, may reduce episodes of SCD crisis associated with severe pain.

REE (kJ/d) 5461  77.7  weight (kg) 233.2  hemoglobin (g/dL)


Females: REE (kcal/d) 1100  13.3  weight (kg) 30.2  hemoglobin (g/dL) REE (kJ/d) 4603  55.6  weight (kg) 126.2  hemoglobin (g/dL)

• Maintain adequate hydration. • Promote normal growth and development, which tend to be stunted in children. • Prevent chronic hypoxia, which can lead to lower intellectual performance. • Improve quality of life and ability to participate in the activities of daily life.

FOOD AND NUTRITION • Include food sources of omega-3 fatty acids; vitamins D, C, A, B12, and B6; folic acid; and HBV proteins; ensure adequate zinc and riboflavin. • Estimate fluid and energy needs; increase diet as needed (Table 12-17). • A multivitamin–mineral supplement should be recommended; one without excess iron is important when transfusions are used. Avoid excesses of iron, including from tube feedings or parenteral nutrition. • Energy deficits are common in this population. Nightly tube feeding can help to improve nutritional status. While supplementation with arginine has been suggested, more studies are needed.

Common Drugs Used and Potential Side Effects • Pain medicines (such as ibuprofen) may be used. Monitor for all side effects and GI distress. • Hydroxyurea therapy (Droxia, Hydrea) can be used to increase Hgb production. • Rofecoxib is a cyclo-oxygenase-2 (COX-2) inhibitor approved for pain and has been tested in children with no adverse effects. • Rituximab may be used to prevent delayed hemolytic transfusion reaction disorder in SCD.


• Indicate which foods are good sources of folic acid, HBV proteins, zinc, riboflavin, and vitamins A, C, D, E, B6, and B12. • Discuss ways for easy meal preparation because fatigue tends to be a problem. • Quality of life is often decreased among adults with SCD, and health professionals should try to offer assistance that will help improve this quality (McClish et al, 2005).

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

American Sickle Cell Association

National Institutes of Health (NIH)–Genes and Disease

NIH–Sickle Cell Anemia

SICKLE CELL ANEMIA—CITED REFERENCES Adams RJ. Big strokes in small persons. Arch Neurol. 64:1567, 2007. Buchowski MS, et al. Defects in postabsorptive plasma homeostasis of fatty acids in sickle cell disease. JPEN J Parenter Enteral Nutr. 31:263, 2007. Edwards CL, et al. A brief review of the pathophysiology, associated pain, and psychosocial issues in sickle cell disease. Int J Behav Med. 12:171, 2005. McClish DK, et al. Health related quality of life in sickle cell patients: the PiSCES project. Health Qual Life Outcomes. 3:50, 2005. Mehta SR, et al. Opportunities to improve outcomes in sickle cell disease. Am Fam Physician. 74:303, 2006. Raffini LJ, et al. Prolongation of the prothrombin time and activated partial thromboplastin time in children with sickle cell disease. Pediatr Blood Cancer. 47:589, 2006. Ren H, et al. Patients with sickle cell disease have reduced blood antioxidant protection. Int J Vitam Nutr Res. 78:139, 2008. Roseff SD. Sickle cell disease: a review. Immunohematology. 25:67, 2009. Sebastiani P, et al. Genetic modifiers of the severity of sickle cell anemia identified through a genome-wide association study. Am J Hematol. 85:29, 2009. Steinberg MH. Sickle cell anemia, the first molecular disease: overview of molecular etiology, pathophysiology, and therapeutic approaches. Scientific World Journal. 8:1295, 2008. Thein SL, et al. Control of fetal hemoglobin: new insights emerging from genomics and clinical implications. Hum Mol Genet. 18:216, 2009. Vichinsky E, et al. Comparison of organ dysfunction in transfused patients with SCD or beta thalassemia. Am J Hematol. 80:70, 2005.

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THALASSEMIAS NUTRITIONAL ACUITY RANKING: LEVEL 1 Recent advances have been beneficial. Bone marrow transplants can be curative for some children with beta thalassemia major. Cord blood is the blood that remains in the umbilical cord and placenta following birth; it is a rich source of stem cells that reproduce into RBCs for the immune system. Stem cell transplantation offers opportunities for individuals with thalassemia to lead a more normal life.


CLINICAL INDICATORS Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND The thalassemias are inherited hematologic disorders caused by defects in the synthesis of one or more of the Hgb chains. Alpha thalassemia is caused by reduced or absent synthesis of alpha globin chains, and beta thalassemia is caused by reduced or absent synthesis of beta globin chains (Muncie and Campbell, 2009). Hemolysis and impaired erythropoiesis occur. Collectively, the thalassemias are among the most common inherited disorders. Alpha-thalassemic syndromes have an increased frequency in African, American Indian, and Asian populations. Beta thalassemia is well recognized in persons of Greek and Italian descent; Cooley’s or Mediterranean anemia is most severe. The beta thalassemias are more common and are a worldwide clinical problem due to an increasing immigrant population (Hahalis et al, 2005). Silent carriers of alpha thalassemia and persons with alpha or beta thalassemia trait are asymptomatic and require no treatment. Alpha thalassemia intermedia (Hgb H disease) causes hemolytic anemia (Muncie and Campbell, 2009). The RBCs are fragile and contain abnormal Hgb. Beta thalassemia major causes hemolytic anemia, poor growth, and skeletal abnormalities during infancy. Symptoms can begin as early as 3 months of age. In the first year or two of life and in the absence of transfusion, a child can demonstrate severe anemia and expansion of the facial and other bones. These children may be pale or jaundiced, have a poor appetite, fail to grow normally, and have an enlarged spleen, liver, or heart. The incidence of gallstones is unusually common in this population. Affected children will require regular lifelong blood transfusions (Hahalis et al, 2005). Blood transfusions and increased gastrointestinal iron absorption result in iron overload and tissue damage. If splenomegaly occurs, a splenectomy may be needed. Excess iron accumulates, leading to liver, heart, and pituitary damage and failure of these organs. Cardiac complications caused by iron deposition, such as cardiomyopathy, are major causes of death (Hahalis et al, 2005). Chelation therapy may be needed.

Genetic Markers: In thalassemia, variations are caused by the severity of the genetic mutations. In thalassemia major or intermedia, reduction in the number of alpha globin genes can ameliorate the disease phenotype; conversely, excess alpha globin genes convert beta thalassemia trait to a clinical picture of thalassemia intermedia (Rund and Fucharoen, 2009). An increase in Hgb F level is variably associated with the presence of beta thalassemia trait. Levels relate to the presence of a polymorphism in the (G)gamma-158 (CT) gene (Mosca et al, 2009). Quantitative Hgb A2 and Height Hgb F Weight Serum Fe BMI (increased) Diet history FEP BP Transferrin iron Growth failure saturation Jaundice percentage I&O (increased) Leg ulcers Serum lead Bone Transferrin abnormalities (decreased) Enlarged spleen SuperconductHypogonadism ing Quantum Anemia Interference Jaundice Device (SQUID) Lab Work Serum ferritin (increased) RBC, CBC H & H (low?) Clinical/History

TIBC (decreased) Thyroidstimulating hormone (TSH) Thyroxine (T4) Alkaline phosphatase (Alk phos) Gluc Vitamin B12 Serum zinc Alb CRP Hypoparathyroidism

INTERVENTION OBJECTIVES • Offer temporary relief with blood transfusions; this will improve hematological status with oxygen availability.

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SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment Data: Growth failure in 6-year old, weight loss of 3# in past 12 months. Poor oral intake and anorexia. Hx of thalassemia intermedia, diagnosed at age 2. Nutrition Diagnoses (PES): Unintentional weight loss related to poor oral intake as evidenced by weight loss of 3# in past year and growth failure (previously 40th percentile, now at 25th percentile for age). Interventions: Food–nutrient delivery: enhance meals and snacks with high-density foods such as milkshakes with dry milk powder and peanut butter added. Educate parents about ways to enhance energy and nutrient density in meals and snacks. Counsel about when to contact the physician (e.g., signs of jaundice, additional weight loss, or chronic anorexia). Monitoring and Evaluation: Improved intake of energy-dense foods and beverages. Growth chart improving over past 3–6 months, closer to 40th percentile again.

• • • •

Correct side effects of iron overloading from the necessary transfusions. Correct failure to thrive and GI problems. Prevent slow or stunted growth. Impaired growth is a problem in children. Reduce or correct infections. Promote healing of any ulcerations. Manage any hyperglycemia.


of this disease (Taher et al, 2005). Side effects include allergic reactions, tinnitus, and erythematous rash. Overchelation may cause growth retardation and mineral deficiency. • Oral iron-binding agents are capable of preventing dietary iron absorption from the diet; oral chelator deferiprone (Ferriprox) is one.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss ways to improve nutritional intake, when deficient. • Discuss importance of diet in the maintenance of hematological health. • Persons with thalassemia should be referred for preconception genetic counseling. Women with alpha thalassemia trait should consider chorionic villus sampling to diagnose infants with Hgb Bart’s, which increases the risk of toxemia and postpartum bleeding (Muncie and Campbell, 2009).

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information

FOOD AND NUTRITION • A diet high in quality protein, energy, B-complex vitamins (especially folic acid and vitamin B12), and zinc will be beneficial. To prevent iron overloading, avoid use of multivitamin–mineral supplements that contain iron and vitamin C in large amounts. • Provide adequate fluid intake. • If hyperglycemia and diabetes are present, use carbohydrate counting and other accepted techniques for managing glucose levels.

Common Drugs Used and Potential Side Effects • Iron-chelating therapy with deferoxamine in patients with thalassemia major has dramatically improved the prognosis

Cooley’s Anemia Foundation

Cord Blood Information

Thalassemia International Federation

THALASSEMIA—CITED REFERENCES Hahalis G, et al. Heart failure in beta-thalassemia syndromes: a decade of progress. Am J Med. 118:957, 2005. Mosca A, et al. The relevance of hemoglobin F measurement in the diagnosis of thalassemias and related hemoglobinopathies. Clin Biochem. 42: 1797, 2009. Muncie HL Jr, Campbell J. Alpha and beta thalassemia. Am Fam Physician. 80:339, 2009. Rund D, Fucharoen S. Genetic modifiers in hemoglobinopathies. Curr Mol Med. 8:600, 2008. Taher A, et al. Comparison between deferoxamine and deferiprone (L1) in iron-loaded thalassemia patients. Eur J Haemetol. 67:30, 2005.

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BLEEDING DISORDERS: HEMORRHAGE AND HEMOPHILIA NUTRITIONAL ACUITY RANKING: LEVEL 2 DEFINITIONS AND BACKGROUND The circulatory system is a closed system, with low volume and high pressure. It provides efficient delivery of nutrients to all tissues. When there is volume loss, a large decrease in nutrient delivery occurs. Hemorrhage is the excessive discharge of blood from a ruptured vessel. Bleeding (bright red in spurts from an artery; dark red and steady flow from a vein) can be external, internal, or into skin or other tissue. When massive, a hemorrhage can cause such symptoms as rapid, shallow breathing; cold, clammy skin; thirst; visual disturbances; and extreme weakness. Loss of more than 20% of blood volume causes hypotension and tachycardia; loss of more than 1 quart of blood may lead to shock. Peptic ulcer, hemophilia, spontaneous liver rupture, or stroke may lead to a hemorrhage. In some cases, surgery may be necessary. In chronic myelogenous leukemia (CML), a slowly progressive disease, platelets are increased in number and easy bleeding occurs. To stop a hemorrhage, blood must clot properly. Blood clots when its fibrinogen is converted to fibrin by action of thrombin. Vitamin K works as a coenzyme that converts glutamic acid to gamma-carboxyglutamic acid; this helps to bind calcium and is required for the activation of the seven vitamin K–dependent clotting factors in the coagulation cascade (Table 12-18). Hemophilia is an inherited bleeding disorder. Diagnosis may be early in life, or later after surgery or trauma. In severe cases, serious bleeding may occur without any cause. While internal bleeding may occur anywhere, bleeding into joints is common. Standard treatment involves replacing the missing clotting factor. In pregnant women who carry the trait, a C-section is often recommended. Von Willebrand disease is the most common hereditary bleeding disorder,

TABLE 12-18

where bleeding gums, abnormal menstrual bleeding, nose bleeds, and bruising are the symptoms. Desamino-8-arginine vasopressin (DDAVP) is given to raise the levels of von Willebrand factor, which reduces the bleeding tendency. The immune response to coagulation factors VIII or IX with formation of inhibitory antibodies complicates the treatment of hemophilia; regulatory T cells (Treg) are an important component of the mechanism by which tolerance is maintained (Cao et al, 2009). New gene therapy and immune tolerance protocols are under study.


CLINICAL INDICATORS Genetic Markers: Hemophilia A, which affects 80–90% of cases, shows a mutation in the FVIII gene. People with Hemophilia B have low or missing levels of clotting factor IX. Hemophilia affects mostly males, although women carry the trait. Clinical/History Height Weight BMI Diet history BP Pulse

Temperature I&O Blood in urine or stool? Petechiae Hemophiliac arthropathy

Excessive or easy bleeding Excessive bruising Nose bleeds Abnormal menstrual bleeding

Blood Clotting Factors That Involve Nutrition

The coagulation cascade involves a series of steps that stop bleeding through clot formation. Vitamin K–dependent coagulation factors are synthesized in the liver. Consequently, severe liver disease results in lower blood levels of vitamin K–dependent clotting factors and an increased risk of uncontrolled bleeding (hemorrhage). The following factors involve nutrition: I. Fibrinogen II. Prothrombin III. Thromboplastin IV. Calcium In hemostatic (bleeding) disorders, it is important to evaluate for bleeding problems in the family history, history of heavy menses or easy bruising, and prior blood transfusions. Bleeding disorders include a number of conditions in which people tend to bleed longer. Clotting involves about 20 different plasma proteins (clotting factors). Normally, clotting factors form fibrin that stops bleeding. In bleeding disorders, the process does not occur normally Some bleeding disorders are present at birth (hemophilia and von Willebrand’s disease), or they can be acquired (such as vitamin K deficiency, severe liver disease, use of anticoagulant drugs or prolonged use of antibiotics, bone marrow problems, leukemia, pregnancy-associated eclampsia, or snake bite). In these disorders, vision loss can occur from bleeding into the eye, or anemia may result, or there may be neurological problems or even death. Gene therapy may one day be available to treat the bleeding disorders.

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Lab Work Coagulation testing PT, International normalized ratio (INR)— prolonged? Activated partial thromboplastin time (aPTT)

Thrombin time (thrombin added to plasma, and time to clot measured) Fibrinogen Platelet count (may be normal) Von Willebrand factor level (reduced?)

Transferrin RBC Alb BUN CBC H&H Serum Fe Serum folic acid and B12 TIBC (increased) Creatinine CRP

INTERVENTION OBJECTIVES • Medical management is designed to control bleeding, take care of the underlying cause of the bleeding, and replace lost blood. Transfusions may be needed. Less severe hemorrhages may require iron, vitamin B12, and folic acid to help replace RBCs. • Support erythropoiesis. • Control intestinal impact of gastrointestinal bleeding, which can cause a protein overload. • Prevent hypovolemic shock (low cardiac output, decreased blood pressure, and decreased urinary output) from uncontrolled bleeding.

FOOD AND NUTRITION • Ensure that diet is rich in proteins, iron, folic acid, vitamin B12, and copper. • Check need for vitamin K. Patients with intestinal or liver disease may become deficient. If medications to replace

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake Assessment Data: Bleeding disorder (Hemophilia A) with easy bruising and blood in urine and stool. Currently taking Alphanate; scheduled for dental surgery in 2 weeks. Serum vitamin K levels low. Diet hx shows little intake of any vitamin K–rich foods. Nutrition Diagnoses (PES): Inadequate vitamin K intake related to hereditary bleeding disorder and minimal dietary intake as evidenced by low serum vitamin K levels, easy bruising and blood in urine and stool even while taking Alphanate. Interventions: Food–nutrient delivery: identify foods that could be included and tolerated. Educate about the sources of vitamin K from diet. Counsel about multivitamin–mineral supplements that contain a desired dose of vitamin K (10–120 g per dose). Monitoring and Evaluation: Fewer episodes of blood in urine and stool; less easy bruising. Tolerance for multivitamin–mineral supplement and foods. Improved serum levels of vitamin K. No difficulty with dental surgery and excessive bleeding.

TABLE 12-19 Food

Food Sources of Vitamin K Serving

Vitamin K (g)

Kale, raw

One cup (chopped)


Broccoli, cooked

One cup (chopped)


Parsley, raw

One cup (chopped)


Swiss chard, raw

One cup (chopped)


Spinach, raw

One cup (chopped)


Leaf lettuce, raw

One cup (shredded)


Watercress, raw

One cup (chopped)


Soybean oil

One tbsp


Canola oil

One tbsp



One tbsp


Olive oil

One tbsp


Source: U.S. Department of Agriculture. USDA national nutrient database for standard reference, release 16. Available at SR16/wtrank/wt_rank.html.

vitamin K are used, diet should provide a balance without excess. Monitor content of meals or enteral feedings and multivitamin supplements carefully to ensure that all RDAs are met without excesses (Table 12-19).

Common Drugs Used and Potential Side Effects • Avoid aspirin, NSAIDs, and other blood thinners. Oral anticoagulants, such as Warfarin, inhibit coagulation through antagonism of the action of vitamin K. Inadequate gamma-carboxylation of vitamin K–dependent proteins will inhibit clot formation. Patients taking these drugs are cautioned against consuming very large or highly variable quantities of vitamin K in their diets; they need a reasonably constant dietary intake. • If vitamin K is needed, it is available in multivitamins and other supplements in doses that range from 10 to 120 g per dose. • Alphanate (antihemophilic factor) is approved to decrease bleeding in patients with bleeding diseases who must have surgery or other invasive procedures. People with hemophilia and their families can be taught to give factor VIII concentrates at home at the first signs of bleeding. XYNTHA is a new recombinant factor VIII product for both the control and prevention of bleeding episodes and surgical prophylaxis. • FEIBA therapy, consisting of activated prothrombin complex concentrate (aPCC) and recombinant activated factor VII (rFVIIa), is effective and safe for reducing bleeding in hemophilia A (Valentino, 2009).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Potential adverse effects of high vitamin E intakes in humans, such as bleeding, are not clear (Hathcock et al, 2005).

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Blood donors should be alerted to the need to replace daily iron intake by 0.7 mg for a year. Every pint is equivalent to 250 mg of iron lost. • Discuss adequate dietary replacement for lost nutrients. A multivitamin–mineral supplement may be indicated.

Blood Line

International Society on Thrombosis and Haemostasis

National Hemophilia Foundation

World Federation of Hemophilia Gudelines_Mng_Hemophilia.pdf

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

All About Bleeding

Anemia from Excessive Bleeding

HEMORRHAGE AND BLEEDING DISORDERS—CITED REFERENCES Cao O, et al. Role of regulatory T cells in tolerance to coagulation factors. J Thromb Haemost. 7:88S, 2009. Hathcock JN, et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr. 81:736, 2005. Valentino LA. Assessing the benefits of FEIBA prophylaxis in haemophilia patients with inhibitors. Haemophilia. 2009 Dec 16. [Epub ahead of print]


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

DEFINITIONS AND BACKGROUND Hereditary hemochromatosis (HH) is one of the most common autosomal recessive disorders among Caucasians. One in 200–400 individuals of Northern European ancestry is at risk for hemochromatosis (Camaschella and Merlini, 2005). It is also common in Hispanics or people of Mediterranean descent and is 10 times more common in males than

females. Irish Americans and African–Americans have double the usual frequency. Tragically, hemochromatosis remains underdiagnosed. In hemochromatosis, iron stores are deposited in excess, often from excess intake or liver/pancreatic diseases, renal dialysis, or frequent and long-term transfusions. Healthy people may accumulate up to 1 g of iron, but people with this condition accumulate 15–30 g. Increased iron absorption leads to excessive accumulation of iron deposits within cells of the liver, heart, pituitary gland, pancreas, and other organs, gradually causing tissue damage. Because hemochromatosis has many possible symptoms, it often goes undiagnosed. However, early detection is important and may prevent organ failure that can occur if it is left untreated. Long-term complications include liver cirrhosis, diabetes, cardiomyopathy, hypogonadism, arthropathy, skin pigmentation, and susceptibility to liver cancer (Camaschella and Merlini, 2005) (Table 12-20). Iron overload patients may have diagnoses other than HH: non-alcoholic fatty liver disease (NAFLD), chronic hepatitis C, and chronic alcohol use are most common (Dever et al, 2009). Iron toxicity can also occur in aplastic anemia, chronic hemolytic anemia, porphyria cutanea tarda, sideroblastic anemia, thalassemias, diabetes, rheumatoid arthritis, or transfusional iron overload. Sometimes, individuals with Alzheimer’s or Parkinson’s disease may have heavy metal toxicities that contribute to an iron overload. Free iron is destructive to cells, and too much iron can be a carcinogen because cancer cells need it for their DNA synthesis. With chronic kidney disease, keep serum ferritin levels below 500 ng/dL. Porphyrias are rare disorders caused by lack of the enzymes necessary for production of heme; this causes heme precursors, porphyrins, to accumulate in the bone marrow, liver, and bloodstream (MedlinePlus, 2009). The porphyrins may also

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TABLE 12-20


Facts About Hemochromatosis

1. Undetected or untreated excess iron kills after inflicting injury to a variety of body organs. The physician’s concern must be to detect any excess iron instead of establishing the diagnosis 2. Some literature suggests treatment when ferritin alone is elevated. Giving blood does no harm and, instead, is beneficial to health. About one fourth of patients have low hemoglobin; treatment is the same unless the anemia is so severe that blood transfusions are required. Severely anemic patients require iron removal by an iron chelator, Desferal 3. Iron overloading is preventable. When diagnosis is in doubt, the patient should begin a trial of weekly phlebotomies at the blood bank. Four to 6 weeks will usually provide the answer, and getting rid of a little excess iron will improve health 4. The patient should be taken to the blood bank upon the physician’s order for weekly phlebotomies 5. A liver biopsy is not always necessary, and waiting can delay important treatment. DNA testing is not useful because it cannot detect all of the known mutations 6. When iron levels test low, the cause must be found. It is dangerous to medicate with iron without testing first and then finding the reason for any deficiency 7. Symptoms vary. Chronic fatigue, arthritis, anemia (iron-loading anemia is one symptom), and elevated liver enzymes must not be ignored. Hemoglobin level does not indicate iron status. A disorder of thyroid or any part of the body can be a symptom of iron overload 8. Excess iron lowers immunity. Many diseases (such as cancer, hepatitis, and AIDS) will show a poor outcome unless any excess iron is removed. Excess iron stored in the brain exacerbates severity in Alzheimer’s, multiple sclerosis, Lou Gehrig’s disease, Parkinson’s disease, psychological problems, autism, and other diseases Adapted from: Iron Overload Diseases Association,, accessed December 23, 2009.

be excreted in the urine or stool. Most porphyrias are hereditary, but attacks may also be triggered by drugs, alcohol, hormones, or infections. Acute, hepatic porphyrias affect the nervous system. Symptoms include nerve damage with pain or paralysis, abdominal pain and liver damage, red or brown urine, anxiety and delirium, muscle pain or weakness, numbness or tingling, tachycardia, loss of deep tendon reflexes, low blood pressure, and electrolyte imbalances. Constipation or diarrhea may occur. A diet high in carbohydrate (55–60% of total kilocalories) and beta carotene may be beneficial (MedlinePlus, 2009). Porphyria cutanea tarda (PCT) can occur without an inherited enzyme deficiency. The porphyrins accumulate in the liver and skin, causing photosensitivity, skin damage, and cirrhosis. Phlebotomy removes excess iron, and chloroquine or hydroxychloroquine removes the excess porphyrins from the liver (Anderson, 2007).

Profound fatigue (in HH) Arthralgia (in HH) Loss of body hair Loss of libido Lack of menstruation or early menopause Abdominal pain Chronic intermittent diarrhea Irregular heartbeat Cardiomegaly with congestive failure Hepatomegaly


Serum Cu (increased) Alb Serum Fe Ferritin (increased 1000 ng/ Lab Work mL?) Hgb (desirable

Transferrin-Iron 10 g/dL) Saturation Hct (desirable

a Percentage 30–35%) (normal Gluc 25–35%)— Serum B6 best test Serum B12 TIBC Serum folic acid (normal, Thyroid tests 12–45%) Liver function Transferrin tests (increased) CRP Enlarged spleen Hypothyroidism Depression Liver biopsy Bone marrow studies


Divide total serum iron by TIBC for percentage of tissue saturation (TS). Divide the serum iron level by TIBC for percentage of transferrin saturation.

CLINICAL INDICATORS INTERVENTION Genetic Markers: HH is recessive, requiring the gene from two carrier parents. There are several types of genetic hemochromatosis: type I or classic (HHC); type II a, b, or juvenile (JHC); type III or transferrin receptor mutation; and type IV or ferroportin mutation. Iron overload can also occur in individuals with the HFE C2824 gene in 1 out of 200 people. Clinical/History Height Weight

BMI Diet history BP

I&O Bronzing of the skin

OBJECTIVES • Remove excess iron from body (usually with phlebotomies of 500 mL weekly, performed by the physician over several months). Then therapy is repeated several times annually for rest of the life. • Prevent liver cancer, heart attack, or stroke by unloading storage iron as fast as possible; keep serum ferritin at low normal range. • If excess iron intake is a chronic problem, discontinue use in supplements and fortified foods (such as iron-fortified cereals). Read labels carefully.

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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Mineral Intake Assessment Data: Male with transferrin-iron saturation percentage (46%), ferritin (160 ng/mL), elevated H & H. Diagnosis of iron overloading. Diet hx reveals high intake of animal proteins and heme iron (about 20 g/day). Nutrition Diagnoses (PES): Excessive iron intake related to diet high in animal proteins and heme iron as evidenced by transferrin-iron saturation percentage (46%), ferritin (160 ng/mL), elevated H & H. Interventions: Food–nutrient delivery—encourage more vegetarian meals and fewer ounces of meats at mealtime. Educate about the role of heme iron intake in iron overloading disorders. Counsel and provide meal planning tips and portion guides for intake of meats. Monitoring and Evaluation: Improvement in serum laboratories (transferrin-iron saturation percentage, ferritin, and H & H) with levels closer to normal. Diet hx reveals improved intake of 8–10 g/day.

• Teach principles of nutrition and menu planning to incorporate adequate intake of other nutrients that may be depleted with excessive phlebotomies (e.g., folate and other B-complex vitamins, protein).

FOOD AND NUTRITION • Provide a normal diet unless renal or hepatic function is altered. Do not consume foods or take supplements high in vitamin C. Read cereal labels and avoid those with 100% or more of the daily allowance for iron and vitamin C. A low-iron diet is not recommended. • Ensure adequate protein and sufficient energy intake to meet estimated needs and activity levels. • Avoid alcohol because of potential damage to a vulnerable liver.

Common Drugs Used and Potential Side Effects • Avoid use of multivitamin supplements that contain iron and vitamin C because these can increase iron absorption.

• An iron chelator may be needed, such as deferoxamine (DFO). This is given intravenously 8–12 hours for up to five times in a week. It can be neurotoxic.

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

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • All blood relatives of the patient must be evaluated and monitored yearly for iron overloading. • Genetic testing of other family members is also recommended for those with inherited type. • Discuss avoidance of alcohol and raw seafood. Vibrio vulnificus in some raw seafood kills people every year; many are those with undetected iron overload. • Discuss nutrient sources as appropriate for the individual.

Patient Education—Food Safety • If tube feeding or CPN is needed, careful handwashing procedures should be followed. • Avoid eating raw seafood.

For More Information •

Iron Disorders Institute

Iron Facts

Iron Overload Diseases Association, Inc.

Iron Tests

HEMOCHROMATOSIS—CITED REFERENCES Anderson K. The porphyrias. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:229. Camaschella C, Merlini R. Inherited hemochromatosis: from genetics to clinics. Minerva Med. 96:207, 2005. Dever JB, et al. Phenotypic characteristics and diagnoses of patients referred to an iron overload clinic. Dig Dis Sci. 2009 Dec 24. [Epub ahead of print] MedlinePlus. Porphyrias. Web site accessed December 28,2009, at http://

POLYCYTHEMIA VERA NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Polycythemia vera (PV) is a chronic, progressive disease in which increased blood volume and increased erythrocyte production occur. Other names include erythremia,

Osler–Vasquez disease, and polycythemia rubra vera. Hematological disorders like PV can result in elevated levels of cobalamin, which is released during hepatic cytolysis. The cause of PV is unknown, and the disease is considered a hematological malignancy. The disease develops

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slowly and may progress to acute myelogenous leukemia. The average age at diagnosis is 50–60 years. Incidence is highest among those of Jewish ancestry, occurring in 2 of 100,000 of the population. Increased viscosity of the blood and number of platelets result in a high risk for clot formation and stroke, hemorrhage, or myocardial infarction. Patients with PV frequently develop hyperhomocysteinemia due to discrete depletion of cobalamin or folate; vitamin therapy should be considered. With treatment, individuals with this condition may live for 15–20 years. Phlebotomy or medications may be used.



SAMPLE NUTRITION CARE PROCESS STEPS Abnormal GI Function Assessment Data: BMI 20. Constipation, flatulence, history of gastric bleeding, and ulceration. Nutrition Diagnoses (PES): Abnormal GI function related to discomfort and pain as evidenced by constipation, flatulence, GI ulceration, and bleeding. Interventions: Food–nutrient delivery—use comfort foods and adequate CHO, fiber, and fluid intake; reduce acidic foods and items not well tolerated. Educate about good nutrition and inclusion of B-complex vitamins. Counsel about individualizing tolerance for medications with appropriate food, fluid, and snacks. Monitoring and Evaluation: Daily use of prescribed medications. Improvement in GI function; resolution of constipation and flatulence. No additional GI bleeding.

CLINICAL INDICATORS Genetic Markers: The somatic V617 F mutation in the Janus kinase (JAK) 2 gene, which causes a valine to phenylalanine substitution at position 617, has recently been found in the majority of patients with PV (Meyer, 2009). Clinical/History Height Weight BMI Diet history I&O BP (hypertension?) Belching, fullness Flatulence Peptic ulcer? Constipation Headache Vertigo Lassitude Tinnitus Pruritus after bathing Transient blurred vision, diplopia Dyspnea Chest pain

Dusky reddish skin on face and hands Hemorrhagic tendency Seizures, confusion Splenomegaly Tinnitus Paresthesias Gout Lab Work Hgb (18 g/dL) Hct (52% for men; 47% for women) Platelets (elevated) Leukocytes (elevated) Serum B12 (elevated)

Erythropoietin (low) TIBC Erythrocyte sedimentation rate (ESR) Leukocyte Alk phos Serum ferritin Gluc RBC (7–12 million) Oxygen saturation 92% CRP Alb, transthyretin CRP Chol, Trig BUN, Creat Uric acid (elevated) Bone marrow biopsy


• Correct or control condition. • Manage any side effects such as heart failure, peptic ulcer disease, gastric bleeding, gout, leukemia, and seizures.

FOOD AND NUTRITION • A high CHO diet with preferred foods and balanced meals should be offered. Monitor for the need for vitamin or mineral supplementation. Include foods rich in beta carotene. • Extra fluids will be helpful (35–40 mL/kg, unless contraindicated, as with heart failure). • Changes in dietary texture or content may be needed if radiation or chemotherapy alters nutrient or dietary needs.

Common Drugs Used and Potential Side Effects • Myelosuppressive agents may be prescribed. Anagrelide hydrochloride (Agrylin) is an oral imidazoquinazoline agent that has been shown to reduce elevated platelet counts and the risk of thrombosis. Interferon alpha may be used in younger patients; pegylated interferon alpha-2a (PEG-IFN-alpha-2a) is beneficial (Quintas-Cardama et al, 2009). • The antimetabolite hydroxyurea may be used. Side effects include anemia and skin ulcers. • Chemotherapeutic agents (busulfan, chlorambucil, and cyclophosphamide) may cause nausea and vomiting or weight loss. • Low-dose aspirin is sometimes used in patients with thrombotic or ischemic conditions. It can relieve some of the burning sensations in the feet and hands. Antihistamines can help reduce itching sensation.

OBJECTIVES • Prepare patient for phlebotomy by ensuring adequate nutrient stores. • Prepare, as needed, for chemotherapy or radiation therapy, which may be provided.

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

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NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss need to maintain a healthy lifestyle and to eat adequate protein and calories because of the frequent phlebotomies, where completed. • Discuss ways to make meals that are nutritious yet simple to prepare. • Tepid oatmeal baths may help reduce pruritus.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

Mayo Clinic – PV

Merck Manual–Blood Disorders

Myeloproliferative Disorders

POLYCYTHEMIA VERA—CITED REFERENCES Meyer T. Activated STAT1 and STAT5 transcription factors in extramedullary hematopoietic tissue in a polycythemia vera patient carrying the JAK2 V617 F mutation. Int J Hematol. [Epub ahead of print] Quintas-Cardama A, et al. Pegylated interferon alfa-2 a yields high rates of hematologic and molecular response in patients with advanced essential thrombocythemia and polycythemia vera. J Clin Oncol. 27:5418, 2009.

THROMBOCYTOPENIA NUTRITIONAL ACUITY RANKING: LEVEL 1 missing enzyme. Mortality of TTP has decreased from 90% to 10% (George, 2009); survival improved dramatically with plasma exchange treatments after the 1980s (KremerHovinga et al, 2009). Unfortunately, adults with TTP of any etiology have a high risk for persistent minor cognitive abnormalities (George, 2009).


CLINICAL INDICATORS Adapted from: Anderson’s Atlas of Hematology; Anderson, Shauna C., PhD. Copyright 2003, Wolters Kluwer Health/Lippincott Williams & Wilkins.

DEFINITIONS AND BACKGROUND Thrombocytopenia purpura, a myeloproliferative disorder, is a blood disease affecting the clotting factor (platelets) of the blood, with an abnormally low platelet count and shorter than normal (10 days) platelet survival time. Thrombocytopenia is the most common cause of bleeding, usually from small capillaries. Women are more affected than men. There are many reasons for the development of decreased marrow production or platelet destruction that causes thrombocytopenia, including some hereditary causes. These can sometimes be determined by examination of bone marrow. Idiopathic thrombocytopenic purpura (ITP) is caused by platelet destruction by antibodies. Thrombotic thrombocytopenic purpura (TTP) is manifested by vascular lesions. Plasma exchange (plasmapheresis) is used to remove the abnormal antibody from the blood and replace the

Genetic Markers: Mutations in the ADAMTS13 gene cause the familial form of TPP. Alterations in the ADAMTS13 gene reduces instructions for the normal process of blood clotting. Clinical/History Height Weight BMI Diet history I&O BP Nosebleeds Bleeding from other sites Bruising Pinpoint red spots on skin Headache

Slurred speech Numbness and weakness of extremities Fever? Pallor Jaundice Shortness of breath Lab Work CBC (low platelets)

H&H (decreased) Alb, transthyretin N balance PT and PTT (normal) Casts in urine Proteinuria CRP Ca Na, K

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SAMPLE NUTRITION CARE PROCESS STEPS Self-Feeding Difficulty Assessment Data: BMI at lower end of normal, but some weight loss noted. Dx of TPP with numbness and weakness in hands and feet. Inability to feed self and remain independent; depression and easy frustration noted at mealtimes. Nutrition Diagnoses (PES): Self-feeding difficulty related to numbness in hands as evidenced by inability to hold traditional utensils.


• Corticosteroids such as prednisone may be used to control bleeding. Side effects are numerous and may affect nutritional status (e.g., decreased serum calcium, potassium, and nitrogen; increased serum sodium; and glucose intolerance may occur). • Myelosuppressive agents are often prescribed. Anagrelide hydrochloride (Agrylin) is an oral imidazoquinazoline agent that has been shown to reduce elevated platelet counts and the risk of thrombosis. Interferon alpha may be used. • Rituximab seems to be a promising drug in the treatment of refractory autoimmune thrombocytopenia.

Interventions: Food–nutrient delivery—alter food choices to simplify options and offer more finger foods. Educate about use of adaptive feeding equipment that can be used for more independence. Counseling with tips on meal simplification.

Herbs, Botanicals, and Supplements

Monitoring and Evaluation: Improved ability to feed self independently. No further weight loss. Less depression and frustration at mealtimes.

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


INTERVENTION OBJECTIVES • Avoid infections, especially upper respiratory infections and flu to prevent coughing, which increases intracranial pressure. • Reduce bleeding tendency and complications, such as intracranial hemorrhage or GI bleeding (Goldman, 2007). • Rest frequently. • Prepare patient for splenectomy, if indicated. Ensure adequate nutrient stores.

FOOD AND NUTRITION • Maintain diet of preference. Use small, frequent feedings if patient has nausea or vomiting. • Adequate folic acid will be needed. • Increase fluids (e.g., 3 L/d) unless contraindicated. • After splenectomy, patient will need adequate protein, energy, zinc, and vitamins A and C for wound healing. Vitamin K from the diet and supplements may need to be monitored.

Common Drugs Used and Potential Side Effects • Most drugs are stopped because nearly any drug may aggravate the condition.

• Discuss altering nutrients as needed, depending on medications ordered and their use over time; surgery, if required; and ability to eat adequately.

Patient Education—Food Safety If tube feeding or CPN is needed, careful handwashing procedures should be followed.

For More Information •

The ITP Society of the Children’s Blood Foundation

Platelet Disorder Support Foundation

THROMBOCYTOPENIA—CITED REFERENCES George JN. The thrombotic thrombocytopenic purpura and hemolytic uremic syndromes: evaluation, management, and long-term outcomes experience of the Oklahoma TTP-HUS Registry, 1989–2007. Kidney Int Suppl. 112:52S, 2009. Goldman L. Ausiello D. Cecil Textbook of Medicine. 23rd ed. Philadelphia, Pa: WB Saunders; 1291–1299, 2007. Kremer-Hovinga JA, et al. Survival and relapse in patients with thrombotic thrombocytopenic purpura. Blood. 2009 Dec 23. [Epub ahead of print]

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CHIEF ASSESSMENT FACTORS American Cancer Society’s Seven Warning Signs of Cancer

• • • • • • •

Change in Bowel/Bladder Habits Indigestion or Dysphagia Nagging Cough or Hoarseness Obvious Change in Wart or Mole Sore That Does Not Heal Thickening or Lump in Breast or Elsewhere Unusual Bleeding or Discharge

Other Factors

• • • • • • • • • • • • • • • • •

Anorexia or Chronic Nausea Changes in Food Intake, Usual Functional Capacity, Energy Levels Depression Diarrhea Dry Mouth Dysphagia, Esophagitis, Mouth Sores, Mucositis Edema or Ascites Fever of Unknown Origin (Hematological, Liver, Pancreatic, Brain, Kidney Cancers) History of Carcinogen Exposure, Tobacco Use, Excessive Alcohol Use Intolerance for Nauseating Odors Muscle Wasting Nutrient Intake and Immune Function Pain Participation in Complementary and Alternative Medicine Treatments Side Effects of Medications Vomiting Weight Changes—Unintended Weight Loss or BMI Less Than 22

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TABLE 13-1

Cancer Definitions






Cancer that starts in the glands.



Benign growth that may or may not transform into cancer.

Cancer where bone marrow–produced abnormal white blood cells crowd out normal white blood cells, red blood cells, and platelets.


Process of stopping a tumor from growing new blood vessels.



Proteins in the immune system; in cancer, antibodies are used to recognize specific cancer cell receptors and to act as smart bombs.

AIDS-related lymphoma; cutaneous T-cell lymphoma; Hodgkin’s lymphoma; mycosis fungoides; non-Hodgkin’s lymphoma; primary central nervous system lymphoma; Sézary’s syndrome; and Waldenstrom’s macroglobulinemia.

Basal cell carcinoma

Most common form of skin cancer, affecting 800,000 Americans each year. Chronic exposure to sunlight causes most basal cell carcinomas, which occur most frequently on exposed parts (e.g., face, ears, neck, scalp, shoulders, and back).

Male reproductive cancers

Penile, testicular cancers, prostate cancers.


Tumors affecting the meninges.


Rare cancer affecting the lining of the chest, heart, and abdominal cavity from exposure to asbestos.

Treatment to stimulate or restore the ability of the immune system to fight infection and disease and to lessen side effects that may be caused by some cancer treatments; also known as immunotherapy, biological therapy, or biological response modifier (BRM) therapy.


Transfer of disease from one organ to another that is not directly connected to it; particularly the spread of carcinoma.

Monoclonal antibodies

Targeted therapy to locate and bind cancer cells. May be used alone or used to deliver drugs, toxins, or radioactive material directly to tumor cells.


Abnormal, uncontrolled growth of cells in a lump or mass that also destroys normal tissue. Oncogenes in a tumor cell may be identifying markers.


A tumor composed of nerve cells, which may occur along any nerve.

Oat cell carcinoma


Cancer involving epithelial tissue and coverings of internal and external surfaces; lungs, colon, breast, stomach, uterus, skin, and tongue cancers. 80–90% of all cancers.

A rapidly spreading, highly fatal cancer of the bronchus.


Scientific study of tumors.


Most common bone cancer, which develops in new tissue in growing bones, affecting young people and more males.

Palliative therapy

Pain relief but not expected to cure the disease. Given to improve quality of life as much as possible.


Treatment with high-energy rays to kill or damage cancer cells. May be external rays or internally placed radioactive material.


Cancer arising from bone or connective tissue, which sometimes spreads into blood or lymphatic tissues.

Small cell carcinoma

Carcinoma that most commonly arises in the lung but can occur as a cancer in other body sites including the prostate, cervix, and head and neck; responsive to chemotherapy and radiation therapy.


To stimulate the immune system to mount a defense against cancer cells. Example – the cervical cancer vaccine.



Use of medications to kill malignant cells.

Curative Therapy

Permanent removal of the cancer from the body.

Endocrine system cancers

Adrenocortical carcinoma; gastrointestinal carcinoid tumor; pancreatic islet cell carcinoma; parathyroid cancer; pheochromocytoma; pituitary tumor; and thyroid cancer.


Carcinoma consisting of many epithelial cells.

Gastrointestinal (GI) cancers

Anal cancer; bile duct cancer; colon cancer; esophageal cancer; gallbladder cancer; GI carcinoid tumor; liver cancers; pancreatic cancer; rectal cancer; small intestine cancer; stomach cancer.

Gynecological cancer

Hormonal therapy

Female reproductive system: cervical cancer; endometrial cancer; gestational trophoblastic tumor; ovarian epithelial cancer; ovarian germ cell tumor; ovarian low malignant potential tumor; sarcoma; vaginal cancer; and vulvar cancer. Treatment by surgery or by shrinking or killing hormone-dependent cancers.

Definitions: and Types of cancers:, accessed December 29, 2009.

For More General Information on Cancer: Table 13-1 provides a list of cancer definitions.

American Institute for Cancer Research (AICR)

AMC Cancer Research Center and Foundation

Cancer Care

American Cancer Society

Cancer Screening Guidelines

American Dietetic Association Oncology Nutrition Dietetic Practice Group

Caring 4 Cancer

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Eating Hints for Cancer Patients

National Coalition for Cancer Survivorship

Genetics 101 project/info.shtml

National Institutes of Health Gene Testing

Harvard–Dana-Farber Cancer Institute

National Toxicology Program

Harvard Center for Risk Analysis

North American Cancer Registry

Hospice Net

Oncology Association of Naturopathic Medicine

Human Carcinogens

Oncology Nursing Society

Journal of the National Cancer Institute

Online Human Genome Resources

Lance Armstrong Foundation

Vital Options

National Cancer Institute


CANCER PREVENTION AND RISK REDUCTION Cancer results from dysregulated cell growth control and is caused by an interaction of dietary, genetic, and environmental risk factors. There are over 100 variations of cancer. Cancer has a strong genetic component, associated with initiation, promotion, and metastatic growth. The Human Genome Project has identified 30,000 human protein-coding genes. Individualized DNA methylation helps to control gene expression. Genotyping resources allow cancer prevention investigators to identify which genetic subsets of patients are likely to benefit most from chemoprevention and interventions. This emerging science of nutritional genomics is very promising (Kauwell, 2005). Natural carcinogens include ultraviolet (UV) radiation, dyes, environmental chemicals from smoke or mines, viruses, nitrosamines, aflatoxins, and safrole. The most consistent carcinogen is tobacco. Approximately 30% of cancers also have a nutrition or dietary component (Williams and Hord, 2005). Functional food components greatly impact the incidence and treatment of cancer. In addition, food intake, aging, and immune function share a complex relationship; selenium, EPA, DHA, vitamin A, and sodium seem to be particularly important (Wardwell et al, 2008). Nutritive and nonnutritive dietary constituents can either promote or hinder the development of cancer, individualized by genetic predisposition. Diets rich in carotenoids, antioxidative vitamins, phenolic compounds, terpenoids, steroids, indoles, and fibers reduce the risk of cancer and related chronic diseases (Aggarwal and Shishorida, 2004). Studies support the role of flavonoids, carotenoids, curcumin, ascorbic acid, and citrus liminoids (Patil et al, 2009). Polyphenols are the most abundant antioxidants in the average diet and are constituents of fruits, vegetables, cereals, dry legumes, chocolate, tea, coffee, and wine. The strongest evidence linking specific foods to a decreased risk of certain cancers is related to the consump-

tion of fruits, vegetables, and whole grains. Antioxidants protect against free radical damage, improving the resistance of cells to oxidative stress. In a study using HANES data, daily intakes of antioxidants from both diet and supplements averaged 208 milligrams of vitamin C, 20 milligrams of alpha-tocopherol, 223 retinol activity equivalents (RAE) of carotenes, 122 micrograms of selenium, and 210 milligrams of dietary flavonoids (Chun et al, 2009). Women, older adults, Caucasians, nonconsumers of alcohol, nonsmokers, and those with a higher income and exercise level than other tended to have better intakes (Chun et al, 2009). Key nutrients, chemoprotective phytochemicals, and functional food ingredients are listed in Table 13-2. Promoting fruits, vegetables, and whole grains is the key message. Choose “better for you” foods, and make vegetables the central focus of the plate. Minimize meats, or use leaner cuts. Enhance the diet with nuts and whole grains (insoluble types to increase stool bulk and push bile out; soluble types for their cholesterol-lowering effect). A complete “anticancer” grocery list includes dark green, yellow, and orange fruits or vegetables; red grapes; cruciferous vegetables; orange juice; tomatoes; olive and canola oils; garlic; legumes; strong coffee; whole grains; soy; and other plant estrogens. Dietary factors and physical inactivity contribute to approximately one-third of all cancers. Table 13-3 provides a list of important dietary factors. Excess body weight increases the risk of several cancers. There are five lifestyle habits to promote: maintain BMI 25, get 30 minutes of exercise, limit alcohol to—one to two drinks daily, do not smoke, and choose a healthy diet rich in phytochemicals. Many cancer patients try CAM therapies; fish oil is the leading choice of adults. Yet the emphasis remains on food sources, not supplements or pills. The intake of whole foods and fortified, enriched, or enhanced foods has the most beneficial impact on health (American Dietetic Association, 2009).

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TABLE 13-2

Phytochemicals, Functional Food Ingredients, and Cancer

Phytochemicals are functional foods or ingredients that occur naturally in fruits and vegetables and whole grains, often to protect against microorganisms. They are not “essential� nutrients, but some phytochemicals function as antioxidants to squelch free radicals. Food

Functional Ingredient

Possible Roles in Reducing Cancer Risk

Apples (MALUS sp., Rosaceae)

Hydroxycinnamic acids, dihydrochalcones, catechins and oligomeric procyanidins

Also contain triterpenoids in apple peel and anthocyanins in red apples. Protect against skin, lung, breast, and colon cancer (Gerhauser, 2008).

Apples, black tea, grapefruit, onions, arugula

Quercetin, kaempferol, myricetin, isorhamnetin (flavonols)

Decreases ascorbate-dependent free radical oxidation; decreases inflammation and tumorigenesis. May be protective against colorectal cancer. Since apple skins retain pesticides, choose organic.

Beans and legumes, soybeans, whole grains, alfalfa, lentils, bean sprouts

Saponins: oleanic acid, hedagenin (terpenes)

Triterpene glycosides that neutralize enzymes in the intestine that may cause cancer; they boost immunity. Consume only moderate amounts of soy as part of a healthy plant-based diet.

Beef, lamb, yogurt, some cheeses and dairy products

Conjugated linoleic acid

Maintains immune function and normal body composition; some antitumor properties. Marinate meats in red wine or beer to cut heterocyclic amine exposure; do not burn meats.

Bell peppers, citrus fruits

Vitamin C

Protects against damage from free radicals.

Blueberries (particularly skins), blackberries, raspberries, strawberries, cherries, red grapes, red cabbage, eggplant, red onion, kidney beans, red beans, beets, black currants, elderberries, purple sweet potato skin, prunes

Anthocyanins (polyphenols/ flavonols)

Bolsters cellular antioxidant defenses particularly against UV radiation; maintain brain function and motor function; neutralize free radicals; have antimicrobial action.

Brazil nuts, lean meats, tuna, salmon, seafood

Selenium and Glutathione

Increases immune cell functioning, DNA methylation, and regulation of cytokine production. Protects from damage from free radicals. SELECT study found that a 200-milligram selenium supplement actually promotes prostate cancer.

Broccoli, broccoli sprouts, horseradish, cauliflower, cabbage, bok choy, Brussels sprouts, kale

Sulforaphane; thiols

Isothiocyanates (ITCs) protect the body from cancer by inducing detoxification enzymes such as quinone reductase. They increase periods of cancer latency and are effective agents against fungi such as Aspergillus. Protects against stomach and skin cancers. Lightly cooked broccoli has more; use a mix of raw and cooked vegetables.

Broccoli, peas, beans, and other vegetables; soybeans, clover, alfalfa

Coumestans (phytoestrogen)

High level of estrogenic activity that may reduce the risk for lung cancer. Estimated daily intake of coumestans is 0.6 micrograms; broccoli is the main source.

Cabbage, sauerkraut


May lower the risk of hormonal cancers

Carrots, American ginseng roots

Falcarinol, falcarindiol, panaxydol (polyacetylenes)

Inhibits cell proliferation in normal and cancer cells through synergism of bioactive polyacetylenes. More effective if whole and not chopped before cooking.

Carrots, sweet potatoes, pumpkin, butternut squash, cantaloupe, mangoes, apricots, peaches, papaya, watermelon

Beta-carotene (terpenes)

Beneficial effects on human cancer prevention; increases the activity of killer cells slightly; photoprotective; neutralize free radicals; serves as antioxidants. Avoid excesses of supplements as they act as pro-oxidants. Dietary fat is needed for proper absorption. Boil or steam to protect the antioxidants.

Cereals, legumes, nuts, sesame seeds, soybeans, brown rice, corn and wheat brans


Found as phytic acid in plants. Used by all cells to relay outside messages to the cell nucleus. Aids in the metabolism of calcium and other minerals.

Cherry juice

Chlorogenic acid (phenolic acid)

Strong antioxidant properties.

Cinnamon, cocoa, apples, strawberries, purple grapes and wines, peanuts, cranberries


Decreases oxidative stress; supports urinary tract health.

Citrus fruits, lemon, cantaloupe, pomegranate, potato skins, wild leafy greens, celery stalks, lettuce, chili and sweet peppers, spinach, parsley, watermelon, whole grains, tomato sauce, red wines

Apigenin, luteolin (flavones)

Tumor growth inhibition and chemoprevention; may protect against skin cancer and ultraviolet damage. May protect women against ovarian cancer.

Caffeic acid, ferulic acid (flavanones)

Bolsters antioxidant defenses.

Citrus fruits, apples, pears Some vegetables


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TABLE 13-2 Phytochemicals, Functional Food Ingredients, and Cancer (continued) Food

Functional Ingredient

Possible Roles in Reducing Cancer Risk

Corn, soy, wheat, wood oils

Plant stanols

Inhibits cholesterol absorption.

Cruciferous vegetables: Broccoli, cabbage, sauerkraut, Brussels sprouts, bok choy, arugula, Swiss chard, watercress, cauliflower, kale, kohlrabi, turnips, rutabaga

Indoles (indole-3-carbinol); glucosinolates (thiols)

Antimutagenics that may enhance detoxification of undesirable compounds. May contribute to a healthy immune system; downregulate estrogen and tumor formation. May yield a lower risk of breast, colon, prostate, and cervical cancers.

Cruciferous vegetables (Brassica family)

Jasmonates (thiols)

Plant signaling compounds that activate the coordinated gene expression in ascorbate and glutathione metabolic pathways. Important in defense responses to oxidative stress and biosynthesis of glucosinolate, a defense compound.

Dairy products

Vitamin D3, calcium, sphingomyelin

May inhibit tumor cell growth and aid in cell death. Vitamin D3 may protect against some skin cancers, but not melanoma. A level of 2000–4000 IU per day of vitamin D3 is considered necessary for most adults. Sun exposure, diet, and supplements may be needed.

Flaxseed, rye, whole grains, berries, carrots, spinach, broccoli, tea, asparagus, linseeds; alcoholic beverages (red and white wines).

Lignans: matairesinol and secoisolariciresinol

Phytoestrogens attach to estrogen receptors and block real estrogen, lower cholesterol levels, and decrease cancer activity. Lignans may prevent prostate or lung cancer. Median intake of lignans is 578 micrograms (mainly from berries).

Garlic, onions

Allyl sulfides; selenium

Boosts levels of naturally occurring enzymes that may help maintain a healthy immune system. Garlic also contains arginine, oligosaccharides, sulfur and flavonoids. May be protective against cancers of the stomach, esophagus, colon, breast, and pancreas.

Ginkgo biloba

Ginkgolide A and B

Taken for 6 months or longer, may lower the risk of ovarian cancer. Involved in anti-inflammation processes.


Triterpene glycoside

Radioprotective capability, attributed to the ginsenosides, which are saponins with antioxidant properties. May increase lymphocyte production, stimulate natural killer cells and other immune activity; inhibit cancer cell growth; antioxidant.

Grapes, wine, raspberries, strawberries, tomatoes, citrus fruits, carrots, whole grains, nuts

Ellagic acid, Ferulic acid (phenolic acids)

May block the production of enzymes needed for cancer cells to reproduce. Protect against Salmonella and Staphylococcus aureus infections (particularly ellagitannins in raspberries).

Grape juices from green and black grapes

Gallic acid (phenolic acids)

Strong antioxidant properties

Green tea, oolong tea, black teas, dark chocolate, red wines, licorice root, cranberries and cranberry products

Catechins: epigallocatechin gallate (EGCG); glycyrrhizin; procyanidins/tannins (flavonols)

Decreases the growth of hydroquinone oxidase; decreases COX-2 gene expression and cancer cell growth; and neutralizes free radicals. Tannins in green and black tea and strong coffee inhibit the proliferation of cancer cells in prostate, ovarian, breast, lung, and possibly other sites. Avoid excesses of caffeine, which dilute the effect of the tea.

Green tea extract, watermelon, prunes, raisins, plums, eggplant, grapes, berries, cherries, apples, cantaloupe


May neutralize free radicals to help block damage to DNA. Superoxide anion radical (SOR) has scavenging activity; protects against oxidation of low-density lipoprotein and protects vision.

Green vegetables: Turnip, collard, and mustard; kale, spinach, broccoli. Green peas, kiwi, cilantro, parsley, lettuce. Corn; egg yolk.

Lutein and zeaxanthin (terpenes)

Antioxidants; anti-inflammatory; DNA repair. Good for healthy vision (protects against macular degeneration). Raw spinach is higher than cooked. Lutein may improve skin health and protect against skin cancer.

Leafy greens

Folic acid

Role in DNA synthesis, mitosis, and gene expression.

Legumes, whole grains, bananas, fish, chicken

Vitamin B6

Supports a healthy immune system and increases lymphocyte numbers.

Licorice Glycyrrhiza uralensis and orange Citrus spp.

Coumarins; benzo-alpha-pyrones

Inhibits proteolysis and lipoxygenase; anti-inflammatory and antitumor effects.

Milk and dairy products, fish, liver

Vitamin A

Protects cells against free radical damage.

Nuts, nut butters, wheat germ, whole grains, oils, mayonnaise, creamy salad dressings, egg yolks, cereals, seeds

Vitamin E

Increases antibody production and B- and T-cell functioning; protects cells against free radical damage. SELECT study found that a 400 IU supplement actually promotes prostate cancer.


Avenanthramides; selenium

These polyphenols have strong antioxidant, anti-inflammatory properties (Meydani, 2009). (continued)

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TABLE 13-2

Phytochemicals, Functional Food Ingredients, and Cancer (continued)


Functional Ingredient

Possible Roles in Reducing Cancer Risk

Oats, lima beans, navy beans, black beans, Brussels sprouts, ground psyllium seeds, peas, carrots, apples, barley, pectins, gums, mucilages

Soluble fiber

May lower cancer risk; helps lower cholesterol levels.

Olive and canola oils; tree nuts


Monounsaturated fats decrease tumorigenesis. Virgin olive oil phenols may reduce colorectal carcinogenesis.

Onions, garlic (particularly oil), leeks, chives, scallions, shallots

Allium and allicin (allyl sulfides, S-allylcysteine [SAC])

Organosulfurs decrease tumor cell growth; inhibit kinase activity; may protect the immune system, assist the liver in rendering carcinogens harmless, and reduce cholesterol production in the liver. Diallyl sulfide (DAS) inhibits the effects of PhIP that can cause DNA damage or transform substances into carcinogens.

Onions, garlic, leeks, shallots, inulin, Jerusalem artichokes, fructooligosaccharides (FOS); polydextrose in whole grains, some fruits, honey


Support GI health and improve calcium absorption. Inulin may help protect against colon cancer.

Orange, grapefruit, lemon; cherries; citrus fruit peel

Limonoids/limonene (Terpenes); Naringenin, Hesperetin, Eriodictyol (flavanones)

Citrus glycosides decrease bacterial and fungal growth; decrease cancer cell growth by detoxifying enzymes in liver. Also cause cell apoptosis with certain types of cancers. Stimulate DNA repair with naringenin. Avoid grapefruit in estrogen breast cancer.

Oranges, grapefruit, lemons, tangerines, peaches, apricots, broccoli, tomatoes

Bioflavonoids, vitamin C

Minimizes damage to neutrophils; induces apoptosis; inhibits histamine

Pomegranate fruit and juice

Punicalagin (phenolic acid)

Potent antioxidant; protective against prostate cancer.

Red pepper, paprika

Capsaicin (8-methyl-N-vanillyl6-nonenamide)

Red peppers of the genus Capsicum; it contains carotenoids that may be protective against cancer.

Salmon, mackerel, sardines

Coenzyme Q10 (ubiquinone) Omega-3 fatty acids

May reduce chemotherapy-related heart damage.

Seafood, canola oil, walnuts, flaxseed, marine and other fish oils

Omega-3 PUFAs

Reduce inflammation; may reduce cancer cachexia. Genetic variations affect response of COX-2 and its inflammatory impact on cancers such as prostate.

Soybean, corn and safflower oils

Omega-6 PUFAs

Keep omega-6 to omega-3 at a ratio of 5–10:1.

Soybeans (tofu, vegetable soy milk, soy nuts); legumes such as chick peas, beans, peas; nuts; grain products, coffee, tea; raisins and currants

Isoflavones: genistein, daidzein, biochanin A

Phytoestrogens attach to estrogen receptors and block real estrogen. Red clover and soy extracts contain isoflavones, with high affinity to estrogen receptor-alpha (ER), estrogen receptor-beta (ER), progesterone receptor (PR), and androgen receptor (AR). Daily dose may be 40–50 milligrams of isoflavones (biochanin A, daidzein, formononetin, and genistein). Avoid excesses.

Spices: Cumin and turmeric, ginger, mint, rosemary, garlic, thyme, oregano, sage, basil, coriander, caraway, fennel, chili powder, black pepper, mint


Neutralizes free radicals, supports antioxidant defense system; preserves alpha-tocopherol, decreases inflammation; decreases ATPase; protects plasma DNA from radiation damage. May protect against prostate cancer.

Supplements, herbal

Astralgus, Echinacea, Silymarin

May increase macrophage activity and enhance immunity (interferon, killer cells, Interleukin-2). Silymarin protects the liver.

Sweet potatoes, carrots, turnips, spinach, papaya, tomato, red or green bell peppers, oranges

Retinoids; beta carotene

Important for cell growth, differentiation and death. May prevent some leukemias. Sweet potatoes are high in fiber, potassium, choline, vitamin C, magnesium, iron, and calcium as well.

Tomatoes and tomato products, ketchup, peppers; pink grapefruit; watermelon

Lycopene; vitamin C

Potent antioxidant; may reduce risk of prostate cancer. Tomato products must be cooked.

Vegetable oils, soy, peanuts, rice bran

Sterols: beta-sitosterol, campesterol, stigmasterol, squalene

Can reduce the risk of lung cancer and may reduce the tumor growth of other cancers. Sterols are found in vegetable oils. Sitosterol is the most studied.


Phytosterols, omega-3 fatty acid (ALA)

Antioxidant, anti-inflammatory properties that reduce tumor growth.

Wheat germ, lean beef, seafood, black-eyed peas


Increases neutrophil function and killer cell numbers; decreases cytokines.

Whole grains, beans, seeds (soybeans, oats, barley, brown rice, whole wheat, flaxseed)

Phytates; insoluble fiber; vitamin E

Decreases oxidative damage to cells. Reduces the risk for breast or colon cancer. (continued)

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TABLE 13-2 Phytochemicals, Functional Food Ingredients, and Cancer (continued) Food

Functional Ingredient

Possible Roles in Reducing Cancer Risk

Whole grains

Oligosaccharides; protease inhibitors

These increase short-chain fatty acid formation; decrease cholesterol and lower insulin levels; inhibit action of proteinsplitting enzymes. May prevent cancer cell formation or decrease tumor size.

Wine, red grapes, grape juice, peanuts

Resveratrol; stilbenes (flavonoids)

Phytoalexin produced in plants in response to exposure to ultraviolet light or fungi. Decreases platelet activity, lowers cholesterol, suppresses proliferation of a variety of tumor cells.

Yogurt with Lactobacilli, Bifidobacteria; fermented milk such as Kefir.

Probiotic bacteria

Normalizes the intestinal microflora, blocks the invasion of potential pathogens in the gut, prevents colon cancer, modulates immune function, inhibits H. pylori, enhances calcium absorption; synthesizes niacin, folic acid, vitamin B6, and biotin.

REFERENCES American Cancer Society (ACS). Accessed December 31, 2009, at http://www.cancer/org Gerhauser C. Cancer chemopreventive potential of apples, apple juice, and apple components. Planta Med. 74:1608, 2008. International Food Information Council. Functional foods fact sheet: antioxidants Accessed December 30, 2009, at Detail.aspx?topicFunctional_Foods_Fact_Sheet_Antioxidants. Linus Pauling Institute. Micronutrient information center. Accessed January 1, 2010, at Medline Plus. Antioxidants. Accessed January 1, 2010, at Meydani M. Potential health benefits of avenanthramides of oats. Nutr Rev. 67:731, 2009. Seeram NP. Berry fruits for cancer prevention: current status and future prospects. J Agric Food Chem. 56:630, 2008. USDA Phytochemical Database. Dr. Duke’s Phytochemical and Ethnobotanical Databases. Accessed January 1, 2010, at

TABLE 13-3 Cancer Risk Factors by Site Factors That are Known to Increase the Risk of Cancer

Factors That May Affect the Risk of Cancer

Cigarette Smoking and Tobacco Use


• Acute myelogenous leukemia (AML). • Bladder cancer. • Cervical cancer. • Esophageal cancer. • Kidney cancer. • Lung cancer. • Oral cavity cancer. • Pancreatic cancer. • Stomach cancer. Infections

• Oral cancer. • Esophageal cancer. • Breast cancer. • Colorectal cancer (in men). • Liver cancer • Female colorectal cancer. Diet

Human papillomavirus (HPV) increases the risk for cancers of the cervix, penis, vagina, anus, and oropharynx. • Hepatitis B and hepatitis C viruses increase the risk for liver cancer. • Epstein-Barr virus increases the risk for Burkitt lymphoma. • Helicobacter pylori increases the risk for gastric cancer. Two vaccines to prevent infection by cancer-causing agents have already been developed and approved by the U.S. Food and Drug Administration (FDA). One is a vaccine to prevent infection with the hepatitis B virus. The other protects against infection with strains of human papillomavirus (HPV) that cause cervical cancer. Scientists continue to work on vaccines against infections that cause cancer. Radiation • •

Ultraviolet radiation from sunlight: This is the main cause of nonmelanoma skin cancers. Ionizing radiation from medical X-rays and radon gas in our homes: Scientists believe that ionizing radiation causes leukemia, thyroid cancer, and breast cancer in women. Ionizing radiation may also be linked to myeloma and cancers of the lung, stomach, colon, esophagus, bladder, and ovary.

Foods may protect against cancer and other foods may increase the risk of cancer. •

Fruits and nonstarchy vegetables may protect against cancers of the mouth, esophagus, and stomach. • Fruits may protect against lung cancer. • Diet high in fat, protein, calories and red meat may increase risk of colorectal cancer, but studies have not confirmed this. • It is not known if a diet low in fat and high in fruits, vegetables and fiber lowers the risk of colorectal cancer. Physical Inactivity • Colorectal cancer • Postmenopausal breast cancer • Endometrial cancer. Obesity • • • • • • •

Postmenopausal breast cancer. Colorectal cancer. Endometrial cancer. Esophageal cancer. Kidney cancer. Pancreatic cancer. Gallbladder cancer

Adapted from: National Cancer Institute,, accessed December 29, 2009.

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For More Information on Cancer Prevention •

Cancer Prevention and Control

Cancer Research and Prevention

Complementary Treatments for Cancer

Patient Advocate Foundation

Wellness Community

American Dietetic Association. Position paper on functional foods. J Am Diet Assoc. 109:735, 2009. Chun OK, et al. Estimation of antioxidant intakes from diet and supplements in U.S. adults [Published online ahead of print December 23, 2009]. J Nutr. Kauwell GP. Emerging concepts in nutrigenomics: a preview of what is to come. Nutr Clin Pract. 20:75, 2005. Patil BS, et al. Bioactive compounds: historical perspectives, opportunities, and challenges. J Agric Food Chem. 57:8142, 2009. Wardwell L, et al. Nutrient intake and immune function of elderly subjects. J Am Diet Assoc. 108:2005, 2008. Williams MT, Hord NG. The role of dietary factors in cancer prevention: beyond fruits and vegetables. Nutr Clin Pract. 20:451, 2005.

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.


CANCER: TREATMENT GUIDELINES DEFINITIONS AND BACKGROUND Cancer patients can be divided into three groups: those receiving standard or experimental therapy, those who have become unresponsive to these therapies, and those in remission who are at risk for recurrence or a second new cancer.

Cancer cachexia—a wasting syndrome characterized by weight loss, anorexia, early satiety, progressive debilitation, and malnutrition—may lead to organ dysfunction and death (Mattox, 2005). Fatigue is the most common experience among cancer patients. Otherwise, each type of cancer has its own set of treatments and side effects.

TABLE 13-4 Use of Nutrition Support in Cancer Patients ASPEN Cancer Guideline Updated (2009) Nutrition support therapy should not be used routinely in patients undergoing major cancer operations. • Grade: A Perioperative nutrition support therapy may be beneficial in moderately or severely malnourished patients if administered for 7–14 days preoperatively, but the potential benefits of nutrition support must be weighed against the potential risks of the nutrition support therapy itself and of delaying the operation. • Grade: A Nutrition support therapy should not be used routinely as an adjunct to chemotherapy. • Grade: B Nutrition support therapy should not be used routinely in patients undergoing head and neck, abdominal, or pelvic irradiation. • Grade: B Nutrition support therapy is appropriate in patients receiving active anticancer treatment who are malnourished and who are anticipated to be unable to ingest and/or absorb adequate nutrients for a prolonged period of time. • Grade: B The palliative use of nutrition support therapy in terminally ill cancer patients is rarely indicated. • Grade: B Omega-3 fatty acid supplementation may help to stabilize weight in cancer patients on oral diets experiencing progressive, unintentional weight loss. • Grade: B Indications for Enteral Feeding

Contraindications for Enteral Feeding

Inability to consume 50% of estimated needs orally for 1 week or longer—estimated or actual

Severe malabsorption that cannot be corrected with enteral nutrition

Functioning gastrointestinal (GI) tract with adequate capacity for nutrient absorption

Intestinal obstruction below feeding placement site

Patient willingness to use tube feeding method

Condition such as high-output fistula or high aspiration risk

Adapted from: ASPEN Guidelines., accessed January 1, 2010. Dixon SW. Nutrition care issues in the ambulatory (outpatient) head and neck cancer. Support Line. 27:3, 2005.

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Weight loss and cachexia are common. Malnourished cancer patients commonly have high protein turnover and loss of nitrogen, significant loss of muscle mass, and impaired physical capacity. Tumor factors such as proteolysis-inducing factor (PIF), tumor necrosis factor (TNF), and lipid mobilizing factor (LMF) all tend to promote catabolism. Nutritional inadequacy mobilizes protein stores and, thus, causes a loss of lean body mass. Altered nutrient utilization causes glucose intolerance, insulin resistance, increased glucose turnover, lipolysis, hyperlipidemia, and increased protein turnover. Properly nourishing patients, particularly when malnourished, is essential therapy. The Subjective Global Assessment tool and scoring sheet is used for cancer patients. Indications for use of nutrition support are listed in Table 13-4. Parenteral nutrition (PN) should not be used to prolong life for patients at the end stages


of disease but may be appropriate for patients with responsive cancers when enteral and oral feedings are poorly tolerated. Many cancer therapies cause unpleasant side effects. Table 13-5 defines the types of side effects and treatments in cancer therapy. Patients who are unresponsive to standard or experimental therapies have few treatment options and usually experience poor quality of life for the remainder of their lives. An active nutritional protocol including high doses of multiple dietary antioxidants (vitamin C, alpha-tocopherol, and natural beta-carotene), when administered as an adjunct to other therapies, may increase tumor response and decrease toxicity. A maintenance nutritional protocol with lower doses of antioxidants, in addition to a modified diet and lifestyle, may reduce the risk of recurrence of the original tumor and development of a second cancer among survivors.

TABLE 13-5 Side Effects of Treatment and Common Problems of Cancer Side Effect



About half of the patients coming to cancer treatment are anemic. Use a balanced diet with high-quality proteins, B-complex vitamins, and vitamin C. Eat small meals every 2–3 hours. Heme sources of iron will increase iron bioavailability. Use beef, chicken, fortified grains, dried fruits such as prunes, nuts, and seeds, and blackstrap molasses. Avoid the long-term use of iron supplementation.


Medications, GI distress, altered sensory experiences often leads to cachexia. Treat symptoms, such as pain, constipation, and GI symptoms. Encourage small, frequent feedings. Consider pharmacological therapy with appetite-enhancing medications. Rinse mouth with baking soda or water before eating. Ginger ale or mint can mask metallic tastes; use plastic utensils if needed. Add flavorings to food, or suck on hard candy. Try chilled, frozen, sweet, or tart foods. Avoid unpleasant odors.

Aversion to foods or flavors

A lower threshold for urea causes aversion to meat; it “smells rotten.” Substitute milk, cottage cheese, eggs, peanut butter, legumes, poultry, fish, and cheese. In addition, patient may have a decreased ability to taste salt and sugar. Add other seasonings, sauces, and more salt or sugar as desired by the patient; however, do not allow sweet foods to replace nourishing foods. Clear palate prior to meals by brushing teeth, gums, and oral cavity. Rinse with baking soda and salt water.


Cachexia is the clinical consequence of a chronic, systemic inflammatory response. Depletion of skeletal muscle and redistribution of the body’s protein occur. Nutritional deprivation at diagnosis can lead to further depletion with treatments. Anorexia cachexia syndrome (ACS) is caused by numerous factors. Use small, frequent feedings and supplements. Teach ways to increase calories and protein. Fortify foods when possible. Relieve symptoms before meals whenever possible. Anabolic and anticatabolic agents, such as Megace and Oxandrin, may help. Use of omega-3 fatty acids (EPA and DHA) can disrupt the cachexia.


With all types (given daily, weekly, monthly for 1–2 months or even years), prompt attention to side effect management and appropriate use of supportive care (medications, nutrition, etc.) will be needed. Increase fluid intake for adequate hydration. After chemotherapy, cardiac, kidney, or pulmonary toxicity may occur. Some chemotherapy agents may cause infertility in both men and women. Nausea and vomiting can now be well controlled with Zofran (ondansetron), Kytril (granisetron), and Anzemet (dolasetron). Hemopoietic agents (e.g., Neupogen, Procrit, granulocyte colony-stimulation factor, granulocyte-macrophage colony-stimulating factor) may be needed if red blood cell production is too low; transfusions are a last resort. Avoid the risk of infection and cuts during chemotherapy. Monitor for nosebleeds, bruising, black or bloody stools, or reddish urine. Glutamine supplementation has been used with some success.

Cold food preference

Cold foods may be better accepted than hot foods. Use cold, clear fluids, carbonated beverages, ices, gelatin, watermelons, grapes and peeled cucumbers, cold meat platters, ice cream, and salted nuts. Serve supplements over ice between meals. Shakes, puddings, and custards are other alternatives.


Establish an appropriate bowel program, including regular use of pharmacological agents. Add fiber and extra fluids to the diet. Milk is beneficial, if tolerated. Fresh or dried fruits, all vegetables, bran and a hot drink may help. Get adequate exercise, such as walking. Drink hot beverages, or use prunes or prune juice. Over-the-counter bulking agents may be useful in some cases. Avoid gas-forming foods in excess. Report any blood, vomiting, or no stool for 3 days to the doctor.

Dental Caries

Avoid sweets and use sodium fluoride three times daily. Mouth care should be provided several times daily. Persons receiving irradiation to the head and neck area may benefit from use of fluoride trays and stannous fluoride. (continued)

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TABLE 13-5

Side Effects of Treatment and Common Problems of Cancer (continued)

Side Effect



Evaluate all medications carefully. Assess hydration status and associated symptoms. Alter fiber in diet. Beware of lactose intolerance secondary to disease process, drug therapy, or abdominal or pelvic radiation therapy. Increase fluids that contain sodium and potassium; use of Gatorade or Pedialyte may be helpful. Use cool or room temperature foods. Avoid dairy products if lactose-intolerant. Consume small amounts of food throughout the day instead of three large meals. Decrease fatty, spicy, or acidic foods; caffeine; gas-forming vegetables; or carbonated beverages. Plain rice, potatoes, eggs, mild fish or skinless chicken may be well tolerated. Limit sorbitol and sugar substitutes. Oral glutamine may be useful.

Difficulty swallowing (dysphagia)

Modify diet consistency and follow swallowing techniques provided by speech pathologist. Use moist foods; add sauces or gravies. Semi-solid foods may be better tolerated than liquids, and pureed foods rather than regular items. Patient should sip fluids throughout meal. To prevent aspiration, try placing liquid under the tongue. Some patients find that tilting their heads back helps. Thickeners are available for liquids, if thin beverages are not tolerated well (as with choking, coughing with each swallow). Use of a straw may be beneficial. Spoons are easier to control than forks in the mouth. Avoid very hot or very cold foods. Chew sugarless gum or candy. Use artificial saliva if needed. Consider feeding tube if needed.

Dry mouth (xerostomia)

Surgical removal of salivary glands, atrophy of mucous membranes, or permanent damage from radiation to salivary glands may cause difficulty in eating and swallowing. Use salivary substitutes, lip balm, sugarless gum and candies, gravies, and sauces. Increase fluids and use softened, moist foods (custard, stews, and soups). Cut food into small pieces, or use pureed foods. Ice chips and popsicles also can help. Avoid salty foods. Tart foods, lemon drops, and lemonade may help to stimulate saliva production; avoid tart items if there are oral lesions. Sip on water or other fluids frequently throughout the day and with each bite of food. Synthetic saliva products such as Optimoist or MouthKote may help. Patients benefit from a thorough dental examination before treatment. Use fluoride trays, rinses, other measures. Avoid caffeine, alcohol and tobacco products. Salagen (pilocarpine) is approved to reduce radiation-related dry mouth.

Early Satiety

Rather than serving plain water, encourage a calorie-containing beverage. Take liquids between meals. Avoid fatty, greasy foods because they are more slowly digested and absorbed. Use small meals and frequent snacks between meals. Add protein and calories using extra butter, margarine, cheese, dry milk powder.


Fluid retention may require elevating the legs at rest, staying physically active (walking), and reducing salt intake overall. The doctor may prescribe a diuretic.


Fatigue is very common. Assess and treat causes such as anemia, infection, pain, neutropenia, depression, or medication side effects. Meals may be prepared in quantity when the patient is less tired. Use foods that require less chewing and provide frequent rest periods, particularly before meals. Exercise daily to build stamina. Maintain adequate sleep/nap patterns.

Graft-versus-host disease (GVHD), neutropenia

Fever, chills, sweating, coughing, shortness of breath, diarrhea. Avoid people with colds or flu. Wash hands frequently and use safe food handling procedures. Wash all produce carefully and cook thoroughly. Avoid raw eggs. Cook meats well.

Insulin resistance

Insulin resistance is common from the tumor itself, or may occur after pancreatic surgery. Control of CHO intake and oral agents may be indicated.

Loneliness, Emotional Changes

Social eating may improve food intake. Visitors should be encouraged to bring gifts of food, as appropriate. If anxiety occurs, discuss with healthcare provider.

Loss of lean body mass

Protein wasting and unintentional weight loss are common. Exercise is extremely helpful. Endurance activities can counteract loss of physical performance and improve lower and upper body strength. Patients who exercise also have less fatigue and depression. Taking hormones such as growth hormone, insulin-like growth factor (IGF-I), thyroid hormone, androgens, and cortisol makes a difference as well. Muscle protein synthesis can be increased accordingly.


Elemental diets can only be used if patient has an intact duodenum and jejunum. Total parenteral nutrition should be used only in some cases, considering risk of infection. Tart beverages such as lemonade can be mixed with elemental products if they are to be taken orally.

Meal interruptions

Encourage a good breakfast and snacks to make up for interrupted meals. Keep kitchen well stocked. Meals-on-Wheels may be a useful way to serve meals to this population at home.

Mouth blindness (dysgeusia)

To alleviate disinterest and aversion to foods, emphasize the aroma and colors of foods. Foods that are served warm or hot have more flavor and aroma. Provide a variety of foods and use garnishes. Acidic foods (such as lemonade) may help stimulate patient’s ability to taste foods. Use highly flavored foods and sauces. Try milk shakes that are coffee or mint flavored. Fresh vegetables, special breads, highly flavored snacks, olives and pickles may be well received.

Mouth or throat soreness or dry mouth (stomatitis, mucositis, esophagitis)

Swish mouth with lidocaine, mild saline, or sodium bicarbonate before meals. Changes in taste or enjoyment of foods may occur. Avoid acidic juices, salty foods or soups, dry toast, and coarse or grainy breads or cereals. Grind meats; use a “mechanical soft diet” as needed. Offer cold or tepid fluids frequently; use a straw if needed. Popsicles may help. Smaller meals are useful. Cut foods into small pieces; grind or puree if needed. Mix food with sauces or gravies to make it easier to swallow. Avoid smoking and use of alcohol. Oral glutamine has been used with some success. Avoid alcohol-based mouthwashes. Salagen (pilocarpine) reduces dry mouth and throat sprays or cough drops may be useful. (continued)

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TABLE 13-5 Side Effects of Treatment and Common Problems of Cancer (continued) Side Effect


Muscle wasting

Muscle weakness is frequently associated with tumor growth. Include adequate amounts of protein and amino acids in the diet or in enteral feeding, particularly arginine, glutamine and leucine. Depression, altered moods, immobility, and bed rest contribute to loss of muscle mass. Structured exercise, including resistance training and aerobic exercises, can improve muscle mass and strength. Increased physical activity improves emotional stability, self-confidence, and independence. Active patients have less fatigue, nausea, and insomnia; quality of life improves.


Treated with slow, deep breathing, ice chips, or sips of ginger ale, tea, or candied dried ginger. Try a dry diet with liquids between meals. Eat small meals; rest upright afterward. Offer toast, yogurt, sherbet, popsicles, pretzels, angel food cake, canned fruit, baked chicken, lemonade, hot cereal such as oatmeal, clear liquids, or broth. Cut down on greasy, spicy, fried, fatty foods; foods with strong odors and excessive sweetness. Sit upright for meals and snacks; avoid tight clothing. If breakfast is the best meal, it can also be the largest of the day. Keep crackers or light snacks at hand; do not skip meals. Use antiemetics as directed by physician; underusage may aggravate the nausea. Drink plenty of water/liquids the day before and after chemotherapy.


Prevention is the key. Give pain medications with the first few bites of a meal or have the patient eat when pain is lowest. Encourage trying foods again after time lapse. Try biofeedback, acupuncture, massage, muscle relaxation techniques. Keep a pain journal and report any side effects to the doctor.

Radiation therapy

Radiotherapy may involve high-energy radiation from x-rays, cobalt-60, or radium. Brachytherapy provides internal, continuous local delivery of radiation to site of malignancy (concealed). Teletherapy provides external radiation to a localized area; 7000 rads usually causes damage, particularly to small intestine (radiation enteritis). Radiation therapy (daily for 2–8 weeks) can cause nausea or vomiting if administered to the brain or abdominal/pelvic fields. A light meal is encouraged before treatment. Diarrhea may occur in radiation enteritis; glutamine may be useful in supplements or in tube feeding (TF)/CPN. Formulas containing multiple antioxidants for biological protection against radiation damage in humans are needed. Use of oral glutamine has been used with some success. **In head and neck cancer: anorexia, dysgeusia, weight loss, odynophagia, dysphagia, difficulty chewing, xerostomia. In the thorax: nausea, esophagitis, vomiting. In abdominal, intestinal: lactose intolerance, diarrhea, distention, abdominal pain, nausea and vomiting; later–intestinal stenosis, edema, fluid and electrolyte loss, weight loss.

Radiation enteritis or colitis

About 50–80% of patients who have radiation to the pelvis end up with radiation enteritis; onset can occur up to years later. Symptoms include nausea, vomiting, mucoid diarrhea, abdominal pain, and bleeding; later, there may be colic, a decrease in stool caliber, and progressive obstipation with stricture and fibrosis. Serious injury to the intestinal epithelium and arterioles of the small or large intestines results in cell death, fibrosis, and obstruction. Radiation to the ileum is particularly devastating. If radiation must be given chronically, resection may be needed and the ability of the intestines to become hyperplastic and increase absorptive capacity is thus prevented. Of these persons, many will require home CPN.

Surgery, curative

Direct efforts at restoring nutritional health to pre-illness status. After GI surgery, effects include—Oropharynx: Difficulty with chewing and swallowing, dysgeusia, xerostomia. Esophagus: Heartburn, loss of normal swallowing, decreased motility, obstruction. Stomach: Dumping syndrome, delayed emptying, anemia, malabsorption. Small intestines: Lactose intolerance, bile acid depletion, steatorrhea, fat malabsorption, vitamin B12 deficiency and anemia, short-gut syndrome. Colon: Loss of electrolytes and water; diarrhea, constipation, gas, bloating.

Thick saliva

Thick, ropy saliva can produce more caries. Use less bread, milk, gelatin, and oily foods. Puree foods such as fruits and vegetables. Encourage the intake of plenty of fluids to decrease the viscosity of oral secretions. Encourage good oral intake and regular oral rinses.

Tooth loss

Loss of teeth makes the patient’s mouth more sensitive to cold, heat, and sweets. Try serving foods at room temperature. Use ground, chopped, or pureed foods as needed until dental repair is possible.


Sip clear liquids every 10–15 minutes after vomiting episodes cease; keep head elevated. “Flat” carbonated beverages are useful. Call doctor if abdominal pains persist. Take antiemetic medications prior to meals. Use small feedings, avoid spicy or acidic foods and those with strong odor, use liquids between meals. Use low fat, light meals.

Weight loss

Calculate 40–45 kcal/kg for repletion. Add fats to foods, dry milk to mashed potatoes and shakes, and extra sugar to coffee and cereals. Use small, frequent feedings and the patient’s favorite foods. Add cream sauces, extra meat or cheeses in casseroles, and gravies. Encourage patients to be as physically active as possible, particularly using long muscles to promote lean body mass.

Derived from: National Cancer Institute,, accessed January 5, 2010.

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CLINICAL INDICATORS Genetic Markers: HMGB1 protein—a danger signaling protein—can act as a proinflammatory and proangiogenic mediator when actively secreted by macrophages or passively released from necrotic cells; this plays an important role in the pathogenesis of cancer (Winter et al, 2009). Other genetics information for cancer can be found at cancertopics/genetics-terms-alphalist/a-e. Sample Clinical/ X-ray Dual-energy History x-ray absorpHeight tiometry Weight (DEXA) scan Weight changes Computed Body mass index tomography (BMI) (CT) scan or Diet history magnetic resInput and onance imagoutput ing (MRI) (I & O) Pain? Lab Work Limited use of affected area Glucose (Gluc) Hemoglobin Fatigue and Warmth in a hematocrit local area? (H&H) Fever, temperaSerum Fe, ture ferritin Cough

Serum folate, B12, B6 Serum homocysteine Ca, Mg Na, K Albumin (Alb) C-reactive protein (CRP) Total lymphocyte count (TLC) (varies)

• Coordinate total care plan with doctor, nurse, patient, family, caregivers, and other team members. • Review each case individually and honor patient’s wishes regarding more aggressive intervention. • Prevent or minimize weight changes. Some patients are hypometabolic; others are hypermetabolic by 10–30% above normal rates. Greatest losses occur from protein stores and body fat. • Use indirect calorimetry to determine energy requirements; Resting Metabolic Rate (RMR) or Resting Energy Expenditure (REE) is measured after 30 minutes of recumbent rest, preferably fasting but not necessarily early in the morning, with as little physical activity as possible before the measurement (American Dietetic Association, 2010). • Diminish toxicity of treatments and improve quality of life. Good nutritional status early on is a good prognostic indicator. • Correct cachexia from weakness, anorexia, redistribution of host nutrients, and nutritional depletion. • Prevent depletion of humoral and cellular immunity from malnutrition. Improved nutritional status may allow neoplastic cells to become more susceptible to medical treatment. • An improved nutritional status reduces side effects, promotes better rehabilitation, and improves quality of life while perhaps increasing survival rates. Malnutrition can potentiate the toxicity of antineoplastic agents. • Prevent infection or sepsis, further morbidity, or death. • Control complications such as anemia or multiple organ dysfunction. • Preserve body mass through structured exercise programs and specialized nutritional supplementation. • Control gastrointestinal symptoms, which are more common with weight loss greater than 10%. • Work with the interdisciplinary team using a sample algorithm (courtesy of (See Algorithm on page 743)


FOOD AND NUTRITION Knowledge Deficit Assessment: Medications, lab values, current use of herbs and botanical products. Nutrition Diagnosis (PES): Knowledge deficit as evidenced by patients requesting information regarding the proper use of herbs and botanicals for cancer treatment. Intervention: Education about herbs and botanical products in cancer; resources and Web sites; label reading. Counseling with responses to specific questions according to type of cancer, prevention versus treatment, side effects. Monitoring and Evaluation: No reports of adverse side effects with herbs and botanicals, medications, or foods (such as allergic reactions).

• Determine cancer-specific energy and protein requirements (American Dietetic Association, 2010). • If indirect calorimetry is not available, calculate energy as 30 kcal/kg body weight to maintain and 35–45 kcal/kg body weight to replete lost stores or if the patient is febrile, septic, or very active. • In general, the intake of protein should be high (1–1.5 g/kg body weight to maintain; 1.5–2 g/kg body weight to replete lean body mass) to protect from muscle wasting, malnutrition, cachexia, and treatments. • Provide appropriate and adequate, but not excessive, micronutrient supplementation. Avoid excesses of iron, but correct anemias when diagnosed. There is no evidence for use of vitamin E or arginine prior to radiation

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Initiated by:


SCREEN Nutrition Screen diagnosis: Cancer

GOALS (Check any/all):


 Maintain or improve nutritional status in_____ (goal time).


 Prevent hospitalization due to dehydration/poor nutrional intake in ____ (goal time).

 Avoid delay of cancer therapy due to poor nutrition in _____ (goal time).

MODERATE RISK INTERVENTIONS (Check any/all)  Build Up Your Diet provided and explained  Food Record provided and explained  Fluid intake encouraged Obtain Dr. orders as needed:  RD chart consult  Monitor weight q:_____  BID/TID supplements  Other:________________________ (See notes for documention.)

Date: 1 or more


Date: Next visit

1 or more

HIGH-RISK INTERVENTIONS (Check any/all)  Build Up Your Diet provided and explained  Food Record provided and explained  Fluid intake stressed Obtain Dr. orders as needed:  RD referral for home visit(s)  Monitor weight q:_____  Monitor I & O q: _____  BID/TID supplements  Other:________________________ (See notes for documention.)

ASSESS RESPONSE (Check any/all)  Further weight loss  Exhibiting Nutrition Impact Symptoms*  Dehydration  Other:________________________ (See notes for documention.)



 Prevent or alleviate nutrition-related complications of cancer or cancer therapy in ____ (goal time).


ASSESS (Check any/all)  Receiving chemotherapy/radiation therapy  Weight loss: _____lb/wk  Receiving enteral or parenteral nutrition or complex diet order  Dehydration Nutrition Impact Symptoms*  Problems chewing/swallowing  Mouth pain/dryness  Nausea/vomiting  Diarrhea/constipation  Fatigue  Anorexia  Altered taste perception

OUTCOMES ACHIEVED  Weight stabilized or improved  Hydration status maintained or improved  Cancer therapy initiated without delay  Other:________________________ (See notes for documention.)  Repeat Nutrition Risk Screen in ____ days

Signed: Signed: Signed:




ASSESS RESPONSE (Check any/all)  Further weight loss  Continued dehydration  Exhibiting Nutrition Impact Symptoms*  Other:________________________ (See notes for documention.)


Next visit OUTCOMES ACHIEVED  Weight stabilized or improved  Hydration status maintained or improved  Cancer therapy initiated without delay  Other:________________________ (See notes for documention.)  Repeat Nutrition Risk Screen in ____ days

Signed: Signed:


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, Inc.


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• • •


or chemotherapy (American Dietetic Association, 2010). Use foods that are high in phytochemicals and antioxidants. Use adequate fluid for hydration. Schedule larger meals earlier in the day. If needed, schedule five to six small meals daily, with tube feeding or intravenous feeding. If the gut works, use it. Parenteral nutrition (PN) is not likely to benefit advanced cancer patients who are unresponsive to treatment and should be used with caution in current or potentially septic patients because of the risks (American Dietetic Association, 2010). Use CPN if enteral nutrition is contraindicated and if the patient is at low risk for infection. After surgery or abdominal radiation, glutamine may be useful to protect from enteropathy, lower morbidity, augment tumor cell kill, and boost natural killer (NK) cell activity.

Common Drugs Used and Potential Side Effects • Drugs used will be matched to the specific type of cancer. Tables 13-6 and 13-7 list drugs and some common side effects. • See the NCI list available at drugdictionary/.

Herbs, Botanicals, and Supplements • Answer questions about the use of herbs and botanicals in cancer treatment plans. Use of complementary and alternative medicine (CAM) therapy is common in the cancer population. • Some products are harmless, but some may lead to serious problems. Table 13-8 describes herbs that are commonly used and some general comments.

TABLE 13-6 Cancer Drugs and Chemotherapy Agents There are many chemotherapy drugs available. With chemotherapy, patients may suffer severe side effects such as nausea, hair loss, infection, and injury to the GI tract. Serotonin antagonists such as Anzemet (dolasetron), if administered at the same time as chemotherapy, can prevent nausea and vomiting, but abdominal pain, headache, and constipation may occur. Biologic therapies such as interferon and interleukin may cause flu-like symptoms and myalgias, shortness of breath, or edema. Monoclonal antibodies such as Herceptin and Rituxan are also used to treat cancer and may cause chills, fever, lethargy and muscle aches. With antineoplastic agents, side effects include nausea, anorexia, stomatitis, diarrhea, taste alterations, some vomiting, and possibly sloughing of colonic mucosa (see Table 13-7 also). Drug


Alkylating agents: cyclophosphamide, fluorouracil

These drugs kill cancer cells by stopping their growth or by making it hard for cancer cells to repair damage. Nausea, vomiting, hyperuricemia.

Antiangiogenic agent: humanized monoclonal antibody bevacizumab (Avastin)

Tumors require nutrients and oxygen in order to grow; angiogenesis provides access to these nutrients.

Antimetabolites: flucytosine

This is a DNA substrate analog that leads to incorrect DNA synthesis affecting the cancer cells. Nausea, vomiting, diarrhea, and stomatitis can occur.

Antiemetics: granisetron or ondansetron; medical cannabis, Marinol; domperidone, promethazine (Phenergan); metoclopramide (Reglan)

May be useful for anorexia/cachexia syndrome. Also used to relieve nausea and vomiting after chemotherapy. Headache may result. Other side effects include nausea, diarrhea, increased gastric emptying, or drowsiness.

Aspirin and anti-inflammatory agents

May prevent some types of cancer, including colon cancer. The use of herbal nonsteroidal anti-inflammatory drugs (NSAIDs) may be recommended with these medications to enhance effectiveness.

Irinotecan (Camptosar)

For the treatment of stage 1–4 breast, lung, prostate, colon, skin, and most other metastatic or nonmetastatic forms of cancer.

Corticosteroids: prednisone

Hyperglycemia, sodium and fluid retention, weight gain, and calcium losses can occur.

Folate antagonist: methotrexate

Use of folate preparations can alter drug response. Folate, lactose, vitamin B12, and fat are less well absorbed. Mouth sores are common.

Immunotherapy: interleukin-2 and interferon

Lymphokine is administered to decrease tumor growth. Nausea, vomiting, abdominal pain, fatigue, and anorexia can result. In addition, low levels of folate and vitamins A and B6 may result.

Monoclonal antibodies (MAbs): cetuximab, Campath-1 H, rituximab (Rituxan), and Bexxar

These drugs correct the abnormal enzyme that causes cancerous cells to grow out of control. These attack only abnormal elements of cells (“kinder and gentler” cancer therapies). Cetuximab specifically binds to the epidermal growth factor receptor with high affinity.

Vinca alkaloids: vincristine, vinblastine

Nausea and vomiting can occur.

Derived from: American Cancer Society,, accessed January 3, 2010. Chemotherapy Drugs National Cancer Institute Oncology Channel

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TABLE 13-7 Antineoplastic Agents: Generic and Brand Names Generic






Interferon-2 a











TheraCys, TICE BCG



Bleomycin sulfate


Leucovorin calcium





Lupron, Lupron-Depot













Cisplatin (cis-platinum, cis-diamminedichloroplatinum)

Platinol, Platinol-AQ

Melphalan, L-phenylalanine mustard, L-sarcolysin

Alkeran (R)

Cladribine, 2-chlorodeoxyadenosine


Melphalan hydrochloride

IV Alkeran


Cytoxan, Neosar


Purinethol Tablets

Cytarabine, cytosine arabinoside




Dacarbazine, imidazole carboxamide


Mechlorethamine, nitrogen mustard





Solumedrol, Medrol

Daunorubicin, daunomycin


Methotrexate, amethopterin



Decadron, Tobradex











Etoposide (epipodophyllotoxin)


Plicamycin, mithramycin











Fluorouracil Injection

Streptozocin, streptozotocin












Thiotepa, triethylene thiophosphoramide






Idarubicin HCL






Vinorelbine tartrate

Navelbine Injection


Roferon-A, Intron-A

Source: Medicine Online. Antineoplastic agents generic abbreviations,, accessed January 3, 2010.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Educate family about special patient needs (Dixon, 2005). • There is evidence that cancer survivors who adopt a healthy lifestyle reap physical and emotional benefits. See Table 13-9 for more guidance and patient education tips.

Patient Education—Food Safety for Cancer Patients • Clean: Wash hands and surfaces often. • Separate: Don’t cross-contaminate. Keep raw meat and poultry apart from cooked foods. • Cook: Use a food thermometer to be sure meat and poultry are safely cooked.

• Chill: Refrigerate or freeze food promptly. • Avoid: • Hot dogs, luncheon, and deli meats unless they are reheated until steaming hot. • Refrigerated plate, meat spreads from a meat counter, smoked seafood, and raw or undercooked seafood. • Raw (unpasteurized) milk and foods that contain unpasteurized milk. • Soft cheeses such as Feta, queso blanco, queso fresco, Brie, Camembert cheeses, blue-veined cheeses, and Panela unless it is labeled as made with pasteurized milk. • Salads made in the store such as ham salad, chicken salad, egg salad, tuna salad, or seafood salad. • Soft-boiled or “over-easy” eggs, as the yolks are not fully cooked.

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TABLE 13-8

Herbs, Dietary Supplements, and Cancer

Most patients diagnosed with cancer explore complementary and alternative medicine (CAM), particularly herbal medicine. Dietetics professionals must evaluate the risks and benefits of the use of herbs and botanical products in various cancers; indicate whether “guidance” or “promotion” is being offered. Alternative therapies should be reviewed in the light of potential harm. Herbs should be appropriately labeled to alert consumers to potential interactions when used with drugs, and consultation with a general practitioner is recommended. Ashwagandha (Withania somnifera)

Used for cancer treatment, diabetes, epilepsy, fatigue, gastrointestinal (GI) disorders, pain, rheumatoid arthritis (RA), skin infections, and stress.

Should not be used in pregnant women because it is an abortifacient.


Stimulates interferon and positively impacts the immune system. Possibly reduces the effectiveness of chemotherapy. Strong immune booster.

A type of legume used for years in Chinese medicine. No convincing evidence in cancer.

Black cohosh (Remifemin)

May relieve the symptoms of menopause. No known side effects with chemotherapy. Source of vitamin A and pantothenic acid. Drug interactions: may increase the toxicity of doxorubicin and docetaxel.

Used to lower hot flashes, which can be a challenge for breast cancer patients.


Bromelain (from pineapple extract) positively impacts the immune system. Improved tumor boundaries.

Studies have not demonstrated evidence in cancer therapy.

Cat’s claw

May have some effect on the immune system, but more comprehensive studies are needed. Antioxidant.

Contains alkaloids.


No proven efficacy in cancer. May promote sedation or allergic reactions.

Chili powder

Capsaicin may actually have tumor-promoting effects; chili powder has been implicated in several GI cancers, but the results are conflicting.

In Mexico, higher use of chili powder is related to more stomach cancer.

Chinese herbal medicine

Chinese herbal medicine uses a variety of herbs, in different combinations, to restore balance to the body.

See Astragalus, Ginkgo, Ginseng, Green tea, and Siberian ginseng.

Chinese PC-SPES

Contains chrysanthemum, isatis, licorice, Panax ginseng, saw palmetto, skullcap; Rabdosia rubescens is the most potent ingredient. PC-SPES contains flavonoids, alkaloids, polysaccharides, amino acids, and trace minerals such as selenium, calcium, magnesium, zinc, and copper.

Antiestrogenic effects.


Contains eugenol, which reduces lipid peroxidation and reduces cancer cell proliferation.

Dehydroepiandrosterone (DHEA)

DHEA is a steroid hormone produced by the adrenal gland and converted into estrogen and testosterone.

It is normally found in humans, plants, and animals. DHEA extracted from a wild yam plant is available as a dietary supplement.


No evidence of usefulness in reducing incidence or symptoms of cancer.

May reduce colds or flu for some people.

Eleuthero (Siberian ginseng)

May boost energy. More studies are needed.


Mixture of four herbs: burdock root (Arctium lappa), sheep sorrel (Rumex acetosella), slippery elm bark (Ulmus rubra), and Indian rhubarb root (Rheum officinale) to make a tea.

Potent antioxidant and DNA-protective activity. Possibly estrogenic, antioxidant, anti-inflammatory, antimicrobial, and anticarcinogenic.

Watercress (Nasturtium officinale R. Br.), blessed thistle (Cnicus benedictus L.), red clover (Trifolium pratense L.), and kelp (Laminaria digitata [Hudson] Lamx.) have been added to a product sold as Flor Essence. Evening primrose oil or gamma linolenic acid (GLA)

Proposed to reduce the effects of cancer treatments. GLA is an omega-6 unsaturated fatty acid made in the human body from other essential fatty acids. The main supplemental sources of GLA are oils of the seeds of evening primrose, borage, and black currant plants.

GLA is found in human breast milk. Claimed to slow cancer cell growth. Increases effectiveness of chemotherapy; boosts efficiency of tamoxifen; antioxidant; boosts immune system.


A cancer-fighting substance found only in carrots.

Human studies are needed.


Flaxseed supplements along with low-fat diets may be useful in men with early-stage prostate cancer.

Controlled clinical studies are needed.


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TABLE 13-8 Herbs, Dietary Supplements, and Cancer (continued) Garlic

Seems to have reduced gastric and prostate cancers. Sulfur compounds tend to be the most chemoprotective. Useful in treatment as well as prevention. Garlic appears to induce cytochrome P-450 3A4 and may enhance metabolism of many medications such as cyclosporine and saquinavir. Antimicrobial properties are helpful.

Supplements are not as effective as real garlic for allicin and S-allylcysteine activity. Garlic poultices may cause burns in infants. Used as spice and to treat hyperlipidemia, hypertension, atherosclerosis, cancer, and infections, but sustained response has not been found. Mixed effects regarding reduction of blood glucose levels, blood pressure, or cardiovascular diseases. Garlic should not be used in patients on anticoagulants and patients with platelet dysfunction.

Ginger (6-gingerol)

May help to reduce the side effects of cancer treatments as an antiemetic, anti-inflammatory agent. Effective in preventing nausea and vomiting in some patients. It is a relatively safe herb, but patients taking blood thinners or about to undergo surgery should avoid ginger supplements. Interaction with many drugs including antacids, anticoagulants and antiplatelets, antidiabetics, antihypertensives, H2 blockers, proton pump inhibitors (PPI), and barbiturates.

Ginger may be effective in treating chemotherapy-induced nausea and vomiting.

Ginkgo biloba (maidenhair tree)

Antioxidant and anti-inflammatory effects; role in cancer is being studied (see Table 13-2). Stimulates blood circulation and helps improve memory.

Ginkgo causes bleeding when combined with warfarin or aspirin (acetylsalicylic acid), raises blood pressure when combined with a thiazide diuretic, and causes coma when combined with trazodone. Lowers the threshold for seizures in seizure-prone individuals.

Ginseng, Asian (Panax ginseng)

The dried roots of the plants are used in some traditional medicines to treat a variety of conditions, including cancer. Rh2 is a ginsenoside extracted from ginseng that has effects on cell proliferation, induction of apoptosis, and stimulation of natural killer cells and other immune activity.

Asian ginseng may prevent some cancers. Proposed to give strength and stamina. Interactions with monoamine oxidase (MAO) inhibitors.

Ginseng, American (Panax quinquefolius)

A plant with similar (but not exactly the same) properties, is grown mainly in the United States.

Used for health maintenance, strength, stamina, and immunostimulation. Contraindicated in patients with hypertension and in premenopausal women.

Glucarate (calcium glucarate)

Proponents claim that glucarate may reduce the risk of colon, lung, liver, skin, prostate, and other cancers by increasing the body’s ability to eliminate cancer-causing toxins that come from diet and the environment. May help the body remove excess estrogen and other hormones that promote these diseases.

Glucarate is found in many fruits and vegetables including apples, grapefruit, broccoli, Brussels sprouts, and bean sprouts. It also occurs naturally in the body in very small amounts.

Green tea (Camellia sinesis)

Contains polyphenols and may slow the delivery of nutrients to cancer cells by inhibiting the formation of new blood vessels (angiogenesis). Recent research has focused on green tea for the prevention of breast, prostate, skin, esophagus, stomach, colon, pancreas, lung, and bladder cancers.

The use of skin products that contain green tea may be somewhat protective against skin cancers. Epigallocatechin gallate (EGCG). EGCG may cause cancer cells to die and may stop new blood vessels from forming, thereby cutting off the supply of blood to cancer cells. Do not use with pregnant or lactating mothers. Use with caution with many drugs particularly anticoagulants.

Isatis root (Ban lan gen, Radix isatidis baphicacanthi, Isatis tinctoria, Isatis indigotica)

Used for common cold, sore throat, mumps, respiratory ailments, and malignant tumors. Leaves are used in one of the herbal formulas to treat prostate cancer. No adverse reactions known.

This herb is also used to treat chronic myelogenous leukemia. Studies also indicate that this plant has antiviral and immunostimulatory effects.


Licorice root is an ingredient in many traditional Chinese herbal remedies. More research is needed to find out whether licorice extract has any role in cancer prevention or treatment.

May cause serious side effects, including hypertension or muscle weakness or paralysis.


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TABLE 13-8

Herbs, Dietary Supplements, and Cancer (continued)

Lipoic acid (alpha lipoic acid)

Lipoic acid plays an important role in metabolism. Recent research has shown that it is beneficial in treating nerve damage in diabetics. It may be helpful for other conditions as well. There is currently no evidence that lipoic acid prevents the development or spread of cancer.

Lipoic acid is an antioxidant found in certain foods including red meat, spinach, broccoli, potatoes, yams, carrots, beets, and yeast. It is also made in small amounts in the human body. Its possible role as a form of complementary therapy to reduce the side effects of radiation therapy or chemotherapy is still unclear.

Lyprinol (green-lipped mussel)

This is a fatty acid complex extracted from Perna canaliculus—a green-lipped mussel (shellfish) native to New Zealand. It contains omega-3 fatty acids. Lyprinol is promoted as a dietary supplement with anti-inflammatory properties to work against leukotrienes.

It is available in capsule form as a dietary supplement.

Macrobiotic diet

The standard macrobiotic diet today consists of 50–60% organically grown whole grains, 20–25% locally and organically grown fruits and vegetables, and 5–10% soups made with vegetables, seaweed, grains, beans, and miso (a fermented soy product). Early versions of the diet included no animal products at all.

Potatoes, tomatoes, eggplant, peppers, asparagus, spinach, beets, zucchini, and avocados are excluded. The diet also advises against eating bananas, pineapples, and other tropical fruits. The use of dairy products, eggs, coffee, sugar, stimulant and aromatic herbs, red meat, poultry, and processed foods is discouraged.


May aid in the effectiveness of chemotherapy and in improving survival in numerous types of cancer. Melatonin inhibits tumorigenesis with the suppression of tumor linoleic acid (LA) uptake and its metabolism. Melatonin may also stimulate natural killer cells, which attack tumors. Inhibits cachexia.

Circadian rhythm may be enhanced with use of melatonin; this may help to alleviate fatigue associated with cancer.

Milk thistle (Silymarin)

Antioxidant for treating liver diseases such as cirrhosis or chronic hepatitis. May help with cancer prevention; human studies are needed.

It contains flavonolignans; perhaps has a role in decreasing skin or prostate cancer.

Mistletoe (Iscador)

Lectin-rich mistletoe extract should be further evaluated.

There may be toxic side effects.


Anthocyanins in mulberry have an anticancer effect.

More research is needed.

Mustard seed (Brassica campestris)

Mustard seeds enhance the antioxidant defense system and provide protection against the toxic effects of carcinogens.

May protect against stomach and uterine cancers.

Oleandrin, odoroside (Nerium odorum)

Raw leaves are toxic. May cause apoptosis in various cancer cell lines.

Side effects include nausea, vomiting and diarrhea, tachycardia, and arrhythmia.

Noni juice (Morinda citrifolia)

An immunomodulatory polysaccharide-rich substance from the fruit juice is rich in potassium.

Common in Polynesian diets. High sugar content.

Pokeweed (Poke salad)

Pokeweed antiviral protein has anti-tumor effects in mice and laboratory studies. Clinical trials have not yet been done.

All parts of the mature plant contain chemically active substances such as phytolaccine, formic acid, tannin, and resin acid; all are mildly poisonous when eaten.


Evidence suggests the following beneficial effects: normalization of the intestinal microflora, the ability to block the invasion of potential pathogens in the gut, prevention of colon cancer, modulation of immune function, inhibition of H. pylori.

Regular use of yogurt and other natural functional foods may be useful for cancer patients. Daily intake of Bifidobacterium lactis enhances natural immune function.

Pycnogenol; pine bark extract (Pinus pinaster)

Pycnogenol is the name of a group of bioflavonoids with proanthocyanidins taken from a number of natural sources, such as grape seeds.

The maritime pine tree contains naturally occurring proanthocyanidins.


Quercetin is promoted to help prevent or treat different types of cancer.

See Table 13-2.

Reishi mushroom (Ganoderma lucidum)

The medicinal mushroom Reishi has been widely used to treat cancer, diabetes, and neurasthenia in many Asian countries. Used for fatigue, high cholesterol, HIV and AIDS, hypertension, immunostimulation, inflammation, strength and stamina, and viral infections.

Can interfere with immunosuppressants and chemotherapeutic drugs. Adverse reactions may include dry throat and nose, GI upset, itchiness, nausea, and vomiting.

Rosemary and marjoram (ursolic acid)

Terpenoids in these spices provide anticancer effects.

Triterpenoid compound that occurs naturally in a large variety of vegetarian foods, medicinal herbs, and plants. (continued)

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TABLE 13-8 Herbs, Dietary Supplements, and Cancer (continued) Saffron (Crocus sativus)

This spice contains glutathione and crocetin, which decreases tumor growth and protects platelets from aggregation.

Being studied for effects on depression and Parkinson’s disease also.

Saw palmetto (Serenoa repens)

Permixon, a phytotherapeutic agent derived from the saw palmetto plant, is a lipid/sterol extract; mixed research results.

Often used to prevent prostate cancer; no side effects noted.

Shark cartilage

It seems to have a role in inhibiting angiogenesis. Frequently recommended to cancer patients by family members.

No evidence that it plays a role in cancer. Prolonged use can have adverse side effects.

Shark oil

Alkylglycerols, found in shark liver oil, may fight cancer by killing tumor cells indirectly and activating the immune system by stimulating macrophages.

Depending on the supplement, it may be rich in omega-3 fatty acids and vitamin A.

Shiitake mushrooms

Contains lentin, which stimulates T-cell and natural killer cell production; antitumor, cholesterol-lowering, and virus-inhibiting effects.

Additional research is needed.

Skullcap (Scutellaria barbata)

It seems to play a role in the reduction of aflatoxin toxicity. Contains flavanone compounds such as scutellarein, scutellarin, carthamidin, and isocarthamidin.

Do not take orally.

Soy isoflavones

Role in cancer prevention is not clear. Exact dosage and effects on specific genes are not currently known. The best advice is to encourage usual dietary use and not to change drastically. Reduces menopausal symptoms.

Soy should not be used in estrogen-dependent breast cancer or with endometrial cancer. Avoid with use of tamoxifen.

Spirulina; blue–green algae (Spirulina spp)

Adverse effects are uncommon unless contaminated. Used to treat cancers, viral infections, weight loss, oral leukoplakia, increased cholesterol.

If contaminated, it is hepato-, nephro-, and neurotoxic.

St. John’s wort (Hypericum perforatum)

Not effective against acute depression. Avoid with all types of chemotherapy; cyclosporine, midazolam, tacrolimus, amitriptyline, digoxin, indinavir, warfarin, and theophylline.

It accelerates the effects of tamoxifen and must be used cautiously. May cause breakthrough bleeding and unplanned pregnancy when used with oral contraceptives. Avoid with selective serotonin reuptake inhibitors and in pregnancy or lactation.

Turkey tail mushroom (Coriolus versicolor; Yunzhi)

A mushroom used in traditional Asian herbal remedies. Polysaccharide K (PSK) and polysaccharide peptide (PSP), are being studied as possible complementary cancer treatments.

Turmeric (Curcuma longa)

Turmeric and other phenols have an anticancer effect. Additional research is needed about the efficacy of turmeric as a cancer treatment).

Warn breast cancer patients on cyclophosphamide to restrict the intake because it inhibits the antitumor action of these chemotherapeutic agents.


Used to promote natural sleep; 2–4 weeks of use is needed. People who are going to have surgery should not use valerian or should taper down slowly, starting several weeks before surgery.

Avoid taking with alcohol, certain antihistamines, muscle relaxants, mental health drugs, sedatives, antiseizure drugs, or narcotics. Talk with their doctors or pharmacists about possible drug interactions before taking valerian.


Few scientific studies in humans to support claims made for wheatgrass.

Proponents suggest that wheatgrass strengthens the immune system.

White Birch (betulinic acid)

Potential role in treating melanoma and certain brain cancers; clinical trials are needed.

Birch bark, buds, and leaves are used as folk medicines but have not been studied to find out if they are safe or effective.


Avoid oral use:

May have serious side effects.

Aconite (bushi, monkshood) aloe vera arnica (wolfbane, mountain tobacco) aveloz (pencil cactus) belladonna (deadly nightshade) blue cohosh (squaw root) boragebroom (broom tops, Irish broom) calamus (sweet root/flag) cesium chloride chaparral (creosote bush; Larrea tridentate) (continued)

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TABLE 13-8 Herbs, Dietary Supplements, and Cancer (continued) HARMFUL

Avoid oral use: coltsfoot comfrey (bruisewort; Symphytuen officinale) Convallaria (lily of the valley) DiBella (DMB) ephedra (ma huang) germander germanium horse chestnut Hoxsey herbal treatment jimson weed jin bu huan Kava (Piper methysticum) Kombucha tea krebiozin (creatine) laetrile (amygdalin)–cyanide toxicity licorice (Glycyrrhiza glabra) liferoot (golden senecio, ragwort) lobelia (Indian or wild tobacco) mandrake oleander Pau d’Arco (Taebuia) pennyroyal periwinkle poke root sassafras sea cucumber tea tree oil wormwood (madder, mug or Ming wort, Artemisia) yohimbe

This table was developed with assistance of Dr. Vijay Erankl and Valerie Kogut, MS, RD. See also: American Cancer Society. Herbs, vitamins, and minerals. National Center for Complementary and Alternative Medicine

TABLE 13-9 General Patient Education Tips For cancer treatment, start “where the patient is.” Instruct patient to use unscientific treatments with caution. Discuss these issues with compassion and an understanding of patient’s perspective. Patients want faith in their health provider, hope for coping and for strength, and respect for their wishes. For cancer survivors, optimal attention to physical activity and nutrition should continue. Because there are different phases of cancer survivorship, from active treatment to advanced disease, existing evidence must be reviewed and informed decisions made regarding dietary choices. Obese and overweight patients can pursue modest weight loss provided that close monitoring occurs. Healthy food intake, low in energy density but high in nutrient and phytochemical content, is the goal. This translates into 5–9 fruits and vegetables, more fish, and plenty of whole grains. Teach good sources of folate, vitamin A, calcium and iron; highlight antioxidant foods rich in selenium, vitamins C and E, and beta-carotene. Excellent resources are available from the cancer survivor Web site at and from the American Institute for Cancer Research Web site For family member counseling, teach that nutrition is fundamental in the molecular basis of cancer. Tailor interventions according to nutritional status, genotype, current health status, and nutritional requirements of the individual. Changes in diet, lifestyle and behaviors may be required. For terminal, palliative care, emotional support and comfort may be the best treatment. The counselor should be aware of the stages of death and dying to identify where the patient is: (a) denial, (b) anger, (c) bargaining, (d) depression and loss, or (e) acceptance. The patient must be included in all decisions. If not competent, follow the living will or advanced medical directives to follow. A court-appointed legal guardian may be needed. Evaluate the benefits and burdens of the illness on the patient, as well as any court or family decisions. Forego heroic measures, including tube feeding and CPN, if so chosen. Otherwise, maintain measures and re-evaluate at a later date. Hydration is the priority when “palliative care” orders are written.

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For More Information •

Cancer Information

Cancer Treatments

Clinical Trials

Food Safety for Cancer Patients

Medicine Online

OncoLink: University of Pennsylvania Cancer Center

Supportive Treatments

Texas Cancer Data Center

Treatment Decisions


CANCER: TREATMENT GUIDELINES—CITED REFERENCES American Dietetic Association (ADA). Evidence analysis library–Oncology. Accessed October 5, 2010, at topic.cfm?cat1058. Dixon SW. Nutrition care issues in the ambulatory (outpatient) head and neck cancer. Support Line. 27:3, 2005. Mattox TW. Treatment of unintentional weight loss in patients with cancer. Nutr Clin Pract. 20:400, 2005. Winter N, et al. Elevated levels of HMGB1 in cancerous and inflammatory effusions. Anticancer Res. 29:5013, 2009.


Adapted from: Yochum TR and Rowe LJ.Yochum and Rowe's Essentials of Skeletal Radiology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.

DEFINITIONS AND BACKGROUND Bone is a fertile ground for cancer cells to flourish (Clines and Guise, 2005). Bone cancers include osteosarcomas, chondrosarcomas, and the Ewing family of tumors. The correct diagnosis depends on an evaluation of clinical, radiologic, pathologic, and genetic features (Li and Siegel, 2010).

Osteosarcoma involves a rapidly growing malignant bone tumor of unknown origin, occurring most often in the long bones of young people. It is most common in males between 10 and 25 years of age. People who have had previous high doses of radiotherapy to a bone or Paget’s disease have an increased risk of developing bone cancer. This type of cancer often spreads to the lung. When metastases from other organs occur, it is considered a secondary bone cancer. Patients with metastasis to the spine may present with pain, neurological deficit, or both. Optimal treatment should include consideration of the patient’s neurological status, general health, age, quality of life, and the anatomical extent of the disease (Ecker et al, 2005). Staging on bone cancer is as follows: stage 1 – low grade, no spread; stage 2 – high grade but not spread; stage 3 – bone cancer of any grade that has spread beyond the bone in which it started to other organs in the body, such as the lungs. In recurrent bone cancer, the cancer has returned after initial treatment. The most common treatment for bone cancer pain is radiation. Radiation decreases bone cancer pain by direct effects on tumor cells (Goblirsch et al, 2005). Chemotherapy may also be needed; sore mouth or anemia may result. Surgery is reserved for neurological compromise, radiation failure, or spinal instability (Ecker et al, 2005). When possible, limbsparing surgery is effective. Occasionally, amputation is necessary when the cancer has spread from the bone into the surrounding blood vessels. Quality of life in this population is affected by depression, socialization problems, and physical limitations (Rustoen et al, 2005). Bisphosphonates are the standard of care for preventing skeletal morbidity and treating hypercalcemia of malignancy in patients with bone metastases; zoledronic acid may be given intravenously at the rate of 4 milligrams monthly (Gnant, 2009).

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CLINICAL INDICATORS Genetic Markers: Bone morphogenetic proteins (BMPs) may impact tumorigenesis and promote tumor spread (Thawani et al, 2009). Specific Clinical/ Fever and cough Bone scan History CT scan Height Weight Lab Work BMI H&H Weight loss Leg, shin, shoul- Alkaline phosphatase der pain? (Alk phos) Limited use of (increased) the extremity Glucose (Gluc) Fatigue Ca Warmth in a Mg local area

Na, K Albumin (Alb) C-reactive protein (CRP) Total lymphocyte count (TLC) (varies) Alanine aminotransferase (ALT) (increased)

• Cisplatin, carboplatin (Paraplatin), cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), high-dose methotrexate with leucovorin, ifosfamide (Ifex) may be used. • Dry mouth, anemia, stomatitis, nausea, esophagitis, or vomiting may occur.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss ways to make meals more attractive and appetizing. • Discuss with the patient and family how to adjust diet for therapies given. • Encourage the patient to address depression or other issues that affect quality of life. • Offer suggestions according to side effects such as sore mouth or dry mouth.

INTERVENTION Patient Education—Food Safety


Prevent dehydration; correct fever. Relieve pain; prolong and improve quality of life. Correct side effects, such as sore mouth or anemia. Counteract effects of surgery (perhaps limb amputation), radiation therapy, or chemotherapy. • Meet needs related to growth or elevated metabolic rate in children.

FOOD AND NUTRITION • A balanced diet (high in energy and protein) will be needed. • Extra fluids are used, unless contraindicated. • Supplement with nutrients that are low in the patient’s dietary intake. A diet rich in zinc, vitamins A and C, and other key nutrients will help with wound healing after surgery. A multivitamin–mineral supplement may be suggested. • Small, frequent feedings may be better tolerated than large meals.

Common Drugs Used and Potential Side Effects • Bisphosphonates may be used to restrict the action of the osteoclasts, help reduce the breakdown of the bone, reduce the risk of fracture and hypercalcemia, and reduce bone pain.

• Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

American Cancer Society – Bone Cancer

Bone Cancer Information

Bone Tumor

Clinical Guidelines for Bone Cancer

Medicine Net – Bone Cancer

BONE CANCER AND OSTEOSARCOMA—CITED REFERENCES Clines GA, Guise TA. Hypercalcaemia of malignancy and basic research on mechanisms responsible for osteolytic and osteoblastic metastasis to bone. Endocr Relat Cancer. 12:549, 2005. Ecker RD, et al. Diagnosis and treatment of vertebral column metastases. Mayo Clin Proc. 80:1177, 2005. Gnant M. Bisphosphonates in the prevention of disease recurrence: current results and ongoing trials. Curr Cancer Drug Targets. 9:824, 2009. Goblirsch M, et al. Radiation treatment decreases bone cancer pain through direct effect on tumor cells. Radiat Res. 164:400, 2005. Li S, Siegel GP. Small cell tumors of bone. Adv Anat Pathol. 17:1, 2010. Rustoen T, et al. Predictors of quality of life in oncology outpatients with pain from bone metastasis. J Pain Symptom Manage. 30:234, 2005. Thawani JP, et al. Bone morphogenetic proteins and cancer: review of the literature [Published online ahead of print Dec 29, 2009]. Neurosurgery.

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BONE MARROW OR HEMATOPOIETIC STEM-CELL TRANSPLANTATION NUTRITIONAL ACUITY RANKING: LEVEL 4 DEFINITIONS AND BACKGROUND Hematopoietic stem cells are cells from which all blood cells evolve. Since bone marrow contains the greatest concentration of blood stem cells, most transplantations, historically, have been bone marrow transplantations. However, with the administration of an artificial growth factor called granulocyte colony-stimulating factor (G-CSF), stem cells are stimulated to grow and leave marrow and can be collected from the bloodstream by apheresis. The terms “hematopoietic stem-cell transplantation” and “peripheral-blood stem-cell transplantation” are used when referring to bone marrow transplantation. Peripheral-blood stem-cell transplantations are being used with increased frequency because it is much less invasive. Traditional bone marrow harvest requires the use of general anesthesia. Treatment consists of a preparative regimen that includes high-dose chemotherapy and may also include total-body irradiation. An infusion of autologous (the patient’s own), syngeneic (from an identical twin), or allogeneic (from a histocompatible related or unrelated donor) marrow follows. Hematological malignancies, including leukemias, lymphomas, multiple myeloma, and aplastic anemia, are the main indications for stem-cell transplantation. Nonhematological malignancies, such as testicular cancer and some autoimmune conditions, are also indications for stem-cell transplantation. Stem-cell transplantations are performed in both adult and pediatric populations. Stem-cell transplantations in patients with matched siblings versus unrelated donors have been associated with significantly better longterm survival (Talano et al, 2006). After transplantation, the patient is often neutropenic, and nutritional status may decline rapidly. Children undergoing bone marrow transplantation may have suboptimal nutritional status; body mass index (BMI) is not an accurate indicator in these cases (White et al, 2005). Hospitalized transplantation patients resume oral intake sooner than ambulatory patients. Treatment is aggressive and has many side effects. Early side effects are basically the same as those of any other type of high-dose chemotherapy and are caused by damage to bone marrow and other rapidly reproducing tissues of the body. Hepatic veno-occlusive disease (VOD) occurs after high doses of chemotherapy in preparation for bone marrow transplantation. Rapid weight gain, elevated bilirubin, right upper quadrant (RUQ) pain, ascites, jaundice, and hepatomegaly can occur. Long-term side effects could include radiation damage to the lungs with shortness of breath, graft-versus-host disease (GVHD), damage to the ovaries causing infertility and loss of menstrual periods, damage to the thyroid gland causing problems with metabolism, cataracts, bone damage, and growth changes in children. GVHD causes erythroderma, jaundice, abdominal pain, emaciation, pneumonitis, infec-

tions, and gastrointestinal tract problems. Hemolytic uremic syndrome (HUS) is an uncommon but potentially lifethreatening complication of stem-cell transplantation.


CLINICAL INDICATORS Genetic Markers: Umbilical cord blood may be used in children born after a genetic diagnosis for human leucocyte antigen (HLA) matching for donation to a sick sibling. Specific Clinical/ Gluc Mg, Ca History Complete blood Height count (CBC) Weight Absolute BMI neutrophil Weight changes count (ANC) Diet history to evaluate I&O engrafting Temperature Na, K Ascites, jaundice Alb, Frequent transthyretin infections Viral hepatitis Hepatomegaly? screening RUQ pain? CRP Rectal biopsy for Serum phosphoGVHDa rus (low from cyclosporine Lab Work A) Uric acid H&H Bilirubin

Cholesterol (Chol) Triglycerides (Trig) TLC (varied reliability) Ferritin Transferrin Blood urea nitrogen (BUN) Creatinine (Creat)


Severe colonic crypt loss predicts severe clinical GIGvHD that is more likely to be refractory to steroid treatment and have high mortality (Melson et al, 2007).

INTERVENTION OBJECTIVES Pretransplantation • Replace the malignant or defective hematopoietic system for the production and development of blood cells. • Provide adequate nutrient stores (glucose, calories, vitamins, minerals, and protein). Supplementation with EPA

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TABLE 13-10

Decreased Oral Food–Beverages Intake

To reduce the introduction of pathogenic organisms into the gastrointestinal tract of immunocompromised patients, food safety practices and dietary changes are in order. The following are practices that may be helpful to patients after bone marrow transplantation (for 3 months or until immunosuppressive therapies are complete):

Assessment Data: Analysis of oral intake compared to requirements from nursing flow sheet; patient states pain while eating; physical examination of the oral cavity. Nutrition Diagnosis (PES): NI-2.1 oral intake related to pain and mucositis as evidenced by the refusal of food at mealtimes. Intervention: Diet modification for consistency. Education about foods that may be better tolerated. Counseling about taking pain medicines ahead of meals. Monitoring and Evaluation: Follow-up in 24 hours to evaluate improvement and changes in oral intake.

fish oil improves energy intake and may reduce complications and inflammatory markers when compared with usual care (Elia et al, 2006). • Assure adequate hydration.

Posttransplantation • Restore normal hematopoiesis and immunological function. • Individualize needs; promote engraftment of marrow. • Prevent or manage gastrointestinal Graft-Versus-Host Disease (GI-GvHD). Rejection occurs less often in wellnourished patients. • Prevent infections, viral hepatitis, mucositis, gastroenteritis, and pneumocystosis. • Reduce nausea, vomiting, diarrhea, appetite loss and fatigue, which can seriously affect nutritional status (Iversen et al, 2009). • Improve weight status; promote anabolism. Most patients are in the hospital for 4–6 weeks. • Correct early satiety, anorexia, stomatitis, xerostomia, and depression—all of which reduce total intake. • Provide nutrition support due to hypermetabolism and side effects of treatments. Promote positive nitrogen balance when possible. • Correct hyperglycemia from metabolic stress, insulin resistance, and medication side effects. • Monitor closely for renal insufficiency and necessary changes for diet. • Prevent or prepare for long-term complications such as hyperphagia and obesity, insulin resistance and diabetes, hyperlipidemia, hypertension, and osteoporosis. • Maximize quality of life. Health-related quality of life (HRQoL) is reduced before, during, and after intensive therapy (Iversen et al, 2009).

FOOD AND NUTRITION • Protective isolation may be needed. A low-bacteria (neutropenic) diet may be useful for several months before and after transplantation. A neutropenic diet guide is found in Table 13-10. • CPN may be needed to initiate recovery after transplantation or with severe intestinal GVHD. Where possible,

• • • • • • • • • • • • • • • • • • • • • • • •

Neutropenic Diet Guidelines

Ensure careful hand washing. Keep foods at a safe temperature to prevent food infection. Microwave hot foods immediately before service. Avoid foods that fall into the following categories: All moldy or outdated food products Deli cheeses and foods Hot dogs, bacon, sausage, luncheon meats Miso and tempeh products Pickled fish, cold smoked salmon, and lox Powdered infant formula Raw and unpasteurized milk and dairy products Raw brewer’s yeast Raw honey Raw or undercooked meats, fish, shellfish, poultry, eggs, game meats Raw vegetable sprouts Salad dressings made with raw eggs Soft or mold-containing cheese (Brie, feta, blue) Stir fried vegetables or fruits Tofu Unboiled well water (it should be boiled at least one minute) Unpasteurized beer or fruit juices Unrefrigerated cheese-based salad dressings Unwashed fruits or vegetables Yogurt and other dairy products with active cultures

Adapted from: Oncology Nutrition Practice Group. The clinical guide to oncology nutrition. 2nd ed. Chicago, IL: American Dietetic Association, 2006.

the use of intravenous fluids and oral diet should be considered as a preference to parenteral nutrition; however, with severe gastrointestinal failure, even with a trial of enteral feeding, use PN (Murray and Pindoria, 2009). A naso-jejunal (NJ) feeding is associated with less vomiting and aspiration. The use of glutamine to decrease oral mucositis or diarrhea among patients receiving autologous or allogeneic HCT is not necessary (American Dietetic Association, 2010). • Use indirect calorimetry to determine energy requirements where possible (American Dietetic Association, 2010). Provide 30–35 kcal/kg for the first month; increase for weight gain, infection, GVHD, or neutropenia. • Protein intake should be 1.5–2 g/kg of weight; increase during corticosteroid therapy. • Fat intake should be 25–30% of total kilocalories to prevent fatty acid deficiency and to support blood glucose control (American Dietetic Association, 2010). Monitor for hyperlipidemia. An olive oil-based lipid emulsion compared with a MCT/LCT emulsion can be well tolerated; maintain essential fatty acids, and support a favorable plasma lipid profile (Hartman et al, 2009).

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• If there is hyperglycemia, keep carbohydrate intake at a steady amount each day. • Sterile water may be used for hydration and renal health. Maintain 1 mL/Kg intake. • A multivitamin–mineral supplement may be useful. Assure adequate intake of vitamin D and calcium with long-term steroid use. Potassium and magnesium can be depleted by some medications; monitor carefully. Avoid iron in supplements if transfusions have been frequent; iron overload may occur. • Patient may need a low-lactose, low-fiber, low-fat diet. Progress, as tolerated, to normal diet. • As patient recovers and no longer requires a protective setting, the use of live-culture pasteurized yogurt may be beneficial to increase bowel flora. Lactobacillus acidophilus therapy can also be helpful.

Common Drugs Used and Potential Side Effects • See Table 13-11.

TABLE 13-11


Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. • St. John’s wort and echinacea should not be taken with cyclosporine, because they alter drug functioning.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The neutropenic, low-bacteria diet protocol should be made available, as appropriate. • Help the patient and family to manage signs of gastrointestinal GVHD; this usually includes anorexia, nausea, vomiting, watery diarrhea, abdominal pain, and GI bleeding (Xu et al, 2008). • Small, frequent meals of bland, cold consistency may be well-tolerated. • Discuss any necessary nutritional support methods and procedures to be used at home or in discharge planning.

Drugs Commonly Used in Bone Marrow or Stem-Cell Transplantation

Conditioning chemotherapy or irradiation is given immediately before the transplant to suppress immune reactions. Drug


Analgesics, antihistamines, and antidepressants

Monitor for specific side effects.


Amphotericin may be used to fight infections. Nausea, stomach pain, or vomiting may occur.


Acyclovir may be given prophylactically to resolve oral ulcers. Headaches, gastrointestinal(GI) distress, or diarrhea may occur.


These may be needed if there is osteopenia or osteoporosis.


Busulfan (to destroy marrow stem cells) and cyclophosphamide (Cytoxan) are given to prevent rejection of the transplant. They can cause nausea, vomiting, diarrhea, and anorexia. Methotrexate, fludarabine, carmustine, and cyclophosphamide may cause anorexia, mucositis, and esophagitis; some also cause diarrhea. Gleevec interferes with an abnormal enzyme that sends signals to the nucleus of a cancer cell. Nausea, extensive diarrhea, and vomiting are potential side effects. Useful for leukemia or advanced stomach cancer.

Immunosuppressive therapy (graft-versus-host disease [GVHD] prophylaxis)

GVHD prophylaxis consists of T-cell depletion (antibody T10B9 or OKT3 and complement) with posttransplantation cyclosporine (Talano et al, 2006). Antithymocyte globulin may cause vomiting, nausea, diarrhea, and stomatitis. Azathioprine may cause vomiting, nausea, diarrhea, mucosal ulceration, esophagitis, and steatorrhea. Beclomethasone can lead to thrush, nausea, and xerostomia. Corticosteroids cause sodium and fluid retention, weight gain, hyperglycemia, skeletal muscle wasting, growth retardation in children, peptic ulceration, and elevated triglycerides. Cyclosporine (Sandimmune) may cause nausea and vomiting, skin rashes, hemorrhagic cystitis, and altered potassium metabolism. Methotrexate causes nausea and vomiting, mucositis, esophagitis, diarrhea, renal and liver changes, decreased absorption of vitamin B12, fat, and D-xylose, and taste changes. Monoclonal antibodies cause nausea and vomiting. Sirolimus elevates triglycerides. Tacrolimus can be nephrotoxic or cause hyperglycemia, hyperkalemia, or hypomagnesemia. Ursodeoxycholic acid can cause nausea and vomiting, diarrhea, and GI distress.

Filgrastim (Neupogen)

Neutropenia secondary to immune suppression may be managed with Neupogen and a low-bacteria diet.


May be needed if there is hyperglycemia.

Oral hygiene

Clotrimazole (Mycelex) may cause nausea or vomiting; it is used for oral hygiene and prevention of oral candidiasis.

Total-body irradiation (TBI)

Side effects vary for each individual, but anorexia, diarrhea, and mucositis or esophagitis are common.

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Transition from CPN and PN to enteral nutrition or oral diet will be helpful. • Physical therapy may be helpful to maintain strength and to regain mobility.

National Cancer Institute – BMT bone-marrow-transplant


Patient Education—Food Safety • Educate about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly. • The neutropenic, low-bacteria diet includes the careful use of raw fruits and vegetables, milk, and shellfish—all of which may be contaminated easily with bacteria. These diets are often used in bone marrow transplantation units.

For More Information •

Bone Marrow Support Group

Medline Plus – BMT

National Bone Marrow Transplant Link

American Dietetic Association (ADA). Evidence analysis library: Oncology. Accessed January 3, 2010, at Elia M, et al. Enteral (oral or tube administration) nutritional support and eicosapentaenoic acid in patients with cancer: a systematic review. Int J Oncol. 28:5, 2006. Hartman C, et al. Olive oil-based intravenous lipid emulsion in pediatric patients undergoing bone marrow transplantation: a short-term prospective controlled trial. Clin Nutr. 28:631, 2009. Iversen PO, et al. Reduced nutritional status among multiple myeloma patients during treatment with high-dose chemotherapy and autologous stem cell support [Published online ahead of print Dec 29, 2009]. Clin Nutr. Melson J, et al. Crypt loss is a marker of clinical severity of acute gastrointestinal graft-versus-host disease. Am J Hematol. 82:881, 2007. Murray SM, Pindoria S. Nutrition support for bone marrow transplant patients. Cochrane Database Syst Rev. 1:CD002920, 2009. Talano JM, et al. Alternative donor bone marrow transplant for children with Philadelphia chromosome ALL. Bone Marrow Transplant. 37:135, 2006. White M, et al. Nutritional status and energy expenditure in children prebone-marrow-transplant. Bone Marrow Transplant. 35:775, 2005. Xu CF, et al. Endoscopic diagnosis of gastrointestinal graft-versus-host disease. World J Gastroenterol. 14:2262, 2008.

BRAIN TUMOR NUTRITIONAL ACUITY RANKING: LEVEL 3 Corpus callosum astrocytoma oligodendroglioma lipoma Third ventricle and area ependymoma

Lateral ventricle ependymoma glioblastoma multiforme

Cerebrum astrocytoma oligodendroglioma lymphoma metastatic tumors

Pineal area pineocytoma pineoblastoma Optic chiasm astrocytoma

Pituitary area craniopharyngioma pituitary adenoma epidermoid cyst

Acoustic nerve neuroma

Brain stem astrocytoma glioblastoma multiforme metastatic tumors Fourth ventricle ependymoma

Cerebellum medulloblastoma astrocytoma hemangioblastoma metastatic tumors

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DEFINITIONS AND BACKGROUND Tumors are either primary or secondary when they are found in the brain. Primary brain tumors start their growth in the brain and can be benign or malignant. They can occur in children, particularly girls between the ages of 5 and 9. Approximately 17,000 Americans each year are diagnosed with a primary brain tumor. Secondary brain tumors are more common, with about 90,000 cases diagnosed each year. These tumors result from cancer that has metastasized to the brain from the lung, breast, melanoma, kidney, or other part of the body. Brain tumors destroy or damage brain cells by producing inflammation, compressing other parts of the brain as the tumor grows, and causing swelling and pressure inside the skull. Headache is the most common symptom. Brain tumor headaches are usually worse upon awakening and do not respond to the usual headache medicines. Depression, fatigue, and memory and personality changes may complicate care (Stewart-Amidei, 2005). Table 13-12 describes types of brain tumors and cells of origin. The nerve cells (neurons) carry signals, and the cells that support them are called glial cells. There are a number of different types of glial cells, all with different names and functions, and they outnumber the neurons by a ratio of 10:1. A glioma is a tumor of neurological origin; it constitutes over 50% of all brain tumors. Glioblastoma multiforme (GBM) is the most frequent and devastating primary malignant brain tumor in adults. Surgery followed by standard radiotherapy with temozolomide chemotherapy is the standard of care, but the prognosis remains poor with survival in the range of 12–15 months

TABLE 13-12

Types of Brain Tumors

Type of Tumor

Location, Cell Origin, or Function

CNS Lymphoma

Affects the body’s immune system, which defends against infection and foreign substances.


Located around the pituitary gland.


Germ cell tumors.


Originate in the glial supporting tissues. Types include astrocytoma; brain stem glioma; oligodendroglioma that affects myelin production; ependymoma affects the ventricles that aid in the circulation of cerebrospinal fluid.


The meninges cover and protect the brain and spinal cord.


These cells normally do not remain in the body after birth; primitive neuroectodermal tumors (PNET).


Originate in the brain.

Pineal gland tumors

Pineocytoma or pineoblastoma are around the pineal gland.


Affects the myelin that protects the acoustic nerve for hearing; acoustic neuromas are in this category.

Source: National Cancer Institute,, accessed January 5, 2010.


(Minniti et al, 2009). While fruit, vegetables, and carotenoids do not increase the risk of glioma (Holick et al, 2007), adequate GLA and DHA fatty acids, lycopene, beta carotene, and other antioxidants are under study. There is also no evidence that the intake of meat, nitrate, nitrite, or nitrosamines is related to the risk of glioma (Michaud et al, 2009). Meningiomas are also common and may be classified as benign, atypical, or malignant. While surgical excision is curative for most patients, up to 20% recur (Lee et al, 2009). Because malignant brain tumors are largely dependent on glycolysis for energy, normal neurons and glia readily transition to ketone bodies (beta-hydroxybutyrate) for energy when glucose levels are reduced (Seyfried and Mukherjee, 2005). Increased melanocortin activity and reduced neuropeptide Y function lead to catabolism with reduced energy intake, increased energy expenditure, increased muscle proteolysis, and adipose tissue loss (Laviano et al, 2008). Nutritional status and weight decline early in treatment (Ward et al, 2009). Anorexia, early satiety, changes in taste/ smell, and nausea are frequently reported. Ghrelin has antiinflammatory properties that may help to alleviate cachexia and improve weight gain; ghrelin receptor agonists show promise (DeBoer 2008). Some brain tumors can be treated successfully with surgery, radiation therapy, and chemotherapy. Emerging technologies allow physicians to target and treat brain tumors more precisely. Antiangiogenesis approaches have the potential to be particularly effective in the treatment of glioblastoma tumors (Anderson et al, 2008). Convection-enhanced delivery (CED) has emerged as a leading investigational delivery technique for the treatment of brain tumors (Bidros et al, 2010).


CLINICAL INDICATORS Genetic Markers: Five “classes” of meningiomas have been detected by gene expression analysis where chromosomes 22q, 6q, and 14q are involved (Lee et al, 2009). Genomic deletion of chromosomes 6, 21, and 22 represents new targets for further research (Lassman et al, 2005). Specific Clinical/ Aphasia Cerebral edema, History headaches Height Vertigo Weight Altered BMI consciousness Weight changes or convulsions Diet history Mental or BP (hypertenpersonality sion?) changes Inability to Unequal pupil follow response commands

Hemianopsia, blurred or decreased vision Ptosis Altered gait or immobility Dysphagia Vomiting (with or without nausea) Tinnitus

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Loss of sense of smell CT scan Diffusion MRI Skull x-ray Electroencephalogram (EEG) Lumbar puncture

TLC, white blood cell Gluc (elevated) count (WBC) Cerebrospinal (altered) fluid (CSF)— WBC in CSF elevated (normal or protein increased) levels Transferrin Alb, ALT (elevated) transthyretin NA, K CRP Serum folate Lab Work

INTERVENTION OBJECTIVES • Provide adequate energy (30 kcal/kg or more if needed). • Provide adequate protein for surgery: 1.2–1.5 g/kg body weight; for radiation: 1.0–1.2 g/kg body weight. Adjust for renal/hepatic dysfunction; obesity; skin breakdown or wound healing. • Avoid constipation and straining. • Prevent lower respiratory infections; coughing can increase intracranial pressure. • Counteract side effects of therapy (e.g., radiation, surgery). • Monitor carefully for elevated blood glucose levels, which may occur with corticosteroids that are used to control brain edema. • Prevent complications such as the loss of ability to interact, care for self, or permanent neurological losses.

• Offer meal setup and assistance with eating, altered liquid/ food textures, and/or enteral tube feedings for patients with cognitive deficits, swallowing difficulties, or limited function of upper extremity.

Common Drugs Used and Potential Side Effects • Seizures are best managed with antiepileptic drug therapy (Stewart-Amidei, 2005). Levetiracetam (Keppra), an anticonvulsant, reduces seizures in malignant brain tumors and may help improve chemotherapy outcomes. Monitor for decreased serum folic acid levels and other nutrients. • The use of procarbazine (an antineoplastic) may warrant the restriction of tyramine-containing foods that are secondary to its monoamine oxidase (MAO) inhibitor–like action. • Nonsteroidal anti-inflammatory agents may help to reduce inflammation (Byrne, 2005). • Steroid therapy may be used. Decrease sodium and increase potassium if appropriate. Negative nitrogen balance or hyperglycemia may result. Maintain near-normal blood glucose levels if possible. • Osmotic diuretics may be needed for edema. Antacids or antihistamines may be needed for stress ulcers. • Temozolomide (Temodar) was approved for brain cancer and GBM in particular.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician.

FOOD AND NUTRITION • Maintain diet, as ordered. Include extra fluid, unless contraindicated. • If oral diet is possible, include fish, fruits, vegetables, and adequate fiber. Include green tea, food sources of beta carotene, and fish oil to enhance neuroprotection. • Alter texture and liquids, if necessary, for dysphagia. If necessary, tube feed or offer CPN. • Limit sodium to 4–6 g/d to correct cerebral edema.

SAMPLE NUTRITION CARE PROCESS STEPS Swallowing Difficulty Assessment Data: Weight loss of 10# in 6 weeks; cognitive changes; brain tumor. Mealtime observation shows choking on thin liquids and inability to swallow solids. Nutrition Diagnosis (PES): NC-1.1 Swallowing difficulty related to neurological changes as evidenced by inability to consume solids, choking on thin liquids, and 10# weight loss in 6 weeks. Intervention: Enteral nutrition support with gastrostomy. Educate the patient and family about the benefits of tube feeding. Monitoring and Evaluation: Recovery of lost weight; tolerance for chemotherapy and radiation treatments.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • The importance of regular and attractive meals should be stressed to help appetite if fair or poor. Keep in mind that sense of smell may have declined recently. • Discuss the importance of a balanced diet with good sources of protein at meals. • Early discussion about end-of-life issues is necessary because the disease can impair the patient’s decisionmaking ability (Stewart-Amidei, 2005). • A multidisciplinary approach using physical, occupational, and speech therapies is essential to maximize neurological function and activities of daily living.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Brain Tumor Clinical Trials: Musella Foundation

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Interactive Tour of the Brain

National Brain Tumor Foundation

OncoLink—Brain Cancer 25&id9534

BRAIN TUMOR—CITED REFERENCES Anderson JC, et al. New molecular targets in angiogenic vessels of glioblastoma tumours. Expert Rev Mol Med. 10:e23, 2008. Bidros DS, et al. Future of convection-enhanced delivery in the treatment of brain tumors. Future Oncol. 6:117, 2010. Byrne TN. Cognitive sequelae of brain tumor treatment. Curr Opin Neurol. 18:662, 2005. DeBoer MD. Emergence of ghrelin as a treatment for cachexia syndromes. Nutrition. 24:806, 2008. de Meijia EG, et al. Bioactive components of tea: cancer, inflammation and behavior. Brain Behav Immun. 23:721, 2009.

Holick CN, et al. Prospective study of intake of fruit, vegetables, and carotenoids and the risk of adult glioma. Am J Clin Nutr. 85:877, 2007. Lassman AB, et al. Molecular study of malignant gliomas treated with epidermal growth factor receptor inhibitors: tissue analysis from North American brain tumor consortium trials. Clin Cancer Res. 11:7841, 2005. Laviano A, et al. NPY and brain monoamines in the pathogenesis of cancer anorexia. Nutrition. 4:802, 2008. Lee Y, et al. Genomic landscape of meningiomas [Published online ahead of print November 20, 2009]. Brain Pathol. Michaud DS, et al. Prospective study of meat intake and dietary nitrates, nitrites, and nitrosamines and risk of adult glioma. Am J Clin Nutr. 90:570, 2009. Minniti G, et al. Chemotherapy for glioblastoma: current treatment and future perspectives for cytotoxic and targeted agents. Anticancer Res. 29:5171, 2009. Seyfried TN, Mukherjee P. Targeting energy metabolism in brain cancer: review and hypothesis. Nutr Metab (London). 2:30, 2005. Stewart-Amidei C. Managing symptoms and side effects during brain tumor illness. Expert Rev Neurother. 5:71S, 2005. Ward E. et al. Nutritional problems in children treated for medulloblastoma: implications for enteral nutrition support. Pediatr Blood Cancer. 53:570, 2009.


The Stages of Cancer The earlier cancer is found and treated, the better the chances of getting well. The diagnosis of cancer is done by a microscopic test (biopsy) of a piece of tissue. Measuring the amount the cancer has spread (grown), called staging, can be done using medical imaging techniques. The stage of a cancer tells the doctor how far it has spread. It is important because treatment is often decided according to the stage of a cancer. Doctors use different systems to stage cancers.

Cancer tumor Large intestine (cut to reveal inside)

Stage I: The cancer is small, localized, and limited. Stage II: Local spreading occurs within the organ and Small intestine lymph nodes.

Asset provided by Anatomical Chart Co.


Stage IV: Metastasis (spread) of the tumor occurs in other tissues of Lymph nodes Stage III: the body. Cancer cells invade through the organ and lymph nodes.

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DEFINITIONS AND BACKGROUND Colorectal cancer (CRC) is the third most common type of cancer in the United States, but the second leading cause of cancer deaths. Family history of colorectal cancer is a risk factor in 25% of cases. Hereditary nonpolyposis colorectal cancer (HNPCC, or Lynch syndrome) is one inherited form. High risk for CRC exists among patients with ulcerative colitis and Crohn’s disease after 8 or more years of duration. The incidence of colorectal cancer rises significantly after age 50 and doubles with each successive decade. Cyclooxygenase2 (COX-2) and its proinflammatory metabolite, prostaglandin E2 (PGE2), enhance colon cancer progression (Castellone et al, 2005). Obesity is a risk factor (Fuemmeller et al, 2009). Bile acid deoxycholic acid (DCA) promotes the hyperproliferation of colonic epithelial cells and the risk of colon cancer (Zeng et al, 2009). Table 13-13 lists other factors that either promote or prevent CRC. The adenomatous polyp is the precursor of most colorectal cancers. In Stage 0 CRC, early cancer is on the innermost layer of the intestine; in Stage 1, it is in the inner layers of the colon; in Stage 2, cancer has spread through the muscle wall of the colon. In Stage 3, the cancer has spread to the lymph nodes and in Stage 4, it has spread to other organs and is usually incurable.

TABLE 13-13

Biomarkers may become a way to find or treat CRC. The 8OH-dG in colorectal crypts is a biomarker of risk from oxidative DNA damage (Fedirko et al, 2010). Ibuprofen-type drugs, IL6 polymorphisms (rs1800796), and dietary alpha-tocopherol and lycopene significantly decrease the effects of TP53 mutations; beta-carotene and ibuprofen lower the risk of KRAS2 tumors (Slattery et al 2009). The interactions between genes, inflammation, and diet have been elucidated. Fecal occult blood test and flexible sigmoidoscopy are used for diagnosis. Either standard colonoscopy (optical) or computed tomography (CT) colonoscopy may be used, but the CT (virtual) colonoscopy is not available at all facilities. In cancer of the small intestine, malignancy generally is found in the lower duodenum and lower ileum, with a high rate of mortality and few early symptoms; it presents in only 5% of cases. Rectal cancer is more common in men than in women and often occurs after middle age, with bleeding, pain, and irregular bowel habits. In the colon, slow-growing malignancies are usually found in the cecum, lower ascending colon, and sigmoid colon. Few early symptoms are found, but the prognosis is optimistic. The right side of the colon (ascending) absorbs fluids and salts; cancer spreads upward here and obstruction is rare. The left side of the colon (the descending colon) stores feces; cancer here tends to encircle the bowel and cause obstructions. If surgery is required, maintaining the ileocecal valve is crucial.

Risks and Protective Factors for Colorectal Cancer

Protective Factors

Risk Factors

Alpha-tocopherol and beta carotene (Slattery et al, 2009) Aspirin or nonsteroidal anti-inflammatory drugs (Kaur Saini et al, 2009; Slattery et al, 2009)

Age 50

Calcium and vitamin D3 (Fedirko et al, 2010; Jenab et al, 2009)

Alcohol intake, excessive (Emmons et al, 2005)

Folic acid (Ulrich, 2005)

Chronic inflammatory and inflammatory cytokines (Bowen et al, 2009)

Lutein and lycopene (Slattery et al, 2009)

Family history of familial adenomatous polyposis (FAP) or hereditary non-polyposis colon cancer (HNPCC)

Green tea

Medical history of colon polyps, inflammatory bowel disease, other types of cancer

Omega-3 fatty acids

Overweight and obesity

Selenium; methylselenol is a critical metabolite (Zeng et al, 2009)

Smoking, particularly at an early age (Botteri et al, 2008; McCleary et al, 2010)

Sulforaphane (broccoli, cruciferous vegetables)

Western-style diet, high in red meat and fat; low in vegetables, folic acid, calcium and vitamin D (Emmons et al, 2005)

REFERENCES Botteri E, et al. Smoking and colorectal cancer: a meta-analysis. JAMA. 300:2765, 2008. Bowen KA, et al. PTEN loss induces epithelial–mesenchymal transition in human colon cancer cells. Anticancer Res. 29:4439, 2009. Emmons KM, et al. Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer. Cancer Epidemiol Biomarkers Prev. 14:1453, 2005. Fedirko V, et al. Effects of supplemental vitamin D and calcium on oxidative DNA damage marker in normal colorectal mucosa: a randomized clinical trial. Cancer Epidemiol Biomarkers Prev. 19:280, 2010. Jenab M. Vitamin D receptor and calcium sensing receptor polymorphisms and the risk of colorectal cancer in European populations. Cancer Epidemiol Biomarkers Prev. 18:2485, 2009. Kaur Saini M, et al. Chemopreventive response of diclofenac, a non-steroidal anti-inflammatory drug in experimental carcinogenesis. Nutr Hosp. 24:717, 2009. McCleary NJ, et al. Impact of smoking on patients with stage III colon cancer: results from Cancer and Leukemia Group B 89803 [Published online ahead of print Jan 5, 2010]. Cancer. Ulrich CM, et al. Polymorphisms in the reduced folate carrier, thymidylate synthase, or methionine synthase and risk of colon cancer. Cancer Epidemiol Biomarkers Prev. 14:2509, 2005. Zeng H, et al. Deoxycholic acid and selenium metabolite methylselenol exert common and distinct effects on cell cycle, apoptosis, and MAP kinase pathway in HCT116 human colon cancer cells. Nutr Cancer 62:85, 2010.

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SAMPLE NUTRITION CARE PROCESS STEPS Abnormal Gi Function Assessment Data: Recent weight loss (10# in 2 months). Diarrhea and constipation; hx of dark, thin stools and blood. Dx of colon cancer.

CLINICAL INDICATORS Genetic Markers: Both cellular factors and genetic changes enhance tumor invasion. Vitamin D receptor (VDR) genes regulate the epithelial changes that initiate tumor cells; the BB genotype of the VDR polymorphism is associated with a reduced risk of colon cancer (Jenab et al, 2009). Chemokine receptor CCR5 expression and increased CD8() T-cell infiltration may be found (Zimmermann et al, 2010). While folate status may be linked with CRC because of its role in DNA synthesis, the CT MTHFR polymorphism decreases risk by 15–18% (Levine et al, 2010). Finally, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is associated with late stage CRC (Bowen et al, 2009). Specific Clinical/ Dehydration, electrolyte History imbalances Height Intestinal Weight obstruction, BMI bowel abscess Obesity? Fistula Unintentional Proctoscopy weight loss? Colonoscopy Diet history Digital rectal Rectal bleeding, examination pain Irregular bowel Lab Work habits CEA level Alternating (CEA 125) diarrhea and constipation 8-OH-dG in colorectal crypts Abdominal Colon lavage distention, cytology bloating Serum folate, Thin, pencil B12 stools Serum homocysWeakness teine Anorexia

MTHFR genotyping Fecal occult blood test (FOBT) H&H (decreased) Serum Fe Transferrin Na K (often decreased) Chol, Trig TLC (varies) WBC, ESR (increased) Alb, transthyretin CRP Mg, Ca Serum zinc

INTERVENTION OBJECTIVES • Decrease residue, particularly with obstruction, until fiber is better tolerated. • Prevent rapid weight loss; correct anemia. Maintain hydration. • Counteract side effects of therapies: chemotherapy, resection, or radiation. Nutrition counseling improves patient outcomes in radiotherapy (Ravasko et al, 2005). • Provide nutrients in a tolerable form—oral, parenteral, or enteral.

Nutrition Diagnosis (PES): Abnormal GI function related to alternating diarrhea and constipation as evidenced by dark stools, and constipation 3 weekly on average followed by bloody diarrhea. Intervention: Food-nutrient delivery—oral nutritional supplement between meals; mild fiber supplement as tolerated. Educate the patient about dietary changes that can be beneficial. Provide counseling about possible nutritional procedures (i.e., colostomy) after surgical resection. Monitoring and Evaluation: No further weight loss before surgery. Tolerance for fiber in diet and from supplement. Adequate preparation for surgery, followed with appropriate changes in feeding method and counseling after colostomy.

• Include sufficient total amounts of folate and vitamin B6 since disrupted DNA synthesis affects carcinogenesis (Sharp et al, 2008). • Provide sufficient vitamin D3 (Grant, 2009). • Prevent or ameliorate starvation diarrhea. • Protect against recurrence by dietary changes indicated in Table 13-13.

FOOD AND NUTRITION • CPN or TF may be needed for an extended period of time; include glutamine. • Administer parenteral fluids with adequate electrolytes, vitamins C and K, and selenium (if used over a long time). Monitor vitamin D, calcium, iron, zinc, and fat intakes for adequacy. • With ileal resection, vitamin B12 deficiency can occur, and bile salts may be lost in diarrhea. Hyperoxaluria and renal oxalate stones can be a problem. With massive bowel resection, malabsorption, malnutrition, metabolic acidosis, and gastric hypersecretion may result. • With ileostomy and colostomy, salt and sodium/water balance are problems. Ostomy diets may be needed (see ileostomy and colostomy entries in Section 7). Increase energy and ensure adequate protein. • Decrease fiber until tolerated. Eventually, increase whole grains including rye bread, cereals, fruits, and vegetables. • Consume less alcohol and more folic acid from spinach, broccoli, asparagus, avocado, orange juice, dried beans, and fortified cereals (Kim, 2007). • Eat less red meat; use more poultry, fish, tofu, and beans as protein sources. • Discuss the inclusion of other protective foods, such as calcium-rich foods; lutein and lycopene (tomato products, watermelon, spinach, kale, greens, broccoli, romaine lettuce, and pink grapefruit); cumin; cereal, bean, vegetable, and fruit fiber; flavonoids (apples, onions, green tea, and chamomile tea); cruciferous vegetables; coffee; omega-3

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fatty acids from fish and walnuts; selenium foods such as Brazil nuts; and unsaturated fats such as flaxseed, salmon, and canola and olive oils. • A multivitamin supplement is beneficial, particularly for folic acid and vitamins B6 and D3. • Monitor carefully for lactose intolerance. Use lactase enzyme products when indicated. • Physical activity should be encouraged as much as possible.

• •

Common Drugs Used and Potential Side Effects • Chemotherapy may be used for 6–8 months, particularly with stage 3 colon cancer. Monitor for side effects because these agents may further impact bowel function. • The multidrug combination of oxaliplatin, fluorouracil, and leucovorin is standard treatment for metastatic colorectal carcinoma (Caraglia et al, 2005). Fluorouracil plus levamisole, methotrexate, mitomycin, lomustine, and vincristine may lead to diarrhea, nausea, vomiting, low WBC, and mouth sores. • Bevacizumab (Avastin) use leads to a significant decrease in colon cancer deaths. Cetuximab (Erbitux), when added to chemotherapy, will shrink tumors and delay progression. • COX-2 inhibitors may be helpful because 50% of polyps and 85% of colonic tumors in humans overexpress COX-2 (Samoha and Arber, 2005). The nonsteroidal antiinflammatory drug, Diclofenac, is a preferential COX-2 inhibitor, which can be an effective chemopreventive agent in colon cancer (Kaur et al, 2009). • Regular low doses of aspirin may reduce prostaglandin production; GI bleeding can result.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. • Folate vitamers (tetrahydrofolate, 5,10-methylenetetrahydrofolate) should be studied further for their roles in CRC (Sharp et al, 2008). • With methotrexate (Rheumatrex), avoid echinacea; it may damage the liver. • A vitamin D3 supplement, such as 1100 IU daily, seems to be of benefit (Grant, 2009). • Low-dose fish oil supplementation may be useful to reduce inflammation. • Sea cucumber extract contains Frondanol A5—a glycolipid extract with potential chemopreventive properties (Janakiram et al, 2009). • Sour orange (cirtus aurantium) has protective liminoid properties (Perez et al, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • At first, limit foods that may cause gas, such as corn, broccoli, cauliflower, beans, cabbage, melon, and carbonated beverages. Provide instruction on hydration and the use

• •

• • • •

of fiber to help with bowel management, particularly for rectal cancer patients. Family members (offspring and other first-degree relatives) should have a digital examination annually at 40 years of age, stool tests for blood after 50 years of age, and sigmoidoscopy or colonoscopy after age 50 every 3–5 years. Medical advice may include regular use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Discuss an appropriate dietary regimen for any specific problems. Weekly Medical Nutrition Therapy (MNT) that includes an individualized nutrition prescription and counseling improves calorie and protein intake, nutrition status, quality of life (QOL), and reduces symptoms of anorexia, nausea, vomiting and diarrhea (American Dietetic Association, 2010). Encourage family participation in all levels of care. Discuss how to prevent future polyps. High compliance with a low-fat, high-fiber diet is associated with a reduced risk of adenoma recurrence (Sansbury et al, 2009). Omit trans-fatty acids as much as possible (Vinikoor et al, 2009). A high intake of flavonols, which are at greater concentrations in beans, onions, apples, and tea, is also associated with decreased risk (Bobe et al, 2008). Suggest an intake of berries, chocolate, coffee, soy foods, folate from foods and supplements, lutein and carotenoids from fruits or vegetables, and whole grains such as rye. Encourage dairy products for calcium, vitamin D, and lactose content. If necessary, use lactase enzymes. Encourage physical activity when feasible. Surveillance following curative treatment generally includes history and physical exams every 6 months for 5 years, then every 3 months for 2 years, and then every 6 months for 3–5 years (Sunga et al, 2005).

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Colon Cancer Page

Medline Information–Colorectal Cancer

National Colorectal Cancer Action Campaign

COLORECTAL CANCER—CITED REFERENCES American Dietetic Association (ADA). Evidence analysis library: Oncology. Accessed January 8, 2010, at topic.cfm?cat3250. Bobe G, et al. Dietary flavonoids and colorectal adenoma recurrence in the Polyp Prevention Trial. Cancer Epidemiol Biomarkers Prev. 17:1344, 2008. Bowen KA, et al. PTEN loss induces epithelial–mesenchymal transition in human colon cancer cells. Anticancer Res. 29:4439, 2009. Caraglia MD, et al. Chemotherapy regimen GOLF induces apoptosis in colon cancer cells through multi-chaperone complex inactivation and increased Raf-1 ubiquitin-dependent degradation. Cancer Biol Ther. 4:1159, 2005. Castellone MD, et al. Prostaglandin E2 promotes colon cancer cell growth through a novel Gs-axin-beta-catenin signaling axis. Science. 310:1504, 2005.

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Fedirko V, et al. Effects of supplemental vitamin D and calcium on oxidative DNA damage marker in normal colorectal mucosa: a randomized clinical trial. Cancer Epidemiol Biomarkers Prev. 19:280, 2010. Fuemmeller ER, et al. Weight, dietary behavior, and physical activity in childhood and adolescence: implications for adult cancer risk. Obes Facts. 2:179, 2009. Grant WB. A critical review of Vitamin D and cancer: a report of the IARC Working Group. Dermatoendocrinol. 1:25, 2009. Janakiram NB, et al. Chemopreventive effects of Frondanol A5, a Cucumaria frondosa extract, against rat colon carcinogenesis and inhibition of human colon cancer cell growth. Cancer Prev Res (Phila Pa). 3:82, 2010. Jenab M. Vitamin D receptor and calcium sensing receptor polymorphisms and the risk of colorectal cancer in European populations. Cancer Epidemiol Biomarkers Prev. 18:2485, 2009. Kaur Saini M, et al. Chemopreventive response of diclofenac, a non-steroidal anti-inflammatory drug in experimental carcinogenesis. Nutr Hosp. 24:717, 2009. Kim DH. The interactive effect of methyl-group diet and polymorphism of methylenetetrahydrofolate reductase on the risk of colorectal cancer. Mutat Res. 622:14, 2007. Levine AJ, et al. Genetic variability in the MTHFR gene and colorectal cancer risk using the colorectal cancer family registry. Cancer Epidemiol Biomarkers Prev. 19:89, 2010. Perez JL, et al. Limonin methoxylation influences the induction of glutathione S-transferase and quinone reductase. J Agric Food Chem. 57:5279, 2009.


Ravasko P, et al. Dietary counseling improves patient outcomes: a prospective, randomized, controlled trial in colorectal cancer patients undergoing radiotherapy. J Clin Oncology. 23:1431, 2005. Samoha S, Arber N. Cyclooxygenase-2 inhibition prevents colorectal cancer: from the bench to the bed side. Oncology. 69:33S, 2005. Sansbury LB, et al. The effect of strict adherence to a high-fiber, high-fruit and -vegetable, and low-fat eating pattern on adenoma recurrence. Am J Epidemiol. 170:576, 2009. Sharp L, et al. Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene, intakes of folate and related B vitamins and colorectal cancer: a case-control study in a population with relatively low folate intake. Br J Nutr. 99:379, 2008. Slattery ML, et al. Tumor markers and rectal cancer: support for an inflammation-related pathway. Int J Cancer. 125:1698, 2009. Sunga AY, et al. Care of cancer survivors. Am Fam Physician. 71:699, 2005. Vinikoor LC, et al. Trans-fatty acid consumption and its association with distal colorectal cancer in the North Carolina colon cancer study II [Published online ahead of print October 20, 2009]. Cancer Causes Control. Zeng H, et al. Deoxycholic acid and selenium metabolite methylselenol exert common and distinct effects on cell cycle, apoptosis, and MAP kinase pathway in HCT116 human colon cancer cells. Nutr Cancer. 62:85, 2010. Zimmermann T, et al. Low expression of chemokine receptor CCR5 in human colorectal cancer correlates with lymphatic dissemination and reduced CD8() T-cell infiltration [Published online ahead of print Jan 7, 2010]. Int J Colorectal Dis.


Mouth and Throat Cancer Cancer-causing chemicals from tobacco products increase the risk of cancer of the lip, cheek, tongue, and larynx (voice box). The removal of these cancers can be disfiguring and can result in loss of the larynx.

Thyroid Nodules and Cancer

Nodules Cancer

Asset provided by Anatomical Chart Co. Cancer of the tongue

Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Head and neck cancers affect esophageal, hypopharyngeal, laryngeal, lip and oral cavity, nasopharyngeal, oropharyngeal, paranasal sinus and nasal cavity, parathyroid, or salivary glands. Annually, approximately 38,000 people in the United States are diagnosed with a head or neck cancer; the highest overall incidence rate is in black males. Tobacco is linked with 85% of these cancers; alcohol is another risk.

Obesity is a factor in many cases (Steffen et al, 2009). See Table 13-14 for more details. Damage from acid reflux may contribute to esophageal cancer. Folate and homocysteine derangements are common. A diet rich in fruits, vegetables, selenium, zinc, and folate is associated with a reduced risk of head and neck cancer (Falciglia et al, 2005; Kane, 2005; Steevens et al, 2010). Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer with low survival rates in advanced stages.

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TABLE 13-14

Key Factors in Types of Head and Neck Cancer



Oral cavity

Caused by sun exposure (lip); possibly human papillomavirus (HPV) infection; paan (betel quid) used by Southeast Asians; intake of mate, a tea-like beverage habitually consumed by South Americans. May present with gingival swelling, pain, bleeding, and loosening teeth. The disorder is rare in persons younger than age 40. Risk of metastasis is great; only about half of these individuals will live longer than 5 years.


More common in Chinese ancestry. Caused by Epstein-Barr virus infection; occupational exposure to wood dust; and consumption of certain preservatives or salted foods. Signs include unilateral obstruction, epistaxis, pain, otological changes, and nasal obstruction.


Caused by poor oral hygiene; HPV infection and the use of mouthwash that has a high alcohol content are possible, but not proven, risk factors. There may be a dull ache, dysphagia, referred otalgia, and trismus.

Paranasal sinuses and nasal cavity

Caused by industrial exposures, such as wood or nickel dust inhalation. Tobacco and alcohol use play less of a role in this type of cancer.


Plummer-Vinson syndrome is a rare disorder that results from iron and other nutritional deficiencies with severe anemia. Dysphagia results as webs of tissue grow across the upper part of the esophagus.


Caused by exposure to airborne particles of asbestos, particularly in the workplace. Voice changes, dysphagia, odynophagia, and dyspnea occur.

Parotid and salivary glands

Caused by radiation to the head and neck. This exposure can come from diagnostic X-rays or from radiation therapy for noncancerous conditions or cancer. Unilateral symptoms and impaired jaw mobility can occur. The parotid gland is the largest salivary gland. Cancer here is rare. Surgery is often curative.

Esophageal cancer

Develops in the middle or lower third of the esophagus. It is one of the more common types of head and neck cancer. It presents as adenocarcinoma or squamous cell cases that require surgical resection. This condition is more common in persons older than 50 years of age, particularly males. Barrett’s esophagus (BE) is a premalignant condition associated with esophageal cancer; cyclooxygenase-2 (COX-2) is overexpressed. Aspirin and other nonsteroidal anti-inflammatory drugs may help prevent esophageal cancer. Stage 0 is very early and affects only the first layer of cells; in Stage V, the cancer has metastasized.

Thyroid cancer

A lump on the side of the neck, hoarseness, and dysphagia can be signs. Thyroidectomy may be used, or radioactive iodine (RDI) can be used to destroy cancerous cells that remain after surgery. A low-iodine diet may be needed about 2 weeks before the RDI treatment.

Derived from: National Cancer Institute,, accessed January 9, 2010.

The prognosis for cure worsens as the depth of tumor invasion increases. Surgery is possible for some cases. Cervicofacial and cervicothoracic rotation flaps provide a reliable means to reconstruct complex defects of the face, lateral skull base, and neck (Moore et al, 2005). Many head and neck cancer patients are malnourished before treatment begins, and those who are treated with radiotherapy are at an increased risk of malnutrition due to the severe side effects (Moore et al, 2005; Wood, 2005). Radiation therapy side effects may include odynophagia, dysphagia, mucositis, esophagitis, xerostomia (with occasional osteoradionecrosis), dental caries, weight loss, taste changes, and decreased appetite. Prophylactic placement of a gastrostomy feeding tube is useful. Thyroid cancer affects approximately 26,000 people in the United States. Thyroid-stimulating hormone (TSH) from the pituitary causes the thyroid gland to produce thyroid hormones and to release thyroglobulin. Papillary tumors are the most common type; they arise as an irregular, solid, or cystic mass from otherwise normal thyroid tissue. Distant metastasis is uncommon, but lung and bone are the most common sites. Tumors that invade or extend beyond the thyroid capsule have a worse prognosis. Often, the thyroid gland is surgically removed as a cure. Thyroxine medicine (Synthroid, Levoxyl, and Unithroid) is needed to keep TSH levels low.


CLINICAL INDICATORS Genetic Markers: An epigenome-wide screen has revealed a set of genes that are commonly methylated and downregulated in head and neck cancers (SEPT9, SLC5A8, FUSSEL18, EBF3, and IRX1). All five interact with components of the TGF-beta pathway; their silencing results in a coordinated decrease in apoptosis, increased proliferation, and decreased differentiation (Bennett et al, 2009). Specific Clinical/History Height Weight BMI Obesity? Unplanned weight loss

Diet history BP I&O Dehydration? Temperature Dysphagia, painful swallowing

Substernal pain or feeling of fullness Regurgitation of undigested food Malaise Malnutrition Anemia

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Regurgitation after eating Hiccups, foul breath Aspiration Increased salivation Hoarseness and coughing Gingival swelling, pain, bleeding, or hyperplasia Nonhealing ulcerative oral lesions Mucositis, esophagitis Xerostomia Dental caries

Taste changes, decreased appetite Loosening teeth Oral biopsy Esophageal webs with achalasia? Palpable mass Barium swallow Endoscopy Nasopharyngoscopy Direct laryngoscopy, esophagoscopy Biopsy Lab Work

CRP Transferrin H&H ALT (increased) Gluc Serum zinc (low?) Triiodothyronine (T3) Thyroxine (T4) Thyroidstimulating hormone (TSH) Ca, Mg Na, K Alb, transthyretin Chol Bicarbonate

Alb, transthyretin

INTERVENTION OBJECTIVES • Prepare for treatments such as surgery, radiation, or chemotherapy. The dietitian should provide a pretreatment evaluation and weekly visits for 6 weeks during chemoradiation treatment to reduce weight loss,


• • • • • • •


unplanned hospitalization, length of stay, and tolerance for full treatment (American Dietetic Association, 2010). Prevent malnutrition, further weight loss, cachexia, and aspiration. Weight loss, caused by acute mucositis and dysphagia, is common during concurrent chemotherapy and irradiation (chemoradiotherapy) of head and neck cancer (Lin et al, 2005). Because nutrition support for patients with head and neck cancer is associated with a significant increase in total energy ingestion, placing gastrostomy tubes prophylactically prevents disruption to treatment plans (Moore et al, 2005; Wood, 2005). Meet nutritional needs with tube feeding, as needed. Progress to goal with minimal signs and symptoms of intolerance (nausea, fullness). Transition to full or partial oral intake when feasible. If resection is needed, fat malabsorption, reflux, dumping syndrome, increased mediastinal pressure, and increased food transit time may be side effects. Hydrate adequately; encourage fluids between meals and limit fluid intake at meals to improve intake of other foods. Promote adequate wound healing, positive nitrogen balance, and retention of lean body mass. Prevent or correct anemia, sepsis, abscesses. Monitor for dysphagia, difficulty chewing, mucositis, xerostomia, fibrosis, and dental caries after treatments. Assure adequate mouth care. Omit alcoholic beverages and abstain from tobacco, including chewing snuff. In patients with advanced cancer: reduce symptoms, preserve organ function, and improve quality of life as much as possible. Provide palliative care if needed.


Involuntary Weight Loss Assessment: Recurrent squamous cell carcinoma of the larynx; s/p emergency tracheostomy, radiation and chemotherapy. NPO due to swallowing difficulty; on GT bolus feeding. Elevated BUN & creatinine levels. On oxycodone for pain. Nutrition Diagnosis (PES): Involuntary weight loss (NC-3.2) related to decreased oral intake and dysphagia as evidenced by weight loss of 21% in 17 months. Interventions: Nutrient delivery—ND 2.41 enteral feeding tube; ND 3.21 multivitamin supplement. Education: Discuss home tube feeding that is appropriate for the patient’s condition. Counseling: C-2.2 goal setting: minimize weight loss, maintain adequate hydration, prevent aspiration, and improve quality of life. Coordination of Nutrition Care: RC-1.1 Interdisciplinary team meeting with nursing, speech therapy, social worker, and recreational therapy. Monitor and Evaluation: Monitor for weight improvement. No GI problems or enteral nutrition intolerance. Improvement in renal lab values. Reassess nutritional needs via GT. Reassess with speech evaluation for possible transition to full or partial oral intake when feasible.

• Adjust diet individually to meet the patient’s needs. Nutrition support enhances desirable outcomes (Odelli et al, 2005). After radiation: xerostomia, ulceration, bleeding, and pain may result; after chemotherapy, nausea, vomiting, weakness, and fatigue may occur (Dixon, 2005). • Be careful not to create refeeding syndrome, which is potentially fatal. Progress slowly in patients who have been malnourished for a week or longer. Begin with 10 kcal/kg per day and increase slowly; use thiamin and other B-complex vitamins in a supplement (Mehanna et al, 2009). • Eventually, provide a diet high in energy and protein with bland or pureed foods as required: 30–35 kcal/kg; 1.0–1.5 g protein/kg. • A dysphagia diet (thick pureed foods, decrease in thin liquids) may be needed. Tolerance will vary for hot and cold foods and drinks; monitor and alter intake accordingly. • Patients are often fed with gastrostomy or jejunostomy feedings. Cellular and morphological changes follow a period of malnutrition; enteral feeding is an important strategy for maintaining gut integrity and function (Sica et al, 2005). Use enteral feeding formulas that are high in omega-3 fatty acids (Aiko et al, 2005) and arginine (De Luis et al, 2009). • Increase fluid intake as tolerated; dehydration is common.

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• Increase intake of vitamins D3, A and C; zinc; and other nutrients that may be low. Otherwise, a multivitamin– mineral supplement is indicated if oral intake is not possible. • If esophagectomy has been performed, gastric stasis or dumping syndrome may occur. The use of needle catheter jejunostomy (NCJ) is safe, with an extremely low rate of complications over a prolonged period at low costs (Sica et al, 2005). • If an oral diet is possible, omit irritants such as black pepper and chili powder and dilute acidic fruits or juices such as orange, grapefruit, and tomato. • Use protective foods to prevent recurrence; use beans, vegetables, fish, foods rich in zinc and lycopene, whole grains, citrus fruits, and vitamin C–rich foods. • Polyphenols show great promise; EGCG in green tea is particularly beneficial (Baumeister et al, 2009). • With thyroid cancer, a low-iodine diet may be needed prior to surgery or treatment. • In advanced cases, offer palliative care. Hydration and comfort are the focus.

Common Drugs Used and Potential Side Effects • Aspirin can lower esophageal cancer risk by 90% by reducing prostaglandin production. Some doctors will prescribe a low daily dose to prevent recurrence. • Chemotherapy with cisplatin may be used, along with radiation therapy. Cisplatin can cause nausea, vomiting, altered taste, changes in renal function, and diarrhea. Weight loss during cisplatin-containing chemoradiotherapy is associated with reduced kidney function; findings highlight the importance of intensive supportive measures of nutrition and hydration beyond standard measures, and these steps should be started before 10% weight loss occurs (Lin et al, 2005). • Bleomycin and methotrexate can lead to nausea, vomiting, anorexia, or stomatitis. • Steroids may be used to reduce inflammation; hyperglycemia, sodium retention, potassium depletion, and negative nitrogen balance can result. • Pilocarpine may be used as a saliva substitute for xerostomia.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss a diet rationale that is appropriate for the patient’s condition. If the patient can eat orally, encourage him or her to chew slowly. • If jejunostomy feeding is required after esophagastric surgery, teach the patient/family/caretaker how to prepare feedings and how to produce the item in a clean environment. • During radiation therapy/surgical recovery, patients with gastrostomy tubes should be encouraged to practice swallowing exercises, as prescribed by the speech pathologist, to maintain swallowing function and reduce the risk of fibrosis. Encourage help from speech therapy. • Hypothyroid status can cause dysphagia; counsel accordingly. • If oral diet is possible, discuss the use of protective foods. • Relaxation therapy or biofeedback can be beneficial. • Radiation-induced fibrosis (RIF) is caused by reduced blood supply months or years later. Rinse with vitamin E solutions and use 1000 IU tocopherol with pentoxifylline to decrease mucositis (Chiao and Lee, 2005; Haddad et al, 2005). Use small frequent feedings and oral supplements.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly. • For home tube feeding or CPN, teach the principles of safe handling and administration. Discuss the signs of infection or intolerance and when to contact the health team.

For More Information •

CancerLinks USA–Esophageal Cancer

Liquid Diets

Low Iodine Cookbook

Medline–Esophageal Cancer

National Cancer Institute–Esophageal Cancer – Nutrition

Herbs, Botanicals, and Supplements (see Table 13-8)

National Institutes of Health Cancer Information

Thyroid Cancer Survivors’ Association

• Herbs and botanical supplements should not be used without discussing it with the physician. • Avoid the use of echinacea with cyclosporine or methotrexate (Rheumatrex) because of potential damage to the liver. Avoid St. John’s wort also. • Curcumin is a powerful inhibitor of COX-2 expression (Khafif et al, 2009). • L-carnitine is sometimes used to decrease toxicity from agents such as bleomycin. • Zinc supplementation helps in managing mucositis after radiation.

Thyroid Cancer – Mayo Clinic

ESOPHAGEAL, HEAD AND NECK, AND THYROID CANCERS—CITED REFERENCES Aiko S, et al. The effects of immediate enteral feeding with a formula containing high levels of omega-3 fatty acids in patients after surgery for esophageal cancer. J Parent Enter Nutr. 29:141, 2005. American Dietetic Association (ADA). Evidence analysis library: Oncology. Accessed January 9, 2010, at

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Baumeister P, et al. Epigallocatechin-3-gallate reduces DNA damage induced by benzo[a]pyrene diol epoxide and cigarette smoke condensate in human mucosa tissue cultures. Eur J Cancer Prev. 18:230, 2009. Bennett KL, et al. Disruption of transforming growth factor-beta signaling by five frequently methylated genes leads to head and neck squamous cell carcinoma pathogenesis. Cancer Res. 69:9301, 2009. Chiao TB, Lee AJ. Role of pentoxifylline and vitamin E in attenuation of radiation-induced fibrosis. Ann Pharmacother. 39:516, 2005. DeLuis DA, et al. High dose of arginine enhanced enteral nutrition in postsurgical head and neck cancer patients. A randomized clinical trial. Eur Rev Med Pharmacol Sci. 13:279, 2009. Dixon SW. Nutrition care issues in the ambulatory (outpatient) head and neck cancer. Support Line. 27:3, 2005. Falciglia GA, et al. A clinical-based intervention improves diet in patients with head and neck cancer at risk for second primary cancer. J Am Diet Assoc. 105:1609, 2005. Haddad P, et al. Pentoxifylline and vitamin E combination for superficial radiation-induced fibrosis: a phase II clinical trial. Radiother Oncol. 77:324, 2005. Kane MA. The role of folates in squamous cell carcinoma of the head and neck. Cancer Detect Prev. 29:46, 2005. Khafif A, et al. Curcumin: a potential radio-enhancer in head and neck cancer. Laryngoscope. 119:2019, 2009.


Lin A, et al. Metabolic abnormalities associated with weight loss during chemoirradiation of head-and-neck cancer. Int J Radiat Oncol Biol Phys. 63:1413, 2005. Mehanna H, et al. Refeeding syndrome – awareness, prevention and management. Head Neck Oncol. 1:4, 2009. Mercuri A, et al. The effect of an intensive nutritional program on daily setup variations and radiotherapy planning margins of head and neck cancer patients. J Med Imaging Radiat Oncol. 53:500, 2009. Moore BA, et al. Cervicofacial and cervicothoracic rotation flaps in head and neck reconstruction. Head Neck. 27:1092, 2005. Odelli C, et al. Nutrition support improves patient outcomes, treatment tolerance and admission characteristics in oesophageal cancer. Clin Oncol. 17:639, 2005. Sica GS, et al. Needle catheter jejunostomy at esophagectomy for cancer. J Surg Oncol. 91:276, 2005. Steevens J, et al. Selenium status and the risk of esophageal and gastric cancer subtypes: the Netherlands cohort study [Published online ahead of print Jan 6, 2010]. Gastroenterology. Steffen A, et al. Anthropometry and esophageal cancer risk in the European prospective investigation into cancer and nutrition. Cancer Epidemiol Biomarkers Prev. 18:2079, 2009. Wood K. Audit of nutritional guidelines for head and neck cancer patients undergoing radiotherapy. J Hum Nutr Diet. 18:343, 2005.

GASTRIC CANCER NUTRITIONAL ACUITY RANKING: LEVEL 3–4 DEFINITIONS AND BACKGROUND Gastric cancer (GC) is a carcinoma that most commonly occurs in the pyloric segment and along the lesser curvature. Cancer that begins in the glandular cells is an adenoma; this type is over 90% of gastric cancers. If the cancer starts in the immune system, it is a lymphoma; if it starts in the hormonal system, it is called carcinoid syndrome. Another very rare form starts in the nervous system and is called a gastrointestinal stromal tumor (GIST). Diffuse forms have a poor prognosis. In GC, early definitive signs are rare. GC may follow longterm pernicious anemia, Ménétrier’s disease, or chronic gastritis. It is generally found in males aged 50–70 years and among smokers. While frequency is low in the United States, it is high in Japan and China. Gastric carcinoma is the second leading cause of cancer-related deaths in the world, accounting for more than 700,000 deaths each year (Hatakeyama, 2009). Helicobacter pylori infection plays a role. Chemokine production and antiapoptosis are mediated by H. pylori and may drive lymphocytes to malignancy. Infection with cagA-positive H. pylori plays an essential role; this protein is delivered into gastric epithelial cells via the bacterial secretion system where it contributes to the transformation of gastric epithelial cells (Hatakeyama, 2009). See Table 13-15 for other risk factors. A recent study shows a protective role for riboflavin and vitamin B6 (Eussen et al, 2010). Physical activity and eating a diet high in fruits, vegetables, beta-carotene, and vitamin C may also decrease the risk for GC (Kim et al, 2005; Vigen et al, 2006). Greater adherence to a Mediterranean dietary pattern is associated with a significant reduction in the risk of incident GC (Buckland et al, 2009).

Surgery is the most common treatment. Very small, stage 1 cancers that are limited to the inside lining of the stomach may be removed using endoscopy. In a subtotal gastrectomy, only the affected stomach portion is removed. In stages 3 or 4, it may be necessary to remove the entire stomach and connect the esophagus to the small intestine. Laparoscopic surgery is less invasive and recovery is faster. Neoadjuvant radiation may be used before surgery to shrink a stomach tumor, or it can also be used after surgery to kill any remaining cancer cells. Radiation therapy may cause diarrhea, nausea, or vomiting. Chemotherapy may also be used along with radiation therapy or for advanced cancers that cannot be treated through surgery. TABLE 13-15

Risks for Gastric Cancer

Advanced age Chronic atrophic gastritis, pernicious anemia, gastric polyps Diet high in red meat Diet high in salt, salted foods, smoked and preserved foods Diet low in vitamin E or selenium Eating foods contaminated with aflatoxin fungus Ethnicity—young white and Hispanic males; African-Americans from poor socioeconomic backgrounds Family history of gastric cancer, Ménétrier’s disease, intestinal metaplasia H. pylori gastric infection Low use of fruits and vegetables Male gender Smoking

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CLINICAL INDICATORS Genetic Markers: Genetic predisposition is a risk factor in gastric cancer. Aberrant methylation of several genes is noted; some have a poor prognosis. Ecadherin is involved with diffuse forms; and SNP analysis (including IL1B) may elucidate the role of inflammation and stem cells in premalignant lesions (Milne et al, 2009). Specific Clinical/ Anorexia Anemia, pallor History Vertigo Height Nausea or Weight vomiting BMI Melena Weight loss? MRI or CT Diet scan history Barium swallow I&O Endoscopy Dehydration? BP Lab Work Feeling of H. pylori fullness Low serum Indigestion, pepsinogen belching I/II ratio Dysphagia

Alb, transthyretin CRP Ca, Mg Na, K Gluc H&H Transferrin ALT (increased) Melena, occult blood Serum folic acid, B12

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Mineral Intake Assessment Data: Diagnosis of gastric cancer, stage 1; several small polyps found on endoscopy. BMI normal, no sign of H. pylori. Lives in region known to have low levels of selenium in the soil (coastal Carolinas). Diet history indicates no intake of seleniumrich foods or multivitamin–mineral supplementation. Some nausea and melena noted. Nutrition Diagnosis (PES): Inadequate selenium intake related to poor diet and supplementation as evidenced by diet history and residence in area known to have selenium-poor soil. Intervention: Food-Nutrient Delivery—Provide foods high in selenium; encourage the use of a daily multivitamin supplement that contains the daily value for selenium. Educate—teach the patient and family about food sources of selenium. Counseling—provide tips on other cancer preventive factors. Coordinate care with the medical team after the surgical removal of the gastric polyps. Monitoring and Evaluation: Successful minor surgery. Improvement in intake of selenium from food and daily supplement; better intake of other protective factors. Able to maintain BMI within desirable range. No further melena or nausea.

• Prevent or reverse weight loss and further malnutrition. • Encourage fluids. • Counteract side effects of chemotherapy, radiation, or gastrectomy. If gastrectomy is performed, dumping syndrome or hypochlorhydria may result. • Promote wound healing. Replete visceral proteins as stress level decreases. • Correct protein-losing enteropathy. • Prevent cancer recurrence by including protective foods. • Improve quality of life.

FOOD AND NUTRITION • Parenteral therapy may be used, particularly before surgery. • If oral diet is possible, include protective foods such as Allium in garlic (raw or lightly cooked), carotenoids and lycopene (Ito et al, 2005), fish, fruits, nonherbal tea, indoles and sulforaphane from cruciferous vegetables, and quercetin from apples and yellow onions. Vitamin B6 and riboflavin should be included (Eussenn et al, 2010) as should selenium and vitamin E (Qiao et al, 2009). • After resection, patients are often volume-sensitive and need small meals and snacks with fluids between meals. When oral intake is allowed, try light meals that are nutrient-dense, high-protein/high-energy. Drink 35 mL/kg of fluid or more, unless contraindicated. • After gastrectomy, manage dumping syndrome, where undigested food enters the small intestine too quickly. Small, frequent feedings may be better tolerated. Concentrated carbohydrates, alcohol, and carbonated beverages should be severely limited or omitted. See entry in Section 7 also. • Jejunostomy feeding may be needed at the time of a resection. Monitor tolerance carefully. • Be sure that dietary intake and supplementation includes selenium, zinc, vitamin C, and other key nutrients for wound healing and correction of anemia. Take supplements with food.

Common Drugs Used and Potential Side Effects • Antibiotic therapy is needed to eradicate H. pylori bacteria where present. • Cytotoxic drugs such as mitomycin C may cause fever, nausea, vomiting, anorexia, and stomatitis. • With fluorouracil (FU), anorexia and nausea are common. Sore mouth, taste changes, and vomiting also may result. Added thiamin is recommended, and leucovorin is often used with FU. • In a rare form of gastrointestinal stromal tumor (GIST), imatinib (Gleevec) is useful; it interferes with an abnormal enzyme that sends signals to the nucleus of a cancer cell. Nausea and vomiting are potential side effects. Imatinib shrinks tumors by more than half with minimal side effects (Heinrich and Corless, 2005).

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• Sunitinib (Sutent) is useful in stomach cancer when imatinib is not effective.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. • Treatment with a combination of 50 micrograms of selenium, 30 milligrams of vitamin E, and 15 milligrams of beta-carotene leads to decreased mortality from gastric cancer (Qiao et al, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Feeding tubes such as jejunostomy may be useful in the home setting. • If eating orally, instruct patient on postgastrectomy diet. Encourage patient to chew slowly and well. • Discuss protective foods and phytochemicals. • If the stomach was resected, vitamin B12 anemia is likely to occur within several years; monitor carefully. Injections will likely be needed for life.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.


• With tube feeding, discuss the safe handling of formula and tubing.

For More Information •

H. pylori and Cancer Fact Sheet

Memorial Sloan-Kettering Cancer Center

National Cancer Institute–Gastric Cancer healthprofessional

OncoLink–Gastric Cancer

GASTRIC CANCER—CITED REFERENCES Buckland G, et al. Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study [Published online ahead of print Dec, 2010]. Am J Clin Nutr. Eussen SJ, et al. Vitamins B2 and B6 and genetic polymorphisms related to one-carbon metabolism as risk factors for gastric adenocarcinoma in the European prospective investigation into cancer and nutrition. Cancer Epidemiol Biomarkers Prev. 19:28, 2010. Hatakeyama M. Helicobacter pylori and gastric carcinogenesis. J Gastroenterol. 44:239, 2009. Heinrich MC, Corless CL. Gastric GI stromal tumors (GISTs): the role of surgery in the era of targeted therapy. J Surg Oncol. 90:195, 2005. Ito H, et al. Polyphenol levels in human urine after intake of six different polyphenol-rich beverages. Br J Nutr. 94:500, 2005. Kim HJ, et al. Effect of nutrient intake and Helicobacter pylori infection on gastric cancer in Korea: a case-control study. Nutr Cancer. 52:138, 2005. Milne AN, et al. Nature meets nurture: molecular genetics of gastric cancer. Hum Genet. 126:615, 2009. Qiao YL, et al. Total and cancer mortality after supplementation with vitamins and minerals: follow-up of the Linxian General Population Nutrition Intervention Trial. J Natl Cancer Inst. 101:507, 2009. Vigen C, et al. Occupational physical activity and risk of adenocarcinomas of the esophagus and stomach. Int J Cancer. 118:1004, 2006.



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

Liver cancer (hepatocellular carcinoma, HCC) is the fifth most common cancer and is one of the leading causes of cancer death worldwide (Yam et al, 2010). Primary hepatic tumors are common with alcohol abuse, aflatoxin ingestion, chronic hepatitis, or low weight at birth (see Table 13-16). HCC may develop after years of chronic inflammation and persistent mucosal or epithelial cell colonization by hepatitis B or C viruses. Malignant hepatic tumors are common due to metastatic lesions from other organs. HCC accounts for almost half a million cancer deaths a year, and the incidence is escalating in the Western world and in developing countries. HCC progresses in a stepwise manner, mostly regulated by gene expression; untreated liver cancer may rapidly lead to death within a year. Early identification of malnutrition status is required for proper intervention. In one study, over 60% of hospitalized patients were malnourished; the prevalence was higher in

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TABLE 13-16

Risk Factors for Liver Cancer

Aflatoxins (Voight, 2005) Anabolic steroids Arsenic in drinking water Cirrhosis from alcohol abuse or hemochromatosis (Kuper et al, 2001)

Aspartate aminotransferase (AST) – altered? ALT (abnormal)

Sedimentation rate (ESR), increased? Ca, Mg Na, K Ammonia

Alb (decreased), transthyretin CRP Gluc (decreased) Alk phos TLC (varies)

Male gender Liver disease: hepatitis B virus (HBV) and hepatitis C virus (HCV)


Obesity Oral contraceptive use (higher dose estrogen)


Tobacco use Vinyl chloride and thorium dioxide (Voight, 2005)

male patients with long hospital stays, readmitted patients, and patients who had liver cancer (Wie et al, 2009). Surgical resection is sometimes possible in some cases; laparoscopic procedures are becoming more common. Laserinduced thermotherapy for the treatment of liver metastases may be an option. In some cases, liver transplantation may be possible. Chemotherapy may be administered. Where radiation is used, radioactive substances are sent into the artery that leads directly to the liver. Computed tomography–guided focal liver irradiation combined with chemotherapy delivered via the hepatic artery may extend the lives of patients with unresectable cancer.


CLINICAL INDICATORS Genetic Markers: HCC is strongly linked to increases in allelic losses, chromosomal changes, gene mutations, epigenetic alterations, and alterations in molecular cellular pathways (Yam et al, 2010). Specific Clinical/ Steatorrhea, diarrhea History Abdominal Height fullness Weight Low-grade fever BMI Anemia, malnuProgressive trition weight loss Portal hypertenI & O, dehydrasion tion Dyspnea Anorexia, Jaundice, ascites weakness Hepatic coma? Nausea and/or Melena vomiting Hepatomegaly Increased Temperature flatulence (fever?)

Alcohol abuse? Pesticide exposure? CT or MRI Lab Work Alphafetoprotein (AFP) Prothrombin time (PT) (prolonged) H&H Transferrin

• Reduce fluid retention and ascites. • Correct serum protein levels and improve hepatic production capacity. • Prevent further nausea and vomiting, weight loss, anorexia, and malnutrition. • Counteract side effects of therapy (e.g., surgery, chemotherapy, radiation). • Improve overall nutritional and hematologic status. • Maintain adequate hydration. • Improve prognosis and prolong life as long as possible. Improve quality of life.

FOOD AND NUTRITION • Tube feed if oral diet is not feasible; patients with hepatic cancer usually have significant fluid balance/overload/ retention problems. Avoid CPN. • Progress, if and when tolerated, to high-protein diet with sufficient carbohydrate intake. Managing weight will be important to prolong life; a carefully planned weight loss diet is needed in those patients who are obese. • If hepatic coma occurs, decrease protein and supplement with amino acids (see hepatic encephalopathy in Section 8). Branched-chain amino acids may be beneficial (Togo et al, 2005).

SAMPLE NUTRITION CARE PROCESS STEPS Poor Nutritional Quality of Life Assessment Data: Liver cancer patient, weight loss of 5# in the past 2 weeks. Anorexia, nausea, and vomiting while on chemotherapy. Very fatigued. Nutrition Diagnosis (PES): Poor nutritional quality of life related to chemotherapy treatments as evidenced by fatigue, anorexia, nausea, and vomiting. Intervention: Food and nutrient delivery—offer preferred foods and beverages. Educate the patient about ways to enhance nutrient and energy density in smaller, more frequent meals. Counsel about ways to manage nausea and vomiting during chemotherapy weeks. Monitoring and Evaluation: Improvement in intake. Tolerance of chemotherapy. No further weight loss. Improved nutritional quality of life.

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• Reduce sodium if ascites and edema are significant; extra protein may be needed if albumin is also low. Monitor serum levels of other electrolytes to determine if other restrictions are needed. • Supplemental vitamins may be beneficial. Monitor serum levels of vitamins A, D, and K because of poor hepatic clearance. • With surgery, monitor nutritional intake for adequate wound healing and recovery. • Encourage small meals and snacks as tolerated throughout the day. • Decreased calcium absorption may occur after surgery. Calcium supplementation is needed, particularly in postmenopausal women.

Common Drugs Used and Potential Side Effects • Antiemetics may be used for vomiting. • Diuretics are used commonly; monitor side effects carefully. • Chemotherapy may include cisplatin, interferon, doxorubicin, and fluorouracil.


• Discuss signs of hepatic coma that require dietary alterations. • Encourage hepatitis B virus vaccination and offer information. • Provide education related to diet (regular, six small feedings) or jejunostomy tube feeding. • Community-based programs to discourage and deal with excessive alcohol intake, to promote tobacco smoking awareness, and to avoid exposure to aflatoxin and other food toxins and measures taken to reduce the pandemic of obesity and diabetes are vital for lowering the incidence of HCC from nonviral liver disease (Fan et al, 2009).

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly. • Offer tips for managing jejunostomy tube feeding safely at home under sanitary preparation and storage methods.

For More Information

Herbs, Botanicals, and Supplements (see Table 13-8)

American Liver Foundation

• Herbs and botanical supplements should not be used without discussing it with the physician. • Use of prebiotics (inulin and oligosaccharides) and silymarin may be protective. • Polyphenols, mainly flavonoids and tannins, prevent oxidative stress-induced injury (Soory, 2009). Resveratrol has anti-inflammatory action through hepatic cyclooxygenase (COX-2) inhibition (Luther et al, 2009). • Vitamin D3 can be used to treat HCC, but hypercalcemia limits its use; a lower dose is possible if fish oil is given at the same time (Chiang et al, 2009).

Liver Cancer in Children

Medline–Liver Cancer

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Hepatic cancer from hepatitis C virus infection warrants maintaining a lean weight to prolong life. • Teach the patient about the signs of deficiency of vitamins K and C, such as bleeding gums and easy bruising.

HEPATIC CANCER—CITED REFERENCES Chiang KC, et al. Fish oil enhances the antiproliferative effect of 1alpha, 25-dihydroxyvitamin D3 on liver cancer cells. Anticancer Res. 29:3591, 2009. Fan JG, et al. Prevention of hepatocellular carcinoma in nonviral-related liver diseases. J Gastroenterol Hepatol. 24:712, 2009. Luther DJ, et al. Chemopreventive doses of resveratrol do not produce cardiotoxicity in a rodent model of hepatocellular carcinoma [Published online ahead of print Oct 8, 2009]. Invest New Drugs. Soory M. Relevance of nutritional antioxidants in metabolic syndrome, ageing and cancer: potential for therapeutic targeting. Infect Disord Drug Targets. 9:400, 2009. Togo S, et al. Usefulness of granular BCAA after hepatectomy for liver cancer complicated with liver cirrhosis. Nutrition. 21:480, 2005. Wie GA, et al. Prevalence and risk factors of malnutrition among cancer patients according to tumor location and stage in the National Cancer Center in Korea [Published online ahead of print Aug 7, 2009]. Nutrition. Yam JW, et al. Molecular and functional genetics of hepatocellular carcinoma. Front Biosci (Schol Ed). 2:117, 2010.

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Cortex Medulla

Adenocarcinoma Renal artery Renal vein


hypertension, fever, anemia, and abdominal pain. A cure may be possible if metastasis has not occurred before nephrectomy. There is now an overall survival rate of 85%, and treatmentrelated morbidity has been reduced by chemotherapy (Gommersall et al, 2005). Metastasis to lungs, liver, and brain can occur. Bladder cancer can be caused by factors such as smoking, exposure to chemicals at work (such as hair dyes, textiles, and paint), old age, chronic bladder infections, and infectious parasites. Well water should be tested for arsenic. Bladder cancer is more common in Caucasians. It can often be cured in the early stages using surgery, radiation, chemotherapy, or immunotherapy. If dual nephrectomy is needed, as in a stage 5 tumor, permanent dialysis may be required until a transplant is possible.

Transitional-cell carcinoma


Asset provided by Anatomical Chart Co.

DEFINITIONS AND BACKGROUND Urinary tract cancers affect more than 50,000 Americans each year. Men are more prone to this type of cancer than women. Surgery is usually required; prognosis with early intervention is good. Survival has improved. Fruit, extra fluids, vitamin C, retinol, daily multivitamin supplements, and green and nonherbal tea tend to be protective. It is likely that vitamin D3 plays a role as well (Grant, 2009). Renal cell cancer (RCC) accounts for approximately 2% of cancers worldwide. It is most common in persons over 45 years of age, particularly among blacks. Blood in the urine and an increased frequency of urination are the most common symptoms. Smoking, long-term dialysis, occupational exposure to dyes, rubber, and leather products are risk factors. Hypertension increases the risk of RCC in both sexes, while effective blood pressure control may lower the risk (Weikert et al, 2008). Finally, obesity contributes to morbidity and mortality in renal cancer (Anderson and Caswell, 2009). Total consumption of fruits, vegetables, fat, red meat, processed meat, poultry, and seafood are not associated with the risk of RCC (Lee et al, 2008; Weikert et al, 2006). RCC can often be cured if it is diagnosed and treated when still localized to the kidney. Fortunately, the majority of patients are diagnosed at that time. Surgical resection or nephrectomy may be needed. Wilms’ tumor (nephroblastoma or embryoma of the kidney) is a highly malignant tumor occurring almost exclusively in children younger than 6 years of age. It is more common in girls than in boys, and in African-American children. Symptoms and signs include weight loss, anorexia, enlarged kidney,

CLINICAL INDICATORS Genetic Markers: Mutation of the VHL gene is associated with the development of RCC and the overexpression of the angiogenesis pathway (George and Bukowski, 2009). Some cases of Wilms’ tumor are related to defects in either Wilms’ tumor 1 (WT1) or Wilms’ tumor 2 (WT2) or to several other genes. Specific Clinical/ Smoking history History Painful Height urination Weight Frequent Weight urinary changes tract BMI infections (obesity?) Incontinence Growth Abdominal percentile in CT scan child Cystoscopy Diet history X-ray BP (increased) (intravenous I & O; pyelogram) dehydration? Bone scan for Hematuria metastasis Anorexia Urine cytology Enlarged kidney? Lab Work Fever? Urinalysis Abdominal or Ca, Mg lower back Na, K pain

Alb, transthyretin CRP BUN Creat Gluc H & H (low?) Serum Fe, ferritin Transferrin Liver function tests ALT

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SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment Data: BMI 20, down from the usual BMI of 24. Poor appetite, stomatitis. Taking temsirolimus for renal cancer. Nutrition Diagnosis (PES): Unintentional weight loss related to anorexia and stomatitis as evidenced by a BMI of 20 when the usual is 24. Intervention: Food-Nutrient Delivery—Suggest small, frequent meals of low-acid, mild foods and beverages. Educate the patient about foods that are more easily tolerated with stomatitis. Counsel about the long-term efforts to regain lost weight to tolerate cancer therapies; surgery is a possibility. Monitoring and Evaluation: No further weight loss; tolerating medication and treatments while managing side effects.

INTERVENTION OBJECTIVES • If needed, prepare patient for surgery and for postsurgical wound healing. • Control the side effects of radiotherapy and chemotherapy. • Promote normal growth and development, as far as possible, in children and teens. • Control hypertension; correct anemia, which is common. • Maintain adequate hydration. • Minimize unplanned weight loss. • Promote adequate bowel function.

FOOD AND NUTRITION • Provide adequate energy and protein according to age and to compensate for weight loss. In obese adults, weight loss regimens are not recommended until several months after surgery. • Restrict excessive sodium with hypertension. Provide sufficient potassium, calcium, and magnesium; supplement if necessary. • Monitor protein tolerance and adjust according to lab values, blood pressure, edema, and other signs of renal failure. • Ensure adequate fluid intake, particularly water. • Follow the Mediterranean or DASH diets, which encourage plenty of fruits and vegetables that are rich in antioxidants. Include fish that contains omega-3 fatty acids.

Common Drugs Used and Potential Side Effects • Rapamycin (mTOR) controls translation of key proteins during cancer cell proliferation; temsirolimus is the first mTOR inhibitor approved for the treatment of advanced RCC (Hudes et al, 2009). Side effects may include hyperglycemia, hyperlipidemia, stomatitis, rash, or even pneumonitis.


• Interferon and interleukin-2 may also be used in advanced kidney cancer. Interferon often causes patients to have flulike symptoms, and nausea and vomiting are common; interleukin-2 can cause nausea and vomiting or fluid retention. Sunitinib (Sutent) is useful in advanced kidney cancer where chemotherapy has not been effective. • Zoledronic acid is a bisphosphonate that is approved for preventing fractures after bone metastasis from renal cancer. • For bladder cancer, chemotherapy often involves carboplatin, fluorouracil, cisplatin, cyclophosphamide, methotrexate, or vinblastine. Many side effects are common, including nausea, anorexia, diarrhea, or vomiting. The use of gemcitabine and cisplatin is as useful as older treatments. • Wilms’ tumor requires perioperative vincristine and dactinomycin, with or without doxorubicin or radiotherapy (Gommersall et al, 2005).

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. Herbal preparations are subject to contamination with metals such as mercury or may contain potassium—all of which can be harmful to the kidney. • Some studies promote the use of green tea for prevention, but others have not identified its efficacy.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the side effects that the patient is experiencing in light of the therapies used (e.g., radiation therapy, chemotherapy, or surgery). • Discuss normal growth and/or desirable weight for the patient. Obesity is a concern. • Highlight meals that are attractive so that the patient eats as well as possible. Cut down on fried meats and fats. • Discuss how to manage anemia through appropriate medications or dietary measures. • There is no risk for bladder or renal cancers from the use of artificial sweeteners.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly. • In some countries, schistosomiasis infestation is a risk. Monitor for water and food safety.

For More Information •

Bladder Cancer

Kidney Cancer Association

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Medine – Bladder Cancer

Medline–Kidney Cancer

National Kidney Foundation – Council on Renal Nutrition

Wilms’ Tumor – Mayo Clinic

KIDNEY, BLADDER, AND URINARY TRACT CANCERS—CITED REFERENCES Anderson AS, Caswell S. Obesity management–an opportunity for cancer prevention. Surgeon. 7:282, 2009.

George S, Bukowski RM. Role of everolimus in the treatment of renal cell carcinoma. Ther Clin Risk Manag. 5:699, 2009. Gommersall LM, et al. Current challenges in Wilms’ tumor management. Nat Clin Pract Oncol. 2:298, 2005. Grant WB. How strong is the evidence that solar ultraviolet B and vitamin D reduce the risk of cancer? An examination using Hill’s criteria for causality. Dermatoendocrinol. 1:17, 2009. Hudes GR, et al. Clinical trial experience with temsirolimus in patients with advanced renal cell carcinoma. Semin Oncol. 36:26S3, 2009. Lee JE, et al. Fat, protein, and meat consumption and renal cell cancer risk: a pooled analysis of 13 prospective studies. J Natl Cancer Inst. 100:1695, 2008. Weikert S, et al. Blood pressure and risk of renal cell carcinoma in the European prospective investigation into cancer and nutrition. Am J Epidemiol. 167:438, 2008. Weikert S, et al. Fruits and vegetables and renal cell carcinoma: findings from the European prospective investigation into cancer and nutrition (EPIC). Int J Cancer. 118:3133, 2006.


Bronchiolar carcinoma infiltrating growth

Adapted from: Moore KL, PhD, FRSM, FIAC & Dalley AF II, PhD. Clinical Oriented Anatomy, 4th ed. Baltimore, Lippincott Williams & Wilkins 1999.

DEFINITIONS AND BACKGROUND Lung (bronchial) cancer begins in the lungs and is the most common type of cancer in the Western world. There are two main types of lung cancer: non–small-cell lung cancer and small-cell lung cancer. Non–small-cell lung cancer (NSCLC) has three major subtypes: adenocarcinoma (40% of cases), squamous carcinoma (30–35% of cases, slow growing, and

formerly called epidermoid carcinoma), and large-cell carcinoma (affecting 5–15% of cases). NSCLC is the leading cause of cancer-related death in the United States (Budde and Hanna, 2005). Small-cell lung cancer (SCLC) is a more aggressive type of lung cancer that comprises 15% of all lung cancer diagnoses. It is highly correlated to smoking. SCLCs grow quickly but tend to respond to specific chemotherapy protocols. Oat cell cancer is a highly fatal form of SCLC; aggressive chemotherapy is needed. In 85% of cases, smoking causes lung cancer. Heavy tobacco or marijuana smokers are 25 times more susceptible to lung cancer. Other causes include exposure to industrial chemicals, radon, and passive smoke. Smoking is associated with lower levels of vitamin C. The best protection against lung cancer is the avoidance of airborne carcinogens and increased consumption of fruits and vegetables (Cranganu and Camporeale, 2009). Foods rich in flavonoids may protect against certain types of lung cancer. Onions and apples have quercetin. Vitamin E food sources (gamma-tocopherol) are protective; supplemental alpha-tocopherol is not. Resveratrol may be beneficial, but excess alcohol is not (Barnardi et al, 2010). Antioxidant sources seems to be an important issue. The focus should be on food; supplemental beta-carotene is a concern (Roswall et al, 2010) whereas dietary betacarotene is protective against lung cancer. Cryptoxanthin, alpha-carotene, and ascorbic acid need to be investigated further as potentially protective factors (Comstock et al, 2008). Isothiocyanates from cruciferous vegetables are anticarcinogenic. Because the glutathione S transferase M1 (GSTM1) gene promotes urinary isothiocyanate excretion, the reduced lung cancer risk with higher isothiocyanate intake may be slightly stronger among individuals with a deletion of GSTM1 and GSTT1 (Carpenter et al, 2009; Lam et al, 2009). Novel interventions to prevent lung cancer should be developed based on the ability of diet and dietary supplements to affect reprogramming of the epigenome (Stidley et al, 2010).

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Lung cancer’s 5-year survival rate is only 15%, which is worse than many other types of cancer. Cancer cells of the lung often spread to the brain, bone, liver, and skin. Radiation and chemotherapy are needed, but surgery after standard chemotherapy and radiation can be an option for some patients. Medical nutrition therapy is often required for the nutrition-related side effects of cancer treatment, which include anorexia, nausea and vomiting, and esophagitis (Cranganu and Camporeale, 2009).


SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Intake From Parenteral Infusion Assessment Data: Inability to eat due to esophagitis over the past 1–2 days. Patient has been receiving chemotherapy treatment for lung cancer. Patient is only on PPN. Patient’s weight has been stable at home; lung cancer is a recent diagnosis yet quite advanced. Labs: WBC 1.8, slightly below normal for Na, phosphorus, magnesium, Hgb and Hct. Nutrition Diagnosis (PES):


2- Inadequate oral food intake (NI 2.1) related to esophagitis as evidenced by the inability to swallow and decreased food intake over the past 2–3 days.

CLINICAL INDICATORS Genetic Markers: Eight genes are commonly silenced in lung cancer and are associated with risk. Smokeinduced methylation may reduce HtrA3 expression, which is one concern (Beleford et al, 2010). Promoter methylation factors are controlled with the use of leafy green vegetables, folate, and the use of multivitamins (Stidley et al, 2010). Epidermal growth factor receptor (EGFR) mutations in tumors are prognostic markers in patients with early stage lung cancer. Tumor microRNAs may help to predict SCLC patients who are resistant to chemotherapy. Specific Clinical/History Height Weight BMI Diet history I&O Weight loss? Fever of unknown cause Persistent cough Bloody sputum Chest pain

Recurring pneumonia or bronchitis Fatigue Hoarseness Shortness of breath Swelling of neck or face Bronchoscopy Biopsy MRI, CT scan Thoracentesis Chest x-ray Sputum cytology

1- Inadequate intake from parenteral infusion (NI 2.3) related to limitations of peripheral access as evidenced by the inability to meet energy requirements through PPN.

Lab Work Partial pressure of carbon dioxide (pCO2) Partial pressure of oxygen (pO2) CEA Alb, transthyretin Gluc CRP Ca, Mg Na, K ALT (increased)

Interventions: Food and Nutrient Delivery: ND 4.2 Insert enteral nutrition feeding tube; NPO until PEG is surgically placed. ND 2.2 Modify rate, concentration, composition, or schedule. Once the PEG was placed, Jevity 1.5 was started 8 hours later at a rate of 35 ml/h. This was increased as tolerated by 10 milliliters every 8 hours until the goal rate of 65 ml/hr was reached. Education: Discuss appropriate feeding using a PEG tube; safe handling; signs of intolerance. Counseling: Adequate intake of tube feeding and how to adjust when oral intake is possible. Coordination of Care: RC 1.3 Collaboration/referral to other providers; patient to have home health; instruct patient on tube feeding at home. Monitoring and Evaluation: Patient tolerating goal rate of 65 ml/hr; discharged from hospital. Follow patient weight, tolerance, and intake status in 1 week. Evaluate for progress back to oral diet if esophagitis subsides.

• Maximize intake through side-effects management. Cachexia, infections, atelectasis, syndrome of inappropriate antidiuretic hormone (SIADH), esophagitis, weight loss, and anorexia may occur. • Minimum weight loss. • Maximize pulmonary health and improve quality of life. Increase disease-free time.

FOOD AND NUTRITION INTERVENTION OBJECTIVES • Patient must stop smoking, avoid passive smoke, or discontinue exposure to radon or other contributors. • Prepare patient for therapy (e.g., surgery, radiation, or chemotherapy). • Meet energy needs, which are often elevated as much as 30% above normal. The use of indirect calorimetry to measure REE is more accurate than estimation (American Dietetic Association, 2010).

• Increase the intake of protein, CHO, energy, and fluids. • Tube feedings are highly recommended if weight loss, decreased appetite, dehydration, or electrolyte imbalance occurs. • Alter diet as appropriate for side effects (see general cancer entry). Adequate vitamin-mineral intake should come from diet as much as possible. Providing medical nutrition therapy may help to improve protein and calorie intake, which may prevent weight loss and improve quality of life (American Dietetic Association). • Small, frequent meals may be beneficial.

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• If oral diet is possible, promote a protective diet. Include citrus fruits, vegetables, sesame seeds and pecans (for gamma-tocopherol), quercetin (apples and onions) and other flavonoids, selenium, lycopene, carotenoids, and natural estrogens (such as soy foods). Use curcumin as seasoning if tolerated. • Include phytosterols from sunflower seeds, pistachio nuts, sesame seeds, and wheat germ (Phillips et al, 2005). • Include more omega-3 fatty acids from fish, shellfish, flaxseed, and walnuts. • Include resveratrol from red grapes and juice, berries, peanuts, or red wine if tolerated.

Common Drugs Used and Potential Side Effects • Cytotoxic drugs are often used. Vincristine can cause severe constipation. • With methotrexate, nausea and vomiting are common; doxorubicin (Adriamycin) causes stomatitis, anorexia, hair loss, and diarrhea. Coadministration of methotrexate with intravenous glucose may alleviate some of the toxic gastrointestinal (GI) effects. • Cyclophosphamide (Cytoxan) and other combinations of therapy may cause anorexia, stomatitis, nausea, or vomiting. • Toxicity is far less than with docetaxel if vitamin B12 and folate supplements are used (Budde and Hanna, 2005). • Tarceva modestly improves survival in NSCLC patients. • With immunotherapy, bacillus Calmette-Guérin (BCG) vaccine is often used.

Herbs, Botanicals, and Supplements (see Table 13-8) • The use of complementary and alternative medicine by lung cancer patients is prevalent. Clinicians should investigate to avoid any potential side effects and interactions with conventional therapies (Cranganu and Camporeale, 2009). Herbs and botanical supplements should not be used without discussing with the physician. • Five promising herbs have been identified in Chinese herbal medicine (CHM) that, when used in conjunction with chemotherapy, may improve quality of life in NSCLC (Chen et al, 2009). • Luteolin, 3 ,4 ,5,7-tetrahydroxyflavone, exists in many types of plants and in Chinese medicinal herbs; it functions as an antioxidant with anticancer properties (Lin et al, 2009). Luteolin is found in carrots, celery, olive oil, oregano, peppers, peppermint, rosemary, and thyme. • Avoid beta-carotene supplements. Diet is more protective. • Clinical trials using dietary garlic, selenium, N-acetylcysteine, vitamins B6 and C are needed.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss alternate methods of intake if oral is not feasible. • A diet high in antioxidant-rich foods such as fruits, vegetables, and spices is protective and a prudent preventive strategy (Roswall et al, 2010).

• Discuss the side effects of drugs being used. • Dietary acrylamide affects carcinogenesis but not through genetic alterations (Hogervorst et al, 2009). Researchers are reviewing its role from heat-treated foods. • Self-reported smoking consistently explains approximately 50% of the inequalities in lung cancer risk due to differences in education (Menvielle et al, 2009). Smokers who quit will allow their lung tissues to repair much of the damage. • Smokers who cannot quit should use a brand of cigarettes with lower nicotine and low tar. Avoid smoking prior to or with meals; smoking may decrease appetite. • Chewing tobacco or snuff is also carcinogenic and should be stopped. • Offer tube feeding or nutritional build-up education as appropriate.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly. • If tube feeding is needed, safe preparation, handling, storage, and administration will be important.

For More Information •

Alliance for Lung Cancer

Cancer Net–Lung Cancer

Focus on Lung Cancer

Lung Cancer Information Library

Lung Cancer Online

National Cancer Institute – Small Cell Cancer small-cell-lung/patient

LUNG CANCER—CITED REFERENCES American Dietetic Association (ADA). Evidence analysis library: Oncology. Accessed January 14, 2010, at topic.cfm?cat3250. Bagnardi V, et al. Alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) study. Am J Epidemiol. 171:36, 2010. Budde LS, Hanna NH. Antimetabolites in the management of non-small cell lung cancer. Curr Treat Options Oncol. 6:83, 2005. Carpenter CL, et al. Dietary isothiocyanates, glutathione S-transferase M1 (GSTM1), and lung cancer risk in African Americans and Caucasians from Los Angeles County, California. Nutr Cancer. 61:492, 2009. Chen S, et al. Oral Chinese herbal medicine (CHM) as an adjuvant treatment during chemotherapy for non-small cell lung cancer: A systematic review [Published online ahead of print Dec 16, 2009]. Lung Cancer. Comstock GW, et al. The risk of developing lung cancer associated with antioxidants in the blood: ascorbic acids, carotenoids, alpha-tocopherol, selenium, and total peroxyl radical absorbing capacity. Am J Epidemiol. 168:831, 2008. Cranganu A, Camporeale J. Nutrition aspects of lung cancer. Nutr Clin Pract. 24:688, 2009. Hogervorst JG, et al. Lung cancer risk in relation to dietary acrylamide intake. J Natl Cancer Inst. 101:651, 2009. Lam TK, et al. Cruciferous vegetable consumption and lung cancer risk: a systematic review. Cancer Epidemiol Biomarkers. 18:184, 2009.

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Lin Y, et al. Luteolin, a flavonoid with potential for cancer prevention and therapy. Curr Cancer Drug Targets. 8:634, 2008. Menvielle G, et al. The role of smoking and diet in explaining educational inequalities in lung cancer incidence. J Natl Cancer Inst. 101:321, 2009. Phillips KM, et al. Phytosterol composition of nuts and seeds commonly consumed in the United States. J Agric Food Chem. 53:9436, 2005.


Roswall N, et al. Source-specific effects of micronutrients in lung cancer prevention [Published online ahead of print Jan , 2010]. Lung Cancer. Stidley CA, et al. Multivitamins, folate, and green vegetables protect against gene promoter methylation in the aerodigestive tract of smokers. Cancer Res. 70:568, 2010.

PANCREATIC CANCER NUTRITIONAL ACUITY RANKING: LEVEL 3–4 Upregulation of antiapoptostic proteins

Downregulation of proapoptotic proteins

Mutations of apoptotic proteins

Pancreatic Cancer


Antisense Oligoconstructs nucleotides

Specific inhibitors ChemoRetroviral of apoptotic therapeutics vectors proteins

DEFINITIONS AND BACKGROUND Pancreatic cancer is the fourth most common cause of death from cancer in men and the fifth for women, primarily occurring between 65 and 79 years of age. Development of pancreas cancer progresses over many years before symptoms appear, and many people with pancreatic cancer die within 6 months of diagnosis. Nearly all pancreatic cancers are primary pancreatic adenocarcinomas. About 50–70% of patients have cancer in the head of the pancreas, and 50% have cancer in the body and tail. Patients who have cancer in the head of the pancreas often present with cholangitis, nausea, anorexia, weight loss, new-onset diabetes, light-colored stools, dark urine, steatorrhea, jaundice, and pruritus. Those who have cancer in the body or tail of the pancreas present with vague abdominal pain, dyspepsia, nausea, intermittent diarrhea, unexpected diabetes, and constant back pain. When there are spontaneous blood clots in the portal blood vessels, this may be associated with pancreatic cancer; this thrombophlebitis is called Trousseau sign. Risks for pancreatic cancer increase with age. It is slightly more common in men, in smokers, in African-Americans, and in people who are obese. Almost a third of the cases of pancreatic cancer are due to cigarette smoking. Persons with a history of pancreatitis are also at risk; type 2 diabetes is not a true risk factor. Diets high in red meat or low in fruits

and vegetables may also be linked to pancreatic cancer. Doses of alcohol greater than 30 grams per day contribute to only a modest increase for this type of cancer. Exercise, such as walking 4 hours or more weekly, may protect against this cancer. Good folate, B12, and pyridoxine status also helps (Schernhammer et al, 2007), as does an increased intake of citrus fruits (Bae et al, 2009). Lifestyle choices are the most preventive steps; cut down on smoking, alcohol and poor food choices (Whitcomb and Greer, 2009). Nutrition intervention together with chemotherapy improves outcomes in these patients. An increased risk has been found for dietary intakes of saturated and polyunsaturated fat (Thiebault et al, 2009; Zhang et al, 2009). A diet high in omega-3 fatty acids may mitigate pancreatic precancer by inhibition of cellular proliferation through induction of cell cycle arrest and apoptosis (Strouch et al, 2009). DHA may be the primary fatty acid that is beneficial. However, the use of supplemental omega-3 fatty acids is not recommended (American Dietetic Association, 2010). Malignancy in the pancreas has a high mortality rate from a lack of early symptoms, symptoms that mimic other conditions, and rapid metastasis to other organs. Medical treatment consists of radiation, chemotherapy, immunotherapy, or vaccine therapy. When the tumor has spread (metastasized) to other organs such as the liver, chemotherapy alone is usually used. The standard chemotherapy drug is gemcitabine, which can help some patients.

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Unfortunately, only about 20% of patients with pancreatic cancer have a form that can be resected. Whipple’s procedure (pancreaticoduodenectomy) involves many operations. The entire duodenum is usually removed, and the pancreas, gallbladder, and spleen may also be removed. It has many nutritional implications (Petzel, 2005; Tang et al, 2005). After surgery, the diet can be liberalized after 10–14 days, adding one new food at a time and using supplements when appetite is poor. Survival rates have improved; approximately 30% will live for 3 years after diagnosis and treatment. But the 5-year survival rate is low; 95% of the people diagnosed with it will not be alive 5 years later.


SAMPLE NUTRITION CARE PROCESS STEPS Undesirable Food Choices Assessment Data: BMI 20, recent weight loss of 2#. Diet history reveals high red meat and saturated intake, low use of fruits and vegetables. Dx pancreatic cancer in past month. Nutrition Diagnosis (PES): Undesirable food choices related to nutrient density and cancer diagnosis as evidenced by diet history showing high intake of red meats and low intake of fruits and vegetables. Intervention: Food-nutrient delivery—offer acceptable fruit and vegetable choices and juices. Educate the patient and family about the role of diet in cancer. Counsel about tips for managing symptoms, weight changes, and anorexia while including protective food choices. Coordinate care with the medical team for home care and potential hospice care. Monitoring and Evaluation: No further weight loss; good tolerance for small meals that are nutrient-dense but not high in fat.

CLINICAL INDICATORS Genetic Markers: Five to ten percent of cases are related to family history, such as mutations in BRCA2 or PALB2 genes, Lynch syndrome, PeutzJeghers syndrome, familial atypical mole-malignant melanoma (FAMMM), familial adenomatous polyposis, or mutations in the CDKN2 A tumor suppressor gene. Much research is going toward understanding the genes in pancreatic cancer (Hruban et al, 2008). Folate genes may be involved, but more studies are needed. Specific Clinical/ Thrombophlebitis History (Trousseau Height sign). Weight Fatigue BMI Ascites Rapid weight Angiography loss Abdominal CT Midepigastric scan or MRI pain Endoscopic Temperature ultrasound BP Fine-needle Jaundice, biopsy pruritus Endoscopic Dark urine? retrograde Biliary cholangiopanobstruction? creatography Pancreatic (ERCP) insufficiency (indigestion, Lab Work cramping, Ca 19–9 bloating) (37 U/mL) Belching Elevated Steatorrhea microRNAs or loose (miR-155, stools miR196a) Anorexia Alk phos Nausea and (increased) vomiting

Bilirubin (increased) PT (increased) Gluc (increased) Serum lipase (increased) Secretin PSCA levels Serum amylase (increased) ALT, AST (increased) Transferrin Serum insulin TLC (varies) Serum B12, folic acid Homocysteine levels Cholecystokinin Alb CRP Chol, Trig H&H Ca, Mg Na, K

INTERVENTION OBJECTIVES • Reduce or control nausea and vomiting. • Prevent or correct weight loss, which is associated with poor outcomes, and restore lean body mass. • Control side effects of therapies and the disease such as diabetes, anemia, pancreatic fistula, wound infection, bile leak, cholangitis, dumping syndrome, weight loss, and lactose intolerance (Petzel, 2005). • Provide foods or supplements that include all necessary nutrients to prolong health. Augment nutritional intake; correct anemia. Include protective foods. • Monitor for depression; encourage the use of antidepressants if needed to help with appetite. • Manage problems such as pancreatic cancer–related diabetes and vitamin B12 malabsorption. • Parenteral nutrition (PN) is indicated mainly for perioperative use in patients with known malnutrition preoperatively. Postoperatively, tube feeding is the nutrition support method of choice. • Wean off tube feeding with increasing oral intake and resolving gastroparesis, usually 4–6 weeks postoperatively.

FOOD AND NUTRITION • For pancreatic insufficiency: Medium-chain triglycerides (MCT), fat-soluble vitamins (water-miscible form), and essential fatty acids (EFAs) should be included. Calcium, selenium, zinc, and iron may become deficient unless supplemented. • After Whipple’s procedure, if pain is severe, tube feeding should be attempted before CPN. If possible, feed after bowel sounds return. Pancreatic enzyme replacement will be needed. Use a low-lactose, low-fat diet (40–60 g) and omit fried foods, nuts, and seeds.

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• Small meals are best tolerated—six to eight feedings may be better tolerated than three large meals. Delayed gastric emptying is common, so avoidance of simple sugars and hot liquids may also be needed. • Increased energy and protein intake should be provided to restore lost weight, unless the patient is hyperglycemic or has extensive liver impairment. Carbohydrate control may be needed to manage diabetes. • Include protective foods, particularly tomato products for lycopene, other vegetables, and citrus fruits (Bae et al, 2009; Nkondjock et al, 2005). Onions, garlic, beans, orange and yellow vegetables, spinach, broccoli, kale, and raw vegetables are particularly protective.

Common Drugs Used and Potential Side Effects • Chemotherapy may include gemcitabine. • Pancreatic enzymes (pancrelipase and pancreatin) are given. Enteric coating aids in maintaining the integrity of enzymes until they reach the small intestine. If a pork allergy is present, there may be a reaction to these enzymes; a pork-free product is PAN-2400. As much as 20,000–30,000 units of lipase may be needed per meal; 10,000 units may be needed with snacks. They must be swallowed whole and not chewed. • Insulin may be needed if the patient is hyperglycemic. In islet cell tumors, hypoglycemia may occur instead. Monitor with meal timing. • Acid-reducing medications (such as proton-pump inhibitors or H2 blockers) are usually needed. • Vitamin B12 supplements may be required with total pancreatectomy, particularly with steatorrhea. • Water-miscible fat-soluble vitamins A, D, E, and K will be needed until intake of pancreatic enzymes is sufficient. Brands may include Vitamax, Source CF, and ADEKs. • Antiemetics, diuretics, and analgesics may be needed. Monitor side effects according to medications prescribed. • Calcium carbonate twice daily may be useful to help bulk stools that are loose. Antidiarrheal medications (e.g., Lomotil, opiates, or Imodium) may be needed if loose stools are persistent. Guar gum and psyllium can be used to add soluble fiber. • Targeted drug therapy blocks chemicals that signal cancer cells to grow and divide. Erlotinib (Tarceva) is usually combined with chemotherapy for advanced pancreatic cancer. • A pancreatic cancer vaccine is under study.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. • There are potential drug-nutrient interactions (e.g., anticoagulant and anti-hypertensive medications/herbal supplements) with the use of EPA fish oil supplements; they are not recommended for pancreatic cancer (American Dietetic Association, 2010).


NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss specific dietary recommendations appropriate for the patient’s condition and therapies. • Discuss the use of pancreatic enzymes. • Provide education for diet and jejunostomy feeding. • With pancreatectomy, a diabetic diet may be absolutely essential. Discuss the rationale with the patient. • Explain how diet affects malabsorption in regard to fat, protein, vitamins, and minerals. • Research does not support the theory that high intakes of sugar or sugar-sweetened beverages cause this cancer. • Lactase enzymes may be helpful if lactose intolerance persists. • Family members may need genetic counseling. The fundamental problem underlying pancreatic cancer is altered genetics (Whitcomb and Greer, 2009).

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

JAMA Patient Page – Pancreatic Cancer

Johns Hopkins–Pancreatic Cancer Home Page

Lustgarten Foundation for Pancreatic Cancer Research

Mayo Clinic – Pancreatic Cancer

Medline–Pancreatic Cancer

National Pancreas Foundation

Pancreatic Cancer Action Network

PANCREATIC CANCER—CITED REFERENCES American Dietetic Association (ADA). Evidence analysis library: Oncology. Accessed January 14, 2010, at topic.cfm?cat3250. Bae JM, et al. Citrus fruit intake and pancreatic cancer risk: a quantitative systematic review. Pancreas. 38:168, 2009. Hruban RH, et al. Emerging molecular biology of pancreatic cancer. Gastrointest Cancer Res. 2:10S, 2008. Nkondjock A, et al. Dietary intake of lycopene is associated with reduced pancreatic cancer risk. J Nutr. 135:592, 2005. Petzel M. Nutrition support of the patient with pancreatic cancer. Nutr Support. 27:11, 2005. Schernhammer E, et al. Plasma folate, vitamin B6, vitamin B12, and homocysteine and pancreatic cancer risk in four large cohorts. Cancer Res. 67:5553, 2007. Strouch MJ, et al. A high omega-3 fatty acid diet mitigates murine pancreatic precancer development [Published online ahead of print May 15, 2009]. J Surg Res. Tang CN, et al. Endo-laparoscopic approach in the management of obstructive jaundice and malignant gastric outflow obstruction. Hepatogastroenterology. 52:128, 2005. Thiebault AC, et al. Dietary fatty acids and pancreatic cancer in the NIHAARP diet and health study. J Natl Cancer Inst. 101:1001, 2009. Whitcomb D, Greer J. Germ-line mutations, pancreatic inflammation, and pancreatic cancer. Clin Gastroenterol Hepatol. 7:S29, 2009. Zhang J, et al. Physical activity, diet, and pancreatic cancer: a populationbased, case-control study in Minnesota. Nutr Cancer. 61:457, 2009.

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DEFINITIONS AND BACKGROUND Skin cancer is the most common cancer in the United States, and the incidence is increasing. Vitamin D is made in the skin upon exposure to solar radiation; regular use of a tanning bed that emits vitamin D–producing ultraviolet (UV) radiation is associated with higher 25-hydroxyvitamin D concentrations, which may benefit the skeleton but not necessarily the skin. UVB–induced skin damage places individuals more at risk for basal cell and squamous cell carcinomas than for malignant melanoma. Risk factors for skin cancer include certain types or a large number of moles; excessive exposure to sun and ultraviolet light with susceptible vitamin D receptor genes; family or personal history of skin cancer; freckles; light skin color, hair color, or eye color; and sunburns early in life. Since carcinogenesis and photoaging are multistep processes, tumor development may be halted at several points. The intake of flavonols may be protective (McNaughton et al, 2005). Deficiency of the prohormone calcidiol (25OH vitamin D3) seems to be associated with cancer, but not calcitriol (Tuohimaa, 2008). Daily brief exposure of a substantial area of the skin to ultraviolet light, climate allowing, provides adults with a safe, physiologic amount of vitamin D, equivalent to an oral intake of approximately 10,000 IU vitamin D3 per day; the plasma 25-hydroxyvitamin D (25(OH)D) concentration potentially reaches 88 ng/mL (Vieth, 2009). The occupational sun exposure rate is positively correlated with a lower risk of overall organ mortality. Adequate vitamin D3 is protective; benefits of sunlight may outweigh some risks (Krause et al, 2006). Skin cancer and photoaging are the result of excessive ultraviolet radiation exposure. UVB (280–315 nm) in natural

sunlight is associated with skin cancer through keratinocyte proliferation and cell cycle progression (Han and He, 2009). Excessive UVB light exposure in childhood promotes the development of melanomas (Wolpowitz and Gilchrest, 2006). Basal cell cancer (BCC) starts as small, shiny, firm nodules that enlarge slowly, bleed and scab, then heal, and finally repeat the cycle. These are the most common type of skin cancer. Basal cell tumors should be removed to avoid destruction to other tissues. Most basal cell carcinomas occur on parts of the body that are excessively exposed to the sun—particularly the face, ears, neck, scalp, shoulders, or back. Rarely, these tumors come from exposure to arsenic or radiation, open sores that will not heal, chronic inflammatory skin conditions, and complications of burns, scars, infections, vaccinations, or tattoos. Squamous cell carcinoma (SCC) originates in the middle layer of the epidermis and may develop on sun-damaged skin or even in the mouth lining or tongue. This type begins as a reddened area with a scaly, crusted surface that does not heal. A precursor is often an actinic keratosis (solar keratosis) that appears on the bald scalp, face, ears, lips, backs of the hands and forearms, shoulders, neck, or any other areas of the body that are frequently exposed to the sun. SCC may have the appearance of a wart and eventually becomes an open sore. Removal is important before it can spread. Leukoplakia anywhere in the mouth may be an early sign. SCC is more common in men than in women and is most likely to occur after age 50. In addition, people who use tanning beds are twice as likely to get SCC. Melanoma, the deadliest type of skin cancer, originates in the melanocytes and tends to spread rapidly. Biopsy is essential. It is the most common cancer for women aged 25–29 years and the second most common cancer for women aged 30–34 years. Most melanomas are black or brown, but some may even be skin-colored, pink, red, blue, or white. Early warning signs of melanoma have been identified by the acronym “ABCDE” (A stands for Asymmetry, B stands for Border, C for Color, D for Diameter, and E for Evolving or changing was recently added). Individuals who have had breast cancer are at risk for melanoma and vice versa. Disfiguring surgery is no longer necessary to remove a melanoma. Mohs micrographic surgery is available.


CLINICAL INDICATORS Genetic Markers: The melanocortin 1 receptor (MC1R) is a highly polymorphic G protein-coupled receptor; MC1R alleles have been associated with a red hair/fair skin phenotype, increased incidence of skin cancer, and altered sensitivity to ultraviolet (UV)

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radiation (Smith et al, 2007). Specific alleles of the gene that codes for the melanocortin 1 receptor are also predictive of skin cancer risk, independent of skin type and hair color (Lynde and Sapra, 2010). Specific Clinical/ Changes in skin or mole History Itching, bleeding Height of mole Weight Nausea and Weight vomiting changes Anorexia BMI Diet history Lab Work Light-colored Alb hair, skin, CRP eyes

H&H Serum ferritin Transferrin Ca, Mg Na, K Serum 25(OH)D


• A high-fat diet may influence the UV-induced inflammatory responses in the skin (Meeran et al, 2009). Choose a diet that is moderate in fat while controlled in saturated fat and cholesterol. Include good sources of omega-3 fatty acids regularly (i.e., salmon, tuna, mackerel, herring, and sardines). • Use sugars, salt, and alcoholic beverages in moderation. • If anemic, a diet that meets at least DRI requirements for blood-forming nutrients will be needed. • Weight gain caused by fluid retention is commonly seen in patients receiving biological therapy (immunotherapy). Use a diet with 2–4 grams of sodium or fluid restriction if needed. • Provide adequate amounts of vitamin D3 and dietary beta carotene. Consumption of 40 IU/d of vitamin D(3) raises plasma 25(OH)D by approximately 0.4 ng/mL (Vieth, 2009).

Common Drugs Used and Potential Side Effects INTERVENTION OBJECTIVES • Maintain appropriate weight for height. • General healthy dietary guidelines should be followed. • Prevent or correct nutritional deficiencies and improve patient tolerance of treatment. • Minimize potential treatment side effects. • Optimize immune function to increase effectiveness of therapy. • Enhance quality of life. • Ensure appropriate healing of surgical sites, if applicable.

FOOD AND NUTRITION • Eat a variety of foods, particularly fruits and vegetables and whole grains such as oats. Use flavonols such as apples, tea, and coffee.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Bioactive Substance Intake Assessment Data: Diagnosis of skin cancer. Hx of tanning bed use for psoriasis. Diet history indicates low intake of fruits and vegetables. Patient has been following a macrobiotic diet to lose weight for 6 months, eating mostly rice. Nutrition Diagnosis (PES): Inadequate bioactive substance intake related to low consumption of fruits and vegetables as evidenced by diet history. Intervention: Food-nutrient delivery—Provide a nutrient-dense diet that includes flavonols and anti-inflammatory foods. Educate the patient about the role of bioactive substances in reducing future skin cancer risks. Counsel about returning to a balanced diet with plenty of phytochemicals. Monitoring and Evaluation: Improved diet with balanced intake of nutrients and phytochemicals.

• Aldara skin cream reduces basal cell lesions without surgery. • Interferon-2b (Intron-A) is used in adult patients who have surgically treated melanoma considered at high risk of recurrence. This immunotherapy (biologic therapy) makes use of chemicals that occur naturally in the body. • Immunomodulating agent histamine dihydrochloride (Maxamine), when used in combination with interleukin-2 (IL-2), improves survival for stage 4 malignant melanoma patients.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. • Evidence from clinical trials shows that a prolonged intake of 10,000 IU/d of vitamin D(3) poses no risk of adverse effects for adults (Vieth, 2009).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the rationale for spacing meals throughout the day to avoid fatigue. • Offer recipes and meal plans that provide the nutrients required to improve status and immunological competence. • Patients undergoing treatment should be allowed flexibility in their food selections, while focusing on high-energy, high-quality protein, and phytochemical-rich choices whenever possible. • Offer recipes and menu options for individual planning. • Use sunscreen with sun protective factor (SPF) 15 or higher and both UVA and UVB protection; apply sunscreen after about 10–15 minutes in the sun. • Biofeedback and stress management techniques may be useful. • Dietary protection is provided by carotenoids, tocopherols, ascorbate, flavonoids, or omega-3 fatty acids.

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Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

CDC – Skin Cancer

Melanoma Research Foundation

Mohs Micrograhic Surgery

Web MD

SKIN CANCERS—CITED REFERENCES Benlloch M, et al. Bcl-2 and MnSOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by TNF-alpha and chemotherapy. J Biol Chem. 281:69, 2006.

Bergomi M, et al. Trace elements and melanoma. J Trace Elem Med Biol. 19:69, 2005. Han W, He YY. Requirement for metalloproteinase-dependent ERK and AKT activation in UVB-induced G1-S cell cycle progression of human keratinocytes. Photochem Photobiol. 85:997, 2009. Krause R, et al. UV radiation and cancer prevention: What is the evidence? Anticancer Res. 26:2723, 2006. Lynde CW, Sapra S. Predictive testing of the melanocortin 1 receptor for skin cancer and photoaging. Skin Therapy Lett. 15:5, 2010. McNaughton SA, et al. Role of dietary factors in the development of basal cell cancer and squamous cell cancer of the skin. Cancer Epidemiol Biomarkers Prev. 14:1596, 2005. Meeran SM, et al. High-fat diet exacerbates inflammation and cell survival signals in the skin of ultraviolet B-irradiated C57BL/6 mice. Toxicol Appl Pharmacol. 241:303, 2009. Smith G, et al. Melanocortin 1 receptor (MC1R) genotype influences erythemal sensitivity to psoralen-ultraviolet A photochemotherapy. Br J Dermatol. 157:1230, 2007. Tuohimaa P. Vitamin D, aging, and cancer. Nutr Rev. 66:S147, 2008. Vieth R. Vitamin D and cancer mini-symposium: the risk of additional vitamin D. Ann Epidemiol. 19:441, 2009. Wolpowitz D, Gilchrest BA. The vitamin D questions: how much do you need and how should you get it? J Am Acad Dermatol. 54:301, 2006. Woolcott CG, et al. Plasma 25-hydroxyvitamin D levels and the risk of colorectal cancer: the multiethnic cohort study. Cancer Epidemiol Biomarkers Prev. 19:130, 2010.



DEFINITIONS AND BACKGROUND Breast (mammary) carcinoma is the second most common cancer in women, with over 200,000 cases diagnosed annually in the United States. It affects one in eight women. Having routine breast screenings for cancer is important. When a woman has specific family history patterns that put her at risk for gene mutations, her primary care physician should suggest DNA testing, but only about 2% of women have this level of risk. Age 30, health history related to fertility, ovar-

ian function, and estrogen exposure play a role in the onset of breast cancer. Exposure to diets that produce high levels of estrogen seems to be most important in utero and after menopause; high estrogen levels during reproductive years seems to be protective. A longer duration of breastfeeding may be associated with a reduced risk. Breast cancer in men is less common and is generally preceded by gynecomastia. Some breast cancer cells have a high proportion of estrogen and/or progesterone receptors in the nucleus. Those women who are ER/PR positive might benefit from hormonal therapy with tamoxifen or aromatase inhibiters; these drugs block hormone receptors in the cancer cell. Protein phosphatase 2A (PP2A) is a major cellular phosphatase that plays key regulatory roles in growth, differentiation, and apoptosis; its role in the suppression of breast cancer is being studied (Dupont et al, 2009). Breast cancer may be related to oxidative stress. Receptor CXCR1 (IL-8) is a protein produced during chronic inflammation and tissue injury; it may play a role in breast cancer. Recent studies show that the intake of anthocyanins and ellagic acid can prevent cancer cells from developing (Stoner et al, 2009). Berries and pomegranates are particularly protective. Being physically active is also protective, whereas obesity and Western dietary patterns increase cancer risk. Weight gain in the years preceding the onset of puberty is a promoter; increased fat cell adiposity increases estrogen availability at this time (Michels et al, 2006). Overweight breast cancer survivors commonly have metabolic syndrome (MetS) and elevated CRP (Thomson et al, 2009). Weight reduction is a reasonable goal.

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TABLE 13-17

Staging of Breast Cancer

Stage 0

In situ—Cancer cells are present in either the lining of a breast lobule or a duct, but they have not spread to the surrounding fatty tissue.

Stage 1

Rarely metastasizing/noninvasive (2 cm or 1 inch in diameter)—Cancer has spread from the lobules or ducts to nearby tissue in the breast; cancer has not spread to the lymph nodes.

Stage 2

Rarely metastasizing/invasive—The tumor can range from 2 cm to 5 cm in diameter (approximately 1–2 inches); sometimes, cancer may have spread to the lymph nodes.

Stage 3

Moderately metastasizing/invasive ( 2 inches)—Cancer cells have grown extensively into axillary (underarm) lymph nodes.

Stage 4

Highly metastasizing/invasive into other parts of the body, such as bone, liver, lung, or brain.

Eating soy foods yields greater benefits than taking isoflavone supplements (Li et al, 2005). Early exposure in childhood or early adolescence to phytoestrogens may be protective (Duffy et al, 2007). Alcohol intake is a problem if folic acid intake is low; 600 micrograms of folic acid is protective. High intake of welldone meat and high exposure to meat carcinogens, particularly HCAs, may increase the risk of breast cancer (Zheng and Lee, 2009). Breast cancer can be treated very effectively, particularly when it is diagnosed in the early stages. Staging of breast cancer is described in Table 13-17. Tumors are frequently found in the upper/outer quadrant of the breast (45%) and nipple area (25%), with 30% identified in other breast areas. In the early stages, a single nontender, firm, or hard mass with poorly defined margins may exist. Later, skin or nipple retraction, axillary lymphadenopathy, breast enlargement, redness, mild edema, and pain may occur. In the late stages, ulceration, moderate edema, and metastases to bone, liver, or brain are common. Four standard types of therapy are used to treat breast cancer: surgery for the removal of cancerous tissue and, sometimes, other tissue; radiation therapy; chemotherapy; and hormonal therapy. New therapies are being researched through clinical trials.


CLINICAL INDICATORS Genetic Markers: Mutations in the BRCA1 gene (on chromosome 17) result in an elevated risk of breast cancer and ovarian cancer (Kroiss et al, 2005). The HER2 (Her2/neu, c-erb-2 or erb-2) gene produces a protein that acts as a receptor on the surface of all cells; some cancer cells have more receptors than normal, and they receive more messages to grow and


divide. The C677 T polymorphism of the folic acid (MTHFR) genotype increases the risk of postmenopausal breast cancer, particularly with low intakes of folate and vitamin B6 (Maruti et al, 2009). Specific Clinical/ Breast enlargement History Redness, mild Height edema, pain Weight Ulceration, BMI moderate Weight changes edema Diet history I&O Anorexia, Temperature nausea Breast self-examLab Work ination— Estrogen recepmasses tors (positive Calcifications or negative) Biopsy Serum estrogen Skin or nipple Carcinoembryretraction onic antigen Axillary (CEA) lymphadenop Prolactin athy

Serum carotenoid levels Mg, Ca H&H Gluc Alk phos Erythrocyte sed rate (ESR) to evaluate metastasis Complete blood cell count (CBC) Chol, Trig Alb, transthyretin CRP Mammography

INTERVENTION OBJECTIVES • Control side effects of therapy and treatments (e.g., local or extensive mastectomy, chemotherapy, external-beam radiation therapy, brachytherapy). • Promote intake of phytochemicals and protective foods to reduce inflammation. • Promote good nutritional status to reduce future incidents and recurrence. Encourage regular breast selfexaminations, physical activity, and other healthy behavior changes. • Maintain or attain appropriate weight for height. Obese patients should lose weight before treatment; be careful not to lose lean body mass (LBM). • Increase the likelihood of survival, wellness, and improved quality of life. • For mastectomy patients, promote wound healing and prevent infection.

FOOD AND NUTRITION • Because most studies have found that exercise, weight reduction, low-fat diet, and reduced alcohol intake are associated with a decreased risk of breast cancer, a diet with controlled total energy and fat is helpful (Cummings et al, 2009). While the Western style of diet should be discouraged (Adebamowo et al, 2005), meat, eggs and lowfat dairy foods can be used in moderation (Pala et al, 2009). Use fewer processed meats and less red meat, particularly if well-done (Zheng and Lee, 2009).

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SAMPLE NUTRITION CARE PROCESS STEPS Poor Nutrition Quality of Life Assessment Data: Status post partial mastectomy; dysphagia and cachexia noted. Poor appetite and BMI dropped to 18.5 from 24 over the past 6 months. Nutrition Diagnosis (PES): Poor nutrition, quality of life (NB2.5) related to dysphagia, depression, and cachexia as evidenced by appetite 50% and BMI of 18.5. Nutrition Intervention: Food and Nutrient Delivery: ND 1.3 specific food/beverage: Puree, nectar, thick liquids and thinned soft foods. ND 3.1.1 commercial beverage supplement: 1 can 2 daily. ND 3.2.1: MVI. Counseling: C-2.2 Goal setting: Minimize weight loss, maintain adequate weight loss, monitor for signs and symptoms of aspiration, improve quality of life with exercise, and improve intake of phytochemical and nutrient-dense foods and tea. Coordination of Nutrition Care: RC 1.1 Interdisciplinary team meeting with nursing, social worker, recreational therapy, physical therapy, speech therapy. Monitoring and Evaluation: No signs of aspiration, nausea, vomiting, speech evaluation follow-up, promote wound healing and prevent infection; reassess nutrition and quality of life.

• Promote use of the Mediterranean diet (Cottet et al, 2009; Masala et al, 2006). Olive/sunflower/canola oils, grape juice, red wine, and cheese are beneficial. Calorie restriction and use of omega-3 fatty acids decrease inflammation (Jolly, 2005). • High fiber diets reduce hormone production and decrease cancer risk (Gaskins et al, 2009). At least 5–9 fruits and vegetables (Ahn et al, 2005; Rock et al, 2005) and 6 grain foods daily should be encouraged. The fruits and vegetables should include sources of alpha- and beta-carotene, zeaxanthin, and lycopene. Berries, pomegranate, garlic, and spices such as curcumin should be used often. Use cruciferous vegetables often (Warin et al, 2009). • Sources of choline and betaine should be included (Xu et al, 2009). Choline is found in beef liver, wheat germ, and eggs. Betaine is found in beets. • Alcohol may promote estrogen receptor–positive tumors (Suzuki et al, 2005). Red wine and resveratrol may be acceptable; limit to one drink per day. • While some women are estrogen-sensitive (Fang et al, 2005; Li et al, 2005), overall, soy-enhanced diets are significantly associated with a decreased risk of death and recurrence (Shu et al, 2009; Steiner et al, 2008). This may be due to a new phytochemical found in soy called glyceollin I (Zimmermann et al, 2010). An isoflavone-rich diet might include wild leafy greens (as in the Greek diet), celery stalks, shredded lettuce, sweet peppers, raw spinach, fresh lemon, and sprigs of fresh parsley. • A general supplement also may be safely recommended for folic acid (Zhang et al, 2005), calcium, vitamin D, vitamin A, vitamin C, and vitamin E as alpha-tocopherol.

Common Drugs Used and Potential Side Effects • For patients who are estrogen receptor positive, hormonal therapy may be a breast cancer promoter; oral contraceptive use should be monitored or discontinued. Estrogen replacement (to prevent osteoporosis) increases risk levels. • Antiestrogen therapy with tamoxifen (Noraldex) may be prescribed to treat estrogen-dependent breast cancer or be used in women at high risk. Nausea, vomiting, and hot flashes are common side effects. Avoid high doses of soy when using tamoxifen. • For patients who are estrogen receptor negative, hormonal therapy actually may be recommended (e.g., progesterone and androgen therapy). Megestrol acetate (a hormonal antineoplastic drug and a synthetic derivative of progesterone) may reverse anorexia and weight loss. • Chemotherapy may be used. Cyclophosphamide (Cytoxan) requires extra fluid intake. Doxorubicin, fluorouracil, and methotrexate are also commonly used; many gastrointestinal (GI) side effects are noted. Taste alterations are common for beef, chicken, and coffee. Anastrozole (Arimidex) can cause anorexia, weight changes, nausea, vomiting, dry mouth, constipation, and diarrhea. Gemcitabine (Gemzar) in combination with paclitaxel is used with metastatic breast cancer after failure of other chemotherapy. • Trastuzumab (Herceptin) helps with early-stage HER2 breast cancer as an adjunct to chemotherapy to decrease recurrence. • Repertaxin, originally developed to prevent organ transplant rejection, blocks receptor CXCR1 and kills breast cancer stem cells. It is under study in humans.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician. Women with a history of breast cancer may seek out “natural” phytoestrogens in the belief that they are safe or perhaps even protective against recurrence, but studies do not support a protective role (Duffy et al, 2007). The following herbal/botanical supplements should be avoided by patients with breast cancer because of their phytoestrogen content: Ginseng, Gingko biloba, Licorice root, Black cohosh, Wild yam root, DHEA. • Grape seed extract, berry powder, and pomegranate products are beneficial (Kim, 2005; Stoner, 2009). Dietary sources of omega-3 fatty acids, vitamin C, vitamin E, betacarotene, selenium, and coenzyme Q10 may be of particular value. • With the use of methotrexate (Rheumatrex), avoid echinacea because of potential damage to the liver.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Breast cancer detection projects are available throughout the United States; check with local chapters of the National Cancer Institute (NCI) and the American Cancer Society (ACS). Early detection of new tumors is crucial because lower stage tumors are much easier to control.

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• Attain or maintain healthy body weight. Low total energy or lower fat dietary patterns may also be helpful (Elias et al, 2005). Reduce intake of sweets and high-glycemic index foods (Tavani et al, 2006). Eat a diet high in whole grains, fruits, and vegetables (Ahn et al, 2005). • Discuss ways to make meals more appetizing, particularly if appetite is poor. • Use of moderate amounts of soy may be encouraged. Increase use of cruciferous vegetables (Warin et al, 2009). • Exercise and consumption of tea are important preventive factors to reduce depression among breast cancer survivors (Chen et al, 2010). Yoga and hypnosis may also be beneficial. • Daughters of women with breast cancer should have a first mammogram before 40 years of age as a baseline and annually every 1–2 years thereafter. Lumps and changes should be reported immediately to a physician. • Limit alcoholic beverages to one drink per day (Suzuki et al, 2005) and avoid high intakes of well-done meats and processed meats (Zheng and Lee, 2009). • Calcium and vitamin D3 supplementation may be indicated for patients who are menopausal or postmenopausal as they are at increased risk for developing osteoporosis.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Breast Cancer

Cornell University

National Alliance of Breast Cancer Organizations

National Breast Cancer Coalition

Sisters Network

Y-Me National Breast Cancer Organization

BREAST CANCER—CITED REFERENCES Adebamowo CA, et al. Dietary patterns and the risk of breast cancer. Ann Epidemiol. 15:789, 2005. Ahn J, et al. Associations between breast cancer risk and the catalase genotype, fruit and vegetable consumption, and supplement use. Am J Epidemiol. 162:943, 2005. Chen X. Exercise, Tea Consumption, and Depression Among Breast Cancer Survivors [Published online ahead of print Jan 4, 2010]. J Clin Oncol.


Cottet v, et al. Postmenopausal breast cancer risk and dietary patterns in the E3 N-EPIC prospective cohort study. Am J Epidemiol. 170(10):1257, 2009. Cummings SR, et al. Prevention of breast cancer in postmenopausal women: approaches to estimating and reducing risk. J Natl Cancer Inst. 101:384, 2009. Duffy C, et al. Implications of phytoestrogen intake for breast cancer. CA Cancer J Clin. 57:260, 2007. Dupont WD, et al. Protein phosphatase 2 A subunit gene haplotypes and proliferative breast disease modify breast cancer risk [Published online ahead of print Nov 4, 2010]. Cancer. Elias SG, et al. The 1944–1945 Dutch famine and subsequent overall cancer incidence. Cancer Epidemiol Biomarkers Prev. 14:1981, 2005. Fang CY, et al. Correlates of soy food consumption in women at increased risk for breast cancer. J Am Diet Assoc. 105:1552, 2005. Gaskins AJ, et al. Effect of daily fiber intake on reproductive function: the BioCycle Study. Am J Clin Nutr. 90:1061, 2009. Jolly CA. Diet manipulation and prevention of aging, cancer and autoimmune disease. Curr Opin Clin Nutr Metab Care. 8:382, 2005. Kim H. New nutrition, proteomics, and how both can enhance studies in cancer prevention and therapy. J Nutr. 135:2715, 2005. Kroiss R, et al. Younger birth cohort correlates with higher breast and ovarian cancer risk in European BRCA1 mutation carriers. Hum Mutat. 26:583, 2005. Li Y, et al. Inactivation of nuclear factor kappaB by soy isoflavone genistein contributes to increased apoptosis induced by chemotherapeutic agents in human cancer cells. Cancer Res. 65:6934, 2005. Maruti SS, et al. MTHFR C677 T and postmenopausal breast cancer risk by intakes of one-carbon metabolism nutrients: a nested case-control study. Breast Cancer Res. 11:91, 2009. Masala G, et al. Dietary and lifestyle determinants of mammographic breast density. A longitudinal study in a Mediterranean population. Int J Cancer. 118:1782, 2006. McCann SE, et al. Dietary lignan intakes in relation to survival among women with breast cancer: the Western New York Exposures and Breast Cancer (WEB) Study [Published online ahead of print Dec 22, 2010]. Breast Cancer Res Treat. Michels KB, et al. Preschool diet and adult risk of breast cancer. Int J Cancer. 118:749, 2006. Pala V, et al. Meat, eggs, dairy products, and risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Am J Clin Nutr. 90:602, 2009. Rock CL, et al. Plasma carotenoids and recurrence-free survival in women with a history of breast cancer. J Clin Oncol. 23:6631, 2005. Shu XO, et al. Soy food intake and breast cancer survival. JAMA. 302:2437, 2009. Steiner C, et al. Isoflavones and the prevention of breast and prostate cancer: new perspectives opened by nutrigenomics. Br J Nutr. 99:78S, 2008. Stoner GD. Foodstuffs for preventing cancer: the preclinical and clinical development of berries. Cancer Prev Res (Phila Pa). 2:187, 2009. Suzuki R, et al. Alcohol and postmenopausal breast cancer risk defined by estrogen and progesterone receptor status: a prospective cohort study. J Natl Cancer Inst. 97:1601, 2005. Tavani A, et al. Consumption of sweet foods and breast cancer risk in Italy. Ann Oncol. 17:341, 2006. Thomson CD, et al. Metabolic syndrome and elevated C-reactive protein in breast cancer survivors on adjuvant hormone therapy. J Womens Health (Larchmt). 18:2041, 2009. Warin R, et al. Prevention of mammary carcinogenesis in MMTV-neu mice by cruciferous vegetable constituent benzyl isothiocyanate. Cancer Res. 69:9473, 2009. Xu X, et al. High intakes of choline and betaine reduce breast cancer mortality in a population-based study. FASEB J. 23:4022, 2009. Zhang SM, et al. Folate intake and risk of breast cancer characterized by hormone receptor status. Cancer Epidemiol Biomarkers Prev. 14:2004, 2005. Zheng W, Lee SA. Well-done meat intake, heterocyclic amine exposure, and cancer risk. Nutr Cancer. 61:437, 2009. Zimmermann MC, et al. Glyceollin I, a novel antiestrogenic phytoalexin isolated from activated soy. J Pharmacol Exp Ther. 332:35, 2010.

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CHORIOCARCINOMA NUTRITIONAL ACUITY RANKING: LEVEL 3 (Alvarez et al, 2005). A hysterectomy is rarely indicated but may be used for some women under age 40.


CLINICAL INDICATORS Genetic Markers: Trophoblast factors are activated by hypoxia; interleukin (IL)-6, CD126, CD130, vascular endothelial growth factor (VEGF), and hypoxia inducible factor-1alpha (HIF-1alpha) are silenced in JEG-3 choriocarcinoma cells (Dubinsky et al, 2010). Adapted from: Michael S. Baggish, Rafael F. Valle, Hubert Guedj, Hysteroscopy: Visual Perspectives of Uterine Anatomy, Physiology and Pathology. Philadelphia: Lippincott Williams & Wilkins, 2007.

DEFINITIONS AND BACKGROUND Choriocarcinoma involves a highly malignant neoplasm of the placenta with a secretion of human chorionic gonadotropin (hCG). It may develop in women after a molar pregnancy (where the fetus does not develop but a tumor develops instead), a miscarriage, or a full-term delivery. Gestational choriocarcinoma occurs in approximately 1 in 20,000–40,000 pregnancies (Alvarez et al, 2005). It is more common among Asian women. Alternative names include chorioblastoma, trophoblastic tumor, chorioepithelioma, gestational trophoblastic disease, and gestational trophoblastic neoplasia. Rarely, a hydatidiform mole grows as a mass inside the uterus at the beginning of a pregnancy. When choriocarcinoma occurs in males, it presents as a testicular neoplasm, with skin hyperpigmentation (from excess beta hCG cross-reacting with the alpha MSH receptor), gynecomastia, and weight loss. Diet affects the development of this type of cancer, because the placenta has such a large role in nutrient availability (Briese et al, 2005). Placental trophoblasts and immunomodulatory molecules are under investigation (Petroff et al, 2005). Phytoestrogens (PEs) induce biologic responses by mimicking or modulating the action or production of endogenous hormones; isoflavonoids and coumestrol increase progesterone receptor protein expression and decrease ERalpha expression (Taxvig et al, 2010). Fatty acid synthase (FASN) is a tumor-associated marker found in all choriocarcinomas (Ueda et al, 2009). After the initial diagnosis, a careful examination is done to rule out metastasis. It can be fatal if there is metastasis to the kidney. Gestational choriocarcinoma is responsive to chemotherapy; surgical excision or D & C is reserved for acute emergencies

Specific Clinical/ Cough, hemoptysis History Chest pain Height Headache Weight Chest X-ray BMI Weight loss? Lab Work Diet history Human Nausea, chorionic vomiting gonadotropin I&O -hCG levels BP; hypertension? Elevated TSH Vaginal bleeding

Alb, transthyretin CRP Transferrin Gluc H&H Serum Fe, ferritin Mg, Ca Na, K ALT (increased) Kidney function tests

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Bioactive Substance Intake Assessment Data: Pregnancy 6 months ago; still breastfeeding but showing high levels of -hCG. Diagnosis of choriocarcinoma. BMI 25. No other unusual medical history. Diet history completed. Nutrition Diagnosis (PES): Inadequate bioactive substance intake related to phytoestrogens as evidenced by food frequency records showing no intake of soy or other isoflavonoids. Intervention: Food-nutrient delivery—Offer recipes and tips for ways to increase the intake of isoflavonoids from soy, legumes, spinach, and Brussels sprouts. Educate the patient about the role of bioactive substances in isoflavonoids in the prevention of relevant forms of cancer. Coordinate care with the medical team for the methotrexate treatment. Monitoring and Evaluation: No undesirable outcomes (e.g., no renal metastasis); methotrexate treatment successful.

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• Phytoestrogens from isoflavonoids may prove to be quite effective in the treatment of this cancer.

OBJECTIVES • Maintain appropriate weight for height. Correct weight loss and cachexia. • Increase intake of isoflavonoids and other bioactive substances. • Correct side effects of chemotherapy if used. • Treat and correct all other side effects of therapy and disease state. • Prepare patient for surgery, if necessary.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Nausea or vomiting may require small, frequent feedings and control of fluid intake at mealtimes. • With the high hCG levels, menstrual periods stop; periods start again when the levels are normal again. Delay pregnancy for 6 months or longer after treatment. With chemotherapy, periods will stop temporarily, and there may be early menopause.

FOOD AND NUTRITION • Modify diet to patient preferences. Include isoflavonoids and coumestrol from soy products, legumes, spinach, and Brussels sprouts. • Increase liquids as needed. • Provide adequate protein, B-complex vitamins, iron, calories, and other nutrients for wound healing, as appropriate. Use RDA and DRI levels as a guide. • Alter the texture of the diet if the patient is fatigued at mealtimes or if stomatitis occurs after chemotherapy.

Common Drugs Used and Potential Side Effects • Methotrexate or actinomycin D may be used; nausea and vomiting are common side effects. Administer with glucose to reduce toxicity. • Combined EMACO therapy (etoposide, methotrexate, actinomycin D, cyclosphosphamide, and oncovin) may be used with high-risk disease; thinning hair or GI distress can occur. • A new FASN inhibitor, C93, is being developed to initiate apoptosis in these cells (Ueda et al, 2009).

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Cancer Help – UK about/index.htm

Family Practice Notebook–Choriocarcinoma


CHORIOCARCINOMA—CITED REFERENCES Alvarez NR, et al. Metastatic choriocarcinoma to the pancreas. Am Surg. 71:330, 2005. Briese J, et al. Osteopontin expression in gestational trophoblastic diseases: correlation with expression of the adhesion molecule, CEACAM1. Int J Gynecol Pathol. 24:271, 2005. Dubinsky V, et al. Role of regulatory and angiogenic cytokines in invasion of trophoblastic cells [Published online ahead of print Dec 29, 2009]. Am J Reprod Immunol. 63:193, 2010. Petroff MG, et al. The immunomodulatory proteins B7-DC, B7-H2, and B7H3 are differentially expressed across gestation in the human placenta. Am J Pathol. 167:465, 2005. Taxvig C, et al. Effects of nutrition relevant mixtures of phytoestrogens on steroidogenesis, aromatase, estrogen, and androgen activity. Nutr Cancer. 62:122, 2010. Ueda SM, et al. Trophoblastic neoplasms express fatty acid synthase, which may be a therapeutic target via its inhibitor C93. Am J Pathol. 175:2618, 2009.

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PROSTATE CANCER NUTRITIONAL ACUITY RANKING: LEVEL 2 The cancer is not found during a digital rectal examination, but found when doing a biospy for increased PSA or surgery for another reason. It is located only in the prostate. T1, N0, M0


Seminal vesicle



Stage I The cancer can be felt on digital rectal examination but has not yet spread outside the prostate. T2, N0, M0


Stage II The cancer has spread outside the prostate, perhaps to the seminal vesicles, but not to the lymph nodes. T3, N0, M0

DEFINITIONS AND BACKGROUND Prostate cancer is third to lung and colon cancer as the cause of cancer-related deaths in American men (Colli and Amling, 2009). Prevalence is high in northwestern Europe and the United States, highest among African-American males worldwide. Men also at great risk are those with abdominal obesity, those with family history of the disease, and those whose diets are low in fiber and high in saturated fats or red meats. High serum cholesterol levels may be linked with the progression of prostate cancer (Freedman and Aronson, 2009). An effective chemoprevention strategy for prostate cancer serves as a model for chemoprevention of other adult malignancies (Canby-Hagino and Thompson, 2005). Diets rich in specific vitamins, grains, fish, fruits, and vegetables may be associated with lower cancer rates (Chan et al, 2005; Lamb and Zhang, 2005). Chemoprotective factors are listed in Table 13-18. Surgical intervention, radiation, and hormonal therapy are used. Radiation therapy may cause temporary changes in bowel habits (such as increased frequency, increased flatulence, and bowel cramping). Brachytherapy is internal radiation therapy in which small radioactive pellets are inserted or implanted into the prostate gland.



Genetic Markers: Overexpression of the AMACR gene is associated with prostate cancer risk (Xu et al, 2005). Strict nutritional interventions can change gene expression (Ornish et al, 2008). Secondary analyses of two randomized, controlled phase III trials have demonstrated that selenium and vitamin E could reduce prostate cancer incidence through cell type- and zonespecific tissue effects (Tsavachidou et al, 2009).

Stage III The cancer may have spread to nearby muscles, organs, lymph nodes, or other parts of the body. T4 or N1 or M1

Lymph nodes


Stage IV


Pathways of spreading cancer

Height Weight BMI Weight changes Diet history I&O Urine testing (infections, enlarged prostate)

Urinary dribbling, frequency, pain, burning Persistent pain (pelvis, lower back, upper thighs) BP Transrectal ultrasound Doppler scan

Digital rectal examination Bone scan, chest x-ray CT scan, MRI Lab Work Prostate-specific antigen (PSA) (2.5 ng/mL is a concern)

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Alb, transthyretin CRP

BUN, Creat H&H Serum vitamin D Ca, Mg Na, K Transferrin

INTERVENTION OBJECTIVES • Prepare patient for surgery, radiation, medications, chemotherapy, or hormone therapy. • Prevent or correct side effects such as nausea, vomiting, and diarrhea. • Prevent or correct weight loss.

TABLE 13-18 Preventive Dietary Factors for Prostate Cancer Allium vegetables (garlic, scallions, onions, chives, and leeks)


SAMPLE NUTRITION CARE PROCESS STEPS Increased Energy Needs Assessment Data: 90-year-old male resident in a long-term care facility; diagnosed with prostate cancer 1 year ago. Gradual weight loss, recently 5# in past month. Intake records show 25–50% at mealtime in the past month; previously 50–75% at all meals and taking oral supplements between meals. Nutrition Diagnosis (PES): NC-3.2 Increased energy needs related to the inflammatory process and diagnosis of prostate cancer as evidenced by the insidious weight loss over six months. Intervention: Food and Nutrient Delivery—Provide fortified foods such as super oatmeal and potatoes because of increased energy needs; MVI with minerals to ensure adequate nutrients are available. Coordinate care—Continue high calorie supplements between meals and with medication passes by nursing. Monitoring and Evaluation: No further weight loss. Improved intake of kilocalories as noted on 3-day calorie count.

Apigenin Cruciferous vegetables (Chan et al, 2005) Curcumin Epigallocatechin gallate (EGCG) Grains, nuts, cereals Grape seed extract Green tea (Trottier et al, 2010)

• Promote intake of protective foods and phytochemicals. Support intensive nutrition and lifestyle intervention to change gene expression, where appropriate (Ornish et al, 2008). • Maintain or achieve a healthy body weight.

Herbs and herbal supplements (saw palmetto) Lignans Lower fat diet Lycopene, other carotenoids (Trottier et al, 2010) Omega-3 fatty acids, EPA and DHA (Chan et al, 2005) Physical activity and exercise (Jian et al, 2005; Zeegers et al, 2005) Polyphenols (Chan et al, 2005) Pomegranate (Trottier et al, 2010) Quercetin Resveratrol Selenium (Chan et al, 2005; Trottier et al, 2010) Soy genistein and isoflavones (Chan et al, 2005; Trottier et al, 2010) Statins, 5-alpha-reductase inhibitors, and NSAIDs Vegan diet Vitamin D3 (Schwartz, 2005; Tokar and Webber, 2005; Trottier et al, 2010) Vitamin E as gamma-tocopherol in walnuts, pecans, sesame seed, corn and sesame oils (Chan et al, 2005; Trottier et al, 2010) REFERENCES Jian L, et al. Moderate physical activity and prostate cancer risk: a case-control study in China. Eur J Epidemiol. 20:155, 2005. Schwartz, GG. Vitamin D and the epidemiology of prostate cancer. Semin Dial. 18:276, 2005. Tokar EJ, Webber MM. Cholecalciferol (vitamin D3) inhibits growth and invasion by upregulating nuclear receptors and 25-hydroxylase (CYP27A1) in human prostate cancer cells. Clin Exp Metastasis. 22:275, 2005. Trottier G, et al. Nutraceuticals and prostate cancer prevention: a current review. Nat Rev Urol. 7:21, 2010. Zeegers MP, et al. Physical activity and the risk of prostate cancer in the Netherlands cohort study, results after 9.3 years of follow-up. Cancer Epidemiol Biomarkers Prev. 14:1490, 2005.

FOOD AND NUTRITION • Provide adequate calories and protein; avoid excesses. • It may be beneficial to have some weight loss prior to surgery using a low-fat, low glycemic index diet (Schenk et al 2009). • After surgery, a multiple vitamin—mineral supplement may be indicated to promote wound healing. • Monitor the need for lower sodium if corticosteroids are prescribed. • Increase the use of fruits and vegetables, particularly green and yellow-orange, and sources of folic acid. Tomato products, pizza sauce, strawberries, and salsa provide lycopene. Pomegranate juice may reduce the likelihood of recurrence (Malik et al, 2005). • Increase the use of isoflavonoids (Haddad et al, 2006; Steiner et al, 2008). Choose beans, soybeans, lentils, tofu, tempeh, soy nuts, soymilk, and dried fruit often. • Low-fat, vegan, and high-fiber diets may be indicated (Dewell et al, 2008; Van Patten et al, 2008). • Increased use of omega-3 fatty acids has been shown to be useful; include salmon, sardines, tuna, mackerel, and herring in the diet. • Vitamin D3 is needed; drink fortified milk, get a modest exposure to the sun, and take a vitamin pill that contains cholecalciferol.

Common Drugs Used and Potential Side Effects • Aspirin improves survival after prostate cancer. NSAIDs and statins may also be beneficial.

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TABLE 13-19

Antioxidant Color Link


Examples of Fruits-Vegetables



Grapes, red wine



Tomatoes, pink grapefruits, watermelon



Pomegranates, grapes, plums, berries



Carrots, mangoes, apricots, cantaloupes, pumpkin, sweet potato

Alpha and beta carotenes


Oranges, peaches, papaya, nectarines



Spinach, collard, yellow corn, green peas, avocado, honeydew melon

Lutein and zeaxanthin


Broccoli, Brussels sprouts, cabbage, bok choy, kale

Sulforaphane, isothiocyanates, indoles


Garlic, onions, asparagus, leeks, shallots, chives

Allyl sulfides

Source: Prostate Cancer Foundation,, accessed January 15, 2010.

• Chemotherapy drugs have varying side effects; monitor closely. Fatigue, nausea and vomiting, mouth sores, hair loss, and a low white blood cell count are common. • The Prostate Cancer Prevention Trial (PCPT) identified the benefits of reducing prostate cancer risk with the use of 5alpha-reductase inhibitors (Crawford et al, 2009). Finasteride lowers prostate cancer risk and can be available to men who are at high risk (Kaplan et al, 2009). • Hormonal therapy may be used as the treatment of choice (Bracarda et al, 2005). Luteinizing hormone–releasing hormone (LH-RH) agonists can decrease the amount of testosterone produced by a man’s testicles as effectively as surgical removal. Lupron Depot (leuprolide acetate for depot suspension), an LH-RH agonist, is used in the palliative treatment of advanced prostate cancer.

Herbs, Botanicals, and Supplements (see Table 13-8) • Complementary and alternative medicine (CAM) includes the use of vitamin and mineral supplements, herbs, antioxidants, saw palmetto, selenium, vitamin E, and lycopene (Chan, Elkin et al, 2005). Herbs and botanical supplements should not be used without discussing it with the physician. • Saw palmetto has some efficacy. Avoid taking it with estrogens, testosterone, anabolic steroids, oral contraceptives, or finasteride because the herb and drugs function in similar ways and additive effects are possible. • Phytoestrogens found in common herbal products are effective inhibitors of prostate tumor cell growth through different mechanisms; these include quercetin, genistein, epigallocatechin gallate (EGCG), curcumin, apigenin, resveratrol, and isoflavones in soy and red clover. • Pygeum and nettle are being studied at this time.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the side effects of therapy and the long-term plans for recovery. • Maintain adequate hydration.

• Discuss lifestyle and dietary changes. This may include lowering the intake of red meats and saturated fats, increasing fruits and vegetables and tomato products, increasing fiber and whole grains, and consuming vitamin D–fortified milk. • Chemopreventive agents include 5-alpha-reductase inhibitors; statins; NSAIDs; selenium; vitamins E and D; lycopene; allium vegetables (garlic, scallions, onions, chives, and leeks); soy/isoflavones; pomegranate and green tea polyphenols (Colli and Amling, 2009; Trottier et al, 2010; Van Patten et al, 2008). Table 13-19 provides a color chart to remember the antioxidant foods. • Lifestyle changes tend to correlate with quality of life after prostate cancer treatments (Sheriff et al, 2005). Diet and exercise changes are important. • Offer menu plans for sufficient intake of protective nutrients. Lycopene can be found in foods such as tomatoes, watermelon, guava, and red grapefruit. Include pomegranates, soy, fish, and more vegan or plant-based choices. • Help to maintain a positive, optimistic outlook to yield favorable results (Kronenwetter et al, 2005).

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Association for the Cure of Prostate Cancer


Minorities and Underserved Populations

Prostate Cancer Research Institute

Prostate Cancer Support Group

PROSTATE CANCER—CITED REFERENCES Bracarda S, et al. Cancer of the prostate. Crit Rev Oncol Hematol. 56:379, 2005. Canby-Hagino ED, Thompson IM. Mechanisms of disease: prostate cancer— a model for cancer chemoprevention in clinical practice. Nat Clin Pract Oncol. 2:255, 2005.

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Chan JM, et al. Role of diet in prostate cancer development and progression. J Clin Oncol. 23:8152, 2005. Colli JL, Amling CL. Chemoprevention of prostate cancer: what can be recommended to patients? Curr Urol Rep. 10:165, 2009. Crawford ED, et al. Reduction in the risk of prostate cancer: future directions after the prostate cancer prevention trial [Published online ahead of print Dec 24, 2009]. Urology. Dewell A, et al. A very-low-fat vegan diet increases intake of protective dietary factors and decreases intake of pathogenic dietary factors. J Am Diet Assoc. 108:347, 2008. Freedland SJ, Aronson W J. Dietary intervention strategies to modulate prostate cancer risk and prognosis. Curr Opin Urol. 19:263, 2009. Haddad AQ, et al. Novel antiproliferative flavonoids induce cell cycle arrest in human prostate cancer cell lines. Prostate Cancer Prostatic Dis. 9:68, 2006. Kaplan SA, et al. PCPT: Evidence that finasteride reduces risk of most frequently detected intermediate- and high-grade (Gleason score 6 and 7) cancer. Urology. 73:935, 2009. Kronenwetter C, et al. A qualitative analysis of interviews of men with early stage prostate cancer: the prostate cancer lifestyle trial. Cancer Nurs. 28:99, 2005. Lamb DJ, Zhang L. Challenges in prostate cancer research: animal models for nutritional studies of chemoprevention and disease progression. J Nutr. 135:3009S, 2005.


Malik A, et al. Pomegranate fruit juice for chemoprevention and chemotherapy of prostate cancer. Proc Natl Acad Sci USA. 102:14813, 2005. Ornish D, et al. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A. 105:8369, 2008. Schenk JM, et al. A dietary intervention to elicit rapid and complex dietary changes for studies investigating the effects of diet on tissues collected during invasive surgical procedures. J Am Diet Assoc. 109:459, 2009. Sheriff SK, et al. Lifestyle correlates of health perception and treatment satisfaction in a clinical cohort of men with prostate cancer. Clin Prostate Cancer. 3:239, 2005. Steiner C, et al. Isoflavones and the prevention of breast and prostate cancer: new perspectives opened by nutrigenomics. Br J Nutr. 99:78S, 2008. Trottier G, et al. Nutraceuticals and prostate cancer prevention: a current review. Nat Rev Urol. 7:21, 2010. Tsavachidou D, et al. Selenium and vitamin E: cell type- and interventionspecific tissue effects in prostate cancer. J Natl Cancer Inst. 101:306, 2009. Van Patten CL, et al. Diet and dietary supplement intervention trials for the prevention of prostate cancer recurrence: a review of the randomized controlled trial evidence. J Urol. 180:2314, 2008.



Adapted from: McClatchey KD M.D., D.D.S. Clinical Laboratory Medicine, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2002.

DEFINITIONS AND BACKGROUND Leukemia involves the uncontrolled proliferation of leukocytes and their precursors in blood-forming organs, with infiltration into other organs (Table 13-20). The blood has a grayish-white appearance. Leukemia incidence is highest among whites and lowest among American Indians/Alaskan natives and Asian and Pacific Islander populations. Acute leukemia progresses rapidly, with an accumulation of immature, functionless cells in the marrow and blood. Then, the marrow stops producing enough normal red cells, white cells and platelets and anemia develops. Chronic leukemias progress more slowly.

Leukemia is the most common childhood cancer. Because chromosomal abnormalities are present at birth in children who later develop leukemia, nutrition during pregnancy affects their risk. Insulin-like growth factor I (IGF-I) is associated with high birth weight and an increased risk of childhood leukemia (Tower and Spector, 2007). Both insulin and IGF-I act to promote cell proliferation and to inhibit apoptosis (Fair and Montgomery, 2009). Obesity is a well-known problem in children with ALL; it may be the result of an excess in energy intake, reduced energy expenditure, or both (Jansen et al, 2009). Dietary exposures to cured/smoked meat or fish, nitrites, and nitrosamines are associated with leukemia in children and adolescents (Liu et al, 2009). It may be prudent for women to consume a diet rich in vegetables, fruit, iron, soybean curd, and protein (particularly fish and seafood) prior to and during pregnancy to reduce the ALL risk in their children (Kwan et al, 2009; Liu et al, 2009; Petridou et al, 2005). Phytochemicals, such as grape extract, apigenin, quercetin, kaempferol, and myricetin, are protective against cancer cell survival (Chen et al, 2005). Red wine polyphenolic extract may inhibit leukemia cell growth (Sharif et al, 2010). In adults with AML, individuals who smoke, do not drink coffee, and eat more meat have a higher risk (Ma et al, 2009). The primary treatment of leukemias currently involves chemotherapy to kill attacking abnormal blood cells. Bone marrow transplantation may be feasible in some cases. Table 13-21 lists various types of leukemias, relevant signs and symptoms, and treatments.

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CLINICAL INDICATORS Genetic Markers: FLT3 is a receptor tyrosine kinase that plays an important role in hematopoietic stem cell proliferation, differentiation and survival; alterations have a role in leukemia. BCR-ABL cancer gene is another gene of importance in leukemias. Persons with Down syndrome, Fanconi’s anemia, and other genetic disorders have a high risk of leukemia. Lack of maternal folate causes DNA hypomethylation and increased DNA strand breaks; MTHFR gene polymorphisms have been associated with adult and childhood ALL (Smith et al, 2005; Tower and Spector, 2007). Chronic lymphocytic leukemia (CLL) is a malignancy of B cells of unknown etiology; deletions of the chromosomal region 13q14 are commonly associated with CLL (Klein et al, 2010). Specific Clinical/ Cough, sternal tenderness History Splenomegaly, Height hepatomegaly Weight Hemorrhages, BMI nosebleeds Weight changes Headache (slight weight Anorexia loss?) Nausea and Diet history vomiting BP Mouth ulcers Fever (over Bleeding 101 F?) Enlarged lymph Frequent infecnodes? tions Night sweats? Malaise, irritabilLumbar ity puncture Pallor Hemorrhage Lab Worka Petechiae, WBC (increased) ecchymosis, Ferritin purpura (increased) Palpitations Platelets Shortness of Lactate dehydrobreath genase (LDH) Bone or joint (elevated) pain

Zinc (decreased) Uric acid (increased) Immunocytochemistry Cytogenetics (FISH test) Molecular genetic studies Alb, transthyretin CRP Serum copper (increased) Gluc H & H, Serum Fe, Ferritin Transferrin PT or International Normalized Ratio (INR) Na, K Ca, Mg


A useful Web site describing lab tests is available at br_1216925469.pdf.

INTERVENTION OBJECTIVES • Prevent hemorrhage and infections. • Promote recovery and stabilization before bone marrow transplantation, if performed.

Assessment Data: Status post bone marrow transplant for ALL in a 14-year old male. Now at the emergency room, complaining of gastric pain and vomiting after eating items at a restaurant salad bar. BMI normal for age. Labs all within normal limits. Nutrition Diagnosis (PES): Intake of unsafe foods related to raw vegetables and salad items at public restaurant following BMT procedure, as evidenced by gastric pain and vomiting. Intervention: Education about the benefits of the low bacteria (neutropenic) diet for a few months longer until the immune system and tolerance improves. Counseling about the use of cooked fruits and vegetables and avoidance of salad bars until tolerance is better. Monitoring and Evaluation: No further episodes of vomiting and GI pain with the use of the neutropenic diet. Good acceptance of the restrictions until immunity improves.

• Correct anorexia and nausea or vomiting. • Prevent complications and further morbidity, such as veno-occlusive disease (VOD). • Alter diet according to medications and therapies such as chemotherapy. A low-bacteria (neutropenic) diet may be useful, particularly if bone marrow transplant is used. • Maintain weight that is appropriate for height. Correct weight loss and cachexia. • Maintain adequate hydration.

FOOD AND NUTRITION • Serve attractive meals at temperatures that are tolerated. • Choose soft foods or foods that can be cooked until tender. Cut foods into bite-sized pieces; grind or blend them so that less chewing is needed. • Follow neutropenic diet guidelines for BMT. Avoid all uncooked vegetables, most uncooked fruits, raw or rare-cooked meat, fish. All eggs should be thoroughly cooked. Avoid salad bars and deli counters. Buy vacuumpacked luncheon meats rather than freshly sliced meats. Eat or drink only pasteurized milk, yogurt, cheese, or other dairy products. Avoid soft mold-ripened and blueveined cheeses including Brie, Camembert, Roquefort, Stilton, Gorgonzola, and Blue. At home, use tap water or bottled water; avoid well water or boil it for one minute before using. • Small meals may be better tolerated than large ones. In some cases, cold or iced foods may be preferred. • A high-protein, high-energy, high-vitamin/mineral intake should be offered. Tube feeding in these patients is often useful, but intolerance due to treatment side effects may be an obstacle. • Extra fluids will be important during febrile states or with the use of interferon, but avoid overload. Sip water and

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TABLE 13-20


Various Forms of Leukemia



Acute Leukemias

Sx: easy fatigue, malaise, irritability, fever, pallor, petechiae, bruising, purpura, hemorrhage, palpitations, shortness of breath, slight weight loss, bone or joint pain, painless lumps in underarm or stomach, cough, sternal tenderness, splenomegaly, hepatomegaly, anemia, hemorrhages or nosebleeds, headache, nausea, vomiting, and mouth ulcers.

Acute lymphocytic leukemia (ALL)

ALL affects bone marrow and lymph nodes. It progresses rapidly and mainly affects children; it accounts for 50% of all childhood leukemias. Control of bone marrow and systemic disease is the goal. Treatment may include monthly lumbar punctures. ALL often spreads to the coverings of the brain and spinal cord; patients may receive chemotherapy into spinal fluid, or radiation therapy to the head. Bone marrow transplantation (BMT) treatment or peripheral-blood stem-cell transplant (PBSCT) may lead to bloody diarrhea, fever, and other symptoms of graft-versus-host disease (GVHD).

Acute myelogenous leukemia (AML)

AML starts in the bone marrow but moves into the blood and to the lymph nodes, liver, spleen, central nervous system, and testes. AML consists of proliferation of myeloblasts, which are immature polynuclear leukocytes. AML is more common in adult males but also accounts for just under half of cases of childhood leukemia. Average onset of AML is the sixth decade. Smoking, obesity, chronic workplace exposure to benzene, large doses of irradiation have been established as causes. Treatments vary according to the age of the patient and according to the specific subtype. The goal is to control bone marrow, CNS, and systemic disease.

Chronic Leukemias

Sx: anemia, increased infections, bleeding, enlarged lymph nodes (in lymphatic form), night sweats, fever, weight loss, and anorexia.

Chronic lymphocytic leukemia (CLL)

CLL involves a crowding out of normal leukocytes in lymph glands, interfering with the body’s ability to produce other blood cells. CLL is more common in people older than 50 years of age and in males. It is twice as common as CML. Treatment depends upon the stage and symptoms of the individual patient. Low-grade disease does not benefit from treatment. With complications or more advanced disease, treatment may be needed. Hairy cell leukemia is a subtype of CLL.

Chronic myelogenous leukemia (CML)

CML affects mostly adults and is very rare in children. The standard of care for newly diagnosed patients is oral administration of imatinib (Gleevec), which has few side effects and makes CML a chronic, manageable condition.

T-cell prolymphocytic leukemia

Has similar overproduction of white blood cells in the bone marrow; less common than the other types. Difficult to treat and does not respond well to chemotherapy drugs. Alemtuzumab (Campath) is a monoclonal antibody that attacks white blood cells with some success.

other clear liquids such as broth, ginger ale, or lemonade frequently. • Vitamins A and D may be beneficial (Trump et al, 2005) but avoid excesses above the UL levels. • Include protective foods such as isoflavones in soy and flavonoids in grapes, coffee, tea, nuts, seeds, fruits, and vegetables.

TABLE 13-21

Common Drugs Used and Potential Side Effects • See Tables 13-22. • Methadone kills leukemia cells while not affecting the normal ones; it activates the mitochondrial pathway, which activated specific enzymes within the cancer cell, causing pre-programmed death. This is a great breakthrough in leukemia research.

Medications for Acute Leukemias

Induction: The first phase destroys as many cancer cells as quickly as possible to bring about a remission. Consolidation: The goal is to get rid of leukemia cells where they reside. Maintenance: After the number of leukemia cells has been reduced by the first two phases of treatment, lower doses of chemotherapy drugs are given over 2 years. CEP-701 (lestaurtinib) inhibits the receptor tyrosine kinase FLT3 in AML patients Chemotherapy often includes methotrexate, 5-azacitidine, cytarabine, thioguanine, and daunorubicin, which may cause stomatitis, nausea, or vomiting. Coadministration of these agents with glucose and adequate fluid is needed. When methotrexate is used, neurotoxicity is a concern; use low-dose folinic acid rescue (Leucovorin). Gemtuzumab ozogamicin (Mylotarg) may be added. Granulocyte colony-stimulating factors (Neupogen, Leukine) may improve response to chemotherapy. This intensive therapy, which usually takes place in the hospital, typically lasts 1 week. L-asparaginase

(Elspar) may be used; hepatitis or pancreatitis may result; watch carefully.

Pegaspargase (Oncaspar) can cause nausea, vomiting, anorexia, and glucose changes. Interferon may be used. Prednisone may be used, with side effects related to steroids with chronic use. Alter diet and intake accordingly to manage hyperglycemia, hypokalemia, and nitrogen losses.

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TABLE 13-22

calorie liquids such as gravy, milk, cream or broth instead of water.

Medications for Chronic Leukemias

Chemotherapeutic agents may be used with varying side effects. Chlorambucil (Leukeran) and busulfan are common; nausea, severe fatigue, flulike symptoms, low-grade temperature, vomiting, glossitis, and cheilosis may occur. Avoid hot, spicy, or acidic foods, if not tolerated. Pegaspargase (Oncaspar) can cause nausea, vomiting, anorexia, and glucose changes. Imatinib (Gleevec), for CML, interferes with an abnormal enzyme that sends signals to the nucleus of a cancer cell. Nausea and vomiting are potential side effects. Dasatinib (Sprycel) and nilotinib (Tasigna) block the BCR-ABL cancer gene, but each works in a different way than Gleevec. Sprycel and Tasigna are approved for certain CML patients who are resistant or intolerant to prior therapy including Gleevec. All three drugs are given orally. For CLL: Multiple treatments include purine analogs, monoclonal antibodies, and stem-cell transplantation. Antifungals, antivirals, or antibiotic drugs may be used; side effects vary.

Patient Education—Food Safety • People who are being treated for leukemia have weakened immune systems and increased risk for food-borne illness. • Keep hands, counters, dishes, cutting boards, and utensils clean. Change sponges and dishtowels often. • Keep foods at proper temperatures, reheating foods properly. • Wash fruits and vegetables thoroughly. • Use separate dishes, cutting boards, and utensils for preparing raw meat, fish, or poultry. • Thaw frozen items in the microwave or refrigerator, not on the kitchen counter. • Use a food thermometer to make sure that meat is fully cooked. • Read the expiration dates on food products. Look for signs of food spoilage; if in doubt, throw it out.

For More Information

Herbs, Botanicals, and Supplements (see Table 13-8)

Leukemia and Lymphoma Society

• Herbs and botanical supplements should not be used without discussing it with the physician. • For CML, bioflavonoids, vitamin A, Retin-A, vitamin D3, vitamin E, vitamin B12, indirubin (found in herbs including Indigofera tinctoria and Isatis tinctoria), and Curcuma longa have shown promise (Matsui, 2005). • Omega-3 fatty acid supplements may increase the bloodthinning effects of aspirin or warfarin. • St. John’s wort reduces the effectiveness of imatinib, which is used to treat CML and Philadelphia-positive ALL.

People Living With Cancer

Partnership for Food Safety Education (PFSE)

University of Virginia Health System hessidb/leukemias.cfm

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • A well-balanced diet is essential; discuss ways to improve or increase intake. • Tumor lysis syndrome is a side effect caused by the rapid breakdown of leukemia cells. When these cells die, they release substances into the bloodstream that can affect the kidneys, heart, and nervous system. Giving patient extra fluids or certain drugs that help rid the body of these toxins can prevent this problem. • Offer guidelines to transition from CPN or PN to enteral nutrition and oral intake. • Discuss guidance for graft-versus-host disease (acute vs. chronic symptoms). • Discuss alternative ways to make meals more attractive and appealing. • Instruct patient on nutrition repletion if appropriate. For extra calories, blend cooked foods or soups with high-

LEUKEMIAS—CITED REFERENCES Chen D, et al. Dietary flavonoids as proteasome inhibitors and apoptosis inducers in human leukemia cells. Biochem Pharmacol. 69:1421, 2005. Fair AM, Montgomery K. Energy balance, physical activity, and cancer risk. Methods Mol Biol. 472:57, 2009. Jansen H, et al. Acute lymphoblastic leukemia and obesity: increased energy intake or decreased physical activity? Support Care Cancer. 17:103, 2009. Klein U, et al. The DLEU2/miR-15 a/16–1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia [Published online ahead of print Jan 6, 2010]. Cancer Cell. Kwan ML, et al. Maternal diet and risk of childhood acute lymphoblastic leukemia. Public Health Rep. 124:503, 2009. Liu CY, et al. Cured meat, vegetables, and bean-curd foods in relation to childhood acute leukemia risk: a population based case-control study. BMC Cancer. 9:15, 2009. Ma X, et al. Diet, lifestyle, and acute myeloid leukemia in the NIH-AARP Cohort [Published online ahead of print Dec 30, 2009]. Am J Epidemiol. Matsui J, et al. Dietary bioflavonoids induce apoptosis in human leukemia cells. Leuk Res. 29:573, 2005. Petridou E, et al. Maternal diet and acute lymphoblastic leukemia in young children. Cancer Epidemiol Biomarkers Prev. 14:1935, 2005. Sharif T, et al. Red wine polyphenols cause growth inhibition and apoptosis in acute lymphoblastic leukaemia cells by inducing a redox-sensitive upregulation of p73 and down-regulation of UHRF1 [Published online ahead of print Jan 12, 2010]. Eur J Cancer. Smith MT, et al. Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol. 206:237, 2005. Tower RL, Spector LG. The epidemiology of childhood leukemia with a focus on birth weight and diet. Crit Rev Clin Lab Sci. 44:203, 2007. Trump DL, et al. Anti-tumor activity of calcitriol: pre-clinical and clinical studies. J Steroid Biochem Mol Biol. 90:519, 2005.

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LYMPHOMAS NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Chronic antigenic stimulation leads to lymphoid malignancy (Anderson et al, 2009). There are two types: Hodgkin’s lymphoma (HL) and non-Hodgkin’s lymphoma (NHL), which is far more common. In HL, patients present with enlarged lymph nodes that are firm and rubbery, severe pruritus, jaundice, night sweats, fatigue and malaise, weight loss, slight fever, alcohol-induced pain, cough, dyspnea, and chest pain. It presents most commonly in males between the ages of 15 and 34 or after age 60 in persons who have lupus, EpsteinBarr virus (mononucleosis) or HIV infection. Abnormal B cells, called Reed-Sternberg cells, develop and enlarge. The treatment of HL involves radiation and chemotherapy. Stage 1 is limited to one body part; stage 2 involves two or more areas on the same side of the diaphragm; stage 3 involves lymph nodes above and below the diaphragm; and stage 4 involves lymph nodes and other areas such as the lungs, marrow, and liver. Patients who present with weight loss initially have a worse prognosis than those without weight loss. The 5year survival rate for Hodgkin’s disease is 84%; it is one of the more curable forms of cancer. Unfortunately, survivors may have a stroke later in life, and young women who receive high-dose radiation for Hodgkin’s disease are more at risk for breast cancer. Non-Hodgkin’s lymphoma (NHL) is a malignant tumor of lymphoid tissue, resulting from an invasion of the lymph nodes and other tissues by lymphocytes. NHL is relatively common among individuals whose immune system is suppressed. Rheumatoid arthritis, Sjögren syndrome, T-cell lymphoma with hemolytic anemia, psoriasis, discoid lupus erythematosus, and celiac disease are associated with an increased risk of NHL (Anderson et al, 2009). H. pylori is associated with the development of lymphoma in the stomach wall. Burkitt’s lymphoma is most common in children, young adult males, and patients with AIDS; it originates from a B lymphocyte and requires chemotherapy. This lymphoma is associated with a prior infection with the Epstein-Barr virus. Exposure to certain chemicals (such as nitrates) in herbicides and pesticides promotes risk. Enteropathy-associated T-cell lymphoma (EATL) is a rare form of high-grade, T-cell NHL of the upper small intestine that is specifically associated with celiac disease (Catassi et al, 2005). Capsule endoscopy is used to evaluate this celiac disease–associated enteropathy (Joyce et al, 2005). Strict adherence to the gluten-free diet protects against NHL, particularly if started early (Hervonen et al, 2005). Symptoms and signs of NHL include difficulty breathing, swelling of face, thickened or dark, itchy skin areas, increased incidence of bacterial infections, night sweats, weight loss, fever, anemia, and pleural effusion. It is possible, as well, to develop chylous ascites or chyloperitoneum. By the time of NHL diagnosis, it is often widely spread. It may spread to the cervix, uterus, and vagina in women. Radiation is a common treatment for the early stages. A cure is less likely for those over age 60.


CLINICAL INDICATORS Genetic Markers: HL and NHL have several gene mutations. The presence of the Reed-Sternberg cell in HL is an expression of the CD30 antigen. In NHL, t(14;18)(q32;q21) chromosomal translocations occur in the BCL2 gene. Specific Clinical/History Height Weight BMI Weight loss? Diet history Enlarged, rubbery lymph nodes Painless adenopathy Pruritus, severe Jaundice Night sweats Fatigue and malaise Slight fever, temperature

Alcohol-induced pain Cough, dyspnea, and chest pain Diarrhea I&O Lymphangiogram X-ray or CT scan Bone marrow biopsy Lab Work Ceruloplasmin (increased) Reed-Sternberg cells (more than one nucleus)

ESR Uric acid (increased) PT (increased) Gluc CRP Serum Cu (increased) H&H Bilirubin (increased) Alk phos (often increased) Ferritin (increased) ALT (increased) Serum lipids— Chol, Trig Ca, Mg Na, K

SAMPLE NUTRITION CARE PROCESS STEPS Obesity Assessment Data: BMI 42, new diagnosis of NHL. Diet hx indicates low intake of whole grains and vegetables and high intake of sugary, refined foods and beverages. Nutrition Diagnosis (PES): Obesity related to poor food choices as evidenced by BMI 42 and preference for sugary, refined foods. Intervention: Food-Nutrient Delivery—Promote the use of low energy foods and beverages. Educate the patient about the risks of obesity in cancer promotion. Counsel about ways to safely lose weight, with the focus on a healthy body weight and nutrient density. Monitoring and Evaluation: Reasonable amount of weight lost, slowly and without loss of lean body mass but with tolerance for chemotherapy treatments. Improved BMI.

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INTERVENTION OBJECTIVES • Prevent or correct weight loss, fever, malaise, and infections such as candidiasis. • Correct dysphagia, nausea and vomiting, and anorexia. • Control protein-losing enteropathy, chylous ascites, and other side effects. • Control enteropathy in patients who also have celiac disease. • Modify diet according to the side effects of therapy (e.g., radiation or chemotherapy). • If obese, a gradual weight loss plan may be indicated.

FOOD AND NUTRITION • Increase protein and fluids. Balance energy intake to meet the needs of treatments without causing weight gain. • Six small feedings are generally better tolerated than three large meals. Alter diet according to symptoms. • Bland, low acidic foods may be better accepted for a while. • With celiac disease, the gluten-free diet is required. • With hyperglycemia, control carbohydrates and overall energy intake. • Support the use of a protective diet with folate and B vitamins, vegetables, and legumes. Include vitamin D3, particularly from sunlight (Grant, 2009; Kelly et al, 2009).

• Lymphoma survivors tend to use CAM therapies more than the general population (Habermann et al, 2009). Chiropractic, massage, and use of St. John’s wort and shark cartilage have been noted. • Acupuncture, coenzyme Q10, and polysaccharide K are under study.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss methods of improving appetite by the use of attractive meals. • Encourage rest periods before and after meals to reduce fatigue. • Encourage a diet that is protective with plenty of vegetables and legumes. • Vitamin D3 may protect against both types of lymphomas (Grant, 2009; Kelly et al, 2009).

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information

Common Drugs Used and Potential Side Effects HL • Chemotherapy is often given in combination. The regimen MOPP, which includes mechlorethamine (nitrogen mustard), vincristine (Oncovin), procarbazine, and prednisone may cause nausea, vomiting, diarrhea, weakness, constipation, and mouth sores. The regimen ChlVPP, which includes chlorambucil, vinblastine, procarbazine, and prednisone, may cause similar side effects. After chemotherapy, young women may have amenorrhea. • Corticosteroids can aggravate the electrolyte status and will decrease the calcium, potassium, and nitrogen balance over time. Hyperglycemia may also occur; monitor blood glucose levels.

NHL • Chemotherapy is often given as a regimen called CHOP, which includes cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisone. CHOP may cause nausea, vomiting, anorexia, diarrhea, and other gastrointestinal (GI) side effects. Single agents may also be used. Methotrexate causes GI pain, mouth ulcers, nausea, and folic acid depletion.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician.

Cancer Information Network

Leukemia and Lymphoma Society

Lymphoma Information Network

National Cancer Institute–Hodgkin’s Lymphoma

National Library of Medicine

Non-Hodgkin’s Lymphoma

Wellness After Treatment

LYMPHOMAS—CITED REFERENCES Anderson LA, et al. Population-based study of autoimmune conditions and the risk of specific lymphoid malignancies. Int J Cancer. 125:398, 2009. Catassi C, et al. Association of celiac disease and intestinal lymphomas and other cancers. Gastroenterology. 128:S79, 2005. Grant WB. How strong is the evidence that solar ultraviolet B and vitamin D reduce the risk of cancer? An examination using Hill’s criteria for causality. Dermatoendocrinol. 1:17, 2009. Habermann TM, et al. Complementary and alternative medicine use among long-term lymphoma survivors: a pilot study. Am J Hematol. 84:795, 2009. Hervonen K, et al. Lymphoma in patients with dermatitis herpetiformis and their first-degree relatives. Br J Dermatol. 152:82, 2005. Joyce AM, et al. Capsule endoscopy findings in celiac disease associated enteropathy-type intestinal T-cell lymphoma. Endoscopy. 37:594, 2005. Kelly JL. et al. Vitamin D and non-Hodgkin lymphoma risk in adults: a review. Cancer Invest. 27:942, 2009. Yee KW, O’Brien SM. Chronic lymphocytic leukemia: diagnosis and treatment. Mayo Clin Proc. 81:1105, 2006.

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MYELOMA NUTRITIONAL ACUITY RANKING: LEVEL 3 Frequent urinary tract infections Pneumonia? Skeletal survey Lab Work Ca (increased) Mg Na, K

Adapted from: Raphael Rubin, David S. Strayer, Rubin’s Pathology: Clinicopathologic Foundations of Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

DEFINITIONS AND BACKGROUND Myeloma is the second most common blood cancer. Multiple myeloma (MM) is a malignant cancer in which plasma cells proliferate, invade bone marrow, and produce abnormal immunoglobulin. Different types of myeloma are classified by the type of immunoglobulin produced by the abnormal cells. The condition is rare, affecting only 4/100,000 persons and representing only 1% of all cancers. Males are affected more often than females, and the disorder usually strikes after age 50. African-Americans are twice as likely to acquire MM as Caucasians, Hispanics, or Asians. Obesity promotes this type of cancer. MM affects several areas of bone marrow. If significant bone lesions, renal failure, or hypercalcemia occur, chemotherapy or transplantation is recommended. Stem-cell transplantation or radiation therapy may be administered (Iversen, 2009).

Total protein Parathormone (PTH) (increased) TLC (varies) Hypercalciuria Alb (often increased) CRP Transferrin H&H

Proteinuria (Bence Jones proteins) Sedimentation rate (increased) Uric acid (increased) RBP ALT (increased)


Avoid fasting. Space meals and snacks adequately. Counteract episodes of fatigue and weakness. Manage pain effectively. Counteract side effects of antineoplastic therapy, steroid therapy, and radiotherapy. • Avoid infections and febrile states. • Prevent spontaneous fractures, as far as possible. • Correct anorexia, nausea and vomiting, and weight loss.

FOOD AND NUTRITION • Provide diet as usual, with six small feedings rather than large meals. • A higher protein intake may be useful to counteract losses. • Provide adequate energy to meet requirements of weight control, preventing unnecessary losses.



Inadequate Oral Food and Beverage Intake

Genetic Markers: The premalignant condition of monoclonal gammopathy of undetermined significance (MGUS) precedes all cases of MM (Jagannath, 2010). Specific Clinical/History Height Weight BMI Weight loss? Shortened stature? I&O

BP Bone pain Pathological fractures Nausea and vomiting Anorexia History of bleeding

Fatigue, weakness, apathy Sudden confusion Renal disorders Bleeding tendency (particularly gums)

Assessment Data: Mucositis following chemotherapy for the treatment of multiple myeloma. Unable to chew and swallow comfortably because of inflamed oral tissues. Nutrition Diagnosis (PES): Inadequate oral food and beverage intake (NI-2.1) related to sore mouth as evidenced by mucositis after chemotherapy and difficulty finding tolerated foods and beverages. Intervention: Food-nutrient delivery—offer soft, ground, or pureed foods that are low in acid and spices. Educate the patient about the use of a soft, easily tolerated diet that has nutrientdensity. Counsel with tips for gradually increasing the oral diet as mucositis subsides. Monitoring and Evaluation: Resolution of mucositis with an improvement in oral intake.

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• Avoid dehydration by including adequate fluid intake (e.g., 3 L daily). This is important. • Ensure sufficient intake of omega-3 fatty acids, vitamins, minerals, and phytochemicals, particularly from fruits and vegetables.

Herbs, Botanicals, and Supplements (see Table 13-8) • Herbs and botanical supplements should not be used without discussing it with the physician.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT Common Drugs Used and Potential Side Effects • Arsenic trioxide (Trisenox), carmustine (BiCU, BCNU), cyclophosphamide (Cytoxan), doxorubicin (Adriamycin, Rubex), idarubicin (Idamycin), interferon-alpha (Roferon-A, Intron-A), lenalidomide (Revlimid), pamidronate (Aredia), vincristine (Oncovin), or zoledronic acid (Zometa) may be given as chemotherapy, often with several in a mixture. Melphalan (Alkeran) or nitrosoureas may also be used; monitor for anorexia, anemia, nausea, vomiting, and stomatitis. • Bisphosphonates may be used to prevent bone fractures. • Pamidronate may be used. Ensure adequate fluid intake but not excess. Avoid use with calcium and vitamin D supplements. Extra phosphorus may be needed. Nausea, vomiting, gastrointestinal bleeding or distress, and constipation can occur. • Prednisone, if used chronically, can increase nitrogen losses and potassium and magnesium depletion and can cause hyperglycemia and sodium retention. • Lenalidomide delays disease progression in late-stage multiple myeloma. It also helps to reduce the need for blood transfusions. • The immunomodulatory agents thalidomide and lenalidomide and the proteasome inhibitor bortezomib are now routine components of MM therapy (Jagannath, 2010). However, all patients with MM eventually relapse; efforts to identify novel synergistic combinations and agents are ongoing (Jagannath, 2010). • Bortezomib (Velcade), a proteasome inhibitor, delays disease progression and extends survival.

• Discuss the rationale for spacing meals throughout the day to avoid fatigue. • Offer recipes and meal plans that provide the nutrients required to improve status and immunological competence.

Patient Education—Food Safety • Educate the patient about food safety issues. Discuss safe food handling and preparation, keeping foods at proper temperatures, the use of sterile water, and reheating foods properly.

For More Information •

Cleveland Clinic–Multiple Myeloma Programs

International Myeloma Foundation

Mayo Clinic Myeloma

Multiple Myeloma Foundation

National Library of Medicine

MYELOMA—CITED REFERENCES Iversen PO, et al. Reduced nutritional status among multiple myeloma patients during treatment with high-dose chemotherapy and autologous stem cell support [Published online ahead of print Dec 29, 2009]. Clin Nutr. Jagannath S, et al. The current status and future of multiple myeloma in the clinic. Clin Lymphoma Myeloma. 10:1E, 2010. Pan SL, et al. Association of obesity and cancer risk in Canada. Am J Epidemiol. 159:259, 2004.

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Surgical Disorders




• • • • • • • • • • • • • •

Anemia, Blood Loss Appetite Changes Blood Pressure, Abnormal Electrolyte Status History of Illness—Acute or Chronic (Such as Diabetes, Cerebrovascular Disease, Coronary Heart Disease) Hydration Status Infections Nausea, Vomiting Obesity and Anesthesia Risk Recent Starvation or Prolonged Malnutrition Recent Weight Changes, Especially Unintentional Loss Respiratory Function, Oxygen Saturation Serum Albumin, Transferrin, Retinol-Binding Protein, and C-Reactive Protein (CRP) (Inflammation) Surgical Procedure with Gastrointestinal (GI) Impact

Postsurgical Status

• • • • • • • • • • • •

Abnormal GI Function (diarrhea, constipation, obstruction) Altered Labs Such as Glucose, CRP, Electrolytes Breathing Rate Fever Impaired Skin Integrity, Wound Dehiscence Infection or Sepsis Nausea, Vomiting Pain, Sleep Disturbance Paralytic Ileus, Abdominal Distention Pneumonia or Lung Collapse Respiratory Function, Oxygen Saturation Urinary Tract Infection

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Adapted from: Smeltzer SC, Bare BG. Textbook of Medical-Surgical Nursing, 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2000.

DEFINITIONS AND BACKGROUND Nutritional risk from surgery is related to the extent of surgery, prior nutritional state of the patient, and the effect of surgery on the patient’s ability to digest and absorb nutrients. Weight loss is one of the most important assessment tools to predict surgical risk as related to nutritional status. Techniques to assess body composition help to quantify weight loss and clarify the impact of malnutrition on postsurgical status. Surgery is the term used for treatments that involve cutting or stitching tissue, laser surgery, and robotic surgical procedures. Major surgery involves opening a major body cavity, such as the abdomen (laparotomy) or the skull in a craniotomy. “General anesthesia,” a surgical team, and a hospital stay are required. Minor surgery may be done in an outpatient or emergency room setting, often with minimal anesthetic treatment. Surgeries with high risk include hip replacement, open heart surgery, and prostatectomy. Patients who are at high surgical risk include those with heart or renal failure, those who have had a recent heart attack, those who are severely malnourished, and those with chronic lung or liver diseases. After surgery or injury with extensive tissue damage, plasma cortisol generally increases rapidly and fat breaks down rapidly to fatty acids and glycerol. The metabolic

response to surgical or accidental injury leads to breakdown of skeletal muscle protein and the transfer of amino acids to visceral organs and the wound. At the wound site, substrate serves to enhance host defenses and support vital organ function and wound repair. Increased excretion of nitrogen and sodium retention occur, but these are reversed in approximately 5–7 days or as late as 12–14 days in elderly individuals and after severe burns. Increased excretion of potassium occurs but begins to reverse itself 1–2 days after surgery. Malnutrition is prevalent among surgical patients and is associated with higher surgical complication rates and mortality (Figure 14-1). Some causes of poor nutritional status are related to the underlying disease, socioeconomic factors, age, and length of hospitalization. If medical teams overlook malnutrition, patients are at risk for malnutrition and complications. Use of tools such as the Subjective Global Assessment identifies malnutrition in many patients. Elective surgery involves minimal increases in nitrogen loss and a 10–15% increase in energy requirements. Major surgery involves greater intensity and duration that will increase catabolic effects. Prevention of hypoxia in surgical wounds is especially important and preventable; fluid and temperature management are key factors. Table 14-1 defines the average length of time and stages of catabolic response after surgery, followed by anabolism. The presence of cancer, infection, age more than 60 years, upper gastrointestinal (GI) disease, and longer length of hospital stay all negatively influence nutritional status. Nutritional status plays an important role in determining outcome after many types of operations. Enteral immunonutrition is an important consideration preoperatively as well, if time permits. Early postoperative enteral nutrition with a formula supplemented with arginine, omega-3 fatty acids, and RNA increases hydroxyproline synthesis and improves surgical wound healing in patients undergoing gastric surgery (Farreras et al, 2005). Fever causes increased nutritional needs; for every 1F increase, there is an increased energy requirement of 7–8% and the need for extra fluid. Optimal wound healing requires integration of responses to inflammatory mediators, growth factors, cytokines, and mechanical forces (Falanga, 2005). Extra protein is needed for wounds, burns, and hemorrhage; major wounds and burns can cause a loss of greater than 50 g of protein per day. With hemorrhage

TABLE 14-1 Postsurgical Phases in Nutrition 3–7 days

Marked catabolic response

2–5 weeks

Turning point and anabolic phase at which spontaneous improvement begins

6 weeks

Fat gain phase; vigorous nutritional support could promote excessive fat stores

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or major blood loss, or even when much blood is drawn for laboratory tests, loss of iron and plasma protein may be significant; loss of 1 L of blood equals a loss of 500 mg of iron and 50 g of plasma protein. C-reactive protein (CRP) is a risk factor for cardiovascular outcomes and mortality in the general population; it predicts all-cause mortality (Winklmayer et al, 2005). Preoperative serum albumin concentration may predict surgical outcomes such as sepsis, renal failure, and major infections. Early identification of high-risk patients undergoing major surgery allows aggressive management. After surgery, the presence of systemic inflammatory response syndrome is a predictor of later sepsis (Mokart et al, 2005). Other patient risk factors predictive of postoperative morbidity include anesthesia and complexity of the operation. A complete, balanced diet is recommended after surgery. A clear liquid diet has about 600 kcal/d and D5W solutions have only 170 kcal/L. Early postoperative oral feeding has been demonstrated to be safe (Lucha et al, 2005). Enhanced rate of recovery can be achieved by enhancing the metabolic status of the patient before (e.g., carbohydrate and fluid loading), during (e.g., epidural anesthesia), and after (e.g., early oral feeding) surgery (Fearon and Luff, 2003). Healing of wounds involves blood cells, tissues, cytokines, growth factors, and metabolic demand for nutrients. Vitamin A is required for epithelial and bone formation, cellular differentiation, and immune function. Vitamin C is necessary for collagen formation, for proper immune function, and as a tissue antioxidant. Adequate protein is absolutely essential for proper wound healing. Tissue levels of the amino acids arginine and glutamine (GLN) influence wound repair and immune function. GLN depletion in skeletal muscle is an outstanding metabolic marker related to acute skeletal muscle wasting (Roth and Oehler, 2010.) Energy-saving signals may be switched on to protect organs in a mode similar to hibernation; this may explain the low energy expenditure in septic patients (Roth and Oehler, 2010.) Its use in various enteral or parenteral products is accepted in many facilities. Patients who receive enteral immunonutrition with multiple nutrients before and after major GI surgery often have lower treatment costs. Arginine is helpful in wound healing after trauma (Wilmore, 2004; Wittman et al, 2005). Major surgery, skeletal trauma, prolonged immobilization, and soft tissue damage are followed by increased calcium loss. Vitamin C may be destroyed by extensive inflammation in postoperative conditions. Table 14-2 indicates the extent of body reserves of nutrients. Higher nutrient reserves are advantageous in most surgeries.


CLINICAL INDICATORS Genetic Markers: Surgery may be needed to repair a genetic condition, such as a congenital heart disorder.

History of dehydration or Height slow wound Weight healing Body mass index Transfusions (BMI) Weight changes Lab Work Diet history Blood pressure Glucose (Gluc) C-reactive (BP) protein (CRP) Intake and outPlatelet count put (I & O) Albumin (Alb), Nausea, vomittransthyretin ing Blood urea Constipation nitrogen Anorexia (BUN) Urinary tract Creatinine infection (Creat) Skin integrity; Na pressure K ulcers Clinical/History


Ca Mg Phosphorus (P) Urinary electrolytes Serum osmolality (Osm) N balance Transferrin Prothrombin time (PT) or international normalized ratio (INR) Hemoglobin and hematocrit (H & H) Serum Fe Vitamin B12

INTERVENTION OBJECTIVES Preoperative • Maintain or enhance reserves. Many patients admitted to hospitals are malnourished; therefore, proper presurgical assessment and nourishment should be emphasized.

TABLE 14-2 Time Required to Deplete Body Nutrient Reserves in Well-Nourished Individuals Nutrient


Amino acids

Several hours


13 hours


2–3 days


4 days


5 days


20–40 days


30–60 days

Vitamin C

60–120 days


60–180 days


60–180 days

Vitamin A

90–365 days


125 days (women); 750 days (men)


1000 days


2500 days

From: Guthrie H. Introductory nutrition. 7th ed. St Louis: Times Mirror/Mosby College Publishers, 1989.

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TABLE 14-3 Measuring Energy Expenditure in Critical Illness

Involuntary Weight Loss Assessment Data (sources of info): Food records, input and output reports, medication history, assessment of depression. Nutrition Diagnosis (PES): NC-3.2 Involuntary weight loss related to depression and poor intake after above-knee (AK) amputation as evidenced by weight loss of 6% in past 2 weeks and statement that “I just don’t feel like eating any more.” Intervention: Food-Nutrient Delivery—Offer nutrient and energydense foods until appetite improves. Counsel about desired food and beverage intake for wound healing. Coordinate care—Discuss status of depression and medications or counseling with health care team. Monitoring and Evaluation: Improved food intake as per I & O records. Better weight status and rate of wound healing. Improvement in symptoms of depression with medication.

Some facilities use glucose and potassium intravenous loading in nondiabetic, nonrespiratory patients for surgical preparation. • Identify risks for cardiac events after surgery, which are common and costly (Maddox, 2005). • Prepare patients who are morbidly obese. Fatty tissues are not resistant to infections, hard to suture, and prone to dehiscence. A large amount of anesthesia is needed in the morbidly obese patients, and it is difficult to awaken them. Controlled weight loss should be instituted before surgery whenever possible. • Elevated serum glucose on admission is an accurate predictor of postoperative infection, length of stay, and mortality (Bochicchio et al, 2005). Reducing hyperglycemia is important.

Measuring energy expenditure via indirect calorimetry (IC) is the most accurate method of determining needs. For short-term use, predictive equations such as the Ireton-Jones calculation for nutrition support are recommended. Ireton-Jones Equations for Estimated Energy Expenditure (EEE) (Ireton-Jones and Jones, 1998) 1. Spontaneously Breathing Patient: EEE  629  11(A)  25(W)  609(O) 2. Ventilator-Dependent Patient: EEE  1784  11(A)  5(W)  244(G)  239(T)  804(B) Key: A  age in years; W  weight in kg; 0  obesity (130% ideal body weight); G  gender (female  0, male  1); T  diagnosis of trauma (absent  0, present  1); B  diagnosis of burn (absent  0, present  1).

• • •

• •

Postoperative • Replete nutrient stores, such as protein and iron from hemorrhage or other blood losses. Replace important vitamins and minerals (vitamin C, 100–200% recommended amounts; vitamin K, zinc, and vitamin A). • Correct imbalances in fluid, sodium, potassium, and other electrolytes. • Promote wound healing. The surgical wound has priority only for the first 5–10 days. Wound tensile strength peaks at 40–50 days. • Use enhanced immunonutrition where needed to provide sufficient amounts of protein and energy to preserve muscle function; stimulate and protect enterocytes while limiting bacterial translocation; keep liver function as normal as possible; and prevent or compensate for disturbances in the immune response. Arginine triggers anabolic hormones (e.g., insulin, growth hormone) and speeds wound healing (Zaloga et al, 2004). Arginine is important for growth, wound healing, cardiovascular function, immune function, inflammatory responses, energy metabolism, urea cycle function, and other metabolic processes (Zaloga et al, 2004). While

somewhat controversial, it may be helpful to select an immune-enhanced tube feeding (TF) product for GI surgeries. Attend to special needs such as fever, trauma, pregnancy, and growth in infants and children. Prevent infection and sepsis, which can occur in more than 10% of surgical cases. Prevent aspiration, a leading cause of pneumonia and the most serious complication of enteral TF. Traditional clinical monitors of glucose oxidase strips and blue food coloring (BFC) should never be used; evaluation of gastric residual volumes is recommended. Minimize weight loss, which is not obligatory. Prevent or correct sarcopenia and protein—energy malnutrition (PEM). Table 14-3 describes the use of estimated energy requirement calculations when indirect calorimetry is not available. With complete bed rest, young adults lose about 1% of their muscle per day; seniors lose up to 5% per day because of lower levels of growth hormone, which maintains muscle tissue. Sitting up in bed, moving, standing, and exercising as soon as possible and safe is good for surgical patients. Manage pain, blood clots, and other complications. Constipation or difficulty urinating may also occur, especially with opioids and anticholinergic drugs, inactivity, and not eating.

FOOD AND NUTRITION Preoperative • Because malnutrition is a recognized risk factor for perioperative morbidity, the Nutrition Risk Screening 2002 score should be used to identify patients at nutritional risk who may benefit from nutritional support therapy; it has been officially adopted by the European Society of Parenteral and Enteral Nutrition (Schiesser et al, 2008.)

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• Use a high-protein/high-energy diet, a TF, or parenteral nutrition, if needed. Enteral nutrition is effective, poses lower risks than parenteral nutrition, reduces infection rates, and shortens hospital length of stay of critically ill patients (Grimble, 2005). • If patient is obese, use a low-energy diet that includes carbohydrates adequate for glycogen stores and protein to protect lean body mass. Elevated serum glucose on admission is an accurate predictor of postoperative infection, length of stay, and mortality (Bochicchio et al, 2005). • Ensure that intakes of zinc and vitamins C and K are adequate. • Bowel cleansing regimens commonly require adherence to liquid diets for 24–48 hours before examination, which often leads to poor compliance. Offering patients a regular breakfast and a low-residue lunch before bowel cleansing with sodium phosphate oral solution may be better tolerated. • Gradually restrict diet to clear liquids and then nothing by mouth (NPO).

Postoperative • Immediately after surgery, use intravenous glucose, insulin, or electrolytes as needed (Bossingham et al, 2005). As treatment progresses, advance diet as tolerated to a combination of liquid and solid items. • A complete, balanced mix of nutrients is best. Excessive vitamin and mineral supplements do not increase rate of healing. In fact, because zinc and iron are bacterial nutrients, excesses may be detrimental. • If oral feeding is not possible, use enteral nutrition. Initiate TF within 12–18 hours for less sepsis and fewer complications. The gut can generally tolerate early feedings, even in patients with pancreatitis (Gabor et al, 2005; Lucha et al, 2005; Marek and Zaloga, 2004). Early postoperative feeding is generally safe, effective, and costeffective (Braga and Gianotti, 2005). • When necessary, because of prolonged GI compromise or short bowel syndrome, use central parenteral nutrition (CPN). Use caution with intravenous lipids due to proinflammatory omega-6 fatty acids. Omega-3 fatty acids are acceptable and not inflammatory. The adaptive role of the small intestine after surgery is described in Table 14-4. • For elective GI surgery, specialized immunonutrition does not have to be routine (Klek et al, 2008.) Enteral nutrition is preferred over parenteral nutrition when the GI tract is functional (Zaloga, 2006). GLN-enhanced products are useful, especially in malnourished patients; they improve antioxidant levels (Grimble, 2005; Luo et al, 2008). If PN is needed, glutamine-supplemented parenteral nutrition (GLN-PN) significantly decreases infections in surgical intensive care patients after cardiac, vascular, and colonic surgery (Estivarez et al, 2008.) • With oral diet, offer increased fluid and include sources of protein, zinc, and vitamins C and A for wound healing. Use 25–45 kcal/kg and 1–1.5 g protein/kg; this varies depending on extent of surgical intervention and degree of catabolism. Losses of 5–15 g of nitrogen daily may occur. • An analysis of clinical studies using enteral formulas with supplemental arginine suggests overall benefits (Zaloga

TABLE 14-4


The Small Intestine After Surgery

The small intestine has a large adaptive capacity, with resection of small segments generally not causing nutritional problems. • If the terminal ileum is removed, vitamin B12 and bile salts will not be reabsorbed. • Diarrhea can be massive if the ileocecal valve is removed with the terminal ileum, with great electrolyte losses and hypovolemia. • Cholestyramine may be needed to bind bile salts. • Fat malabsorption with steatorrhea and inadequate vitamin A, D, E, and K absorption may also occur. Medium-chain triglycerides (MCT) and water-miscible supplements may be necessary. • Hyperoxaluria and renal stones may occur. Calcium supplements, altered polyunsaturated fatty acid (PUFA) intake, and aluminum hydroxide binders may be needed.

et al, 2004). Arginine is found in shrimp, lean ground beef, pumpkin seeds, garbanzo beans, cottage cheese, peanuts, and soymilk. • Hyperglycemia is associated with poor wound healing, increased susceptibility to infection, and other complications. While perioperative hyperglycemia has been associated with increased surgical site infections, there is insufficient evidence to support strict versus conventional glycemic control (Kao et al, 2009.) • Electrolyte imbalances are common after surgery; see Table 14-5. • Fluid imbalances are also common. Monitor for changes in urine output or concentration. Check labs such as BUN, albumin, sodium, and glucose. Check for

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

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fever. Calculate fluid needs; evaluate using I & O records. Be sure that medications are given with 4 oz of fluid and that sufficient fluid is served with and between meals. • Intravenous therapy will likely be used to give fluids directly into a vein. IVs can be intermittent or continu-




5% dextrose

2/3D & 1/3 S

3.3% dextrose/0.3% saline

Normal saline Ringer’s lactate

Na (mmol/L)

ous. Risks of IV therapy may include infiltration, fluid overload, electrolyte imbalances, phlebitis, or infection. It is important to calculate the content of IV fluids when they contain glucose, as indicated in this example:

Cl (mmol/L)

K (mmol/L)

Ca2 (mmol/L)

Glucose (mg/dL)











0.9% NaCl






Lactated Ringer






Follow an interdisciplinary protocol for managing dehydration, as shown on the following page.

Common Drugs and Anesthesia Used with Surgery and Potential Side Effects • Anesthesia delays peristalsis; eat ice chips or sip carbonated beverages until nausea subsides. • Analgesics should provide effective pain relief. Epidural analgesia in GI surgery yields shorter duration of postoperative ileus, attenuation of the stress response, fewer pulmonary complications, and improved postoperative pain control and recovery (Fotiadis et al, 2004). Pain medications should be taken sufficiently in advance of meals to allow a pleasant, pain-free mealtime. • Antibiotics may be needed; monitor specific side effects for selected medication. • Insulin may be needed if hyperglycemia persists. • Laxatives may deplete electrolytes. When able to progress, use a higher fiber intake and plenty of liquids. • Metoclopramide (Reglan) may help with postoperative ileus (Chan et al, 2005). Dry mouth or nausea can result after prolonged use. • Vitamin K can help with clotting. There are generally no side effects with this injection. Warfarin (Coumadin), a blood thinner used to prevent emboli, requires that patients maintain steady intake of vitamin K foods (cabbage, kale, and spinach) to control levels. Heparin has no dietary consequences.

Herbs, Botanicals, and Supplements • Interactions between herbs, anesthesia, and surgery must be noted. For surgical patients, herbs can affect sedation, pain control, bleeding, heart function, metabolism, immunity, and recovery. As many as one third of presurgical patients take herbal medications, and many of those patients fail to disclose herbal use during preoperative

assessment, even when prompted. Table 14-6 describes these potential interactions. • Antioxidant foods are protective. Consume plenty of tea and foods listed in Table 13-2. Coenzyme Q10 may help to lower angiogenesis markers and lipid levels; studies are ongoing.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Immobilization of the patient can produce unwanted side effects. Have patient drink plenty of fluids and ambulate as soon as possible. • Patients tend to lose 0.5 lb daily early in postoperative period. Weight gain during this time suggests fluid excess. • Eat and drink slowly to prevent gas formation from swallowed air. • Discuss the role of surgery as “planned trauma,” allowing adequate time for return to homeostasis. Discuss wound healing priority, tensile strength, and role of nutrients (zinc, vitamin C, vitamin A, and amino acids). Note that poor nutrient intake can decrease anabolism, delaying scar formation. B-complex vitamins are also beneficial. While zinc deficiency impairs wound healing, supplementation in people who are not deficient does not accelerate wound healing and an excess can interfere with immune system function and copper absorption. • During the rehabilitative anabolic stage (3 months to 1 year postoperatively), energy intake should be adequate but not excessive. • With amputation, determine the percentage of body mass lost and decrease estimated energy needs accordingly; see Table 14-7. • Table 14-8 lists other types of surgeries and their specific nutritional impact.

Patient Education—Food Safety Surgical patients may be vulnerable to foodborne illness; safe food handling and handwashing are essential.

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Initiated by:


SCREEN Nutrition Screen diagnosis: Dehydration

GOALS (Check any/all):


❑ Assure intake of minimum daily water need of _____ mL in _____(goal time). (Calculate using Daily Water Need for Adults.)



❑ Maintain or improve hydration status as indicated by weight gain, fluid intake greater than or equal to output and normalization of biochemistries in ____ (goal time). ❑ Prevent dehydration-related adverse events in ____ (goal time). ❑ Reduce or eliminate dehydration risk factors in _____ (goal time).


ASSESS (Check any/all) Hydration status ❑ Fluid intake ≤ fluid output ❑ Diuretics’ multiple medications ❑ Ostomy* ❑ Increased environmental temperature/ no air conditioning/low humidity Biochemistries ❑ BUN ❑ Serum sodium Complex diet order ❑ High-protein, high-calorie diet ❑ Fluid restriction Infection/Wounds ❑ Fever ❑ Pneumonia, UTI, URI ❑ Pressure ulcers, wounds Poor Oral Intake Symptoms ❑ Anorexia ❑ Nausea/vomiting* ❑ Poor appetite ❑ Diarrhea*

MODERATE RISK INTERVENTIONS (Check any/all) Getting the Fluid You Need provided and explained Food Record provided and explained Obtain Dr. orders as needed: ❑ RD chart consult ❑ Monitor weight q:_____ ❑ Other:________________________ (See notes for documention.)

Date: 1 or more




ASSESS RESPONSE (Check any/all) ❑ Weight loss ❑ Fluid intake less than fluid output ❑ Onset of new infection ❑ Dehydration ❑ Exhibiting Poor Oral Intake symptoms ❑ Other:________________________ (See notes for documention.)


Next visit

1 or more

HIGH-RISK INTERVENTIONS (Check any/all) ❑ Getting the Fluid You Need provided and explained ❑ Food Record provided and explained ❑ Assure intake of a 2qt (2L) of appropriate fluids/day Obtain Dr. orders as needed: ❑ RD referral for home visit(s) ❑ Monitor weight q:_____ ❑ Monitor I & O q: _____ ❑ Oral rehydration fluid if diarrhea, vomiting, ostomy are present ❑ Other:________________________ (See notes for documention.)

OUTCOMES ACHIEVED ❑ Hydration status maintained or improved ❑ Weight maintained or improved ❑ Nutrition status maintained or improved ❑ Other:________________________ (See notes for documention.) ❑ Repeat Nutrition Risk Screen in ____ days

Signed: Signed:




ASSESS RESPONSE (Check any/all) ❑ Further weight loss ❑ Fluid intake less than fluid output ❑ Onset of new infection ❑ Dehydration ❑ Exhibiting Fewer Oral Intake symptoms ❑ Other:________________________ (See notes for documention.) Signed:

Date: 1 or more


Next visit

OUTCOMES ACHIEVED ❑ Hydration status maintained or improved ❑ Weight maintained or improved ❑ Nutrition status maintained or improved ❑ Other:________________________ (See notes for documention.) ❑ Repeat Nutrition Risk Screen in ____ days



* Requires replacement of water and electrolytes.

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


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TABLE 14-5

Managing Electrolyte Imbalances

Three variables regulate pH in blood plasma: carbon dioxide, electrolyte concentrations, and total weak acid concentrations. Acid–base balance is when blood pH is out of the normal range (7.35–7.45). An excess of acid leads to acidosis (pH  7.35) and an excess of base leads to alkalosis (pH  7.45). Imbalance is classified according to the source: respiratory or metabolic. There are four basic conditions: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. Dietitians typically address electrolyte imbalances, which involve calcium, potassium, magnesium, and sodium and are discussed here. Normal Range

Causes of Elevation

Causes of Decline

Sodium (Na): 135–145 mEq/L

Hypernatremia: Excessive loss of water through GI system, lungs, or skin; fluid restriction, certain diuretics, hypertonic IV solutions, tube feeding; hypothalamic lesions, hyperaldosteronism, corticosteroid use, Cushing's syndrome, diabetes insipidus

Hyponatremia: Congestive heart failure, cirrhosis, nephrosis, excess fluid intake, syndrome of inappropriate antidiuretic hormone secretion (dilutional hyponatremia); sodium depletion, loss of body fluids without replacement, diuretic therapy, laxatives, nasogastric suctioning, hypoaldosteronism, cerebral salt-wasting disease

Potassium (K): 3.5–5.0 mEq/L

Hyperkalemia: Aldosterone deficiency, sodium depletion, acidosis, trauma, hemolysis of red blood cells, potassiumsparing diuretics

Hypokalemia: Lack of dietary intake of potassium, vomiting, nasogastric suctioning, potassium-depleting diuretics, aldosteronism, salt-wasting kidney disease, major GI surgery, diuretic therapy with inadequate potassium replacement

Calcium (Ca): 8.5–10.5 mg/dL

Hypercalcemia: Excessive vitamin D, immobility, hyperparathyroidism, potassium-sparing diuretics, ACE inhibitors, malignancy of bone or blood

Hypocalcemia: Hypoparathyroidism, malabsorption, insufficient or inactivated vitamin D or inadequate intake of calcium, hypoalbuminemia, diuretic therapy, diarrhea, acute pancreatitis, bone cancer, gastric surgery

Magnesium (Mg): 1.5–2.5 mg/dL

Hypermagnesemia: Excessive use of magnesium-containing antacids and laxatives, untreated diabetic ketoacidosis, excessive magnesium infusions

Hypomagnesemia: Malabsorption related to GI disease, excessive loss of GI fluids, acute alcoholism/cirrhosis, diuretic therapy, hyper- or hypothyroidism, pancreatitis, preeclampsia, nasogastric suctioning, fistula drainage

Kee J, et al. Fluids and electrolytes with clinical applications: a programmed approach. 7th ed. Clifton Park, NY: Delmar Learning, 2004.

Signs and Symptoms

Comments and Nutritional Concerns

HYPONATREMIA Lethargy, anorexia, nausea, vomiting, cramping, muscular twitching, confusion, fingerprinting over the breastbone, seizures, and coma. Hyponatremia is associated with increased morbidity and mortality.

Distinguish between the different types of hyponatremia and their treatments. Contracted extracellular fluid volume may occur; a hypertonic or isotonic saline solution is given (perhaps salty broth). Avoid giving large water flushes with isotonic tube feeding. Fluid restriction and low-sodium diet with diuretics may cause hyponatremia. D5W used in excess can cause hyponatremia with water intoxication.

HYPERNATREMIA Thirst, dry and sticky mucous membranes, fever, dry and swollen tongue, disorientation, and seizures. Flushing, fever, loss of sweating, dry tongue and mucous membranes, tachycardia, hallucinations, or coma.

High-protein tube feedings without adequate water flushes, excessive diaphoresis, diabetes insipidus, or watery diarrhea may cause problems. Correct dehydration. Monitor thirst, the first sign of water loss. High doses of steroids, solutions that contain NaCl, other sodium additives, and sodium-containing analgesics should be managed or omitted. Determine patient's fluid needs (generally 30 mL/kg or 1 mL/kcal given in enteral or total parenteral infusions. Adjust according to the renal or cardiovascular status, especially in seniors. Patients with dysphagia may have difficulty obtaining enough fluid; monitor closely.

HYPOKALEMIA Severe muscle weakness, electrocardiogram (ECG) changes and arrhythmias, lethargy, hypotension, shallow breathing, fatigue, anorexia, constipation, confusion, and impaired carbohydrate (CHO) tolerance. Chloride depletion usually accompanies hypokalemia; alkalosis is also common.

Replace potassium (generally done with intravenous or oral KCl, except in renal tubular acidosis). Kaochlor, Kay-Ciel, K-Lor, K-Lyte, K Tab, Klotrix, Micro-K, K-Dur, Klor-Con, Ten-K, and Slow-K are all sources of potassium. Some products are slow release. Diarrhea, nausea, or vomiting may occur; take with meals. A potassium-rich diet may also be needed. Monitor serum levels and adjust accordingly. Be sure fluid intake is adequate. (continued)

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TABLE 14-5 Managing Electrolyte Imbalances (continued) Signs and Symptoms

Comments and Nutritional Concerns

HYPERKALEMIA Weakness, anxiety, altered ECGs (with 7 mEq/L, a fatal arrhythmia can occur), flaccid muscle paralysis, or even respiratory arrest, if severe.

Immediate treatment is needed to prevent arrhythmias, bradycardia, heart block, and respiratory arrest. If all else fails, dialysis may be needed. Intravenous feedings are likely to be used (glucose, insulin, bicarbonate) to shift potassium intracellularly. Sodium or calcium may also be needed as physical antagonists; infusions will be given until serum potassium is corrected. Monitor closely. Avoid high-potassium foods and K in salt substitutes. Kayexalate may be needed and should be given with sorbitol to prevent constipation; take separately from calcium or antacids. Read labels of oral supplements to be sure total K is calculated.

HYPOCALCEMIA Tetany, seizures, and cardiac arrest. In the long term, bone demineralization with bone pain and compression fractures may result.

Correct symptomatic condition (usually calcium gluconate intravenously). Supplement with vitamin D3 as needed. When able to eat orally, provide a high-calcium intake; dry milk can be added to foods. Avoid excesses of caffeine, oxalate, fiber, and aluminum-containing antacids. Calcium carbonate (as in Tums) provides 40% elemental calcium. Drink extra water. Avoid use of iron supplements at the same time. Beware of bone meal and dolomite because of their toxic metal content.

HYPERCALCEMIA Drowsiness, lethargy, stupor, muscle weakness, decreased reflexes, nausea and vomiting, anorexia, constipation, ileus, polyuria, renal stones, azotemia, nocturia, hypertension, bradycardia, pruritus, and eye abnormalities.

Correct underlying condition with rehydration (usually with normal saline) and hemodilution. Correct nausea, vomiting, constipation, and other side effects. Avoid excesses of milk, vitamins A or D, calcium supplements and antacids, and lactose. Potassium and magnesium may also be depleted; monitor carefully. Extra caffeine, oxalates, fiber, and phytates can help to decrease calcium absorption and can help excretion. Sometimes furosemide or prednisone is used to excrete calcium also. Intravenous etidronate (Didronel) may be used; nausea and vomiting could occur.

HYPOMAGNESEMIA Anxiety, hyperirritability, confusion, hallucinations, seizures, tremor, hyperreflexia, tetany, tachycardia, hypertension, arrhythmias, vasomotor changes, profuse sweating, muscle weakness, grimaces of facial muscles, and refractory hypocalcemia.

Correct low serum magnesium levels to prevent sudden death. Discuss longterm measures to prevent further episodes. Long-term use of magnesiumfree CPN can be one aggravating source of the problem. Monitor intake from all sources (oral, TF, CPN.) Milk of magnesia (MOM) can be used for liquid form of magnesium hydroxide; nausea, cramps, or diarrhea may result. Normal renal function is needed for use of magnesium sulfate; diarrhea can occur. Chocolate, nuts, fruits and green vegetables, beans, potatoes, wheat, and corn are considered good sources.

HYPERMAGNESEMIA Lethargy, hyporeflexia, and respiratory depression. Bradycardia, myocardial infarction, and respiratory failure may be fatal.

Reduce or eliminate sources of exogenous magnesium from diet, supplements, CPN solutions, and medications until resolved. Calcium-containing medications may be given to help with excretion of excessive magnesium. Avoid megadoses of multivitamin–mineral supplements.

HYPOPHOSPHATEMIA Anorexia, weakness, bone pain, dizziness, and waddling gait may be observed. In severe cases, elevated creatine phosphokinase (CPK) levels are seen, with rhabdomyolysis superimposed on myopathy. Hypophosphatemia may result in sudden death, rhabdomyolysis, red cell dysfunction, and respiratory insufficiency. Heart failure can result if phosphorus is not administered. Low serum phosphorus levels will result in lowered 2,3-diphosphoglyceric acid (2,3-DPG), which facilitates oxyhemoglobin dissociation and leads to tissue hypoxia and low partial pressure of oxygen.

Phosphorus is a major component of bone and is one of the most abundant constituents of all metabolic processes and tissues; 85% is found in the skeleton. Only about 12% is bound to proteins; a typical laboratory assessment is of elemental phosphorus, with some values for HPO4 and NaHPO4 as well. Prevent further complications. Use appropriate measures according to the cause; for example, low-phosphorus diet with high calcium and adequate vitamin D will be needed in renal osteodystrophy. Note that 50–60% of dietary phosphorus is absorbed, and more is absorbed in depleted persons. If potassium phosphate (K-Phos) is used as an acidifier, it may cause nausea, vomiting, or diarrhea.

HYPERPHOSPHATEMIA Phosphorus levels tend to be higher in children and to rise in women after menopause.

Provide appropriate levels of phosphorus according to age and serum status. Monitor glucose and phosphorus intake, especially from enteral or parenteral nutrition. Monitor dietary intake of milk, meat, and other foods high in phosphorus. Observe serum levels regularly, especially in renal patients. Antacids containing aluminum will prevent phosphorus absorption in intestinal lumen. Calcium acetate is useful in dialysis patients.

Resources: FreeMD,, accessed January 19, 2010. Medline Plus,, accessed January 19, 2010. Merck Manual,, accessed January 19, 2010.

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TABLE 14-6

Herbal Medications and Recommendations for Discontinued Use before Surgery

Most commonly used herbs and antidepressant medications have potentially deleterious effects on the patient during surgery, ranging from increased risk of bleeding to fatal interactions (Chin et al, 2009.) The top four used by the general public are Echinacea, garlic, ginseng, and ginger (Heller et al, 2006.) Herb

Relevant Effects

Perioperative Concerns



Boosts immunity

Allergic reactions, impairs immune system, especially for transplantation patients

Discontinue as far in advance as possible.

Ephedra (ma huang)

Increases heart rate and increases blood pressure

Risk of heart attack, arrhythmias, stroke, kidney stones, interaction with other drugs

Discontinue 24 hours before surgery.


Prevents clotting

Risk of bleeding, especially when combined with other drugs that inhibit clotting

Discontinue at least 7 days before surgery.


Prevents clotting

Risk of bleeding, especially when combined with other drugs that inhibit clotting

Discontinue at least 36 hours before surgery.


Lowers blood glucose, inhibits clotting

Increases risk of bleeding; interferes with warfarin (an anticlotting drug)

Discontinue at least 7 days before surgery.


Sedates, decreases anxiety

May increase sedative effects of anesthesia

Discontinue 24 hours before surgery.

St. John’s wort

Inhibits reuptake of neurotransmitters

Alters metabolisms of other drugs

Discontinue at least 5 days before surgery.



Could increase effects of sedatives. Long-term use could increase amount of anesthesia needed.

If possible, taper dose weeks before surgery. Withdrawal symptoms resemble diazepam (Valium) addiction.

Sources: Ang-Lee M, et al. Herbal medicines and perioperative care. JAMA. 286:208, 2001. Chin SH, et al. Perioperative management of antidepressants and herbal medications in elective plastic surgery. Plast Reconstr Surg. 123:377, 2009. Heller J, et al. Top-10 list of herbal and supplemental medicines used by cosmetic patients: what the plastic surgeon needs to know. Plast Reconstr Surg. 117:436, 2006. Yuan CS, et al. Brief communication: American ginseng reduces warfarin’s effect in healthy patients: a randomized, controlled Trial. Ann Intern Med. 141:23, 2004.

TABLE 14-7 Percentage of Body Weight in Amputees Body weight is a good indicator of a person’s size and is widely used in assessments. Body mass index (BMI) values in subjects with limb amputation are not useful unless lost weight of the limbs is not considered in the calculation. To reduce the underestimation of nutritional status in persons with limb amputation, estimation of body weight is necessary so that BMI can be reliably estimated for persons with limb amputation. Estimated body weight after amputation uses the following formula: Estimated Ideal Body Weight (IBW)  (100  % amputation)/100  IBW for original height. Body Part and % Loss from Amputation Below knee 6.5% Bilateral below knee (BK) 13% Bilateral above knee (AK) 16% BK  AK 14.5% Foot 1.5% Both feet 3% Hand 0.7% Both hands 1.4% Forearm and hand 3% Both forearms/hands 6% Entire arm 5% Both entire arms 10% Entire leg 16% Both entire legs 32% Adapted from: Osterkamp LK. Current perspective on assessment of human body proportions of relevance to amputees. J Am Diet Assoc. 95:215, 1995. Amputee BMI calculator,, accessed January 20, 2010.

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TABLE 14-8 Surgeries, Level of Nutritional Acuity, and Nutritional Recommendations Background

Specific Objectives

Food and Nutrition Recommendations

Amputation, Level 2 Amputations may result from poorly controlled diabetes, trauma, peripheral artery disease, congenital deformity, chronic infections, gangrene, or tumors such as osteosarcoma.

Postoperative: Determine percentage of body weight of amputated area and calculate changes from preoperative to postoperative status in height, weight, and body mass index (BMI). Provide adequate protein, calories, zinc, vitamins C, K, and A for healing. Low albumin levels, serum carotene, zinc, and vitamin C are commonly found.

Postoperative: Use a high-protein/high-energy diet for healing. Supplement diet with vitamins and minerals, especially zinc, vitamins A, C, and K, and arginine. Use tube feeding (TF) if necessary; consider use of an immuneenhanced product. For hand or arm amputations, consider adaptive feeding equipment with Occupational therapy (OT) specialists.

Long Term: Provide a low-calorie diet, if needed. For patients who lose too much weight, a higher energy diet should be used. Otherwise, immobilized patients tend to gain weight and will need weight control measures.

Long Term: Discuss how to control or increase calories in diet for energy use. Patients with an AK amputation who walk with or without prosthesis use 25% more energy than a nondisabled person who walks at the same speed; these patients have difficulty maintaining weight.

Preoperative: White blood cell count and erythrocyte sedimentation rate may be increased.

Postoperative: Use a balanced diet with adequate amounts of zinc and vitamins C, K, and A.

Postoperative: Reduce fever. Lower risks of infection or sepsis, peritonitis, or abscess formation.

Long-Term: After recovery, include more fruits, vegetables, and whole grain for fiber.

Cesarean delivery (C-section), Level 1 C-section is performed for numerous reasons, including HIV infection, maternal diabetes, or edema-proteinuriahypertensive (EPH) gestosis.

Postoperative: Manage nausea, which is common after anesthesia. Replenish stores of nutrients from blood and fluid losses. Reduce likelihood of complications such as hemorrhage, infection, fever, drainage, cystitis, anemia, or pneumonia after the operation.

Postoperative: Nothing by mouth (NPO) with intravenous or clear liquids and ice chips will be given until nausea subsides. Progress to usual diet, with increased fiber and fluid to soften stools. Promote wound healing with protein and energy; include iron, vitamins C and A, and zinc in diet or supplemental form.

Coronary Artery Bypass Graft (CABG), Level 3 Open heart procedures require use of a cardiopulmonary machine for extracorporeal circulation. Narrowed or blocked arteries are bypassed; the vein usually comes from the leg. Blood can then flow directly into the heart muscle. CABG usually takes 4–5 hours.

Preoperative: Monitor serum levels of electrolytes, albumin, and glucose. Provide the diet as prescribed (may be sodium, energy, or fluid restricted). Provide ample amounts of glycogen for stores. Use nutrition support, if needed, for malnourished cardiac patients.

Postoperative: Control fluid intake by measuring previous day’s output plus 500 mL for insensible losses. Provide adequate protein, kilocalories, and micronutrients for wound healing. Use TF or CPN if severely malnourished. Replete slowly and keep head of bed elevated 30° to prevent worsening of heart failure. Low-sodium, high-calorie, low-volume TF products may be useful.

Heart valve replacement involves replacing the damaged valve with a mechanical prosthesis (St. Jude valve) or biological tissue valve. This may be done with robotic techniques, which are less invasive than open heart procedures.

Postoperative: Promote wound healing and restore normal fluid and electrolyte balance. Promote weight control. Wean from ventilator support when possible. Prevent hyperglycemia, coma, sepsis, renal failure, cardiac tamponade, wound dehiscence, and atelectasis. Maintain comfort and educate regarding follow-up.

Appendectomy, Level 1 Appendectomy generally is an uncomplicated procedure with minimal recovery time. A low-fiber diet may contribute to appendicitis.

Long Term: Avoid excessive weight gain, which can further aggravate heart condition. Teach appropriate measures for changes in daily diet to prevent further problems while wound is healing. Discuss need to alter lifestyle (diet, exercise, and stress) to prevent additional problems; many patients have atherogenic effects even after heart surgery. Control carbohydrates in patients with diabetes or hypertriglyceridemia.

Long-Term: Modify diet to control sodium and potassium intake, lessen edema, and improve blood pressure. Diuretics and digoxin may deplete potassium; anorexia, nausea, and diarrhea may occur. Beta-blockers, ace inhibitors, and other cardiac drugs may require use of low-sodium, low-calorie diets. Hypoalbuminemia can cause digoxin toxicity. National Cholesterol Education Program guidelines may be used if serum cholesterol remains high. (continued)

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TABLE 14-8

Surgeries, Level of Nutritional Acuity, and Nutritional Recommendations (continued)


Specific Objectives

Food and Nutrition Recommendations

Craniotomy, Level 2 Craniotomy involves removing and replacing the bone of the skull to provide access to intracranial structures, usually for a brain tumor.

Postoperative: Prevent aspiration. Prevent or correct dysphagia, constipation, urinary tract infection (UTI), nausea and vomiting, and diabetes insipidus. Normalize electrolyte levels. Prevent blood clots using anticoagulant therapy. If anticonvulsants are used, prevent folic acid depletion. Prevent or manage nausea, vomiting, facial or extremity paralysis, wound drainage, hyperthermia, dysphagia, diabetes insipidus, and syndrome of inappropriate antidiuretic hormone (SIADH). Monitor consciousness, gag reflex, results of examinations such as ECG and cerebrospinal fluid (CSF) levels.

Postoperative: NPO is needed until nausea and vomiting subside. Progress from liquids to soft diet as tolerated. Patient should be fed while lying on his/her side or with his/her head elevated 30° to prevent aspiration. Check swallowing reflex. Assist with feeding if needed, and TF may be required. Adequate fiber may be beneficial. If steroids are used, reduce sodium intake to 4–6 g/d (or less).

Preoperative: Enhance nutritional intake in preparation for surgery.

Preoperative: Nutritional status before arthroplasty is a good predictor of surgical outcomes after surgery; albumin levels 3.4 often predict a better outcome.

Postoperative: Replenish stores. Prevent side effects of immobilization (renal calculi, pressure ulcers, and UTIs). Promote adequate wound healing. Regain maximum mobility. Use small, frequent meals if nausea is a problem.

Postoperative: Use a high-protein/high-energy diet. Supplement diet with zinc and vitamins A, C, and K. Determine whether blood loss can cause anemia; provide sufficient iron and protein in cooperation with medical team.

Long-Term: Promote early ambulation, when possible, to promote healing and increase strength.

Long-Term: If weight loss is needed, provide a balanced, low-energy diet after wound healing is completed. Include calcium and phosphorus.

Hysterectomy, abdominal, Level 1 Abdominal hysterectomy is the surgical removal of the uterus through an abdominal incision. This approach is used if the uterus is enlarged or if an oophorectomy (ovary removal) and salpingectomy (removal of the fallopian tubes) are also performed.

Postoperative: Promote wound healing and rapid recovery. Replete nutrient reserves and glycogen stores. Replace protein, iron, and vitamin K if blood loss was extensive. Prevent complications such as UTIs, incisional infections, fever, nausea, vomiting, or diverticular colovaginal fistula.

Postoperative: Use a high-protein/high-calorie diet. Ensure that adequate fiber and fluid are provided to alleviate constipation. Provide a diet with adequate iron, zinc, and vitamins K, C, and A.

Long-Term: Support gradual return to normal activity; exercise improves nutrient repletion and tissue repair.

Long-Term: Emphasize the importance of a good diet for wound healing.

Pancreatic Surgery, Level 3 This may include total pancreatectomy with or without islet cell autotransplantation for chronic pancreatitis and cancer; subtotal or pancreatoduodenectomy (Whipple’s procedure) for islet cell tumors.

Preoperative: Monitor for history of ethanol (ETOH) abuse with resulting malnutrition and malabsorption; replete if possible.

Preoperative: Use enteral nutrition or CPN to prepare patient for a major operation.

Postoperative: Prevent or correct sepsis, which is a common complication. Encourage nourishing and well-balanced meals; control CHO if diabetes occurs or is present. Determine pancreatic function according to type and extent of resection and underlying disorder. Whipple’s procedure results in dumping syndrome, diarrhea, dyspepsia, ulceration at gastroenterostomy site, and extensive weight loss unless a pylorus-saving technique is used.

Postoperative: Enteral nutrition, CPN, or oral intake may progress as tolerated. Enteral nutrition has better outcomes if the tube is placed in the jejunum. Standard treatment following major pancreatic surgery includes the administration of pancreatic enzymes and inhibition of acid secretion by proton pump inhibitors; monitor effects on vitamin B12 status.

Long-Term: Monitor impact of medications and replacement enzymes or hormones that are ordered. Alter fat source with malabsorption or steatorrhea. Offer resources for control of diabetes or for alcohol addiction, as needed.

Long-Term: A carbohydrate-controlled diet may be needed, along with small, frequent feedings. Most patients develop diabetes that may require insulin; hypoglycemia is the most difficult problem to manage.

Hip Replacement, Level 2 A total hip replacement (arthroplasty) is the formation of an artificial hip joint. Prostheses are either cemented in place or uncemented. The procedure is performed for severe degenerative joint disease, rheumatoid arthritis, or congenital deformities.

Long-Term: Discuss importance of diet in correcting any malnutrition or anemia. As needed, teach family about a diet for dysphagia (e.g., thick, pureed foods with reduced thin liquids). When oral intake is possible, suggest slow chewing and eating. Aphasia occurs in some patients, making it hard to communicate their needs.


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TABLE 14-8 Surgeries, Level of Nutritional Acuity, and Nutritional Recommendations (continued) Background

Specific Objectives

Food and Nutrition Recommendations

Parathyroidectomy, Level 1 Surgical removal of the parathyroid glands

Preoperative: Prepare patient for surgery. Postoperative: Manage hypoparathyroidism (with tingling, tetany, hoarseness, and seizures.)

Postoperative: IV or TF may be needed. Avoid CPN because of high risk for sepsis in the neck area. Provide extra fluids.

Long-Term: Vitamin D, calcium, and chemotherapy are often required. A low-phosphorus diet with aluminum hydroxide (Amphojel) may be needed; constipation is one side effect.

Long-Term: A high-calcium/low-phosphorus diet may be necessary. Monitor carefully. Counsel about follow-up measures and potential medication interactions.

Preoperative: A low-residue or elemental diet may be needed, regressing to clear liquids, NPO. Vitamin K may be needed 24–48 hours before the procedure.

Postoperative: Parenteral fluids with electrolytes may be needed (3–4 L/d unless contraindicated). CPN or TF may also be appropriate. If nausea is an extensive problem, give fluids between meals.

Pelvic Exenteration, Level 1 This surgery involves removal of all female reproductive organs and adjacent tissues (i.e., radical hysterectomy, pelvic node dissection, cystectomy and formation of an ileal conduit, vaginectomy, and rectal resection with colostomy). Cancer is usually the reason.

Spinal Surgery, Level 2 This surgery generally is performed to relieve pressure on spinal nerves or cord due to herniated discs, trauma, displaced fractures, osteoporosis, or incomplete vertebral dislocation from rheumatoid arthritis. Laminectomy, discectomy, or spinal fusion may be performed.

Tonsillectomy/Adenoidectomy, Level 1 These tissues are considered to be part of the protective immune system; removal is for severe and chronic ear, throat, and sinus infections.

Postoperative: Colonic stasis occurs after major abdominal surgery and persists for approximately 3 days. Prevent hemorrhage, infection, urinary or GI problems, shock, fever, anemia, and sepsis. Long-Term: Promote wound healing and recovery. Provide colostomy teaching if needed.

Long-Term: Progress, as tolerated, to a high-protein/high-calorie intake with snacks (eggnog, custard, oral supplements). Adequate iron, zinc, and vitamins A and C help with wound-healing process.

Preoperative: Nutrients may be needed for adequate stores (e.g., glucose, protein, vitamins A, C, and K, and zinc).

Postoperative: Parenteral fluids may be given as ordered. A balanced diet, when patient is ready, with control of total energy intake to prevent excessive weight gain, may be used. If patient has been malnourished, a gradual increase in calories may be beneficial. Adequate hydration will be necessary unless contraindicated.

Postoperative: Correct nausea and vomiting if a problem. Prevent calculi, UTIs, and pressure ulcers. Fluid and fiber will be important, but prevent overhydration. Long-Term: Avoid weight gain.

Long-Term: Increase fiber intake if constipation is a problem; prune juice, crushed bran, and other items may be used. If tolerated, extra fruits and raw vegetables may be used.

Preoperative: Supply adequate nourishment for glycogen stores.

Postoperative: Give cold liquids (sherbet, ginger ale, nectars, and gelatin). Do not use red gelatin as it may mask blood if there is any vomiting. Use extra fluid intake; large swallows are less painful than many small ones. Avoid milk products only if patient cannot tolerate them. On day 2 or 3, use soft, smooth foods (pudding, strained cereals, soft-cooked eggs). Progress to regular diet when tolerated.

Long-Term: Help patient select nonirritating foods for use at home. Avoid hot, spicy foods, raw vegetables, toast and crackers, citrus juices, and other related foods until full recovery.

Long-Term: Use supplements of vitamin C if patient cannot tolerate juices. Evaluate zinc intake and encourage dietary sources when possible.

For More Information •

American Academy of Physical Medicine and Rehabilitation


Amputee Resource Foundation of America

National Library of Medicine—Surgery

Refeeding Syndrome

SURGERY—CITED REFERENCES Bochicchio GV, et al. Admission preoperative glucose is predictive of morbidity and mortality in trauma patients who require immediate operative intervention. Am Surg. 71:171, 2005. Bossingham MJ, et al. Water balance, hydration status, and fat-free mass hydration in younger and older adults. Am J Clin Nutr. 81:1342, 2005. Braga M, Gianotti L. Preoperative immunonutrition: cost-benefit analysis. JPEN J Parenter Enteral Nutr. 29:S57, 2005. Chan DC, et al. Preventing prolonged post-operative ileus in gastric cancer patients undergoing gastrectomy and intra-peritoneal chemotherapy. World J Gastroenterol. 11:4776, 2005.

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Estivarez CF, et al. Efficacy of parenteral nutrition supplemented with glutamine dipeptide to decrease hospital infections in critically ill surgical patients. JPEN J Parenter Enteral Nutr. 32:389, 2008. Falanga V. Wound healing and its impairment in the diabetic foot. Lancet. 366:1736, 2005. Farreras N, et al. Effect of early postoperative enteral immunonutrition on wound healing in patients undergoing surgery for gastric cancer. Clin Nutr. 24:55, 2005. Fearon KC, Luff R. The nutritional management of surgical patients: enhanced recovery after surgery. Proc Nutr Soc. 62:807, 2003. Fotiadis RJ, et al. Epidural analgesia in gastrointestinal surgery. Br J Surg. 91:828, 2004. Gabor S, et al. Early enteral feeding compared with parenteral nutrition after oesophageal or oesophagogastric resection and reconstruction. Br J Nutr. 93:509, 2005. Grimble RF. Immunonutrition. Curr Opin Gastroenterol. 21:216, 2005. Kao LS, et al. Peri-operative glycaemic control regimens for preventing surgical site infections in adults. Cochrane Database Syst Rev. (3):CD006806, 2009. Klek S, et al. The impact of immunostimulating nutrition on infectious complications after upper gastrointestinal surgery: a prospective, randomized, clinical trial. Ann Surg. 248:212, 2008. Lucha PA Jr, et al. The economic impact of early enteral feeding in gastrointestinal surgery: a prospective survey of 51 consecutive patients. Am Surg. 71:187, 2005. Luo M, et al. Depletion of plasma antioxidants in surgical intensive care unit patients requiring parenteral feeding: effects of parenteral nutrition

with or without alanyl-glutamine dipeptide supplementation. Nutrition. 24:37, 2008. Maddox TM. Preoperative cardiovascular evaluation for noncardiac surgery. Mt Sinai J Med. 72:185, 2005. Marek PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ. 328:1407, 2004. Mokart D, et al. Predictive perioperative factors for developing severe sepsis after major surgery. Br J Anaesth. 95:776, 2005. Roth E, Oehler R. Hypothesis: Muscular glutamine deficiency in sepsis-A necessary step for a hibernation-like state? [published online ahead of print January 11, 2010]. Nutrition. 26:571, 2010. Schiesser M, et al. Assessment of a novel screening score for nutritional risk in predicting complications in gastro-intestinal surgery. Clin Nutr. 27:565, 2008. Wilmore D. Enteral and parenteral arginine supplementation to improve medical outcomes in hospitalized patients. J Nutr. 134:2863S, 2004. Winkelmayer WC, et al. C-reactive protein and body mass index independently predict mortality in kidney transplant recipients. Am J Transplant. 4:1178, 2005. Wittman F, et al. L-arginine improves wound healing after trauma-hemorrhage by increasing collagen synthesis. J Trauma. 59:162, 2005. Zaloga GP. Parenteral nutrition in adult inpatients with functioning gastrointestinal tracts: assessment of outcomes. Lancet. 367:1101, 2006. Zaloga GP, et al. Arginine: mediator or modulator of sepsis? Nutr Clin Pract. 19:201, 2004.



Surgical staples



Jejunum Colon

Surgical staples Stomach

Jenunum bypass


The gastric bypass procedure has replaced the jejunal bypass, which had many undesirable nutritional consequences. Adapted from: Neil O. Hardy. Wesport, CT. Stedman's Medical Dictionary, 27th ed. Baltimore: Lippincott Williams & Wilkins, 2000, p. 1249.

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DEFINITIONS AND BACKGROUND More than 10 million Americans are severely obese. Bariatric surgery is a viable option for the treatment, resulting in longterm weight loss and improved health risk factors. Bariatric surgery is expensive, $20,000 and $25,000, but is an effective weapon against the consequences of morbid obesity. Candidates should be 100 lb or more over ideal weight range, have a BMI greater than 40, or a BMI greater than 35 in addition to serious medical comorbidities. Obesity surgery is superior to medical intervention in this population (Leslie et al, 2007.) Results show lower incidence rates of diabetes, hypertriglyceridemia, and hyperuricemia. In fact, bariatric surgery should be considered for adults who have type 2 diabetes and a BMI greater than 35 kg/m2, especially if the diabetes is difficult to control with lifestyle and pharmacologic therapy (American Diabetes Association, 2009.) Bariatric surgery may be implemented in carefully selected, older, severely obese adolescents ( Jen et al, 2010). However, surgical treatment should be considered only when adolescents have tried for at least 6 months to lose weight and have not been successful, have a BMI greater than 40, have reached their adult height (usually 13 or older for girls and 15 or older for boys), and have serious weight-related health problems such as T2DM, heart disease, or sleep apnea (NIDDK, 2010). Teens should be referred only to specialized adolescent bariatric centers. Gastric bypass (GBP) achieves permanent and significant weight loss. The Roux-en-Y gastric bypass (RYGB) induces long-term remission of type 2DM, returning impaired glucose tolerance to euglycemia in a matter of days (Pories and Albrecht, 2001). Exclusion of food and alteration in signals from the antrum, duodenum, and proximal jejunum to the pancreatic islet cells improve glucose tolerance. While altered gut and pancreatic hormone secretion may resolve insulin resistance after RYGB, the independent effects of weight loss and hormonal secretion on peripheral glucose disposal are observed only after substantial weight loss (Campos et al, 2010.) GBP procedures reduce capacity to 40–60 mL and induce physiological and neuroendocrine changes that affect the weight regulatory centers in the brain. Major adverse events include anastomosis leakage, pneumonia, pulmonary embolism, band slippage, and band erosion (Picot et al, 2009.) Laparoscopic Roux-en-Y gastric bypass (LRYGB) has fewer side effects, but anastomotic leak is one of them. Biliopancreatic diversion with duodenal switch reduces the stomach to 20%, like a thin sleeve. The duodenal switch (valve) remains along with a limited portion of the duodenum; the intestine is connected to the duodenum near the stomach (biliopancreatic diversion). This weight loss leads to more malnutrition and vitamin deficiencies and requires close monitoring. Lap-band adjustable gastric banding uses an inflatable band to divide the stomach into two parts by wrapping a band around the upper part and tightening it like a belt. Lap-band adjustable gastric banding is simple, has a lower complication rate, and can be adjusted or removed if necessary. Most patients lose more than 60% of their excess weight after bariatric surgery. GBP and laparoscopic isolated sleeve gastrectomy are more effective for weight loss than vertical banded gastroplasty and adjustable gastric banding; more


research is needed (Picot et al, 2009.) Because gallstones are common after the surgery, cholecystectomy may be done at the same time as the bariatric procedure. Bariatric surgery appears to be a clinically effective and cost-effective intervention for moderately to severely obese people compared with nonsurgical interventions (Picot et al, 2009.) Expected long-term outcomes include improvement or resolution of diabetes, metabolic syndrome, coronary artery disease, dyslipidemia, gastroesophageal reflux disease, sleep apnea, hypertension, osteoarthritis, and cardiovascular mortality (Jhaveri et al, 2009; Madan et al, 2006; Torquati et al, 2005.) Deficiencies in protein, iron, vitamin B12, folate, calcium, fat-soluble vitamins (A, D, E, and K), and other micronutrients are common and become clinically significant if not recognized and treated with supplements (Carlin et al, 2006.) Copper deficiency, for example, has been noted in this population with cardiovascular and neurological changes (Tan et al, 2006). Rhabdomyolysis is a risk from extended immobilization. It is accompanied by pain in the region of the referred muscle group, increase in creatine phosphokinase levels, myoglobinuria, severe renal failure, multiorgan system failure, and death if not treated in time (Filis et al, 2005). Another rare complication is hyperfunction of the pancreatic beta cells (nesidioblastosis) which can lead to life-threatening hypoglycemia (Service et al, 2005). Weight regain after RYGB occurs in approximately 20% of patients and constitutes another serious complication; failure to sustain elevated plasma PYY concentrations occurs (Meguid et al, 2008.) Quality assurance produces better outcomes (Rendon and Pories, 2005). A multidisciplinary clinical pathway, preprinted orders, discharge home instruction sheet, and daily guidelines are important aspects of treatment. As long as obesity and the popularity of bariatric surgery continue, medical practitioners must be aware of preexisting nutritional deficiencies and treat any nutritional deficiencies that may arise or worsen following surgery (Xanthakos, 2009.) Monitoring and follow-up with a dietitian should be standard procedure. Tips are available in Table 14-9.


CLINICAL INDICATORS Genetic Markers: The usual reason for GBP is morbid obesity, some of which may be genetically related, but it is believed that environment plays a greater role. Clinical/History Height Weight Postoperative weight BMI (pre-/postsurgery)

Diet history Waist-hip ratio (WHR) Waist circumference Vomiting I&O BP

Sleep apnea Endoscopy Lab Work Gluc Hemoglobin A1c CRP

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TABLE 14-9

Tips for Diet after Gastric Bypass

Diet Order


Beverage and Food Choices

Clear Liquids (no more than 1/2 cup total)

1–2 days after surgery

Water, unsweetened drinks, sugar-free gelatin or popsicles, and clear broths. Diluted (pulp-free) juices (1 part juice to 10 parts water.) Decaffeinated tea. NO CARBONATED BEVERAGES. Sip at least 48–64 oz of liquid (especially water) each day. Take a prescribed multivitamin every day.

Full Liquids (gradually increase to no more than 3/4 cup total)

Days 3–21

Items listed above, plus: Use nonfat acidophilus milk, sugar-free Carnation Instant Breakfast drink, plain soymilk, low-fat cream soups made with skim milk for protein in this stage. May also add cream of wheat or rice cereal; sugar-free yogurt or pudding; unsweetened applesauce or strained infant fruits; sugar-free powdered drinks or iced tea. Sip at least 48–64 oz of liquid (especially water) each day. Take a prescribed multivitamin every day.

Pureed (gradually increase to no more than 1 cup total)

3–6 weeks after surgery

Items listed above, plus: Low-fat cottage cheese, eggs, tofu, baby food chicken or turkey for protein in this stage. May also add hummus, regular unflavored oatmeal, baby food or toddler fruits and vegetables, blended fruit smoothies, chicken or vegetable broth. Sip at least 48–64 oz of liquid (especially water) each day. Take a prescribed multivitamin every day.

Regular (small meals and snacks with no more than 1 cup total; 2 oz total meat)

6 weeks on

Items listed above, plus: Low-fat foods (5 g fat per serving) such as plain rice, well-cooked pasta. Avoid concentrated sweets and sugar (10 g sugar per serving). For protein, use lean chicken or deboned fish and most tender meats except for tough meats like beef or pork. Allow 30–45 minutes for each meal. Take small bites, and chew food until fairly liquefied before swallowing. Sip at least 48–64 oz of liquid (especially water) each day. Take a prescribed multivitamin every day.

Interleukin-6 Na, K Ca, Mg Alb, transthyretin H&H

Serum Fe Alkaline Serum B12 phosphatase Serum folic acid Cholesterol Serum vitamin D Triglycerides Serum copper

INTERVENTION OBJECTIVES Preoperative • Provide adequate glycogen stores and vitamins C and K for surgical procedure. Consider enteral immunonutrition. • Patients with diabetes should be under fairly good glucose control or at least stable.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Vitamin Intake Assessment Data: Medication history. Intake records after GBP surgery indicating no animal protein sources. Not taking prescribed vitamin–mineral supplement. BMI 50 before surgery; 6-month postoperation, BMI 48. Low serum B12 level. Recent complaints of tingling and numbness in extremities. Nutrition Diagnosis (PES): NI-5.9.11 Inadequate vitamin B12 intake related to inadequate intake and not taking vitamin supplement as evidenced by diet history, low serum B12 level, and symptoms of neurological changes (tingling in hands and feet.) Intervention: Food-nutrient delivery—Encourage use of milk products as tolerated throughout the day. Educate—Discuss the importance of vitamin B12 from supplemental intake when dietary intake is poor. Counsel about acceptable sources of B12 while on the highly restricted GBP diet. Coordinate care with medical team and family members to emphasize improving the diet. Monitoring and Evaluation: Pill count for prescribed vitamin supplements. Improvement in neurological symptoms; normalized vitamin B12 lab values within 1–2 months of therapy.

Postoperative • Promote wound healing and restoration of depleted glycogen in the liver. • Prevent side effects during weight loss. The weight loss results of GBP surgery average 10 lb per month and stabilize between 18 and 24 months after surgery. Most patients will never achieve an ideal body weight, but they will be closer to a healthy body weight. • Prevent complications such as alkaline reflux gastritis, esophagitis, perforation, gastric dilation, stomal obstruction, peptic ulcer, staple line disruption, and excessive vomiting. • Monitor and manage rare conditions such as rhabdomyolysis, nesidioblastosis, bowel obstruction, and acute renal failure (Capella et al, 2006; Sharma et al, 2006.) • At 4–6 weeks postoperatively, patients often report that foods taste sweet and will modify intake accordingly. Aversions to meat may occur. Pica may be found in some patients who also have iron deficiency anemia (Kushner and Shanta Retelny, 2005). • Have patient eat and sip liquids slowly to prevent vomiting; take meat and toast in small bites.

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• Prevent neurological, hematological, and cardiovascular side effects of thiamin, vitamin B12 deficiency, and other nutrients that may be inadequate (Bloomberg et al, 2005).

FOOD AND NUTRITION Preoperative • Use a balanced diet with adequate energy, protein, vitamins, and minerals. Enteral immunonutrition may be useful. • Diet should regress from liquids to NPO.

Postoperative • Over several days, progress from clear to full liquids. Enteral feeding with a high-protein intake may be useful to promote healing. Provide at least 1000 kcal/d with 1.5–2.0 g protein/kg. • Until weight loss is achieved, add semisolid or pureed foods in small amounts. Initial gastric capacity is 30–60 mL; progression is up to 250 mL. Three meals and two snacks are better tolerated than three meals. • Include 60–80 g of protein per day when possible. Highprotein, low-fat foods such as milk, eggs, yogurt, boneless fish, and skinless poultry are important for maintaining adequate lean body mass while losing weight. • Carbohydrate should be less than 30 g total per meal. A minimum of 130 g of carbohydrate per day should be included to meet Dietary Reference Intakes (DRIs). • Patients will vomit if they eat too rapidly, drink fluids right after eating, lie down after eating, or overeat. Recommend chewing slowly and consuming liquids 30 minutes before or after meals. • Dumping syndrome may also occur. Avoid alcoholic beverages, soft drinks, high-fat food such as fried foods and pastries, and high-carbohydrate foods such as cookies, cake, and candies. • Ensure adequate fluid intake to prevent dehydration. Use at least 40 mL/Kg of noncaffeinated/noncaloric fluid daily, especially water. • Meet micronutrient requirements, such as a daily liquid multivitamin–mineral supplement and a monthly vitamin B12 injection (Johnson et al, 2005). Monitor for iron and calcium deficiencies. Progress to a chewable supplement that meets 100% of the DRIs. • Avoid obstructive foods, such as popcorn, celery, nuts, seeds, and membranes of citrus fruits.


NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Preoperative evaluations include: all weight loss attempts and outcomes; usual eating patterns and nutritional intake evaluations; frequency of eating away from home; cooking and shopping habits; reasons and motives for surgery; knowledge about protein, vitamins, and minerals; awareness of signs of dehydration; and food allergies and intolerances. Keeping a food diary and sharing it with the dietitian is important. Continuous nutrition monitoring can prevent poor outcomes if the patient and the dietitian work together. • Postoperative education includes: use of high-protein supplemental beverages, especially for wound healing. Thinned baby food, low-fat and sugar-free milk shakes, thinned hot cereals, blenderized soups, vegetable juices, and sugar-free instant breakfast drinks are useful. • Patients require close monitoring, with special regard to the rapidity of weight loss and vigilant screening for signs and symptoms of subclinical and clinical nutritional deficiencies (Bloomberg et al, 2005.) • Discuss appropriate quantities and qualities of foods that will be consumed; overeating may stretch the stoma or cause dumping syndrome. Have patient take small bites and sip liquids slowly to prevent vomiting. • Help patient progress to normalized diet with 120–200 mL per meal. Increase awareness of the eating and satiety process. • A multivitamin–mineral preparation is definitely needed. Vitamin B12, folacin, iron, potassium, copper, and vitamins A and D are special risks for deficiency. Nutritional deficiencies may become apparent, including PEM (Shuster and Vasquez, 2005). • Discuss methods for blenderizing foods and recipes. • Avoid fasting, as it may cause hypoglycemia. • Promote adequate sleep, exercise, and other lifestyle measures that support a sense of well-being. • Discuss how to manage dumping syndrome by avoiding simple sugars. • Most patients lose a significant amount of weight and maintain their weight loss for long term, thereby having an improved quality of life. Unfortunately, between 5% and 30% of patients lose little weight or are unable to maintain their weight loss postoperatively (Puzziferri, 2005). Encourage exercise to help with weight loss and self-esteem.

Common Drugs Used and Potential Side Effects Patient Education—Food Safety • Drugs used will be for the specific condition and side effects of surgery. • Combining RYGB with pharmacologic stimulation of PYY secretion may increase long-term success of surgical weight reduction in morbidly obese adults (Meguid et al, 2008.)

Herbs, Botanicals, and Supplements • Answer questions about the use of herbs and botanicals; stop them before surgery.

Surgical patients may be vulnerable to foodborne illness; safe food handling and handwashing are essential.

For More Information •

American Society for Metabolic & Bariatric Surgery

Cleveland Clinic

Consumer Guide to Bariatric Surgery

Gastric Bypass

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Longitudinal Assessment of Bariatric Surgery (LABS)

Mayo Clinic

Presurgical Psychological Assessment

Weight-Control Information Network

GASTRIC BYPASS—CITED REFERENCES American Diabetes Association. Standards of Medical Care in Diabetes 2009. Diabetes Care. 32:25S, 2009. Bloomberg RD, et al. Nutritional deficiencies following bariatric surgery: what have we learned? Obes Surg. 15:145, 2005. Campos GM, et al. Improvement in peripheral glucose uptake after gastric bypass surgery is observed only after substantial weight loss has occurred and correlates with the magnitude of weight lost. J Gastrointest Surg. 14:15, 2010. Capella RF, et al. Bowel obstruction after open and laparoscopic gastric bypass surgery for morbid obesity. J Am Coll Surg. 203:328, 2006. Carlin AM, et al. Prevalence of vitamin D depletion among morbidly obese patients seeking gastric bypass surgery. Surg Obes Relat Dis. 2:98, 2006. Filis D, et al. Rhabdomyolysis following laparoscopic gastric bypass. Obes Surg. 15:1496, 2005. Jen HC, et al. Trends and outcomes of adolescent bariatric surgery in California, 2005–2007. Pediatrics. 126:746, 2010. Jhaveri RR, et al. Cardiac remodeling after substantial weight loss: a prospective cardiac magnetic resonance study after bariatric surgery. Surg Obes Relat Dis. 5:648, 2009. Johnson JM, et al. Effects of gastric bypass procedures on bone mineral density, calcium, parathyroid hormone, and vitamin D. J Gastrointest Surg. 9:1106, 2005.

Kushner RF, Shanta Retelny V. Emergence of pica (ingestion of non-food substances) accompanying iron deficiency anemia after gastric bypass surgery. Obes Surg. 15:1491, 2005. Leslie D, et al. Bariatric surgery primer for the internist: keys to the surgical consultation. Med Clin North Am. 91:353, 2007. Madan AK, et al. Metabolic syndrome: yet another co-morbidity gastric bypass helps cure. Surg Obes Relat Dis. 2:48, 2006. Meguid MM, et al. Weight regain after Roux-en-Y: a significant 20% complication related to PYY. Nutrition. 24:832, 2008. NIDDK. Web site accessed January 22, 2010 at publications/gastric.htm#adolescent. Picot J, et al. The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation. Health Technol Assess. 13:1, 2009. Pories W, Albrecht R. Etiology of type II diabetes mellitus: role of the foregut. World J Surg. 25:527, 2001. Puzziferri N. Psychologic issues in bariatric surgery—the surgeon’s perspective. Surg Clin North Am. 85:741, 2005. Rendon SE, Pories WJ. Quality assurance in bariatric surgery. Surg Clin North Am. 85:757, 2005. Service GJ, et al. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med. 353:249, 2005. Sharma SK, et al. Acute changes in renal function after laparoscopic gastric surgery for morbid obesity. Surg Obes Relat Dis. 2:389, 2006. Shuster MH, Vasquez JA. Nutritional concerns related to Roux-en-Y gastric bypass: what every clinician needs to know. Crit Care Nurs Q. 28:227, 2005. Tan JC, et al. Severe ataxia, myelopathy, and peripheral neuropathy due to acquired copper deficiency in a patient with history of gastrectomy. JPEN J Parenter Enteral Nutr. 30:446, 2006. Torquati A, et al. Is Roux-en-Y gastric bypass surgery the most effective treatment for type 2 diabetes mellitus in morbidly obese patients? J Gastrointest Surg. 9:1112, 2005. Xanthakos SA. Nutritional deficiencies in obesity and after bariatric surgery. Pediatr Clin North Am. 56:1105, 2009.

BOWEL SURGERY NUTRITIONAL ACUITY RANKING: LEVEL 3 DEFINITIONS AND BACKGROUND Small bowel surgery may be needed for inflammatory bowel disease, intestinal blockage, precancerous polyps, cancer, necrotizing enterocolitis, and other problems. Emergency surgical procedures in patients with inflammatory bowel disease are rare but can have a high morbidity unless carefully managed. Patients with short bowel syndrome (SBS) may have a higher than average prevalence of small intestinal bacterial overgrowth and may be at risk for septicemia due to bacterial translocation while on PN (Walzer and Buchman, 2010.) Failure to provide enteral nutrients creates a physiologic profile that exacerbates oxidative stress and increases the systemic inflammatory response syndrome (McClave and Heyland, 2009.) After small bowel surgery, SBS occurs. Earlier feeding may reduce the risk of postsurgical complications after gastrointestinal (GI) surgery (Andersen et al, 2006.) When possible, early enteral feeding should be attempted (Lewis et al, 2009.). Residual small bowel length remains an important predictor of duration of the need for PN.

Most people with SBS experience spontaneous small bowel adaptation over time, when they can be weaned from PN. There are some individuals who cannot be weaned and are potential candidates for techniques to promote intestinal adaptation. Small bowel transplantation has become the treatment of choice for patients with chronic intestinal failure, whose illness cannot be managed with medications or who cannot be maintained on home parenteral nutrition. Rejection, bacterial translocation, and sepsis rates are high. Colectomy removes part or all of the colon. A colostomy or ileostomy creates an opening on the abdomen (stoma) for the drainage of feces; it may be permanent or temporary. Patients who have an ileostomy lose a considerable amount of fluid that contains sodium and potassium. Fat and vitamin B12 absorption is reduced. See section 7 for more details on nutritional management. Patients who have had a hemorrhoidectomy usually tolerate a low-residue diet to delay defecation and allow healing at operative site. After patient is healed, it is important to have patient return to a high-fiber diet to prevent constipation.

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CLINICAL INDICATORS • Clinical/History Height Weight Body mass index (BMI) Weight changes Diet history Blood pressure (BP) Intake and output (I & O)

Nausea, vomiting, anorexia Constipation Infection or pressure ulcers History of dehydration? Lab Work Gluc CRP Platelet count

Alb, transthyretin BUN, Creat Na, K Ca, Mg Serum Osm N balance PT, INR H&H Serum Fe, ferritin Vitamin B12

INTERVENTION OBJECTIVES Preoperative • Replenish depleted reserves by using special immuneenhanced formulas. Uninterrupted enteral nutrition (before, during, and after surgery) is popular in practice to achieve energy intake goals. • Mechanical bowel preparation before surgery offers no major benefits.

Postoperative • Restore enteral autonomy (Weseman and Gilroy, 2005). • Early enteral feeding is generally recommended; this downregulates systemic immune responses, reduces oxidative


• •


stress, and improves patient outcome (McClave and Heyland, 2009.) Slowly progress back to a normal diet. Progress from clear liquids to soft—solid diet and avoid dairy products if there is lactose intolerance. Modify diet, as needed, for part of bowel that was affected. Correct inadequate digestion or absorption of fluid, electrolytes, and nutrients (Matarese et al, 2005). Prevent complications, such as peritonitis or ileus. Chewing gum can prevent ileus in some patients. Coordinate efforts with a transplantation team to restore nutritional autonomy to transplantation recipients (Weseman and Gilroy, 2005). Successful transplantation recipients can resume unrestricted oral diet eventually. Fight surgical infections by adding probiotics to enteral nutrition (EN) improve the immune status of the colon.

FOOD AND NUTRITION Preoperative • Regress from soft diet to full liquids and then clear liquids. • If needed, use a hydrolyzed formula or jejunostomy.

Postoperative • Enteral nutrition is a primary therapy. Growth hormone, GLN, short-chain fatty acids, and fermentable fiber sources are useful. Intestinal rehabilitation regimens provide specialized oral diets, soluble fiber, oral rehydration solutions, and tropic factors to enhance absorption (Matarese et al, 2005). • Probiotics may be beneficial (Floch et al, 2006). • Slowly progress from a low-residue diet to a normal diet. Suggest that patient eat slowly and chew foods well. Excesses of fiber should be avoided. Probiotics may be included (Jenkins et al, 2005). • Focus on adequate fluids; needs are usually greater than normal. • Long-term nutritional support may be needed; CPN may be required for a short time.

Common Drugs Used and Potential Side Effects

Inadequate Fluid Intake Assessment Data: Food records, input and output reports showing poor fluid intake, medication history, assessment of depression following bowel surgery for cancer. Showing signs of dehydration. Nutrition Diagnosis (PES): Inadequate fluid intake related to semiconscious state after bowel surgery and decreased oral intake as evidenced by I & O records showing only 800 mL intake for the past 3 days. Poor skin turgor, sunken eyeballs. Intervention: Food-Nutrient Delivery—Add extra fluids to meal trays; encourage nursing to provide at least 4–5 oz with each medication given. Educate family and nursing staff about desired fluid intake; ensure that I & O records are kept accurately. Counsel about the dangers of dehydration. Coordinate care with medical team to increase fluid intake. Monitoring and Evaluation: Improved fluid intake as per I & O records; achieving 35 mL/Kg fluid goal.

• Drugs used will be for the specific condition and side effects of surgery. New medications to reduce rejection in transplant patients are under study.

Herbs, Botanicals, and Supplements • Answer questions about the use of herbs and botanicals; stop them before surgery. • Patients may benefit from prebiotics and probiotics to decrease sepsis. Use with caution.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Evaluate and discuss preoperative weight loss, eating problems and fears, nutritional intake evaluations, frequency

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of eating away from home, and cooking and shopping habits. Discuss changes that will be needed after the specific bowel surgery. See section 7 for ileostomy and colostomy guidance.

Society for American Gastroenterological and Endoscopic Surgeons

Society for Surgery of the Gastrointestinal Tract

Patient Education—Food Safety


Surgical patients may be vulnerable to foodborne illness; safe food handling and handwashing are essential.

Andersen AK, et al. Early enteral nutrition within 24 h of colorectal surgery versus later commencement of feeding for postoperative complications. Cochrane Database Syst Rev. (4):CD004080, 2006. Floch MH, et al. Recommendations for probiotic use. J Clin Gastroenterol. 40:275, 2006. Jenkins B, et al. Probiotics: a practical review of their role in specific clinical scenarios. Nutr Clin Pract. 20:262, 2005. Lewis SJ, et al. Early enteral nutrition within 24 h of intestinal surgery versus later commencement of feeding: a systematic review and meta-analysis. J Gastrointest Surg. 13:569, 2009. Matarese LE, et al. Short bowel syndrome: clinical guidelines for nutrition management. Nutr Clin Pract. 20:493, 2005. McClave SA, Heyland DK. The physiologic response and associated clinical benefits from provision of early enteral nutrition. Nutr Clin Pract. 24:305, 2009. Walzer N, Buchman AL. Development of Crohn’s disease in patients with intestinal failure: A role for bacteria? [published online ahead of print January 5, 2010]. J Clin Gastroenterol. 44:361, 2010. Weseman RA, Gilroy R. Nutrition management of small bowel transplant patients. Nutr Clin Pract. 20:509, 2005.

For More Information •

The American College of Gastroenterology

Atlas of Gastrointestinal Endoscopy

Bowel Sounds

Ileostomy, Colostomy, and Other Surgery


Small Bowel Resection

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AIDS and Immunology, Burns, Sepsis and Trauma




• • • • • • • • • • • • • • • • • • •

Accidents or Trauma Altered Breathing Altered White Blood Cell (WBC) Count and Differential Anemia Anorexia, Malnutrition Culture Results, Specimens Environmental Sanitation and Level of Personal Hygiene Fever, Chills Fluid Status, Edema Infection, Sepsis (Heat, Pain, Redness, Swelling, or Drainage in Any Area) Indicators of Immunity (T Cells, Other Lymphocytes) Medications, Prescription and Over-the-Counter Metabolic Rate (Indirect Calorimetry or Estimated) Multiple Organ Dysfunction Syndrome (MODS) Nutritional Status for Zinc, Iron, Selenium; Vitamins A, C, E; Albumin, CRP Presence of Chronic Diseases Pulse Rate Recent Illness or Surgery Urinary Changes (Frequency, Urgency, Burning)

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OVERVIEW OF NUTRITION AND IMMUNOCOMPETENCE The interdependency between the disciplines of nutrition and immunology has been recognized for many decades. Fetal and early infant programming of thymic function suggests that early environments have long-term implications for immunocompetence and adult disease risk. Nutrition and physical growth affect immunocompetence and morbidity from infections. Common diseases such as atopy and allergy, autoimmunity, chronic infections, and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th) 1 versus Th2 cytokine balance. Proinflammatory cytokines promote atherosclerosis, major depression, visceral-type obesity, metabolic syndrome, and sleep disturbances (Elenkov et al, 2005). Studies regarding the role of nutrients on gene expression and cytokine production have established the importance of maintaining a balanced immune system throughout life. Lack of adequate macronutrients or selected micronutrients, especially zinc, selenium, iron, and the antioxidant vitamins, can lead to clinically significant immune deficiency and infections, especially in children (Cunningham-Rundles et al, 2005). Reduced number of lymphocytes causes loss of host defense in zinc deficiency. In turn, infections aggravate micronutrient deficiencies by reducing nutrient intake, increasing losses, and altering metabolic pathways (Wintergerst et al, 2007). See Table 15-1 and Table 15-2. Large variations in immunity relate to genetics, age, gender, smoking habits, exercise habits, alcohol consumption,

TABLE 15-1

diet, stage in the female menstrual cycle, stress, history of infections, vaccinations and early life exposures. Sound nutritional practices, stress management, good hygiene and sanitation, adequate rest and sleep, and maintaining healthy physical activity can enhance immunocompetence and reduce risks of infection in any population. Even in older adults, improved nutrition can decrease risks for infection. Nutritional supplementation may reduce this risk and reverse some of the immune dysfunction associated with advanced age. The role of calorie restriction and zinc on immunity, aging, autoimmunity, and malignancy has been studied extensively; adding omega-3 fatty acids (fish oil) is also beneficial (Fernandes, 2008). Hospital admission screening that best identifies patients who are at risk for malnutrition-related complications include presence of a wound, poor oral intake or evident malnutrition, low serum albumin or hemoglobin values, and low total lymphocyte count (TLC) (Brugler et al, 2005). The ability of admission information to accurately reflect malnutrition-related complication risk is crucial to early initiation of restorative medical nutritional therapy (Brugler et al, 2005). New approaches exploring the link through nutrigenomics, proteomics, and metabolomics may provide insight into controlling age-related diseases by following a balanced diet intake (Fernandes, 2008). Table 15-3 provides a list of key nutrients for immunocompetence. Table 15-4 provides important factors to consider in critical illness. Table 15-5 lists nutritional implications in some specific conditions, and Table 15-6 lists virulence increased by iron supplementation.

How the Immune System Works

The immune system is designed to provide protection from invading organisms, including bacteria and viruses, tumor cells, dirt, pollen, and other foreign material. Normally, barriers from the skin and linings of the lungs and gastrointestinal (GI) and reproductive tracts protect the underlying tissues from the outside environment. Whenever there is a breakdown in the protective lining, germs and other irritants can enter the body. The immune system is designed to conquer these foreign molecules by engulfing them or by destroying them with enzymes or other detoxifying means. In addition to fighting off these foreign invaders, the immune system has evolved to destroy abnormal cells (such as tumor cells) but occasionally reacts against the body’s own normal tissues (autoimmunity). Innate and Acquired Immunity The two principal types of immune response, innate and adaptive (acquired) immunity, are distinguished from one another by both their speed and specificity. The innate immune system, present from birth, involves nonspecific responses that are the first line of defense against common infectious agents, including bacteria and viruses. This system is generally able to recognize foreign organisms but is unable to distinguish between particular invaders. Thus, an innate response does not require stimulation by sophisticated cell-to-cell interactions to remove bacteria or other foreign material and degrade it. The more specific adaptive (acquired) immune system must be triggered by a specific virus, bacterium, or other foreign material, which stimulates lymphocytes to produce antibodies that can combat the foreign substance. At the next exposure, the preformed antibodies will allow the person to respond with an even stronger, more specific response known as immunological memory. Cells of the Immune System The immune system consists of white blood cells (WBCs, leukocytes), which are produced in the bone marrow and mature there or in the thymus and other lymphoid organs. Leukocytes circulate in the blood along with oxygen-carrying red blood cells. Under normal conditions, leukocytes leave the circulation and migrate into organs where germs can appear, including the skin, lungs, intestine, and reproductive tract. There, they can wait for infectious agents, or they can migrate back through the circulation to other organs. (continued)

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TABLE 15-1 How the Immune System Works (continued) There are three major types of leukocytes. Neutrophils are the most plentiful and are the first line of defense; they contain an arsenal of preformed enzymes that are capable of destroying bacteria. In addition, they are phagocytic, and they engulf viruses, bacteria, or other foreign material, protecting the host from further damage. Neutrophils are very short-lived, often destroyed during the fight. Monocytes are leukocytes that migrate to tissues and mature into macrophages. Macrophages are phagocytic and can remove foreign material and parts of dead cells from the tissues. They contain enzymes that can destroy infectious material but live longer than neutrophils and do not tend to self-destruct as easily. The tissue macrophage in the liver is called the Kupffer cell. Lymphocytes are selective, specialized WBCs that combat specific infectious agents. The two types of lymphocytes are B cells and T cells. B cells are responsible for humoral immunity in the body fluids (classically known as the humors); they release specialized, soluble protein antibodies into the blood and other body fluids. The antibodies recognize and bind to the surface of foreign substances (i.e., pathogens), immobilizing them and further labeling them as foreign so that they can be more readily taken up by phagocytic cells. T cells, in contrast, act directly on other cells rather than manufacturing antibodies. Because of this direct interaction with other cells, T cells are responsible for cellular immunity. They can be further divided into helper T cells, which recognize foreign invaders and stimulate immune responses from other cells, and cytotoxic T cells, which destroy infected cells. Some of these cells are extremely long-lived “memory cells,” capable of remembering certain features on the foreign molecules so that, if the organism encounters that foreign molecule in the future, it can quickly stimulate a response. Communication Between Immune Cells: Cytokines One form of communication between immune cells is direct cell-to-cell contact, which can occur either as a loose, transient association or as a tighter, longlasting encounter. Either way, cells must make physical contact with one another. In the second form of contact, cells release small proteins called cytokines, which bind to specific receptors on the surface of target cells. Cytokines interact only with the appropriate target cell and not with surrounding cells. Although many of the effects of cytokines are local, they have been called the hormones of the immune system because they are transported by the circulating blood. Cytokines can affect the same cell that produced them, a neighboring cell, or a cell far away. They stimulate or dampen cell proliferation (replication), production of other cytokines, killing of damaged cells or tumor cells (cytotoxicity), and cell migration (chemotaxis). The latter response is controlled by a subset, chemokines. Just as there are cells that can stimulate or inhibit immune response, cytokines can regulate a variety of cell functions either positively or negatively. Interleukin-6 is an important cytokine. Excessive production of proinflammatory cytokines or their production in the wrong biological context may lead to chronic inflammation and negative health consequences. Gut Immunity An extremely important function of the GI tract is its ability to regulate the flow of macromolecules between the environment and the host through a barrier mechanism. The GI immune response maintains critical pathways in the body. Gut-associated lymphoid tissue (GALT) is the dominant location for initiation of mucosal immune response and is dependent on fats, amino acids, and micronutrients. A healthy GI mucosal immune system provides barriers against systemic access for food antigens and microbes. Changes in the GALT immune response may contribute to intestinal dysfunction and susceptibility to postinjury gut-derived sepsis. Together with GALT and the neuroendocrine network, the intestinal epithelial barrier controls the equilibrium between tolerance and immunity to non–self-antigens (Fasano and Shea-Donohue, 2005). Because genetic and mucosal immunity strongly influence the composition and function of enteric bacteria, strategies are needed to correct dysfunctional microbiota in genetically susceptible individuals and to correct dysbiosis in many inflammatory disorders (Hansen et al, 2010). REFERENCE Fasano A, Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol. 2:416, 2005. Hansen J, et al. The role of mucosal immunity and host genetics in defining intestinal commensal bacteria. Curr Opin Gastroenterol. 26:564, 2010.

TABLE 15-2 Immunocompetence and Immunity Concerns Almost all nutrients in the diet play a crucial role in maintaining an optimal immune response. Thus, deficient and excessive intakes can have negative consequences on immune status and susceptibility to a variety of pathogens. In addition, botanical and herbal products can be a concern. While Echinacea is used to reduce symptoms of the “common cold” or flu, there is a risk of hepatotoxicity, exacerbation of allergies or asthma, and even anaphylactic reactions. Garlic is also used to relieve cough, colds, and rhinitis but gastrointestinal disturbances, allergic reactions, or hypoglycemia can occur. Other agents, including angelica, German chamomile flower, ephedra, ginkgo, grape seed extract, licorice root, St. John’s wort, kava-kava rhizome, peppermint, stinging nettle, and ginseng, may also have undesirable side effects (see Section 2). Nutrition and dietary patterns have been shown to have direct impact on health of the population and of selected patient groups, related to a reduction of oxidative damage from free radical production (Berger, 2005). Insufficient intake of micronutrients occurs in people with eating disorders, in smokers (both active and passive), in individuals with chronic alcohol abuse, in patients who are immunocompromised or malnourished, during pregnancy and lactation, and in the elderly (Wintergerst et al, 2007; Happel and Nelson, 2005). Concerns are listed here. Infants

Undernutrition in critical periods of gestation and neonatal maturation and during weaning impairs the development of a normal immune system. There is a high prevalence of micronutrient deficiencies and infectious diseases in infants in developing countries. Breastfed infants have lower morbidity and mortality due to diarrhea than those fed formula; human milk oligosaccharides protect against pathogens (Newburg et al, 2005). (continued)

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TABLE 15-2

Immunocompetence and Immunity Concerns (continued)

Young children

Risks and adverse functional and health outcomes may be associated with deficient and excessive intakes and nutrition status of iron, iodine, zinc, vitamins A and D, folate, vitamin B12, and riboflavin in children. Altered growth and development, mental and neuromotor performance, immunocompetence, physical working capacity, and morbidity can result. Vitamin C and zinc may reduce the incidence and improve the outcome of pneumonia, malaria, and diarrhea infections, especially in developing countries (Wintergerst et al, 2005).

Older adults

Adults 65 years and older comprise the fastest-growing segment of the U.S. population. Older adults experience greater morbidity and mortality due to infection than do young adults (High et al, 2005). Nutritional factors can modify susceptibility to disease and promote healthy aging. Interleukin-6 (IL-6), a cytokine, is tightly controlled by hormonal feedback (estrogen, testosterone) that is lost in the aging process. Elevated IL-6 levels progressively increase and may promote tumorigenesis, osteoporosis, neurodegenerative diseases, and sarcopenia. Zinc is important for immune efficiency (innate and adaptive), antioxidant activity (superoxide dismutase), and cell differentiation (Mocchegiani et al, 2007). Use of a daily multivitamin/mineral supplement that contains 100% of the Dietary Reference Intakes (DRIs) may be encouraged.

Upper respiratory infections

The role of large doses of vitamin C to reduce duration or severity of cold symptoms has been inconclusive. Vitamin E supplementation may reduce the incidence of respiratory infections among the elderly. Echinacea or ginseng may also be modestly protective (Predy et al, 2005).

Immunocompromised persons (cancer, AIDS, tuberculosis)

Supplementation of vitamin C improves antimicrobial and natural killer cell activities, lymphocyte proliferation, chemotaxis, and delayed-type hypersensitivity (Wintergerst et al, 2005). Glutamine, arginine, fatty acids, and vitamin E provide some additional benefits for immunocompromised persons or patients who suffer from various infections but avoid excesses of arginine in septic patients. Chronic undernutrition and infection further weaken the immune response. Assessment of immunocompetence by available methods can identify individuals who are most in need of appropriate nutritional support to enhance host defense to infectious pathogens


Iron and vitamin A deficiencies and protein–energy malnutrition are highly prevalent worldwide. Vitamin A and zinc play important roles in protecting individuals from severity in illnesses such as diarrhea and HIV infection. Zinc undernutrition or deficiency impairs cellular phagocytosis, natural killer cell activity, and the generation of oxidative burst (Wintergerst et al, 2005).


Obesity caused by excess nutrition or excess storage of fats relative to energy expenditure is a form of malnutrition. Leptin is a cytokine-like immune regulator that has complex effects in both overnutrition and in the inflammatory response in malnutrition.

Surgical patients

Preoperative oral intake of immunonutrition containing omega-3 fatty acids, arginine, and nucleotides at home may prevent the risks of hospitalization and may lead to immunomodulating effects, which can improve nutritional status (see Section 14). Postsurgical or septic patients given branched-chain amino acids intravenously show improved immunity and improved outcomes (Calder, 2006).


Sepsis and multiple organ failure have mortality rates of up to 80%. Vitamin C concentrations in the plasma and leukocytes rapidly decline during infections and stress (Wintergerst et al, 2005).

REFERENCES Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 24:172, 2005. Calder PC. Branched-chain amino acids and immunity. J Nutr. 136:288S, 2006. Happel KI, Nelson S. Alcohol, immunosuppression, and the lung. Proc Am Thorac Soc. 2:428, 2005. High KP, et al. A new paradigm for clinical investigation of infectious syndromes in older adults: assessment of functional status as a risk factor and outcome measure. Clin Infect Dis. 40:114, 2005. Mocchegiani E, et al. Zinc, metallothioneins, and longevity—effect of zinc supplementation: zincage study. Ann N Y Acad Sci. 1119:129, 2007. Newburg DS, et al. Human milk glycans protect infants against enteric pathogens. Annu Rev Nutr. 25:37, 2005. Predy GN, et al. Efficacy of an extract of North American ginseng containing poly-furanosyl-pyranosyl-saccharides for preventing upper respiratory tract infections: a randomized controlled trial. CMAJ. 173:1043, 2005. Wintergerst ES, et al. Immune-enhancing role of vitamin C and zinc and effect on clinical conditions. Ann Nutr Metab. 50:85, 2005. Wintergerst ES, et al. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 51:301, 2007.

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TABLE 15-3 Nutritional and Host Factors in Immunity Nutrient status is an important factor contributing to immune competence; undernutrition impairs the immune system, suppressing immune functions that are fundamental to host protection. Both macronutrients and micronutrients are essential. Protein is very important. Branched-chain amino acids (BCAAs) and other essential amino acids support synthesis of protein, RNA, and DNA in lymphocytes to respond to pathogens. Arginine and glutamine support a healthy gut and healing processes, but excesses are to be avoided. To prevent protein use for energy, sufficient carbohydrate intake is needed. Fats, especially omega-3 fatty acids, provide needed calories and support the immune system. Vitamin A deficiency impairs both innate and adaptive immune responses to infection. Carotenoids such as beta-carotene, lycopene, and zeaxanthin protect the immune system. As a precursor of NAD, the substrate for DNA repair, niacin contributes to genomic stability (Moccegiani et al, 2008). Antioxidant vitamins C and E counteract damage caused by reactive oxygen species and modulate immune cell function (Wintergerst et al, 2007). Excesses of vitamin E must be avoided as they can also be immunosuppressive. Vitamin D3 regulates the differentiation, growth, and function of monocytes, dendritic cells, and T and B lymphocytes (Equils et al, 2006). Vitamins B6, folate, B12, C, and E support the Th1 cytokine-mediated immune response with sufficient production of proinflammatory cytokines (Wintergerst et al, 2007). Protection against macular degeneration has been noted with prescriptions that contain omega-3 fatty acids, lutein and zeaxanthin, vitamins C, E, beta-carotene, zinc and copper (Krishnadev et al, 2010). Minerals and other substances also play an important role. Chromium can enhance the ability of white blood cells to respond to infection. Iron, as lactoferrin, deprives invading cells of their defense systems. Manganese can enhance natural killer cells and macrophage activity; CoQ10 is thought to do the same. Selenium deficiency may allow viruses to mutate into more dangerous pathogens. Selenium, copper, and zinc modulate immune cell function; they, along with iron, help to produce proinflammatory cytokines (Wintergerst et al, 2007). A summary of important factors is listed here. Infectious Disease Determinants • •

Environmental sanitation Microorganismic virulence

• •

Host immunity, including nutritional status Personal hygiene

• • • •

Oligosaccharides and other prebiotics Phagocytes (leukocytes, macrophages) Physical barriers (skin, mucous membranes) Probiotic bacteria

• • • •

Peyer patches in gut Spleen Thymus gland (T cells) Tonsils


Folic acid, vitamin B6, vitamin B12

• Arginine and glutamine • Dietary nucleotides (RNA) • Essential amino acids (especially BCAAs) • Linoleic acid (essential fatty acid) • Omega-3 fatty acids Micronutrient Vitamins • Vitamin A; carotenoids • Iron • Magnesium and CoQ10 • Manganese

• • • • •

Niacin Vitamin C Vitamin D Vitamin E Micronutrient Minerals • Chromium • Copper • Selenium • Zinc

Host-Resistance Factors • • • • •

Cell-mediated T cells Complement system Immunoglobulins, antibodies (B cells) Monocytes and dendritic cells Mucus and cilia on epithelial surfaces

Immune System • • • •

Bone marrow (B cells) GALT Luster patches in bronchioles Lymph nodes

Nutrients of Immunocompetence •

Immunonutrition • • • •

To provide immunonutrition, enteral feeding can be supplemented with arginine, glutamine, omega-3 polyunsaturated fatty acids (PUFAs), and nucleotides. Immunonutrition is a less invasive alternative to immunotherapy to lessen chronic inflammation. Excessive intravenous lipid can be deleterious due to the proinflammatory effects of omega-6 fatty acids. Omega-3 fatty acids are anti-inflammatory and, combined with medium-chain triglycerides and olive oil, they are more desirable (Grimble, 2005). Antioxidants, plant fibers, and live lactic acid bacteria are also important to boost the immune system and reduce inflammation (Bengmark, 2005). (continued)

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TABLE 15-3

Nutritional and Host Factors in Immunity (continued)

Nutrient–Nutrient Interactions, Excesses, and Immunocompetence • • • • • •

Under most circumstances the systemic inflammatory response is beneficial to the host, improving the eventual outcome of injury or infection. Chronic, excessive inflammation may lead to cardiac, hepatic, and mitochondrial dysfunction. Excessive counterinflammation leads to immune depression; excesses of iron, zinc, vitamin E, and PUFA interfere with immunity, especially if given intravenously or intramuscularly. Excess calcium interferes with leukocyte function by displacing magnesium. Long-term parenteral nutrition reduces immune functions (Bengmark, 2005). Parenteral iron and zinc are to be used with great caution; central parenteral nutrition is contraindicated in septic patients. Associations for “zinc plus selenium and niacin” have a role in healthy immunity, especially in the aging process (Moccegiani et al, 2008).

REFERENCES Bengmark S. Bio-ecological control of acute pancreatitis: the role of enteral nutrition, pro and synbiotics. Curr Opin Clin Nutr Metab Care. 8:557, 2005. Grimble RF. Immunonutrition. Curr Opin Gastroenterol. 21:216, 2005. Krishnadev N, et al. Nutritional supplements for age-related macular degeneration. Curr Opin Ophthalmol. 21:184, 2010. Moccegiani E, et al. Zinc, metallothioneins and longevity: interrelationships with niacin and selenium. Curr Pharm Des. 14:2719, 2008. Wintergerst ES, et al. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 51:301, 2007.

TABLE 15-4

Factors of Importance in Critical Care

Metabolic complications can occur from overfeeding critically ill patients. In general, current practice is to underfeed slightly rather than to overfeed: 20–25 kcal/kg actual body weight ABW is recommended; use 30% fat. Indirect calorimetry (IC) remains the best method of determining a patient’s energy needs. IC decreases complications from overfeeding and saves costs by reducing length of stay. Use a combination of prediction equations, clinical judgment, and monitoring of the appropriateness of the nutrition prescription. • Harris–Benedict equation: using ABW or IBW in the calculation tends to underestimate energy needs (Campbell et al, 2005). • Ireton–Jones formula: tends to overestimate the energy needs of mechanically ventilated patients (Campbell et al, 2005). Maintain protein at approximately 1.5 g/kg. In critical illness, glutamine levels are much higher in the duodenal mucosa than during starvation; glutamine supplementation may be beneficial (De-Souza and Greene, 2005). Arginine is a conditionally essential amino acid. It is a substrate for protein synthesis but can also be metabolized to various compounds, including nitric oxide, ornithine, and creatine phosphate, that are important for growth, wound healing, cardiovascular function, immune function, inflammatory responses, energy metabolism, urea cycle function, and other metabolic processes. Arginine supplementation improves outcomes with sepsis, wounds, ischemiareperfusion injury, and burns. The use of specific nutrients to modify immune, inflammatory, and metabolic processes offers the possibility for reducing morbidity following major surgery (Heys et al, 2005). Trace elements and antioxidant nutrients, especially selenium, are important for use in critical care and may reduce mortality (Heyland et al, 2005). Vitamin E levels tend to be low and may be supplemented accordingly. Use of omega-3 fatty acids is also important. In general, enteral nutrition poses fewer risks than parenteral nutrition. Calories and protein that are delivered early by the enteral route have a significant effect on outcome in patients in critical care units; specific nutrients may also be needed to replace acute deficiencies brought on by specific injury or disease states (Wischmeyer and Heyland, 2010). Control of hyperglycemia is very important to lessen infection and sepsis (Butler et al, 2005). REFERENCES Butler SO, et al. Relationship between hyperglycemia and infection in critically ill patients. Pharmacotherapy. 25:963, 2005. Campbell CG, et al. Predicted vs measured energy expenditure in critically ill, underweight patients. Nutr Clin Pract. 20:276, 2005. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 33:1125, 2005. Heyland DK, et al. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 31:327, 2005. Heys SD, et al. Nutrition and the surgical patient: triumphs and challenges. Surgeon. 3:139, 2005. Wischmeyer PE, Heyland DK. The future of critical care nutrition therapy. Crit Care Clin. 26:433, 2010.

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TABLE 15-5 Infections and Febrile Conditions and Nutritional Implications Emergence of new infectious diseases and old diseases with new properties may affect the whole world; severe acute respiratory syndrome and avian flu are examples. Condition, Nutritional Acuity, Background

Nutritional Implications

Bacterial endocarditis, Level 3 Bacterial endocarditis is an infection (often Streptococcus) of the membrane lining the heart chambers, often occurring after rheumatic fever. It accounts for 2% of all cases of organic heart disease. Symptoms and signs include fever, chills, joint pain, lassitude, anorexia, weight loss, and malaise.

Restore patient’s nutritional status to normal. Replenish electrolytes and fluids. Reduce edema, if present. Prevent heart failure, infections, anemia, embolism, and nephritis. Penicillin, erythromycin, and other antibiotics may be used; monitor for timing of meals and drugs. Use a high-energy and high-protein diet. If patient’s appetite is poor, encourage intake of favorite foods. Ensure adequate intake of fluids, vitamins, and minerals, especially vitamins A and C. Antibiotic prophylaxis is generally needed before dental work.

Candidiasis, Level 2 Candida albicans is normally found in the mouth, feces, and vagina. Greater colonization occurs in debilitated persons in whom thrush or vaginitis or cutaneous lesions are common. Susceptible individuals are those with leukemias, those who are immunosuppressed or on long-term central parenteral nutrition, and those who are obese or have diabetes.

Prevent or treat systemic infections. Prevent endocarditis, emboli, splenomegaly, and other complications. Correct underlying conditions when possible. Ensure a diet high in quality proteins, fluid, and calories. Use regular meals and small, frequent snacks; avoid skipping meals or fasting. Increase vitamin and mineral intake from tolerated fruits and vegetables, especially for vitamins A and C. Nystatin or amphotericin B may be used; diarrhea, nausea, and stomach pain may occur. Synthetic antimicrobial peptides are under development for use in oral candidiasis.

Clostridium difficile–infection, Level 3 The common name is Clostridium difficile–associated disease (CDAD;) it is hard to treat. Suppression of gastric acid with proton pump inhibitor drugs such as Prilosec (omeprazole) or Nexium (esomeprazole) is associated with a 2–3 times increase in community-acquired CDAD. C. difficile causes one fourth of nosocomial antibiotic-associated diarrheas. The incidence is rising, with more colectomy and mortality.

Repeat antibiotics are indicated, either metronidazole or vancomycin. Tapering the dose after a 10-day course decreases the incidence of recurrences compared with abruptly stopping antibiotics. Long-term use of metronidazole may cause neurotoxicity. Vancomycin followed by rifaximin or immune therapy are treatments under study. Probiotics such as Saccharomyces boulardii may decrease recurrences when combined with high-dose vancomycin.

Chronic fatigue and immune dysfunction syndrome (CFIDS), Level 1 CFIDS is a serious health concern affecting more than 800,000 Americans of all ages, races, socioeconomic groups, and genders. CFIDS involves severe exhaustion, weakness, headaches, sore throat, tender lymph nodes, unrefreshing sleep, fever, muscle aches, inability to concentrate, and depression. Symptoms tend to mimic lupus or even cancer. Testing for viral load is helpful. There may be a link to Hodgkin disease or multiple sclerosis; patients may have neurally mediated hypotension.

Improve immunological status and prevent malnutrition. Lessen severity of symptoms. Avoid infections and stress to prevent recurrent attacks, where possible. Discourage use of high fat diets. Provide adequate protein (0.8–1 g/kg) and 35 kcal/kg. Include adequate vitamins, minerals, and antioxidant foods. Extra salt or fluids may be needed for hypotension. Fludrocortisone promotes sodium retention. Use analgesics for aches and pain. A multidisciplinary approach is beneficial. Traditional Chinese medicine has shown some merit in reducing sleeplessness and fatigue.

Encephalitis and Reye syndrome, Level 2 Encephalitis involves an inflammation of brain cells, usually by a virus such as measles, mumps, mononucleosis, or herpes simplex. If caused by the tsetse fly, it is known as African sleeping sickness. Reye syndrome is a disease of the brain and liver, affecting mostly children and teenagers after viral illness. Symptoms include headache, lethargy, nightmares, heavy vomiting; stupor and fatty liver; coma, double vision; hypoglycemia; multiple organ failure, or even death.

Ease symptoms. Allow natural defense system to work. Assist breathing with respirator if necessary. Control any pernicious vomiting. Tube feed if patient is comatose. A ketogenic diet may help when there are seizures. Otherwise, use a high-protein, high-calorie diet with a multivitamin–mineral supplement and extra fluids. If steroid therapy is used, monitor glucose, potassium, and nitrogen levels carefully; reduce sodium in foods if there is edema. Aspirin should be avoided.

Fever, Level 2 Fever is considered to be elevated body temperature 37.5–38.3C (100–101F). Fever (pyrexia) may be caused by acute (pneumonia, measles, flu, or chicken pox) or chronic causes (tuberculosis, hepatitis, or malaria). Disturbed thermoregulation is controlled by the hypothalamus. Prostaglandin E2 (PE2) is released from the arachidonic acid pathway and can help increase leukocyte, phagocyte, T cell and interferon activity. Hyperpyrexia is considered to be 41.5C (106.7F). Fever of unknown origin (FUO) involves illness for more than 3 weeks with a temperature higher than 101F. Approximately 40% of FUO is from infections, 20% from cancer, 15% from connective tissue disease, and 25% from undetermined causes.

Meet increased nutrient needs caused by patient’s hypermetabolic state, especially energy requirements. Each 1F elevation causes a 7% increase in metabolic rate. Replace nitrogen losses. Replenish carbohydrate since liver stores last only 18–24 hours. Normalize electrolyte status, replace losses from perspiration, and facilitate toxin elimination through increased urine output. Prevent dehydration but avoid water intoxication. Treat anorexia, nausea, or vomiting. Adults need 30–40 kcal/kg/day; infants and children need additional calories as well. Monitor weight changes closely. Adults need 1.5–2 g protein/kg if temperature is high and chronic. If fever is acute, patient may prefer liquids. With longer duration, thiamin and vitamins A and C may be depleted, and a supplement may be used. Parenteral zinc or iron supplementation may significantly increase temperature in patients with recent injury or infection; avoid until fever improves. As treatment progresses, a diet with small, frequent feedings can be used. Offer preferred foods according to appetite, such as puddings, shakes, and soups. (continued)

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TABLE 15-5

Infections and Febrile Conditions and Nutritional Implications (continued)

Condition, Nutritional Acuity, Background

Nutritional Implications Take antipyretics/aspirin with food or milk and avoid alcoholic beverages. Take erythromycin with a full glass of water on an empty stomach to avoid sore mouth, nausea, or diarrhea. Penicillins should not be taken with acidic food or fluids such as fruit juice; so use adequate protein. Take tetracycline on an empty stomach with a full glass of water; avoid milk and dairy products for 2 hours before or after taking tetracycline. Avoid use in pregnancy and in children.

Herpes simplex, Level 1 Herpes simplex involves a viral infection of skin or mucous membranes (herpes simplex I for oral lesions, whereas herpes simplex II usually involves genital/anal area) with vesicular eruptions of repeated frequency. Oral lesions (“cold sores” or “fever blisters”) are latent in the nerve cell ganglia of the trigeminal nerve and are triggered by stress. This virus is similar to the chicken pox virus. Testing includes polymerase chain reaction, herpes simplex virus test, and swollen lymph nodes. Herpetic outbreaks are common in HIV-positive and other immunocompromised patients.

Reduce inflammation and duration. Lessen recurrences and virulence. Reduce stress, febrile states, or further complications such as encephalitis or aseptic meningitis. Highlight relaxation and stress reduction techniques. Use high-quality protein and adequate calories. Increase intakes of vitamins A and C. Discuss relationship of nutrition to immune status. Take prescribed medication at first sign of an outbreak. Acyclovir (Zovirax), famciclovir (Famvir), and antiviral agents such as Valtrex are available; nausea, vomiting, or headaches may occur. If interferon is used, gastrointestinal (GI) distress, stomatitis, nausea and vomiting, abdominal pain, and diarrhea may be side effects. A herpes vaccine is being tested.

Herpes zoster (shingles), Level 1 Herpes zoster is an acute viral infection with vesicles, usually confined to a specific nerve tract, and neuralgic pain in the area of the affected nerve. It is a reactivation of the Varicella virus (chicken pox); severity correlates with age. Symptoms include pain along the affected nerve tract, fever, malaise, anorexia, and enlarged lymph nodes. Bacterial infection of the lesions, poor nutritional status, and risk of dehydration may occur if rehabilitation requires a long period. There is a comprehensive, sensitive assay that detects simultaneous HSV-1, HSV-2, varicella-zoster virus, human cytomegalovirus, and Epstein–Barr virus (EBV). The Zostavax vaccine is effective.

Facial nerves may be affected; alter diet as needed. Prevent further systemic infection; reduce fever. Correct or prevent malnutrition, constipation, and encephalitis. Hydrate adequately. Prevent or correct unplanned weight loss. Prevent or reduce severity of postherpetic neuralgia, which is a very painful complication. A balanced diet with frequent, small feedings may be needed. Increased fiber may be useful to correct constipation. Adequate vitamins E and B12 have been suggested for postherpetic neuralgia. Use adequate vitamins A and C. Acyclovir or famciclovir may shorten the duration and decrease pain. Monitor for GI distress, nausea and vomiting, or diarrhea. Valacyclovir is effective at facilitating healing lesions, reducing pain and postherpetic neuralgia. Narcotics and analgesics are needed to reduce pain. Capsaicin cream from hot peppers has proven to be useful for pain relief. Injecting lidocaine and prednisone directly into spinal column for pain relief of postshingles neuralgia has been tested. Oral prednisone may be used; alter sodium intake and monitor for glucose intolerance.

Infection, Levels 1–2 Infection results from successful invasion, establishment, and growth of microorganisms in a host. Responses involve general and antigen-specific immunological defense systems. In infectious processes, vitamin A is excreted in large amounts from the urine. Correct iron-deficiency anemia, but do not use excesses as microbes depend on iron for growth and proliferation. Iron is mostly protein bound as transferrin. Avoid parenteral or intravenous iron and zinc until fever is resolved.

Provide adequate nourishment to counteract hypermetabolic state. Support body’s host defense system. Prevent or correct dehydration, hypoglycemia, complications, and anorexia. Replace nutrient losses (potassium, nitrogen, magnesium, phosphorus, and sulfur). Discuss role of nutrients in maintaining skin and mucous membrane integrity and preventing bacterial invasion and subsequent infections. Use a high-protein, high-calorie diet, rich in vitamins, minerals, and fluids. Needs increase up to 20% in mild infection, 20–40% in moderate, or 40–60% in septic conditions. Administration of antibiotics with or without food is specific to the type of drug used. Avoid caffeine, sodas, and fruit juices when taking penicillins. For tetracycline, avoid milk and dairy products 2 hours before and after taking drug. With amoxicillin (Augmentin), diarrhea, nausea, and vomiting may occur. Cephalosporins (e.g., Ceclor, Cephalexin, Duricef) may cause diarrhea, nausea and vomiting, sore mouth, hypokalemia, and vitamin K deficiency. Griseofulvin for fungal infections should be taken with a high-fat meal; dry mouth, nausea, and diarrhea are common effects. Ketoconazole (Nizoral) is used in fungal infections and should be taken with an acidic liquid such as orange juice; avoid taking ketoconazole within 2 hours of use of calcium or magnesium. Metronidazole (Flagyl) may cause nausea and vomiting, diarrhea, and anorexia; avoid alcoholic beverages.

Influenza (flu) and the common cold, Level 1 The common cold and influenza are the most common syndromes of infection in human beings. Influenza virus is transmitted by respiratory route, generally in the fall and winter months. Incubation is 1–4 days, with abrupt onset. Signs and symptoms include chills, fever for 3–5 days, malaise lasting 2–3 weeks, muscular aching, substernal soreness, nasal stuffiness, sore throat, some nausea, nonproductive cough, and headache. Annual vaccinations are suggested for high-risk populations, including elderly individuals and those individuals with pulmonary diseases. Low humidity, cold weather, or psychological stress may increase susceptibility. Adequate rest and hydration are essential. Discuss infection control.

Reduce fever and relieve symptoms. Chicken soup is actually useful by providing potassium and sodium, as well as fluid; it increases mucus flow. Prevent complications such as Reye syndrome, secondary bacterial infections (especially pneumonia), otitis media, and bronchitis. Promote bed rest, adequate hydration, and calorie intake. Replace fluid and electrolyte losses. Increase fluids from salty broths, juices, and other fluids. A high-energy and protein intake should be encouraged. Small meals and snacks may be better tolerated than three large meals. Adequate vitamins A and C, sodium, and potassium should be considered. Adequate zinc and low zinc status may be a risk factor for pneumonia in the elderly Barnett et al, 2010). Antibiotics may be needed if secondary bacterial infections occur; monitor for proper timing of administration with food and beverages. Amantadine or rimantadine may be helpful, especially in type A flu. Nausea, dry mouth, and constipation may occur. Avoid use of aspirin in children. (continued)

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TABLE 15-5 Infections and Febrile Conditions and Nutritional Implications (continued) Condition, Nutritional Acuity, Background

Nutritional Implications

Meningitis, Level 1 Infection of the meninges causes inflammatory reactions, usually in the pia mater or arachnoid membranes. The condition may be viral or bacterial. Bacterial forms are more likely to be fatal if left untreated. Bacterial forms include Listeria monocytogenes, Neisseria meningitidis, Haemophilus influenzae, or Streptococcus pneumoniae. Meningitis can be caused by lung or ear infections or by a skull fracture. Symptoms and signs include headache, neck rigidity, fever, tachycardia, tachypnea, nausea and/or vomiting, disorientation, diplopia, altered consciousness, photophobia, petechial rash, irritability, malaise, seizure activity, and dehydration. Spinal tap or lumbar puncture is needed to assess cerebrospinal fluid. Meningitis could lead to septic shock, respiratory failure, or death. It most commonly affects children aged 1 month–2 years. Chronic meningitis can affect people with cancer or HIV/AIDS.

Prevent or correct weight loss. Force fluids but do not overhydrate, especially if there is cerebral edema. Prevent or correct constipation, fever, and other symptoms. Maintain intravenous feedings as appropriate; prevent overhydration. Progress diet, as possible, to high-calorie, high-protein intake. Unless contraindicated, provide 2–3 L of fluid. Adequate fiber will be beneficial to correct or prevent constipation. Gradually return to normal caloric intake for age. Ensure adequate intake of vitamins A and C from fruits, juices, and vegetables. In the long term, control obesity. Antibiotics (penicillin, ampicillin, and cephalosporin) may be used in bacterial forms or to prevent complications in viral forms; nausea, vomiting, and diarrhea can result. If corticosteroids are used, side effects may include nitrogen and calcium losses and sodium retention.

Mononucleosis, Level 1 Infectious mononucleosis is an acute disease caused by EBV; it causes gland swellings in the neck and elsewhere (“glandular fever”). It causes fatigue, malaise, headache, chills, and other symptoms such as sore throat, fever, abdominal pain, jaundice, stiff neck, chest pain, breathing difficulty, cough, and hepatitis. Incubation is 5–15 days. It is most common in those between ages 10 and 35 years. Lab work may include evaluation of increased cerebrospinal fluid pressure, EBV titer, uric acid, and liver enzymes. It is also useful to evaluate a serum agglutination test.

Use a high-protein, high-calorie diet. Use liquids when swallowing solid foods is difficult. Use small, frequent feedings to improve overall nutritional quality and quantity. Ensure adequate intakes of vitamins A and C, especially from fruits and vegetables. Modify food textures when swallowing is difficult. Emphasize importance of exercise in restoring lean body mass. Restore fluid balance. Replenish glucose stores. Spare protein. Restore lost weight. Reduce fever. Prevent complications such as myocarditis, hepatitis, and encephalitis. Acyclovir (Zovirax) may be useful in initial infection, preventing typical persistence; nausea, anorexia, and vomiting may occur. Other antibiotics may be needed for related infections.

Pelvic inflammatory disease (PID), Level 1 PID involves inflammation of the pelvic cavity, affecting the fallopian tubes (salpingitis) and ovaries (oophoritis) with acute pelvic and abdominal pain, low back pain, fever, purulent vaginal discharge, nausea and vomiting, urinary tract infection (UTI), diarrhea, maceration of the vulva, and leukocytosis. Long-term sequelae may include tubal infertility or chronic pelvic pain.

Promote good nutritional status to maintain weight and immunity. Increase hydration as tolerated. Lessen diarrhea, nausea, and vomiting. If nausea or vomiting is extensive, discuss need for small meals and consumption of fluids separately from meals. Provide diet as tolerated with small, frequent feedings until nausea and vomiting subside. Alter fiber and fluid, as needed. Increase energy and protein if needed to improve patient’s nutritional status. Ensure adequate intake of all vitamins and minerals, especially vitamins A and C. Antibiotics may be used; quinolones, cephalosporins, metronidazole, and doxycycline may be prescribed. Analgesics are generally used to reduce pain; chronic use may cause GI distress.

Poliomyelitis, Level 1 A highly contagious enterovirus, poliomyelitis attacks the motor neurons of the brain stem and spinal cord; it may or may not cause paralysis. Polio is transmitted by personal contact, by eating contaminated food, or by drinking contaminated fluids. Polio is rare in areas where the vaccine is available, but there are risks in areas where the vaccine is not administered to all members of the population. Extra immunization may be needed for persons traveling to tropical areas. Symptoms and signs include headache, sore throat, fever, and neck and back pain. For breathing problems, a ventilator may be needed. Postpolio syndrome produces neuromuscular symptoms 25–30 years after attack; serious swallowing difficulties can ensue. Beware of possible choking or aspiration in the bulbar type of paralysis; patient may be unable to swallow. Provide adequate nourishment. Correct electrolyte imbalances.

For patient with acute paralysis, use a high-protein, high-calorie diet in liquid form. Use intravenous feeding and tube feeding when needed. Use vitamin supplements with 1–2 times the DRI; extra calcium and potassium may be needed to replace losses. As the treatment progresses, diet may be changed from a liquid to a solid diet as tolerated. A dysphagia diet may be useful, with varying levels of thickened liquids to enhance swallowing. Wean to oral diet as intake increases. Frequent high nutrient–density snacks are recommended. Instruct patient regarding how to puree or blend foods as needed, including how to add thickeners to liquids. Discuss appropriate recipes for high-energy and high-protein foods. Prevent complications of prolonged immobilization: renal stones, pressure ulcers, and negative N balance. Current antiviral drugs do not work; polio has no cure.


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TABLE 15-5

Infections and Febrile Conditions and Nutritional Implications (continued)

Condition, Nutritional Acuity, Background

Nutritional Implications

Rheumatic fever, Level 1 Rheumatic fever is an inflammatory condition affecting the connective tissues that causes joint pain, swelling, fever, rash, jerky movements (Sydenham chorea), facial grimacing, and carditis. It usually ensues 3 weeks after streptococcal infection. Lab work includes testing for serum antibodies to streptococci; albumin, transthyretin, and cholesterol may be decreased; erythrocyte sedimentation rate and white blood cell (WBC) level may be increased. Heart inflammation usually disappears but may cause permanent damage to the valves (especially the mitral valve), with a resulting heart murmur. Long-term effects are called rheumatic heart disease.

Use a full-liquid diet for acute rheumatic fever. As treatment progresses, gradually change diet, first to a soft diet, then to a regular diet. Restrict sodium intake if edema is present or if steroids are used. Increase intake of vitamin C, protein, and calories. Include adequate vitamin A as well. Reduce inflammation in joints and heart. Decrease physical activity and encourage rest while heart is inflamed. Recover lost weight. Reduce fluid retention, if present. Cure the infection and prevent its recurrence. Prevent complications such as bacterial endocarditis, atrial fibrillation, and heart failure. Explain increased need for calories and protein. Adequate rest, exercise, and nutrition are essential to prevent recurrence. Explain increased need for calories and protein. Adequate rest, exercise, and nutrition are essential to prevent recurrence. Restrict sodium if prednisone or adrenocorticotropic hormone is given for severe heart inflammation. Side effects include depletion of nitrogen, calcium, potassium, and hyperglycemia. Antibiotics are used. Monitor for specific side effects such as GI distress. Penicillin may be needed for 10 days. Lifelong use of antibiotics before surgery and dental work protects against bacterial invasion of heart valves. Aspirin or nonsteroidal anti-inflammatory drugs may be used to reduce joint pain and inflammation.

Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (MRSA) infection, Level 1 Staphylococcus aureus is a gram-positive bacterium that developed resistance to the penicillin-derivative methicillin. MRSA emerged as a bacterium that became less susceptible to the actions of methicillin and thus developed the ability to colonize and cause life-threatening infections. S. aureus and MRSA population estimates are in the millions of persons.

MRSA colonization should be contained by infection control measures and not treated. Hand-washing technique is very important. The most potent anti-MRSA drug at the present time is daptomycin, especially to treat endocarditis.

Toxic shock syndrome (TSS), Level 1 TSS is an acute bacterial infection caused by S. aureus and most often is associated with prolonged use of tampons during menses. Symptoms include sudden onset of high fever, severe headache, red eyes, myalgia, vomiting, watery diarrhea, red rash on palms and soles (with desquamation), decreased circulation to fingers and toes, disorientation, peripheral edema, pulmonary edema, respiratory distress syndrome, and sudden hypotension progressing to shock. Anemia, kidney, liver, and muscle damage; septic shock; respiratory distress can occur. Monitor labs for increased levels of WBC, blood urea nitrogen, creatinine, bilirubin, liver enzymes, and creatine phosphokinase. Platelets may be decreased.

Increase fluid intake to 3 L daily, unless contraindicated. Discuss need for adequate fluid intake and small meals, especially with vomiting or nausea. Control diarrhea and vomiting. Improve well-being. Stabilize hydration and electrolyte balance. Prevent renal, heart, and lung problems and other complications. Antibiotics are required. Monitor for GI side effects. Determine how to administer specific drugs (such as with food, water, or milk).

Typhoid (enteric) fever, Level 2 Enteric fever includes typhoid and paratyphoid fever. It is a systemic infection caused by Salmonella enterica, and it is most common among travelers. This infectious fever is spread by contamination of food, water, or milk with S. typhi or paratyphi, which can come from sewage, flies, or faulty personal hygiene. The problem practically has been eradicated in areas of proper sanitary practices. Most infections are found in people who are in contact with carriers who have persistent gallbladder or UTIs. Incubation is 5–14 days. Symptoms include malaise, headache, cough, sore throat, “pea soup” diarrhea, constipation, rose spots, and splenomegaly. Lab work includes stool and urine for Widal test.

Reduce fever and prevent irritation. Replace nutrient losses from diarrhea. Replace tissue losses. Prevent complications such as intestinal hemorrhage or shock and pulmonary or cardiac side effects. Gradually add pectin and other fiber. Especially, include good dietary sources of vitamins A and C. Explain which foods are highprotein, high-calorie sources. Discuss how to prevent future reinfection. For patients with acute fever, use a diet of high-protein, high-calorie liquids. A lowresidue diet may be needed temporarily. As treatment progresses, gradually add soft, bland foods. Try small, frequent feedings. First-line therapy is ceftriaxone, and fluoroquinolones can also be given. Monitor for GI distress. Preventive measures include educating travelers about hygiene precautions and vaccinations.

REFERENCE Barnett JB, et al. Low zinc status: a new risk factor for pneumonia in the elderly? Nutr Rev. 68:30, 2010.

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TABLE 15-6 Virulence Increased by Iron To successfully sustain an infection, nearly all bacteria, fungi, and protozoa require a continuous supply of host iron. Iron is a cofactor in oxidation– reduction reactions. Iron deficiency has opposing effects on infectious disease risk, decreasing susceptibility by restricting iron availability to pathogens, and increasing susceptibility by compromising cellular immunocompetence (Wander et al, 2009). Studies suggest that moderate iron deficiency protects against acute infection and may represent a nutritional adaptation to endemic infectious disease stress (Wander et al, 2009). Zinc and manganese may also play a role in host defense mechanisms. Acid-fast and gram-positive bacteria

Bacillus, Clostridium, Listeria, Mycobacterium, Staphylococcus, Streptococcus


Candida, Cryptococcus, Histoplasma, Mucor, Pneumocystis, Rhizopus

Gram-negative bacteria

Campylobacter, Chlamydia, Escherichia, Klebsiella, Legionella, Proteus, Pseudomonas, Salmonella, Shigella, Vibrio, Yersinia


Entamoeba, Leishmania, Plasmodium, Toxoplasma, Trypanosoma

REFERENCES Robien M. Iron and microbial infection. Support Line. 22:23, 2000. Wander K, et al. Evaluation of iron deficiency as a nutritional adaptation to infectious disease: an evolutionary medicine perspective. Am J Hum Biol. 21:172, 2009.

CITED REFERENCES Brugler L, et al. A simplified nutrition screen for hospitalized patients using readily available laboratory and patient information. Nutrition. 21:650, 2005. Cunningham-Rundles S, et al. Mechanisms of nutrient modulation of the immune response. J Allergy Clin Immunol. 115:1119, 2005.

Elenkov IJ, et al. Cytokine dysregulation, inflammation and well-being. Neuroimmunomodulation. 12:255, 2005. Fernandes G. Progress in nutritional immunology. Immunol Res. 40:244, 2008. Wintergerst ES, et al. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 51:301, 2007.


GP120 GP41


P 24

Reverse transcriptase

Adapted from: Porth CM. Pathophysiology: Concepts of altered health states, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 1998.

DEFINITIONS AND BACKGROUND The human immunodeficiency virus (HIV) infects T cells (CD4) and macrophages. Levels of CD41 (helper) and CD81 (nonhelper) subsets of T cells are used to evaluate immunological competency. After levels have been identi-

fied, staging is identified to plan therapeutic interventions; see Table 15-7. Many people will develop acquired immunodeficiency syndrome (AIDS) after a decade, following an opportunistic infection or a decline in the immune system. Prognosis for AIDS ranges from 1 year, if not treated with antiretroviral therapy (ART), to 5 years, if treated. HIV is not easily transmitted except by exchange of bodily fluids during sexual contact, by receipt of infected blood through a blood transfusion, by sharing contaminated needles with intravenous drug injection, or from an HIVinfected mother to neonate (children represent 15–20% of the affected population). Persons at high risk include homosexual and bisexual males, hemophiliacs, intravenous drug addicts, heterosexuals with multiple partners, and infants of HIV-positive mothers. Breastfeeding by HIVinfected mothers can result in HIV transmission to the infant, especially with mastitis. In some developing countries, the relative risk of HIV transmission may be less significant than malnutrition for the infant; risks and benefits must be weighed individually. HIV infection involves multiple organs. It targets the immune system and impairs the ability to mount an adequate immune response. Malnutrition and its complications further impair the body; HIV often depletes nutritional status (Sztam et al, 2010). Immune reconstitution inflammatory syndrome develops in a substantial percentage of HIV-infected patients who have an underlying opportunistic infection and receive ART (Danaher et al, 2010). AIDSrelated malignancies are another major complication.

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TABLE 15-7

WHO Clinical Staging of HIV/AIDS for Adults and Adolescents

Clinical stage 1—Asymptomatic

Clinical stage 4—Clinical signs

Acute retroviral syndrome

Chronic herpes simplex infection (orolabial, genital, or anorectal 1 month)

Persistent generalized lymphadenopathy

Central nervous system toxoplasmosis

Clinical stage 2

Esophageal candidiasis

Angular cheilitis

Extrapulmonary TB

Fungal nail infections of fingers

HIV encephalopathy

Herpes zoster

HIV wasting syndrome

Moderate unexplained weight loss (10% of body weight)

Kaposi sarcoma

Papular pruritic eruptions

Pneumocystis pneumonia

Recurrent oral ulcerations

Recurrent severe or radiological bacterial pneumonia

Recurrent respiratory infections (sinusitis, bronchitis, otitis media, pharyngitis)

Diagnostic testing needed for:

Seborrheic dermatitis


Clinical stage 3—Clinical signs Acute necrotizing ulcerative stomatitis, gingivitis, or periodontitis

Cytomegalovirus infection (retinitis or of an organ other than liver, spleen, or lymph nodes)

Oral candidiasis

Disseminated mycosis (e.g., histoplasmosis, coccidiomycosis, penicilliosis)

Oral hairy leukoplakia

Disseminated non–tuberculous mycobacteria infection

Pulmonary tuberculosis (TB) diagnosed in last 2 years

Extrapulmonary cryptococcosis including meningitis

Severe infections (e.g., pneumonia, empyema, pyomyositis, bone/joint infection, meningitis, bacteremia)

Invasive cervical carcinoma

Severe weight loss (10% of body weight)

Lymphoma (cerebral or B-cell non-Hodgkin)

Unexplained chronic diarrhea 1 month

Progressive multifocal leukoencephalopathy

Unexplained persistent fever 1 month

Recurrent non-typhoidal salmonella septicemia

Diagnostic test needed for: anemia (8 g/dL), neutropenia (500/mm3), or thrombocytopenia (50,000/mm3)  1 month

Visceral herpes simplex infection

Kaposi sarcoma and Hodgkin and non-Hodgkin lymphomas are the most common malignancies (Wood and Harrington, 2005). HIV infections are considered pandemic, and AIDS has killed more than 25 million people, especially in the subSahara. Worldwide, hepatitis B virus affects 370 million people, hepatitis C virus (HCV) affects 130 million, and HIV affects 40 million (Alter, 2006). Fortunately, ART has reduced mother-to-child transmission rates. HIV infection requires lifelong, vigilant polypharmacy. Nutrition directly impacts immune-cell triggering and indirectly impacts DNA and protein synthesis in HIV progression. Decline in body cell mass and deficiencies in vitamins and minerals occur; some clinicians recommend a series of antioxidant supplements to augment cellular immunity. Because of the crucial role that nutrition plays throughout the course of HIV, medical nutrition therapy (MNT) is an integral part of disease management. During starvation, there is generally a loss of adipose tissue with maintenance of lean body mass (LBM); in HIV/AIDS, there is loss of LBM (wasting) while maintaining body fat. Wasting syndrome is defined by the World Health Organization as the involuntary loss of at least 10% of body weight and is a common AIDS-defining diagnosis. Weight loss is an independent prognostic indicator of outcomes, including mortality. Weight loss, fatigue, anorexia, diarrhea, and low-grade fevers may occur. As long as an infection

remains untreated, nutritional support regimens will meet needs with only limited success. Body composition measures should be accurate, ideally taken prior to the initiation of ART. Bioelectrical impedance analysis is useful, whereas skinfold measurements tend to overestimate fat-free mass and underestimate fat mass. Fat redistribution is part of a syndrome known as peripheral lipodystrophy in patients receiving ART; they lose facial and extremity fat with redeposition into visceral and truncal adiposity. Abnormal fatty deposits are disfiguring and are found in the neck and dorsocervical area (“buffalo hump”). These changes can be accompanied by development of hyperlipidemia or diabetes. Gastrointestinal (GI) complications are common. Weight loss is often multifactorial in etiology, and reduced oral intake is common. Malnutrition further compromises those who have tuberculosis (TB) or persistent diarrhea (Wanke, 2005). Nutritional supplements, dietary counseling, and use of specific nutrients such as vitamin D3, are critically important (Villamor, 2006). While central parenteral nutrition (CPN) is often indicated with HIV patients experiencing severe GI dysfunction, there is a concern over infection with the use of central venous catheters in patients with advanced HIV/AIDS. Medication interactions, coinfection with other infections and diseases, wasting, lipodystrophy, and other issues make individualized nutrition care plans extremely important

Candida of trachea, bronchi or lungs


Visceral leishmaniasis

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TABLE 15-8 Guidelines for Nutrition Therapy in HIV Management I. High risk (see RD within 1 week)

F. Hypertension

A. Poorly controlled diabetes mellitus

G. Evidence for hypervitaminoses or excessive supplement intake

B. Pregnancy (mother’s nutrition; infant: artificial infant formula)

H. Inappropriate use of diet pills, laxatives, or other over-the-counter medications

C. Poor growth, lack of weight gain, or failure to thrive in pediatric patients

I. Substance abuse in the recovery phase

D. 110% unintentional weight loss over 4–6 months

J. Possible food—drug–nutrient interactions

E. 15% unintentional weight loss within 4 weeks or in conjunction with the following:

K. Food allergies and intolerance L. Single medical comorbidity

1. Chronic oral (or esophageal) thrush

M. Oral thrush

2. Dental problems

N. Dental problems

3. Dysphagia

O. Chronic nausea or vomiting

4. Chronic nausea or vomiting

P. Chronic diarrhea

5. Chronic diarrhea

Q. CNS disease resulting in a decrease in functional capacity

6. Central nervous system (CNS) disease

R. Chronic pain other than oral/gastrointestinal tract source

7. Intercurrent illness or active opportunistic infection

S. Eating disorder

F. Severe dysphagia G. Enteral or parenteral feedings H. Two or more medical comorbidities, or dialysis

T. Evidence for sedentary lifestyle or excessive exercise regimen U. Unstable psychosocial situation (especially in children) III. Low risk (see RD as needed)

I. Complicated food–drug–nutrient interactions

A. Stable weight

J. Severely dysfunctional psychosocial situation (especially in children)

B. Appropriate weight gain, growth, and weight-for-height in pediatric patients

II. Moderate risk (see RD within 1 month)

C. Adequate and balanced diet

A. Obesity

D. Normal levels of cholesterol, triglycerides, albumin, and glucose

B. Evidence for body fat redistribution

E. Stable HIV disease (with no active intercurrent infections)

C. Elevated cholesterol (1200 mg/dL) or triglycerides (1250 mg/dL) levels, or cholesterol level 100 mg/dL

F. Regular exercise regimen

D. Osteoporosis E. Diabetes mellitus, controlled or new diagnosis

G. Normal hepatic and renal function H. Psychosocial issues stable (especially in children)

Source: Hayes C et al. Integrating nutrition therapy into medical management of human immunodeficiency virus. Web site accessed February 5, 2010, at

(American Dietetic Association, 2010). Although the incidence of most AIDS-defining opportunistic infections, including HIV wasting syndrome, has dramatically decreased since the introduction of ART, weight loss and wasting are still common in HIV-infected persons who use injected drugs; live below the federal poverty level; have a lower CD4 cell count or higher HIV viral load; or have diarrhea, nausea, or fever (Tang et al, 2005). Work on an HIV vaccine is important. The International AIDS Vaccine Initiative has established a consortium to elucidate mechanisms of protection from such a vaccine (Koff et al, 2006). In addition, a new, inactivated mycobacterial vaccine may significantly reduce TB cases among HIV-positive individuals. MNT for HIV/AIDS patients can reduce illness, hospital stays, and related medical costs. MNT helps the patient have an improved quality of life along with better CD4 counts and weight gain (American Dietetic Association, 2010). See Table 15-8 for guidelines on risk levels. The American Dietetic Association has recommended three MNT visits per year for adults with stage 1 HIV/AIDS; three to six visits per year for adults with stage 2 or 3 HIV/AIDS; and a minimum of five

visits per year for children or adolescents with HIV/AIDS. Through the Ryan White Comprehensive AIDS Resources Emergency (CARE) Act, treatment is available even when other funds have been depleted.


CLINICAL INDICATORS Genetic Markers: HIV-1 has a minimal genome of only nine genes, which encode 15 proteins; the virus depends on the human host for every aspect of its life cycle (Balakrishnan et al, 2009). Polymorphisms cause the 15% of variation in viral load between individuals during the asymptomatic phase of infection. Alleles of the HLA-B5701 gene and the HLA-C gene are affected.

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Opportunistic infections Height (in AIDS) Pre-illness Stool tests for weight malabsorption Current weight Biopsies (lymph Waist to hip nodes, skin ratio lesions) Body mass index Dual-energy (BMI) x-ray absorpSkinfolds; tiometry scan fat-free mass Bioelectrical (low?) impedance Blood pressure analysis (BP) Intake and outLab Work put (I & O) Complete blood Weight count with changes differential Swollen lymph Platelets nodes Cholesterol Rash (Chol) Sore throat, Triglycerides headache (Trig) Night sweats (increased) Dyspnea on Glucose (Gluc) exertion, CD4 rales, or lymphocytes rhonchi (active AIDS, Nausea, 200 T cells) vomiting CD8 Anorexia lymphocytes Temperature (fever, chills) TLC Viral load Dysphagia, Polymerase chewing chain problems reaction for Stomatitis herpes virus Diarrhea Cyanosis, pneu- P24 antigen Albumin monia (Alb) or Frequent viral transthyretin or herpes (decreased) infections Clinical/History

C-reactive protein (CRP) Prealbumin:CRP ratio Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Bilirubin Prothrombin time (PT), international normalized ratio Hemoglobin and hematocrit (H & H) (decreased?) Ferritin (increased?) Creatine (Creat), blood urea nitrogen (BUN) Transferrin Lactose test Serum B12 and folate (decreased?) Schilling test Serum vitamin A Serum testosterone

INTERVENTION OBJECTIVES • Improve nutrition-related immunity to prevent opportunistic infections, such as oral candidiasis; cirrhosis or hepatocellular carcinoma from chronic infection with hepatitis B or C; and other conditions such as immune reconstitution inflammatory syndrome. • Enhance response to therapy through continuous counseling, nutritional alterations, and drug effectiveness monitoring. Follow guidelines according to levels of risk (see Table 15-8). • Use 3-day food records rather than food frequencies (American Dietetic Association, 2010).

SAMPLE NUTRITION CARE PROCESS STEPS Increased Nutrient Needs Assessment Data: Three-day food records. Input and output, weight loss, and medication records. Diagnosis of AIDS 3 years ago. Complaints of GI distress after meals. Nutrition Diagnosis (PES): NI 5.1 Increased nutrient needs related to unintentional weight loss of 21% in 5 months as evidenced by weight only 80% of desirable BMI range. Interventions: Food-Nutrient Delivery. ND 1.3 Specific foods (yogurt) 2 times daily. ND 3.1.1 Commercial beverage 3 times daily. Education: E 1.1 Purpose of nutrition education: to explain importance of adequate nutrient intake and compliance with all medical/ nutritional/emotional care. Counseling: C2.2 Goal setting—Gain 1–1⁄2 lb per week until ideal body weight (IBW) range is reached. Coordination of Care: RC 1.1 Team meeting—Discuss interventions with interdisciplinary team. Monitoring and Evaluation: Weight records, fewer reports of GI distress and symptoms. Greatly improved intake on 3-day food records.

• Maintain body weight at 95–100% of usual body weight levels. LBM is especially affected; increased resting energy expenditure occurs (American Dietetic Association, 2010). • Prevent weight loss from fever, poor intake with oral pain, infection, nausea, diarrhea, malabsorption, swallowing difficulties, effects of medications, inflammation, viral load, and lipodystrophy, and vomiting; offer early nutritional intervention (American Dietetic Association, 2010). • Reduce mealtime fatigue to encourage better intake. Avoid unnecessary distractions and stresses. • Lower the temperature when febrile. • Manage altered GI function including diarrhea, malabsorption, vomiting, and HIV-induced enteropathy. • If necessary, use CPN to prevent further weight loss and potential malnutrition. CPN will stop weight loss, but it will not prevent further immunodeficiency. • Keep body well hydrated. Fluids are critical to prevent kidney stones and other complications. • Support depleted levels of nutrients such as linoleic acid, selenium, and vitamin B12. • Counteract problems such as dysphagia, mouth pain, taste alterations (dysgeusia), or difficulty chewing. Alleviate nutritional effect of fatigue, anemia, anorexia, depression, and dyspnea. Optimize nutritional status. • Maintain fat intake at prudent levels (30–35% total kcal) to maintain or achieve normal lipid levels. • Alter dietary regimen if there is renal or hepatic impairment. • Maintain honest discussions regarding use of alternative therapies such as herbs, special diets, and megavitamin therapy.

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• Encourage physical activity, which has been shown to improve cardiopulmonary fitness and to reduce symptoms of depression (American Dietetic Association, 2010). • Comply with food and water safety guidelines.

FOOD AND NUTRITION • Maintain diet as appropriate for patient’s condition; use a high-energy/high-protein diet with adequate nutritional supplements. Weight gain or maintenance is possible in patients with HIV infection and early stages of AIDS by use of oral liquid supplements. • From 2–2.5 g protein/kg and 35–45 kcal/kg are needed. Fever and infection may further elevate need for these nutrients. Increase energy intake in cases of infection, fever, and pneumonia. Use indirect calorimetry when available; estimates are often incorrect (Frankenfield et al, 2005). • Keep the body well hydrated. Estimate 35–40 cc/kg unless there is a reason to restrict fluids. • Use TF, especially gastrostomy, if warranted. Low-lactose/ low-fat TF products may need to be fed continuously to reduce gastroenteritis or reflux. CPN may be necessary if weight loss exceeds 20% of usual body weight. • Increase use of omega-3 fatty acids and decrease saturated fat intake. There may be advantages to using a medium-chain triglyceride formula in the presence of AIDS-associated malabsorption (American Dietetic Association, 2010). • Small, frequent feedings (6–9 times daily) are usually better tolerated but may be difficult to achieve given complex medication regimens. • A general multivitamin–mineral supplement should be recommended, not to exceed 100% of the recommended dietary allowances (RDAs). Low serum micronutrient levels are common and have been associated with immune impairment, HIV disease progression, or mortality (Mehta and Fawzi, 2007). Use of vitamin A and beta-carotene may reduce some of the gut permeability and lessen watery diarrhea (American Dietetic Association, 2010). Vitamin K deficiency is common with antibiotic use. • Use nutrient-dense snacks, such as pudding, if tolerated, nonacidic juices for sore mouth, ices made with tolerated juices, and sandwiches made with cold meat salads. Add protein powders and glucose polymers, if desired. Use oral supplements when needed. • With bouts of diarrhea, use small meals and avoid extremes in temperatures; room temperature is often best. Avoid excesses of caffeine, alcohol, and fried and high-fat foods. Use soft cooked chicken, turkey, fish, and lean beef. Replace electrolytes with foods such as broth soups or Gatorade for sodium, potassium, magnesium, and chloride. • If lactose intolerant, avoid milk and use a low-lactose diet. • Sucrose and gluten may not be tolerated. Individualize as needed. • Children present unique nutritional needs, further compounded by HIV infection; see Section 3.


Common Drugs Used and Potential Side Effects (see Table 15-9) • Antiretroviral regimens are complicated and difficult. Because nonalcoholic fatty liver disease is a prominent feature induced by ART, hepatitis A and B virus vaccinations and close monitoring of liver parameters are suggested (Kahraman et al, 2006). Malabsorption can occur if antiretroviral agents are taken improperly with regard to meals or if they are taken with certain other drugs or herbal remedies. Suboptimal use of antiretrovirals because of noncompliance or malabsorption can result in viral resistance. • Recombinant human growth hormone and growth hormone–releasing hormone are options for reducing visceral adipose tissue and coronary heart disease (Cofrancesco et al, 2009).

Herbs, Botanicals, and Supplements • Ethical dilemmas may be presented by CAM use. HIVinfected patients often seek complementary therapies due to unsatisfactory side effects, high cost, nonavailability, or adverse effects of conventional medicines (Liu et al, 2005). • CAM use is nearly 100% in the HIV-infected population, with half reporting daily use of a dietary supplement (especially vitamin C, vitamin E, and soy) as an adjunct to other treatments (Milan et al, 2008). However, there may be risks for herb–drug and herb–nutrient interactions. Many herbals may also interact with prophylactic medicines, such as antibiotics. • Herbs and botanical supplements should not be used without discussing with the physician. Older, collegeeducated, or insured patients are more likely to disclose their CAM use to health care providers, and there is a need to find ways to discuss CAM between more patients and their providers (Liu et al, 2009). • Licorice, capsaicin, astragalus, and burdock are not confirmed; large, rigorous trials are needed (Liu et al, 2005). • Rosemary and marjoram have pentacyclic triterpenoic acids with anti-inflammatory, hepatoprotective, gastroprotective, antiulcer, anti-HIV, cardiovascular, hypolipidemic, antiatherosclerotic, and immunoregulatory effects. There would be no harm in seasoning foods with these herbs. • Echinacea is not recommended as an antiviral agent. Do not use with warfarin or immunosuppressants. • Garlic and St. John’s wort may make saquinavir or indinavir less effective.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the role of nutrition in infection and immunity; patients should also decrease the use of drugs and cigarettes because of their effects on overall health status and immunocompetence. They should avoid sharing razors, toothbrushes, tweezers, nail clippers or piercing jewelry with others.

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TABLE 15-9

Medications Used for HIV Infections and AIDS

Class and Purpose

Generic Name

Brand and Other Names

Nutritional Implications and Comments Can cause severe bone marrow depletion and anemia, altered taste, constipation, nausea, indigestion, or vomiting. Adequate folate and vitamin B12 may prevent toxicity. NRTIs can cause lactic acidosis, hypersensitivity reactions, neuropathies, pancreatitis, anemia, and neutropenia.

Nucleoside reverse transcriptase inhibitors (NRTIs)—faulty versions of building blocks that HIV needs to make more copies of itself; when HIV uses an NRTI instead of a normal building block, reproduction of the virus is stalled Abacavir

Ziagen, ABC

Diarrhea may be a side effect. Malaise, fever, rash, and liver inflammation can occur.

Abacavir, lamivudine


Diarrhea may be a side effect. Malaise, fever, rash, and liver inflammation can occur.

Abacavir, lamivudine, zidovudine


Diarrhea may be a side effect. Malaise, fever, rash, and liver inflammation can occur.


Hepsera, ADV, Preveon

Often used in chronic hepatitis B virus treatments. Has nephrotoxic potential. Nausea, diarrhea, and vomiting can occur.



For the adjunctive treatment of HIV-1 infections.


Videx, ddI Videx EC

May cause liver toxicity in low-weight patients. Neuropathy and pancreatitis may result.


Emtriva, FTC, Coviracil

Well tolerated. Anorexia and fatigue are side effects.

Emtricitabine, tenofovir DF


May cause diarrhea, nausea, and vomiting. Take with food.


Epivir, 3TC

May cause nausea and vomiting, pancreatitis, and depression. Avoid alcohol. Take without regard for meals.

Lamivudine, zidovudine


Headache, liver inflammation, and fatigue can occur. Take with meals.


Zerit, d4 T

Severe anemia may occur. Avoid alcohol.

Tenofovir DF

Viread, TDF

Gastrointestinal (GI) distress, hypophosphatemia, acute renal failure.


Hivid, ddC

Can cause oral ulcers, nausea, vomiting, dry mouth, and neuropathy. Take on empty stomach. Avoid taking with antacids.


Retrovir, AZT, ZDV

Can cause severe bone marrow depletion and anemia, altered taste, constipation, nausea, indigestion, or vomiting. It works better in sequence with acyclovir. Adequate folate and vitamin B12 may prevent toxicity. Take with food.

Nonnucleoside reverse transcriptase inhibitors (NNRTIs)—bind to and disable reverse transcriptase, a protein that HIV needs to make more copies of itself

Nausea, vomiting, and diarrhea are common side effects. Liver inflammation may occur; avoid alcohol and St. John’s wort. NNRTIs can cause rashes and hepatotoxicity. Delavirdine

Rescriptor, DLV

Monitor for abnormal liver enzymes. Headaches are common.

Efavirenz, emtricitabine, and tenofovir DF


Hyperlipidemia can occur. Contains two NRTIs and one NNRTI.


Viramune, NVP

Take with food or on an empty stomach; fever, headache, hepatitis, general fatigue, mouth sores, and rash can occur.

Protease inhibitors (PI)—disable protease, a protein that HIV needs to make more copies of itself

Associated with hyperlipidemia, hyperglycemia, GI symptoms, and body fat distribution abnormalities. Disguising their taste is important; add a small amount to cold foods such as ice cream, shakes, and fruit ices; thick sweet foods such as honey, jellies, and frozen juice; or small amounts of peanut butter, pudding, applesauce, or yogurt. Atazanavir


May cause a tendency to bleed. Take with food.



May cause GI distress.


Lexiva, FPV

May cause a tendency to bleed. Take without regard for meals. (continued)

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TABLE 15-9 Medications Used for HIV Infections and AIDS (continued)

Class and Purpose

Generic Name

Brand and Other Names


Crixivan, IDV

Best absorbed on an empty stomach or with a light, nonfat snack and increased fluids (but not skim milk, coffee, or tea), even juice if calories are needed. Nausea and vomiting, change in taste, and diarrhea can occur.

Lopinavir/ ritonavir

Kaletra, LPV/r

Elevated lipid levels and GI distress may occur. Take with food. Abnormal mouth sensations are noted. Hyperglycemia can occur.


Viracept, NFV

Take with food; flatulence, loose stools, or diarrhea can occur. Hyperglycemia may result.


Norvir, RTV

Take with a high-energy, high-fat meal. Side effects include weakness, diarrhea, nausea and vomiting, loss of appetite, abdominal pain, abnormal mouth sensations of burning or prickling, dyslipidemia, and coronary events.



Best absorbed after a high-energy, high-fat meal; contains some lactose; may cause GI distress, diarrhea, or nausea. May cause GI distress.

Nutritional Implications and Comments



Entry inhibitors: Integrase inhibitors—stop HIV from inserting its own genetic code into the cell by slowing integrase, the chemical HIV needs to unlock the CD4 command center.



Entry inhibitors: Fusion inhibitors—prevent HIV entry into cells.


Fuzeon, T-20

Pneumonia has been one side effect. Take without regard for meals. Nausea, diarrhea, fatigue, and pancreatitis are possible side effects.



May cause GI distress.

Antineoplastic agents—for Kaposi sarcoma

Other medications—to manage other side effects of HIV.

Adriamycin, bleomycin, vincristine

Numerous side effects include nausea and vomiting, diarrhea, anorexia, stomatitis, and weight loss.


Administer with riboflavin to decrease toxicity. Dry mouth, esophagitis, stomatitis, nausea, and vomiting are common.



May cause headache, nausea, anorexia, sore throat, fatigue, altered taste, and diarrhea.


Zoloft, Wellbutrin, others

May be useful before interferon therapy if there is a history of depression.


Amphotericin-B, clotrimazole, flucytosine, ketoconazole

May cause nausea and vomiting, diarrhea, weight loss, metallic taste, and GI distress.


Multivitamin– mineral supplement that meets 100% DRI levels

Antioxidant supplementation may decrease markers of oxidative stress. Selenium may enhance immune function by modulating cytokine production.



A cytosine nucleotide analog for treatment of cytomegalovirus (CMV), herpes simplex, papilloma, and pox viruses.


Prednisone, others

Sodium retention and potassium, calcium, and vitamin C depletion can occur; protein malnutrition can occur with extended use. Glucose intolerance also may result.



Used for CMV retinitis (used intravenously only) and may cause anorexia, nausea and vomiting, abdominal pain, and diarrhea.



Approved for use with CMV. May cause diarrhea, fever, neuropathy, elevated blood urea nitrogen and creatinine levels, and hypoglycemia. (continued)

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TABLE 15-9

Medications Used for HIV Infections and AIDS (continued)

Class and Purpose

Generic Name Pancreatic enzymes

Brand and Other Names

Nutritional Implications and Comments


May be used with malabsorption.

Peginterferon- plus ribavirin

Standard for hepatitis C virus/HIV coinfection. Flu-like symptoms, fatigue, weight loss, and depressive mood changes are frequent.

Topical microbicides

Many microbicides are in development. Alkyl sulfate microbicides, such as sodium dodecyl sulfate agents

Proposed to break the chain of transmission by providing chemical, biological, and physical barriers to infection by blocking or inactivating pathogens at the mucosal surface.

Trimethoprim– sulfamethoxazole

Bactrim, Septra

Used for Pneumocystis carinii pneumonia for 1 month; may cause hepatitis, azotemia, anorexia, stomatitis, and thrombocytopenia. Monitor carefully. Folate may be needed.



Approved for CMV.

Appetite stimulants and anabolic steroids—to improve appetite and intake

Appetite stimulants and anabolic steroids lead to significant increase in body weight and fat-free mass. Dronabinol

Marijuana derivative

Takes 4–6 weeks to show effects; somnolence and impaired memory can occur.

Megestrol acetate


Useful for stimulating appetite.

Anabolic steroids: oxandrolone, nandrolone decanoate


Synthetic testosterone (anabolic steroid) that promotes weight gain, linear growth in children, and increased muscle mass. Hepatic changes or tumors have been reported. Elevation of low-density lipoprotein can occur with prolonged use; this may have cardiovascular effects. Nutritional status and the quality of life can improve.

For more information, see the FDA Web site. Accessed February 6, 2010, at

• Patients and caregivers should report all weight loss, anorexia, and fever to doctor. Even a 5% weight loss in 6 months markedly increases the risk of death (Tang et al, 2005). • Diet must be altered whenever necessary. Evaluation of nutrition assessment parameters on a regular basis requires a comprehensive process. Continuing contact with a dietitian is essential regarding alternative feeding methods, changes in medications, need for home-delivered meals, simplified menu planning, and treatment of GI side effects. • Aversion to meat may be countered by use of cold protein foods such as cottage cheese, yogurt, skim milk, and cheeses. • Education should address any decline in self-care abilities, as well as alternative therapies and consequences. • Address the consequences of protease-inhibiting therapy, such as hyperlipidemia. Studies show that managing fat, alcohol, and fiber intakes and increasing exercise can be very beneficial (American Dietetic Association, 2010). • Resistance and strengthening exercises should be maintained. Twenty minutes three times weekly is quite effective (American Dietetic Association, 2010; Cade et al, 2007).

• New mothers who are HIV positive will want to use formula or milk from a surrogate mother instead of breastfeeding. • In the short term, nutrition counseling and oral supplements can achieve a substantial increase in energy intake. Importance of maintaining a balanced, nutritious diet should be addressed. Dietary patterns in HIV-positive individuals may be reflected in changes in BMI, CD4 counts, and viral load (Hendricks et al, 2008). Rest periods before and after meals are suggested. • Patients are living longer because of ART therapy, and they may be susceptible to other age-related diseases (Gerrior and Neff, 2005). They should receive appropriate nutrition counseling to meet their individual needs. A new standard of care is also needed where malnourished patients may easily access nutritional therapies within HIV treatment (Sztam et al, 2010). • Patients should be screened and treated for depression (Kacanek et al, 2010). • Use of stress management and coping mechanisms will be important to maintain nutritional health (Tromble-Hoke et al, 2005). Massage therapy may also be beneficial. • In home care, continuing education should be offered to caregivers to prevent transmission of the disease and to reduce other infections.

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Patient Education—Food Safety

• Educate about food safety issues. Studies show that education helps to reduce the instances of foodborne illness in this vulnerable population (American Dietetic Association, 2010). • Reducing infections is very important. Meticulous hand washing is essential because immune-compromised individuals are more susceptible to foodborne illness. Preparation and home delivery methods must also be scrupulously clean (American Dietetic Association, 2010). • Tips include the following: • Separate raw meats from other raw foods such as fruits and vegetables. • Avoid cross-contamination from raw meats by storing and preparing raw meat so it does not come in contact with fruits, vegetables, and uncooked foods. • Use separate cutting boards and cooking utensils so that juices from raw meats are not allowed to contact uncooked foods. • Keep hot foods hot (140F) and cold foods cold (40F). Limit the amount of time that food is left at room temperature to prevent germs from growing in it. • Wash all fruits and vegetables with warm water and a soft bristle brush. • Thaw frozen meat or poultry in a refrigerator or under cold running water, not at room temperature. • Avoid raw fish or shellfish, unpasteurized juices or milk, and uncooked eggs (and dishes containing uncooked eggs). • Exceptional hand-washing techniques should be used by all caregivers and by patient. Safe food-handling techniques are imperative to reduce exposure to Cryptosporidia, Giardia, and Salmonella.

International AIDS Vaccine Initiative

National AIDS Information Clearinghouse (NAIC)

For More Information •

AEGIS (AIDS Education Global Information System)

AIDS Clinical Guidelines


American Foundation for AIDS Research

Body: An AIDS and HIV Information Resource

HIV InSite


AIDS AND HIV INFECTION—CITED REFERENCES Alter MJ. Epidemiology of viral hepatitis and HIV co-infection: epidemiology of viral hepatitis and HIV co-infection. J Hepatol. 44:S6, 2006. American Dietetic Association. Evidence Analysis Library: HIV infection. Web site accessed February 5, 2010 at topic.cfm?cat1404. Balakrishnan S, et al. Alternative paths in HIV-1 targeted human signal transduction pathways. BMC Genomics. 10:30S, 2009. Cade WT, et al. Blunted lipolysis and fatty acid oxidation during moderate exercise in HIV-infected subjects taking HAART. Am J Physiol Endocrinol Metab. 292:E812, 2007. Cofrancesco J Jr, et al. Treatment options for HIV-associated central fat accumulation. AIDS Patient Care STDS. 23:5, 2009. Danaher RJ, et al. inflammatory syndrome? HIV protease inhibitors alter innate immune response signaling to double-stranded RNA in oral epithelial cells: implications for immune reconstitution. AIDS. 24:2587, 2010. Frankenfield D, et al. Comparison of predictive equations for resting metabolic rate in healthy nonobese and obese adults: a systematic review. J Am Diet Assoc. 105:775, 2005. Gerrior JL, Neff LM. Nutrition assessment in HIV infection. Nutr Clin Care. 8:6, 2005. Hendricks KM, et al. Dietary patterns and health and nutrition outcomes in men living with HIV infection. Am J Clin Nutr. 88:1584, 2008. Kacanek D, et al. Incident depression symptoms are associated with poorer HAART adherence: a longitudinal analysis from the nutrition for healthy living study. J Acquir Immune Defic Syndr. 53:266, 2010. Kahraman A, et al. Non-alcoholic fatty liver disease in HIV-positive patients predisposes for acute-on-chronic liver failure: two cases. Eur J Gastroenterol Hepatol. 18:101, 2006. Koff WC, et al. HIV vaccine design: insights from live attenuated SIV vaccines. Nat Immunol. 7:19, 2006. Liu C, et al. Disclosure of complementary and alternative medicine use to health care providers among HIV-infected women. AIDS Patient Care STDS. 23:965, 2009. Liu JP, et al. Herbal medicines for treating HIV infection and AIDS. Cochrane Database Syst Rev. 3:CD003937, 2005. Mehta S and Fawzi W. Effects of vitamins, including vitamin A, on HIV/AIDS patients. Vitam Horm. 75:355, 2007. Milan FB, et al. Use of complementary and alternative medicine in inner-city persons with or at risk for HIV infection. AIDS Patient Care STDS. 22:811, 2008. Sztam KA, et al. Macronutrient supplementation and food prices in HIV treatment. J Nutr. 140:213S, 2010. Tang AM, et al. Increasing risk of 5% or greater unintentional weight loss in a cohort of HIV-infected patients, 1995 to 2003. J Acquir Immune Defic Syndr. 40:70, 2005. Tromble-Hoke SM, et al. Severe stress events and use of stress-management behaviors are associated with nutrition-related parameters in men with HIV/AIDS. J Am Diet Assoc. 105:1541, 2005. Villamor E. A potential role for vitamin D on HIV infection? Nutr Rev. 64:226, 2006. Wanke C. Nutrition and HIV in the international setting. Nutr Clin Care. 8:44, 2005. Wood C, Harrington W Jr. AIDS and associated malignancies. Cell Res. 15:947, 2005.

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Adapted from: Fleisher GR, MD, Ludwig S, MD, Baskin MN, MD. Atlas of Pediatric Emergency Medicine. Philadelphia: Lippincott Williams & Wilkins, 2004.

DEFINITIONS AND BACKGROUND Electrical, thermal, chemical, or radioactive agents can cause burns. Burns are the third leading cause of accidental death in the United States; 35% of burn victims are children. Unfortunately, a significant proportion of critically ill children admitted to pediatric intensive care units (ICUs)present with nutritional deficiencies; younger age, burn injury, and need for mechanical ventilation support are some factors that are associated with worse nutritional deficiencies (Mehta and Duggan, 2009). With a first-degree burn, simple redness of epidermis occurs. In a second-degree burn, redness and blistering occur. In a third-degree burn, skin and tissue destruction occurs. The hypermetabolic response to burn injury is mediated by hugely increased levels of circulating catecholamines, prostaglandins, glucagon, and cortisol. This response causes profound skeletal muscle catabolism, immune deficiency, peripheral lipolysis, reduced bone mineralization, reduced linear growth, increased energy expenditure, and marked increase in metabolic rate. Local cytokines are released from inflammatory cells, attracting more to the affected area. Interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF) are involved. Fever, evaporative losses, and infections may occur. Determination of total body surface area (TBSA) burned is often documented in the medical record by using charts such as the Lund-Browder chart, shown in Figure 15-3 (http://www.rch. Before the modern era of early enteral nutrition therapy, significant weight loss led to impaired wound healing, infectious morbidity, and increased mortality (Lee et al, 2005). Loss of 1 g of nitrogen equals a 30 g loss of LBM. Therefore, nitrogen balance becomes a matter of life and death in a major burn victim. Survival depends on medical treatment and early, effective nutritional support. Weight loss of up to 10% is acceptable; 40–50% shows great catabolism and hypermetabolism. Systemic inflammation, acute lung injury,

and multiple organ failure (MOF) are common causes of mortality (Magnotti and Deitch, 2005). Early institution of enteral feeding can attenuate the stress response, abate hypermetabolism, and improve patient outcome (Lee et al, 2005). Adding high doses of ascorbic acid (25 mg/mL) to resuscitation fluid during the first 24 hours after severe burns significantly reduces edema and severity of respiratory dysfunction. Thermal injury produces a profound hypermetabolic and hypercatabolic stress response characterized by increased endogenous glucose production via gluconeogenesis and glycogenolysis, lipolysis, and proteolysis (Jeschke, 2009; Jeschke et al, 2005). Severity of thermal injury and presence of systemic infection increase risk for developing ischemic bowel disease. If the GI tract becomes nonfunctional, parenteral support may be needed. Estimating the percentage of total body burned is important because total burn thickness affects metabolic rate more than body surface area. A 25–30% TBSA burn leads to systemic edema and catabolic responses. A 90% TBSA burn is usually fatal; 60% or more in an older person is also usually fatal. The Harris–Benedict equation (with or without activity and stress factors), the Mifflin–St. Jeor equation, the 1997 Ireton–Jones equation, and the Fick equation should not be considered for use in resting energy expenditure (REE) determination, as these equations do not have adequate prediction accuracy (American Dietetic Association, 2010). If a

Figure 3. LifeART image copyright © 2010 Lippincott Williams & Wilkins. All rights reserved.

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metabolic cart is not available, the following Penn State equation may be used for nonobese patients, where V is ventilation per minute (American Dietetic Association, 2010): PENN STATE EQUATION RMR  BMR (0.85)  VE (33)  Tmax(175)  6433. The liver, with its metabolic, inflammatory, immune, and acute phase functions, plays a pivotal role in patient survival and recovery by modulating multiple pathways (Jeschke, 2009). Healing takes place in three stages: establishment of the epithelial barrier, scar tissue formation (dermal replacement), and contraction (shrinkage). Eschars cut off blood supply to an extremity or may impair breathing; they are often cut open in a surgical escharotomy. Bleeding occurs, but because the burn causing the eschar has destroyed the nerve endings in the skin, there is little pain. Hepatic acute phase proteins are strong predictors for postburn survival (Jeschke, 2009). The burn patient is best cared for in a dedicated burn center where resuscitation and monitoring focus is on the pathophysiology of burns, inhalation injury, and edema management (Latenser, 2009). Most dietitians working in burn centers report having advanced training or education (Graves et al, 2009).



SAMPLE NUTRITION CARE PROCESS STEPS Unintentional Weight Loss Assessment Data: Analysis of preferences, dislikes, and allergies; intake compared with measured or estimated requirements; confirmation of severity and extent of burn from medical record; recorded weights. Nutrition Diagnosis (PES): NC-3.2 Unintentional weight loss related to inadequate intake after burns of 45% of upper extremities as evidenced by weight loss of 10 lb in past 14 days. Intervention: Food-Nutrient Delivery—If needs cannot be met by oral route due to extent and severity of burn, patient will need nutrition therapy or feeding assistance. Eliminate distractions at mealtime and avoid lab work and painful procedures before meals. Educate family and nursing staff about not using empty-calorie foods or beverages and offering nutrient-dense beverages, especially with medication passes. Counsel about long-term nutritional implications, as appropriate. Monitoring and Evaluation: Monitor and evaluate weights. Determine whether nutritional needs are being met. Anticipate 2–3 months total for optimal recovery time.


CLINICAL INDICATORS Genetic Markers: Burns are an injury and not genetic in origin. Clinical/History Height Preburn weight Weight changes Daily weight (beware of heavy exudate, edema) BMI Diet history Measured energy expenditure (MEE) Percentage body burned Burn classification (first, second, third degree) Edema I&O BP Temperature

Urine acetone, sugars Ability to chew Ability to swallow Hypovolemic shock  tachycardia, low BP, decreased urinary output Lab Work Alb Prealbumin: CRP ratio CRP Transthyretin (decreased) BUN, Creat H&H Gluc (increased) AST (increased) Na+ (decreased)

Chloride K+ Total urinary N (TUN) Ca++, Mg++ Partial pressure of carbon dioxide (pCO2) Partial pressure of oxygen (pO2) Transferrin Chol, Trig WBC, TLC Serum catecholamines (increased) Ceruloplasmin Alkaline phosphatase (Alk phos) N balance

• Restore fluid and electrolyte balance to prevent hypovolemic shock and to stabilize body temperature. Fluid resuscitation during the first 24–48 hours after injury remains a significant challenge (White and Renz, 2008). • Prevent renal insufficiency or failure from decreased plasma volume, cardiac output, and excessive pigment overload from necrosis, toxins, or hemolysis. Exudate losses may be as high as 20–25% of total daily nitrogen losses. • Promote wound healing and graft retention while minimizing loss of LBM (Lee et al, 2005). Close wound surface with grafts to reduce the likelihood of organ failure. Grafts may be autograft (own body) or from cultured keratinocytes. • Provide early operative intervention and wound closure, metabolic interventions, early enteral nutrition, and intensive glucose control (Latenser, 2009). • Anabolic steroid, glutamine, and glucose protocols (120 mg/dL) are widely used (Graves et al, 2009). • Avoid weight losses greater than 10% of preburn weight. Minimize catabolism of protein tissues to avoid consequences of impaired immunity, decreased wound healing, decreased vigor and muscle strength, retarded synthesis of blood proteins and hemoglobin, and increased rates of infection. • Use indirect calorimetry where possible. Patients require only small adjustment for physical activity levels; bedridden patients may need only 1.0–1.2 times the determined REE. Patients who are also malnourished benefit from a gradual increase in intake of 1.1–1.3 times the REE. • Achieve positive nitrogen balance and minimize losses. Albumin therapy may be considered for the management

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• • • • • • •


of ascites and volume resuscitation (Mendez et al, 2005). In children, growth must continue. Prevent ischemic gut, sepsis, and organ failure (Magnotti and Deitch, 2005). Prevent hypothermia and other complications. Reduce evaporative water losses, especially with occlusive wound dressings. Correct syndrome of inappropriate antidiuretic hormone, hypertonic dehydration, or overhydration. Relieve pain and alleviate problems such as postburn pruritus, deep venous thrombosis, peptic ulceration, or pressure ulcers. Manage psychosocial problems such as acute stress syndrome, depression, and posttraumatic stress syndrome, and reduce their effect on intake. Avoid overfeeding and minimize the negative consequences of hyperglycemia. Restore skin’s protection to reduce infection. Sepsis is a major cause of mortality, often occurring 2–3 weeks after injury.

• •

FOOD AND NUTRITION • Immediately use intravenous fluids to replace deficits; prevent gastric distention and paralytic ileus. Prevent overhydration (Kattelmann et al, 2006). Add vitamin C (25 mg/mL) to promote healing. • If hemodynamically stable with a functional GI tract, then EN is recommended over parenteral nutrition (PN) to lower sepsis and complication rates (American Dietetic Association, 2010; Chan and Chan, 2009). Start within a few hours to decrease the hypermetabolic response to injury (Magnotti and Dietch, 2005). • A duodenal placement, especially in the early postburn phase, is superior to gastric feeding. Use specialty immunoenhanced products with peptides and glutamine to preserve gut function (De-Souza and Greene, 2005). Provide the feeding at a 45-degree angle, where possible, to reduce risks for pneumonia and aspiration; do not use blue dye to test for aspiration (American Dietetic Association, 2010). • Protein intake should be from 2–3 times the RDA or 1.5–3 g/kg body weight; adjust for children. Add modular protein supplements as needed, especially glutamine. Leucine-supplemented nutrition is also very promising (De Bandt and Cynober, 2005). • Use 20% protein, 50–60% carbohydrates (CHOs), and 20–30% fat (2–4% essential fatty acids and slight increase in omega-3 fatty acids). CHO may be given at rate of 5 mg/ kg/min. Intravenous lipids can be given at 4 g/kg maximum in pediatric population. • Gradually progress to oral diet when possible; use a highcalorie, high-protein diet with 5–6 small meals and snacks. Add CHO additives as needed. Suitable snacks may include peanut butter cookies, brownies, cake, shakes, pasteurized eggs in milkshakes or eggnog, protein in broths, and dextrins added to coffee. (See tips for adding protein and calories to the diet in Section 5). • Supplemental glutamine granules with oral feeding or TF can abate glutamine depletion, promote protein syn-

thesis, inhibit protein decomposition, improve wound healing, and reduce hospital stay (Peng et al, 2005). Provide adequate fluid intake: encourage intake of fruit juices (cranberry, grapefruit, prune, or orange juice) for adequate supplies of potassium. Water losses may be 10–12 times normal during first few weeks. Supplement diet with 5–10 times the RDA of vitamin C; 2 times the RDA of zinc sulfate; and 2–3 times the RDA of B-complex vitamins. Two times the RDA for vitamins A and D may be useful at first. Vitamins K and B12 may need to be given weekly; check serum levels as needed. For children, vitamins should be given at twice the RDA until recovery. Provide adequate copper (for collagen cross-linkage). Arginine (up to 2% of kilocalories) and carnitine also may be beneficial. Phosphorus should be added intravenously as potassium phosphate, enterally, or orally as Neutra-Phos. Essential fatty acids are included to reduce inflammation and promote wound healing. Omega-3 fatty acids help to promote a healthy balance of proteins in the body and to reduce inflammation. Administration of high-calorie total enteral nutrition in any highly septic phase should be avoided. Avoid large doses of linoleic acid, iron, and zinc, which can depress immunocompetence. Do not discontinue nutritional support because of watery diarrhea; this type of diarrhea is likely to occur for reasons other than CHO intolerance (Thakkar et al, 2005).

Common Drugs Used and Potential Side Effects • See Table 15-10.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Large amount of vitamin C supplements may be considered in severe burns because of increased requirements resulting from oxidative stress and wound healing; a 3-g dose/day may be needed to restore normal plasma ascorbate concentrations (Berger, 2009). • Calendula may be used topically as an ointment or a tea. Gotu kola and bee resin (propolis) may also be useful. Aloe vera has some merit but should never be taken orally. • Probiotic supplements containing Lactobacillus acidophilus can help restore GI and immune health. • Vitamin E helps to promote healing; it may also be recommended for topical use. However, avoid excessive doses before any surgery.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Considering possible consequences of long-term immobilization (renal calculi, pneumonia, contractures, and pressure ulcers), increase activity as pain tolerance allows. Discuss importance of the balance between appetite, nutritional intake, and physical activity.

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TABLE 15-10


Pharmacotherapy for Burns

Antimicrobial control, analgesia, sedation, and anxiety management are required for burn management. Given acutely and during rehabilitation, supportive therapy uses growth hormone, insulin and related proteins, oxandrolone, and propranolol. Medication


Anabolic steroids

Oral oxandrolone 0.1 mg/kg twice daily increases protein synthesis, lean body mass accretion, and muscle strength; improves serum visceral protein concentrations; promotes weight gain; and increases bone mineral content (Miller and Btaiche, 2008). Close monitoring of liver transaminase levels should be undertaken.


Pain medications may have some effect on gastrointestinal (GI) function and appetite.


Used to prevent Curling ulcer. Cimetidine is also useful.

Antibiotic ointments

Early burn wound excision and complete coverage with autograft will reduce septic complications. Bacitracin may be used for first-degree burns, but other ointments (silver sulfadiazine, silver nitrate, mafenide, or povidoneiodine) may also be used. If Silvadene is used, nutrients may be leached out (i.e., sodium, copper, potassium, magnesium, calcium, and B-complex vitamins).

Antibiotics, oral

Oxacillin, mezlocillin, and gentamicin are used to treat infection.

Growth hormone

Growth hormones may be used to decrease the catabolic effect of burns.


Used for stress-induced hyperglycemia.

Interferon-gamma or -alpha-2b

Used to decrease keloid formation. Dry mouth, stomatitis, nausea and vomiting, diarrhea, and abdominal pain may result.

Pain medicine

Prescription medications (acetaminophen with codeine, morphine, or meperidine) are used for severe burns.

Promotility agents (metoclopramide)

If the patient has gastroparesis or repeated high gastric residuals, a promotility agent may help increase GI transit and improve feeding tolerance.

From Miller JT, Btaiche IF. Oxandrolone in pediatric patients with severe thermal burn injury. Ann Pharmacother. 42:1310, 2008.

• Review the fact that fat is high in energy while low in volume. Fat is helpful in normalizing elimination; however, excesses may negatively affect immunocompetence. • Explain that adequate intake of fiber is important. • The family’s attitude toward patient’s dietary intake should be firm but understanding. A daily nutrient intake record may be a good way to track goals and to assess total intake. Discuss problems to monitor and report, such as fever or wound drainage. • Offer a written care plan for home use.

• Wash all fruits and vegetables with warm water and a soft bristle brush. • Thaw frozen meat or poultry in a refrigerator or under cold running water, not at room temperature • Avoid raw fish, shellfish, unpasteurized juices, and uncooked eggs (and dishes containing uncooked eggs).

For More Information •

American Burn Association

Burn Care Foundation

Patient Education—Food Safety

Burn Prevention

• Educate about food safety, reducing risk of infection, and meticulous hand washing. • Reinforce kitchen fire safety issues. Clean cooking surfaces to prevent food and grease buildup. Turn pan handles inward to avoid hot food spills. Avoid wearing loose clothing while cooking. Stay in the kitchen while cooking. • Burn patients are more susceptible to minor illnesses, including foodborne illness. Tips include the following: • Separate raw meats from other raw foods such as fruits and vegetables. • Avoid cross-contamination from raw meats by storing and preparing raw meat so it does not come in contact with fruits, vegetables, and uncooked foods. • Use separate cutting boards and cooking utensils so that juices from raw meats are not allowed to contact uncooked foods. • Keep hot foods hot (140F) and cold foods cold (40F). Limit the amount of time that food is left at room temperature to prevent germs from growing in it.

Centers for Disease Control and Prevention (CDC) Emergency Treatment of Burns

Fire Safety

Mayo Clinic


National Library of Medicine—Burns

BURNS—CITED REFERENCES American Dietetic Association. Evidence Analysis Library: critical illness. Web site accessed February 7, 2010 at topic.cfm?cat2809. Berger MM. Vitamin C requirements in parenteral nutrition. Gastroenterology. 137:70S, 2009. Chan MM, Chan GM. Nutritional therapy for burns in children and adults. Nutrition. 25:261, 2009.

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De Bandt JP, Cynober L. Therapeutic use of branched-chain amino acids in burn, trauma, and sepsis. J Nutr. 136:308S, 2006. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 33:1125, 2005. Graves C, et al. Actual burn nutrition care practices: an update. J Burn Care Res. 30:77, 2009. Jeschke MG. The hepatic response to thermal injury: is the liver important for postburn outcomes? Mol Med. 15:337, 2009. Jeschke MG, et al. Endogenous anabolic hormones and hypermetabolism: effect of trauma and gender differences. Ann Surg. 241:759, 2005. Kattelmann K, et al. Preliminary evidence for a medical nutrition therapy protocol: enteral feedings for critically ill patients. J Am Diet Assoc. 106:226, 2006. Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care Med. 37:2819, 2009.

Lee JO, et al. Nutrition support strategies for severely burned patients. Nutr Clin Pract. 20:325, 2005. Magnotti LJ, Deitch EA. Burns, bacterial translocation, gut barrier function, and failure. J Burn Care Rehabil. 26:383, 2005. Mehta NM, Duggan CP. Nutritional deficiencies during critical illness. Pediatr Clin North Am. 56:1143, 2009. Mendez CM, et al. Albumin therapy in clinical practice. Nutr Clin Pract. 20:314, 2005. Peng X, et al. Clinical and protein metabolic efficacy of glutamine granulessupplemented enteral nutrition in severely burned patients. Burns. 31:342, 2005. Thakkar K, et al. Diarrhea in severely burned children. JPEN J Parenter Enteral Nutr. 29:8, 2005. White CE, Renz EM. Advances in surgical care: management of severe burn injury. Crit Care Med. 36:318S, 2008.


Adapted from: Koval KJ, MD and Zuckerman, JD, MD. Atlas of Orthopaedic Surgery: A Multimeidal Reference. Philadelphia: Lippincott Williams & Wilkins, 2004.

DEFINITIONS AND BACKGROUND Stress fractures occur from prolonged stress on normal bones. Here, broken bones result from a physical force

greater than stress that cannot be withstood. They are common in athletes, especially gymnasts, runners, and basketball or tennis players. Simple (closed) fractures involve bones that do not protrude. A compound (open) fracture allows bone to protrude. A long-bone fracture generally is an emergency and may be complicated by shock, wound infection, bleeding, or inadequate hydration; traction is used for internal immobilization. The most commonly broken bones are the collarbone (clavicle) and the bones of the wrist. In persons older than 75 years, the hip is more commonly broken. A complete fracture has separated bone fragments complete, whereas they are still partially joined in an incomplete fracture. In comminuted fractures, the bones are split into multiple pieces. Orthopedic surgeons have elaborate nomenclature for the type of fracture, its location, and its geometric shape (transverse, oblique, spiral, and so on). After a break, edema of surrounding tissue causes discomfort, and muscle spasms occur to hold the bone in place. Healing occurs in stages, starting with the inflammation phase; a blood clot (fracture hematoma) between the bone fragments, followed by new blood vessels with phagocytosis to remove dead tissue. Fibroblasts can then produce collagen fibers and new tissue. The second, reparative stage begins approximately 2 weeks after the fracture. In this stage, proteins produced by the osteoblasts and chondroblasts form new bone matrix (soft callus) from calcium hydroxyapatite crystals. This healing shows on a radiograph after approximately 4–6 weeks. The soft callus hardens forms into a hard callus over a 6- to 12-week period. In the third, remodeling phase, mature lamellar bone replaces the woven bone in the period of 3–18 months after the injury. Both osteoblasts and osteoclasts are involved. Good nutrition is essential during all phases of healing. With multiple fractures, metabolic rate may increase by 20% or more for several weeks. Aggressive refeeding can decrease morbidity and mortality in malnourished patients (Bonjour, 2005). Compression fractures involve weakened bones breaking from osteoporosis or from bone cancer. Incidence increases

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after 60 years of age, especially in women. Osteoporosis is responsible for more than 1.5 million fractures annually, including more than 300,000 hip fractures; 700,000 vertebral fractures; 250,000 wrist fractures; and 300,000 fractures at other sites. Bone resorption markers at levels above the upper limit of the premenopausal range are associated with an increased risk of hip, vertebral, and nonvertebral fracture; the most sensitive markers include serum osteocalcin, bone-specific alkaline phosphatase, the N-terminal propeptide of type I collagen for bone formation, and the crosslinked C- (CTX) and N- (NTX) telopeptides of type I collagen for bone resorption (Garnero, 2008). A broken hip includes fractures of the femur head (intracapsular), femur neck (extracapsular), and greater Hesser trochanter. Osteoporotic fractures lower one’s quality of life. Up to 50% of women and 20% of men at the age of 50 years may have a fragility fracture in their remaining lifetimes (Earl et al, 2010). The most common risk factors for osteoporotic fracture are advanced age, low bone mineral density, and previous fracture as an adult (NAMS, 2010). Women with one hip fracture are at a fourfold greater risk of having a second one. Maternal nutrition may have critical and far-reaching persistent consequences for offspring health; reduced maternal fat stores and low levels of circulating 25-hydroxyvitamin D in pregnancy are associated with reduced bone mass in the offspring (Earl et al, 2010). Low birth-weight and poor childhood growth are also linked to risk of hip fracture later in life (Cooper et al, 2006). Clearly, optimizing nutrition throughout life is protective. Deficiency in dietary proteins causes marked deterioration in bone mass, microarchitecture, and strength (Bonjour, 2005). Vitamin A in amounts greater than 5000 IU/day may increase the risk of hip fractures; intake should be limited to 100% RDA levels. After hip fracture, aligning the bone through an open “reduction” with internal fixation (ORIF) may be necessary. In spinal fracture, vertebroplasty involves inserting glue (methylmethacrylate) into the center of the collapsed spinal vertebra to stabilize and strengthen the crushed bone. Here, adequate nutrition must be provided to heal and to reduce infectious processes. Sometimes the medical team uses electrical bone growth stimulation or osteostimulation to support bone recovery. Once healed, it is important to return to some level of physical activity if possible.


CLINICAL INDICATORS Genetic Markers: Bone density and family history can predict fracture risk (Cosman, 2005). Many genes are implicated. BMD candidate genes, ADAMTS18 (ADAM metallopeptidase with thrombospondin type 1 motif, 18) and TGFBR3 (transforming growth factor, beta receptor III) seem to predict bone density and risk for skeletal fracture (Xiong et al, 2009).


Lab Work

Height Weight (may need chair scales) Weight changes BMI Diet history I&O BP Temperature

Serum Ca++ Urinary Ca++ Mg++ BUN, Creat H&H Serum Fe N balance Alb, transthyretin


Prealbumin: CRP ratio CRP Gluc WBC, TLC Total ironbinding capacity (TIBC) Alk phos (increased) Na+, K+

INTERVENTION OBJECTIVES • Support formation of bone matrix. Complete union may take 4–8 months. • Supply adequate nutrition for collagen formation and calcium deposition. • Prevent side effects of long-term immobilization, such as renal calculi, pressure ulcers, urinary tract infections, embolus, contractures, and neurovascular dysfunction. • Use fluoridated water. Monitor bottled waters and well water, which are often not fluoridated. • For long-bone fracture, meet energy needs, which are increased by 20–25%. Keep nearby joints as active as possible and prevent complications such as pressure ulcers, renal calculi, and effects from spinal anesthesia.

SAMPLE NUTRITION CARE PROCESS STEPS Inadequate Oral Food and Beverage Intake Assessment Data: Diet history and intake records showing intake of 50% at most meals following hip fracture and ORIF. Weights not available at that time. Medications include morphine and heparin. Patient shows signs of depression and anorexia. Nutrition Diagnosis (PES): NI-2.1 Inadequate oral food and beverage intake related to anorexia and depression as evidenced by food records showing 50% oral intake at most meals for past 5 days. Intervention: Food-Nutrient Delivery—Consider use of tube feeding if oral intake continues to be low. Offer liquid nutritional supplements between meals to enhance protein and calorie intake. Educate patient and family about the importance of nutrition for healing. Counsel about ways to increase nutrient density without increasing the total amount of food consumed. Coordinate care with medical team for gradual increments of physical activity, which should help with depression and anorexia; review medications and determine whether morphine can be decreased to lessen sleepiness during the day. Monitoring and Evaluation: Improved oral intake for total protein and calories. Gradual improvement in cognition and the ability to participate in physical activity. Decline in signs of depression.

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FOOD AND NUTRITION • Use a high-protein, high-energy diet; needs may increase as much as 20–25%. • Use adequate levels of calcium, phosphorus, and vitamins D, C, and K. Encourage these nutrients to be taken in diet; if a supplement is used, avoid levels 100% RDA for vitamin A. • Although the main source of dietary calcium is dairy products, calcium contained in mineral water is highly bioavailable and can provide another valuable source. • Supply zinc for wound healing after surgical procedures. • Prevent or correct fever, pneumonia, and possible embolism. • Ensure adequate fluid intake to excrete calcium excesses.

• Refer to appropriate agencies, such as home health, Visiting Nurses Association, or Meals-on-Wheels, as needed. • All women should have a bone density test by the age of 65 years or at the time of early menopause. • Discourage smoking. Smoking cigarettes hinders the healing of bones by decreasing collagen production and oxygen availability. • Prevention focuses first on measures such as a balanced diet, adequate calcium and vitamin D intake, adequate exercise, smoking cessation, avoidance of excessive alcohol intake, and fall prevention (NAMS, 2010). Encourage frequent fish consumption, especially in winter, for vitamin D (Nakamura, 2006).

Patient Education—Food Safety

Common Drugs Used and Potential Side Effects • Pharmacological therapy can reduce the risk of fractures, but many patients take their medication incorrectly, stop it prematurely, or have malabsorption (Hamdy et al, 2010). • Bisphosphonates (alendronate, risedronate, and ibandronate), selective estrogen-receptor modulators (raloxifene), parathyroid hormone, estrogens, and calcitonin may be necessary (NAMS, 2010). Parathyroid hormone (teriparatide) is an anabolic agent that stimulates new bone formation, repairs architectural defects, and improves bone density. • Some drugs, such thiazolidinedione, anticonvulsants, and opioids, significantly reduce bone mineral density. Selective serotonin reuptake inhibitors may also have an undesirable effect on bone health; their use should be carefully monitored (Haney et al, 2010). • Pain medications such as morphine or meperidine (Demerol) may cause vomiting, nausea, and constipation. When analgesics are needed, monitor for GI distress or bleeding.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. • Creatine supplementation, with and without resistance training, has the potential to influence bone biology; however, the longer-term effects of creatine supplementation are not known (Candow and Chilibeck, 2010).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Emphasize nutrition, especially adequate calcium, vitamin D, protein, and vitamin K (Earl et al, 2010). • Encourage activity and the use of physical therapy after the healing has progressed. Use of oral supplements with resistance training can be very beneficial (Miller et al, 2006).

• Educate about basic food safety and hand washing.

For More Information •

American College of Physicians—Guidelines for Reducing Fractures

Fracture Healing


Orthopedic Trauma Association

Penn State University—Hershey Medical Center

Web MD understanding-fractures-basic-information WHO On-Line Risk Assessment Tool: FRAX

FRACTURES—CITED REFERENCES Bonjour JP. Dietary protein: an essential nutrient for bone health. J Am Coll Nutr. 24:526S, 2005. Candow DG, Chilibeck PD. Potential of creatine supplementation for improving aging bone health. J Nutr Health Aging. 14:149, 2010. Cooper C, et al. Review: developmental origins of osteoporotic fracture. Osteoporos Int. 17:337, 2006. Cosman S. The prevention and treatment of osteoporosis: a review. Med Gen Med. 7:73, 2005. Earl S, et al. Session 2: other diseases: dietary management of osteoporosis throughout the life course. Proc Nutr Soc. 69:25, 2010. Garnero P. Biomarkers for osteoporosis management: utility in diagnosis, fracture risk prediction and therapy monitoring. Mol Diagn Ther. 12:157, 2008. Hamdy RC, et al. Algorithm for the management of osteoporosis. South Med J. 103:1009, 2010. Haney EM, et al. Effects of selective serotonin reuptake inhibitors on bone health in adults: time for recommendations about screening, prevention and management? Bone. 46:13, 2010. Miller MD, et al. Nutritional supplementation and resistance training in nutritionally at risk older adults following lower limb fracture: a randomized controlled trial. Clin Rehabil. 20:311, 2006. Nakamura K. Vitamin D insufficiency in Japanese populations: from the viewpoint of the prevention of osteoporosis. J Bone Miner Metab. 24:1, 2006. NAMS. Management of osteoporosis in postmenopausal women: 2010 position statement of The North American Menopause Society. Menopause. 17:25, 2010. Xiong DH, et al. Genome-wide association and follow-up replication studies identified ADAMTS18 and TGFBR3 as bone mass candidate genes in different ethnic groups. Am J Hum Genet. 84:388, 2009.

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INTESTINAL PARASITE INFECTIONS NUTRITIONAL ACUITY RANKING: LEVEL 1 DEFINITIONS AND BACKGROUND Intestinal parasite infections cause significant morbidity and mortality. These infections, especially from helminths and untreated water, represent major health problems that increase iron-deficiency anemia in developing countries (Alaofe et al, 2008). Protein–energy malnutrition causes immune deficiency, especially in developing countries. Newborns are especially vulnerable, where morbidity is often secondary to intestinal parasites (Steer, 2005). In addition, transmission of parasites is common in refugee or displacement camps. Cryptosporidium parvum, Giardia lamblia, Entamoeba histolytica, Ascaris lumbricoides, hookworm infection, Schistosoma haematobium, S. mansoni and Strongyloides stercoralis are important intestinal parasites that are common among children, the immunocompromised, and displaced populations (Gbakima et al, 2007). Infections caused by Enterobius vermicularis, G. lamblia, Ancylostoma duodenale, Necator americanus, and E. histolytica occur in the United States (see Table 15-11). TABLE 15-11

Mucin-secreting intestinal goblet cells are an important component of the innate defense system (Hasnain et al, 2010). Parasites modulate GI immunity, possibly by inhibiting migration of CD8 to the draining lymph nodes while increasing IL6, TNF- , and, in particular, IL-10 (Balic et al, 2009). Activation of the mucosal immune system of the GI tract results in altered intestinal physiology, which changes in intestinal motility and mucus production (Kahn and Collins, 2004). The protective immune response that develops following infection with intestinal parasites is characterized by increased numbers of CD4 T cells, granulocytes, and macrophages (Patel et al, 2009). Toxoplasmosis is considered to be the third leading cause of death attributed to foodborne illness in the United States. More than 60 million men, women, and children in the United States carry the Toxoplasma parasite, but very few have symptoms because their healthy immune system usually keeps the parasite from causing illness. Washing vegetables thoroughly before eating them and cooking meat to the recommended temperatures are just a few ways to reduce risk of toxoplasmosis.

Intestinal Parasites and Treatments


Description and Treatment

Ancylostoma duodenale, Necator americanus (hookworms)

Cause blood loss, anemia, pica, and wasting. Finding eggs in the feces is diagnostic. Treatments include albendazole, mebendazole, pyrantel pamoate, iron supplementation, and blood transfusion. Preventive measures include wearing shoes and treating sewage.

Ascariasis (intestinal roundworms)

Common in warm or humid climates or when personal hygiene is inadequate. Adult worms live in the small intestine, with eggs that pass out in human feces. These eggs become infective within 2–3 weeks. When ingested by humans through fecally contaminated food or water, the eggs hatch and penetrate the intestines. Eventually, they reach the heart. Larvae mature within 2–3 months, and adult worms may live for 1 year or more. Hemorrhage can occur in lung tissue and cause pneumonitis. Vague abdominal discomfort can occur with small intestine involvement. Malnutrition can cause an imbalance in T-cell subpopulations that may lead to a defective T-cell maturation, thereby increasing susceptibility to parasitic infection (Di Pentima, 2009).

Enterobius vermicularis (pinworm)

Causes irritation and sleep disturbances. Diagnosis can be made using the “cellophane tape test.” Treatment includes mebendazole and household sanitation.


Giardia intestinalis is one of the most common intestinal parasites in the world, and it contributes to diarrhea, nutritional deficiencies, stunting, and cognitive impairment in children in developing regions (CDC, 2010). It causes nausea, vomiting, malabsorption, diarrhea, and weight loss. Stool ova and parasite studies are diagnostic. Treatment includes metronidazole. Sewage treatment, proper hand washing, and consumption of bottled water can be preventive.

Entamoeba histolytica

Can cause intestinal ulcerations, bloody diarrhea, weight loss, fever, gastrointestinal obstruction, and peritonitis. Amebas can cause abscesses in the liver that may rupture into the pleural space, peritoneum, or pericardium. Stool and serological assays, biopsy, barium studies, and liver imaging have diagnostic merit. Therapy includes luminal and tissue amebicides to attack both life-cycle stages. Metronidazole, chloroquine, and aspiration are treatments for liver abscess. Careful sanitation and use of peeled foods and bottled water are preventive.

Trichinella spiralis

T. spiralis is a roundworm that causes an acute infection (trichinosis) and is usually acquired by eating encysted larvae in raw or undercooked pork. Larvae mature and mate in the small intestine; larvae reaching striated muscle will encyst and live for years. Usual incubation is 5–15 days. The disorder has a 4% prevalence in the United States. Symptoms and signs include swelling of the upper eyelids, bleeding under the nails, skin rash, diarrhea, abdominal cramps, and malaise; later, low-grade fever, edema, sweating, dyspnea, cough, and muscle pain occur. In nonstriated muscle tissues such as the heart, brain, kidney, or lung, death can follow in 4–6 weeks, if untreated. Most symptoms disappear by the third month.

REFERENCES CDC. Centers for Disease Control. Website accessed 10/16/10 at Di Pentima C. Burden of non-sexually transmitted infections on adolescent growth and development in the developing world. Adolesc Med State Art Rev. 20:930, 2009.

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Risks are more significant for individuals with AIDS and for pregnant women. Most intestinal protozoan infections can cause acute or chronic diarrhea in healthy individuals but may result in intractable, life-threatening illness in patients with immunosuppressive diseases such as AIDS (Escobedo et al, 2009). Vaccines or immunotherapies may be developed to treat these pathogens.


CLINICAL INDICATORS Genetic Markers: The T-helper (Th) 2–type immune response causes infection-induced intestinal muscle hypercontractility and goblet cell hyperplasia (Kahn and Collins, 2004). The genetics of this form of immunity are under study. Clinical/History Height Weight BMI Diet history Temperature I&O BP Lab Work Stool examination

Positive skin and serological tests for eosinophilia and leukocytosis Trichinosis— biopsy of skeletal muscle after fourth week (for larvae or cysts)

Alb, transthyretin Prealbumin:CRP ratio CRP H&H Serum Fe, ferritin Transferrin TIBC Na+, K+, Cl Ca++, Mg++ TLC, WBC Gluc

SAMPLE NUTRITION CARE PROCESS STEPS Altered GI Function Assessment Data: Diet history and intake records showing normal intake of all macronutrients. History of (Hx) explosive diarrhea for the past month. Tested positive for G. lamblia after a camping trip where patient drank untreated water from a stream. Other family members tested negative. Nutrition Diagnosis (PES): NC-1.4 Altered GI function related to infection with Giardia as evidenced by explosive diarrhea for the past month and no changes in usual dietary intake. Intervention: Food-Nutrient Delivery—discuss options for decreasing fiber and tolerating medications while under treatment for Giardia. Educate patient and family about the importance of drinking only treated water while camping. Counsel about monitoring tolerance for fiber-rich foods when infection has resolved. Coordinate care with medical team for pharmacotherapy and any nutritional side effects. Monitoring and Evaluation: Resolution of Giardia infection and diarrheal disease. No undesirable side effects from medications.

INTERVENTION OBJECTIVES • Differentiate symptoms and correctly identify condition as rapidly as possible; treat as needed. • Treat infections and diarrhea. • Prevent or correct malnutrition; prevent stunting and allow growth in children. • Prevent blockage, inflammation, volvulus, and bowel perforation. • Correct any complications such as anemia, pneumonia, and cardiac failure. • Teach ways to prevent further infections.

FOOD AND NUTRITION • Provide balanced intake of all macronutrients. Protein intake, especially lysine, is important. Adequate, but not excessive, iron and zinc are also useful. • Encourage adequate intake of food sources of vitamins A and C, especially from fruits, juices, and vegetables. Vitamin E and selenium may be especially protective (Smith et al, 2005). Supplements with retinol may be used in some cases. • Ensure an adequate fluid intake, especially with diarrheal losses. Replace electrolytes with broths and juices. • With poor appetite, offer small, frequent meals and snacks to correct malnutrition or weight loss that is undesirable. • Ensure safe food handling at all meals.

Common Drugs Used and Potential Side Effects • The albendazole–praziquantel combined regimen is a useful single-dose therapy for giardiasis in children. • Pyrantel pamoate (Povan) may be used for ascariasis. Rarely, vomiting or diarrhea may occur. • For trichinosis, mebendazole or thiabendazole may be used. GI distress is a common side effect. Aspirin or analgesics may be needed for muscular pain. • Corticosteroids such as prednisone are often used temporarily to reduce inflammation of the heart or brain.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. Chincona, elecampane, golden seal, ipecac, and papaya are not proven through clinical trials.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Discuss the importance of personal hygiene in maintaining a sanitary environment and in preventing reinfestation. • Children who play outside should always wash their hands before eating meals or snacks. Diarrhea caused by

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parasites such as Cryptosporidium may be severe in malnourished or immunodeficient children; recovery is achieved only after sufficient nutritional repletion. • Protozoa intestinal infection is still frequent in some marginalized populations; improvement in sanitation might decrease the prevalence of these diseases (Korkes et al, 2009). A mass campaign to educate about the role of sanitation in reducing intestinal parasite infection is recommended (Mehraj et al, 2008).

Patient Education—Food Safety • Educate about food safety issues. Reducing new infection is very important. Meticulous hand washing is essential. • Many of these parasites can be transmitted by food, water, soil, or person-to-person contact. Occasionally, helminthic roundworms, tapeworms, and flukes are transmitted in foods such as undercooked fish, crabs, and mollusks; undercooked meat; raw aquatic plants such as watercress; raw vegetables that have been contaminated by human or animal feces; and foods contaminated by food service workers with poor hygiene or working in unsanitary facilities.

For More Information •

CDC—An Ounce of Prevention

Index of Parasitic Diseases

National Center for Emerging and Zoonotic Infectious Diseases


INTESTINAL PARASITES—CITED REFERENCES Alaofe H, et al. Intestinal parasitic infections in adolescent girls from two boarding schools in southern Benin. Trans R Soc Trop Med Hyg. 102:653, 2008. Balic A, et al. Dynamics of CD11 c() dendritic cell subsets in lymph nodes draining the site of intestinal nematode infection. Immunol Lett. 127:68, 2009. Escobedo AA, et al. Treatment of intestinal protozoan infections in children. Arch Dis Child. 94:478, 2009. Gbakima AA, et al. Intestinal protozoa and intestinal helminthic infections in displacement camps in Sierra Leone. Afr J Med Med Sci. 36:1, 2007. Hasnain SZ, et al. Mucin gene deficiency in mice impairs host resistance to an enteric parasitic infection. Gastroenterology. 138:1763, 2010. Kahn WI, Collins SM. Immune-mediated alteration in gut physiology and its role in host defence in nematode infection. Parasite Immunol. 26:319, 2004. Korkes F, et al. Relationship between intestinal parasitic infection in children and soil contamination in an urban slum. J Trop Pediatr. 55:42, 2009. Mehraj V, et al. Prevalence and factors associated with intestinal parasitic infection among children in an urban slum of Karachi. PLoS One. 3:e3680, 2008. Patel N, et al. Characterisation of effector mechanisms at the host:parasite interface during the immune response to tissue-dwelling intestinal nematode parasites. Int J Parasitol. 39:13, 2009. Smith A, et al. Deficiencies in selenium and/or vitamin E lower the resistance of mice to Heligmosomoides polygyrus infections. J Nutr. 135:830, 2005. Steer P. The epidemiology of preterm labor—a global perspective. J Perinat Med. 33:273, 2005.


Adapted from: Sherwood L. Gorbach, John G. Bartlett, et al. Infectious Diseases. Philadelphia: Lippincott Williams & Wilkins, 2004.

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DEFINITIONS AND BACKGROUND Multiple organ dysfunction syndrome (MODS) involves two or more systems in failure at the same time (e.g., renal, hepatic, cardiac, or respiratory). The condition is also called MOF. Etiology may be from sepsis (gram-positive/negative bacteria, fungal or viral,) shock, hemorrhage, allergy, burns, or trauma. Conditions leading to MOF may also include unnecessary deep sedation, excessive blood glucose levels, prolonged immobilization, or corticosteroid use (de Jonge et al, 2009). Cytokines are direct mediators. MODS is triggered by TNF- and by a cytokine cascade with IL-6 and other ILs, platelets, endothelial cells, and leukocytes. Lactate level is often used as a prognostic indicator of problems with tissue perfusion. High baseline serum cortisol level is also a marker of severity and poor prognosis. Cortisol levels 20 g/dL in a highly stressed patient (with respiratory failure, hypotension) may diagnose adrenal insufficiency, which should be treated (Marik et al, 2005). Early aggressive resuscitation of critically ill patients limits or prevents progression to MODS. Gut injury and impaired gut barrier function have a high impact on the development of MODS. Mucosal lesions and increased intestinal permeability cause translocation of bacteria and endotoxins and initiate a local or systemic inflammatory response syndrome (SIRS). There are sequential metabolic changes following induction of SIRS, with an elevation in REE from 4–21 days and loss of LBM. Some experts suggest use of the phrase “nutrition therapy” versus “nutrition support” to strengthen the role in attenuating this metabolic response, preventing oxidative stress, and modifying the immune response with the use of appropriate lipids, glutamine, arginine, and antioxidants. Indeed, the quality of nutrition therapy is more important than the quantity. Specific nutrients to modify immune, inflammatory, and metabolic processes have been helpful (Heys et al, 2005). In critical illness, glutamine levels are much higher in the duodenal mucosa; glutamine supplementation may be beneficial (De-Souza and Greene, 2005). While arginine supplementation may improve outcomes, controversy continues surrounding its long-term use in septic patients. In general, immune-enhanced products do not decrease ICU length of stay or improve rates of recovery (American Dietetic Association, 2010). Maintaining adequate tissue oxygenation and cellular nutrition are priorities. Trace elements, omega-3 fatty acids, and antioxidant nutrients, especially vitamin E and selenium, are important and may reduce mortality (Grimble, 2005; Heyland et al, 2005). Enteral nutrition provides the intestinal mucosa with nutrients, which reduces bacterial translocation and septic complications. There may be beneficial effects of immune-enhancing diets for MODS, especially after trauma or surgery. However, overall mortality remains high at 30–100%, especially if multiple organs are involved. The treatment of MODS is complex. Treatment includes correction of ischemia through fluid resuscitation and mechanical ventilation; antibiotics; and stabilization of water, electrolyte, and acid–base imbalance. Stress hyperglycemia promotes the proinflammatory response, whereas insulin has the opposite effect; therefore, tight glycemic control is important.


CLINICAL INDICATORS Genetic Markers: The development of techniques for measuring the expression level of all of a person’s genes may make it possible to develop an injury scoring system based on the degree of gene activation related to having more infections and organ failure (Warren et al, 2009). Clinical/History

Lab Work

Height Weight BMI Dry weight Weight changes Edema, ascites Diet history Temperature I&O BP Acute Physiology and Chronic Health Evaluation (APACHE) Injury Severity Score (ISS) Ultrasonography Echocardiography Electroencephalogram (EEG)

Serum procalcitonin (PCT) BUN (often elevated) Creat (often elevated) ALT, AST (elevated) Alb, transthyretin Albumin:CRP ratio CRP Na+, K+ Ca++, Mg++ Cl Creatine kinase (CK) Phosphorus Gluc—serum, urine Serum insulin

Lactic acid (elevated?) Serum pH 7.35 (acidosis) Alanine, pyruvate (retention?) Serum cortisol pCO2, pO2 Chol, Trig Glomerular filtration rate TLC, WBC H&H Serum Fe TIBC Serum phosphorous Serum folate Serum zinc

INTERVENTION OBJECTIVES • Stabilize electrolyte and hemodynamic balances. Remove or control sources of organ dysfunction, such as bacterial translocation. Early identification and aggressive management of MODS is essential. • Provide continuous administration of at least minimal enteral nutrition to prevent gut mucosa atrophy. • In patients with a functional GI tract, enteral nutrition is preferred over parenteral nutrition (Casaer et al, 2008). Enteral or oral nutrition preserves the gut and immune system integrity. • Support organs with appropriate substrate. “Immunonutrition” provides formulas supplemented with arginine, omega-3 fatty acids, ribonucleic acids, and glutamine; however, there is no clear evidence that these products promote faster recovery (American Dietetic Association, 2010). • Control hyperglycemia to decrease infection and sepsis.

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SAMPLE NUTRITION CARE PROCESS STEPS Excessive Infusion of Parenteral Nutrition Assessment Data: Patient in ICU for 3 days, on CPN with order changed Day 2 to provide CHO and lipid in excess of estimated requirements. Indirect calorimetry identifies needs as 1400 kcal/ day; patient receiving 1800 kcal/day. Admitted with acute pancreatitis; now showing signs of heart and liver failure. Glucose 200 mg/dL; fever with temperature of 102 F. Nutrition Diagnosis (PES): Excessive infusion of parenteral nutrition related to current CPN order as evidenced by solution providing 1800 kcal/day with CHO and lipid exceeding daily requirements. Intervention: Food-Nutrient Delivery—Decrease CPN order to 1400 kcal/day; lipid calculated at 30% total calories and CHO calculated as 50% total kilocalories. Patient may benefit from jejunostomy instead of CPN because of MODS. Coordinate care with medical team—discuss importance of not overfeeding CPN solution. Discuss merits of using jejunostomy feeding instead of parenteral feeding. Monitoring and Evaluation: CPN order discontinued. Jejunostomy tube placed; new feeding order that meets needs of 1400 kcal and 50% CHO, 30% fat, and 20% protein with extra fluid. Glucose monitoring and use of insulin to bring levels back below 120 mg/dL. Patient tolerating jejunostomy. Fever gradually subsiding. Signs of improvement in MODS.

• Promote prompt and immediate responses to all changing parameters. Until organ dysfunction resolves, monitor weight, relevant laboratory parameters, and nutrient intake. • Consider short- and long-term consequences of all actions (e.g., treatments must incorporate a consensus of opinions about which therapy precedes another). • Manage complications such as anemia, gastric reflux, or delayed bowel motility. • Promote wound healing if surgery is required. Prevent additional sepsis. • Promote recovery and improved well-being.

FOOD AND NUTRITION • If there is gastric reflux or delayed bowel motility, a nasoduodenal or jejunal feeding tube or feeding jejunostomy is required. Ensure that the formula is appropriate. • The recommended energy intake is 20–30 kcal/kg/day with a protein intake of 1.2–1.5 g/kg/day (Casaer et al, 2008). Evaluate organ function and provide a correctly calculated feeding and product for patient’s diagnosis and condition. • Immunoenhanced or glutamine-enriched products used to preserve gut integrity do not necessarily speed rates of recovery or reduce time in ICUs (American Dietetic Association, 2010). • Review current vitamin and mineral intakes; adjust according to changing needs. Antioxidants may play a role in supporting recovery. • Avoid excesses of iron, zinc, polyunsaturated fatty acids (PUFAs), and linoleic acid—especially parenterally— because of their effects on the immune system.


• When possible, return to oral feeding to acquire the benefits of phytochemicals from whole foods. • Patients requiring ventilator support may need a higher lipid content in their feeding, even with cardiac failure.

Common Drugs Used and Potential Side Effects • Hypertonic saline solution is commonly used. • Anti-inflammatory treatment is vital for intervention in severe infectious disease. • All medications should be reviewed for potential drug– nutrient incompatibility and stability with formulas. Try to avoid inclusion of medications with EN products because of drug–nutrient interactions and because drugs may then be less available to the patient. • Drug metabolism with the liver cytochrome P-450 (CYP450) system can result in drug toxicities, reduced pharmacological effect, and adverse drug reactions. Foods such as grapefruit, alcoholic beverages, teas, and herbs may inhibit or induce the activity of CYP3A4 (Flanagan, 2005). • Review all vitamin and mineral supplements and enteral products to determine whether the potential of hypervitaminosis and mineral toxicities exists. • Insulin may be required because of the hyperglycemia that occurs with stress. • With continuous seizures, lorazepam or anticonvulsants may be needed. Weight and appetite changes are common if used long term.

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with the physician. Herbs often possess the ability to inhibit or induce the activity of CYP3A4. • Chinese herbs for reducing inflammatory reaction are being studied.

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • When possible, discuss implications of MODS in relation to nutritional support. Include a realistic assessment of potential for recovery and use of EN in the home setting, as discussed with the physician. • Family should be included in discussions about nutritional support measures that are taken. As appropriate, prepare patient and family for home nutritional needs and total parenteral nutrition/EN/oral diet requirements. • Alleviate fears associated with eating or nutritional support therapies. • Discuss any signs or problems that should require professional intervention.

Patient Education—Food Safety • Educate about food safety issues. Reducing more infection is very important.

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• Meticulous hand washing is essential because immunocompromised individuals are more susceptible to minor illnesses, including foodborne illness.

For More Information •



MULTIPLE ORGAN DYSFUNCTION SYNDROME— CITED REFERENCES American Dietetic Association. Evidence Analysis Library: critical illness. Web site accessed February 11, 2010 at topic.cfm?cat2809.

Casaer MP, et al. Bench-to-bedside review: metabolism and nutrition. Crit Care. 12:222, 2008. de Jonge B, et al. Intensive care unit-acquired weakness: risk factors and prevention. Crit Care Med. 37:309S, 2009. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 33:1125, 2005. Flanagan D. Understanding the grapefruit-drug interaction. Gen Dent. 53:282, 2005. Grimble RF. Immunonutrition. Curr Opin Gastroenterol. 21:216, 2005. Heyland DK, et al. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 31:327, 2005. Heys SD, et al. Nutrition and the surgical patient: triumphs and challenges. Surgeon. 3:139, 2005. Marik PE, et al. The hepatoadrenal syndrome: a common yet unrecognized clinical condition. Crit Care Med. 33:1254, 2005. Warren HS, et al. A genomic score prognostic of outcome in trauma patients. Mol Med. 15:220, 2009.


Adapted from: Sherwood L. Gorbach, John G. Bartlett, et al. Infectious Diseases. Philadelphia: Lippincott Williams & Wilkins, 2004.

DEFINITIONS AND BACKGROUND Sepsis involves a SIRS, with infection that has spread to other areas from its original site. Similar to the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time (Elenkov et al, 2005). Sepsis may be a complication of vascular access devices or intravenous catheters and may be bacterial or fungal in origin. The most common sources of infection are lung and abdominal infections (Russell, 2008). The stages of sepsis are listed in Table 15-12. Natural killer cells are a crucial component of the innate immune response to various viruses, fungi, parasites, and bacteria (Fauci et al, 2005). Systemic inflammation stimulates an

acute-phase reaction and the stress response, mediated by the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system (Elenkov et al, 2005). GI tract dysmotility increases permeability of intestinal mucosa and bacterial translocation, contributing to sepsis and MODS (Ukleja, 2010). Synergistic effects of TNF- , IL-1 , other cytokines, and nitric oxide are also implicated. In SIRS, reduced TNF production occurs; this is immunosuppression rather than an excessive inflammatory response (Cavaillon et al, 2005). In sepsis, activated phagocytes release leukocytic endogenous mediators; hepatic uptake of amino acids and increased prostaglandin synthesis occur. Hormonal responses include increases in adrenocorticotropic hormone (ACTH), aldosterone, and catecholamines (with increased gluconeogenesis, glycolysis, proteolysis, and lipolysis). Decreased triiodothyronine (T3) cause tissue degradation and mobilized triglycerides. Host defense peptides modulate inflammation (Bowdish and Hancock, 2005). While albumin, transthyretin, and transferrin have a transport role in the body, acute-phase proteins (CRP, -acid glycoprotein, and -trypsin) help with host defense. These parameters drop in sepsis independent of nutritional status; monitor all protein levels as markers of inflammation in this population. Vitamin D3 plays a role in immune activation of endothelial cells during gram-negative bacterial infections (Equils et al, 2006). It may enhance the innate immune response by induction of cathelicidin (LL-37), an endogenous antimicrobial peptide produced by macrophages and neutrophils (Jeng et al, 2009). Enteral feeding is preferred over parenteral feeding, where catheter infection is a risk. A key issue in providing nutrition to critically ill patients is intolerance of enteral feeding as a result of impaired GI motility (Ukleja, 2010). Overfeeding sometimes increases sepsis.

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TABLE 15-12

Stages of Sepsis

Definitions of the various stages of sepsis can be summarized as follows: Infection is a microbial phenomenon in which an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by these organisms is characteristic. • Bacteremia is the presence of viable bacteria in the blood. • Systemic inflammatory response syndrome (SIRS) may follow a variety of clinical insults, including infection, pancreatitis, ischemia, multiple trauma, tissue injury, hemorrhagic shock, or immune-mediated organ injury. • Sepsis is a systemic response to infection. This is identical to SIRS, except that it must result from infection. • Septic shock is sepsis with hypotension (systolic blood pressure 90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation. Concomitant organ dysfunction or perfusion abnormalities (e.g., lactic acidosis, oliguria, coma) are present in the absence of other known causes. • Multiple organ dysfunction syndrome (MODS) is the presence of altered organ function in a patient who is acutely ill such that homeostasis cannot be maintained without intervention. Primary MODS is the direct result of a well-defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself. Secondary MODS develops as a consequence of a host response and is identified within the context of SIRS. The inflammatory response of the body to toxins and other components of microorganisms causes the clinical manifestations of sepsis. Sepsis syndrome is recognized clinically by the presence of two or more of the following:


et al, 2005). In the elderly, poor immune response and poor functional status may be indicators of sepsis (Gavazzi et al, 2005).

• Temperature 38C or 36C • Heart rate 90 beats/min • Respiratory rate 20 breaths/min or partial pressure of carbon dioxide in arterial gas 32 mm Hg • White blood cell count 12,000 cells/ L, 4000 cells/ L, or 10% band forms Adapted from: American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines. Web site accessed February 11, 2010 at

Management of septic shock requires an ABCDEF approach: Airway, Breathing, Circulation, Drugs, Evaluate, and Fix the source of sepsis (Russell, 2008). Improvements in the management of sepsis and MODS have resulted from improvements in critical care practices (Sullivan et al, 2005). Yet, the incidence of septic shock is increasing; mortality ranges from 30% to 70% (Russell, 2008). Severe sepsis leading to shock is still a common cause of death in critically ill patients. Sepsis may involve the bloodstream from gram-negative or gram-positive bacteria. Diseases caused by group A Streptococcus include acute rheumatic fever, rheumatic heart disease, poststreptococcal glomerulonephritis, and invasive infections. Pathogenic Escherichia coli causes infections such as urinary tract infection and meningitis, which are prevalent (Kim et al, 2005). Yersinia enterocolitis can cause bacteremia or abdominal abscess, especially in states of iron overload. Neonatal sepsis is a major cause of death, especially in low birth-weight infants. In addition, while sepsis during pregnancy is uncommon, it is potentially fatal (Fernandez-Perez


CLINICAL INDICATORS Genetic Markers: The genetics involved with various inflammatory responses to sepsis are being studied. A variety of polymorphisms may play a role in sepsis. Clinical/History

Lab Work

Height Weight BMI Diet history I&O BP (hypotension?) Fever, chills Fatigue, malaise Decreased urine output Skin rash? Mild confusion Catabolism of lean body mass Tachycardia

Elevated WBC Alb, transthyretin Albumin: CRP ratio CRP Chol (decreased) pO2, pCO2 Gluc (altered) Decreased glucose tolerance? Glucagon (increased) Serum insulin Plasma 25(OH)D— low?

Plasma lactate Transferrin Trig (increased) AST (increased) BUN, Creat Urinary urea nitrogen Na+, K+ Ca++, Mg++ Cl H&H Serum Fe N balance T3 (decreased) 5-Hydroxyindole acetic acid (5-HIAA) (increased) Phosphate (decreased) Osmolality

INTERVENTION OBJECTIVES • Prevent septic shock with increased cardiac output, tachycardia, low blood pressure, decreased renal output, and warm flushed skin. Support medical, goal-directed resuscitation of the septic patient and use of broad-spectrum antibiotic therapy within 1 hour of diagnosis of septic shock (Dellenger et al, 2008). • Support the body’s antimicrobial defense system and keep the environment as germ free as possible to prevent MODS. Use strict guidelines and protocols for insertion, care, and maintenance of any catheters and feeding tubes. • Meet increased energy needs. Mild infection elevates resting energy expenditure between 15% and 40%; sepsis increases it by 40–70% and doubles nitrogen losses. Use indirect calorimetry whenever possible, and do not overfeed.

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Toxins Bacteria

Three Ways Bacteria Cause Damage

Damaged tissue



Tissue Damage Some bacteria may adhere to and invade tissue cells. Other bacteria may produce toxins that alter the chemical reactions in cells. This results in a disruption in the cells’ normal function or causes the cell to die.

Red blood cell Toxins Fibrin (involved with clotting) Blood vessel


Blood Clots (intravascular coagulation)


Fluid Leakage from Vessel

Some bacterial toxins may cause blood to coagulate (clot) in small vessels, forming blockages. The tissue cells normally supplied by these vessels are deprived of blood, resulting in tissue damage.

The walls of small blood vessels may be damaged by bacterial toxins. This leads to fluid leakage from the vessel into the surrounding tissue. The fluid loss results in decreases blood pressure, and the heart is unable to pump an adequate amount of blood to the vital organs. Damaged vessel wall Bacteria Toxin

Fluid leakage

Asset provided by Anatomical Chart Co.

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SAMPLE NUTRITION CARE PROCESS STEPS Increased Nutrient Needs Assessment Data: Nursing home resident with urosepsis; fever with temperature 101F; albumin 2.4 g/dL; requires feeding assistance; hip replacement surgery 1 month ago. Nutrition Diagnosis (PES): NI 5.1 Increased nutrient needs for protein related to urosepsis and recent surgery as evidenced by albumin 2.4 g/dL and intake 50% of dairy-meat items at meals. Intervention Food-Nutrient Delivery—ND 3.1.1 Commercial high-protein beverage Education E 2.1 Adding protein powder, 30 mL BID for increased protein Counseling C2.2 Goal setting—meet protein needs daily (1.5 g/kg) Coordination of Care RC 1.1 Team meeting—nursing to focus on better intake of dairy and meat items on trays. Monitoring and Evaluation: Improved oral intake of protein sources from dairy products, meat group choices, and protein powder; 75–100% at meals. Meeting daily protein needs of 1.5 g/kg. Resolution of urosepsis. Wound healing continues.

• Promote tissue repair and wound healing. Protein turnover is often 30–50% higher than normal. • Treat nausea, vomiting, and anorexia. • Prevent or treat metabolic derangements such as hyperglycemia, glycosuria, hyperosmolar/nonketotic coma, electrolyte abnormalities (e.g., decreased potassium, decreased phosphate, elevated chloride), osmotic diarrhea, and fluid overload. Glycemic control, targeting a blood glucose 150 mg/dL after initial stabilization (Dellenger et al, 2008). • Correct anemia, which prevents tissue oxygenation. Target a hemoglobin level of 7–9 g/dL (Dellenger et al, 2008). Prevent or manage stress ulcers and upper GI bleeding.

FOOD AND NUTRITION • Protein should be provided in levels of 1.5–2.0 g/kg daily. Branched-chain amino acids (BCAAs) are useful for energy because they do not need to be metabolized to glucose. • Provide calories at 30–35 kcal/kg. Monitor daily actual intake. • Enteral nutrition should be initiated within 48 hours of injury or admission and average intake actually delivered within the first week should be at least 60–70% of total estimated energy requirements as determined by patient assessment (American Dietetic Association, 2010). • When patient can eat, soft diet and liquids of high nutrient and energy value are beneficial. • Vitamins A, C, D, K, thiamin, and folic acid may become depleted with infection. Urinary excretion of phosphorus, potassium, magnesium, zinc, and chromium also occur; monitor for signs of malnutrition. Replace in feedings or diet as appropriate.


• Include omega-3 fatty acids (Babcock et al, 2005). Inclusion of fish oil in parenteral nutrition provided to septic ICU patients increases plasma eicosapentaenoic acid, modifies inflammatory cytokine concentrations, improves gas exchange, and shortens the length of hospital stay (Barbosa et al, 2010). • Monitor fluid requirements and intake carefully to excrete wastes properly. • If tube feeding is needed, there are no benefits for using immune-enhancing formulas (American Dietetic Association, 2010).

Common Drugs Used and Potential Side Effects • Antibiotics are used for bacterial sepsis; monitor for side effects and GI distress. • Activated protein C, a vitamin K–dependent serine protease, is an anticoagulant that is also cytoprotective and has anti-inflammatory role for use in septic shock (Russell, 2008). • Antiseptic-impregnated catheters, such as those with minocycline–rifampicin or chlorhexidine/silver sulfadiazine, may be needed to reduce catheter-related sepsis. • Insulin may be needed for hyperglycemia; glucose control is important. • Iron and zinc are bacterial nutrients; omit them in CPN solutions in septic patients. • Prevent upper GI bleeding by using H2 blockers or proton pump inhibitors (Dellenger et al, 2008). • Steroids may be used. Greater nitrogen depletion and hyperglycemia, sodium retention, and potassium losses can occur. Monitor carefully. Corticosteroid therapy induces potentially detrimental hyperglycemia in septic shock (COIITSS Study Investigators, 2010).

Herbs, Botanicals, and Supplements • Herbs and botanical supplements should not be used without discussing with physician. • Optimal vitamin D is important for innate immunity in the setting of sepsis (Jeng et al, 2009). • Fish oil may play an important role in reducing the hospital length of stay in septic patients (Barbosa et al, 2010).

NUTRITION EDUCATION, COUNSELING, CARE MANAGEMENT • Use of aseptic techniques for feedings and meals will be essential. • Need for a well-managed convalescence and gradual refeeding process will be needed to support patient’s resistance and immunity. Terminate the cycle of infection, malnutrition, reinfection, and further protein–energy malnutrition.

Patient Education—Food Safety • Educate about food safety issues. Reducing infections is very important.

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• Meticulous hand washing is essential; immunocompromised individuals are more susceptible to minor illnesses, including foodborne illness.

For More Information •

JAMA—Sepsis Page