A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS
■■Substituting MDs With APPs in Nursing Homes ■■Hawaii Repeals Physician Chart Reviews for PAs LEGAL ADVISOR
Medical Errors and Negligence
Chronic Pancreatitis: Challenging to Diagnose, Difficult to Treat Computed tomography is important for visualizing calcifications in chronic pancreatitis.
Hair Loss on the Scalp
Erythematous, Pruritic Plaques Salary Survey Are you being fairly compensated? See page 24
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EXPERTS If a patient has you stumped, write us and we’ll forward your query to one of our consultants and publish the response in Advisor Forum.You can also use this space to contribute a clinical pearl of your own or comment on another letter.
Advisor Forum the color of the affected area was normal, the skin CLINICAL PEARLS felt quite thick and inflexible. These skin changes stopped abruptly at the collar line, below which POISON IVY PREVENTION the skin was entirely normal. Poison ivy season is starting! I recommend that Abundant evidence of sun damage — includ- people take an old pair of knee-high tube socks ing weathering, telangiectasias, solar lentiginosis, and cut off the foot part above the heel. Pull the and numerous actinic keratoses on prominent socks over the arms up to the start of their sleeve areas of his cheeks and ears — was noted. Similar (assuming they are wearing a T-shirt) and tuck changes were noted on the dorsa of both hands into gloves. Use the socks to protect arms when but were not present on his arms and trunk working in the yard or other high-risk poison because he wore long-sleeved shirts when in the ivy areas. They can be rolled off the arms and sun. Although he had worn a wide-brimmed hat thrown away, or washed and re-used. I remind while in the sun during his adult life, he had never people to always wear gloves, and to remove worn anything, such as a bandana, on his neck. the gloves before touching anything, including Always wear The posterior neck is especially susceptible door handles. This significantly reduces the gloves to to the effects of the sun, evidence of which fre- exposure area of skin to poison ivy. —JUDITH protect the quently manifests as it did in this patient. This MCINTOSH, MSN, Kokomo, Indiana skin from condition is called cutis rhomboidalis nuchae weath- VERRUCA VULGARIS TREATMENT exposure to (CRN), which represents thickening and weath ering of the epidermis as well as solar elastosis I always recommend candida albicans skin anti- poison ivy, and of the underlying dermis caused by the sun. gen test injections for patients who are not remove them Although this condition is clear evidence of responding well to liquid nitrogen +/- paring for before touching chronic overexposure to the sun, CRN has no verruca vulgaris. A 0.1-mg injection every month anything. malignant potential, and treatment is neither for about 3 months creates an immune response required nor does it exist. against the warts. I have seen resolution of some Besides being common, CRN is unique in its recalcitrant cases that seemed most impossible! presentation, as well as in the patient population —SARAH LUP, PA-C, Chicago, Illinois it affects (eg, older patients with sun damage confined to the posterior neck), so the differen- RETHINKING PRESCRIBING tial is quite narrow. Punch biopsy would resolve DICLEGIS Diclegis is the only FDA-approved prescription any confusion. CRN puts this patient at higher risk for the medication for nausea and vomiting of pregdevelopmentThe of skin caused by sun expo- nancy that is classified as Category A (safe for se cancers are lette rssquamous sure, such asand basal cell carcinoma, cell mom and baby). Before writing a prescription, from prac successe titioconsider ners arou carcinoma, melanoma, and s,others. the price tag. Diclegis with a coupon obseThis nd the coun rvatpatient ions, andcosts approximately and others with similar histories require regular $345 try for 60 tablets. The pearls with who their to share their skin checks by a qualified dermatology provider most common dosagecolle is 2 tablets/dwan but tcan agues. We clinical chall at least once a year. Although this patient would be more. Some patients may obtain insurance invite you enges to participa be advised to protect himself from the sun, this coverage for this medication, but it will likely te. will do little to ward off any future skin cancers still cost something. Let’s break down Diclegis that will have been caused by sun overexposure CONSUL into its 2 active ingredients: doxylamine sucTAT occurring decades earlier. Application of sun- cinate IONand S pyridoxine hydrochloride (vitamin screen to his neck would prevent IRO worsening of B 6). Unless you are writing a prescription for N PILL 2. Cohen SM, Kwo PY, Lim, his CRN. a celebrity, recommend that your patients ON LIVE S AND THEIR JK. ACG clinical of abnorm Send us R ENZ al liver chemis ECT guideline: your purchase over-the-counter doxylamine YMESinsteadEFF Can takin evaluat tries. Am J Gastroe 3. Iron. ion g iron pills nterol. 2017;1 al Institute Reference letters with succinate and vitamin B 6 to take Nation at night elevate liver —AGNES 12:18-35. of Health nih.gov/Iron.h ques website. https:// enzymes? MURPHY, tm. Access for nausea. —AMBER PA-C, Bolognia JL, Jorizzo JL,tions Rapini RP. Dermatology. 1st ed. NewDEW, PCA and , Americus, livertox. ed April 3, commen 2019. Georgia Birmingham, Michigan York: Mosby, 2003;1380-1381. ts to: Liver enzym es Advisor Forum aspartate aminosuch as alanine amino , CASE FILE transfe The Clinica l Advisor, phatase are transferase (AST), and rase (ALT), S www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2019 45 275 7th Aven markers of alkaline phosfunction, and hepat ue, 10th CUTIS RHO should be referre ic injury, not hepat Floor, New Albumin, MBO ic York, d to as liver bilirubin, and chemistries. Contributed by Joe Monr IDALIS NY 10001 measures of prothrombin .You oe, MPAS, hepatocellu time are direct A 78-year-old may conta PA-C lar appropriately ct us heavily lined man presented characterized synthetic function and with thick e-mail at edito by skin on enzymes may are as “liver functio r@ be abnormal n tests.” Liver been present for an his posterior neck ened, clinicaladvis liver diseas that had even in patien indet or.com. Although e. The differe ts without the striking erminate period of Letters are ntial for elevat broad with time. skin chang tomatic, edited many be further define potential causative ed enzymes is insiste they were concerning es were asympfor length factors and and d that he be to his relativ d by the patien should risk factors. 1 clarity. The seen es who t’s by a medical histor The Clinical y and the patient had spent dermatology provider. Almost all Advisor’s policy nearl sun, farmi medications ng, ranching, y his whole life small risk of are associated is to print to his in elevat fishing, and the hepatotoxic 2 ed liver chemistries with at least a a histo property in rural tending author’s name Okla ity. Oral with ry homa or of witho iron skin cance . replacement with the letter r and claim He denied doses has little supplementation at typicaut good health. ed to be . liver or serum or No anony in The skin on enzyme elevati no adverse effects on l mous the patien or overdoses, the ons. However, contributio it in high doses lined and thickened t’s nuchal area was ns will of iron poison can cause acute hepato heavily . The multiple overla toxicity as a ing. be accepted. pping rhom lines joined to form result of ferrous sulfate Toxicity occurs after boidal shape ingestion of (approximat ≥3 g s. toxicity with Altho ely 10 tablets ugh aminotransf ). Severe the upper limit erases greate r overdoses and of normal typically than 25 times occurs with high initial larger serum iron dL). Mild levels to usually self-limmoderate cases of iron (>1000 ug/ whereas severe iting and resolve with poisoning are suppo KUSMIN cases become fatal rapidl 3 rtive care, SKY, PA-C y. —LAURA Referenc es
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1. Approach to the patient with abnorm and functio n tests. UptoD al liver bioche mical ate.com websit uptodate.com e. https://www. /contents/app roach-to-theabnormal-liver patient-with-biochemical -and-functionApril 2, 2019. tests. Access ed
44 THE CLINI
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www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2019 5
CONTENTS SEPTEMBER 2019
Newsline ■ Substituting Physicians With NPs or PAs in Nursing Homes ■ Hawaii Legislation Repeals Physician Chart Reviews for Practicing PAs
FEATURE 10 APPs Provide Care Equal to MDs
28 Hypopigmented Macules and Patches
Chronic Pancreatitis: Challenging to Diagnose, Difficult to Treat Chronic pancreatitis is a complicated disease that leads to significant psychosocial and physical disability and reduced quality of life.
Salary Survey Find out how your salary and benefits package compare to those of your peers. The results of the 2019 Salary Survey are in and available to help guide you.
Web Roundup A summary of our most recent opinion, news, and multimedia content from ClinicalAdvisor.com.
Dermatology Clinic ■ Hair Loss on the Parietal Scalp ■ Hypopigmented Macules and Patches
Dermatologic Look-Alikes Erythematous, Pruritic Plaques
Legal Advisor Medical Errors and Negligence
33 Erythematous, Pruritic Plaques
39 Medical Errors and Negligence
Follow us on Twitter @ClinicalAdvisor
Like us on Facebook facebook.com/TheClinicalAdvisor Visit us on the web ClinicalAdvisor.com Download the app ClinicalAdvisor.com/App
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Benzodiazepine Monotherapy Often Used for Depression Contrary to Guidelines
Elements of Successful Medical Care for Transgender Patients The largest barrier to care for transgender persons is a lack of knowledgeable providers who offer appropriate and culturally competent care.
A study found that the most commonly prescribed benzodiazepine monotherapies were alprazolam, lorazepam, clonazepam, and diazepam.
Improved Counseling on Effective Contraception Needed for Women With Epilepsy In a study of women with epilepsy at risk for pregnancy, researchers found that 36.6% were not using highly effective contraception despite the risk of having offspring with congenital malformations.
Rate of Pediatric ED Use After ACA Implementation Between 2014 and 2016, the rate of pediatric emergency department visits increased by 9.7% per year.
Increasing Lung Cancer Screening Eligibility in African American Smokers
FEATURES ClinicalAdvisor.com/Features Family Planning in Multiple Sclerosis Research highlights the need for health care professionals to proactively and directly address the issues and risks of disease-modifying therapies in patients with MS planning to start a family. New Approaches to Care of Women With PAH Renewed focus on the impact of PAH in women — along with evidence that links estrogen to the activity of PAH genetic factors — has led to updated, gender-based definitions regarding the classification, pathophysiology, diagnosis, and treatment of PAH.
CLINICAL CHALLENGE ClinicalAdvisor.com/CaseStudy
Race-specific adjustment of pack-year criteria in lung cancer screening guidelines would result in more equitable screening for African American smokers at high risk for lung cancer.
Recommendations on Caring for Those Who Are Incapacitated, Unrepresented Patients who are incapacitated cannot consent to medical treatment, and if a representative is unavailable, no one can consent on their behalf.
8 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
Brady Pregerson, MD Case Study: Arm Weakness and Paresthesia A 52-year-old man with a history of remote neck surgery presents to the emergency department with weakness and paresthesia in the left arm. He first noted the symptoms when he awoke in the morning. The patient denies any neck pain, headache, speech or vision changes, or other symptoms. Physical examination reveals grip weakness in the left hand. See the full case at: ClinicalAdvisor.com/CaseSept19
Advisor Dx Interact with your peers by viewing the images and offering your diagnosis and comments. To post your answer, obtain more clues, or view similar cases, visit ClinicalAdvisor.com/AdvisorDx. Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues. Check out some of our latest cases below!
Erythematous Plaque With Central Scale on the Calf A 70-year old man presents for evaluation of an asymptomatic rash on his leg that he first noted several months ago. He denies a history of systemic disease or skin cancer. Examination reveals a well-demarcated, erythematous plaque with central scale on his right lateral upper calf. CAN YOU DIAGNOSE THIS CONDITION?
• Psoriasis • Bowen disease
• Sarcoid • B cell lymphoma
● See the full case at ClinicalAdvisor.com/DermDx_Sept19
In partnership with
Journal of Orthopedics for Physician Assistants
Severe Knee Pain and Disability A 67-year-old man presents for evaluation of severe right knee pain and disability. He underwent a right total knee replacement 30 years ago that was complicated by an infection within a year. He has since developed progressive pain and deformity in the knee, with severe stiffness. On examination, a valgus knee deformity of 40° is noted, and range of motion is 0° to approximately 30° of flexion. WHICH IS THE NEXT BEST STEP IN TREATMENT?
• Observation • Revision knee arthroplasty • Above the knee amputation • Knee fusion ● See the full case at ClinicalAdvisor.com/OrthoDx_Sept19
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2019 9
Newsline NURSE practitioners (NPs) and physician assistants (PAs) can autonomously substitute for elderly care physicians (ECPs) in a nursing home setting because of the high level of collaborative care they provide, according to a study published in BMJ Open. Researchers in the Netherlands selected 7 nursing homes in which NPs (n=3), PAs (n=2), and registered nurses (RNs; n=2) were compared with ECPs (n=15) and medical doctors (MDs; n=2). Data collected consisted of observations of the NP/ PA/RN and an ECP/MD;interviews with the participants; questionnaires filled out by the NP/PA/RN, ECPs/MDs, and managing directors/managers of the facility; and analysis of internal policy documents. The clinicians worked in 3 types of units: unit for residents with physical disabilities, dementia special care unit, and geriatric rehabilitation unit. Autonomous substitution for ECPs was present in 4 of the facilities; in 2 cases, the professional was a PA, and the professional was an NP in 2 cases.
In 3 of the cases, 2 PAs and 1 NP worked on their own unit or units with an ECP in the background as an expert colleague rather than a supervisor; in 1 case, the NP and the ECP shared responsibility for residents on a unit and worked together closely. Factors that made substitution successful were organizational factors that acknowledge NPs and PAs as independent clinicians, as well as individual factors such as the proactivity of the clinician. In facilities 3, 4, and 7, the collaboration between the NP, PA, and ECP was based on trust. The ECP shared responsibilities with the NP or PA, and the clinicians all shared the same views on what constituted good resident care, which was established through the use of ad hoc meetings. In certain cases, however, the ECP did not trust the NP or PA, and responsibilities of care were not equally shared. In all cases, the professionals performed tasks such as the structural evaluation of restraints, writing care programs, enhancing
© MORSA IMAGES / GETTY IMAGES
Substituting Physicians With NPs or PAs in Nursing Homes
Acknowledging NPs and PAs as autonomous clinicians promoted successful substitution of physicians.
rehabilitation climate by implementing a breakfast or lunch buffet, educating the care team, and being a member of working groups who discussed specific themes and innovations such as fall prevention. “Our description of three mechanisms of substitution showed that according to participants, the NPs and PAs are able to deliver similar quality of healthcare as the ECPs, based on the condition that the collaboration between the NP or PAs and the ECP is qualified as successful,” the authors concluded.
Hawaii Legislation Repeals Physician Chart Reviews for Practicing PAs HAWAII GOVERNOR David Ige signed the SB 1406 bill on July 2, 2019, which repealed the state’s outdated requirement for 100% chart review by a physician and included other changes to physician assistant (PA) laws currently in place in Hawaii. “Repealing 100% chart review for all PAs within seven days is a huge administrative burden that we’re happy to finally have removed from our state laws,” said Christina Starks, PA-C, president of the Hawaii Academy of PAs. Additional changes implemented in the legislation include allowing chart review to be determined at the practice level
for PAs with >1 year of experience. For PAs with <1 year of experience, 50% chart review should be conducted for the first 6 months and 25% for the second 6 months. A “group of physicians” are among the individuals who may establish a work relationship with a PA. Although the 100% chart review requirement was repealed, the requirement for 100% chart co-signature for all controlled substance prescriptions remains in effect under the Uniform Controlled Substances Act of Hawaii. The bill went into effect on July 1, 2019. ■
10 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
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FEATURE: ANNA WALKER, PA-C; MICHAEL FELZ, MD
Chronic Pancreatitis: Challenging to Diagnose, Difficult to Treat Chronic pancreatitis stems from a variety of pathogenic entities that result in chronic inflammation, fibrosis, and irreversible damage to the pancreas.
hronic pancreatitis (CP) is a debilitating disease that is associated with approximately $150 million in healthcare expense annually.1 It is a complicated disease in that it is multifactorial, problematic to diagnose, and difficult to treat. The majority of patients with CP experience severe abdominal pain; 50% will develop endocrine insufficiency, and 80% will develop exocrine insufficiency within 5 years of diagnosis. Abdominal pain and other myriad symptoms lead to significant psychosocial and physical disability and reduced quality of life.2
© ZEPHYR / SCIENCE SOURCE
Diagnostic imaging for chronic pancreatitis often begins with abdominal CT.
12 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
A variety of pathogenic entities contribute to CP, all of which result in chronic inflammation, fibrosis, and irreversible damage to the pancreas. These etiologies can be remembered according to the mnemonic TIGAR-O: toxicmetabolic, idiopathic, genetic, autoimmune, recurrent, and obstructive.3 Toxic-metabolic triggers include chronic alcohol abuse, tobacco use, hypercalcemia, hyperlipidemia, uremia, and others. Chronic exposure to toxins is responsible for oxidative damage at the cellular level, resulting in parenchymal destruction and reduced pancreatic function.4 Idiopathic CP occurs in 2 patterns based on age: idiopathic chronic juvenile pancreatitis in the pediatric population (early onset) and idiopathic senile chronic pancreatitis in the elderly (late onset).5 One form of early-onset CP is tropical
CP, also known as fibrocalculous pancreatic diabetes; this entity is most common in tropical, southern India.1 The bimodal age distribution in idiopathic CP is poorly understood, but environmental, genetic, and autoimmune factors are likely responsible. To relegate a case of CP as idiopathic requires that all other entities be excluded.4 Genetic causes of CP are the result of mutations primarily involving “premature activation of trypsinogen or failure to inactivate trypsin during pancreatic inflammation,” which ultimately damages the pancreas.5 Trypsin is the active form of the precursor enzyme trypsinogen. Trypsinogen is produced by and stored in the pancreas, and upon stimulation by cholecystokinin, it is released into the duodenum where it is converted to trypsin, an enzyme involved in the breakdown of protein. If this chain of events fails, trypsin promotes autodigestion of acinar tissue, leading to pancreatitis. Genes directly or indirectly related to the trypsin pathway and underlying derangements in the development of CP include: CFTR (codes for cystic fibrosis transmembrane regulator protein), PRSS1 (codes for cationic trypsinogen enzyme), SPINK1 (codes for pancreatic secretory trypsin inhibitor protein), CTRC (codes for chymotrypsin C enzyme), and CASR (codes for calcium sensing receptor protein).3,5 Autoimmune pancreatitis occurs in 2 patterns. Type 1 correlates with deposition of immunoglobulin G4 (IgG4) in pancreatic tissue, leading to subsequent damage to the pancreas. Infiltration of IgG4, however, is not confined to the pancreas; IgG4 may invade the bile duct, salivary glands, retroperitoneum, kidneys, and lymph nodes.5 Type 2, in contrast, is characterized by cellular infiltration of neutrophils, which damage the pancreatic ducts. Both types 1 and 2 respond to treatment with steroids.5 Recurrent pancreatitis is typified by repeated episodes of acute pancreatitis, resulting in cumulative tissue damage. Complete morphologic resolution rarely occurs following numerous attacks. Deposition of collagen and formation of scar tissue interfere with restoration of glandular structure and function, resulting in CP.4 Obstructive CP consists of segmental anatomic blockade in the ductal system by occlusive stones, tumors, or structural entities such as pancreas divisum. Obstruction of enzyme flux in and out of the ductal network results in accumulation of digestive enzymes within the pancreas.This dynamic process creates elevated intraductal and parenchymal pressures, mimicking a compartment syndrome and resulting in ischemic tissue damage.4,6 Clinical Presentation
Because many patients with CP display risk factors associated with certain etiologies, it is important that social and medical
TABLE. Differential Diagnoses for Chronic Pancreatitis7 Cholangiocarcinoma
Peptic ulcer disease
histories be explored for conditions predisposing patients to the disease.7 The most common symptom of CP is epigastric pain, often exacerbated by lying down and alleviated by leaning forward. Radiation to the back also occurs frequently. Pain is typically postprandial, and can be persistent or intermittent. Depending on disease severity, patients may also present with exocrine dysfunction, which manifests as malabsorption (weight loss, diarrhea, and steatorrhea), and endocrine disturbance presenting as hyperglycemia. Signs and symptoms vary depending on the etiology of CP.7 Physical examination in CP often reveals midline epigastric tenderness. Rigidity and rebound are rare. The presence of ascites suggests a pseudocyst, abscess, or other complication. Physical findings may prove beneficial in ruling out conditions that mimic CP (Table).7 No single laboratory test is diagnostic of CP. Amylase and lipase are usually normal in chronic disease but may be elevated in early disease stages or during an acute exacerbation. In late-stage CP, amylase and lipase may be low, signaling exocrine insufficiency, although this is not sensitive or specific.3,7 Laboratory data are of further value in determining precise etiologies of CP, especially metabolic toxins, and in monitoring disease flares or complications. For example, elevated liver enzymes may suggest alcohol abuse. Azotemia may indicate uremic pancreatitis. Hypercalcemia may indicate calcium deposition in the pancreas.Abnormal blood glucose levels are associated with loss of endocrine function. Elevated white blood cell counts may indicate pancreatic infection or necrosis.7 Diagnostic Testing
Clinical presentation, radiologic imaging, and pancreatic function testing (PFT) are pillars of investigation for the diagnosis of CP, which is a complex illness that often eludes diagnostic certainty. Radiologic modalities are helpful for Continues on page 19
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2019 13
Pancreatic function testing is useful for diagnosing chronic pancreatitis based on quantification of exocrine pancreatic insufficiency. visualizing the pancreas and associated calcifications, which is a common radiologic finding in CP. Imaging is often the first step in diagnostic testing. Noninvasive modalities include computed tomography (CT) and magnetic resonance cholangiopancreatography (MRCP). More invasive tools, such as endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasound (EUS), are helpful in the evaluation of more challenging cases.3 Computed Tomography Diagnostic testing often begins with abdominal CT with pancreatic protocol. CT images are effective for detecting scattered pancreatic calcifications, which is suggestive of late-stage CP. CT is also useful in assessing for disease complications, such as pseudocysts and necrosis, and for differentiating similar diagnoses such as pancreatic adenocarcinoma, cholangiocarcinoma, and other biliary tract pathology. Lack of sensitivity in earlier stages of CP, however, limits the capability of CT to visualize ductal and parenchymal derangements.3 Magnetic Resonance Imaging MRI is additive in diagnosing CP. According to the American Pancreatic Association, MRI is more sensitive than CT in the evaluation of CP in earlier stages, conferring an important advantage for early clinical intervention and enhanced disease outcomes. Although several MRI protocols are available, the MRCP/secretin protocol is regarded as the most accurate.3 MRCP involves an MRI of the abdomen focused on structural images of the pancreas, bile duct, and gallbladder. This method provides more definitive visualization than MRI of the abdomen alone.3 The MRCP/secretin protocol involves intravenous administration of secretin, a hormone that stimulates pancreatic exocrine secretion. Images are generated during secretin administration to qualify pancreatic function while also visualizing pancreatic structure. Furthermore, secretin administration increases the sensitivity and specificity of MRCP.3
criteria are more sensitive, whereas Rosemont criteria are more specific.8 Regardless of the criteria used, EUS remains a useful test. Diagnosis should be established based on signs and symptoms consistent with CP in combination with EUS or other imaging modality.5 Pancreatic Function Testing PFT is useful in diagnosing CP based on quantification of exocrine insufficiency.3 Methodology of PFT may involve either direct or indirect approaches. Direct PFT involves administration of secretin followed by endoscopic collection of stimulated pancreatic secretions while obtaining simultaneous EUS imaging. Direct PFT is distinct from the MRCP/ secretin protocol in that it provides quantitative physiologic assessment. In contrast, MRCP/secretin testing is a qualitative evaluation of exocrine insufficiency wherein no fluid is collected or measured. Since direct PFT is invasive, it is rarely employed today. Indirect PFT is far more commonly performed and involves the assessment of fecal elastase 1 or fecal fat concentrations in a stool specimen. Fecal elastase 1 is a pancreatic enzyme that digests protein and aids in transport of cholesterol.3 Fecal elastase 1 concentrations <200 μg/g of stool are abnormal and indicative of some degree of exocrine insufficiency. Fecal elastase 1 concentrations <100 μg/g of stool indicate severe exocrine insufficiency and are supportive of a diagnosis of CP. Moreover, this assessment
POLL POSITION Which of the following is the most common symptom of chronic pancreatitis? 4.23% ■ Weight loss ■ Epigastric pain
Endoscopic Ultrasound EUS is regarded as the most sensitive imaging tool for the diagnosis of CP and identification of ductal and parenchymal abnormalities early in the disease.8 EUS provides a high sensitivity of 91% depending on which diagnostic criteria are employed, conventional or Rosemont.5,8 The limitation of EUS, however, is low specificity. Yet as with sensitivity, specificity relies on the set of criteria employed.5,8 Conventional
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www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2019 19
Abdominal pain, malabsorption, weight loss, and steatorrhea are indicative of exocrine pancreatic insufficiency. requires only 1 stool sample and is not affected by pancreatic enzyme replacement therapy (PERT).3,5,9 Fecal fat measurements are less specific but still may be considered. Detection of ≥7 g of fat per 24 hours during a 72-hour collection period is abnormal and suggestive of a diagnosis of CP.3,5,9 When interpreting indirect PFTs, confounding elements such as diarrhea and bacterial overgrowth can cause false positives. Likewise, the presence of acute pancreatitis can cause false negatives. Celiac disease and inflammatory bowel disease must be considered in the interpretation of PFTs.3 Endoscopic Retrograde Cholangiopancreatography ERCP is intended primarily for therapeutic purposes and is rarely used for diagnosis of CP. When selected for diagnosis, ERCP allows for performance of diagnostic biopsies. ERCP is invasive and carries significant risk for triggering acute pancreatitis.Additional limitations include visualization restricted to the ductal system, intraoperator bias, and lack of specificity.3 Histology obtained by ERCP lacks sensitivity and specificity due to sampling error.5 Treatment
Initial treatment for CP is lifestyle modification with alcohol and smoking cessation, along with elimination of other metabolic or exogenous toxins. Further treatment is divided into 3 categories: medical, endoscopic, and surgical. Appropriate selection of therapeutic measures depends on the overall health of the patient, as well as the etiology and severity of CP.5 Medical Pain control is the established mainstay of treatment, yet pain management is one of medicine’s most elusive therapeutic measures. In the past, mechanical dysfunction due to pancreatic duct obstruction and resultant ductal hypertension was thought to be responsible for most of the pain associated with CP. More recently, however, neurobiologic mechanisms have been implicated. In theory, recurrent damage to the pancreas results in inflammation of intrapancreatic nerves triggering abnormal pain as organized in the central nervous system.5,6 Concepts based on nerve inflammation support inclusion of neuropathic pain medications to existing treatment regimens. Such novel regimens could prove beneficial in pain control as well as in reduction of opioid use and dependence. Patients with CP are often responsive to medications such as tricyclic antidepressants, gabapentin, pregabalin, and selective serotonin reuptake inhibitors.Therapeutic success with
such regimens lends biologic plausibility to the concept of pancreatic neuropathy.5,6 Some patients, in contrast, achieve adequate pain relief with nonsteroidal anti-inflammatory drugs and acetaminophen.Antioxidant therapy and pancreatic enzyme replacement are available but are of unpredictable efficacy in reducing pain.5 Another medical essential is management of pancreatic exocrine dysfunction. Abdominal pain, malabsorption, weight loss, and steatorrhea are indicative of exocrine insufficiency. Treatment is advisable for patients with these signs and symptoms. Most patients begin therapy with digestive enzyme replacement such as 40,000 units of lipase with meals. Severe insufficiency may require up to 90,000 units 3 times daily. Lesser amounts are appropriate for lighter meals or snacks.5,9 Typical enzyme preparations contain amylase and protease. Histamine-2 receptor antagonists and proton pump inhibitors provide benefit in addition to enzyme supplementation. These agents act by minimizing premature enzymatic breakdown of pancreatic enzymes by stomach acid. Reduction of fat intake and consumption of multiple small meals throughout the day are also effective for some patients. Response to enzyme replacement can be monitored by frequently checking serum levels of fat-soluble vitamins, especially vitamin D.9 A third goal of medical therapy is management of pancreatic endocrine deficiency. Labelled as “pancreatic diabetes,” or “type 3C diabetes,” this entity must be distinguished from type 1 or type 2 diabetes mellitus, although it is treated similarly in early stages.5,9,10 Until insulin is necessary for euglycemia, type 3C diabetes may be successfully treated with metformin. In addition to antidiabetic effects, metformin has antineoplastic properties and has been reported to reduce the risk of pancreatic cancer by as much as 70%.10 Sulfonylurea preparations may also be considered an appropriate choice, but care must be taken to avoid hypoglycemia. If endocrine insufficiency ensues and first-line management is ineffective, insulin will be necessary.5,10 Incretin-based therapies, such as glucagon-like peptide-1 (GLP-1) analogues and dipeptidyl peptidase 4 (DPP-4) inhibitors, are not recommended due to concomitant increased risk of medication-induced pancreatitis and problematic side effects. Likewise, thiazolidinediones should be avoided.10 Endoscopy Endoscopy may be necessary when medical therapy fails. Careful patient selection is prudent to avoid endoscopic
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Continues on page 22
Early recognition of chronic pancreatitis is paramount to preserving quality of life for patients with the condition. complications, such as acute pancreatitis and exacerbation of CP.5 ERCP is usually definitive in removal of obstructing intraductal stones, dilation of intraductal strictures, and drainage of pseudocysts.5,9
3. Conwell DL, Lee LS, Yadav D, et al. American Pancreatic Association practice guidelines in chronic pancreatitis: evidence-based report on diagnostic guidelines. Pancreas. 2014;43(8):1143-1162. 4. Stevens T, Conwell DL, Zuccaro G. Pathogenesis of chronic pancreatitis: an evidence-based review of past theories and recent developments. Am J
Surgery Interventional surgery is reserved for patients for whom medical and endoscopic therapies are unsuccessful. Certain cases of severe CP require surgery as first-line therapy. Surgical indications include poor pain control; duodenal, biliary, and pancreatic duct obstruction; symptomatic pseudocysts (complex or large); extensive necrosis; and suspicion of pancreatic cancer.5 Four common surgical techniques are used: • Pancreaticojejunostomy, for obstructive ductal disease, can be performed using the Frey or Puestow techniques.5 • Pancreaticoduodenectomy, for cases with significant disease of the pancreatic head, can be performed using the Whipple or Beger approaches.5 • Distal pancreatectomy is preferred for disease in the pancreatic tail.5 • Total pancreatectomy with islet auto-transplantation can be performed in patients with nonobstructive disease and atrophy of the acini involving the entire pancreas.5
Gastroenterol. 2004;99(11):2256-2270. 5. Majumder S, Chari ST. Chronic pancreatitis. Lancet. 2016;387(10031):1957-1966. 6. Poulsen JL, Olesen SS, Malver LP, Frøkjær JB, Drewes AM. Pain and chronic pancreatitis: a complex interplay of multiple mechanisms. World J Gastroenterol. 2013;19(42):7282-7291. 7. Huffman J, Wehbi M, Obideen K. Chronic pancreatitis treatment & management: approach considerations, behavior modification, pharmacologic alleviation of abdominal pain. Medscape website. https://emedicine.medscape. com/article/181554- treatment#d10. Updated November 11, 2019. Accessed June 10, 2019. 8. D’Souza SL, Anderson MA, Korsnes SJ, et al. EUS diagnostic criteria for chronic pancreatitis: a comparison of conventional versus Rosemont criteria. Dig Dis Sci. 2015;60(12):3782-3787. 9. Nair RJ, Lawler L, Miller MR. Chronic pancreatitis. Am Fam Physician. 2007;76(11):1679-1688. 10. Ewald N, Hardt PD. Diagnosis and treatment of diabetes mellitus in chronic pancreatitis. World J Gastroenterol. 2013;19(42):7276-7281.
Anna Walker, PA-C, is a physician assistant in the department of medicine, division of gastroenterology, at Augusta University Medical Center, in Augusta, Georgia. Michael Felz, MD, is an associate clinical professor in the department of physician assistant studies at Augusta University, in Augusta, Georgia. References 1. Lew D, Afghani E, Pandol S. Chronic pancreatitis: current status and challenges for prevention and treatment. Dig Dis Sci. 2017;62(7): 1702-1712. 2. Juel J, Olesen SS, Olesen AE, et al. Study protocol for a randomised, double-blinded, placebo-controlled, clinical trial of S-ketamine for pain treatment in patients with chronic pancreatitis (RESET trial). BMJ Open. 2015; 5(3):e007087.
22 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
“Who wants to help me with the fireworks this year?”
© The New Yorker Collection 2019 from cartoonbank.com. All Rights Reserved.
This review has discussed the complex nature of CP and serves to raise awareness of the disease among all providers. It is important to be familiar with risk factors, clinical presentation, diagnostic workup, and treatment. Early recognition of CP is paramount to preserving quality of life for patients with the condition. ■
FEATURE: SALARY SURVEY
Are you being fairly compensated? As Clinical Advisor continues to be a champion for the nurse practitioner (NP) and physician assistant (PA) audiences, we recognize that just as clinical practice has evolved over the past year, so too has compensation. Are you considering a career in a new location or specialty and unsure about how this change may affect your compensation? The results of the 2019 NP/PA Salary Survey are in and available to help guide your next big career move. Similar to the results from previous surveys, more than half of all NPs and PAs who responded to the survey reported earning more in 2018-2019 than in the prior year.
See how your salary compares with those of your peers as reported in the 2019 NP/PA SALARY SURVEY
NPs and PAs reported average annual salaries in the 2019 survey of $107,973 and $115,881, respectively.
Although the wage gap persists between male and female advanced practice providers, it has narrowed in 2019. In 2018, men earned approximately $17,000 more than their female counterparts. In contrast, results from the 2019 salary survey indicate that male NPs earned approximately $11,000 more than female NPs, and male PAs earned approximately $15,000 more than female PAs.
The West Coast remains the region with the highest average yearly compensation, with NPs earning $117,311 and PAs earning $125,307. The majority of NPs surveyed reported practicing in suburban locations (38%); however, those practicing in urban locations (36.8%) earned the highest salary. Like NPs, the majority of PAs surveyed practiced in suburban locations (42.2%), but PAs working in rural areas earned the highest salary ($118,344). Interestingly, family medicine is no longer the specialty in which the majority of NPs and PAs are employed (27% and 13.8%, respectively). Like last year, most NP and PA respondents practice in a stand-alone clinic, but those working in hospitals reported earning the highest salary ($122,598 and $127,173, respectively). Additionally, 40.5% of NPs and 41.1% of PAs report working in more than 1 location, and approximately one-fourth of respondents see 51-75 patients per week. The majority of NPs and PAs anticipate earning as much or more than they currently earn in the year to come, with more than half of all clinician respondents expecting more money in their paychecks in 2020.
24 THE CLINICAL ADVISOR â€˘ SEPTEMBER 2019 â€˘ www.ClinicalAdvisor.com
See the complete survey results online at ClinicalAdvisor.com/2019SalarySurvey
TABLE 1. Average NP salary
TABLE 2. Average PA salary
Average hourly rate
Average hourly rate
TABLE 3. Average NP salary by practice area
TABLE 4. Average PA salary by practice area
TABLE 5. Average NP salary by degree attained
TABLE 6. Average PA salary by degree attained
Certificate of completion
Certificate of completion
TABLE 8. Average PA salary according to gender
TABLE 7. Average NP salary according to gender Female
FIGURE 1. Average NP salary by geographic region West
(n=273) $117,311 average salary
(n=451) $103,059 average salary
FIGURE 2. Average PA salary by geographic region
Northeast (n=311) $111,502 average salary
West (n=125) $125,307average salary
Midwest (n=130) $110,789 average salary
Northeast (n=128) $113,431 average salary
(n=609) $106,255 average salary
(n=174) $115,000 average salary
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FEATURE: SALARY SURVEY
FIGURE 3. Did you earn more this year (NPs)?
FIGURE 4. Did you earn more this year (PAs)?
FIGURE 5. Do you expect to earn more next year (NPs)?
FIGURE 6. Do you expect to earn more next year (PAs)?
TABLE 9. Average NP salary by experience level
TABLE 10. Average PA salary by experience level
Experience in years
Experience in years
FIGURE 7. Do you work in multiple locations (NPs)?
FIGURE 8. Do you work in multiple locations (PAs)? No
TABLE 11. Average NP salary by urban, suburban, or rural location
TABLE 12. Average PA salary by urban, suburban, or rural location
26 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
TABLE 13. Average NP salary according to practice setting
TABLE 14. Average PA salary according to practice setting
Walk-in/ Ambulatory Care
Walk-in/ Ambulatory Care
TABLE 15. Number of patients seen per week (NPs)
TABLE 16. Number of patients seen per week (PAs)
Number of patients
Number of patients
TABLE 17. Hours per week worked (NPs)
TABLE 18. Hours per week worked (PAs)
Hours per week
Hours per week
TABLE 19. How satisfied are you with your compensation (NPs)?
TABLE 20. How satisfied are you with your compensation (PAs)?
www.ClinicalAdvisor.com â€˘ THE CLINICAL ADVISOR â€˘ SEPTEMBER 2019 27
Dermatology Clinic CASE #1
Hair Loss on the Parietal Scalp MAYA FIRSOWICZ, BS; MICHELLE EUGENE LEE, BS; CHRISTOPHER RIZK, MD
A 25-year-old man with no significant medical history arrives at the clinic concerned about a bald patch on his head that has been growing in size. There is no family history of hair loss, and he denies hair-pulling, scratching, or trauma to the area. On examination, a well-demarcated, circular, smooth patch of nonscarring hair loss is noted over the parietal scalp. There is no hair loss on any other part of the body. What is your diagnosis? Turn to page 30
Hypopigmented Macules and Patches EMILY K. BURNS, BA; MICHELLE EUGENE LEE, BS; CHRISTOPHER RIZK, MD
A 30-year-old man presents to the clinic with a mildly itchy rash on his upper back and upper arms for the past week following a trip to the beach, during which time his skin became tanned from exposure to the sun. He is taking antihistamines. On examination, faint hypopigmented macules and patches with areas of fine scale are noted. Some of the lesions coalesce to form irregularly shaped patches. The patient denies pain but finds the lesions unsightly. What is your diagnosis? Turn to page 31 28 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
Dermatology Clinic CASE #1
Alopecia areata is a prevalent autoimmune disease of the hair follicles leading to nonscarring hair loss, commonly presenting as smooth patches of welldefined hair loss on the scalp. It has been frequently described in the literature since the early 20th century, with numerous studies investigating its etiology and treatment. A variety of presentations have been seen, ranging from small patches of hair loss to total body hair loss, and response to treatment has been found to vary widely among patients. After androgenetic alopecia, alopecia areata is the second most common cause of hair loss, affecting an estimated 4.5 million people in the United States, with a worldwide prevalence of 0.1% to 0.2% and an estimated lifetime incidence of 2.1%.1-3 Although it is often seen in children and younger adults, individuals of all ages can be affected with the condition.3 There is no apparent sex predominance, no significant variance among ethnicities, and hair of all colors can be affected.3,4 Alopecia areata is believed to occur as a result of an autoimmune process directed against follicular melanocytes or matrix keratinocytes in which inflammatory cells attack hair follicles in the anagen phase and prematurely propel them into the catagen phase.5 As the hair shaft can then no longer be anchored within the hair canal, it is subsequently shed, leading to visible hair loss.6 Given its underlying autoimmune basis, patients with alopecia areata are at increased risk for other conditions including atopy, vitiligo, thyroid disease, and other autoimmune diseases, as well as depression and anxiety.3,7 Alopecia areata has a strong genetic component, with a family history increasing the risk of developing the condition.7 Likewise, a family history of other autoimmune conditions increases the risk of developing alopecia areata. Patients with Down syndrome have also been found to be at increased risk for alopecia areata.7 The diagnosis of alopecia areata is primarily made clinically, with the classic presentation of well-defined, smooth patches of nonscarring hair loss and absence of any notable epidermal changes.8 Although the skin in the observed patch is typically normal, peachy or mildly reddened discoloration can sometimes be seen. Hair loss most commonly involves the scalp, but other areas such as the eyebrows, eyelashes, beard, extremities, or anywhere else on the body may be affected.4
Patches can be single, multiple, or diffuse, and classification of alopecia areata is typically based on this designation. Alopecia areata can present as patchy alopecia; alopecia totalis, where hair loss involves the entire head; or alopecia universalis, where hair loss involves the whole body.4,8 The latter two of these diagnoses are commonly observed to have high resistance to treatment.9 Other commonly observed patterns include ophiasis type, which is a band-like hair loss of the parieto-temporo-occipital scalp, or ophiasis inversus (sisaipho), which involves hair loss of the fronto-parietotemporal scalp.8 Common clinical findings in alopecia areata can include “exclamation mark hairs,” which are short hairs that taper closer to the skin, and nail pitting, an associated clinical finding observed in two-thirds of cases.4 Upon histologic examination, alopecia areata typically involves an infiltrate of lymphocytes surrounding the hair bulb, sometimes described as a “swarm of bees.”5 This finding may be absent in older alopecia areata lesions; therefore, other clues such as eosinophils, melanin and lymphocytes in fibrous tract remnants, and an increase in catagen-telogen follicles may help in diagnosis.5
Patches of alopecia areata can be single, multiple, or diffuse, and classification is typically based on this designation. The differential diagnosis for alopecia areata includes a variety of hair loss conditions, most notably tinea capitis, trichotillomania, and telogen effluvium.4,8 Several clinical features of these conditions can help differentiate them from alopecia areata. The presence of inflammation and scale as well as postauricular lymphadenopathy can help identify tinea capitis. The finding of hairs broken off at different lengths is more consistent with trichotillomania. Diffuse hair loss as opposed to localized hair loss can help distinguish telogen effluvium. Other potential diagnoses to consider include lupus or secondary syphilis, both of which can be confirmed via serologic testing.8 Although alopecia areata can be treated, no definitive cure is known. Spontaneous remission occurs in approximately 8% to 68% of cases, with the higher remission rates occurring when <25% of the scalp is involved.10 Treatment can often help with hair regrowth and prevent further hair loss.10 Initial treatment may involve topical or intralesional corticosteroids, with the former often preferred for pediatric patients who may not tolerate injections.10 Minoxidil foam or solution is
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sometimes added as adjuvant therapy. Short, 6-week courses of oral corticosteroids can also be effective for hair regrowth; however, the risk of relapse is high, and long-term use is not advised given the associated side effects. Other treatments including methotrexate and topical immunotherapy, such as diphenylcyclopropenone and squaric acid dibutylester, may be considered in refractory cases.9 New therapies including Janus kinase inhibitors such as tofacitinib, ruxolitinib, and baricitinib are currently under investigation.10 With continued development and study of new treatment options for alopecia areata, it is hoped that more effective hair regrowth and sustained disease control will be attainable. Our patient was treated with intralesional triamcinolone acetonide (5 mg/mL × 1 cc). At his return visit 6 weeks later, he was noted to have significant hair regrowth and was happy with the results. Maya Firsowicz, BS, is a medical student; Michelle Eugene Lee, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston,Texas. References 1. Safavi K. Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey. Arch Dermatol. 1992;128(5):702. 2. Mirzoyev SA, Schrum AG, Davis MDP, Torgerson RR. Lifetime incidence
Tinea versicolor, also known as pityriasis versicolor, is a benign, chronic discoloration of the skin caused by the proliferation of yeast. Malassezia furfur, previously known as Pityrosporum, is the dimorphic, lipophilic fungus that causes tinea versicolor.1 In 1853, Robin described the first Malassezia species.2,3 M furfur is a normal component of the skin flora that may opportunistically convert from the yeast to the mycelial form that invades the stratum corneum in tinea versicolor.4 Tinea versicolor occurs more frequently in hot, humid areas and tends to affect the skin of the face, arms, chest, and back. Adolescents and young adults are most commonly affected. Tinea versicolor is primarily a cosmetic concern but when pruritic can affect quality of life.2,5 Although the etiology of tinea versicolor appears to be multifactorial, genetics may predispose some individuals to developing these skin lesions. Adolescents and young adults more frequently develop tinea versicolor because increased sex hormones stimulate sebum production. In contrast, children less frequently experience tinea versicolor; when they do, it is more commonly
risk of alopecia areata estimated at 2.1% by Rochester Epidemiology Project, 1990–2009. J Invest Dermatol. 2014;134(4):1141-1142. 3. Fricke ACV, Miteva M. Epidemiology and burden of alopecia areata: a systematic review. Clin Cosmet Investig Dermatol. 2015;8:397-403. 4. Finner AM. Alopecia areata: clinical presentation, diagnosis, and unusual cases. Dermatol Ther. 2011;24(3):348-354.
Tinea versicolor occurs more frequently in hot, humid areas and tends to affect the skin of the face, arms, chest, and back.
5. Peckham SJ, Sloan SB, Elston DM. Histologic features of alopecia areata other than peribulbar lymphocytic infiltrates. J Am Acad Dermatol. 2011;65(3):615-620. 6. Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl J Med. 2012;366(16): 1515-1525. 7. Goh C, Finkel M, Christos PJ, Sinha AA. Profile of 513 patients with alopecia areata: associations of disease subtypes with atopy, autoimmune disease and positive family history. J Eur Acad Dermatol Venereol. 2006; 20(9):1055-1060. 8. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol. 2010;62(2):177-188. 9. Kassira S, Korta DZ, Chapman LW, Dann F. Review of treatment for alopecia totalis and alopecia universalis. Int J Dermatol. 2017;56(8): 801-810. 10. Strazulla LC, Wang EHC, Avila L, et al. Alopecia areata: an appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol. 2018;78(1):15-24.
found on the face. Other suspected contributing factors include the application of oils, creams, and cosmetics, which provide lipid nourishment for Malassezia. Tinea versicolor is associated with hyperhidrosis, exposure to sunlight, and oral contraceptive use, but it is not linked to poor hygiene.1,5 Immunocompromised individuals are at higher risk for the condition.4 Tinea versicolor typically presents as well-demarcated, hypopigmented, hyperpigmented, or salmon-colored patches, commonly on the back and chest. The lesions differ widely in color, hence the term “versicolor.”1 Oftentimes, a single herald patch precedes the development of multiple smaller lesions that may coalesce into larger patches. Upon scraping, a fine scale is visible, and some patients complain of mild pruritus.1,2,6 The diagnosis of tinea versicolor is made clinically but can be confirmed with a potassium hydroxide (KOH) mount of scrapings. Scales slough off in characteristic sheets with the use
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Dermatology Clinic of a glass slide or scalpel blade.6 Light microscopy of scrapings will reveal hyphae and round budding cells with a “spaghettiand-meatball” appearance.2,5 Wood lamp examination reveals yellow to yellow-green fluorescence of tinea versicolor patches but is not preferred due to decreased sensitivity. A skin biopsy of tinea versicolor is characterized by lymphocytes around the dermal vasculature, mild epidermal hyperkeratosis, and acanthosis; however, it is rarely required to confirm diagnosis.4,5 Differential diagnoses of tinea versicolor include psoriasis, seborrheic dermatitis, pityriasis rosea, mycosis fungoides, secondary syphilis, pityriasis alba, erythrasma, and vitiligo. Seborrheic dermatitis tends to present with a thicker scale, usually on the scalp and face. Results from the KOH
should use monthly topical or oral prophylaxis, particularly during the summertime.2 The diagnosis of tinea versicolor in this case was confirmed via KOH examination, and treatment with topical ketoconazole was initiated. After treatment with 2% ketoconazole shampoo, the patient started to notice resolution of the rash. The discoloration completely faded within a few weeks. ■ Emily K. Burns, BA, is a medical student; Michelle Eugene Lee, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston,Texas. References 1. Mendez-Tovar LJ. Pathogenesis of dermatophytosis and tinea versicolor. Clin
The diagnosis of tinea versicolor is made clinically but can be confirmed with a potassium hydroxide mount of scrapings.
Dermatol. 2010;28(2):185-189. 2. Hudson A, Sturgeon A, Peiris A. Tinea versicolor. JAMA. 2018;320(13):1396. 3. Robin C. Historie Naturelle des Vegeaux Parasites. Paris; Chez H. Bailliere; 1853:438. 4. Gupta AK, Batra R, Bluhm R, Faergemann J. Pityriasis versicolor. Dermatol Clin. 2003;21(3):413-429. 5. Sunenshine PJ, Schwartz RA, Janniger CK. Tinea versicolor. Int J Dermatol. 1998;37(9):648-655. 6. Han A, Calcara DA, Stoecker WV, Daly J, Siegel DM, Shell A. Evoked scale sign of tinea versicolor. Arch Dermatol. 2009;145(9):1078. 7. Lange DS, Richards HM, Guarnieri J, et al. Ketoconazole 2% shampoo in the treatment of tinea versicolor: a multicenter, randomized, double-blind, placebo-controlled trial. J Am Acad Dermatol. 1998;39(6):944-950. 8. Hu SW, Bigby M. Pityriasis versicolor: a systematic review of interventions. Arch Dermatol. 2010;146(10):1132-1140.
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© Harley Schwadron, 2019.
e xamination eliminate pityriasis rosea, pityriasis alba, secondary syphilis, and mycosis fungoides from the differential. Vitiligo presents with completely depigmented macules and patches as opposed to hypopigmented lesions. Erythrasma will fluoresce coral-red on Wood lamp illumination rather than the characteristic yellow-green of tinea versicolor.1,4,5 Treatment of tinea versicolor with topical and oral antifungals is usually successful. Topical antifungals, such as ketoconazole, are first-line therapy due to their targeted activity against Malassezia. Selenium sulfide and zinc pyrithione shampoos act by removing the stratum corneum and are also effective with a shorter required duration of therapy than ketoconazole antifungals.2 One to 3 applications of 2% ketoconazole can be sufficient for treatment.7 Topical treatment is less expensive than systemic treatment; however, application to the back may be difficult for some patients, and topical antifungal shampoos must be applied for extended periods of time before rinsing. Oral therapies are indicated for patients for whom topical therapy is ineffective or those who experience recurrent or widespread tinea versicolor. Oral fluconazole can safely treat extensive or recurrent tinea versicolor. Drug interactions and liver function abnormalities have been reported with the use of oral antifungals.8 Patients using either oral or topical therapies should be advised that the scale quickly resolves after treatment of active infection but dyschromic areas may persist for months. The successful resolution of active infection can be confirmed by KOH examination. Patients who experience multiple recurrences
Dermatologic Look-Alikes Erythematous, Pruritic Plaques KAITLYN LEA STREIGHT, BS; MICHELLE EUGENE LEE, BA; CHRISTOPHER RIZK, MD
A 30-year-old man presents to the office for a mildly itchy rash over a large area of his body that has been worsening for the past 6 months. He states that the rash started on his elbows and knees and has quickly spread to his torso and extremities. He has tried several home remedies to no avail. On examination, the patient has diffuse, erythematous plaques with silvery scale covering his elbows, knees, chest, and back. He has no significant medical history and is otherwise healthy. He is anxious to be rid of the rash.
A 38-year-old man presents to the office with an itchy rash on his wrists and torso. The patient has a medical history that includes asthma and allergic rhinitis. He says that the rash has been worsening for the past few years, has a waxing and waning nature, and is intensely itchy when it flares. The patient has not tried any treatments and cannot think of any factors that make the rash worse or better. On examination, erythematous, excoriated, and annular-like plaques are noted on his wrists and torso.
www.ClinicalAdvisor.com â€˘ THE CLINICAL ADVISOR â€˘ SEPTEMBER 2019 33
Dermatologic Look-Alikes CASE #1
Psoriasis is a chronic, immunemediated disease with a variety of subtypes affecting the skin and joints.1 Prior to the first clinical description by Robert William in 1808, the disease was commonly confused with leprosy.2 Psoriasis affects approximately 2% of people worldwide, with an equal prevalence among men and women.3,4 The disease primarily affects adults in a bimodal distribution, with peaks in diagnoses for patients in their 20s and 50s.4 Although the etiology of psoriasis is not fully understood, immune system overactivation along with genetic and environmental factors have been found to contribute to disease development. Psoriasis is an autoimmune disease historically thought to be predominantly caused by CD4+ helper T cells. More recent research indicates that cell type Th17 secretes the proinflammatory cytokines that cause the inflammation and keratinocyte proliferation associated with the disease. Development of Th17 is maintained in a positive feedback loop by interleukin (IL)-23 produced by dendritic cells of the innate immune system.5 Genetic factors are implicated in the pathogenesis of psoriasis, as 30% of affected individuals have a first-degree relative with the condition.6 Genetic influences are also demonstrated by a concordance rate of approximately 70% in monozygotic twins and 20% in dizygotic twins. Multiple genes including PSORS1, CARD14, and IL36RN have been linked to psoriasis.7 In addition, environmental factors such as medications, smoking, alcohol, obesity, and stress contribute to disease development in genetically susceptible individuals.8 The diagnosis of psoriasis is primarily made clinically. Classic findings include relapsing and remitting, well-demarcated, erythematous plaques with dry, silvery scales.1,9 Other common features are scalp involvement and nail discoloration, pitting, and dystrophy. Plaque psoriasis, also known as psoriasis vulgaris, is the most common subtype, comprising 90% of diagnoses. Lesions can be present on the extensor, periumbilical, and perianal regions in adults, while smaller plaques occurring on the face and flexural regions are seen in children.6 Guttate psoriasis, most commonly seen in children after a recent streptococcal infection, is characterized by small droplet-shaped plaques in a centripetal distribution. While guttate psoriasis accounts for only 2% of all cases, approximately one-third of affected patients will develop plaque psoriasis later on. Another rare form of psoriasis is pustular psoriasis, which is
characterized by a localized eruption of white pustules following steroid withdrawal.1 Early diagnosis and treatment are important to prevent disease progression. Assessment tools, such as The Psoriasis Area and Severity Index (PASI) score, are used following diagnosis to determine disease severity based on the extent of involvement. Because 30% of patients develop psoriatic arthritis as a complication, physicians should assess for joint symptoms at each visit.9 Screening for mental disorders, such as depression and anxiety, is crucial due to the impact of the disease on a patientâ€™s psychological well-being.10 Although biopsy is rarely required for diagnosis, histologic features can distinguish psoriasis from other conditions when
The differential diagnosis of psoriasis includes eczema, tinea capitis, tinea corporis, and seborrheic dermatitis. the diagnosis is unclear. Epidermal changes involve acanthosis, hyperkeratosis, and parakeratosis with thickened rete ridges that form the characteristic plaques. Engorged blood vessels causing erythema are visualized in the tips of the dermal papillae. An inflammatory infiltrate composed of T cells, macrophages, neutrophils, and mast cells is present within the epidermis and dermis.9 The differential diagnosis of psoriasis includes eczema, tinea capitis, tinea corporis, and seborrheic dermatitis.9 Psoriasis can be differentiated from eczema primarily by distribution on the extensor surfaces; the classic appearance of erythematous plaques with dry, silvery scales; and presentation at an older age. The Auspitz sign, seen when bleeding occurs after removal of a silver plaque, and the Koebner phenomenon, observed when psoriatic lesions occur in areas of trauma, make psoriasis a more likely diagnosis over other dermatologic conditions.6 Other diagnoses to consider include lichen planus, pityriasis rosea, secondary syphilis, and cutaneous lymphoma.9 While lichen planus presents as violet papules on the wrists, psoriasis presents as silvery plaques on the extensor surfaces. A negative rapid plasma reagin favors a diagnosis of psoriasis over secondary syphilis. The treatment of psoriasis involves topical medications, phototherapy, and systemic agents. First-line therapy for mild cases often includes topical glucocorticoids, vitamin D analogues, or both. While glucocorticoids provide effective and rapid relief of symptoms, they can lead to skin atrophy with long-term use.9,11 In areas where steroid treatment is often avoided, such as the face and intertriginous areas,
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Dermatologic Look-Alikes topical calcineurin inhibitors may be effective. Although less effective, vitamin D agents are safest for the long-term topical treatment of psoriasis. Phototherapy with ultraviolet (UV) B light can also be used for the short-term treatment of moderate to severe forms of psoriasis due to the suppressive effect of UV exposure on the Th17 immune response.8,9 However, phototherapy must be used with caution due to the risks of premature aging and skin cancer. Systemic agents such as methotrexate, cyclosporine, and acitretin are usually reserved for more severe cases of psoriasis due to the risk of organ toxicities.9,11 Methotrexate is highly effective at treating severe psoriasis and psoriatic arthritis but must be used with caution due to the risk of liver cirrhosis.11 Within recent years, several new biologic therapies have been introduced that target the inflammatory pathways with intermediate effect on the pathogenesis of psoriasis.9 Tumor necrosis factor-α inhibitors, such as etanercept and infliximab, treat psoriasis by blocking proinflammatory cytokines.11 Ustekinumab inhibits IL-12 and IL-23, thus preventing the development of Th17 lymphocytes.9 These agents pose a risk for infections and malignancies due to their immunosuppressive effects. Recent understanding of the molecular mechanisms involved in psoriasis has also enabled the development of newer agents.11 The patient in this case was diagnosed with psoriasis and started on methotrexate and topical corticosteroids. He had a partial response and was eventually transitioned to adalimumab (a tumor necrosis factor-α inhibitor) that led to complete clearance of the psoriasis.
Eczema, or atopic dermatitis, is a chronic inflammatory disorder characterized by intense itching and recurrent skin lesions. Derived from the word atopy, meaning “a propensity for allergic disease,” the term atopic dermatitis was first introduced by Fred Wise and Marion Sulzberger in 1933.12 The incidence of eczema has increased more than 3-fold since the 1960s, for reasons that are largely unknown.13 Unlike psoriasis, eczema is a disease of childhood, affecting 10% to 20% of children but only 1% to 3% of adults worldwide.13 Ninety percent of eczema cases appear in the first 5 years of life. Recent evidence reveals a higher incidence of eczema
in developed countries and a higher vulnerability in people moving to more industrialized areas.14 Eczema is characterized by elevated levels of immunoglobulin E (IgE) in response to environmental antigens, triggering an inflammatory response in the skin.While the causes of eczema are multifactorial, 2 main hypotheses have been proposed to describe the pathophysiology of the disease. The first hypothesis argues that eczema is caused by an imbalance of type-2 helper T (Th2) cells, causing an overabundance of IL-4, IL-5, and IL-13 that leads to an overproduction of IgE.15 The second hypothesis describes mutations in the filaggrin gene (FLG) that encodes a protein involved in the permeability barrier of the stratum corneum. These mutations increase the skin’s permeability to allergens and microbes, triggering a Th2mediated inflammatory response that leads to the typical presentation of eczema.16
Eczema, or atopic dermatitis, is a chronic inflammatory disorder characterized by intense itching and recurrent skin lesions. Risk factors for eczema include genetic, socioeconomic, and environmental influences. Genetic factors are strongly associated with the development of atopic dermatitis, with a concordance rate of approximately 75% in monozygotic twins and only 30% in dizygotic twins. Furthermore, FLG mutations are found in 50% of patients with atopic dermatitis.15 Socioeconomic and environmental risk factors also play a role in the development of eczema, as suggested by the higher incidence of the disease in industrialized countries.14 Environmental factors positively correlated with eczema include colder climates, increased fast-food intake, obesity, pollution, and tobacco smoke. Protective factors include exposure to UV light, consuming fresh fruits, and breastfeeding. Many studies propose a “hygiene hypothesis” of eczema, which posits that a decrease in exposure to microbes in childhood increases susceptibility to allergic diseases. Environmental factors that increase exposure to microbial agents early in life, such as attendance in daycare and exposure to dogs, are considered protective.17 Eczema classically presents as a relapsing dermatitis characterized by intense pruritus and eczematous lesions.18 Acute lesions of eczema are described as erythematous patches with vesicles, oozing, and crusting. Lichenification, excoriations, papules, and nodules are more common in chronic forms of the disease.15 Infantile lesions frequently involve the face, scalp, and extensor surfaces whereas adults and children more
36 THE CLINICAL ADVISOR • SEPTEMBER 2019 • www.ClinicalAdvisor.com
commonly experience flexural involvement.18 Associated disorders include asthma and allergic rhinitis. The diagnosis of eczema requires 3 of the following major diagnostic criteria: pruritus, relapsing course, typical distribution, family or personal history of atopy, and onset at age <2 years.18 Several other minor criteria have been described and include xerosis, white dermatographism, Dennie-Morgan lines, elevated levels of IgE, immediate skin test reactivity, and food intolerance.16 Approximately half of patients with eczema present with allergic sensitivities and elevated IgE levels.15 The differential diagnosis of eczema varies according to the age at presentation. In infants, many primary immunodeficiency diseases present with elevated IgE levels and an eczematous rash similar to eczema. Examples include hyper-IgE syndrome, DOCK8 deficiency, PGM3 deficiency, WiskottAldrich syndrome, IPEX syndrome, and Netherton syndrome. Particular characteristics, such as eczematous rashes occurring immediately following birth, favor these diagnoses over atopic dermatitis.When patients present with eczematous rashes after age 5 years, malignancies such as cutaneous T-cell lymphoma should be included in the differential. Contact dermatitis, nutritional deficiencies, scabies, seborrheic dermatitis, drug eruptions, and psoriasis are other diagnoses to consider.18 The key features that distinguish eczema from other syndromes include infantile onset, intense pruritus, xerosis, age-dependent distribution, and a fluctuating course.19 Although there is no cure for eczema, spontaneous remission occurs prior to adolescence in approximately 75% of
patients.15 Treatment of eczema involves hydration, elimination of aggravating factors, and pharmacologic therapy. First, hydration in the form of emollients should be applied cutaneously to improve the skin’s barrier function and reduce the need for steroid treatment. Patients should also be educated on the avoidance of known aggravating factors, such as irritating soaps, products containing perfumes, and wool. Pharmacologic therapy includes both topical and systemic medications, with the latter reserved for refractory cases.13 Topical glucocorticoids serve as the first-line pharmacologic treatment of eczema and are used both for the treatment of flares and as maintenance therapy.15 Topical calcineurin inhibitors, such as tacrolimus, prevent the production of cytokines from Th2 cells. Antimicrobial agents can be effective in certain cases, as dermatologic infections are associated with eczema and often aggravate the disease.13 Phototherapy can be considered for treatment-resistant cases but can cause premature aging of the skin and increase the risk for skin cancer.15 Systemic immunosuppressants such as cyclosporine, glucocorticoids, methotrexate, mycophenolate, and azathioprine are reserved for patients with severe or refractory eczema due to the risk of side effects.13 An increased understanding of eczema in recent years has led to the development of monoclonal antibodies targeting specific cytokines involved in the pathogenesis of the condition, such as IL-4, IL-13, IL-22, and IL-31. These biologic agents have the potential to decrease the frequency of flares-ups for those with eczema, offering a promising outlook for those affected.20
TABLE. Characteristics of Psoriasis and Eczema Psoriasis1-9,15-20
Age at Onset
Mostly in adulthood
Mostly in childhood
Well-demarcated, erythematous plaques with a dry, silvery scale
Erythematous patches with vesicles, oozing, and crusting
• Extensor, periumbilical, and perianal regions • Scalp and nail involvement in a subset of patients
• Face, scalp, and extensor surfaces in infants • Flexural involvement in children and adults
Food allergies, allergic rhinitis, and asthma (“atopic march”)
Clinical presentation, biopsy rarely necessary
Clinical presentation based on major and minor diagnostic criteria
• Topical steroids • Phototherapy • Systemic immunosuppressants • Biologic agents
• Emollients • Topical steroids • Systemic steroids immunosuppressants
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Dermatologic Look-Alikes The patient in this vignette was diagnosed with eczema and treated with a moderate-strength topical steroid.The lesions resolved within 2 weeks. ■
9. Boehncke W-H, Schön MP. Psoriasis. Lancet. 2015;386(9997):983-994. 10. Jafferany M. Psychodermatology: a guide to understanding common psychocutaneous disorders. Prim Care Companion J Clin Psychiatry. 2007;9(3): 203-213.
Kaitlyn Lea Streight, BS, is a medical student; Michelle Eugene Lee, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston,Texas.
11. Smith CH, Barker JNWN. Psoriasis and its management. BMJ. 2006;
13. Lee JH, Son SW, Cho SH. A comprehensive review of the treatment of
1. Langley RGB, Krueger GG, Griffiths CEM. Psoriasis: epidemiology,
atopic eczema. Allergy Asthma Immunol Res. 2016;8(3):181-190.
clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18-23;
14. Fennessy M, Coupland S, Popay J, Naysmith K. The epidemiology and
experience of atopic eczema during childhood: a discussion paper on the
2. Sauder DN, Sauder MB. Molecular mechanisms in psoriasis: historical
implications of current knowledge for health care, public health policy and
perspective and current pathogenesis. Expert Rev Dermatol. 2014;8(1):1-3.
research. J Epidemiol Community Health. 2000;54(8):581-589.
3. Huerta C, Rivero E, Rodríguez LAG. Incidence and risk factors for psoriasis
15. Thomsen SF. Atopic dermatitis: natural history, diagnosis, and treatment.
in the general population. Arch Dermatol. 2007;143(12):1559-1565.
ISRN Allergy. 2014;2014:354250.
4. Tampa M, Sarbu M-I, Mitran M-I, Mitran C-I, Matei C, Georgescu S-R. The
16. Kaufman AJ. Atopic dermatitis. In: Integrative Medicine. 4th ed. Amsterdam,
pathophysiological mechanisms and the quest for biomarkers in psoriasis, a
NL: Elsevier; 2018;716-725.
stress-related skin disease. Dis Markers. 2018;2018:5823684.
17. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr
5. Ogawa E, Sato Y, Minagawa A, Okuyama R. Pathogenesis of psoriasis and
Metab. 2015;66(Suppl 1):8-16.
development of treatment. J Dermatol. 2017;45(3):264-272.
18. Lyons JJ, Milner JD, Stone KD. Atopic dermatitis in children: clinical
6. Bronckers IMGJ, Paller AS, van Geel MJ, van de Kerkhof PCM, Seyger
features, pathophysiology, and treatment. Immunol Allergy Clin North Am.
MMB. Psoriasis in children and adolescents: diagnosis, management and
comorbidities. Paediatric Drugs. 2015;17(5):373-384.
19. Siegfried EC, Hebert AA. Diagnosis of atopic dermatitis: mimics, overlaps,
7. Lowes MA, Suárez-Fariñas M, Krueger JG. Immunology of psoriasis. Annu
and complications. J Clin Med. 2015;4(5):884-917.
Rev Immunol. 2014;32:227-255.
20. Fabbrocini G, Napolitano M, Megna M, Balato N, Patruno C. Treatment
333(7564):380-384. 12. Kramer ON, Strom MA, Ladizinski B, Lio PA. The history of atopic dermatitis. Clin Dermatol. 2017;35(4)344-348.
8. Zeng J, Luo S, Huang Y, Lu Q. Critical role of environmental factors in the
of atopic dermatitis with biologic drugs. Dermatol Ther (Heidelb). 2018;8(4):
pathogenesis of psoriasis. J Dermatol. 2017;44(8):863-872.
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LEGAL ADVISOR CASE
© FATCAMERA / GETTY IMAGES
Medical Errors and Negligence A series of medical errors and negligence in a nursing home lead to an elderly man’s death. BY ANN W. LATNER, JD
This month we look at a case involving several errors that led to the death of a patient.The case went to trial and resulted in a verdict for the plaintiff that included punitive damages.The defendants appealed, and the Court of Appeals was asked to decide whether punitive damages were appropriate. The patient, Mr K, experienced a stroke in his mid-80s that resulted in memory problems and the inability to manage his own medications or walk without assistance. Mr K had diabetes for which he took insulin. After 2 years of caring for Mr K at home with the help of nurses, his family decided that he needed more supervised care than they could provide. When Mr K was aged 87 years, he was moved into The Pines, a facility that provided memory care. The facility did not request a physician’s medical assessment or admission order prior to admitting Mr K. The patient had been treated at a VA hospital previously, and there was some confusion as to who his primary care physician was. Mr K’s family provided a list of his medications, which included insulin glargine and insulin aspart. However, the facility had difficulty verifying the
It is never acceptable to treat a patient based simply on a family member’s verbal report of the patient’s medical history and medication regimen.
list as no primary physician was identified. The facility assigned one of its contracted physicians to be Mr K’s attending physician. Due to the confusion regarding his medication regimen, Mr K’s son stayed with him at the facility the first night to monitor his blood sugar levels and administer his medications. The next morning, Mr K’s son checked the patient’s blood glucose, gave him his medication, and took him to a scheduled appointment at the VA hospital. Upon returning to The Pines, Mr K’s son checked his father’s blood sugar levels again and administered his medication. He then left his father in The Pines’ dining room for lunch. After lunch, Nurse B checked the patient’s blood sugar level, which showed elevated readings of 358 mg/dL and 398 mg/dL. Concerned, she called Nurse Practitioner (NP) A, who worked with the physician who had been assigned to Mr K. Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2019 39
LEGAL ADVISOR Neither NP A nor the physician had seen Mr K, yet NP A gave a medication order over the phone, changing Mr K’s regimen. She discontinued the insulin glargine and insulin aspart, and instead ordered metformin and insulin detemir twice daily.The new medication regimen meant that the patient went from receiving 10 units of insulin daily to 55 units daily. The facility notified Mr K’s family that the brand of insulin had changed, but the family was not told about the addition of metformin or that the insulin dosage had been changed. Mr K began experiencing episodes of hypoglycemia on the new regimen. Two days after the medication change, Nurse B found Mr K’s blood sugar level to be 51 mg/dL. She did not contact the assigned physician or NP A; instead, she gave Mr K orange juice. When that failed to increase his glucose level,
To protect against liability, never order or change medications for a patient you have not evaluated in person. she administered oral glucose. After the glucose was given, Mr K’s blood sugar level rose to 186 mg/dL. At 2:00 AM the following morning, Nurse B found Mr K incoherent. She noted that verbal stimuli and a sternum rub elicited no response, and he had pinpoint pupils. According to Nurse B’s notes, Mr K’s blood sugar level was 52 mg/dL at that time. She wrote in the chart,“Oral glucose gel was given.After 10 minutes, retook finger stick. Blood sugar was 48. After waiting 5 minutes, remeasured blood sugar, 28.” Nurse B called for an ambulance. Upon arrival, emergency medical technicians administered glucose intravenously. Mr K died at the hospital the next day. Mr K’s family sued the facility, the company that provided the contracted physicians and NPs, and several others. The case went to trial before a jury who decided in favor of Mr K’s family and awarded a small amount of compensatory damages (approximately $5,000) as well as $100,000 in punitive damages. The facility appealed. Legal Background
Because the facility specifically appealed the punitive damages, the Court of Appeals had to decide whether punitive damages were warranted. The facility argued that the award of $100,000 was excessive and in violation of the Due Process Clause of the 14th Amendment. Three criteria are used to examine the appropriateness of the amount of punitive damages: 1) the degree of reprehensibility of the defendants’
conduct; 2) the disparity between the harm suffered and the amount of punitive damages; and 3) the difference between the punitive damages and civil penalties authorized in comparable cases. The facility only argued the first criteria and claimed that its actions did not rise to the level of reprehensible. The Court of Appeals disagreed and pointed out that Mr K had been admitted without a physician’s medical assessment or order, without an accurate verified medication list, and without knowing who his primary physician was. A drastic medication change was made within 24 hours of his arrival without an examination performed by a physician or NP. The Court also pointed out that according to Nurse B’s notes, Mr K was given oral glucose gel, which should never be administered to unconscious patients.The Court noted that expert testimony pointed out numerous missed opportunities by the facility to notice and correct the drastic overmedication of the patient, as well as the failure of Nurse B to notify the physician or NP about the incidents of hypoglycemia. The facility had promised a level of care that it was neither able nor licensed to provide. The family had been paying $6000 per month for memory care, but the facility was only licensed as a personal care home, requiring much lower levels of skilled care under the state’s regulations. The experts also faulted the nurses and staff at the facility for not recognizing that increasing a patient’s insulin from 10 units to more than 50 units should raise a red flag. Finally, the experts faulted Nurse B for giving an unresponsive patient a gel form of glucose when she should have given the patient glucagon, which is administered via injection. The Court of Appeals held that the egregious conduct of the facility, even for the brief time the patient was there, supported the amount of punitive damages and affirmed the award. Because of the patient’s age at his death, his frail health, and his minimal economic prospects, the compensatory damages were low as the economic “value” of a person is often tied to their age. Protecting Yourself
To protect against liability, never order or change medications for a patient you have not evaluated in person. This should be obvious, particularly in this case where NP A didn’t have any medical records on the patient. If you encounter a situation where you do not have access to a patient’s medical records, you must conduct your own examination and work-up. It is never acceptable to treat a patient based simply on a family member’s verbal report of the patient’s medical history and medication regimen. ■ Ms Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, New York.
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