March 2016 Clinical Advisor by The Clinical Advisor

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■ Autism screening ■ Prenatal steroid therapy ■ Diabetes drug for stroke CASE STUDY Pain

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Misdiagnosed heart attack

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A CHRONIC CONDITION

CROHN DISEASE Crohn disease is characterized by inflammation along the GI tract.

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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 These are letters from practitioners around the country who want to share their clinical problems and successes, observations, and pearls with their colleagues. Responding consultants are identified below. We invite you to participate.

YOUR COMMENTS MORE READER COMMENTS ON ETHICAL ISSUES REGARDING USE OF IUDS Regarding “The IUD rumor mill: common misconceptions” [Nov. 2015, p. 32], conception takes place in the fallopian tube near the ovary and then continues its journey to the uterus. The IUD makes the surface of the uterus such that a fertilized ovum cannot attach itself and continue growing and surviving until birth. Therefore, the fertilized ovum cannot survive and is expelled from the mother’s body. In my estimation, this is yet another form of abortion.—JEAN LUCK, LVN, PA, Green Valley Lake, Calif. (208-2) The LNG-IUS also prevents conception. While the progestin affects the endometrium, making it inhospitable to a fertilized egg, it also thickens the cervical mucous—in the words of a lecturer I heard, “turns it into cement.” Thus, the

LNG-IUS also is a barrier method, blocking the entrance of sperm into the uterus.—SUSANNA LEVIN, WHNP, New Rochelle, N.Y. (208-3) The copper IUD also works by disruption of the endometrium and implantation. A previous commenter stated that it works by preventing fertilization. Both are possible, but neither action is acceptable according to certain belief systems.—NANCY SANDROCK, CNM, Weslaco, Texas (208-1)

AVOIDING LABELING PATIENTS AS NONCOMPLIANT Sam Mbugua, MD, wrote about using analogies for education [Advisor Forum, Dec. 2015, p. 54]. I agree that teaching requires visual aids and any other method of teaching and learning that can be used to convey a point of understanding. However, he starts his comment with the word “noncompliance.” Really? I was told in my masters program in the 1980s to never label a patient as noncompliant. My professors said that use of that word only indicates that you do not know why the patient is making the decision that he or she is making. I work hard to educate patients, friends, and families, but if education, lecturing, and pushing information toward people changed behavior, we would not have any overweight healthcare personnel. All physicians and nurses would be

Advisor F orum

Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. You may contact us by e-mail at editor@ clinicaladvisor.com. If you are writing in response to a published letter, please indicate so by including the number in parentheses at the end of each item. Letters are edited for length and clarity. The Clinical Advisor’s policy is to print the author’s name with the letter. No anonymous contributions will be accepted.

This forum is devoted successes, to observations prac titioners who OUR CONSULTANTS want to shar below. We , and pear ls invite you e their clinic to participa with their colleague s. Respond al questions, prob te. lems, ing consultan ts are iden tified CONSUL TATION S

PERTUS SIS VAC YOUR COM CINE EFF With the recent incre ICACY MENTS whole cell ase in pertu pertussis ssis, Abimbola Farinde, PhD, PharmD,XYLLaura A. Foster, CRNP, FNP, Deborah L. Cross, MPH, CRNP, what Abby A. Jacobson, PA-C, vacci a confi role woul ITOL,family ne TOX medicine is a physician assistant ICITY, AND I enjoypractices your with Palmetto Primary at Delaware PETSValley cation and AlternativCarepubli Physicians Group appreDermatology e Meds S.C. inciate Wilmington, Del. the inclu DNP, on in Charleston,Upda g Waters, sion of the IEN, PA-C xylitol [The te column by Sherr W.V. , il Xylitol is The older very toxic Clinical Advisor, AprilSego, FNP-C, whole cell . In dogs, glycemia, pertus protec 2015, p. 86]. sis vaccines 50 THE CLINICAL • FEBRUARY 2016 • www.ClinicalAdvisor.com tion andADVISOR it weak can cause vomi ness, lethar funct vaccines. But effectiveness, compa are thought to offer gy, ataxia, ting, red more lead ion, liver failure, and seizures, abnor hypooffer the combithe key aspect that must with the newer acellu coma, all to death. mal liver of which Because be remembered ar can ultim cell vaccines nation of diphtheria is that both items, including oral xylitol is found ately and tetanu is hygiene produ in many house goods (cook AdvisorForum_CA0216.indd 1/28/16 7:07 PM s. The use and it was 50 believed to be effecti of whole hold ve and genera recent cts, gum, stored safely ies and muffins), it pertussis was ly reported that lly inexpensive is vital that candy, baked protec . If a dog , tooth these items is close to vaccines.— observed among those tion from an outbre a piece of ABIM BOL are ak of that paste, or candy, for given whole dropped photo at many clinic example, gum, bottom of A FARINDE, PhD, cell pertussis it ians can are dog be letha l. etc., this page Dr. Farin Phar mD Given for more de.) (200(See are I suggest that any articl owners, dog sitter infor matio 1) s, volunteers, at risk.— e on xylito n about BAR l mentions BAR New York that dogs Send us City (200- A WALTER, MEd your 2) , RNC, GNP Advisor Forum letters with , , The Clinical questions and York, Philip R. Cohen, MD,

play in slowi ned groupANP-BC, is associate d the is clinical associate professor is a professor (such as a NPprogram ng an outbr phyla xis of dermatology, University prisonProgram, Southern and antibdirector, Gerontology eak populationat Columbia in iotics?—A University of Pennsylvania School of Texas Medical Center, MPH University ) versu , NDR EW pro-Ala. of Nursing, Philadelphia. Houston. DFA APA, Fallin O’BRin Orange sBeach,

NY 10001 comments .You may Advisor, 114 West 26th to: com. If you contac Street, so by includiare writing in respont us by e-mail at editor 4th Floor, New se to a publish @clinicaladvi Letters are ng the number ed sor. in parent heses at letter, please indicat print the edited for length the and clarity. author e will be accept ’s name with The Clinical end of each item. the letter. Advisor’s policy ed. No anonym ous contrib is to utions

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60 THE CLINICAL

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CRNP, C, is associa te program director, Geronto logy NP Program University of Pennsyl vania School , of Nursing , Philadelphia.

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CONTENTS MARCH 2016

NEWS AND COMMENT

FEATURES

18 Newsline ■■The USPSTF finds insufficient evidence to recommend autism screening in all children. ■■Symptoms of myocardial infarction may be different in women than in men, especially among African American and Hispanic women. ■■Use of prenatal steroids can reduce respiratory complications in late preterm infants. ■■A diabetes drug may lower the risk of recurrent stroke and myocardial infarction in insulin-resistant patients without diabetes. ■■Weighing the benefits and harms of transvaginal mesh ■■Once-weekly GLP-1RAs may be beneficial for type 2 diabetes. ■■Past marijuana use is linked to worse verbal memory later in life. ■■How effective are smoking cessation medications? ■■Minimal benzodiazepine use is associated with a higher risk of dementia. ■■The benefits of fiber intake are not equal among patients with IBD. ■■Patients with penicillin allergy are more likely to have chronic hives.

28 Crohn disease: diagnosis and treatment A condition prone to recurrence, Crohn disease has a complicated presentation, but multiple treatment options are available.

Autism screening in children 18

34 CME/CE Using an evidence-based approach to diagnose IPF The importance of ruling out conditions other than idiopathic pulmonary fibrosis is highlighted in this case of a 62-year-old female. 40 CME/CE Feature posttest 64 Cryptogenic organizing pneumonia Patients with COP generally have positive outcomes following a definitive diagnosis and treatment.

Benefits/harms of transvaginal mesh 24

74 Uganda’s clinical officers rise to the challenge In Uganda, clinical officers address public health needs by training to work in rural areas and treating the country’s growing population. Continues on page 14

92 International Stroke Conference 2016 A roundup of news articles from the annual meeting 108 Commentary Keep the care in care coordination

MAKING CONTACT

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Clinical officers at work in Uganda 74

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CONTENTS ADVISOR FORUM

Web Roundup A summary of our most recent opinion, news, and multimedia content from ClinicalAdvisor.com

Your Comments ■ No thanks, on full-practice authority ■ MRI after breast cancer diagnosis

Dermatology Clinic ■ Itchy, burning rash that recurs on the legs every winter ■ Painless, bruise-like hyperpigmentation on a woman with lupus

Consultation A side effect of the flu vaccine?

Case File Hair loss after steroid injections

Clinical Pearl Steroid and rescue inhalers

Dermatologic Look-Alikes Erythematous papules on the face and torso

Case Study Wrist pain after a fall: a simple fracture?

Legal Advisor Heart attack misdiagnosed as heartburn

Stat Consult Acute sinusitis in children and adolescents

105 Alternative Meds Update Bright light therapy

Acute sinusitis in children 99

DEPARTMENTS

“Either cheer up or take off the hat.”

HOW TO CONTACT US THE CLINIC 2016

CASE STU

Pain

Wrist pain

after a fall

LEGAL ADV

Misdiagnosed

ISOR

hear t attac

NERS

MAR CH

2016

| www.Clin icalA

dvisor.com

A CHRO

NIC COND

CROHN D ITION ISEASE Crohn disea se is characterized by inflamm ation along the GI tract.

■ Dermatolo gic

• Send it by e-mail to editor@ClinicalAdvisor.com

ERYTHEMALook-Alikes TOUS PAPULES PAGE 57

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19, NUMB ER 3

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IEWE D FORU M FOR NUR SE PRAC TITIO

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Screening with HPV-Alone invites more risk into women’s lives than you may think. One out of 5 cases of cervical cancer were missed with HPV-Alone screening in a recent landmark, retrospective study—the largest ever conducted to evaluate the effectiveness of cervical cancer screening strategies in women ages 30-65.1* Additionally, screening with Pap+HPV Together™ (co-testing) identified more than 70% of those missed cancers.1 And it only requires one sample. So is HPV-Alone screening really worth the risk? Screen your patients with Pap+HPV Together. Because every woman deserves the best possible protection from cervical cancer. See more data at PapPlusHPV.com.

* A positive HPV screening result may lead to further evaluation with cytology and/or colposcopy. Reference: 1. Blatt AJ, Kennedy R, Luff RD, Austin RM, Rabin DS. Comparison of cervical cancer screening results among 256,648 women in multiple clinical practices. Cancer Cytopathol. 2015 April (Study included ThinPrep®, SurePath, Hybrid Capture 2 assay). ADS-01325-001 Rev. 001 © 2015 Hologic, Inc. All rights reserved. Hologic, Science of Sure, Pap+HPV Together, ThinPrep and associated logos are trademarks and/or registered trademarks of Hologic, Inc. and/or its subsidiaries in the United States and/or other countries. All other trademarks, registered trademarks, and product names are the property of their respective owners. This information is intended for medical professionals in the U.S. and is not intended as a product solicitation or promotion where such activities are prohibited. Because Hologic materials are distributed through websites, eBroadcasts and tradeshows, it is not always possible to control where such materials appear. For specific information on what products are available for sale in a particular country, please contact your local Hologic representative or write to diagnostic.solutions@hologic.com.

EXCLUSIVE TO THE WEB AT

ClinicalAdvisor.com Web Exclusives

Multimedia

ClinicalAdvisor.com/News

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Inappropriate antibiotic prescribing in primary care: the effect of behavioral interventions In outpatient primary care settings, various behavioral interventions can reduce the rate of inappropriate antibiotic prescribing practices. 2016 Child and adolescent immunization schedules available The American Academy of Pediatrics has approved the 2016 immunization schedule for children and adolescents. USPSTF issues final updated mammography screening guidelines In an update to its 2009 recommendations, the U.S. Preventive Services Task Force has presented its final guidelines on mammography screening for breast cancer.

The Waiting Room Official Blog of The Clinical Advisor ClinicalAdvisor.com/WaitingRoom Jillian Knowles, MMS, PA-C Recognizing victims of domestic violence Clinicians should trust their intuition when a patient’s injuries do not match up with their story. Jim Anderson, MPAS, PA-C, DFAAPA, ATC Impaired provider programs give clinicians a safe place to recover For clinicians who struggle with substance abuse and other mental health problems, impaired provider programs offer a safe, supportive space where they can recover.

MAKING CONTACT

Can behavioral interventions reduce inappropriate antibiotic prescriptions? Jason Doctor, PhD, and colleagues conducted a study to determine if behavioral interventions could help curb inappropriate antibiotic prescribing behaviors among primary care clinicians. Watch it here: ClinicalAdvisor.com/ AntiobioticInterventionVid

Assigning a Mallampati score to a patient The Mallampati score is generally used to determine how easy it will be to intubate a patient for anesthesia, but it can also be used as a predictor of obstructive sleep apnea. Watch it here: ClinicalAdvisor.com/ MallampatiVid

Screen all adults for depression, including pregnant and postpartum women Primary care clinicians should screen all adult patients for depression, according to new recommendations from the USPSTF. If a patient screens positively, proper steps should be taken to treat the patient, or they should be directed to the proper treatment services. Watch it here: ClinicalAdvisor.com/ DepressionScreeningVid

USPSTF autism screening recommendations cause controversy The U.S. Preventive Services Task Force (USPSTF) released recommendations for autism screening in young children, stating that they found “insufficient evidence” to support screening all asymptomatic children for autism. Watch it here: ClinicalAdvisor.com/AutismScreeningVid

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Advisor Dx

EXCLUSIVE TO THE WEB

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.

Ortho Dx

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A foot fracture following a car accident A 21-year-old woman presents to the emergency department with severe right ankle pain after being involved in a motor vehicle accident. X-ray and sagittal computed tomography images of the fracture were taken. WHICH DIAGNOSIS IS CORRECT?

• Anterior process fracture • Tongue-type fracture with decreased Bohler angle • Calcaneal body fracture • Joint depression-type fracture with increased Bohler angle ● See the full case at ClinicalAdvisor.com/OrthoDx_March16

Derm Dx Hyperkeratotic lesions of the palms and soles A 58-year-old African American man presents with multiple hyperkeratotic lesions on his palms and soles. The lesions are discrete, firm, and slightly elevated, ranging in diameter from 2 to 5 mm. The condition first manifested at age 16 and requires constant paring because pressure induces pain. CAN YOU DIAGNOSE THE CONDITION?

• Warts • Secondary syphilis • Punctate keratoderma • Lichen planus ● See the full case at ClinicalAdvisor.com/DermDx_March16

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Newsline M A R C H 2 016

Prenatal steroids for respiratory complications page 23

Transvaginal mesh: benefits and harms page 24

Marijuana use and verbal memory decline page 26

THE U.S. Preventive Services Task Force (USPSTF) has found insufficient evidence to recommend screening young children for autism spectrum disorder (ASD) if no concerns have been noted by parents or a clinician, according to a new recommendation statement published in JAMA. The recommendation applies to children aged 18 to 30 months who have not been diagnosed with ASD or other developmental delays. The USPSTF based its recommendations on evidence regarding the accuracy, benefits, and potential adverse effects of brief, formal screening instruments for ASD. The task force

also considered the benefits and potential adverse effects of early behavioral treatment for children diagnosed with ASD through these screening procedures. The potential harms of screening and treatment include misdiagnosis; the time, effort, and mental strain associated with more testing; and the time and monetary burden that behavioral treatments can have on a family. Overall, the USPSTF declared the potential harms of screening to be “no greater than small.” The USPSTF did not find any randomized clinical trials pertaining to the overarching question: Does screening for ASD in young

USPSTF finds insufficient evidence for autism screening in all children Clinicians are advised to use their clinical judgment if further testing is needed.

children improve symptoms, behavior, functioning, or quality of life? While there were studies concerning the efficacy of behavioral and developmental interventions for children with ASD, it was not clear if these studies are applicable to children who would be identified through ASD screening. If a parent is concerned about a child’s development, the USPSTF advises clinicians to use their clinical judgment along with validated diagnostic tools to determine if further testing is needed.

MI risks, symptoms different in women compared with men, per AHA The risks, symptoms, and outcomes of acute myocardial infarction may be different in women than in men, especially among African American and Hispanic women, according to the first scientific statement from the American Heart Association (AHA) on heart attacks in women published online ahead of print January 25 in Circulation. Take-away points from the statement, published by a group chaired by Laxmi S. Mehta, MD, include:

• The most common symptom of heart attack is chest pain or discomfort for both sexes, but women are more likely to have atypical symptoms, such as shortness of breath, nausea or vomiting, and back or jaw pain. • High blood pressure is more strongly associated with heart attacks in women.

• Young women with diabetes have a risk for heart disease that is higher by 4 to 5 times, compared with young men. • African American and Hispanic women have more heart-related risk factors, such as diabetes and high blood pressure, at the time of their heart attack, compared with non-Hispanic white women. • African American women have a higher incidence of heart attacks in all age categories, and young African American women have higher in-hospital death rates, compared with white women. • Women are undertreated, compared with men. Cardiac rehabilitation is prescribed less frequently for women and when prescribed, women are less likely to undertake the therapy. In addition, African American women are also less likely to be referred for important treatments such as cardiac catheterization, compared with white women.

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Newsline LATE PRETERM infants (born at 34 to 36 weeks) have a significantly reduced likelihood of respiratory complications if their mothers undergo prenatal steroid therapy, according to a new study from the National Institutes of Health (NIH) published in the New England Journal of Medicine. “Reducing neonatal respiratory complications could result in less injury to the immature lung, less hospitalizations, earlier infant-mom bonding, and better long-term lung and general health,” said Carol Blaisdell, MD, medical officer at the National Heart, Lung, and Blood Institute. Pregnant women who are likely to deliver before 34 weeks receive steroids as part of standard treatment to reduce their infants’ risk of complications (including

respiratory ones) and death. Now, evidence supports steroid use in pregnant women likely to deliver before 37 weeks to reduce infants’ risk of respiratory complications. The study, conducted by Uma Reddy, MD, MPH, of the Pregnancy and Perinatology Research Branch at the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development, and colleagues, included 2,831 women in their 34th to 36th week of pregnancy who were at high risk of delivering before 37 weeks. Participants were randomly assigned to receive two injections 24 hours apart of either the steroid betamethasone or a placebo. In the betamethasone group, 11.6% of infants met the primary outcome criteria—the need

Prenatal steroids for preterm infants

Respiratory complications are lower in late preterm infants when their mothers undergo prenatal steroid therapy.

for respiratory therapy was 20% less compared with the placebo group. Two infants in the betamethasone group died within 72 hours, but neither death was from respiratory causes. Infants in the betamethasone group were more likely to have low blood sugar, compared with the placebo group.

Diabetes drug may lower recurrent stroke risk THE RISK OF stroke and myocardial infarction is lower in patients without diabetes who have insulin resistance and a recent history of stroke or transient ischemic attack (TIA) and are treated with pioglitazone, compared with a placebo, according to research presented at the 2016 International Stroke Conference and published simultaneously in the New England Journal of Medicine. “This study represents a novel approach to prevent recurrent vascular events by reversing a specific metabolic abnormality thought to increase the risk for future heart

The benefit was found in patients with insulin resistance but without diabetes.

attack or stroke,” said Walter J. Koroshetz, MD, director of the National Institute of Neurological Disorders and Stroke (NINDS), which supported the study. The multicenter, double-blind Insulin Resistance Intervention after Stroke (IRIS) trial focused on patients who had insulin resistance but were not diabetic. Researchers randomly assigned either pioglitazone (45 mg daily) or a placebo to 3,876 participants, all of whom had had either an ischemic stroke or TIA within 6 months prior to study enrollment. Participant insulin resistance was defined as a score

greater than 3.0 on the homeostasis model assessment of insulin resistance (HOMA-IR) index. At median follow-up (4.8 years), the researchers found that either stroke or myocardial infarction occurred in 175 (9%) of the 1,939 participants randomized to the pioglitazone group and in 228 (11.8%) of the 1,937 participants in the placebo group (hazard ratio 0.76). Across both groups, 73 participants (3.8%) and 149 participants (7.7%), respectively, developed diabetes (hazard ratio 0.48); however, pioglitazone reduced the overall risk of diabetes development by 52%.

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Newsline Weighing the benefits and harms of transvaginal mesh A REVIEW of evidence highlighting the benefits and harms of using artificial mesh to repair vaginal prolapse has been published in the Cochrane Database of Systematic Reviews. Led by Christopher Maher, MD, PhD, of the Royal Brisbane Women’s Hospital in Queensland, Australia, a team of researchers conducted an analysis of 37 randomized controlled trials to determine the potential benefits and harms of using artificial mesh versus native tissue to repair vaginal prolapse; use of the mesh studied in these research papers has been disallowed since 2011. “While transvaginal permanent mesh is associated with lower rates of awareness of prolapse, reoperation for prolapse, and prolapse on examination than native tissue repair, it is also associated with higher rates of reoperation for prolapse, stress urinary incontinence, or mesh exposure and higher rates of bladder injury at

A study suggests that transvaginal mesh has limited utility in primary surgery.

surgery and de novo stress urinary incontinence,” the researchers stated. “The risk-benefit profile means that transvaginal mesh has limited utility in primary surgery. While it is possible that in women with higher risk of recurrence the benefits may outweigh the risks, there is currently no evidence to support this position.” The analysis, including low- to moderate-quality evidence gathered from 4,023 women, found that when permanent mesh was used, 10% to 15% of patients were aware of prolapse, compared with 19% of women who were aware of prolapse after undergoing native tissue repair. In addition, women who underwent permanent mesh repair had lower rates of repeat surgery, although 8% of these women did require repeat surgery for mesh exposure. Additional low-quality evidence showed no difference in effectiveness of absorbable mesh when compared with native tissue

repair, and no evidence existed to show a potential difference between biological graft and native tissue repair. “This is a very significant review informing women about the surgical options available for the treatment of this debilitating condition,” said Dr. Maher. “It summarizes the evidence of effectiveness of these approaches and their complications. It provides women with more information to make an informed choice about what treatment is best for them.” According to the researchers, limited evidence suggests that absorbable mesh may reduce rates of recurrent prolapse on examination compared to native tissue repair. “But there was insufficient evidence on absorbable mesh for us to draw any conclusions for other outcomes,” they concluded. “There was also insufficient evidence for us to draw any conclusions regarding biological grafts compared to native tissue repair.”

ONCE-WEEKLY glucagon-like peptide-1 receptor agonists (GLP-1RAs), new therapeutic agents for the treatment of type 2 diabetes, have shown promise in the reduction of hemoglobin A1c (HbA1c) levels, fasting plasma glucose levels, and body weight, according to a systematic review and network meta-analysis published in the January 19 issue of the Annals of Internal Medicine. Senior author Melanie J. Davies, MD, and fellow investigators analyzed 34 randomized, controlled trials (21,126 participants; ≥24 weeks of follow-up) of albiglutide, dulaglutide, once-weekly exenatide, semaglutide, and taspoglutide. They found that all once-weekly GLP-1RAs reduced HbA1c and fasting plasma glucose, when compared with placebo. Compared with other once-weekly GLP-1RAs, dulaglutide (1.5 mg), once-weekly

exenatide, and taspoglutide (20 mg) showed a greater reduction of HbA1c levels, fasting plasma glucose levels, and body weight. Taspoglutide, once-weekly exenatide, and dulaglutide reduced body weight, when compared with placebo. Among the drugs, differences found in blood pressure, blood lipid levels, and C-reactive protein levels were clinically insignificant. Once-weekly exenatide increased heart rate, compared with albiglutide and dulaglutide (1.4 to 3.2 beats/min). Taspoglutide had the highest risk for nausea. The risk for hypoglycemia among the once-weekly GLP-1RAs studied was similar. The study was limited by poor data on semaglutide, and the definitions of outcomes varied among the trials in the analysis, the authors said.

Once-weekly GLP-1RAs beneficial for type 2 diabetes

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Newsline Past marijuana use linked to decline in verbal memory PAST EXPOSURE to marijuana is associated with worse verbal memory in middle age, but it does not seem to affect other areas of cognitive function, according to a study published in JAMA Internal Medicine. In addition, researchers found that current marijuana use is not only associated with worse verbal memory, but it is also associated with reduced processing speed. The study included 3,385 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study, a cohort of black and white men and women aged 18 to 30 years at baseline from March 25, 1985, to June 7, 1986 (year 0). Each participant in the CARDIA study was followed for more than 25 years, from June 7, 1986, to August 31, 2011.

For every 5 years of past exposure, verbal memory declined by 0.13 standardized units.

Reto Auer, MD, MAS, and colleagues analyzed 3 domains of cognitive function that were assessed at year 25: verbal memory (via the Rey Auditory Verbal Learning Test), processing speed (via the Digit Symbol Substitution Test), and executive function (via the Stroop Interference Test).

A total of 2,852 (84.3%) participants reported past marijuana use, with 392 (11.6%) continuing use into middle age. The researchers found an association between current marijuana users and worse verbal memory and processing speed. Initially, cumulative lifetime marijuana use was associated with worse verbal memory, processing speed, and executive function. The researchers then adjusted the results for possible confounders, including demographic and CVD factors and smoking. After adjustment, there was no association between past marijuana use and lower executive function or processing speed; only verbal memory retained its association. For every 5 years of past exposure, verbal memory was reduced by 0.13 standardized units.

AMONG SMOKERS, no significant differences were found in biochemically confirmed rates of smoking abstinence at 26 weeks regarding use of three methods of medication-based cessation, according to research published in JAMA. In a study of 1,086 smokers participating between May 2012 and November 2015, researchers compared the efficacy of varenicline, combination nicotine replacement therapy (C-NRT), and the nicotine patch. “Smoking cessation medications are routinely used in health

Results raise questions about the effectiveness of smoking therapies.

care; it is vital to identify medications that most effectively treat this leading cause of preventable mortality,” wrote study author Timothy B. Baker, PhD, of the Center for Tobacco Research and University of Wisconsin School of Medicine and Public Health in Madison, and colleagues. The 3-group, intention-totreat clinical trial randomized patients to 1 of 3 12-week open label pharmacotherapy groups. The first group was given only a nicotine patch (n = 241). The second group used only varenicline (n = 424), and the third group

was given combination nicotine replacement therapy (C-NRT) comprised of a nicotine patch and nicotine lozenge (n = 421). All participants were offered 6 counseling sessions. All medications were well tolerated by the participants. At 26 weeks, risk differences for abstinence were –0.76% for the patch versus varenicline, –4% for the patch versus C-NRT, and –3.3% for varenicline versus C-NRT. “The results raise questions about the relative effectiveness of intense smoking pharmacotherapies,” stated Dr. Baker.

IMAGES: © THINKSTOCK (TOP), SHUTTERSTOCK (BOTTOM)

How effective are smoking cessation medications?

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Penicillin allergy Minimal benzodiazepine use associated and the risk for with a higher risk of dementia chronic hives colleagues. “We found no signifiDEMENTIA RISK is slightly elevated in patients with minimal exposure to benzodiazepines, according to research published in BMJ. In a population-based prospective cohort study, researchers measured outcomes in 3,434 participants aged 65 years or older who did not have dementia at the time of enrollment. On a biennial basis, the researchers administered the cognitive abilities screening instrument (CASI) to screen for dementia, as well as to examine participants’ cognitive trajectory. “The average CASI score at baseline was 93.4, with similar scores across levels of cumulative benzodiazepine use (range 93.0–93.6),” wrote lead author Shelly L. Gray, PharmD, of the School of Pharmacy, University of Washington in Seattle, and

No risk was found in those with the highest exposure to the drugs.

cant differences for any benzodiazepine use group in mean CASI or rates of decline compared with non-users.” At follow-up, the investigators found that 797 participants (23.2%) developed dementia. Of that group, 637 (79.9%) developed Alzheimer’s disease. The researchers did not find an association between the highest level of benzodiazepine use (≥121 total standard daily doses [TSDDs]) for dementia (hazard ratio [HR], 1.07) or Alzheimer’s disease (HR, 0.95) when compared with non-use. “There was a slightly increased risk for dementia for participants with low (1–30 TSDDs; HR, 1.25) or moderate use (31–120 TSDDs; HR, 1.31),” said Dr. Gray. No increased risk in those with the highest exposure levels was identified.

Benefit of fiber intake not equal in IBD patients DIETARY FIBER is associated with fewer flares in patients with Crohn disease but not in those with ulcerative colitis, according to a report published online ahead of print December 31 in Clinical Gastroenterology and Hepatology. Lead author Carol S. Brotherton, PhD, and colleagues collected a 26-item dietary survey from 1,619 patients with inflammatory bowel disease (IBD)—1,130 patients with Crohn disease and 489 patients with ulcerative colitis—who were in remission at baseline. The researchers conducted a follow-up survey with the participants 6 months later. Patients with ulcerative colitis

consumed more fiber than patients with Crohn disease. Female gender, prior hospitalization, and prior surgery were associated with lower fiber intake. Patients with Crohn disease who reported that they ate highfiber foods were approximately 40% less likely to have a disease flare than those who did not eat high-fiber foods. The researchers found no association between fiber intake and flares in patients with ulcerative colitis. The authors suggested that recommendations that patients with IBD limit how much dietary fiber they consume should be reevaluated. n

PEOPLE ARE MORE likely to report they have a penicillin allergy if they have chronic urticaria (hives) and vice versa, according to a study published online ahead of print January 9 in the Annals of Allergy, Asthma, and Immunology. Senior author Andrea J. Apter, MD, MSc, and fellow investigators examined the medical records of 11,143 patients, 220 of which had both self-reported penicillin allergy and chronic hives. The prevalence of selfreported penicillin allergy in patients with chronic urticaria was found to be approximately 3 times greater than in the general population. The researcher’s analysis found that the prevalence of chronic urticaria in patients with self-reported penicillin allergy was also approximately 3 times higher than in the general population. “This link between chronic urticaria and self-reported penicillin allergy highlights the need for clinicians to inquire about self-reported penicillin allergy in patients with chronic urticaria and to consider penicillin skin testing,” Dr. Apter said. “Furthermore,” he continued, “patients who report penicillin allergy might actually have chronic urticaria, indicating the importance of inquiring about chronic urticaria symptoms in patients with self-reported penicillin allergy.”

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FEATURE: CARLOS A. SALAZAR, MSN, ARNP, FNP-BC

Crohn disease: diagnosis and treatment A condition prone to recurrence, Crohn disease has a complicated presentation and pathophysiology, but multiple treatment options are available.

nflammatory bowel disease (IBD) is believed to result from the interaction of genetic predisposition, environmental triggers, and dysfunctional immune response. IBD may present as ulcerative colitis or Crohn disease (CD). CD is a chronic condition characterized by inflammation anywhere along the gastrointestinal tract.1

Patient history and presentation

Colonoscopy showing Crohn disease, with ulceration of the colonic mucosa.

CD most frequently involves the small intestine alone, the colon alone, or both the small intestine and the colon. Although the mouth, esophagus, stomach, and duodenum may be affected, involvement of these sites is uncommon and rarely occurs without active disease in the small or large intestine. Inflammation develops in the absence of infection, with periods of relapse and remission (Figure 1). A primary symptom of IBD is diarrhea. Because the terminal ileum is inflamed in a large number of patients with CD, they also typically present with right lower quadrant pain that is cramping in nature.2 Additional clinical manifestations of CD vary according to disease location. Esophageal disease may manifest as dysphagia, heartburn, or chest pain, whereas gastrointestinal disease may produce epigastric pain or hematemesis.1 Weight loss is often evident in patients with CD and may be caused by food avoidance or malabsorption that results in malnutrition, especially if inflammation of the small intestine is extensive. Impaired growth and malnutrition are significant complications of CD in children

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and adolescents and can be especially severe in children with stricturing CD.3 Other extraintestinal manifestations of CD include erythema nodosum, pyoderma gangrenosum, uveitis, iritis, peripheral arthritis, sacroiliitis, ankylosing spondylitis, sclerosing cholangitis, cholelithiasis, and hepatitis.2 Genetic and environmental risk factors

Several genetic mutations have been associated with CD, but no single mutated gene is responsible for its development. Many of the genetic mutations associated with the condition involve defects in innate immunity.4 The NOD2 gene, located on chromosome 16q12, is the most studied site of mutations associated with CD. It encodes a protein that modulates mitogen-activated protein kinase pathways and nuclear factor κB in the presence of bacterial cell wall peptidoglycan components.2 Defects in the NOD2 gene may affect the ability of the immune system to locate and destroy invading bacteria. Some mutations more recently associated with CD include those of the IL23R gene5 and the ATG16L gene.4 The first is related to an inflammation pathway, and the second is involved in the process of cell autophagy. In addition to genetic mutations, several environmental triggers have been identified, but evidence points to the absence of a single causative factor. Any break in the mucosal barrier caused by infection, antibiotics, or nonsteroidal anti-inflammatory drugs can serve as a trigger.4 Smoking is also recognized as a risk factor. It is possible that different environmental factors prompt the development of CD in different populations.

results in chronic inflammation. AIEC are thought to take advantage of defects in bacterial recognition related to the NOD2 mutation and in the autophagy pathway related to the ATG16L mutation in affected individuals, and this may be one of the factors leading to CD. The adaptive immune system, T lymphocytes in particular, has been more definitively linked to the pathogenesis of CD. Inflammation is thought to be triggered by the release of interferon-gamma (IFN-γ) from T helper type 1 (Th1) cells, which are usually activated by intracellular pathogens.1 Usually, a Th1 cell is activated by an antigen-presenting cell (APC) in the presence of interleukin 12 (IL-12), which is secreted by the APC.4 In CD, this pathway is thought to be dysfunctional. High levels of IL-12 in the intestinal mucosa lead to increased Th1 production of IFN-γ, which then upregulates macrophages in a cycle of uncontrolled inflammation.1 Several other subsets of T helper cells have been described, such as the Th17 and Th2 cells. Evidence does not conclusively point to a single cell subpopulation as the cause of CD.4 It is rare for only one cell type to be activated during an immune response, and plasticity is usually a characteristic of the reaction.4 After T cells are activated, their cytokines act on the local environment to attract other inflammatory cells. The migrating inflammatory cells are regulated differently from those of the gut and may be more easily activated to secrete destructive and proinflammatory factors.

Pathophysiology

In the presence of triggers and a genetic predisposition, the interaction between a defective innate or adaptive immune system and enteric bacteria can result in the pathologic process responsible for the chronic inflammation of CD. In the intestine, innate immunity includes the epithelial barrier and the phagocytes of the lamina propria. Some bacteria are able to survive within phagocytes and avoid killing. High levels of Escherichia coli have been observed in the small bowel of patients with CD.6 These bacteria have been named adherent-invasive E coli (AIEC) because they can survive and multiply inside macrophages and epithelial cells. They have been found in biopsy specimens of early CD lesions, so they may play a role in the etiopathogenesis of the condition. Although most bacteria cause infected macrophages to undergo apoptosis, AIEC do not. The infected macrophages remain activated and secrete high levels of tumor necrosis factor-alpha (TNF-α). The pathogens may in this way promote chronic antigenic stimulation that

IMPAIRED GROWTH

DIARRHEA

INFLAMMATION WITHOUT INFECTION

Common Presenting Features

MALABSORPTION

PAIN

WEIGHT LOSS

FIGURE 1. Common presenting features of Crohn disease include diarrhea, pain, and weight loss.

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CROHN DISEASE

TABLE 1. Working definitions of Crohn disease activity8 Mild to moderate acute disease

Ambulatory patient who tolerates oral alimentation and has no dehydration, high fever, prostration, abdominal tenderness, painful mass, obstruction, or weight loss of more than 10%.

Moderate to severe acute disease

Patient does not respond to treatment for mild to moderate disease or has fever, significant weight loss, abdominal pain or tenderness, intermittent nausea or vomiting, or significant anemia.

Severe/fulminant acute disease

Patient has symptoms despite outpatient steroid treatment or has high fever, persistent vomiting, evidence of intestinal obstruction or abscess, rebound tenderness, or cachexia.

Remission

Patient is asymptomatic or without inflammatory sequelae; this includes a patient who has responded to acute medical or surgical intervention.

TABLE 2. Management pearls for Crohn disease7,9 • Smoking increases the risk for recurrence, and cessation should be encouraged. • Although frequently prescribed, mesalamine has limited efficacy and is less effective than corticosteroids. • Delayed introduction or underdosing of immunomodulators or anti– tumor necrosis factor (anti-TNF) monoclonal antibody therapy is a common mistake. • Steroids are not indicated for long-term maintenance. • Patients and providers should not view surgery as a failure of therapy but as a fast and effective option when medical therapy is ineffective.

Defective immune regulation may also play a role in CD. The immune system of the gastrointestinal tract, in comparison with the systemic immune system, is suppressed in normal individuals. Regulatory cells prevent immune responses against commensal flora or dietary antigens. It has been proposed that defective T regulatory cells allow active inflammation to be maintained.4 Dysfunction at any of these levels may lead to IBD. What one sees as the disease progresses is the result of multiple factors coming into play, including collagenase, elastase, matrix metalloproteinases, and superoxides, among others, which produce tissue damage.4 The histologic findings of CD include transmural inflammation anywhere along the gastrointestinal tract and the formation of lymphoid aggregates across the layers of the bowel wall.1 Neutrophils infiltrate the epithelial layer overlying lymphoid aggregates. They infiltrate the crypts, form abscesses, and eventually destroy the crypts, leading to atrophy of the colon. Aphthous ulcers are a gross feature of CD. They may enlarge or become stellate, and they may combine to form longitudinal ulcerations. A network of ulcerations surrounding inflamed mucosa may lead to a cobblestone appearance.1 Diagnosis and treatment

Several procedures may be used in the diagnosis of CD. Ileocolonoscopy with biopsy specimens systematically obtained from each anatomical segment is a common procedure, except in patients with fulminant colitis.2 In contrast Continues on page 33

TABLE 3. Recommendations for the treatment of Crohn disease7,9 Mild to moderate acute disease

• Mesalamine 3.2-4 g/d for ileal, ileocolonic, or colonic disease OR sulfasalazine 3-6 g/d for ileocolonic or colonic disease • Budesonide 9 mg/d for ileocolonic disease OR prednisone ≤40 mg/d for distal colonic disease if mesalamine/ sulfasalazine ineffective • Nutritional therapy (first in children) generally ineffective alone in adults • Immunomodulator (methotrexate, azathioprine, or 6-mercaptopurine) should not be delayed when steroids ineffective • Anti–tumor necrosis factor (anti-TNF) monoclonal antibody therapy (infliximab, adalimumab, or certolizumab pegol) when steroids/immunomodulators ineffective/not tolerated

Moderate to severe acute disease

• Prednisone 40-60 mg/d until resolution of symptoms and weight gain • Anti-TNF monoclonal antibody therapy (introduce early for complex fistulizing disease) • Natalizumab when response inadequate or patient unable to tolerate conventional therapy • Treatment of nutritional deficiencies (eg, iron deficiency) • Surgical drainage and antibiotic therapy for perianal and fistulizing disease • Timely surgical intervention

Severe/fulminant acute disease

• Hospitalization and surgical evaluation for patient with persistent disease despite therapy or presenting with high fever, frequent vomiting, signs of gastrointestinal obstruction, rebound tenderness, cachexia, or abscess formation

Maintenance of remission

• Immunomodulator, anti-TNF monoclonal antibody therapy (best combined with immunomodulator), or natalizumab

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CROHN DISEASE

POLL POSITION

Which of the following treatment options do you most frequently recommend for patients with Crohn disease? n=502

■ Steroids

3. Vasseur F, Gower-Rousseau C, Vernier-Massouille G, et al. Nutritional status and growth in pediatric Crohn’s disease: a population-based study. Am J Gastroenterol. 2010;105(8):1893-1900. 4. Mayer L. Evolving paradigms in the pathogenesis of IBD. J Gastroenterol. 2010;45(1):9-16. identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis. Nat Genet. 2007;39(5):596-604.

39.44%

■ Anti-TNF therapy

treatment of IBD. J Gastroenterol. 2010;45(6):571-583.

5. Rioux JD, Xavier RJ, Taylor KD, et al. Genome-wide association study

41.83%

■ Immunomodulators

2. Engel MA, Neurath MF. New pathophysiological insights and modern

6. Caprilli R, Lapaquette P, Darfeuille-Michaud A. Eating the enemy

■ Surgery 1.2%

in Crohn’s disease: an old theory revisited. J Crohns Colitis. 2010;

17.53%

4(4):377-383. 7. Burger D, Travis S. Conventional medical management of inflammatory bowel disease. Gastroenterology. 2011;140(6):1827-1837.

For more polls, visit ClinicalAdvisor.com/Polls.

8. Hanauer SB, Sandborn W; Practice Parameters Committee of the American College of Gastroenterology. Management of Crohn’s disease in

Carlos A. Salazar, MSN, ARNP, FNP-BC, is a student nurse anesthetist at Florida International University and a field nurse practitioner for Altegra Health in Miami, Florida. References 1. Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel disease: an overview. Surg Clin North Am. 2007;87(3):575-585.

adults. Am J Gastroenterol. 2001;96(3):635-643. 9. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of the American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol. 2009;104(2):465-483. All electronic documents accessed February 4, 2016.

to ulcerative colitis, CD can involve the entire gastrointestinal tract, although the lesions are limited to the colon in 20% of patients. About half of patients have involvement of the terminal ileum and colon. A patchy, cobblestone pattern may be noted in the terminal ileum of patients with CD. Granulomas are also characteristic of CD but are not evident in all cases. Biopsies help differentiate between the transmural inflammation of CD and the mucosal inflammation of ulcerative colitis. Additional diagnostic examinations include magnetic resonance imaging, computed tomography, and transabdominal sonography. The treatment of CD is complex and depends on numerous factors, such as the location and severity of the disease (Table 1). Treatment is not curative, and recurrence is common after remission has been achieved. Several approaches are used, including steroids, immunomodulators, anti-TNF therapy, and surgery (Tables 2 and 3).7 The therapy for CD differs from that for ulcerative colitis, although some medications may be used in both conditions. Surgery is usually performed to manage complications such as strictures, fistula, abscess, and perforation. Extraintestinal manifestations and nutritional deficiencies also require adequate management. ■

“Kids, your mother and I have spent so much money on health insurance this year that instead of vacation we’re all going to go in for elective surgery.”

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CME CE FEATURED COURSE

n EDUCATIONAL OBJECTIVES At the conclusion of this activity, participants should be better able to: • Apply an evidence-based clinical assessment of patients for whom idiopathic pulmonary fibrosis (IPF) is suspected, underscoring timely recognition of interstitial lung disease (ILD) • Describe the value of integrating multidisciplinary components into the diagnostic workup of patients with suspected IPF • Interpret usual interstitial pneumonia (UIP) radiological pattern on high-resolution computed tomography (HRCT) n COMPLETE THE POST-TEST: Page 40

Release Date: July 24, 2015 Expiration Date: July 24, 2016 Estimated Time to Complete: 1 hour Accredited Provider: Provided by Postgraduate Institute for Medicine (PIM) in collaboration with Haymarket Medical Education (HME) Commercial Supporter: This activity is supported by an independent educational grant from Boehringer Ingelheim. Program Description: Idiopathic pulmonary fibrosis (IPF) is a form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, primarily occurring in older adults, limited to the lungs. As IPF progresses, lung tissue is replaced by fibrous scar tissue, resulting in declining lung function and, eventually, respiratory failure. IPF is often a diagnosis of exclusion, as initial symptoms (nonproductive cough, dyspnea with exertion) mimic other pulmonary diseases. It is crucial to confirm or eliminate the possibility of diagnoses other than IPF because some alternative conditions may be responsive to steroid treatment, whereas anti-inflammatory agents have a negative effect in IPF. This CME case activity will explain the diagnostic algorithm of IPF, focusing on the exclusion of similar interstitial lung diseases (ILDs), the interpretation of radiological results, and the incorporation of a multidisciplinary discussion in the patient’s workup. Intended Audience: This activity has been designed to meet the educational needs of primary care physicians, pulmonologists, pathologists, and radiologists involved in the care of patients with IPF. Conflict of Interest Disclosure Policy: Postgraduate Institute for Medicine (PIM) requires instructors, planners, managers and other individuals who are in a position to control the content of this activity to disclose any real or apparent conflict of interest (COI) they may have as related to the content of this activity. All identified COI are thoroughly vetted and resolved according to PIM policy. PIM is committed to providing its learners with high quality CME activities and related materials that promote improvements or quality in healthcare and not a specific proprietary business interest of a commercial interest. Faculty Jeff Swigris, DO, MS Associate Professor of Medicine Director, Interstitial Lung Disease Program National Jewish Health Denver, CO Faculty Disclosure: Dr. Swigris has received consulting fees from Boehringer Ingelheim and Genentech.

The following PIM planners and managers, Laura Excell, ND, NP, MS, MA, LPC, NCC, Trace Hutchison, PharmD,Samantha Mattiucci, PharmD, CCMEP, and Jan Schultz, MSN, RN, CCMEP, hereby state that they or their spouse/life partner do not have any financial relationships or relationships to products or devices with any commercial interest related to the content of this activity of any amount during the past 12 months. The HME staff involved in the planning and content review of this activity have no relevant financial relationships to disclose. Accreditation Statement: The Postgraduate Institute for Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Designation Statement: The Postgraduate Institute for Medicine designates this enduring material for a maximum of 1.00 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Disclosure of Unlabeled Use: This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the FDA. The planners of this activity do not recommend the use of any agent outside of the labeled indications. The opinions expressed in the educational activity are those of the faculty and do not necessarily represent the views of the planners. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings. Disclaimer: Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patient’s conditions and possible contraindications and/or dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. Instructions: There are no fees for participating in and receiving CE credit for this activity. During the period July 24, 2015 through July 24, 2016, participants must: 1) read the learning objectives and faculty disclosures; 2) study the educational activity; 3) complete the post-test and submit it online. A statement of credit will be issued only upon receipt of a completed preassessment test, polling questions, activity evaluation form, and post-test with a score of 70% or better. All components must be completed and submitted online at myCME.com/Mar16CAfeature.

Planners’ and Managers’ Disclosures: The planners and managers reported the following financial relationships or relationships to products or devices they or their spouse/life partner have with commercial interests related to the content of this CME activity:

Provided by

In collaboration with

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CME CE FEATURED COURSE: JEFF SWIGRIS, DO, MS

Using an evidence-based approach to diagnose IPF The importance of ruling out conditions other than idiopathic pulmonary fibrosis is highlighted in this case of a 62-year-old female.

Honeycomb appearance of the lungs caused by idiopathic pulmonary fibrosis.

diopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease (ILD) in the subgroup of ILDs called idiopathic interstitial pneumonia (IIP).1 IPF is defined by a combination of the following 2 features: 1) an idiopathic clinical circumstance (ie, the absence of exposures or diseases known to cause pulmonary fibrosis) and 2) a pattern of usual interstitial pneumonia (UIP) on high-resolution computed tomography (HRCT) or surgical lung biopsy.1 “Idiopathic” by name, IPF requires the exclusion of all known causes of ILD in the diagnostic workup. This is a critical step, because a number of respiratory illnesses can mimic the clinical presentation of IPF,2 including connective tissue disease (CTD)-related pulmonary fibrosis, hypersensitivity pneumonia, or asbestosis.1,2 Clinical features of IPF include chronic exertional dyspnea, dry cough, bibasilar inspiratory crackles (“Velcro crackles”), and finger clubbing.1,3 Although IPF has no known cause, risk factors include cigarette smoking and several environmental exposures.1 For example, various dusts (eg, metal, agricultural) have been linked to IPF. Additionally, comorbidities such as gastroesophageal reflux disease (GERD) and diabetes have been described as risk factors for IPF.1 IPF is believed to result from injury to the alveolar epithelium. The currently accepted theory of IPF pathogenesis holds that aberrant wound healing leads to progressive fibrosis and architectural distortion of the lung.1,4 IPF typically affects adults aged ≥50 years and increases in incidence with advancing age, often

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CME CE

FEATURED COURSE

presenting when patients are in their 60s or 70s.1 A recent study of Medicare patients aged ≥65 years revealed a stable incidence of IPF from 2001 to 2011, with an estimated 93.7 cases per 100,000 person-years.5 Over the same time, the cumulative prevalence steadily increased from 202.2 cases per 100,000 person-years to 494.5 cases per 100,000 person-years. There was a higher incidence of IPF (and shorter survival time after diagnosis) in male patients.5 With the US population increasing in age, the number of patients with IPF is expected to increase. Mostly because IPF is not as common as certain other respiratory illnesses, >50% of IPF patients are initially misdiagnosed, and many patients are evaluated by more than 3 physicians before being accurately diagnosed with IPF.2,6 Consequently, by the time a diagnosis is confirmed,

many patients will have already endured irreversible damage in the lungs and experienced profound impairments in quality of life.1,7 IPF has an unpredictable and variable natural history, but results of several studies estimate median survival at only 3 years from the time of diagnosis.1 Management options for patients with IPF include supplemental oxygen as needed to maintain normoxia, pulmonary rehabilitation, and possibly pharmacologic treatment aimed at slowing disease progression. There is no cure for IPF. Lung transplantation is an option for a minority of patients.1 For optimal health outcomes, an early and accurate diagnosis is necessary. Therefore, it is imperative that the index of suspicion of IPF be raised among primary care physicians (PCPs) to enable quick recognition of IPF and exclusion of other causes of pulmonary fibrosis.

Suspected IPF

Identifiable Causes for ILD?

Yes

No HRCT UIP

Possible UIP Inconsistent With UIP Surgical Lung Biopsy

Not UIP

UIP Probable UIP/Possible UIP Nonclassifiable Fibrosis MDD

IPF

IPF/Not IPF

Not IPF

HRCT = high-resolution computed tomography; ILD = interstitial lung disease; IPF = idiopathic pulmonary fibrosis; MDD = multidisciplinary discussion; UIP = usual interstitial pneumonia. Source: Adapted with permission from Raghu G, et al. Am J Respir Crit Care Med. 2011;183(6):788-824. Note: This document was published in March 2011 and is currently in revision. Certain aspects of this document may be out of date and caution should be used when applying these in clinical practice or other usages.

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Achieving a confident diagnosis of IPF is challenging. Current guidelines recommend the exclusion of known causes for pulmonary fibrosis and the presence of a UIP pattern on HRCT or surgical lung biopsy (Figure 1).1 Additionally, guidelines recommend a multidisciplinary discussion of available clinical, HRCT, and pathology data. Introduction to our patient, Mrs. R

Mrs. R is a 62-year-old female with type 2 diabetes and hypertension who has endured a dry cough for the last 10 years and, more recently, shortness of breath. She is an active 7th-grade foreign language teacher who walks her dog Tippy a mile before and after school each day. Over the last 18 months, Mrs. R has noticed gradually increasing shortness of breath. A former 15-pack per year smoker who quit 30 years ago, Mrs. R was overweight (179 lbs with a body mass index [BMI] of 27.4 kg/m2). However, after being diagnosed with type 2 diabetes 10 years ago, Mrs. R has been walking daily and eating a healthy diet. Her BMI is now normal. Similarly, Mrs. R’s cholesterol levels are within normal range, and she has no family history of coronary disease. Mrs. R’s medications include metformin 750 mg twice daily, enalapril 10 mg daily, a daily multivitamin, baby aspirin, and ibuprofen occasionally for knee pain. In an effort to address the chronic dry cough, Mrs. R’s PCP treated her for postnasal drip, GERD, and COPD with a regimen that included loratadine, omeprazole, albuterol, inhaled corticosteroids, and bronchodilators. The dry cough persisted with little to no improvement. To address the shortness of breath, Mrs. R was treated with antibiotics for community-acquired pneumonia twice, each time with no benefit. Her PCP then ordered a cardiac stress test, which revealed no findings concerning for cardiac ischemia. Additionally, her PCP conducted PFTs, which revealed restrictive physiology with a forced vital capacity (FVC) of 72% predicted and a mildly reduced diffusing capacity of the lungs for carbon monoxide (DLCO) of 62% predicted. A chest x-ray revealed lower-zone predominant reticular abnormalities. Based on Mrs. R’s evaluation, the PCP suspects chronic ILD and refers Mrs. R to a pulmonologist. This referral initiates a multidisciplinary conversation about the patient. Multidisciplinary discussion in the diagnosis of IPF

Making the diagnosis of IPF requires more than the simple recognition of disease signs and symptoms by a lone PCP; rather, it takes a collaborative effort by a team of healthcare

providers (HCPs).2 Current guidelines recommend that the IPF diagnostic workup be a multidisciplinary effort involving the PCP and specialists (eg, pulmonologist, radiologist, pathologist) experienced in the diagnosis of ILDs.1,8 Indeed, this multidisciplinary approach has been shown to improve diagnostic accuracy.1,2 Such experienced specialists can be found in medical centers with established ILD programs. Early referral to these centers are associated with improved survival in IPF,9 likely stemming from the multidisciplinary assessment of these patients and particular attention to longitudinal disease and comorbidity management.1,2,8 Differential diagnosis: differentiating IPF from ILDs with similar clinical and radiologic manifestations

Effectively caring for patients with IPF demands, yet frequently def ies, an early and accurate diagnosis. Distinguishing IPF from other similar conditions is critical, given that the 5-year survival in IPF is <20%, compared with >50% for other forms of ILD, including nonspecific interstitial pneumonia.10 Because IPF is a diagnosis of exclusion, ILDs of known origin (including those related to environmental, occupational, TABLE 1. Criteria for a definite, possible, and inconsistent UIP pattern on HRCT scan1 UIP pattern (all 4 features) • Subpleural, basal predominance • Reticular abnormality • Honeycombing with or without traction bronchiectasis • Absence of features that are inconsistent with a UIP pattern (see “Inconsistent With UIP Pattern”) Possible UIP pattern • Subpleural, basal predominance • Reticular abnormality • Absence of features listed as inconsistent with UIP pattern (see “Inconsistent With UIP Pattern”) Inconsistent with UIP pattern (any of the following 7 features) • Upper-lung or midlung predominance • Peribronchovascular predominance • Extensive ground glass abnormality (defined extent > reticular abnormality) • Profuse micronodules • Discrete cysts • Diffuse mosaic attenuation or air trapping (bilateral, in 3 or more lobes) • Consolidation in bronchopulmonary segments or lobes HRCT = high-resolution computed tomography; UIP = usual interstitial pneumonia. Adapted from: Raghu G, et al. Am J Respir Crit Care Med. 2011;183(6):788-824.

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CME CE

FEATURED COURSE

Effectively caring for patients with idiopathic pulmonary fibrosis demands, yet frequently defies, an early and accurate diagnosis.

CREDIT: COURTESY OF DR. JEFF SWIGRIS

or medicinal exposures or systemic autoimmune diseases) must be ruled out with a comprehensive history, thorough physical examination, and integration of results from a targeted laboratory battery. Recall that IPF is diagnosed when there is confirmation of an idiopathic clinical circumstance and identification of a UIP pattern on HRCT or surgical lung biopsy. A UIP pattern identified on HRCT is nearly 100% accurate for a UIP pattern in surgical lung biopsy specimens. Thus, HRCT is the diagnostic cornerstone of testing for patients in whom the diagnosis of IPF is being considered.11,12 On HRCT, a UIP pattern is characterized by the following features: 1) subpleural, basal predominance, 2) reticular abnormality, and 3) honeycombing. Typically, honeycombing occurs as clustered air spaces of 3 mm to 10 mm in diameter and with well-defined walls.1 The presence of ground glass opacities should be very limited or nonexistent.13 Findings consistent with a definite, possible, and inconsistent UIP pattern are listed in Table 1. The current guidelines recommend consideration for performing a surgical lung biopsy in the event of an inconsistent UIP pattern on HRCT scan. While an HRCT pattern may be inconsistent with UIP, a surgical lung biopsy may reveal a UIP pattern and ultimately confirm diagnosis of IPF. Histologically, a UIP pattern is indicated by the presence of heterogeneous lung injury with marked fibrosis, architectural distortion with or without honeycombing in

FIGURE 2. HRCT imaging results for Mrs. R.

a predominantly subpleural distribution, areas of normal lung, and presence of fibroblast foci.1 The UIP pattern (on HRCT or surgical biopsy) is not specific for IPF; it can be found in several other conditions, including CTD, chronic hypersensitivity pneumonitis, and asbestosis.4 Often, the greatest challenge is in distinguishing IPF from other IIPs, particularly idiopathic nonspecific interstitial pneumonia. This is particularly true when the HRCT shows a possible UIP pattern. In these cases, a surgical biopsy is often considered, because the UIP pattern can be identified in biopsy specimens even though the HRCT is not confirmatory. Initial evaluation by pulmonologist

The pulmonologist asks Mrs. R a series of specific questions to help rule out diseases with similar clinical symptoms. Mrs. R expresses no complaints of dry eyes or dry mouth, arthralgias, morning stiffness, rash, skin thickening, or color changes of the fingers or toes consistent with Raynaud phenomenon. Consequently, her pulmonologist rules out CTD. Although results of routine laboratory studies are nonspecific, they may further support the absence of a systemic autoimmune disease. Accordingly, the pulmonologist orders laboratory tests for antinuclear antibody titer, rheumatoid factor, and anti-cyclic citrullinated peptide (anti-CCP) antibody.1 It is important to realize that these tests are not diagnostic for autoimmune disease; indeed, as many as 30% of IPF patients test positive for autoantibodies.14 The presence of autoantibodies, absent other diagnostic features of systemic autoimmunity, does not confirm a diagnosis. In Mrs. R’s case, none of the results were positive. The pulmonologist also questions Mrs. R about various exposures. For example, she asks Mrs. R if she ever raised birds, worked in the area of stone cutting or polishing, or owns/uses an indoor hot tub.1 Mrs. R’s negative responses confirm the absence of an identifiable cause for ILD. Following a thorough physical examination (which fails to reveal anything other than bibasilar Velcro crackles) and considering Mrs. R’s PFT results, the pulmonologist reviews her HRCT. The HRCT reveals lower-zone, peripheral, and subpleural predominant reticular opacities, traction bronchiectasis, and patchy honeycombing, but no ground glass and no air

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Current guidelines recommend that the IPF diagnostic workup be a multidisciplinary effort involving the PCP and specialists experienced in the diagnosis of ILDs. trapping on expiratory imaging (Figure 2). The radiologist says he is confident the HRCT shows a UIP pattern.

6. Schoenheit G, Becattelli I, Cohen AH. Living with idiopathic pulmonary fibrosis: an in-depth qualitative survey of European patients. Chron Respir Dis. 2011;8(4):225-231.

Summary

7. Raghu G, Weycker D, Edelsberg J, et al. Incidence and prevalence of idio-

Mrs. R’s radiologic imaging demonstrated all the features of UIP. Based on the discussion among the PCP, pulmonologist, and radiologist, a multidisciplinary consensus is reached indicating a definitive diagnosis of IPF. ■

pathic pulmonary fibrosis. Am J Respir Crit Care Med. 2006;174(7):810-816. 8. Olson AL, Swigris JJ. Idiopathic pulmonary fibrosis: diagnosis and epidemiology. Clin Chest Med. 2012;33(1):41-50. 9. Lamas DJ, Kawut SM, Bagiella E, et al. Delayed access and survival in idiopathic pulmonary fibrosis. A cohort study. Am J Respir Crit Care Med.

References

2011;184(7):842-847.

1. Raghu G, Collard HR, Egan JJ, et al; ATS/ERS/JRS/ALAT Committee on

10. Bradley B, Branley HM, Egan JJ, et al. Interstitial lung disease guideline:

Idiopathic Pulmonary Fibrosis. An official ATS/ERS/JRS/ALAT statement:

the British Thoracic Society in collaboration with the Thoracic Society

idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and

of Australia and New Zealand and the Irish Thoracic Society. Thorax.

management. Am J Respir Crit Care Med. 2011;183(6):788-824.

2008;63(suppl 5):v1-v58.

2. Spagnolo P, Tonelli R, Cocconcelli E, et al. Idiopathic pulmonary fibro-

11. Bhatti H, Girdhar A, Cury J, Bajwa A. Approach to acute exacerbation

sis: diagnostic pitfalls and therapeutic challenges. Multidisc Respir Med.

of idiopathic pulmonary fibrosis. Ann Thorac Med. 2013;8(2):71-77.

2012;7(1):42.

12. Cicchitto G, Sanguinetti CM. Idiopathic pulmonary fibrosis: the need

3. Cottin V, Cordier JF. Velcro crackles: the key for early diagnosis of idio-

for early diagnosis. Multidiscip Respir Med. 2013;8(1):53.

pathic pulmonary fibrosis? Eur Respir J. 2012;40(3):519-521.

13. Xaubet A, Ancochea J, Bollo E, et al; Sociedad Española de Neumología

4. Moua T, Zamora Martinez AC, Baqir M, et al. Predictors of diagnosis

y Cirugía Torácica (SEPAR) Research Group on Diffuse Pulmonary

and survival in idiopathic pulmonary fibrosis and connective tissue disease-

Diseases. Guidelines for the diagnosis and treatment of idiopathic pulmo-

related usual interstitial pneumonia. Respir Res. 2014;15(1):154.

nary fibrosis. Arch Bronconeumol. 2013;49(8):343-353.

5. Raghu G, Chen SY, Yeh WS, et al. Idiopathic pulmonary fibrosis in US

14. Kang BH, Park JK, Roh JH, et al. Clinical significance of serum

Medicare beneficiaries aged 65 years and older: incidence, prevalence, and

autoantibodies in idiopathic interstitial pneumonia. J Korean Med Sci.

survival, 2001-11. Lancet Respir Med. 2014;2(7):566-572.

2013;28(5):731-737.

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CME CE

POST-TEST Expiration date: July 24, 2016

Credit Designation: The Postgraduate Institute for Medicine designates this enduring material for a maximum of 1.00 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. A statement of credit will be issued only upon receipt of a completed pre-assessment test, polling questions, activity evaluation form, and post-test with a score of 70% or better. All components must be completed and submitted online at myCME.com/Mar16CAfeature.

CREDITS: 1.00

| Using an evidence-based approach to diagnose IPF

1. Which of the following clinical scenarios most likely represents a patient having initial symptoms of idiopathic pulmonary fibrosis (IPF)? a. 51-year-old female presenting with dyspnea, chronic cough, sputum production, fever, and history of cigarette smoking b. 68-year-old male, former smoker with dyspnea and chronic cough c. 58-year-old male with dry mouth, dry eyes, morning stiffness, and rash d. 61-year-old female with cough and chest tightness accompanied by fever, chills, malaise, and headache 2. Mr. Q is a 63-year-old building contractor who presents with a dry cough and breathlessness while climbing the stairs at work. After the pulmonologist rules out connective tissue disease (CTD) and significant exposures, including those common to the construction field, she orders a high-resolution computed tomography (HRCT). Which of the following features on HRCT would suggest a diagnosis of IPF? a. Subpleural, basal predominance; reticular abnormality; and honeycombing b. Extensive ground glass opacities; reticular abnormality; and honeycombing c. Air trapping; ground glass opacities; and honeycombing d. Honeycombing; reticular interstitial thickening; and ground glass opacity 3. The usual interstitial pneumonia (UIP) pattern on HRCT or surgical biopsy can be found in: a. IPF only b. Asbestosis only c. Conditions involving air trapping d. IPF and other interstitial lung diseases (ILDs)

4. The differential diagnosis of IPF is challenging. Current guidelines recommend utilization of which of the following primary algorithmic approaches to confirm a diagnosis of IPF? a. Pulmonary function tests (PFTs) followed by confirming the presence of UIP pattern on HRCT b. PFTs followed by incorporation of a multidisciplinary discussion to confirm the presence of UIP pattern on surgical lung biopsy c. Excluding other causes of ILDs followed by bronchoalveolar lavage cellular analysis d. Excluding other possible causes, confirming the presence of UIP pattern on HRCT or surgical biopsy, and collaborating in multidisciplinary discussion 5. Ms. W is a 55-year-old lounge piano player who is a heavy smoker with dyspnea, for which her primary care physician (PCP) treated her with inhaled corticosteroids. Recently, she has complained of intensified dyspnea. Her PCP referred her to a pulmonologist, who ordered an HRCT that reveals a pattern inconsistent with UIP. According to current IPF treatment guidelines, which of the following is the recommended course of action for the pulmonologist? a. Order another HRCT and compare the results with the first HRCT with a radiologist and histopathologist b. Conduct PFTs (ie, forced vital capacity [FVC] and diffusing capacity of the lungs for carbon monoxide [DLCO]) and discuss results with PCP c. Consider obtaining surgical lung biopsy and engage a radiologist and histopathologist in a multidisciplinary discussion of the results of the HRCT and lung biopsy d. Rule out IPF and test for other ILDs as Ms. W’s age makes her an unlikely candidate for IPF

TO TAKE THE POST-TEST please go to: myCME.com/Mar16CAfeature

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YOUR COMMENTS NO THANKS, ON FULL-PRACTICE AUTHORITY With all due respect, I could not disagree with Ms. Amabile more [“Full practice authority and opiate use,” January, page 110]. I am in my 31st year as a physician assistant and had several years of practice in emergency medicine and addiction medicine during that time. I worked in a facility in my addiction medicine years where the supervising physicians would prescribe Suboxone (which is what Ms. Amabile wishes for all mid-levels to be able to prescribe). If/when mid-levels are able to do this, she might regret her words. I, for one, was grateful that we mid-levels at the facility could NOT prescribe it. There are many tough conversations that surround the prescription of this medicine. It, too, can be abused (sold on the street, etc.). It is not, by any stretch of the imagination, a “benign” medication. Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. You may contact us by e-mail at editor@ clinicaladvisor.com. If you are writing in response to a published letter, please indicate so by including the number in parentheses at the end of each item. Letters are edited for length and clarity. The Clinical Advisor’s policy is to print the author’s name with the letter. No anonymous contributions will be accepted.

Sad to say, I learned of physicians (through our addicts) who viewed this medication as a means to increase the census in their offices. It simply became “Pay $ (fill in the blank) for a visit, and we will continue your Suboxone.” I would want NO part of that. That is not practicing good medicine. In my opinion, agents such as Suboxone and Narcan have their place. But among addicts, these are just tools to help feed an addiction and/or keep them alive for the next time they use. A better usage of our time and money would be to help addicts get off of opiates (and not use any substitutes). That may sound harsh to some. However, I have seen folks stay on Methadone or Suboxone for much longer than was intended and never wish to wean themselves off of either. So, my message, again is to BE THANKFUL that you cannot prescribe it as a mid-level. I have seen numerous problems associated with patients and providers who are in this loop of Suboxone maintnenance. It’s not pretty, and I never wish for any mid-level to be a part of it. This also can be painful for those providers whose work sites are caught up in Press Ganey surveys. If you do not keep the patient(s) happy, your survey scores suffer. We have a local ER that is known for dispensing pain medications. And its mid-levels are, unfortunately, caught up in this primarily because their supervisor values survey results. What a shame. And being able to prescribe Suboxone would just make that whole picture worse.—PATTY PULVER, MPH, PA-C, Albany, N.Y. (209-1)

OUR CONSULTANTS

Philip R. Cohen, MD,

is clinical associate professor of dermatology, University of Texas Medical Center, Houston.

Deborah L. Cross, MPH, CRNP, ANP-BC, is associate program

director, Gerontology NP Program, University of Pennsylvania School of Nursing, Philadelphia.

Abimbola Farinde, PhD, PharmD,

is a professor at Columbia Southern University in Orange Beach, Ala.

Laura A. Foster, CRNP, FNP,

Abby A. Jacobson, MS, PA-C,

practices family medicine with Palmetto Primary Care Physicians in Charleston, S.C.

is an assistant professor at Thomas Jefferson University and a dermatology PA at Family Dermatology of Reading, Pa.

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MRI AFTER BREAST CANCER DIAGNOSIS Unfortunately, there is no documented role for MRI of the breast AFTER someone has been diagnosed with breast cancer, even if the original cancer was not detected with mammography [“Hereditary breast cancer risk assessment in primary care,” January, page 36]. National Comprehensive Cancer Network guidelines do NOT include recommendations for MRI as a part of breast cancer surveillance. It is quite a quandary for the patient, and many providers do order it, especially in women who have dense breasts. I specifically asked about the role of MRI after breast cancer diagnosis and treatment at a national conference for breast cancer, and I was told that there is no role.—ELIZABETH GARBER, MSN, FNP, NP-C, Goshen, Ind. (209-2)

CONSULTATION A SIDE EFFECT OF THE FLU VACCINE? Is there a connection between cardiac arrhythmia and the flu vaccine? Three members of our staff have arrhythmia after receiving the flu shot.—TOM LAJUDICE, ANP, Newark, Del. The flu vaccine is recommended yearly to reduce the risk of the flu, a serious respiratory illness that causes over 3,000 deaths in the United States per year. There is a trivalent vaccine and quadrivalent vaccine (the quadrivalent is available as a nasal spray). The most common adverse event is soreness and swelling at the site of injection. Patients may experience flu-like symptoms, including runny nose, cough, headache, myalgias, and fever. Less commonly, a patient may experience syncope. There is no evidence of cardiac arrhythmias associated with the flu vaccine. A patient may have an increased pulse along with the fever, and this may be interpreted as palpitations, but

Debra August King, PhD, PA,

is senior physician assistant at New York-Presbyterian Hospital, New York City.

Mary Newberry, CNM, MSN,

provides well-woman gynecologic care as a midwife with Prima Medical Group, Greenbrae, Calif.

the heart rate will slow with the resolution of the fever.—Claire O’Connell, MPH, PA-C (See photo at bottom of this page for more information about Ms. O’Connell.) (209-3)

CASE FILE HAIR LOSS AFTER STEROID INJECTIONS An 80-year-old woman presents with a complaint of recentonset marked hair loss. While she says she has never had ‘“thick hair,” she is losing handfuls every day when she combs her hair. The patient’s recent medical history noted a series of epidural steroid injections that were completed about 3 months prior to her hair loss. Hair loss is a known side effect of steroid use, regardless of the route or duration. The etiology and timing involves the stages of hair growth and the impact of the sudden influx of steroid medication into the system. The good news is that the hair growth does gradually return to normal. (209-4) Contributed by Sherril Sego, FNP-C, DNP (See photo at bottom of this page for more information about Dr. Sego.)

CLINICAL PEARL STEROID AND RESCUE INHALERS Many patients mix up their steroid inhalers and rescue inhalers, and at times will use the steroid inhaler when they are short of breath. I teach my patients to keep their steroid inhaler with their toothbrush. It helps them remember to use it twice a day, every day (not p.r.n), and they can brush their teeth afterward instead of rinsing their mouth. I use it to show how the steroid inhaler helps keep their lungs clean, just as the toothbrush helps keep their teeth clean.—LISA SCHWARTZ, NP, Boston (209-5) n

Claire O’Connell, MPH, PA-C,

Katherine Pereira, DNP, FNP,

teaches in the PA Program at the New Jersey Medical School and Rutgers University, Piscataway, N.J.

is assistant professor, Duke University School of Nursing, Durham, N.C.

Sherril Sego, FNP-C, DNP,

is an independent consultant in Kansas City, Mo.

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Dermatology Clinic CASE #1

Itchy, burning rash that recurs on the legs every winter R. BLAKE STEELE, BS, AND ERIN L. REESE, MD

A man, aged 68 years, with no known history of atopy presents with a 4-month history of an itchy and burning rash on the legs that has been recurring every winter for the past 3 years. He notes that he had dry skin at baseline and did not use emollients, but he did try hydrocortisone 1% cream without improvement. Examination revealed ovoid, erythematous, well-marginated plaques on the lower legs and dorsal feet with variable scaling and focal weeping and crusting. There were no nail changes, and the rest of his skin examination was notable only for xerosis. What is your diagnosis? Turn to page 51

CASE #2

Painless, bruise-like hyperpigmentation on a woman with lupus T. PETER NGUYEN, BS, AND MAURA HOLCOMB, MD

An African American woman, aged 50 years, presents with painless “bruises” on her leg. She first noticed bruises on both legs a year ago and reports that they have since become larger. Physical examination reveals blue-black macules and patches on both shins. The macules are asymptomatic. A venous stasis ulcer is seen on her right leg. She has a 10-year history of discoid and systemic lupus erythematosus treated with hydroxychloroquine and does not recall any trauma to her legs. What is your diagnosis? Turn to page 54 48 THE CLINICAL ADVISOR • MARCH 2016 • www.ClinicalAdvisor.com

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Dermatology Clinic CASE #1

Nummular dermatitis

Nummular dermatitis, also known as nummular eczema or discoid eczema, is an inflammatory condition characterized by sharply marginated, coin-shaped, erythematous plaques containing microvesicles that erode with resultant weeping, crusting, and scaling. The morphology of nummular dermatitis lesions differs from those of classic eczema, which generally consists of ill-defined, irregularly shaped, scaling patches and plaques. Devergie initially described this condition in 1857, using the term “l’eczéma nummulaire” to emphasize the distinctive coin-shaped lesions.1 Of note, the word nummular is derived from the Latin word for coin, nummus. The condition continued to be reported by other authors under various names, including orbicular eczema, recurrent eczematoid affection, and neurotic eczema.2 Epidemiologic data regarding nummular dermatitis are limited, as the condition is not often reported in the literature, and many of the studies are decades old. Up-to-date population prevalence data are lacking. The condition is more common in adults, with a peak in the third to fourth decade of life, although children may be affected as well.3 Reports of sex-specific predilection are varied. A majority of studies report male predominance among cases, with the exception being in pediatric patients with nummular dermatitis.3-5 Patients with nummular dermatitis classically present with well-marginated, ovoid, erythematous plaques measuring up to a few centimeters in diameter with variable vesiculation, weeping, crusting, and scaling. There are often multiple lesions, with symptoms of pruritus and/or pain, and they tend to concentrate on the extremities (legs more often than arms). Truncal involvement can occur, but facial lesions are rare. The eruption usually lasts several months with frequent recurrences, and onset in colder months is typical.3-6 Many varied hypotheses on the etiology of nummular dermatitis have been proposed, but the pathogenesis has yet to be determined. Some authors consider nummular dermatitis to be a form of atopic dermatitis, but this is debated because personal or family history of atopy is not commonly reported in patients with nummular dermatitis.3-5 In addition, serum immunoglobulin E levels, which are usually elevated in patients with atopic dermatitis, are generally normal in

those with nummular eczema.3 Given the predominance of lesions on the lower extremities, the role of varicose veins in the pathogenesis of the condition has been proposed, with the thought that the nummular lesions may represent an “id reaction” to stasis dermatitis seen more commonly in patients with varicosities.6 Id reactions are sympathy reactions that manifest as rashes of varying morphology distant to the inciting eruption. The prevalence of xerosis mirrors that of nummular dermatitis in that it is more common in older adults and in winter months; thus, age and weather have also been reported as a predisposing or contributing factor.3,6,7 Emotional distress, which has been reported to trigger or flare many dermatoses, has also been hypothesized to do the same in nummular eczema.6 Contact allergy has also been reported to occur at a higher frequency in patients with nummular dermatitis; it is unclear whether the contact allergy initiates the condition or whether the condition is simply complicated by superimposed contact allergy. Patients with nummular dermatitis have a skin barrier that is not intact, thus predisposing them to contact sensitization. In addition, many of these patients apply a myriad of topical preparations to their lesions, which also makes them more prone to the development of contact allergy.3 Patch testing should be considered in patients with treatment-refractory disease. Similar to the idea that nummular dermatitis may represent an id reaction to stasis dermatitis, some have proposed that nummular dermatitis represents a skin reaction triggered by bacterial antigens released from various infectious foci (including non-skin sites such as teeth and tonsils). Patients with difficult-to-control disease have shown improvement with eradication of the distant infection.8,9 Other reported associations include excessive alcohol intake, nutritional deficiency, and medications, among others.3 The differential diagnosis of nummular dermatitis includes psoriasis, bullous impetigo, tinea corporis, and other variants of dermatitis. Psoriasis is another chronic, inflammatory condition of the skin but can be differentiated from nummular dermatitis by its appearance. Psoriasis also consists of well-marginated plaques, but the borders of psoriasis lesions are often more welldefined than those of nummular dermatitis. Psoriasis lesions are predominantly scaly, whereas nummular dermatitis lesions are typically more crusted. Bullous impetigo is more commonly seen in children and is caused by a staphylococcal infection of the skin that leads to formation of flaccid bullae that erode into ovoid, crusted plaques. Once bullous impetigo lesions have eroded and crusted, they can mimic nummular dermatitis lesions. However, patients with nummular dermatitis usually

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Dermatology Clinic do not have a preceding history of frank bullae; their lesions consist of multiple tiny vesicles. Notably, nummular dermatitis can be complicated by bacterial superinfection, so obtaining cultures of affected skin is important. Tinea corporis is a superficial fungal infection of the skin that presents with annular, erythematous plaques with a peripheral rim of scale (also known as ringworm). Tinea corporis lesions have central clearing,

The prognosis for nummular dermatitis is good, and most patients respond to conservative therapy. which is absent in nummular dermatitis lesions. Depending on the chronicity of dermatitis, the clinical appearance varies. Acute forms of dermatitis (usually irritant or allergic contact dermatitis) can present with vesiculobullous lesions that may resemble nummular dermatitis. Contact dermatitis lesions can be localized in a specific pattern depending on the contactant. Subacute forms of dermatitis are generally erythematous and scaly and usually less well-marginated, so often, these lesions will not look like nummular dermatitis. Chronic dermatitis is usually ill-defined and lichenified, with an appearance that differs from nummular dermatitis. The diagnosis of nummular dermatitis is made clinically. However, if the presentation is not typical or response to treatment is poor, a skin biopsy should be considered for confirmation. Histopathology reveals edema between the keratinocytes in the epidermis (spongiosis) that expands to form intraepidermal vesicles. There is an accompanying lymphohistiocytic infiltrate in the superficial dermis, concentrated perivascularly.3 This is a typical pattern for dermatitis of all types; therefore, a skin biopsy will not necessarily help to differentiate specific etiologies of dermatitis (atopic vs contact vs nummular). Special stains for infection may reveal bacteria within the stratum corneum but results are typically negative for fungus. Topical corticosteroids are the first-line treatment for nummular dermatitis; mid- to high-potency preparations are usually required. Clinicians should keep in mind the side effects of atrophy and striae. To minimize the side effects of steroids, topical tar and topical calcineurin inhibitors have also been used successfully. Phototherapy can also be effective for widespread lesions or in patients who do not respond to conservative management. Systemic immunosuppressive therapy is reserved for the most severe and

treatment-refractory patients and is considered off-label use; prednisone, cyclosporine, methotrexate, mycophenolate mofetil, or azathioprine can be considered. Patients must be closely monitored for side effects. If there is suspicion for superimposed skin infection, bacterial cultures should be obtained, with use of oral antibiotics dictated by results of cultures and sensitivities.10 All patients should be advised on proper skin care measures that include use of emollients and gentle soaps. Pruritus can be managed with antihistamines. The prognosis for nummular dermatitis is good, and most patients respond to conservative therapy. Complications can include skin infection, and lesions usually resolve with postinflammatory hyperpigmentation. In our case, the patient received a diagnosis of nummular dermatitis and was treated with a topical class 1 corticosteroid, with improvement. R. Blake Steele, BS, is a medical student and Erin Reese, MD, is assistant professor and assistant residency program director in the Department of Dermatology at Virginia Commonwealth University in Richmond. References 1. Devergie M. Traité Pratique des Maladies de la Peau. Paris: Librarie de Victor Masson; 1857:238. 2. Weidman AI, Sawicky HH. Nummular eczema; review of the literature: survey of 516 case records and follow-up of 125 patients. AMA Arch Derm. 1956;73(1):58-65. 3. Bonamonte D, Foti C, Vestita M, et al. Nummular eczema and contact allergy: a retrospective study. Dermatitis. 2012;23(4):153-157. 4. Hellgren L, Mobacken H. Nummular eczema—clinical and statistical data. Acta Derm Venereol. 1969;49(2):189-196. 5. Cowan MA. Nummular eczema. A review, follow up, and analysis of a series of 325 cases. Acta Derm Venereol. 1961;41:453-460. 6. Jiamton S, Tangjaturonrusamee C, Kulthanan K. Clinical features and aggravating factors in nummular eczema in Thais. Asian Pac J Allergy Immunol. 2013;31(1):36-42. 7. Aoyama H, Tanaka M, Hara M, et al. Nummular eczema: an addition of senile xerosis and unique cutaneous reactivities to environmental aeroallergens. Dermatology. 1999;199(2):135-139. 8. Pugliarello S, Cozzi A, Gisondi P, Girolomoni G. Phenotypes of atopic dermatitis. J Dtsch Dermatol Ges. 2011;9(1):12-20. 9. Tanaka T, Satoh T, Yokozeki H. Dental infection associated with nummular eczema as an overlooked focal infection. J Dermatol. 2009;36(8);462-465. 10. Roberts H, Orchard D. Methotrexate is a safe and effective treatment for paediatric discoid (nummular) eczema: a case series of 25 children. Australas J Dermatol. 2010;51(2):128-130. Continues on page 54

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Dermatology Clinic CASE #2

Hydroxychloroquine-induced hyperpigmentation Hyperpigmentation is a common side effect of antimalarial drugs, including hydroxychloroquine (HCQ), which is commonly used to treat systemic lupus erythematosus. Hyperpigmentation develops in up to 10% to 25% of patients after they have been on an antimalarial drug for

at least 4 months.1 When this occurs, bruise-like macules (with a blue-black to gray appearance) form.1 The macules appear most often on the anterior aspect of the leg.1 However, they sometimes develop on the forearms, hard palate, face, and neck, and discoloration of the hair and nail beds may also occur.2 In general, drug-induced changes are often exacerbated by exposure to the sun.1 The diagnosis of HCQ-induced hyperpigmentation can be confirmed with punch biopsy showing melanin granules and hemosiderin deposits in the dermis.2 A case-control study of 24 patients with HCQ-induced hyperpigmentation found that pigmentation changes begin after a median of 6.1 years of HCQ treatment, as early as 3 months and as late as 22 years after the first treatment.3 Having observed an increased incidence in patients taking platelet antiaggregants or oral anticoagulants, the study authors also hypothesized that HCQ-induced hyperpigmentation follows the development of ecchymoses or bruising. Accordingly, individuals prone to ecchymoses or bruising may be at high risk for HCQ-induced hyperpigmentation. Although some believe that the risk for hyperpigmentation increases with the cumulative dose, a 2011 study of 209 patients taking antimalarial drugs found no relationship between cutaneous side effects and treatment duration.4 They also found no relationship with ethnic background, gender, or type of antimalarial drug.4 HCQ is a synthetic derivative of quinine, which is naturally found in the cinchona tree and was discovered to be an antimalarial agent hundreds of years ago. Since then, a variety of additional therapeutic effects of antimalarial agents have become known. The most prominent of these is their immunologic activity.5 Because they weaken the immune response to auto-antigens, they are key drugs in the treatment of lupus erythematosus and rheumatoid arthritis.2 Antimalarial agents are also beneficial in the

treatment of skin diseases, such as eosinophilic fasciitis and dermatomyositis.5 The most concerning adverse reaction to antimalarial agents is retinopathy, which can be irreversible.2 In addition to hyperpigmentation, other adverse effects include nausea, vomiting, neuromuscular symptoms, and deafness.5 Disorders of pigmentation are common and can be benign or the symptom of a complicated underlying disease. Even when medically benign, such lesions have the potential to be cosmetically displeasing. The hyperpigmentation is usually the result of increased melanin production, the deposition of iron or other heavy metals, or the formation of drug-melanin complexes.1 Other possible causes of the lesions include postinflammatory hyperpigmentation (PIH), an endocrine disorder such as Addison disease, or a fixed drug eruption.1 PIH often manifests as localized darkening at a site of previous inflammation. The inciting inflammation can be due to an allergic reaction, a physical agent, or another event.6 The color of these lesions ranges from light brown to black, and they tend to be worse in patients with lupus erythematosus because the epidermis is disrupted.6 Even with treatment,

Hyperpigmentation is usually the result of increased melanin production, the deposition of iron or other heavy metals, or the formation of drug-melanin complexes. the lesions can last for more than a year. Addison disease, also known as adrenal insufficiency, may be associated with hypermelanosis, usually with accentuation around scars and main folds.1 A fixed drug eruption is a localized cutaneous response to a drug or chemical and usually begins as an erythematous plaque that leaves behind a hyperpigmented patch.6 In addition to antimalarial agents, many other drugs can induce hyperpigmentation, including minocycline, nonsteroidal anti-inf lammatory drugs (NSAIDs), and chemotherapeutic agents. After onset, darkening and expansion of the lesions is normally slow and progressive over months to years.1 Furthermore, the changes may not occur until more than a decade after the initiation of treatment, so that the diagnosis is often difficult.3 Minocycline, an antibiotic often used to treat acne, is one of the most commonly cited causes of drug-induced hyperpigmentation. Minocycline-induced hyperpigmentation has three Continues on page 56

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Dermatology Clinic classic presentations.1 In type 1, blue-black pigmentation develops in previously inflamed areas and old scars. In type 2, which best matches our introductory case, macules form on otherwise normal skin, usually on the anterior aspect of the legs or on sun-exposed areas. In type 3, a diffuse muddy brown discoloration develops on sun-exposed areas. When a patient presents with acquired hyperpigmentation, it is important to include drug-induced pigmentation in the differential diagnosis even though the connection is often hard to determine. For example, in patients denying trauma, drug-induced blue-black macules have been confused with bruises and mistaken for evidence of elder abuse.7 It is estimated that 10% to 20% of cases of acquired hyperpigmentation are drug-induced.1 Treatment involves discontinuation of the offending drug and sun avoidance, although disappearance of the pigmentation often takes many months and may be incomplete.1,3 If the drug cannot be discontinued, topical depigmenting agents or laser treatments may be considered, but their effectiveness has yet to be proved.1 Areas of hyperpigmentation may also fade over time without changes in the antimalarial dosage.3 In our case, a diagnosis of HCQ-induced hyperpigmentation of the legs was determined. The patient elected not to discontinue the drug or undergo treatment because the HCQ was managing her systemic lupus erythematosus very well and the lesions were a cosmetic problem. ■ T. Peter Nguyen, BS, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston, Texas. References

“I suppose you know you’re spoiling that dog.”

and treatment. Am J Clin Dermatol. 2001;2(4):253-262. 2. Van Beek MJ, Piette WW. Antimalarials. Dermatol Clin. 2001;19(1): 147-160, ix. 3. Jallouli M, Francès C, Piette J-C, et al. Hydroxychloroquine-induced pigmentation in patients with systemic lupus erythematosus: a case-control study. JAMA Dermatol. 2013;149(8):935-940. 4. Skare T, Ribeiro CF, Souza FHM, Haendchen L, Jordão JM. Antimalarial cutaneous side effects: a study in 209 users. Cutan Ocul Toxicol. 2011;30(1):45-49. 5. Ben-Zvi I, Kivity S, Langevitz P, Shoenfeld Y. Hydroxychloroquine: from malaria to autoimmunity. Clin Rev Allergy Immunol. 2012;42(2):145-153. 6. Pandya A, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000;18(1):91-98, ix. 7. Cohen PR. Hydroxychloroquine-associated hyperpigmentation mimicking elder abuse. Dermatol Ther (Heidelb). 2013;3(2):203-210.

1. Dereure O. Drug-induced skin pigmentation. Epidemiology, diagnosis,

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Dermatologic Look-Alikes Erythematous papules on the face and torso EMAN BAHRANI, BA, AND MAURA HOLCOMB, MD

CASE #1

CASE #2

A 42-year-old African American man with no significant medical history presents with a 3-week history of rash that began on his face and neck and spread to his chest. He denies a history of infectious or metabolic disease. He reports intense pruritus but denies fever and pain. Physical examination reveals erythematous, follicular papules and pustules distributed across the face, anterior neck, upper chest, and upper back. There is no associated lymphadenopathy. Results of the remainder of the examination, which included hair, nails, and oral mucosae, were normal.

A 30-year-old Hispanic man with acute lymphoblastic leukemia presents with a new rash for a consultation with the dermatology department. He is on his third week of combination reinduction therapy with oral dexamethasone and imatinib. On physical examination, inflamed, erythematous, and dome-shaped papules and pustules are identified on his back, shoulders, upper arms, chest, neck, and face. Other than observation of a few petechiae on his lower legs, the remainder of the examination is unremarkable.

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Dermatologic Look-Alikes CASE #1

HIV-associated eosinophilic folliculitis

There are three major varieties of eosinophilic folliculitis: classic eosinophilic pustular folliculitis (EPF; Ofuji disease), eosinophilic pustular folliculitis in infancy, and human immunodef iciency virus (HIV)- or immunosuppression-associated eosinophilic folliculitis (HEF). These conditions are rare, and HEF typically occurs in HIV-infected adults with CD4 counts of less than 300 cells/mm3, but is also seen in patients with lymphoma, chronic lymphocytic leukemia, acute myelogenous leukemia, and myeloproliferative disorders.1 Patients who have received allogeneic hematopoietic stem cell transplantation are also at risk.2,3 Although the exact pathogenesis of HEF remains unknown, some studies have reported a Th2 pattern with elevated levels of interleukin (IL)-4, IL-5 and chemokines RANTES (regulated on activation normal T cell expressed and secreted) and eotaxin messenger RNA within lesions.1,4 The mite Demodex folliculorum has been implicated in the pathogenesis of HEF due to an abnormal immune response to the mite as an antigen, but some studies propose that they are separate entities.3,5 Papular follicular eruptions on acne-prone areas, such as the face, scalp, and upper trunk characterize HEF. The papules are chronic, recurrent, erythematous, and often intensely pruritic, but they may or may not present with pustules.1,3,6 There are reports of HEF as the presenting feature of HIV infection.6

HEF is different from EPF in that the papules do not coalesce into plaques or form annular lesions and the individual lesions are more persistent.3,6 The differential diagnosis includes more common causes of erythematous papules, such as acne vulgaris and folliculitis, both bacterial and fungal. Less common causes of folliculitis that could be included in the differential diagnosis include herpes simplex folliculitis, pseudofolliculitis barbae, actinic folliculitis, drug-induced folliculitis, and Demodex folliculitis. Lupus miliaris disseminatus faciei, rosacea, granuloma faciale, drug-induced folliculitis, and graft-versus-host disease after bone marrow transplantation can also be considered. Given their clinical similarities, microscopic examination of follicular contents, as well as punch biopsy, provide a definitive final diagnosis. If the patient has not been tested recently, HIV testing is recommended.1,3,7 Another papular and pruritic dermatosis related to HIV infection is HIV-related pruritic papular eruption (or prurigo). It can present as an eruption clinically similar to HEF but can be differentiated by histopathology and immunohistochemical staining. HEF has a denser perivascular and diffuse inflammatory infiltrate, with high expression of eosinophils and mast cells.8 Histologically, HEF is similar to EPF, but EPF always involves the infundibular region of hair follicles, whereas HEF may only have perifollicular infiltrates. Biopsy of involved follicles in HEF exhibits spongiosis and exocytosis of lymphocytes and eosinophils into the follicular epithelium. A dermal infiltrate of lymphocytes and eosinophils may also be present. Micropustular aggregation may lead to eosinophilic pustules and occasional follicular mucinosis and abscess formation. CD8+ lymphocytes predominate in HEF.1,3,7 No treatment has been uniformly effective for HEF, but management of the underlying disease process, such as

Take-away points for HIV-associated eosinophilic folliculitis Clinical presentation

• Papular follicular eruptions on acne-prone areas, such as the face, scalp, and upper trunk; papules are chronic, recurrent, erythematous, and often intensely pruritic, but may or may not present with pustules • May be a presenting feature of HIV infection

Differential diagnosis

• EPF, acne vulgaris, bacterial and fungal folliculitis, herpes simplex folliculitis, pseudofolliculitis barbae, actinic folliculitis, druginduced folliculitis/acne, Demodex folliculitis, lupus miliaris disseminatus faciei, rosacea, granuloma faciale, HIV-related pruritic papular eruption, and graft-versus-host disease (if occurring after bone marrow transplantation)

Diagnosis

• Punch biopsy: spongiosis and exocytosis of lymphocytes and eosinophils into the follicular epithelium • Dermal infiltrate of lymphocytes and eosinophils may also be present; occasional follicular mucinosis and abscess formation; CD8+ lymphocytes predominate

Management

• Antiretroviral therapy, antipruritic agents, indomethacin, and topical steroids; UVB phototherapy in recalcitrant cases • Other topical agents: tacrolimus and permethrin • Oral therapies cited in the literature include itraconazole (100-400 mg/d), antibiotics, isotretinoin (0.5-1 mg/kg/d × 1-4 wk, then taper), and interferon (beta and gamma)

EPF, eosinophilic pustular folliculitis; HIV, human immunodeficiency virus; UVB, ultraviolet B.

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Dermatologic Look-Alikes HIV, is paramount.1,3 A rise in the CD4 count may lead to resolution of HEF, but eruptions can also be seen in the first 3 to 6 months of antiretroviral therapy with immune reconstitution.7 Oral and topical therapies that are effective in some cases, such as antipruritic agents, indomethacin, and topical steroids, may be inadequate in individuals with other diseases causing immunosuppression or in those who have already failed antiretroviral therapy. Ultraviolet B phototherapy may be curative in such cases. Other topical therapies to consider include tacrolimus and permethrin. Oral therapies cited in the literature include itraconazole (100-400 mg/d), antibiotics, isotretinoin (0.5-1 mg/kg/d × 1-4 wk, then taper), and interferon (beta and gamma).1,3 In our case, punch biopsy confirmed eosinophilic folliculitis in the patient, and the patient tested positive for HIV (CD4<300 cells/mm3). He was referred to the infectious disease department to begin antiretroviral therapy.

CASE #1

Steroid-induced acne

Various drugs have been implicated in causing acne or eruptive acneiform lesions as a side effect of their use. High-dose intravenous or oral corticosteroids are the most common medications implicated in acneiform eruptions that concentrate on the chest and back. Steroid-induced acne (and rosacea) can also result from inappropriate use of topical corticosteroids on the face or after chronic inhalation of steroid-containing medications.1,9,10 Perioral dermatitis, which predominantly affects women, is seen in patients using inhaled and topical corticosteroids for long durations.10,11 Misuse of topical corticosteroids is a widespread cause of acne and telangiectasia, especially among young women worldwide, many of whom view these medications as skin-lightening agents.12 The exact pathogenesis of how corticosteroids cause acneiform eruptions remains unclear because they are anti-inflammatory agents. However, studies have found that dexamethasone and cortisol added to cultured human keratinocytes promote cellular toll-like receptor 2 (TLR2) expression. This increases TLR2’s probability of activation to circulating inflammatory cytokines or to Propionibacterium

Perinatal dermatitis is seen in patients using inhaled and topical corticosteroids for long durations. acnes, the bacteria found in normal skin flora and the most common culprit in classic acne vulgaris. In this context, these drugs may trigger proinflammatory changes in the skin when used incorrectly or for long durations.13 Inflamed, dome-shaped papules and pustules develop on a background of erythema that tends to follow the distribution of corticosteroid application, or they appear on the upper arms and trunk weeks to months after beginning a systemic regimen. The differential diagnosis of steroid-induced acne includes eruptions caused by other medications, acne vulgaris, and folliculitis (including eosinophilic, bacterial, and fungal). Unlike acne vulgaris and acne caused by cosmetics or friction, comedones are typically absent in drug-induced acne, perioral dermatitis, and rosacea.10 To rule out acne caused by other medications, an understanding of when medications were initiated in relation to symptom onset is necessary. Other agents commonly known to cause drug-induced acneiform eruptions include corticotropin, androgens and anabolic steroids, bromides, iodides, isoniazid, lithium, phenytoin, and progestins. Targeted therapies, such as tyrosine kinase inhibitors, monoclonal antibodies, soluble receptors (etanercept), transcription modulators, and proteasome inhibitors, have also been implicated. A thorough medical history is thus indicated for any atypical, nonjuvenile-onset cases of acne or acneiform eruptions.1,9,10 In women, misuse of anabolic androgenic steroids causes hirsutism and deepening of the voice, in addition to acne.14 Histopathologic findings of classic acne lesions reflect the stage of the lesion and clinical findings. In acne vulgaris, microcomedones show keratinocytes plugging the opening to a distended follicle; closed comedones exhibit increased follicular distension due to the cystic structure, with eosinophilic keratin debris, hair, and bacteria. As the follicular epithelium distends due to the increasing infiltrates and disruption of the pilosebaceous unit, the obstructing contents can rupture into the dermis. The keratin, hair, and bacteria provoke a strong inflammatory response, with neutrophils forming pustules leading to eventual granulomatous changes and scarring.1 Perioral dermatitis, however, exhibits histopathologic features similar to those of rosacea: lymphocytes and histiocytes around follicles and their vascular supply with concurrent sebaceous hyperplasia.11

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“Steroid acne” and “steroid-induced acne” are misnomers in that these drugs do not cause a true form of acne and can be differentiated histologically. Their histopathology resembles folliculitis with neutrophils surrounding the hair follicle. Druginduced acne presents abruptly as a monomorphic, inflammatory papular and pustular eruption, unlike the heterogeneous and more common lesions of acne vulgaris. Some physicians therefore refer to drug-induced acne as a form of folliculitis.1,9,10 Eosinophilic folliculitis exhibits eosinophils and lymphocytes rather than neutrophils around the hair follicle; unlike bacterial or fungal folliculitis, steroid use in the past few days to weeks would establish a likely diagnosis of steroid-induced acne. Epidermal growth factor receptor inhibitors (EGFRIs) have also been shown to cause acneiform eruptions in a high proportion of patients on these drugs. This class includes gefitinib, cetuximab, erlotinib, lapatinib, and panitumumab. Monomorphic, follicular pustules and papules erupt on the face, scalp, and trunk 1 to 3 weeks after initiation of the EGFRI. Coinfection with Staphylococcus aureus may occur, causing discharge and honey-colored crusting and scale. Histopathology in these cases shows a folliculitis pattern, including neutrophils within the follicle and lymphocytes aggregated around it.9,10 Medication history and biopsy establish a diagnosis. For most drug-induced acneiform eruptions, lesions gradually resolve following discontinuation of the drug or a decrease in dosage, although steroid dependency can lead to prolonged and severe flares following withdrawal.1,9 Topical agents, such as clindamycin and benzoyl peroxide, can also be used for management.10

The patient described in our case was almost finished with his current cycle of reinduction therapy, so he was advised to complete the course and then discontinue dexamethasone. On follow-up 1 week later, most of his lesions had resolved. ■ Eman Bahrani, BA, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston. References 1. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012. 2. Zitelli K, Fernandes N, Adams BB. Eosinophilic folliculitis occurring after stem cell transplant for acute lymphoblastic leukemia: a case report and review. Int J Dermatol. 2015;54(7):785-789. 3. Long H, Zhang G, Wang L, Lu Q. Eosinophilic skin diseases: a comprehensive review [published online April 16, 2015]. Clin Rev Allergy Immunol. doi: 10.1007/12016-015-8485-8. 4. Amerio P, Verdolini R, Proletto G, et al. Role of Th2 cytokines, RANTES, and eotaxin in AIDS-associated eosinophilic folliculitis. Acta Derm Venereol. 2001;81(2):92-95. 5. Sabater-Marco V, Escutia-Muñoz B, Botella-Estrada R. Eosinophilic follicular reaction induced by Demodex folliculorum mite: a different disease from eosinophilic folliculitis. Clin Exp Dermatol. 2015;40(4):413-415. 6. Basarab T, Russell Jones R. HIV-associated eosinophilic folliculitis: case report and review of the literature. Br J Dermatol. 1996;134(3):499-503. 7. Rajendran PM, Dolev JC, Heaphy MR Jr, Maurer T. Eosinophilic folliculitis: before and after the introduction of antiretroviral therapy. Arch Dermatol. 2005;141(10):1227-1231. 8. Alfonso JP, Tomimori J, Michalany NS, et al. Pruritic papular eruption

Take-away points for steroid-induced acne Clinical presentation

Differential diagnosis

Diagnosis Management

and eosinophilic folliculitis associated with human immunodeficiency virus

• Dome-shaped papules and pustules on a background of erythema in distribution of topical corticosteroid application; abrupt, monomorphic, inflammatory, papular and pustular eruption appearing on the upper arms and trunk weeks to months after starting systemic regimens; comedones are typically absent

(HIV) infection: a histopathological and immunohistochemical comparative

• Acne vulgaris, folliculitis (eosinophilic, bacterial, fungal) • Acneiform eruptions caused by other drugs: corticotropin, anabolic steroids, bromides, iodides, isoniazid, lithium, phenytoin, progestins, tyrosine kinase inhibitors, monoclonal antibodies, soluble receptors (etanercept), transcription modulators, proteasome inhibitors, EGFRIs

11. Lipozenčić J, Hadžavdić SL. Perioral dermatitis. Clin Dermatol.

• Clear history of present illness or punch biopsy; resembles folliculitis with neutrophils surrounding the hair follicle

toll-like receptor 2 expression in human keratinocytes stimulated with

• Discontinue offending agent or reduce dosage; addition of topical clindamycin and benzoyl peroxide optional

EGFRI, epidermal growth factor receptor inhibitor; HIV, human immunodeficiency virus.

study. J Am Acad Dermatol. 2012;67(2):269-275. 9. Du-Thanh A, Kluger N, Bensalleh H, Guillot B. Drug-induced acneiform eruption. Am J Clin Dermatol. 2011;12(4):233-245. 10. Dessinioti C, Antoniou C, Katsambras A. Acneiform eruptions. Clin Dermatol. 2014;32(1):24-34. 2014;32(1):125-130. 12. Dey VK. Misuse of topical corticosteroids: a clinical study of adverse effects. Indian Dermatol Online J. 2014;5(4):436-440. 13. Shibata M, Katsuyama M, Onodera T, et al. Glucocorticoids enhance Propionibacterium acnes or proinflammatory cytokines. J Invest Dermatol. 2009;129(2):375-382. 14. Nieschlag E, Vorona E. Mechanisms in endocrinology: medical consequences of doping with anabolic androgenic steroids (AAS): effects on reproductive functions. Eur J Endocrinol. 2015;173(2):R47-R58.

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FEATURE: JILL ELLIS, PA-C, MPAS, AND MELANIE TIDMAN, DHSC, MA, OTR/L

Cryptogenic organizing pneumonia Patients with COP generally have positive outcomes following a definitive diagnosis and the initiation of appropriate treatment.

Common symptoms of COP include a flulike prodrome and nonproductive cough.

requently, dyspnea is the chief symptom of patients presenting to primary care settings. The differential diagnosis is broad and commonly includes both pulmonary and cardiac disease. Common pulmonary diagnoses for patients with dyspnea include exacerbation of an underlying illness, infectious processes, and inflammatory disease.1 When patients present with acute dyspnea associated with fever and cough, community-acquired pneumonia (CAP) is often diagnosed. A less common, yet clinically important, alternative diagnosis for patients with these symptoms is cryptogenic organizing pneumonia (COP). COP is a relatively uncommon disease process with a presentation that can mimic that of CAP. However, the management of COP differs significantly from the management of CAP, and it is important to distinguish between the two disorders. Clinicians often fail to recognize COP, leading to a delay in diagnosis.2 The purpose of this article is to increase awareness of COP among primary care clinicians. Definition of terms

Organizing pneumonia is both an inflammatory and a fibrotic lung disorder that can occur following a variety of pulmonary insults.3 The term organizing implies that the underlying lung parenchyma remains intact. The term pneumonia is defined as “filling of the alveoli by inflammatory exudate.”4 Organizing pneumonia is not a specific diagnosis, but rather a spectrum of disorders that share histopathologic features.3,5 64 THE CLINICAL ADVISOR • MARCH 2016 • www.ClinicalAdvisor.com

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In the majority of patients with organizing pneumonia, the inciting insult cannot be identified,6,7 and this condition has been designated as cryptogenic organizing pneumonia (COP)8; cryptogenic means of obscure or unknown origin.9 COP has also been identified in the literature by a variety of other terms, including bronchiolitis obliterans organizing pneumonia (BOOP), chronic pneumonia, and organizing diffuse alveolar damage.10 In 2001, the American Thoracic Society and the European Respiratory Society formed a multidisciplinary group to standardize the terminology used to describe interstitial lung diseases. The consensus recommendation of this group was that COP is preferable to other terminology for two primary reasons11: first, it focuses on the essential histologic features of the disorder; and second, it avoids confusion with other airway diseases, including constrictive bronchiolitis obliterans.11 In this article, the recommended term, COP, is used; however, other terms are mentioned because many sources reference them.

TABLE. Causes of secondary organizing pneumonia5,16

Epidemiology

process can extend between the alveoli by means of intraalveolar connections, known as pores of Kohn.15,19 A mild degree of interstitial inflammation and fibrosis may also occur.15 Buds of granulation tissue, known as Masson bodies, develop within affected areas as part of the reparative process.15 The lung is typically affected in a patchy distribution rather than uniformly throughout.17 Cordier describes this process, which does not occur exclusively in COP, as a type of “wound healing that results in a serious lung disorder.”5

COP is a relatively rare pulmonary disorder. Exact incidence and prevalence data are limited.12 Gudmundsson et al. performed an epidemiologic study in Iceland and calculated a mean annual incidence of COP of 1.1 per 100,000 persons,13 yet prevalence estimates have ranged up to 7 per 100,000 persons.10 COP is estimated to account for 1.8% to 13% of all cases of interstitial lung disease.14 Several studies have shown that COP affects men and women equally.14-17 It develops most often in the fifth and sixth decades of life,15 although it has been reported to occur less commonly from adolescence to old age.13 Smoking has not been shown to be a risk factor for the development of COP, and in some studies, it has even appeared to be a protective factor.14-17 Etiology

The etiology of COP is idiopathic, or cryptogenic, as its name implies. Organizing pneumonia can also develop as the consequence of a known insult.2 Known causes include connective tissue disease, autoimmune disorders, infections, malignancies, drugs, radiation injury, organ transplants, aspiration, and inhaled toxic agents.2,16,18 The term secondary organizing pneumonia is applied when an etiologic factor is identified (Table). It is important to differentiate between COP and secondary organizing pneumonia because the treatment and prognosis vary.15 Pathophysiology

The development of COP begins with lung injury. The injury stimulates the migration of inflammatory and fibrotic products into the alveoli, alveolar ducts, and terminal and respiratory bronchioles.19,20 The inflammatory and fibrotic

Etiologic category

Examples

Autoimmune and/or connective tissue disorders

Behçet disease, inflammatory bowel disease, primary biliary cirrhosis, polymyalgia rheumatica

Drugs

Antibiotics, antiepileptics, antineoplastics, antirheumatics, amiodarone, beta-blockers, chelating agents, cocaine, cytotoxins, immunosuppressants, statins

Infection

Bacterial, fungal, protozoal, viral infections

Malignancy

Leukemia, lymphoma

Pulmonary disorders

Hypersensitivity pneumonitis, eosinophilic pneumonia, chronic bronchiolitis

Other

Aspiration, bone marrow transplant, inhalation injury, organ transplant, radiation injury

Clinical presentation

As previously mentioned, the clinical presentation of COP can mimic that of CAP.17,21 Nearly half of all patients with COP are initially given a diagnosis of CAP,22 and many have failed prior courses of antibiotics.16 The most common symptoms associated with COP include a flu-like prodrome, nonproductive cough, and progressive dyspnea.23 The onset of symptoms in patients with COP can vary; however, the presentation most often is subacute, with symptoms of several weeks’ duration.15,19 The median duration of symptoms has been found to be less than 3 months.20 In a minority of patients, the clinical course is more rapidly progressive, developing over 1 to 2 weeks7,24; however, this is more likely to occur in patients with secondary organizing pneumonia.5,24 Another minority of patients are asymptomatic at presentation, with incidentally discovered radiographic abnormalities.7 A prodrome that mimics influenza, or a viral type of illness, may be present for several weeks before presentation, with symptoms including low-grade fever, malaise, and fatigue.5,7,23 Fever has been described as both continuous and intermittent and is usually low grade.6,7 The most common pulmonary

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CRYPTOGENIC ORGANIZING PNEUMONIA

The physical examination findings are often nonspecific, and the diagnosis cannot be established on the basis of the examination alone. symptoms are nonproductive cough and dyspnea.15,16,25 Drakopanagiotakis et al. reported that cough was present in about two-thirds of patients who had a confirmed diagnosis of COP and was predominantly nonproductive.2 The dyspnea is usually mild and often occurs only with exertion, but it can be severe in a minority of cases.5 Mild weight loss is common and has been reported to occur in more than half of affected patients.10 Uncommon symptoms include hemoptysis, chest pain, arthralgias, and night sweats.2,5,15 The physical examination findings are often nonspecific, and the diagnosis cannot be established on the basis of the examination alone. Scattered bilateral crackles are the most common physical examination finding15,26 and have been reported to occur in more than 75% of cases.7 Wheezing and clubbing may also occur but much less frequently.6,12 Cazzato et al. found that wheezing was present in 26% of cases.7 Cordier et al. noted that digital clubbing was found in only 1 of 16 study patients.19 Up to 25% of patients have had normal findings on physical examination.12,25 The history and physical examination should seek to identify underlying causes of organizing pneumonia. For example, the identification of causative drugs in the medication history or exposure to environmental triggers may lead to a diagnosis of secondary organizing pneumonia, rather than COP. The causes of secondary organizing pneumonia are listed in the Table. Differential diagnosis

Diagnostic considerations for patients with the clinical presentation previously described, other than COP, include infection, other types of interstitial and/or inflammatory lung disease, and malignancy. Several types of infection, especially CAP, can present similarly to COP. An important feature for distinguishing between COP and CAP is that COP will not respond to antibiotic therapy because it is does not have an infectious etiology. The presentations of several interstitial lung diseases, including idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, and hypersensitivity pneumonitis, as well as those of certain malignancies, especially pulmonary lymphoma, may mimic the presentation of COP.1,12 Chronic eosinophilic pneumonia is an immunologically mediated lung disease that can imitate COP.1 Because of the similarities between the clinical presentation and radiographic findings of COP and those of numerous other conditions, lung biopsy is frequently needed to establish a definitive diagnosis.2,12

Diagnosis

The diagnosis of COP is complex and not easily established. A definitive diagnosis is based on a combination of clinical and histologic characteristics; thus, COP is considered a clinicopathologic condition.26 It is unusual for a definitive diagnosis to be established before 6 weeks following the onset of symptoms.26 In some instances, the primary care provider will first consider COP as a diagnostic possibility only after a patient has failed to respond to antibiotic therapy for suspected CAP.12 A primary care provider will rarely diagnose this condition on his or her own but can facilitate the diagnosis by remaining alert to COP as a possibility. Radiographic imaging is an integral component of the diagnostic evaluation for patients presenting with symptoms possibly attributable to COP. Previous reports have described distinct patterns that can be seen on radiographic images of the chest.5,7,19 The most common pattern consists of bilateral, peripherally distributed patchy alveolar infiltrates or air space consolidation.15,18,23 The location of affected areas can appear to change when serial radiographic images are obtained, which is known as a migratory sign.15,26 Another pattern consists of bilateral, diffuse interstitial infiltrates with smaller superimposed alveolar infiltrates, or ground glass opacity.5 Other, less common radiographic patterns can include solitary, nodular lesions; multiple nodules; fibrosis; cavitation; pleural effusions; and pleural thickening.7,12,16 High-resolution computed tomography (HRCT) is increasingly used in the evaluation of patients with undiagnosed lung pathology. HRCT can reveal patterns of disease similar to those seen on chest radiographs; however, more extensive disease is often seen on HRCT than on radiographic imaging in patients with COP.12 Pulmonary function tests are a useful adjunct in the diagnosis of COP. The most common defect seen on pulmonary function testing is a mild or moderate restrictive ventilatory pattern.2,27 A combination of restrictive and obstructive defects may also be seen.6,15 The diffusion capacity for carbon monoxide is usually reduced.12,18 Mild hypoxemia, both at rest and with exercise, is common.5 There are no specific laboratory tests to confirm the diagnosis of COP. A complete blood cell count and tests of renal and hepatic function are often obtained during routine evaluation; however, the results are not specific for COP. Variable leukocytosis can be seen. King noted in a literature review that up Continues on page 71

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Patients are typically started on corticosteroid therapy.The outcome of untreated COP can range from spontaneous remission to death. to 50% of patients with COP had associated leukocytosis.12 In their study of 25 patients with COP, Alasaly et al. found that a minority of them had associated leukocytosis (4 patients).6 Other laboratory abnormalities can include an elevated sedimentation rate and C-reactive protein level; however, both of these are nonspecific findings. Cazzato et al. found an elevated sedimentation rate in 81% of patients studied,7 whereas Cordier noted in a review study that about 30% of patients had elevated values.5 Additional laboratory testing may be required to rule out conditions that are known causes of secondary organizing pneumonia, based on the specific clinical presentation. This may include a comprehensive infectious evaluation as well as an evaluation for connective tissue disease. Following these basic diagnostic tests, the primary care clinician will usually refer the patient to a specialist for further diagnostic evaluation and treatment because COP is ideally diagnosed in a multidisciplinary approach.20 Bronchoscopy with bronchoalveolar lavage (BAL) is commonly the next step. BAL fluid most frequently reveals a mixed pleocytosis with lymphocytosis, as well as modest increases in the numbers of neutrophils and eosinophils7,14 and a reduction in the CD4/CD8 ratio.7,15 Mast cells and foamy macrophages may also be seen.10,28,29 BAL often does not lead to a definitive diagnosis6; however, it remains an important diagnostic tool because it may exclude other diagnostic possibilities, especially infections.16 Following BAL, lung biopsy is usually required to establish a definitive diagnosis. Chest imaging should be performed just before biopsy because of the migratory nature of the lesions.5 A histologic diagnosis is made when Masson bodies, which are buds of granulation tissue, are identified within the alveoli and distal airways along with preservation of the underlying lung parenchyma architecture.7 The histologic diagnosis is then combined with the patientâ&#x20AC;&#x2122;s clinical picture to establish a clinicopathologic diagnosis of COP. Both transbronchial lung biopsy and open lung biopsy can be performed to obtain tissue samples, although open lung biopsy remains the gold standard for diagnosis.2,18,30 Transbronchial lung biopsy is less invasive and associated with less morbidity; however, the tissue samples that are obtained are not as large as the samples obtained via open lung biopsy.31 COP affects the lung in a patchy distribution, so that the tissue samples obtained via transbronchial lung biopsy may not include affected portions of the lung.6 Larger tissue samples are often necessary, not only to confirm the

diagnosis of COP but also to exclude other diagnostic possibilities adequately.5 Poletti et al. examined the accuracy of transbronchial lung biopsy in diagnosing COP and found that the probability of obtaining a correct diagnosis was 69%.29 The diagnostic yield of transbronchial lung biopsy may be increased when the findings are combined with the available clinical information and BAL findings.2,6,29 A clinical decision may be made to omit lung biopsy and treat the patient empirically based on a presumptive diagnosis of COP if the risk of biopsy outweighs the potential benefit of a definitive diagnosis.5 Treatment

Once a diagnosis of COP is established, patients are typically started on corticosteroid therapy. The outcome of untreated COP can range from spontaneous remission to death.5 Spontaneous remission is more likely to occur in patients with mild disease and minimal symptoms; thus, close clinical observation may be an option in such cases.12 Studies have shown significantly improved outcomes in patients treated with corticosteroids versus those who do not receive them.6,32 The underlying mechanism by which corticosteroids effectively treat COP remains obscure.5 No randomized trials have defined a standard protocol for the duration and dosage of corticosteroid therapy. Specific therapy is usually initiated by a pulmonary specialist and directed based on clinical experience, case reports, and practice guidelines.12 In the study by Cazzato et al., patients with a diagnosis of COP were treated with a mean dose of 40 mg of methylprednisolone for 6 weeks, followed by a taper over the following 6 to 9 months.7 Cordier reviewed treatment options and noted a range between 0.75 and 1.5 mg/kg per day for 1 to 3 months, followed by a taper over several months.5 More aggressive courses of corticosteroids, including intravenous therapy, may be required to treat patients with more severe symptoms.12,27 Corticosteroid-sparing agents are primarily used when patients do not respond appropriately to standard therapy and/ or when the side effects of corticosteroids limit therapy.15,23,32 These agents can include macrolide antibiotics and cytotoxic agents. Macrolide antibiotics, including erythromycin, clarithromycin, and azithromycin, may be useful for their antiinflammatory properties.6,12,23 Cytotoxic agents, including cyclophosphamide and azathioprine, have been trialed with some success, although reports are limited.12

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Follow-up care

Following their referral to a specialist for care, the primary care provider often plays a supportive role in the management of patients with COP. One task that can be vital in the care of these patients is monitoring for the onset of relapse. Relapses occur frequently as corticosteroids are tapered,5,16 and the presentation is most commonly similar to the initial clinical presentation. Chest radiography and pulmonary function testing should be done every 6 to 8 weeks in the initial follow-up period to allow an early detection of relapse.10 Because of the migratory nature of the disorder, chest radiographic imaging during follow-up may demonstrate infiltrates in a location different from the location identified on initial radiographic imaging.26 Cazzato et al. noted that relapse occurred in 26% of study patients when the corticosteroid dose was lowered.7 Relapses that occur in patients during the tapering phase of treatment do not seem to affect the ultimate prognosis; however, they can have a significant impact on patients in the short term.5,16 Patients with relapse generally respond well to increased doses of corticosteroids, but it is important to recognize the onset of relapse as early as possible to prevent complications.

Ms. Ellis is an assistant professor of physician assistant studies, Grand Valley State University in Allendale, Mich., and Ms. Tidman is an adjunct professor for the DHSc program at AT Still University. References 1. Fauci A, Braunwald E, Kasper D, et al. Harrison’s Principles of Internal Medicine. New York, NY: McGraw Hill Medical; 2008. 2. Drakopanagiotakis F, Paschalaki K, Abu-Hijleh M, et al. Cryptogenic and secondary organizing pneumonia: clinical presentation, radiographic findings, treatment response, and prognosis. Chest. 2011;139(4):893-900. 3. Geddes DM. BOOP and COP. Thorax. 1991;46(8):545-547. 4. Mark EJ, Ruangchira-urai R. Bronchiolitis interstitial pneumonitis: a pathologic study of 31 lung biopsies with features intermediate between bronchiolitis obliterans organizing pneumonia and usual interstitial pneumonitis, with clinical correlation. Ann Diagn Pathol. 2008;12(3):171-180. 5. Cordier JF. Organising pneumonia. Thorax. 2000;55(4):318-328. 6. Alasaly K, Muller N, Ostrow DN, et al. Cryptogenic organizing pneumonia. A report of 25 cases and a review of the literature. Medicine. 1995;74(4):201-211. 7. Cazzato S, Zompatori M, Baruzzi G, et al. Bronchiolitis obliterans-organizing pneumonia: an Italian experience. Respir Med. 2000;94(7);702-708.

Prognosis

8. Davison A, Heard B, McAllister W, Turner-Warwick M. Cryptogenic

Patients with COP generally recover without long-term clinical or radiographic impairment.6,16 They have been shown to have outcomes better than those of patients with secondary organizing pneumonia.5,15 Patients with COP characteristically demonstrate a rapid clinical response to corticosteroid therapy, generally within 1 to 2 weeks.12,17 Radiographic resolution can take up to several weeks.5 There have also been sporadic reports of a minority of patients in whom progressive interstitial fibrosis develops and does not resolve completely, although this is more likely to occur in patients with secondary organizing pneumonia.20,32 The more common radiographic pattern of alveolar infiltrates and the presence of a high lymphocyte count on BAL appear to be associated with a favorable prognosis.5,28

organizing pneumonitis. Q J Med. 1983;52(207):382-394. 9. Merriam-Webster Online Dictionary. Cryptogenic. Retrieved from http://www.merriam-webster.com/dictionary/cryptogenic. 10. King T. Organizing pneumonia. In: Schwarz M, King T, eds. Interstitial Lung Disease. Shelton, CT: People’s Medical Publishing House; 2011:981-994. 11. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001. Am J Respir Crit Care Med. 2002;165(2):277-304. 12. King T. Cryptogenic organizing pneumonia. UpToDate. http://www. uptodate.com/contents/cryptogenic-organizing-pneumonia. Published 2013. Updated October 22, 2015.

Conclusion

13. Gudmundsson G, Sveinsson O, Isaksson HJ, et al. Epidemiology of

Primary care clinicians frequently encounter patients with respiratory symptoms and should be alert to the broad range of diagnostic possibilities, including COP, when patients present with dyspnea. The prompt identification of COP can improve patient outcomes. The burden of diagnosing and managing COP does not rest solely with primary care clinicians; however, it is imperative that they be able to identify and appropriately refer patients with a possible diagnosis of COP. Patients with COP generally have positive outcomes following a definitive diagnosis and the initiation of appropriate treatment. ■

organising pneumonia in Iceland. Thorax. 2006;61(9):805-808. 14. Jara-Palomares L, Gomez-Izquierdo L, Gonzalez-Vergara D, et al. Utility of high resolution computed tomography and BAL in cryptogenic organizing pneumonia. Respir Med. 2010;104:1706-1711. 15. Beardsley B, Rassl D. Fibrosing organizing pneumonia. J Clin Pathol. 2013;66(10):875-881. 16. Roberton B, Hansell D. Organizing pneumonia: a kaleidoscope of concepts and morphologies. Eur Radiol. 2011;21(11):2244-2254. 17. Tetenta S, Chawla H, Trow L, Bandyopadhyay T. Cryptogenic organizing pneumonia with fatal respiratory failure. Connecticut Med. 2012;76(1):23-25.

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18. Vasu TS, Cavallazzi R, Hirani A, et al. Clinical and radiologic distinctions between secondary bronchiolitis obliterans organizing pneumonia and cryptogenic organizing pneumonia. Respir Care. 2009;54(8):1028-1032. 19. Cordier JF, Loire R, Brune J. Idiopathic bronchiolitis obliterans organizing pneumonia. Definition of characteristic clinical profiles in a series of 16 patients. Chest. 1989;96(5):999-1004. 20. Travis WD, Costabel U, Hansell DM, et al; ATS/ERS Committee on Idiopathic Interstitial Pneumonias. An official American Thoracic Society/ European Respiratory Society statement: Update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med. 2013;188(6):733-748. 21. Kolditz M, Halank M, Schulte-Hubbert B, Hoffken G. Procalcitonin improves the differentiation between infectious and cryptogenic/secondary organizing pneumonia [Letter to the editor]. J Infect. 2012;64(1):122-124. 22. Li J, Yen A, Lin G. Recurrent pneumonia, persistent cough, and dyspnea

“Two separate worlds, please.”

in a 41-year-old man. Chest. 2012;142(5):1338-1342. 23. Pathak V, Kuhn J, Durham C, et al. Macrolide use leads to clinical and radiological improvement in patients with cryptogenic organizing pneumonia. Ann Am Thorac Soc. 2014;11(1):87-91. 24. Cohen AJ, King TE, Downey GP. Rapidly progressive bronchiolitis obliterans with organizing pneumonia. Am J Respir Crit Care Med. 1994;149(6):1670-1675. 25. Epler GR, Colby TV, McLoud TC, Carrington CB, Gaensler EA. Bronchiolitis obliterans organizing pneumonia. N Engl J Med. 1985;312(3):152-158. 26. Wells AU. Cryptogenic organizing pneumonia. Semin Respir Crit Care Med. 2001;22(4):449-460. 27. Nishino M, Mathai S, Schoenfeld D, et al. Clinicopathologic features associated with relapse in cryptogenic organizing pneumonia. Hum Pathol. 2014;45(2):342-351.

“Of course the savings on gas are fantastic!”

28. Costabel U, Guzman J, Teschler H. Bronchiolitis obliterans with organising pneumonia: outcome. Thorax. 1995;50(Suppl 1):S59-S64. ML. The diagnostic value of bronchoalveolar lavage and transbronchial lung biopsy in cryptogenic organizing pneumonia. Eur Respir J. 1996;9(12):2513-2516. 30. Luo Q, Han Q, Chen X, Xie J, Wu L, Chen R. The diagnosis efficacy and safety of video-assisted thoracoscopy surgery (VATS) in undefined interstitial lung disease: a retrospective study. J Thorac Dis. 2013;5(3):283-288. 31. Fruchter O, Fridel L, El Raouf B, Abdel-Rahman N, Rosengarten D, Kramer M. Histological diagnosis of interstitial lung diseases by cryo-transbronchial biopsy. Respirology. 2014;19:683-688. 32. Lee J, Cha S, Park T, et al. Adjunctive effects of cyclosporine and macrolide in rapidly progressive cryptogenic organizing pneumonia with no prompt response to steroid. Intern Med. 2011;50(5):475-479. All electronic documents accessed February 19, 2016.

“I tried to make it from the windowsill to the top of the refrigerator. How about you?”

29. Poletti V, Cazzato S, Minicuci N, Zompatori M, Burzi M, Schiattone

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FEATURE: MARIE MECKEL, PA-C, MPH

Uganda’s clinical officers rise to the challenge In Uganda, clinical officers are addressing public health needs by training to work in rural areas and treating the country’s growing population.

Uganda is a pioneer in the field of clinical officers.

was eager to talk to James Ofono about the history of clinical officers in Uganda. I had met Mr Ofono when I worked at Walter Sisulu University in Eastern Cape in South Africa. He has worked as one of the educators there for many years. He has been instrumental in the growth and development of the clinical associate program in Eastern Cape. When I thought about the development of the physician assistant and nurse practitioner professions, I immediately assumed that the United States was one of the first countries to develop these healthcare professions. However, after meeting Mr Ofono, I realized that Uganda has a rich history of not only developing this unique cadre of healthcare professionals, but also implementing them into their healthcare system. After reading about the development of the clinical officer in Africa, I learned that British colonizers were a major force in developing this profession. The British had their own healthcare system in many of the countries they colonized, and African populations did not have access to this system. Although the British essentially prevented access to their medical care, this resulted in the development of the non-doctor healthcare providers in many of these countries. As NPs and PAs, we are aware that our professions have had long and often difficult journeys This article is part of Global Health Rounds, an ongoing series that highlights the successes and challenges faced by advanced medically trained clinicians (AMTCs) in developing countries. For more articles in this series, please visit: ClinicalAdvisor.com/GHR

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from being barely understood by the medical community to one of the fastest-growing and most respected professions in the United States. Likewise, the Ugandan clinical officer has had a long and arduous path, and the current profession greatly benefitted from this journey. Mr Ofono, a clinical officer in Uganda, works as a lecturer in the clinical associate program at Walter Sisulu University in South Africa. When asked about his profession’s role in the country, he said, “It’s very popular and very well respected.” The profession is so popular that schools receive thousands of applicants each year for a small number of available spots. While there is federal financial aid to help students fund their education, Mr Ofono notes that “the population has outrun government resources.” Now, financial aid is awarded to students with the highest grades. Although Mr Ofono believes the future of clinical officers is bright, Uganda faces many challenges in delivering quality health care to its residents. Most developing countries share similar struggles such as poverty, limited access to clean water, urban air pollution, and infectious diseases such as malaria, but Uganda is also experiencing explosive population growth. Fifteen of the world’s youngest populations are in Africa, and Uganda has the 2nd youngest population in the world, with half of the country’s population younger than 15.7 years old. Uganda’s population has been growing at an annual rate of 3.2%, which is the 9th fastest in the world. From 2002 to 2012, Uganda grew from a nation of 24 million to 34 million—and most of that growth is happening in rural areas, where access to health care can be challenging. Mr Ofono estimates that 80% of the population lives in these rural areas, and he emphasized that clinical officer training is focusing on serving these areas. The evolution and education of clinical officers in Uganda

The clinical officer program started in 1918, which makes it one of the oldest programs in the world. However, as Mr Ofono points out, there is no real documentation to support this. The initial title of this profession was medical assistant, and it was changed to clinical officer in 1996. Mr Ofono tells us that Sir Albert Cook, CMG, OBE, MD, and his wife, a nurse, were Christian missionaries living in Uganda in 1918. They recognized that there was a need to train laypeople in treating patients. In 1929 the Ugandan government recognized the importance of this healthcare profession and created an official training school for clinical officers. An official curriculum was established in 1975 for the clinical officer program, which was a major achievement for Uganda. In 1995, public health was incorporated into the clinical officer curriculum, and the profession was clearly

recognized as a means of addressing the public health needs of Uganda. Students spent 10 weeks working in rural communities where they learned environmental health, rural health concerns, irrigation, hygiene, and basic public health issues. The education of the clinical officer is quite different from how NPs or PAs are educated in the United States. There are 2 tracks for the clinical officer. The 1st track is for students who matriculate, followed by 2 years of basic science. The 2nd track is for healthcare professionals such as orthopedic technicians or nurses. Students from both graduate as clinical officers, but what is unique is that the program has different tracks for different learners. Another feature of the clinical officer program is the educational model. The program is 3 years, but it is unique in that students spend time in both the classroom and in the clinical setting throughout their studies. The 1st-year students spend 40% of their time in clinical settings and 60% of their time in lectures. As the years progress, they spend less time in the classroom, so that by their last year they spend 80% of their time in a clinical setting. The role of the clinical officer in Uganda Clinical officers have a huge role in Ugandan health care. They outnumber doctors, are highly respected, and have an impressive amount of autonomy. These healthcare professionals work in all levels of the public health sector, where they are seen managing health centers that cater to districts with populations of 25,000 to 40,000. When I asked Mr Ofono what problems or issues the profession is facing in Uganda, he told me that clinical officers have limitations in their surgical scope of practice. For example, clinical officers run health centers but cannot perform Cesarean sections, a skill greatly needed in rural areas. Fortunately, the government has responded to this concern and has begun to train clinical officers in Cesarean sections. Clinical officers also face the difficult expectation of managing healthcare facilities. They often feel overworked and burdened by having to simultaneously manage the health center and practice medicine. Mr Ofono noted that supplying health centers with management staff to help run these complex centers could potentially improve the workload for clinical officers. Lessons learned and hopes for a brighter future

Mr Ofono hopes that everyone will recognize Uganda as a pioneer in the field of clinical officers and that these professionals are well integrated into the healthcare system. What I find most impressive about Uganda’s clinical officers is their thorough integration of public health, their educational model, and the long history they have had in Uganda.

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UGANDA

Listen to the podcast at: ClinicalAdvisor.com/ UgandaPodcast

The United States could benefit from incorporating more clinical exposure into our educational model. There is a lot we can learn from our Ugandan colleagues. Recently, Pew Research Center conducted a survey of SubSaharan African countries that focused on attitudes toward economic growth as well as other pressing issues. The results indicated that 56% of people in Sub-Saharan Africa believed that the next generation will be financially better off than their parents, a rate much higher compared with other parts of the world. In Uganda, the top 3 problems cited by respondents are lack of employment, poor health care, and poor quality schools. Mr Ofono and the people of Uganda are optimistic about the future and are greatly concerned about improving health care in their country. Young people in the country express a strong interest to enter the healthcare field. This is an exciting time for Uganda to harness the power and enthusiasm of its youthful population, continuing to educate and propel them toward a brighter future. n

“This is money—get ready to worry about it for the rest of your life ”

Marie Meckel, PA-C, MPH, is a physician assistant who works in Western Massachusetts. She spent a year in South Africa at Walter Sisulu University where she taught clinical associates. She has spent the last year interviewing PAs and NPs and their international equivalents and American PAs and NPs working abroad. References

“I’m really going to miss their chips and dip.”

1. Lehmann U. Mid-level health workers. The state of the evidence on review. WHO and Global Health Workforce Alliance 2008. 2. Diamond K. Uganda’s demographic and health challenges put into perspective with newfound oil discoveries [part one]. New Security Beat. April 26, 2012. http://www.newsecuritybeat.org/2012/04/ugandas-demographic-and-health-challenges-put-into-perspective-with-newfound-oildiscoveries-part-one/ 3. Wike R, Simmons K. Health care, education are top priorities in Sub-Saharan Africa. Pew Research Center. September 16, 2015. http://www.pewglobal.org/2015/09/16/ health-care-education-are-top-priorities-in-sub-saharan-africa/ 4. Khosl S. These maps show where the world’s youngest and oldest people live. Global Post. September 8, 2014. http://www.globalpost.com/dispatch/news/ health/140904/map-youth-elderly-world-political-unrest-economy-unemployment. All electronic documents accessed January 22, 2016.

programmes, activities, costs and impact on health outcomes. A literature

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After a fall on an outstretched hand, wrist injuries are common, but clinicians are advised to also consider ligament tears in adults. PAMELA HORN, MS, CNP, RNFA, ONP-C; MATTHEW BERAN, MD

A 58-year-old, right-hand–dominant woman fell in the shower and injured her left wrist. She was seen 3 days later at an outside emergency department (ED) where radiographs were obtained. Her wrist was splinted, and then she was sent to an urban ED to “have her arm set.” No reduction was required. She was evaluated, placed in a volar splint, and referred to a specialty hand clinic where she was seen 4 days later. Her splint was then removed, and she was noted to have moderate edema of the distal forearm and hand with no open wounds or skin injury. There was minimal bruising. Her compartments were soft and compressible. Range of motion of her wrist and fingers was limited, secondary to pain and swelling. Her radial pulse was easily palpated, and motor/sensory function was intact in a median, radial,

FIGURE 1. Left wrist PA view: Distal radius fracture with widening between the scaphoid and lunate carpal bones, highly suspicious for a scapholunate ligamentous tear.

and ulnar distribution. She complained of severe pain with palpation of the distal radius and dorsolateral carpus with minimal snuff box tenderness. Imaging results

Repeat radiographs (Figures 1 and 2) of the left wrist revealed a comminuted distal radius fracture with possible intraarticular extension but no significant displacement or angulation. Osteopenia was noted with soft tissue swelling over the dorsum of the wrist. No other fractures were seen; however, there was evidence of widening between the scaphoid and lunate carpal bones. The patient was placed in a removable thumb spica splint, and an MRI of the left wrist was obtained. The MRI

FIGURE 2. Left wrist lateral view: Distal radius fracture with no appreciable angulation/displacement. Scapholunate angle 90 degrees (normal 30 to 60 degrees)

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(Figure 3) showed a subacute transverse distal radius fracture without malalignment, a small joint effusion, and a widened scapholunate (S-L) space associated with a tear of the SL ligament. The patient ultimately underwent surgical repair of this ligament with an uneventful healing of the fracture. She had no residual wrist pain. Had this patient been casted for the fracture with the ligament injury left untreated, she would have been at risk for lingering pain and potential for future morbidity. Discussion

Wrist injuries after a fall on an outstretched hand (FOOSH) are common in any age group. However, SL ligament tears are more common in adults, especially adult athletes. A myriad of diagnoses are associated with wrist injuries, including sprains, strains, and fractures (single or multiple) of the distal radius, ulna, or any of the carpal bones (with the most common being scaphoid). The most important diagnostic tool is the initial history and physical exam. Acute injuries, if appropriately diagnosed, are easier to treat and result in lower morbidity and subsequent unwanted sequelae.1,2 Patients whose radiographs are read as negative are often thought to have wrist sprains and/or strains. These patients are usually treated conservatively with splints for several weeks to months. If pain persists following immobilization, it may be due to a ligament tear (either partial or complete), which can cause continued pain and/or decreased motion (especially rotation).1-4 Typical acute symptoms of a scapholunate tear are wrist pain in the dorsolateral aspect of the wrist (1 cm distal to the dorsoradial tubercle), swelling and/or bruising, weak hand grip, and loss of wrist motion. There may also be a popping or clicking sound with motion.5 Watson’s maneuver (scaphoid shift test) is a physical exam to assess for SL laxity. The examiner places his or her thumb on the distal aspect of the scaphoid, using the opposite hand to axially load the wrist. The wrist would be passively brought from ulnar to radial deviation. If the test is positive, the pressure exerted dorsally will result in dorsal wrist pain and often a palpable “clunk.” Exam of the contralateral wrist may help differentiate laxity from normal motion.2,5 Initial radiographs consist of a posterior-anterior (PA) wrist film, lateral wrist film, and often an oblique wrist film and/or a scaphoid view (wrist in ulnar deviation looking for an acute scaphoid fracture). With a scapholunate injury, a ≥5-mm space is noted between the scaphoid and lunate bones on the PA view or a >2- to 3-mm difference from the contralateral side. This is also known as the “Terry Thomas”

FIGURE 3. MRI of the left wrist: Distal radius fracture with scapholunate ligamentous widening consistent with an acute tear. Complete disruption seen in additional views with a repairable ligament as noted by the hand surgeon.

sign after a British actor who had a gap between his teeth.3,5 If the radiograph is unremarkable but the history and physical exam are indicative of an SL tear, stress radiographs are warranted. These are completed with a patient clenching his or her fist, then supinating and ulnarly deviating the wrist, which may reveal dynamic SL widening.5 Advanced imaging may consist of an MRI with or without arthrography or a CT scan. A CT scan is more helpful in diagnosing carpal/radial fractures, while an MRI can best assess soft tissue injuries. Some clinicians prefer wrist arthroscopy for diagnosis and treatment, but ongoing research is being conducted in this area.2,5 Misdiagnosis of an SL tear may result in carpal or radiocarpal avascular necrosis, osteoarthritis, decreased wrist function, and/or continuous pain. Scapholunate advanced collapse (SLAC) is an advanced arthritis due to progressive

Wrist exam with concern for SL tear • History of fall on an outstretched hand • Swelling, pain, or bruising about the wrist • There may or may not be a distal radius fracture • Loss of wrist motion • Weak hand grip • Popping or clicking sound with motion • Pain on the distal aspect of the scaphoid when the wrist is axially loaded.

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Case Study instability and results in significant morbidity. When surgical intervention is based on reconstruction rather than initial repair, outcomes are not as optimal for the patient.2,5,6 Office visits for wrist injuries may not always be benign. It is crucial to conduct a careful history and complete physical examination with subsequent radiographs as deemed necessary, especially when there is no fracture associated with the injury and the patient has significant wrist pain. When in doubt, a timely referral to a hand surgery specialist is necessary. ■

References 1. Kulhawik D, Szalaj T, Grabowska, M. Avascular necrosis of the lunate bone (Kienbock’s disease) secondary to scapholunate ligament tear as a consequence of trauma—a case study. Pol J Radiol. 2014;79:24-26. 2. Pappou I, Basel J, Deal D. Scapholunate ligament injuries: a review of current concepts. Hand (N Y). 2013;8(2):146-156. 3. Clark D, von Schroeder H. Scapholunate ligament injury: the natural history. Can J Surg. 2004;47(4):298-299. 4. Rohman EM, Agel J, Putman MD, Adams JE. Scapholunate interosseous ligament injuries: a retrospective review of treatment and outcomes in 82 wrists. J Hand Surg Am. 2014;39(10):2020-2026.

Pamela Horn, MS, CNP, RNFA, ONP-C, is the Orthopaedic Allied Health Professional Lead and Matthew Beran, MD, is a faculty member of the Department of Orthopaedics at the Nationwide Children’s Hospital in Columbus, Ohio.

5. Fufa D, Goldfarb C. Sports injuries of the wrist. Curr Rev Musculosketel Med. 2013;6(1):35-40. 6. Vitale M. SLAC (Scaphoid lunate advanced collapse). Orthobullets. http:// www.orthobullets.com/hand/6043/slac-scaphoid-lunate-advanced-collapse.

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LEGAL ADVISOR CASE

Heart attack misdiagnosed as heartburn

BY ANN W. LATNER, JD

Ms. M, a 28-year-old nurse practitioner, worked in a walk-in clinic that was located on the ground floor of a multi-story office building. She had been working for the clinic for the past year. Due to the clinic’s location, many of the patients were employees in the businesses located in the office building. The clinic was primarily staffed by nurse practitioners with the oversight of a supervising physician. On a typical day, Ms. M would primarily see business people with minor injuries or complaints of flu symptoms, sore throats, or gastrointestinal illness. She administered flu and pneumonia shots as well as regular vaccinations, and she performed the occasional pediatric check-up for kids participating in sports activities or going to camp. In the few times that there was a true emergency, the patient was referred to the local hospital for treatment. The office building opened at 7 a.m. each morning, but the clinic itself did not open until 9 a.m. Ms. M arrived at 8 a.m. to help the office manager prepare for the upcoming day. The

A clinician turns away a man looking for assistance before a walk-in clinic is open for the day.

Signs exhibited by the patient should have alerted Ms. M that the situation should be treated as an emergency.

clinic’s waiting room was open to the building’s lobby, but the reception and exam areas were gated off until the clinic opened. One morning, just past 8 a.m., Ms. M was at the clinic looking over some paperwork when she heard a faint knocking coming from the waiting area. She opened the locked door to the waiting room and saw a somewhat distressed-looking man in a business suit in his mid-50s. The man was pale, with a slight sheen of sweat on his face, although the day was cool. “I’m sorry. We’re not open for another hour,” Ms. M said politely. “Oh,” the man said, clearly disappointed and with a hand across his stomach. “I was hoping someone could see me. I arrived at work this morning, and I’ve just had this terrible stomach ache that is just radiating across my body.” 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.

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LEGAL ADVISOR “I’m very sorry,” Ms. M said, still speaking through the slightly open office door. “I can’t examine you until we open. If I came out there, the only thing I’d be able to do is call an ambulance for you, and I don’t know if your insurance would cover that.” The man frowned. “I can only imagine what something like that would cost. Okay, I guess I’ll just come back down in another hour. I’m just feeling pretty crappy.” “There’s a pharmacy around the corner that is open already,” Ms. M said. “Maybe you want to go pick up an antacid in the meantime.” “Good idea,” the man said. “I’ll do that, and will come back in an hour when you’re open.” “See you then,” Ms. M said cheerfully. However, when the clinic officially opened, the man did not return. Shortly after the clinic opened, Ms. M and the other clinic staff heard a commotion in the lobby of the building and saw an emergency medical team running into the building and heading up in the elevator. A short time later, they wheeled someone out. Later that afternoon, one of the other clinic staff asked Ms. M whether she had heard about the guy on the fifth floor who had died of a heart attack that morning.

Once Ms. M heard the symptoms he was describing, she should have called an ambulance immediately or instructed the patient to take himself to the hospital. Ms. M realized that it was likely the man who had come into the waiting room earlier that day. She felt terrible that she had not called an ambulance for him. After he had tried to get medical help from Ms. M that morning, the man—Mr. D—went to the pharmacy as Ms. M had suggested and bought an antacid. He returned to his office and told his co-worker that he had not been able to get into the clinic yet, but he had spoken to a nurse and he was going to try an antacid in the meantime. The co-worker found Mr. D slumped over in his chair a short time later and called 911. But Mr. D had had a massive cardiopulmonary event and was declared dead on arrival at the hospital. The co-worker told Mr. D’s family about his encounter with the nurse at the clinic that morning. His family hired a plaintiff’s attorney and sued the walk-in clinic.

Ms. M and the supervising physician met with their defense attorney. “We never treated that man,” the physician said. “Ms. M merely talked to him and told him we weren’t open yet. He wasn’t actually a patient.” The attorney asked Ms. M some questions: Was the man exhibiting signs that indicated a heart attack? Did Ms. M suggest calling for emergency medical help? Ms. M described her interaction with the man, including the symptoms he described, his appearance, and her suggestion that he go to the pharmacy and come back in an hour. The attorney consulted with a medical expert who confirmed that the symptoms described were consistent with signs of a heart attack. After some months of negotiations, the case was settled out of court for $900,000. Legal background

Cases may settle out of court for any number of reasons. Taking a case to trial is expensive and time-consuming, and the result is unpredictable, particularly when a jury is involved. In this case, the defense attorney made a tactical decision to settle. Taking the case to trial would have resulted in bad publicity for the clinic and its staff. Although the clinic did not officially treat Mr. D and he was not a patient as such, once Ms. M spoke to him and noted that he was exhibiting cardiac symptoms, she should have called an ambulance. Protecting yourself

Clinicians are well acquainted with the signs and symptoms of a heart attack. Abdominal pain that radiates and pale sweaty skin are signs exhibited by Mr. D that should have been enough to alert Ms. M that the situation should be treated as an emergency. Although Ms. M thought she was doing the right thing by referring Mr. D to the nearby pharmacy for an antacid and expressing concern about whether an ambulance would be covered by Mr. D’s insurance, she was doing him a great disservice. Once she heard the symptoms he was describing and recognized that it could be an indicator of a heart attack, she should have either called an ambulance immediately or instructed the patient to take himself to the nearest hospital right away. Either option might have both saved the patient’s life and prevented a costly lawsuit. n Ms. Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, N.Y.

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Writers’ Guidelines The Clinical Advisor welcomes submissions from its readers. Writing for us is an opportunity to share your knowledge and experience with your colleagues — and to collect a fee in the bargain! We pay an honorarium for every submission we accept. We’ll be glad to work with you to develop your ideas into compelling articles. As for length, that depends on which kind of article you submit. CLINICAL FEATURES update our readers on the latest information about conditions seen in everyday practice. Running approximately 2,500 to 5,000 words, including the references, features can be written either as regular narratives or as a series of questions and answers. Topics should be selected with the busy primary-care clinician in mind; specialists should review specialty topics from the primary-care point of view. If at all possible, articles should be accompanied by clinical photos. Charts, tables, and algorithms are also encouraged. Please include your title and affiliation. CLINICAL CHALLENGE is our popular department comprising histories of difficult cases. Each case is presented as a step-by-step, chronological account, revealing the author’s thought processes along the way. It is divided into sections in this order: the patient presentation; the patient history; the twists and turns eventually leading to a diagnosis; the treatment and outcome; and a discussion of the lessons learned or of the condition in general. The length should be about 1,500 words, and accompanying images are encouraged. Please include your title and affiliation. DERMATOLOGY CLINIC is a department that presents photos of actual cases and asks readers to identify the condition. Each case opens with one or two color photos and a 75-to-100-word description of the patient presentation, without giving away the diagnosis. This is followed by a 750-to-1,000-word summary that includes a fuller description of the ailment, an explanation of how the correct diagnosis was reached, a general review of the condition along with a differential diagnosis, and a description of the patient’s treatment and outcome. Topics must be approved by the editor prior to submission. Please include your title and affiliation. COMMENTARY is our guest editorial page. It gives you the opportunity to sound off on an issue of importance to your colleagues nationwide. A typical Commentary runs about 600 words in length. Please include your title and affiliation. To discuss your editorial ideas, contact us by phone at 646.638.6078; by e-mail to editor@ClinicalAdvisor.com; or by mail to The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2016 87

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Conference Roundup International Stroke Conference 2016

LONG AND SHORT SLEEP DURATION MAY INCREASE STROKE RISK Individuals who sleep between 7 and 8 hours a night have a decreased risk for stroke, whereas those who sleep more or less than this amount have an increased risk for stroke, researchers reported. “We found that there were multiple combinations of sleep duration and physical activity that are associated with risk of having a stroke,” Azizi Seixas, PhD, of the NYU Langone Medical Center, New York, said in an interview. According to Dr Seixas, there were two catalysts for the analysis. “First, there is mounting evidence highlighting the importance of sleep in overall health, particularly with cardiovascular disease,” he said. “Second, sleep makes up one-third of our day and physical activity makes up the other twothirds of our daily lives. We wanted to show how the two together are important behavioral factors in health. We wanted to capture idiosyncratic sleep and physical activity profiles that reduce stroke risk.” Dr Seixas and colleagues hypothesized that average sleep duration (7 to 8 hours a night) and moderate-vigorous physical activity would reduce stroke risk and culled data from 288,888 responders of the 2004 to 2013 National Health Interview Survey. A machine-learning Bayesian Belief Network (BBN) was used to model the probabilistic relationships—both independent and additive—of sleep duration and physical activity to stroke risk. “Utilization of BBN analysis is important, as it provides a more dynamic risk stratification system,” Dr Seixas and colleagues wrote. In the study, they examined several factors, including demographic, behavioral, health/

Individuals who sleep between 7 and 8 hours per night have a lower risk for stroke, while those who sleep more or less than that amount have a higher risk of stroke, according to researchers.

medical, and psychosocial, along with sleep duration and physical activities, such as leisurely walking/bicycling, slow swimming/dancing, and simple gardening activities. Overall, 48.1% of responders were 45 years of age or younger, 77.4% were white, 15.9% were black/African American, and 45.1% reported earning less than $35,000 annually. The precision index of the model was 95.84%. Results suggested that 7 to 8 hours of sleep a night was associated with a stroke risk reduction of 25%, compared with long sleepers (>8 hours) who were 146% more likely to have a stroke and short sleepers (<7 hours) who were 22% more likely to have a stroke. In an analysis that included a model-based adaptive method, the combined effect of health status, hypertension, heart condition, income, and alcohol consumption increased the risk for stroke from 3% to 90%. Furthermore, healthy sleep and vigorous leisurely activity of 30 to 60 minutes 3 to 6 times per week significantly decreased the risk for stroke. Dr Seixas and colleagues used the observational inference technique and created idiosyncratic profiles of protective behaviors—or minutes and frequency of moderate or vigorous exercise per week and short, average, or long sleep—that reduced the likelihood of stroke. “The one size fits all sleep and [physical] activity recommendations are often discordant with the lifestyles of many people who lead busy lives,” he said. “Our study ‘pluralizes’ these recommendations to fit diverse lifestyles.” Dr Seixas cautioned that the study does not establish any causal relationships between sleep, physical activity, and stroke. “However, these are significant findings that can be used as behavioral guidelines,” he said.

American Heart Association / American Stroke Association Los Angeles

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WOMEN AND MINORITIES HAVE WORSE FUNCTIONAL OUTCOMES AFTER STROKE Women and minorities have worse functional status at 3 months following stroke, according to researchers. “Women and non-white minorities had lower Stroke Impact Scale-16 (SIS-16) scores, whereas [patients with] diabetes, depression, prior stroke/[transient ischemic attack (TIA)], and age did not, even after adjusting for stroke severity,” Cheryl Bushnell, MD, MHS, of the Wake Forest School of Medicine in Winston Salem, N.C., said in an interview. Functional outcomes after stroke are important to patients but are not found in administrative data, leading researchers to use a hospital quality improvement program to determine outcomes 3 months after discharge. They evaluated the association between outcomes measured with the SIS-16 and sex, comorbidities, depression, and risk factors. “The catalyst for the study was to see if comorbidities and the management of them might influence functional status,” Dr Bushnell said. “But, we pre-specified gender and race because we knew these could be important predictors of outcome.” The study included patients who had ischemic/hemorrhagic stroke or transient ischemic attack (TIA) and were in an ongoing hospital-supported quality improvement program that concentrated on transitional care and outcomes. Dr Bushnell and colleagues used the SIS-16 to determine self-reported mobility, arm strength, and basic/instrumental activities of daily living. The range of transformed scores was 0 (worst) to 100 (best), and questionnaires were mailed to patients 3 months after discharge or collected by phone if there was no mailed response. In all, 90-day outcomes were obtained from 129 patients (mean age, 66 years; 45.7% women; 73% white) between September 2011 and April 2015. The mean NIH Stroke Scale (NIHSS) score was 4, and 28% of patients had diabetes, 82% had hypertension, 15.6% had coronary artery disease, 35% had prior stroke/TIA, and 7% had pre-stroke depression. Overall, 37% of patients received no therapy, 14.7% received inpatient therapy, 24% received home health therapy, and 23.2% received outpatient therapy. The SIS-16 score was 81.1. Predictors of a lower SIS-16 score included female gender, non-white race, and NIHSS score. Furthermore, in a stepwise linear regression model that adjusted for NIHSS, female gender and non-white race yielded poorer functional status, while a trend was found in patients with prior stroke/TIA. “Women and minorities have poorer functional outcome after stroke, but the reasons for this outcome need to be further explored,” Dr Bushnell said. “Our model showed that we only explained 31% of the variance in SIS-16 with

Women and minorities have worse outcomes 3 months post-stroke.

gender, race/ethnicity, and stroke severity, so unmeasured factors are extremely important. We could speculate from this dataset and other published data that women may be more likely to have functional deficits prior to stroke, be unmarried/widowed, live alone, or be institutionalized after stroke. Non-white stroke survivors may have poorer access to care, have multiple strokes, and more comorbidities.” Dr Bushnell added that she and her colleagues will continue to collect functional outcomes and have a process for doing so among all stroke survivors discharged home. “As we move toward value-based care, these outcomes will become the focal point for our post-acute care processes,” she said. “Knowing which patients might have worse functional outcomes is an important step.”

HRT USE, MIGRAINE SEVERITY ASSOCIATED WITH HIGHER STROKE RISK Women on hormone replacement therapy (HRT) who experience an increase in migraine severity of one grade or more have an increased risk for ischemic stroke, researchers reported. “We found that women who are currently taking HRT and have had a worsening severity of migraines have a 30% increased risk of having strokes, as compared to women who have worsening migraines but are not currently on HRT,” Haseeb A. Rahman, MD, said lead author from the Zeenat Qureshi Stroke Institute in Minneapolis. According to Dr Rahman, a large number of post-menopausal women are on HRT, many of whom with a history of migraines, and women can develop more severe migraines while taking HRT. “We wanted to investigate if a worsening of migraines while taking HRT increases the risk of stroke in these women,” he said. “To our knowledge, a correlation between worsening

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severity of migraines while taking HRT and increased stroke risk had never been studied before.” Although previous studies had addressed the relationship between HRT and migraines as risk factors for stroke, Dr Rahman noted that they had sometimes come to differing conclusions. “There are still certain ‘grey areas’ in our understanding of the correlation of HRT and migraines as stroke risk factors,” he said. For the current study, Dr Rahman and colleagues culled data for 82,208 women who were aged 50 to 79 years and were enrolled in the observational arm of the Women’s Health Initiative study. Researchers defined HRT as unopposed estrogen and/or estrogen plus progesterone and examined the risk for ischemic stroke among women with migraines who were receiving HRT or who had previously or never received HRT. Patients were categorized into two groups: those who had an increase in migraine severity of one grade or more at 3 years, and those who experienced no change or a decrease in migraine severity at that same time point. The researchers compared the relative risk of developing ischemic stroke among patients who were currently on HRT with those who were either previously on HRT or who had never received HRT. Overall, 45.8% of patients were on HRT and 54.2% were either past users or had never used HRT therapy. Results indicated that 20.6% of patients who were currently on HRT demonstrated an increase in migraine severity, compared with 18.7% of those previously on HRT and 17.3% of those never on HRT. Compared with women who were current users of HRT and had experienced no change or a decrease in migraine severity, those who never or only in the past used HRT had a decreased odds ratio (OR) for ischemic stroke (0.91 vs. 1.1). This discrepancy in ischemic stroke likelihood was also observed when researchers compared patients who had never or only in the past used HRT (OR=0.81) with those who were current HRT users and had experienced an increase in migraine severity (OR=1.3). As a result of the findings, Dr Rahman said neurologists should keep a close watch on migraines in post-menopausal women taking HRT. “Aside from addressing the migraines as they worsen, it would be helpful to keep in mind a potential increase in stroke risk that may be related to this,” he said. “It is important to work in collaboration with the prescribing physician, who is often a primary care clinician or gynecologist, to address the potential risks and benefits of placing a patient on HRT, or continuing them on it once started. It is also necessary to identify and improve other stroke risk factors as best as possible.”

Conference Roundup

Stroke in the right frontal lobe caused by an arterial thrombus.

MIGRAINE WITH AURA INCREASES RISK FOR ISCHEMIC STROKE SUBTYPES Patients who have migraine with aura demonstrate increased rates of thrombotic and cardioembolic stroke, compared with patients who have migraine without aura, according to researchers. “Our results indicate migraine with aura is significantly associated with increased risk of stroke both in men and women—twice as likely when compared with migraine without aura,” Souvik Sen, MD, MS, MPH, study investigator from the University of South Carolina School of Medicine, Columbia, South Carolina, said in an interview. “After adjusting for the stroke risk factors, the risk of stroke in migraine with aura remained significant and twice as likely when compared to migraine without aura.” Previous research had indicated that migraine with aura is an independent risk factor for ischemic stroke, leading Dr Sen and colleagues from South Carolina, North Carolina, and Maryland, to evaluate whether migraine with aura is associated with specific ischemic stroke subtypes. “South Carolina, North Carolina, and Georgia are located in the ‘buckle’ of the stroke belt, with one of the highest stroke-related death rates in the country,” said Dr Sen. “An unfortunate trend is that younger patients are having strokes leading to death and disability. As a part of the workup for young stroke, we are interested in migraine with aura and the type of stroke associated with this condition.” The prospective cohort analysis involved 12,844 patients from the Atherosclerosis Risk In Communities (ARIC) study who completed an in-person headache questionnaire. The researchers classified headaches as migraine with aura, migraine without aura, or non-migraine headaches, and strokes

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Conference Roundup as thrombotic brain infarction, lacunar infarction, or cardioembolic stroke, with classification requiring evidence of sudden or rapid onset of neurological symptoms lasting ≥24 hours. In addition, stroke diagnoses were ascertained via computerderived diagnosis and physician medical record review, with a second physician reviewer adjudicating differences. During the third ARIC study visit, Dr Sen and colleagues reported that 12.7% of patients had migraine, of whom 29% had MA, and 8.5% had non-migraine headaches. Between 1987 and 2012, 817 ischemic strokes occurred, of which 51% were thrombotic, 27% cardioembolic, and 22% lacunar. Among those with migraine with aura, there was an increased risk for ischemic stroke compared with patients with migraine without aura (unadjusted odds ratio [OR]=2.4). “These results are in agreement with the previous studies that reported increased risk of stroke in migraine with aura,” Dr Sen said. Moreover, individuals with migraine with aura were at increased risk for cardioembolic stroke (OR=3.3) vs thrombotic stroke (OR=2). No significant association was observed between migraine with aura and lacunar stroke. “As our results point to the significant association of stroke with migraine, it emphasizes the importance of specific diagnostic testing to assess for cardioembolism and stroke prevention in migraine with aura patients,” Dr Sen said. “These individuals should ask their primary care physicians about access to specific diagnostic testing such as echocardiogram with bubble studies or Holter monitoring for cardioembolism and additional stroke risk factors.” He added that migraine with aura patients may benefit from the initiation of an 81-mg aspirin regimen, especially those who have additional stroke risk factors. “Encouraging individuals with a history of migraine with aura to talk with their primary care clinicians about specific cardioembolic stroke risk factors may aid in the effort of preventing stroke in young people,” Dr Sen said.

LONG-TERM SEIZURE RISK HIGHER WITH STROKE VERSUS TRAUMATIC BRAIN INJURY Research suggests that a large portion of stroke patients develop seizures and that the long-term risk for seizure after stroke is higher than after traumatic brain injury (TBI). “As compared to TBI, a disease well known to predispose patients to having seizures, patients with stroke were significantly more likely to develop seizures,” said Alexander E. Merkler, MD, study investigator from the Weill Cornell Medical Center, New York. “This result was surprising to us as TBI has for such a long time been used [as] a disease model to study seizures.”

Dr Merkler and colleagues aimed to better understand the long-term risk for seizures after stroke, postulating that it would be similar to the rate observed in patients with TBI. “Patients with stroke often ask about what type of problems they may expect in the future. As neurologists, we often warn our patients about the risk for recurrent stroke, infections, clots, eating difficulty, and depression,” Dr Merkler said. “Although seizures are a known complication of stroke, there were little data regarding the actual percentage of patients with stroke who develop seizures. Therefore, we sought to evaluate the long-term risk of seizures following stroke to better advise physicians and patients on the likelihood of developing seizures after suffering a stroke.” The researchers used administrative claims data on all acute care hospitalizations and emergency department (ED) visits at nonfederal facilities in California, Florida, and New York between 2005 and 2012. They determined the patients who experienced a first documented stroke and compared them with a control group of patients who had a first documented TBI. Stroke types included ischemic stroke, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). An ED visit or hospitalization with a discharge diagnosis of seizure served as the primary outcome measure. The study population included 568,659 patients with stroke and 270,796 patients with TBI. During follow-up (2.5 ± 2.1 years), patients with stroke had a cumulative risk for seizure of 37.6%, compared with 29.9% in patients with TBI. This resulted in a higher hazard ratio for seizure in the stroke group after adjustment for demographic characteristics and comorbidities (hazard ratio=1.12). A sensitivity analysis, which limited the outcome to primary discharge diagnoses of seizure or diagnoses of status epilepticus, yielded similar findings. In other data, the cumulative rates of any seizure were reported in the following subgroups: after SAH, 26.2%; after ischemic stroke, 33.6%; and after ICH, 35%. “Patients who suffer from a stroke have a significant risk of developing seizures. In particular, patients with hemorrhagic stroke have a significant chance of developing seizures,” Dr Merkler concluded. “The rate of seizures after stroke is higher than the rate of seizures after TBI.” Dr Merkler noted that patients and clinicians should be aware of the high long-term risk of seizures after stroke. n These articles originally appeared on NeurologyAdvisor.com

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Stat Consult

A quick review of common conditions, using the best global evidence

Background

Acute sinusitis in children and adolescents BY ALAN DRABKIN, MD

Dr. Drabkin is a senior clinical writer for DynaMed (www.ebscohost. com/dynamed), a database of comprehensive updated summaries covering more than 3,200 clinical topics, and assistant clinical professor of population medicine at Harvard Medical School.

• Acute rhinosinusitis is inf lammation of mucosal lining of nasal passage and paranasal sinuses <4 weeks in duration • causes ——viruses identified in <10% of childhood sinus infections ——acute bacterial sinusitis is rhinosinusitis complicated by bacterial infection, such as ■■ Streptococcus pneumoniae ■■ Nontypeable Haemophilus influenzae ■■ Moraxella catarrhalis ——uncommon bacterial agents in acute sinusitis include ■■ Staphylococcus aureus (unless orbital or intracranial complication) ■■ respiratory anaerobes (unless dental infections) ——fungal sinusitis (such as Aspergillus species) if immunocompromised or diabetic • common, possibly affecting 6% to 7% of children attending medical care for respiratory symptoms • risk factors ——exposure to tobacco smoke or other irritants ——underlying conditions such as ■■ anatomic abnormalities of nasal passages and sinuses ■■ immunodeficiencies ■■ cystic fibrosis ■■ primary ciliary dyskinesia • pathogenesis ——usually follows URIs or allergic rhinitis ——mucosal edema, decreased mucus transport, and obstruction of ostiomeatal complex lead to stagnation of secretions ——stagnation of secretions, decreased pH, and lowered oxygen tension within sinus promotes bacterial or viral overgrowth ——age of pneumatization of paranasal sinuses based on MRI in 1,452 children with no history of sinus disease ■■ at birth for maxillary and ethmoid sinuses ■■ age 9 months for sphenoid sinus ■■ age ≥5 years for frontal sinus

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Stat Consult Evaluation

• ISDA criteria for diagnosis of acute sinusitis includes presence of at least 2 major or 1 major plus ≥2 minor symptoms. ——Major symptoms include ■■ nasal congestion or obstruction ■■ facial congestion or fullness ■■ facial pain or pressure (may be unilateral, above or below eyes on leaning forward) ■■ purulent anterior nasal discharge ■■ purulent or discolored posterior nasal discharge ■■ hyposmia or anosmia ■■ fever ——Minor symptoms include ■■ Headache ■■ ear pain, pressure, or fullness ■■ halitosis ■■ dental pain ■■ cough ■■ fatigue • percussion of sinuses may elicit tenderness but not useful to distinguish causes of rhinosinusitis • signs favoring acute bacterial sinusitis include ■■ signs or symptoms lasting ≥10 days without clinical improvement ■■ worsening signs or symptoms following initial improvement (“double sickening”) ■■ severe symptoms including fever ≥39 degrees C (102 degrees F) and purulent nasal discharge lasting ≥3 consecutive days • symptoms suggestive of noninfectious rhinitis include ■■ pruritis of eyes, nose, mouth, palate, ears ■■ watery rhinorrhea ■■ sneezing ■■ nasal congestion ■■ postnasal drip • differential diagnosis ——viral URI (may be indicated by absence of either disturbed sleep or green nasal discharge) ——allergic rhinitis ——migraine ——nasal foreign body ——dental disease • testing ——blood tests and imaging studies are not indicated to ■■ confirm uncomplicated acute bacterial sinusitis ■■ distinguish bacterial from viral causes

——Contrast-enhanced CT preferred over MRI to identify suppurative complications (such as orbital or intracranial extension of infection) ——obtain cultures by direct sinus aspiration rather than by nasopharyngeal swab if no response to first- and second-line antibiotics Management

• options for initial management for uncomplicated acute bacterial sinusitis include either ——Initial antibiotic therapy ——3 additional days of observation if ■■ symptoms (nasal discharge and/or cough) for >10 days without improvement ■■ no co-existing illness ■■ follow-up for and begin antibiotics if symptoms worsen at any time or fail to improve within 3 days • Antibiotic therapy ——Indications ■■ severe symptoms ■■ worsening symptoms after initial improvement ■■ orbital or cranial complications ■■ i nfectious complications (co-existing acute otitis media, pneumonia, adenitis, or streptococcal pharyngitis) ——Choices ■■ amoxicillin »»45 mg/kg/day in 2 divided doses for uncomplicated cases »»80–90 mg/kg/day (maximum 2 g/dose) if > 10% local prevalence of resistant Streptococcus pneumoniae ■■ amoxicillin 80 to 90 mg/kg/day plus clavulanate 6.4 mg/kg/day in 2 divided doses for »»age < 2 years »»moderate-to-severe illness »»children attending day care »»antibiotic exposure within prior 4 weeks ■■ Options if penicillin-allergic »»cefdinir 14 mg/kg/day in 1–2 doses (maximum 600 mg/day) »»cefuroxime 15 mg/kg twice daily (maximum 500 mg/dose) »»cefpodoxime 5 mg/kg every 12 hours (maximum 200 mg/dose) »»cefixime 8 mg/kg/day orally in 2 divided doses plus clindamycin 30–40 mg/kg/day orally in 3 divided doses

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Stat Consult

•

• • •

twice daily » ceftriaxone 50 mg/kg intramuscularly or IV in single dose if unable to use oral medication (followed by oral antibiotic therapy upon clinical improvement) IV antibiotic options for severe illness requiring hospitalization ——ampicillin-sulbactam 200–400 mg/kg/day IV in 4 divided doses ——levofloxacin 10–20 mg/kg IV once daily or in 2 divided doses ——ceftriaxone 50 mg/kg/day IV in 2 divided doses ——cefotaxime 100–200 mg/kg/day IV in 4 divided doses If symptoms worsen or fail to improve within 72 hours, change therapy from ——observation to amoxicillin ——amoxicillin to high-dose amoxicillin-clavulanate ——high-dose amoxicillin-clavulanate to either ■■ levofloxacin or ■■ cefixime plus either clindamycin or linezolid ——optimal duration of antibiotic therapy may be either ■■ 10 to 14 days ■■ 7 days after resolution of symptoms Symptomatic treatment may be considered with ——intranasal corticosteroids (especially if allergic rhinitis) ——normal saline nasal irrigation treatments not recommended as adjunctive therapy include ——topical or oral decongestants ——antihistamines (may worsen congestion by drying nasal mucosa) no recommendations regarding mucolytics functional endoscopic sinus surgery (FESS) reserved for recurrent acute or chronic infective sinusitis refractory to medical treatment referral ——consider referral to otolaryngologist if acutely ill with toxic appearance (for consideration of maxillary sinus aspiration to guide antimicrobial therapy) ——refer to a specialist (such as otolaryngologist, infectious disease specialist, or allergist) if ■■ seriously ill and immunocompromised ■■ continued clinical deterioration despite extended courses of antimicrobial therapy ■■ recurrent bouts of acute rhinosinusitis with interval clearing

Prognosis

• most cases resolve without treatment • acute sinusitis symptoms may last up to 30 days in children treated with antibiotics, but majority resolve in <19 days Complications

• orbital inflammation and infection • intracranial complications ——most commonly found in males with frontal sinusitis ——may include ■■ venous sinus thrombosis ■■ bacterial meningitis ■■ brain abscess ■■ subdural or epidural empyema • osteomyelitis and/or Pott puffy tumor (osteomyelitis of frontal bone) Prevention

• practices reported to prevent recurrence or chronicity include ——completing full course of recommended treatment ——limiting exposure to crowded areas (such as day care) and environmental factors (such as cigarette smoke) ——daily saline washes to clear secretions and enhance mucociliary transport ——laparoscopic sinus surgery ——adenoidectomy ——treating underlying risk factors

“I’m between jobs right now, so if you kids would give these business cards to your parents that would be primo helpful.”

» levofloxacin 10 to 20 mg/kg orally once or

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ALTERNATIVE MEDS UPDATE

What you should know about the herbs and supplements patients use By Sherril Sego, FNP-C, DNP Ms. Sego is an independent consultant in Kansas City, Mo.

Bright light therapy

The sun has always held a prominent place in society. It has been worshipped as a god for its lifegiving rays, as well as by those who have desired deep bronze tans on the beach. More recently, sunshine has been recognized for its importance in helping the body manufacture vitamin D, and it has been studied for its potential impact on mood, specifically, on depression. Moderating the hours of sunlight (or the equivalent of brightness) may have an impact on sleep cycle, and those using bright light therapy (BLT) to improve sleep may find improvements in mood.

Background BLT, sometimes known as phototherapy or heliotherapy, is used in multiple ways and for a variety of conditions. Newborns with jaundice are routinely treated with light therapy, often referred to as a bili light,1 and BLT is used extensively in dermatology for conditions such as psoriasis and acne.2 Whereas these applications of BLT have been accepted practice for decades, the impact of BLT on mood disorders is less studied and not well-documented by appropriate clinical trials.

Science The mechanism of action of BLT is thought to be multifaceted. As light contacts the retina, a variety of actions are set in motion. Two key processes are the suppression of melatonin and the activation of serotonergic systems.3 The earliest use of BLT was for seasonal affective disorder (SAD). Commonly called holiday depression, SAD is linked

to the natural decrease in sunlight during the winter season.4 In a study by Reeves et al., participants diagnosed with SAD were randomly assigned to therapy with either low-intensity light (placebo) for 1 hour or BLT for 1 hour.4 Results showed significantly improved Beck Depression Inventory II (BDI II) scores in the BLT group compared with the placebo group. BLT has also been considered for nonseasonal depression. In one small study, researchers randomly assigned 15 patients with confirmed depression, impaired circadian rhythm, and poor sleep quality to either BLT alone or BLT in combination with fluoxetine.5 Both groups were treated with 30 minutes daily of 10,000 lux BLT, and one group also continued taking daily fluoxetine. At the end of 7 days, BDI II and Hamilton Depression Rating Scale (HAM-D) scores showed no statistically significant difference between the two groups. Although this may be an unimpressive result, it does confirm that BLT is at least as effective as fluoxetine for this condition.5 Another study, which used a combination approach to treat major depression, randomly assigned 50 patients to venlafaxine

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ALTERNATIVE MEDS UPDATE alone or venlafaxine plus BLT daily for 8 weeks.6 Both groups had significant improvement in symptoms; however, 76% of patients in the combination therapy group had achieved complete remission by the end of 8 weeks, compared with 64% of the venlafaxine-only group.6 Terao and Hirakawa published two case studies in which patients with bipolar disorder were treated with light deprivation when manic and BLT when depressed and found a shortening of both types of mood aberrancy with modulation toward a more central, stable mood.3 The effect of BLT on suicidality was studied in a 40-year retrospective examination in which researchers compared the number of hours per day of sunshine with the incidence of reported suicide in Austria.7 During that time, nearly 70,000 suicides occurred.8 Extraction of historic meteorologic data detailed the mean hours of sunshine during the previous 10 days and compared the information with each suicide event. The researchers found a highly significant inverse correlation.7 BLT is also being studied for its safety and efficacy in children, adolescents, and pregnant women.8 BLT has been found to be relatively safe and effective for these populations, but more study is needed.8

Summary

Bright light therapy may be safe and effective in children and adolescents.

Bright light therapy may be used for managing patients with depression, sleep disorders, and low mood.

Safety, interactions, side effects

During the winter months, long bouts of dull, dreary weather cause irritability and depressed mood in some people. Studies and empiric evidence have shown that mood is improved with exposure to sunlight, including reports of improvement of clinical depression with BLT. Although there are no clinical data to confirm the finding, it seems reasonable that BLT could improve work productivity and overall daily function. Healthcare providers should consider adding BLT to the treatment toolbox for managing depression, sleep disorders, and low mood. n References 1. University of Maryland Medical Center. Bili lights. http:// umm.edu/health/medical/ency/articles/bili-lights. Reviewed December 4, 2013. 2. Almutawa F, Alnomair N, Wang Y, et al. Systematic review of UV-based therapy for psoriasis. Am J Clin Dermatol. 2013;14(2):87-109. 3. Terao T, Hirakawa H. Light modulation therapy for bipolar disorder. Bipolar Disord. 2015;1(1):e104. 4. Reeves GM, Nijjar GV, Langenberg P, et al. Improvement in depression scores after 1 hour of light therapy treatment in patients with seasonal affective disorder. J Nerv Ment Dis. 2012;200(1):51-55. 5. Ag˘argün MY, Sayar GH, Bulut H, Tan O. Comparison of effects of bright light therapy alone or combined with

Interactions and side effects are minimal; however, persons with migraine or other light sensitivities should use caution until accustomed to therapy.

How supplied, dose, cost

fluoxetine on severity of depression, circadian rhythms, mood disturbance, and sleep quality, in patients with nonseasonal depression. ChronoPhysiol Ther. 2013;3:53-59. 6. Güzel Özdemir PG, Boysan M, Smolensky MH, et al. Comparison of venlafaxine alone versus venlafaxine plus bright light therapy combination for severe major depressive disorder. J Clin Psychiatry. 2015;76(5):e645-e654. 7. Vyssoki B, Kapusta ND, Praschak-Rieder N, et al. Direct effect of sunshine on suicide. JAMA Psychiatry. 2014;71(11):1231-1237. 8. Krysta K, Krzystanek M, Janas-Kozik M, Krupka-Matuszczyk I. Bright light therapy in the treatment of childhood and adolescence depression, antepartum depression, and eating disorders. J Neural Transm (Vienna). 2012;119(10):1167-1172. 9. Wright HR, Lack LC, Kennaway DJ. Differential effects of light wavelength in phase advancing the melatonin rhythm. J Pineal Res. 2004;36(2):140-144.

Light is measured in terms of wavelength, which indicates the color of light, and lux, which indicates intensity. Most light therapy uses wavelengths in the blue to green spectrum (460 nm-525 nm) with an intensity of up to 10,000 lux.9 BLT for mood and behavioral conditions is supplied by a light box. This device, which is often no larger than a book, sits on the desk or work surface at a slightly oblique angle to the eyes. These boxes may be purchased without a prescription for as little as $40. 106 THE CLINICAL ADVISOR • MARCH 2016 • www.ClinicalAdvisor.com

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COMMENTARY Margaret Ackerman, DNP, APRN, is an assistant professor at Salem State University in Salem, Mass.

Keep the care in care coordination Mrs. J lay in her bed, surrounded by men and women in white coats—a team approach to making decisions about her future, care, and treatment. Each of the white coats was a specialist in his or her own area of oncological practice. “The tumor has spread from your lung to your back,” said the lung specialist. “Once the tumor is in your bones, the chemo won’t help,” noted the bone specialist. “So radiation treatment is the next option,” the radiation oncologist commented. “But you can’t stay here,” said the case manager. “Of course, we know this is hard,” commented the social worker. “We will do everything we can,” said the primary oncologist.

In a patientcentric model of care, the effort focuses on the patient’s wishes.

Care coordination—the new buzzword. I recently heard Atul Gawande in a “TED talk” state that during the 1970s, a patient had the equivalent of 2 full-time staff care for him during a hospital stay. In 2012, that number had increased to 15 per patient, largely because of technology and specialty practice. Has all of this helped? In the U.S. healthcare system, outcomes are among the worst in the world, yet costs are among the highest. At the time I met Mrs. J, my job was to train new nurse practitioners (NPs) at the Commonwealth Care Alliance (CCA) Senior Care Options program in Boston. At CCA, the NP was the majordomo for patient concierge care for disenfranchised, vulnerable populations. The NP carried a small caseload and formed tight relationships with her patients, all fragile elders, who had an average of 7 chronic diseases and took an average of 18 medications a day prescribed by an average of 9 different providers. Lena was Mrs. J’s NP and had invited me to her first team conference, which was held in a hospital for the purpose of discharge planning. We stood, the 2 of us, in the corner and listened as each specialist addressed that component of Mrs. J’s illness with which he or she was directly involved. I watched her confused look as she gazed from one face to another and recognized her desire to please each of these specialists, all top-notch doctors. When they

began to discuss transferring Mrs. J to a skilled nursing facility with daily ambulance rides to the radiation suite, Lena interjected, “Mrs. J, tell us what you would like.” The room became strangely silent as everyone paused to reflect on her next words. “I want to go home,” said Mrs. J. Lena developed a discharge plan that included extensive hands-on care and pain management. The hospital care manager advocated for a nursing home, stating that home was not safe. But Lena knew differently. She arranged for Mrs. J to return home with a health aid 12 hours a day, a visiting nurse daily to administer pain medication, and with Lena visiting 3 to 4 times a week to check in on her and to support her daughter’s efforts in caring for her dying mother. Mrs. J died peacefully at home within months. It was what we call a “good death.” Mrs. J was comfortable at home with her cat and with her daughter who was active in her care. CCA spent far less on home care than it would have spent on hospitalization, and Lena learned the true meaning of patient-centric care and doing “all we can.” In a care coordination system, the effort focuses on systems and illness. In a patient-centric model, the effort focuses on the patient’s wishes. We are missing the big picture by buying into this overspecialized, technocratic system. n

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