Clinical Advisor May 2014 by The Clinical Advisor

THE CLINICAL ADVISOR • MAY 2014

A P E E R - R E V I E W E D F O RU M F O R N U R S E P R AC T I T I O N E R S

NEWSLINE

■ New BP goals ■ Lifestyle and vision ■ Imaging for headache ADVISOR FORUM

■ Antibiotics and warfarin ■ BMI as a vital sign ■ Handyman’s wart fix LEGAL ADVISOR

Opinions in chart notes bring on defamation charges.

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■ Dermatology Clinic

DEPIGMENTED SKIN ON ABDOMEN PAGE 75

■ Dermatologic Look-Alikes

VOLUME 17, NUMBER 5

BROWN SPOTS ON THE LIPS PAGE 79 Where do you rank in our Salary Survey? To find out the results, turn to page 50.

M AY 2 014

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EARLY DETECTION OF

MELANOMA Malignant melanoma may or may not be pigmented.

Editor Delicia Honen Yard, editor@ClinicalAdvisor.com Web editor Nicole Blazek Contributing editors Mark P. Brady, PA-C; Philip R. Cohen, MD; Deborah L. Cross, MPH, CRNP, ANP; Sharon Dudley-Brown, PhD, FNP; Abimbola Farinde, PharmD; Laura A. Foster, CRNP, FNP; Abby A. Jacobson, PA; Maria Kidner, DNP, FNP; Joan W. Kiely, MSN, CRNP; Debra August King, PhD, PA; Ann W. Latner, JD; Mary Newberry, CNM, MSN; Claire Babcock O’Connell, MPH, PA; Kathy Pereira, DNP, FNP; Sherril Sego, DNP, FNP; Julee B. Waldrop, DNP, PNP, FNP; Ann Walsh, PA-C, SCT(ASCP); Kim Zuber, PA-C Art director Andrew Bass Group art director, Haymarket Medical Jennifer Dvoretz Production director Kathleen Millea Grinder Circulation manager Paul Silver National accounts manager Alison McCauley, 646.638.6098 alison.mccauley @ haymarketmedical.com Publisher Thomas P. Hennessy, 646.638.6085 tom.hennessy @ haymarketmedia.com Editorial director Jeff Forster Senior vice president, digital products and medical magazines Jim Burke, RPh Senior vice president, clinical communications John Pal CEO, Haymarket Media, Inc. Lee Maniscalco All correspondence to: The Clinical Advisor 114 West 26th Street, 4th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints, contact Wright’s Reprints at 877.652.5295. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Clinical Challenge” are not the actual individuals mentioned in the articles.They appear for illustrative purposes only. The Clinical Advisor® (USPS 017-546, ISSN 1524-7317), Volume 17, Number 5, is published 12 times a year, monthly, for $75.00 per year in the United States; $85.00 in Canada; $110.00 for all other foreign, in U.S. dollars, by Haymarket Media, Inc., 114 West 26th Street, 4th Floor, New York, NY 10001. Single copy: $20 U.S.; $30 foreign. www.ClinicalAdvisor.com. To order or update your paid subscription, call 800.436.9269. Periodicals postage rate paid at New York, NY, and additional mailing offices. POSTMASTER: Send address change to DMD Data Inc. 10255 W. Higgins Rd, Suite 280, Rosemont, IL 60018. Call 800.430.5450 to change your address or make other subscription inquiries. Requests for subscriptions from outside the United States must be accompanied by payment. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2014.

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LEVEL

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LEVEL

CONTENTS M AY 2 0 1 4

NEWS AND COMMENT

59 CME/CE A child’s cough: common presentations and causes Clinicians who recognize various types of pediatric coughs will be better able to identify serious underlying conditions in the young patient.

20 Newsline ■■New guidelines change the BP picture ■■Self-esteem may help senior health ■■Lifestyle changes may preserve vision ■■Stress and springtime don’t mix ■■Antibiotics and C. difficile ■■Benefits seen with 7+ daily fruits, vegetables ■■Gout: securing the diagnosis with CT scans ■■Depression puts kidneys at risk in diabetes ■■Imaging studies overused for headaches ■■More MRSA tied to more skin abscesses

DEPARTMENTS C. difficile tied to office antibiotics 26

71 Legal Advisor A clinician’s opinions of a patient, noted in the patient’s chart, become grounds for charges of defamation. 75 CME/CE Dermatology Clinic n A child with a depigmented patch with overlying brown macules on the abdomen also has a white forelock.

87 Commentary

FEATURES

CT helps make the gout diagnosis. 29

32 Save a life with early detection of melanoma With May being Skin Cancer Awareness Month, the time is right to brush up on melanoma prevention and detection in primary care. 50 Special report: Salary Survey: How does your paycheck compare? The results of our fourth annual survey of nurse practitioner and physician assistant salaries are in. See how your income measures up.

MAKING CONTACT

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70 Derm Dx Read the clinical descriptions, view the images, and make your diagnosis at ClinicalAdvisor.com.

n An ICU patient with traumatic brain

injury develops clear, superficial vesicles from his neck to his abdomen and on his extremities. Continues on page 15

Recognizing different coughs in children 59

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CONTENTS CME/CE Dermatologic

Look-Alikes Two patients present with brown spots on the lips, oral cavity, and elsewhere.

CME/CE Posttest

Alternative Meds Update Activated charcoal may have medicinal uses beyond its role as a treatment for acute poisoning and overdose.

ADVISOR FORUM 66

Consultations ■ Interactions between antibiotics and warfarin ■ Does itching indicate healing? ■ Is petroleum jelly toxic? ■ BMI as a vital sign

Clinical Pearls ■ Written reminder of risky sex ■ Subtle signs of a failing heart ■ The handyman’s wart treatment

“I wanted to be there for you growing up, I really did. But I got a foot cramp. And then a thing came up at the store —anyway, you understand.”

HOW TO CONTACT US THE CLINIC AL ADVISO

TO CONTACT AN EDITOR: • Editor@ClinicalAdvisor.com • Call 646.638.6078

TO SUBMIT A CLINICAL QUESTION FOR PUBLICATION:

MAY 2 014

NEWSLIN

■ New BP goals ■ Lifestyle and vision ■ Imaging for headache ADVISOR

• www.ClinicalAdvisor.com/Advisor Forum • Send it by e-mail to letters@ClinicalAdvisor.com • Fax it to 646.638.6117 • Mail it to The Clinical Advisor, 114 W. 26th St., 4th Floor, New York, NY 10001 VOLUM E

FORUM

■ Antibiot ics and war farin ■ BMI as a vital sign ■ Handym an’s war t fix LEGAL ADV

ISOR

Opinions in char t notes bring on defamati on charges.

| www.Clin icalA

EARLY DE TECTION OF

dvisor.com

MEL ANOM A Malignan t melanom a may or may not be pigmente d.

✶ FREE CE COURS

ES!

■ Dermatolo gy Clini

DEPIGMEN c TED SKIN ON ABDOM EN

PAGE 75

■ Dermatolo gic

Look-Alik es BROWN SPO TS ON THE LIPS PAGE 79

17, NUMBE

Where do you rank in our Sala ry

TO SUBMIT AN ARTICLE: • Editor@ClinicalAdvisor.com • Fax it to 646.638.6117

R • MAY 2014

TO SUBSCRIBE: • www.ClinicalAdvisor.com/subscribe

Survey? To find out turn to pagethe results, 50.

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EXCLUSIVE TO THE WEB AT

ClinicalAdvisor.com Web Exclusives

Derm Dx

CliniAd.com/WyTpbB

Interact with your peers by viewing the images and offering your diagnosis and comments.

No link between labor induction and autism Current evidence does not support a correlation between labor induction and augmentation and the risk of autism spectrum disorders. Out-of-pocket expenses decline for diabetes patients High out-of-pocket costs are decreasing, with significant reductions for poor and near-poor patients. Households a major CA-MRSA reservoir Study provides evidence to support decontamination strategies for patients with MRSA.

Prior to vaccine, most oropharyngeal cancers HPV+ Most oropharyngeal cancers diagnosed in the United States between 1995 and 2005 tested positive for HPV.

CliniAd.com/1hvsVWo A necrotic mass on the back A 57-year-old patient presented with a large, oblong necrotic mass on the left posterior lateral region of his back.

The Waiting Room Official Blog of The Clinical Advisor CliniAd.com/VwgfCl Robyn Carlisle, MSN, CNM, WHNP Creating patient partnerships Follow-up visits can make working through a patient’s list of complaints more manageable. Jim Anderson, MPAS, PA-C, DFAAPA, ATC Understanding the military PA experience Physician assistants who are veterans of the military face unique challenges when integrating back into the civilian workplace.

Cartoon slideshow Cliniad.com/1n6rtNR

Videos CliniAd.com/1gfTZtj Can poor patient memory interfere with informed consent?

“We’d like to switch you from working under the radar to living off the grid.”

MAKING CONTACT

Is informed consent legally valid if the patient wakes up after a procedure and does not remember the risks described? Victor Cotton, MD, JD, responds.

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Newsline

Senior health improves with self-esteem page 22

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Stress may make spring allergies worse page 26

More MRSA tied to more skin abscesses page 31

IF THE EIGHTH Joint National Committee (JNC 8) guidelines ( JAMA. 2014;311[5]:507-520) were followed, many older Americans would be at their target blood pressure (BP). The recently released guidelines relax the BP goal from 140/90 mmHg to 150/90 mmHg in adults aged 60 years and older. They also ease BP goals for adults with diabetes or nondiabetes-related chronic kidney disease. Raising the target BP in older adults is controversial, concedes Ann Marie Navar-Boggan, MD, PhD, of Duke University School of Medicine in Durham, North Carolina, lead author of a new study in JAMA. She and her colleagues looked at data from more than 16,000 participants to gauge the effect of the revised guidelines. They estimated that 13.5 million adults aged 60 years and older would already be at their

New guidelines relax BP goals for older adults and others.

The percentage of adults with no natural teeth was higher in nonmetropolitan areas among all age groups.

Source: National Health Interview Survey, United States, 20102012 (MMWR . 2014 [Mar. 14]; 63[10]:225.)

BP goal, including approximately 5.8 million who would longer require antihypertensive medication, dropping the proportion of adults deemed eligible for treatment from 40.6% to 31.7%. “The new guidelines do not address whether these adults should still be considered as having hypertension,” Navar-Boggan noted in a statement accompanying the release of her team’s study. “But they would no longer need medication to lower their blood pressure.” Further research is needed to determine “the related effects on cardiovascular disease outcomes.” Another recent study on BP control focused on people who have suffered a stroke. Consistent BP control in these individuals may halve the likelihood of a second stroke. Amytis Towf ighi, MD, and fellow

investigators published their findings in the journal Stroke after examining results from the Vitamin Intervention for Stroke Prevention (VISP) trial, which involved more than 3,600 persons with ischemic stroke, aged 35 years and older. BP was measured at the start of the study, a month later, at six months, and then at six-month intervals thereafter for up to 24 months. Less than 30% of stroke survivors maintained consistent BP control more than 75% of the time. BP was considered “controlled” at 140/90 mmHg or lower. Individuals whose baseline BP reading was high (systolic above 153 mmHg), but who were able to keep their BP under control more than 75% of the time, had a second-stroke rate 54% lower than those who kept their BP under control less than 25% of the time.

Persons aged 18 and older who have no more natural teeth 50 Metropolitan Nonmetropolitan

40 Percentage

New guidelines change the BP picture

30 20 10 0

≥18

18-44

45-64 65-74 Age group (yrs)

75-84

≥85

20 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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Newsline HIGHER LEVELS of selfesteem may confer enhanced health benefits on older people. That is the conclusion of researchers at Concordia University in Montreal, Quebec, Canada, who published their study in the journal Psychoneuroendocrinology (2014;41:111-120). The study focused on 147 individuals aged 60 years and older who were followed for a period of four years. Every two years, they were evaluated for symptoms of depression and degree of self-esteem. Self-esteem was assessed by responses to questions such as whether a person felt worthless. Also measured were the participants’ levels of the stress hormone cortisol. Sarah Y. Liu and fellow investigators also took into account personal

and health factors—such as marital status, economic status, and mortality risk. The study team found that sustaining or improving selfesteem could help prevent health problems normally associated with aging. When self-esteem declined, cortisol levels rose, and vice versa. The correlation between self-esteem and cortisol levels was particularly striking in individuals who had a history of stress or depression. However, despite the discovery of an inverse association between seniors’ self-esteem and cortisol levels, the study did not confirm a cause-and-effect relationship. “Because self-esteem is associated with psychological wellbeing and physical health, raising self-esteem would be an ideal

Self-esteem may help senior health

Levels of cortisol rose when selfesteem fell.

way to help prevent health problems later in life,” explained Liu in a statement accompanying the release of the study findings. “Improving self-esteem provides real health benefits in seniors. The ultimate solution may be to prevent self-esteem from declining.”

THREE LIFESTYLE factors— physical activity, alcohol consumption, and smoking—are known to affect overall health. Now add vision to conditions impacted by these variables. By 2020, at least 4 million individuals are expected to suffer from visual impairment or sight loss that cannot be corrected with glasses or contact lenses. To help find strategies to reduce that number, investigators at the University of Wisconsin School of Medicine and Public Health in Madison looked at data on nearly 5,000 adults aged 43 to 84

Only 2% of active people had vision problems.

years. The goal was to identify links between vision loss and modifiable lifestyle factors. As Ronald Klein, MD, MPH, and fellow researchers reported in Ophthalmology, over the course of 20 years only 2% of physically active people developed visual impairment, compared with nearly 7% of their sedentary counterparts. After adjusting for age, this represented a 58% reduction in the risk of visual impairment. A similar benefit was observed among occasional drinkers (those consuming less than one serving

of alcohol weekly): Over 20 years, adjusting for age, a 49% decrease in the risk of visual impairment was noted among occasional drinkers compared with nondrinkers. Although the risks were higher in heavy drinkers and smokers compared with people who were not heavy drinkers or smokers, the associations were not found to be statistically significant. Age is a factor that cannot be changed, pointed out Klein. “Lifestyle behaviors like smoking, drinking, and physical activity, however, can be altered.”

Lifestyle changes may preserve vision

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Newsline

WHILE STRESS itself does not cause allergies, it may contribute to spring flares. That is the word from researchers from The Ohio State University in Columbus, who noted that stress may produce various negative effects throughout the body—including additional symptoms for allergy sufferers. This situation may trigger a vicious cycle, observed Amber M. Patterson, MD, lead author of the Annals of Allergy, Asthma & Immunology study (2014;112[4]:317321), in a statement describing the team’s findings. People who suffer from more frequent allergy flares also may have a greater negative mood which, in turn, may lead to even more flares. The Ohio group followed 179 patients over a period of 12 weeks, during which 39% of participants reported more than one allergy flare. The investigators then compared the average stress level within this subset with that of the remaining sample. The participants who reported having more than one flare were found to have significantly higher stress levels than did those who reported only one or no flares. Nearly two-thirds of the persons with more than one flare reported more than four flares over two separate 14-day periods. “While alleviating stress won’t cure allergies,” commented Patterson, “it may help decrease episodes of intense symptoms.”

Antibiotics and C. difficile ACCORDING to a new study from the Centers for Disease Control and Prevention (CDC), most cases of Clostridium difficile, the bacterial infection that causes severe and even life-threatening diarrhea in children, can be traced to antibiotics prescribed in clinicians’ offices for other conditions. Preliminary information from the CDC indicates that approximately 17,000 children aged 1 to 17 years contract C. difficile each year. Authored by Joyanna M. Wendt, MD, MPH, and colleagues and published in the journal Pediatrics (2014;133[4]:651-658), the CDC study found that 71% of C. difficile infection in children aged 1 to 17 years was community-associated rather than connected with an overnight hospital stay. That differs markedly from the situation in the nonpediatric population: Two-thirds of C. difficile infections in adults are linked with hospital stays. The infection, which has hit an all-time high

Infection in most youths was communityassociated.

level, is responsible for 14,000 deaths every year in children and adults (www.cdc.gov/media/ releases/2014/p0307-severediarrheal-illness.html). Ear, sinus, or upper respiratory infections represented the most common indications for antibiotic prescriptions in children. This finding echoes those of previous studies showing that at least 50% of antibiotics prescribed in the pediatric setting are for respiratory infections, despite the fact that the majority of these infections do not warrant the use of antibiotics. This state of affairs has prompted CDC Director Tom Frieden, MD, MPH, to issue the following statement: “Improved antibiotic prescribing is critical to protect the health of our nation’s children. When antibiotics are prescribed incorrectly, our children are needlessly put at risk for health problems including C. difficile infection and dangerous antibiotic-resistant infections.”

Benefits seen with 7+ daily fruits, vegetables FIVE A DAY may once have been the recommendation, but a new study suggests more is better. To hold off death from any cause—including cancer and cardiovascular disease—people should eat seven or more portions of fruits and vegetables a day. A team of investigators from University College London (London, United Kingdom) reviewed lifestyle information on more than 65,000 adults aged 35 years and older. They found that individuals who ate seven or

more servings of fruits and vegetables per day had a 42% reduced risk of death overall, compared with those who consumed just one portion. The seven-servings-or-more regimen reduced the risk of death from cancer by 25% and from cardiovascular disease by 31%, reported Oyinlola Oyebode and coauthors in Journal of Epidemiology and Community Health. The strongest protective effect came from fresh vegetables, closely followed by salad and then fruit.

Stress and springtime don’t mix

26 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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Newsline THE INCIDENCE of gout, the most common (and painful) form of inflammatory arthritis, is increasing in the United States. The problem is that diagnosis is not always straightforward. The standard approach is needle aspiration to remove fluid from the inflamed joint and to then search for uric acid crystals. But sometimes those aspirates yield false-negative results. Now a study suggests that dual-energy computed tomography (CT) scans may be the answer. The study, performed by researchers from the Mayo Clinic in Rochester, Minnesota, appears in Annals of the Rheumatic Diseases. Using the scanning technique, the Mayo team discovered gout in one-third of patients whose aspirates had been negative. The

CT scans proved especially useful in people who had experienced a number of gout-like episodes but had not been correctly diagnosed. Some had been given diagnoses such as rheumatoid arthritis or unexplained chronic elbow or Achilles tendinitis— misdiagnoses that often resulted in ineffective treatment. Once CT scanning detected the presence of uric acid crystals, ultrasound-guided needle aspiration was performed. These findings should not imply that CT scans be used as the initial diagnostic test, emphasizes Tim Bongartz, MD, lead author of the study. In the majority of cases, needle aspiration is fine and even superior to CT scans in diagnosing patients with their first episode of gout.

Gout: securing the diagnosis with CT scans

CT scans can help make the diagnosis in some gout cases.

“What we are learning from the dual-energy CT scans has really changed our perception of where gout can occur and how it can manifest,” said Bongartz in a statement announcing the study results. “The ability to visualize those deposits clearly broadens our perspective on gout.”

PEOPLE WITH diabetes who suffer from major depression have a nearly twofold risk of developing kidney failure. This finding comes from a University of Washington (Seattle) study reported in the Clinical Journal of the American Society of Nephrology. The Washington team, which was led by Margaret Yu, MD, MS, and Bessie Young, MD, MPH, looked at nearly 4,000 adults with diabetes. Of this group, 448 (11.5%) persons reported major depressive symptoms and 327 (8.4%) reported minor ones. After adjusting the data for numerous

Depression in diabetes was linked to kidney failure.

factors—including age, sex, ethnicity, smoking, body mass index, hypertension, and diabetes compliance—the investigators found that persons with major depressive symptoms had an 85% higher risk of developing kidney failure than did those without such symptoms. Minor depressive symptoms carried no significantly increased risk. Another study involving diabetes evaluated antihypertension treatment in persons with diabetes. The American Diabetes Association recommends either angiotensin-converting enzyme

inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) for people afflicted with both diabetes and hypertension. The study, conducted by Jun Cheng, MD, and fellow investigators and published in JAMA Internal Medicine, analyzed data from 35 clinical trials and indicated that ACEIs reduce the risk of cardiovascular deaths in people with diabetes by 17%, reduce the risk of major cardiovascular events by 14%, and reduce the risk of allcause mortality by 13%. ARBs were found to have no such effect on those outcomes.

Depression puts kidneys at risk in diabetes

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Newsline MOST HEADACHES have harmless causes, but that has not curbed utilization of neuroimaging in outpatients with that complaint. And imaging for headache is increasing—nearly trebling from just over 5% in 1995 to nearly 15% in 2010—despite multiple guidelines opposing this practice. To assess the trend, Brian C. Callaghan, MD, MS, and colleagues from the University of Michigan Health System in Ann Arbor analyzed data from the National Ambulatory Medical Care Survey. They looked at all

Patient demand may be driving imaging for headaches.

headache visits for patients aged 18 years and older from 2007 through 2010, identifying more than 51 million visits for headache including 25.4 million for migraine. Neuroimaging was performed in 12.4% of all headache visits and in 9.8% of migraine visits. The Michigan team, whose findings appear in JAMA Internal Medicine, noted that the unwarranted imaging may be driven more by patient demand rather than provider practices. Another study on headache, this one done by Dawn C. Buse,

PhD, and associates and published in Neurology, offers new insights into migraine and stress. Although stress is often considered a trigger of migraine, many migraine sufferers find the release of stress to be an even greater trigger. In the first six hours of reduced stress, the risk of migraine increases by nearly five times. The explanation may lie with the hormone cortisol, which rises during stress and reduces pain. As cortisol levels drop during relaxation, the protective effect disappears and leads to a migraine.

Imaging studies overused for headaches

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SKIN A BSCESSES are on the rise, a development that is matched closely by the emergence of community-associated methicillin-resistant Staphylococcus aureus (MRSA). MRSA infections now represent the single most common cause of skin abscesses in the United States, prompting new treatment guidelines. When MRSA first appeared, cases were comparatively mild and limited mainly to high-risk patients in hospitals and longterm-care facilities. But over the last decade, a more virulent

strain of community-acquired MRSA has evolved that is more widespread, contagious, and difficult to treat. In extreme cases, MRSA can lead to severe infection—including sepsis, fasciitis, and necrotizing pneumonia. In a report in The New England Journal of Medicine (2014;370:10391047), clinicians offer updated “best practice” guidelines for managing MRSA-related skins abscesses. These concentrate on abscesses on the trunk and extremities, areas that clinicians in general practice routinely treat.

MRSA is now the top cause of skin abscesses.

Ultrasound can be used to enhance diagnostic accuracy for deeper abscesses and can ensure complete drainage. Preferred antibiotics for community-acquired MRSA include trimethoprimsulfamethoxazole (Bactrim, Septra, Sulfatrim), doxycycline, minocycline, and clindamycin (Cleocin). Antibiotic therapy is essential for patients with risk factors such as immunosuppression, recurrent infection, and extensive or rapidly progressive disease, as well as for the very young and the very old. n

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More MRSA tied to more skin abscesses

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FEATURE: ABBY A. JACOBSON, MS, PA-C

Save a life with early detection of melanoma With May being Skin Cancer Awareness Month, the time is right to brush up on melanoma prevention and detection in primary care.

U.S. incidence of malignant melanoma (shown) is on the rise.

ne of every 57 Americans will be afflicted with melanoma (or one in 33, if noninvasive melanoma in situ is included), with one person per hour dying of the disease.1 Melanoma in men is increasing more rapidly than any other malignancy, and in women it is the second most rapidly increasing malignancy, after lung cancer. 2 Even these estimates may be low because melanomas treated in the private outpatient setting are often not reported.3 Melanoma incidence has increased significantly over the past several decades. Predictions forecast a doubling of melanoma rates every 10 to 20 years, making melanoma the most rapidly increasing cancer in white populations.4 So, who needs to be screened? The answer is: everyone. It is widely believed that the total risk factor for melanoma is determined by the interplay between genetic factors and environmental factors, such as exposure to ultraviolet (UV) light.4 Studies suggest that a sunburn during childhood may be a more important risk factor for melanoma than is sunburn as an adult.5 This is an important point for family practice, pediatrics, and obstetrics/gynecology clinicians, who can educate parents on the dangers that sunburns during youth can pose to long-term health. Pigmentation and skin reaction to sun also are risk factors for melanoma.6 In addition, the World Health Organization’s International Agency for Research on Cancer categorized tanning beds as a human carcinogen.4 Continues on page 41

32 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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MELANOMA DETECTION

Melanoma risk factors

The following factors put a person at particularly high risk for melanoma and merit more frequent skin examinations by the provider and by the patients themselves, consideration for referral to a dermatologist for skin surveillance, and direct patient education using smart sun-protection methods: • family history of melanoma, especially for patients who have a first-degree relative with melanoma • lightly pigmented skin • tendency to burn/inability to tan • intense intermittent sun exposure, regardless of whether sunburns are incurred during that exposure • chronic sun exposure • tanning-bed use, especially before age 35 years • immunosuppression • multiple moles (more than 60) • atypical or dysplastic nevi • presence of lentigos (a sign of prior overexposure to UV light) • history of melanoma • history of nonmelanoma skin cancer, such as basal cell or squamous cell skin cancer.7 The skin examination

As a general rule, patients should undergo a baseline skin examination with a dermatology provider, and then ask that provider how frequently future screening should be done as determined by the patient’s skin type, family history, lifestyle, and findings during that initial examination. Yearly is a conservative schedule for someone who is fair, has a family history of skin cancer, or has a history of actinic damage. Someone lacking any risk factors could need a clinical examination as infrequently as once every three years. When conducting a skin examination, providers should look for much the same signs they should advise patients to note when performing a skin self-examination. Clinicians can cover the patient-education piece while performing the clinical skin examination. Showing the patient an example of a finding or nonfinding on the patient’s own skin will further drive home the information. The ABCDEs of skin cancer screening are as follows: Asymmetry. An asymmetric lesion raises the index of concern. Does an imaginary line drawn down the center of the lesion create a mirror image of the two sides? If not, then the lesion is asymmetric. Border. A scalloped, irregular, paisley-like, or vague border should raise the index of concern.

Color. The lesion should be the same color throughout. The clinician should not see different shades of brown and certainly no black, red, or blue. Diameter. As a general rule, melanomas usually are larger than 6 mm. (Explain to patients that 6 mm is approximately the size of the eraser end of a Number 2 pencil.) In reality, many melanomas are much smaller than 6 mm, particularly when the lesion is detected early in its development. Evolution. At one time, the ABCD mnemonic had no “E.” But a new or changing lesion should raise an immediate concern for a skin cancer risk. Change (or evolution) in size, shape, elevation, or color of a mole should be evaluated immediately. Early detection of melanoma also can be aided by both the practitioner’s and the patient’s attention to the so-called ugly duckling syndrome: One lesion that clearly stands out from the rest raises the index of concern. For example, one particular lesion on the skin may be much darker or bigger than the rest. During a first glance at a particular part of the body, one lesion may instantly jump out at the clinician as being atypical. One dermatologist reports a practice in which he routinely quickly glances at a patient’s skin before turning away, then asks himself whether there was a spot that stood out during that brief initial look. A skin lesion that is clearly an outlier is significant cause for concern. Start the clinical examination by evaluating any lesion that is specifically mentioned by the patient, so that the patient’s concern does not get lost in the end-of-appointment rush. The clinician should then perform a full skin examination, following his or her own pattern or sequence of body areas to examine. This pattern should become habit so that the provider never misses an area of the patient’s body, from the scalp to down between the toes and the bottom of the feet. Many dermatology providers, including this author, use a dermatoscope to aid the skin examination. These instruments light up and magnify pigmented lesions and help illuminate benign lesions such as seborrheic keratosis and hemangioma. Lesions of concern

If a lesion of concern is discovered, it should be measured and documented. Photographing it can also help both the practitioner and the patient monitor the lesion for growth or other changes. Electronic medical records may provide a relatively easy location for storing such images. Providers who feel that biopsy is in order should use a lab that has a dermatopathologist rather than a general pathologist available to read the slide. Pigmented lesions and skin biopsies

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MELANOMA DETECTION

in general are difficult specimens to evaluate histologically. If the index of concern for a melanoma is high, a punch or excisional biopsy is ideal for measuring depth and allowing for evaluation of the entire lesion. If the lesion is too large to biopsy in that fashion, then a wide, deep, “scoop biopsy,” also known as a tangential biopsy or a saucerization, should be done for the entire lesion. A biopsy performed on only one small portion of a large lesion may not be representative of the entire histology or future of the lesion. Melanoma types and staging

The various types of melanomas include superficial spreading malignant melanoma, lentigo maligna melanoma, nodular malignant melanoma, acral lentiginous melanoma, ocular melanoma, and malignant melanoma on mucous membranes. Superficial spreading melanoma is the most common in ethnically white individuals, occurring most frequently on the trunk in men and on the legs in women. Superficial spreading melanomas follow the most typical pattern of failing the ABCDE guidelines. Nodular melanoma is the second most common type of melanoma. These lesions are found in white patients, most commonly those in their sixth decade of life. Nodular melanomas are thick and have the potential to progress and metastasize rapidly. These lesions can be nonpigmented (amelanotic). This fact highlights the point that any fast-growing new lesion, even one without pigment, should be evaluated and at least monitored, if not biopsied. Ulceration and bleeding of the amelanotic lesions can be clues to the diagnosis.1 Lentigo maligna melanoma tends to occur on chronically sun-exposed skin such as the head, neck, and arms. Acral lentiginous melanoma appears on the palms, soles, and nail beds, and is more commonly seen among non-white persons than among whites. This is also true for melanoma under the nail bed, a rare disease that appears as brown or black linear pigmentation. Involvement of the proximal nail fold or nail bed, called the Hutchinson sign, is a hallmark for subungual melanoma. Various rare melanoma subtypes exist and include melanomas that develop in the eye or other internal locations. A pathology report will include different measurements in the staging of a melanoma. The stage determines the treatment and is a prognostic factor. A good pathology report on a melanoma should provide at least the following information: diagnosis, tumor site, histologic subtype, Clark level, growth phase, greatest thickness, presence of ulceration or regression, mitotic rate, presence of blood

POLL POSITION

What proportion of your patients do you routinely screen for skin cancer? n=156 6% 12%

n Less than 10% n 10%–25% n 25%–50% n 50%–75% n More than 75%

26% 13%

32% 37%

74%

For more polls, visit CliniAd.com/152aAbQ.

vessel/lymphatic invasion, margins, and presence of any microscopic satellite lesions, plus a description of what was seen under the microscope. Mitotic rate is the measure of tumor proliferation, expressed in millimeters squared. The Clark level refers to the area of invasion within the skin and correlates with Breslow depth, which measures the depth of invasion in millimeters. Clark level 1 involves only intraepidermal invasion of the epidermis, level 2 shows tumor in the papillary dermis, level 3 shows the tumor filling the papillary dermis, level 4 shows the tumor in the reticular dermis, and level 5 shows the tumor entering the fat of the subcutaneous tissue. As with many malignancies, early diagnosis directly corresponds with chances of survival. The staging of melanoma is as follows: localized disease (stages I-II), regional disease (stage III), and distant metastasis (stage IV). In stage I, the three most important factors for predicting outcome are Breslow depth, mitotic factor, and ulceration. For patients with localized metastasis (stage III), the sentinel lymph node biopsy is the key prognostic factor. For patients with distant metastasis, the location of the metastasis is the most important prognostic factor. The presence of ulceration or regression overall usually indicates a poor prognosis. Patient self-examination and education

Patients should be instructed to examine their own skin on a monthly basis, enlisting the help of a partner or loved one if possible. Inform the patient that the skin examination should be performed while the patient is nude and in a well-lit area. A second mirror can help the person examine hard-to-see

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MELANOMA DETECTION

CLINICAL SLIDESHOW For more information on melanoma and its various presentations, please view the slideshow at CliniAd.com/1iAlHSJ.

be cognizant of the warning signs of melanoma. Primarycare clinicians who do not feel comfortable conducting skin examinations should recommend that the patient make an appointment with a dermatology provider for such a check. n Ms. Jacobson is a physician assistant practicing in dermatology at Delaware Valley Dermatology Group in Wilmington, Del. References 1. Swetter SM. Cutaneous melanoma. Medscape. October 8, 2012. Available at emedicine.medscape.com/article/1100753-overview#a0199. 2. Daniel CG, Thompson JA, Andtbacka R, et al. Melanoma, Version 2.2014. National Cancer Care Network Clinical Practice Guidelines in Oncology. NCCN.org. 3. Cockburn M, Swetter SM, Peng D, et al. Melanoma underreporting: why does it happen, how big is the problem, and how do we fix it? J Am Acad Dermatol. 2008;59(6):1081-1085. 4. Miller AJ, Mihm MC Jr. Melanoma. N Engl J Med. 2006;355:51-65. 5. Elwood JM, Jopson J. Melanoma and sun exposure: an overview of published studies. Int J Cancer. 1997;73(2):198-203. Available at onlinelibrary.wiley. com/doi/10.1002/%28SICI%291097-0215%2819971009%2973:2%3C198::A ID-IJC6%3E3.0.CO;2-R/abstract 6. Elwood JM, Gallagher RP, Hill GB, et al. Pigmentation and skin reaction to sun as risk factors for cutaneous melanoma: Western Canada Melanoma Study. Br Med J (Clin Res Ed). 1984;288(6411):99-102. Available at www.bmj.com/content/288/6411/99.pdf%2Bhtml. 7. Cust AE, Armstrong BK, Goumas C, et al. Sunbed use during adolescence and early adulthood is associated with increased risk of early-onset melanoma. Int J Cancer. 2011;128(10):2425-2435. Available at onlinelibrary.wiley.com/ doi/10.1002/ijc.25576/pdf. All electronic documents accessed April 15, 2014..

Conclusion

Melanoma is the deadliest skin cancer, but early diagnosis yields the best chance for long-term survival. It is incumbent upon the medical community to know the risk factors for this disease, to screen all patients on a routine basis, and to teach patients how to perform skin self-examinations and to 48 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

“Forget it. We’re not stopping again.”

areas such as the back, underarms, back of legs, genitalia, buttocks, and bottom of the feet. Remind patients that skin cancers can develop anywhere, not just on areas exposed to sunlight, so they need to check every inch of their skin. Providing information on safe sun exposure goes handin-hand with instructing patients on how to perform a skin self-examination. Encourage patients to enjoy their lives, to be healthy, and to get outdoor exercise, but to do so in a way that does not increase their skin cancer risk. Patients—and providers, for that matter—should use sunscreen with a skin protection factor (SPF) of 30 or higher. The sunscreen should be applied liberally and reapplied at least every two hours. Nevertheless, patients should seek shade whenever possible. Remind them that they are still exposed to UV radiation even when they are in a shaded area or when the weather is slightly overcast. Special attention needs to be devoted to shielding one’s skin with sunscreen as well as with hats and other sun-protective clothing when the person is near water, sand, or snow, as all these elements reflect light back up onto the person. Tell patients that if they are able to read a book outside, then ultraviolet light is touching them. Let patients know that vitamin D may be more safely obtained by means of a healthy diet and, if the clinician deems necessary, supplementation, rather than from sunlight exposure. Be sure they also understand that the concept of slowly getting more sun (or tanning-bed use) as a means of gearing up safely for a vacation in the sun is no more than a dangerous myth, as is the idea that tanning is acceptable as long as one does so only for special occasions.

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 • MAY 2014 49

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SPECIAL REPORT: DELICIA HONEN YARD

SALARYSURVEY How does your paycheck compare?

Let’s get right to the bottom line…or at least the first of several. Based on the data that respondents to The Clinical Advisor 2014 salary survey so generously provided in March and April 2014: • The average salary among all nurse practitioners (NPs) earning between $20,001 and $149,999 per year is $94,881.22. • The average salary among all physician assistants (PAs) earning between $20,001and $149,999 per year is $100,497.78.

Why did we frame the results this way? In order to create an industry snapshot, we asked our readers to indicate their current annual salaries, including base pay plus any bonuses, in increments of $5,000 (inclusive). In other words, a person making $72,500 would fall into the “$71,000-$75,000” category. Salaries for all respondents in that group were then converted to the midpoint of $73,000. A person checking off the “$36,000 to $40,000” box was considered to make $38,000 per year, and so forth. At the lowest and highest salary ranges, however, we offered two much broader choices: “$20,000 or less” and “$150,000 or more” (with approximately 3% of NPs and approximately 9% of PAs falling into the latter category). Because we could not assign an accurate average value to either of those response ranges, and because the vast majority of our participants—approximately 90% of each group—brings home an annual salary of $20,001 to $149,999 per year, we often isolated responses from participants who fell into the very high and very low categories, as you will see when you read through our report. A total of 3,635 NPs and 1,232 PAs—as well as some selfidentified “others” in each category—responded to our survey, but not every participant answered every question. We have indicated total number of respondents for each area addressed below.

Salary related to practice area

After removing 153 NPs making $150,000 or more, or $20,000 or less, from our analysis of salary related to practice area (in total, less than 0.04% of 3,850 total respondents), and after eliminating replies from persons who listed anything other than “nurse practitioner” as their profession or who listed no salary, we were left with 3,502 responses for this category. Table 1 reflects the average annual salaries in the practice areas with the highest response rates to our survey. By far, the most NP respondents identified themselves as family medicine practitioners (24.0%). A steep drop leads to the next largest TABLE 1. Average NP salary by practice area*

TABLE 2. Average PA salary by practice area*

Practice area

Response percent

Average salary

Practice area

Response percent

Average salary

Family Medicine

24.0% (n=842)

$91,699

Family Medicine

18.5% (n=212)

$93,872

Pediatrics

6.3% (n=221)

$88,022

Emergency Medicine

7.8% (n=89)

$113,393

Adult Medicine

5.7% (n=200)

$93,750

Orthopedic Surgery

6.5% (n=74)

$108,878

Psychiatry

4.7% (n=165)

$102,242

Urgent care

4.6% (n=52)

$103,865

Oncology/Hematology

4.5% (n=158)

$100,626

Cardiology

3.1% (n=35)

$102,000

*Based on responses from 3,502 NPs who earn $20,001-$149,999 per year.

*Based on responses from 1,127 PAs who earn $20,001-$149,999 per year.

50 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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group of NP respondents, at 6.3%—those working in pediatrics (not including pediatric surgery), followed by providers of adult medicine, psychiatry, and oncology/hematology services. We compiled the same information for the PAs (Table 2), beginning with 1,271 responses and then eliminating the five participants who make $20,000 or less and the 104 who make $150,000 or more; those 109 respondents constituted 8.6% of the total. (Incidentally, about 40% of PAs earning at least $150,000 per year are working in dermatology or emergency medicine.) We also omitted respondents who listed anything other than PA as their profession or who listed no salary, leaving a sample of 1,127 PA respondents for this analysis. As was the case for NP respondents, family medicine yielded the highest percentage of PA respondents, but the similarities in practice areas harboring high concentrations of survey participants ended there. Salary by experience level

Among our survey respondents, salaries for NPs (Table 3) and PAs (Table 4) varied by only about $10,000 between those with fewer than five years of experience and those with more than 20 years. Although we did not include in our results salaries of $20,000 or lower or $150,000 or higher, an interesting finding from the PA camp was that among those who do make at least $150,000 per year, 35 have been practicing for 11 to 15 years and 34 have been practicing more than 20 years. By comparison with other PAs, the 16-to-20-year category included 10 of these top earners, and the less-than-five-year group boasts eight people making $150,000 or more per year. TABLE 3. Average NP salary by experience level

TABLE 4. Average PA salary by experience level

Years of experience

Response percent

Average salary

Years of experience

Response percent

Average salary

34.3% (n=1,187)

$90,009

28.4% (n=316)

$94,582

6-10

20.5% (n=711)

$96,186

6-10

23.0% (n=256)

$97,570

11-15

17.3% (n=599)

$98,718

11-15

18.7% (n=208)

$106,125

16-20

13.8% (n=479)

$99,138

16-20

9.9% (n=110)

$103,409

>20

14.0% (n=486)

$96,488

>20

20.1% (n=224)

$105,649

*Based on responses from 3,462 NPs who earn $20,001–$14w9,999 per year. Percentages do not add up to 100% due to rounding.

*Based on responses from 1,114 PAs who earn $20,001–$149,999 per year. Percentages do not add up to 100% due to rounding.

Average salary by geographic region

Most of this year’s survey respondents hail from the South, as Figure 1 and Figure 2 illustrate, but the highest salaries for both NPs and PAs can be found in the West. Nevertheless, the variation in salary among PAs across geographic regions is minimal. FIGURE 1. Average NP salary by geographic region*

FIGURE 2. Average PA salary by geographic region*

West

Midwest

Northeast

West

Midwest

Northeast

15.3% response (n=536) $100,715 average salary

24.4% response (n=853) $91,400 average salary

21.3% response (n=744) $95,937 average salary

20.0% response (n=224) $101,883 average salary

22.0% response (n=246) $100,073 average salary

24.0% response (n=270) $99,389 average salary

South 39.0% response (n=1,362) $91,361 average salary *Based on responses from 3,495 NPs who earn $20,001–$149,999 per year.

South 34.0% response (n=383) $100,963 average salary *Based on responses from 1,123 PAs who earn $20,001–$149,999 per year.

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SALARY SURVEY 2014

Salary by practice setting

Although our clinician respondents practice in more than 20 types of settings, the same five venues are featured in both the NP (Table 5) and PA (Table 6) breakdowns for highest average salary based on survey response rate. For both groups of providers, hospital practice delivers the highest salaries. TABLE 5. Average NP salary by practice setting

TABLE 6. Average PA salary by practice setting

Practice setting

Percent response

Average salary

Practice setting

Percent response

Average salary

Office practice

21.7% (n=748)

$89,705

Hospital

23.1% (n=258)

$108,058

Clinic–hospital

19.0% (n=657)

$97,056

Clinic–standalone

21.0% (n=235)

$96,447

Clinic–standalone

17.9% (n=619)

$92,338

Clinic–hospital

18.8% (n=210)

$101,952

Hospital

15.2% (n=523)

$104,147

Office practice

17.4% (n=195)

$96,179

Walk-in/ambulatory

5.5% (n=189)

$95,487

Walk-in/ambulatory

4.0% (n=45)

$102,000

*Based on responses from 3,453 NPs who earn $20,001–$149,999 per year.

*Based on responses from 1,118 PAs who earn $20,001–$149,999 per year.

Salary by practice location— urban, suburban, rural

The majority of respondents who described their work environment to us worked in an urban location, but overall, salary discrepancies across urban, suburban, and rural lines amounted to less than $4,500 for NPs (Table 7) and only about $6,000 for PAs (Table 8). TABLE 7. Average NP salary by urban, suburban, or rural location

TABLE 8. Average PA salary by urban, suburban, or rural location

Practice setting

Percent response

Average salary

Practice setting

Percent response

Average salary

Urban

42.3% (n=1,471)

$96,939

Urban

41.0% (n=462)

$102,437

Suburban

35.5% (n=1,233)

$93,787

Suburban

39.6% (n=446)

$100,601

22.2% (n=771)

$92,514

Rural

19.4% (n=218)

$96,280

Rural

*Based on responses from 3,475 NPs who earn $20,001–$149,999 per year.

*Based on responses from 1,126 PAs who earn $20,001–$149,999 per year.

Gender

As might be expected given the predominance of women in the NP f ield, nearly all NP respondents to the salary survey who identif ied their gender and who earn $20,001 to $149,999 per year are women (3,182, or 92.2%, compared with 270 men, or 7.8% of respondents). The men in this salary range earn more money, at $102,759 per year compared with $94,196 for women. Yet among the NP respondents who reported making $150,000 or more per year, 75 are women and 38 are men. Among NPs who reported making no more than $20,000 per year, 37 are female and just one is male. More of a mix is seen on the PA side: 742 respondents who identified their gender on the survey are women and 372 are men, for a 67%-to-33% split. The average salary for female PAs earning $20,001 to $149,999 per year is $96,585, with their male counterparts bringing down substantially more: $108,228. That trend continued into the highest echelons of PA salary ranges: A total of 40 female PAs reported an annual salary of $150,000 or more, compared with 64 of their male counterparts. 52 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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CME CE

n LEARNING OBJECTIVES: • Describe how a weak cough can be harmful or fatal. • Explain the three phases of cough. • Discuss the differences between cough caused by croup, bronchiolitis, and other sources. • Identify habit cough. • List the treatment options for the various coughs examined. n COMPLETE THE POSTTEST: Page 83

FEATURED COURSE

n ADDITIONAL CME/CE CREDIT: Pages 75, 79

Faculty Disclosures The faculty reported the following financial relationships or relationships to products or devices that they or their spouse/life partner have with commercial interests related to the content of this CME/CE activity: Brian Wingrove, PA-C, has no relevant financial relationships to disclose.

Statement of Need: Cough is one of the most frequent symptoms in children and the most common symptom for which children visit a health-care provider. Acute cough in children can be indicative of asthma, bronchiolitis, whooping cough, and other conditions clinicians need to recognize, manage, and explain to patients and their caregivers.

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

Target Audience: This activity has been designed to meet the educational needs of primary-care physicians, physician assistants, and nurse practitioners who treat pediatric patients for cough. Faculty Brian Wingrove, PA-C Georgia Pediatric Pulmonology Associates Children’s Healthcare of Atlanta at Scottish Rite Atlanta, Ga.

The following HME planners and managers hereby state the following 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: Delicia Yard, Editor; and Nicole Blazek, Web Editor, have no real or apparent conflicts of interest to report.

Accreditation Statements Physician Credit: This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of MER and HME. MER is accredited by the ACCME to provide continuing medical education for physicians. Credit Designation: MER designates this educational activity for a maximum of 0.5 AMA PRA Category 1 Credits TM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Nursing Credit: MER is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Credit Designation: This CE activity provides 0.5 contact hour of continuing nursing education. MER is a provider of continuing nursing education by the California Board of Nursing Registered Nursing, Provider #CEP 12299, for 0.5 contact hours. American Academy of Physician Assistants AAPA accepts certificates of participation for educational activities certified for Category I credit from AOACCME, Prescribed credit from AAFP, and AMA PRA Category 1 Credit™ from organizations accredited by ACCME or a recognized state medical society. Physician assistants may receive a maximum of 0.5 hour of Category I credit for completing this program.

The MER planners and managers, and Veronda Smith, FNP-BC, 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. Method of Participation: There are no fees for participating in and receiving CME/CE credit for this activity. During the period of May 2014 through May 2015, participants must: 1) read the learning objectives and faculty disclosures; 2) study the educational activity; 3) complete the posttest and submit it online (physicians may register at www.myCME.com); and 4) complete the evaluation form online. A statement of credit will be issued only upon receipt of a completed activity evaluation form and a completed posttest with a score of 70% or better. Disclaimer: The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of MER or HME. The authors have disclosed if there is any discussion of published and/or investigational uses of agents that are not indicated by the FDA in their presentations. The opinions expressed in this educational activity are those of the faculty and do not necessarily represent the views of MER or HME. Before prescribing any medicine, primary references and full prescribing information should be consulted. 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 patients’ conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. The information presented in this activity is not meant to serve as a guideline for patient management.

Accreditor Disclosure of Conflicts-of-Interest Policy MER ensures balance, independence, objectivity, and scientific rigor in all our educational programs. In accordance with this policy, MER identifies conflicts of interest with its instructors, content managers, and other individuals who are in a position to control the content of an activity. Conflicts are resolved by MER to ensure all scientific research referred to, reported, or used in a CME/CE activity conforms to the generally accepted standards of experimental design, data collection, and analysis. MER is committed to providing its learners with high-quality CME/CE activities that promote improvements or quality in health care and not a commercial interest.

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BRIAN WINGROVE, PA-C

A child’s cough: common presentations and causes Clinicians who recognize various types of pediatric coughs will be better able to identify serious underlying conditions in the young patient.

The differential diagnosis of cough in children is extensive.

ough is the most common chief complaint in the United States and Australia.1 Although the differential diagnosis of cough in children is extensive, coughs can have very characteristic presentations that can aid the clinician in the diagnosis and management of this problem. This article reviews the pathophysiology of cough, its common presentations in children, and suggested treatments. Cough is an innate defense mechanism of the lungs, used to clear the airways.2 The absence of cough, or the presence of only a weak, ineffective cough, can be harmful or fatal.3 Mucus, pus, fluid, and such inhaled substances as dust, pollen, smoke, and foreign bodies must be cleared from the airways regularly in order to prevent damage to lung tissue that may impair gas exchange. (Figure 1, Figure 2) For example, cough helps to clear the 20 mL to 30 mL of mucus and secretions a person can produce per day on average. This helps explain the frequency of cough: It is estimated that a child can cough up to 11 times per day, increasing to 140 with respiratory infections. City-dwellers cough more on average than do their rural counterparts, being exposed to more air pollution and smog.2

The burden of cough

Cough can be a warning sign of pneumonia, asthma, cystic fibrosis, or other disease. As a symptom, cough can be quite detrimental, interfering with sleep, preventing participation in play or exercise, and causing missed days of school for children as well as missed days of work for their caregivers.2 Cough is a major public health issue, accounting for an estimated 29.5 million outpatients visits per year.1 A cough lasting longer than eight weeks in www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2014 59

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The effectiveness of a cough depends on such factors as the strength of the respiratory muscles, particularly those used in exhalation. adults is the most common reason for referral to a pulmonary specialist; in children, a chronic cough is defined as a cough lasting more than four weeks.4 The annual cost for cough treatment is unknown, as patients often choose to pursue their own remedies without consulting a health-care provider. The money spent on over-thecounter cough and cold preparations alone exceeds billions of dollars.1 Despite high usage levels of these products by consumers, the American Academy of Pediatrics (AAP) holds that they are not effective in children under age 6 years, and may pose a health risk in some cases.5 Studies have indicated that the use of dextromethorphan and diphenhydramine are not superior to placebo in relieving symptoms in children, and do nothing to improve quality of sleep.6 Cough physiology

A cough consists of three phases: inspiratory, compressive, and expiratory (Table 1). The initial phase, inspiratory, is the least critical of the three. It is characterized by an inhalation of air to near total lung capacity. The greater the volume of air inhaled, the greater the positive intrathoracic pressure generated to produce the kinetic energy of a cough. Cough can, however, be generated with low volumes of air.3 The second, compressive phase begins with closure of the glottis at the end of inhalation. However, patients with a tracheostomy or endotracheal tube can still generate a cough with an open glottis through a huffing maneuver.3 This closure maintains the volume of air inhaled into the lungs while simultaneously increasing the intrathoracic pressure. The high pressures that are generated can be transmitted to the nervous, cardiac, gastrointestinal, genitourinary, and musculoskeletal systems, resulting in such secondary symptoms as headache, palpitations, vomiting, incontinence, and pain. The final, expiratory phase is the most dynamic. It is characterized by an explosive release of air and the opening of the previously closed glottis. This blast of turbulent air can reach flow rates of up to 12 liters per second in adolescents and adults, although such rates would not be achieved in younger children. The flow rate rapidly decreases as both pulmonary pressure and lung volume fall. The velocity of the flow rate is directly proportional to the degree of compressive pressures and inversely proportional to the cross-sectional area of the airways involved. 3 The greater the involvement of the more distal, smaller-diameter airways, the greater the end velocity of the cough generated.

The effectiveness of a cough depends on several factors, among them the strength of the respiratory muscles, particularly those used in exhalation, and the rheologic character of the mucus being eliminated from the airway. 3 At high airway velocities within the bronchioles, mucus is torn off from the pulmonary parenchyma and suspended in the lumen. The flow rate can then produce waves of mucus. Additionally, the collapsible nature of the bronchi enhances mucus clearance through vibration. Cilia also play a role in airway clearance, which is enhanced by the vibratory effect of the airways. Mucus lying close to the surface of the cilia becomes less viscous and more easily cleared. Overall, increased viscosity of mucus impairs clearance by airflow alone; however, elimination can be enhanced by ciliary beat frequency. A cough capable of eliminating debris from the lungs is produced by the complex interplay among the pressures generated by respiratory muscle strength, the volume of air inhaled, the rheology of mucus, the rigidity and collapsibility of the airway, and the efficacy of cilia. Certain disorders are characterized by ineffective coughs that have an impaired ability to clear mucus from the alveoli and bronchioles. In cystic fibrosis, for example, mucus becomes inspissated, or thickened, through a defect in the sodium chloride ion channels. Due to the tenacious mucus, children with cystic fibrosis lack the ability to mobilize mucus into the bronchial lumen. A defect in the mobility of cilia, seen in ciliary dyskinesia, will also result in an inability to mobilize mucus out of the respiratory tract. In both instances, the entrapped mucus can lead to atelectasis, pneumonia, and bronchiectasis. Etiology of cough

The differential diagnosis of cough in children is extensive. It has been reported that up to 31% of coughs have no apparent underlying cause.2 Primary among the causes of cough TABLE 1. Phases of cough Inspiratory

Compressive

Expiratory

• Inhalation to near total lung volume • Increase in intrathoracic pressure • Generation of kinetic energy

• Closure of glottis • Maintenance of lung volume • Large increase in intrathoracic pressure

• Opening of glottis • Dynamic release of air • Rapid decline in flow rate, lung volume, and intrathoracic pressure

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As children grow, airways with greater diameter are less susceptible to edema caused by viruses, making the bark of croup less notable. are infectious etiologies of the upper and lower respiratory tract such as sinusitis, viral upper respiratory infection, bronchiolitis, and pneumonia. Aspiration from foreign bodies, dysphagia, and gastroesophageal reflux are also common in children. However, the most frequent cause of a chronic or recurrent cough in children is asthma and may be closely linked to allergic or chronic nonallergic rhinitis. Habit cough as well as tic cough also may be present in children. Inhalation pneumonitis from smoke (tobacco, fire) and hydrofluorocarbons (kerosene, gasoline) are not uncommon. Heritable disorders such as cystic fibrosis, ciliary dyskinesia, and congenital malformations of the airway also should be considered. Rarer causes of cough in children include Wegener granulomatosis and connective-tissue diseases. Croup

Laryngotracheobronchitis, better known as croup, accounts for 15% of all respiratory disease in children. This viral infection occurs most often in the fall and winter and tends to affect children younger than age 6 years, with a peak incidence at age 18 months.7 Croup is caused predominantly by parainfluenza viruses, which are present in 65% of cases. The virus seeds in the nasopharynx, then spreads distally into the respiratory epithelium of the larynx and trachea. It causes diffuse edema of the airway wall and impairs vocal cord mobility, resulting in the harsh, barky or “seal-like” cough of croup. A hoarse voice is also quite common. Stridor is an emergent sign in croup, signaling severe edema and respiratory compromise. Croup is more common in young children because of the much smaller, more compact laryngeal anatomic structures of the airway. As children grow, the airways with greater diameter are less susceptible to the edema caused by viruses, rendering the bark of croup is less notable. The most important step in evaluating children with croup is to keep them calm. Crying or screaming will increase airway resistance and worsen the stridor and respiratory distress. Allow the child to remain with a caregiver and examine him or her in as “hands off” a manner as is reasonable. Steroids are the standard for treatment in even mild croup as edema can progress rapidly.8 In one study of 720 children with croup, the patients receiving steroids had more rapid resolution and less lost sleep, and their parents experienced less stress.9 Systemic dexamethasone (Decadron, Dexamethasone Intensol, Dexpak) and

FIGURE 1. Mucus collected in airway of a child with asthma, shown on bronchoscopy. FIGURE 2. Pus collected in airway of a child with cystic fibrosis, shown on bronchoscopy.

nebulized budesonide (Pulmicort) were found to be equally effective. However, the cost and administration burden of nebulized budesonide makes dexamethasone a more favorable choice. Dexamethasone can be given orally or by injection. Avoidance of injection is clearly the preferred approach when attempting to keep a child calm. Dosing is 0.6 mg/kg; doses up to 10 mg have been used safely.9 Racemic epinephrine should be reserved for use in children who have stridor at rest or those who are in respiratory distress. A child should be observed for several hours after administration of the racemic epinephrine to ensure that symptoms do not return or worsen.8 Patients should be admitted to the hospital if their stridor is refractory to steroids or epinephrine. Doses of these medications should continue to be given to the hospitalized child until stable. Bronchiolitis

Bronchiolitis, inflammation of the lower respiratory tract, is caused by a viral pathogen. Respiratory syncytial virus (RSV) is the most common pathogen identified and is epidemic from November to February, with geographic variations.10 Bronchiolitis almost universally affects children younger than age 2 years, with peak incidence occurring at age 2 months to age 6 months. The viral culprits in bronchiolitis invade the terminal bronchiolar epithelial cells, causing tissue damage and inflammation in the airways. Pathologically, the damage caused includes edema, mucus production, and sloughed epithelial cells, all leading to obstruction and atelectasis. In severe cases these pathologic changes can lead to cell necrosis, ciliary injury, and peribronchial lymphocytic infiltration.11 Characteristically, children with bronchiolitis wheeze due to the obstruction in their narrowed airways. The cough of

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Habit cough is completely absent during sleep and usually during distraction, such as when the child is undergoing lung-function testing. bronchiolitis will produce a wheeze as well as crackles and sputum. Depending on the degree of obstruction, many children are otherwise stable and playful. Nevertheless, the obstruction can be life-threatening. Infants with bronchiolitis should have very close follow-up; hospitalization should be considered for young infants who were born prematurely, because of their heightened risk for apnea. Treatment options for bronchiolitis are limited, with no proven, efficacious therapies identified despite multiple studies. Bronchodilators and steroids are frequently used to manage the condition, especially among hospitalized patients, but have limited impact due to their ineffectiveness against the bronchogenic infiltrates of bronchiolitis.10 Several studies showed some benefit with the use of a nebulized 3% hypertonic saline. This treatment improved symptoms and reduced length of hospital stay by 26%.12,13 Supportive care with hydration, suctioning of excess secretions, supplemental oxygen, and administration of antipyretics are suggested. Prophylaxis for high-risk infants and children is recommended during the epidemic period of RSV disease. Palivizumab (Synagis) is a monoclonal antibody given by injection every 28 to 32 days. Palivizumab does not prevent disease but can inhibit replication of the respiratory syncytial virus.11 Premature infants born at less than 35 weeks’ gestational age, infants with neuromuscular disease or congenital airway abnormalities, and children younger than age 2 years with congenital heart disease or chronic lung disease should be considered for prophylaxis.10 Habit cough

Habit cough is a very disruptive, brash, brassy cough. Many children with this type of cough do not realize they are coughing habitually. Habit cough virtually always has an organic origin. The child will have had a cough from an asthma exacerbation, pneumonia, or a common cold. He or she becomes stuck in a cycle of cough, irritation, throat-clearing, more irritation, and more cough.14 The situation can be likened to a fire alarm that keeps going off despite the fact that the fire has been put out. There is often a very dramatic flourish to the cough with arm waving, back-arching, chest-heaving, and head-bobbing. The cough typically is very annoying and anxiety-provoking for caregivers. The etiology of habit cough is unique from that of other coughs in that lung function is preserved. Habit cough is

completely absent during sleep and usually during distraction, such as when the child is undergoing lung-function testing. Comorbid symptoms are rare and physical examination is entirely normal. Habit cough does not respond to bronchodilators, steroids, antibiotics, or antitussive medications. These options usually have been exhausted by the time the diagnosis of habit cough is reached. Habit cough frequently leads to multiple office or hospital visits with no change in the clinical course.14 Such exercises as breathing through pursed lips, huffing and puffing, or blowing against resistance can help relieve the child’s airway irritation and urge to cough. Having the child suck on sugar-free candy and take frequent sips of water can help keep the youngster’s laryngeal structures lubricated and reduce irritation, and can serve as good distractions from coughing. Caregivers should be encouraged to give the child positive reinforcement by praising or rewarding the patient for controlling the cough. Anecdotally, one simple technique that has been used successfully by this practitioner centers on calling attention to the cough by asking the patient to stop coughing while the clinician talks to the parent. Games can be an effective method for making the child more cognizant of the habit cough. For example, explain to the child that the cough has control of his or her life and the life of their caregivers, and now it’s time to take back control. Then have the child keep score: If he or she can keep from coughing, he or she wins a point; otherwise, the point goes to the cough. Treating habit cough is challenging and requires great patience. No single therapy will always work. It is important to note, however, that absence of a treatment plan can result in prolonged, continued symptoms.14 Asthma

Asthma is by far the most common cause of a chronic or recurrent cough. A diagnosis of asthma should always be considered for any child with recurrent cough, whatever the presumed previous etiology was called (for example, pneumonia, croup, bronchitis). A nighttime cough is the most common type of asthma cough,15 and is included as part of the assessment for asthma control in the National Heart, Lung, and Blood Institute guidelines for the diagnosis and management of asthma.16 A cough first thing in the morning and a cough with exercise are also very characteristic of asthma.

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A nighttime cough is the most common type of asthma cough; cough first thing in the morning or with exercise also is very characteristic. An asthma cough can take one of two forms, bronchospasm or wheezing, but is often a mix of both. Bronchospasm occurs when a deep inhalation provokes coughing fits (three or more coughs in a row). These coughing fits are characterized by spasms of rapid-succession coughs that can make administration of inhaled medications difficult. Wheezing is a hallmark of asthma with a biphasic musical component. There is often a vibratory quality to the cough even if the wheeze is not audible. In these cases the cough is frequently dry, but because excess mucus production is part of the pathophysiology of asthma, the cough can become “wet.” All patients with asthma should have a written asthmamanagement plan in place (Table 2). This document should include specific information on medications to be used, dosage and dosing frequency, and when to seek emergent care. Acutely, the first-line treatment for asthma is the use of fast-acting bronchodilators by means of nebulization or metered-dose inhalation. There is no difference between nebulized or metered-dose inhaler administration, if done technically correctly.17 The fast-acting bronchodilators work on beta-2 receptors in the airway to induce smoothmuscle relaxation and enhance ciliary beat frequency, thereby improving air flow. The beta-2 agonists include albuterol (Accuneb, Proair, Proventil, Ventolin), levalbuterol (Xopenex), and pirbuterol (Maxair); ipratropium bromide (Atrovent) is another fast-acting bronchodilator but must be used in conjunction with one of the beta-2 agonists. Salmeterol (Serevent) and formoterol (Foradil, Perforomist) are long-acting bronchodilators and are not indicated for use in the treatment of acute asthma. Treatment frequency is based on asthma severity but is typically every three to four hours in mild disease. In some cases, clinicians can advise patients to do repeat treatment cycles in a shorter time frame to get symptoms quickly under control, and then resume the administration schedule of every three hours. Our practice uses a “back-to-back-to-back” cycle in which a patient may do a treatment every 20 minutes for one hour, but then must contact the provider on call. When bronchodilators are insufficient to abort asthma symptoms, the next step is to use systemic steroids, either orally or parenterally. Studies indicate that short bursts with dexamethasone have been used successfully in place of longer courses of prednisolone.18 However, dexamethasone has a longer half-life and is more potent, so repeated use should be done with caution.

Access to steroids should be part of every asthma management plan. Patients—particularly those with severe disease—should be advised to keep a supply at home and should be given explicit instructions to contact their health-care provider when using these medications. Use of daily controller medication with inhaled corticosteroids should be considered in any child requiring systemic steroids, or when bronchodilators are used more than three times a week on a regular basis.16 Several adjunct therapies are available for the emergent treatment of acute asthma, including magnesium sulfate, terbutaline, and heliox, a helium/oxygen mixture. Discussion of these treatments is beyond the scope of this article. Neuromuscular cough

Children with neuromuscular diseases such as spinal muscular atrophy, Duchenne muscular dystrophy, cerebral palsy, cervical spine injuries, mitochondrial myopathy, and other hypotonic disorders of unknown etiology may lack sufficient inspiratory muscle strength to generate a large volume of inhaled air into the lungs. As a result, the lungs are not fully expanded to maximal capacity. More critical, however, is decreased expiratory-muscle strength, leading to reduced dynamic airway compression and diminished expiratory pressures and flow rates. 3 Spirometry and plethysmography are essential components of routine assessment that will enable the clinician to determine the child’s respiratory sufficiency by tracking vital capacity, forced expiratory volume in one second and forced vital capacity (FEV1/FVC) ratios, maximum inspiratory pressure (MIP), and maximum expiratory pressure (MEP). The clinician TABLE 2. Key sections of an asthma management plan Daily controller medication: Name: Dosing: Frequency: When experiencing symptoms such as coughing, wheezing, or chest tightness: Fast-acting medication to take: Dosing: Frequency: What to do if your fast-acting medication is not working: • Back-to-back treatments • Start steroids • Call for help

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The absence of effective cough can be a dangerous condition, possibly resulting in atelectasis, pneumonia, and respiratory failure for the patient. also should ask the patient to cough with as much force as possible during the evaluation to hear the strength and effectiveness of the cough.19 The absence of an effective cough can be dangerous, possibly resulting in atelectasis, pneumonia, and respiratory failure. Protussive mechanical aids are essential in the daily management of neuromuscular disease to enhance airway clearance.20 Chest physiotherapy by means of manual cuffing, vibratory wand, or a high-frequency chest compression vest helps to move mucus and fluid into the central airways. Acapella and Flutter devices do not work as well for this purpose because the patient may lack sufficient oral-muscle strength to form a seal, and cannot generate the pressures needed for the device to operate. Insufflation/exsufflation therapy simulates a cough by using pre-set positive pressure to push air into the lungs through a face mask, followed rapidly by negative pressures to pull air out. Suction equipment is then necessary to clean the debris from the oropharynx. Biphasic positive airway pressure (BiPAP) delivered through a face mask, a nasal mask, or nasal pillows can be used to permit lung rest, recruit atelectatic alveoli, and enhance ventilation. Frequently used at night during sleep, BiPAP is beneficial during acute illnesses and during naps for rest. Tracheostomy is an invasive option for providing a means for chronic ventilation and airway clearance with deep suctioning. Long-term expectations and personal desires for end-of-life interventions must be discussed with patients and their families before pursuing tracheostomy.19 Pertussis

Pertussis, also called whooping cough, most commonly affects infants and young children, and can be fatal in children younger than age 1 year. This bacterial infection is caused by Bordetella pertussis, a non-motile coccobacillus that is transmitted by means of aerosolized droplets; transmission is from human to human only. As is the case with many respiratory pathogens, B. pertussis attaches to the respiratory tract, starting in the nasopharynx and migrating distally down to the terminal bronchioles, where it becomes invasive and can be found in alveolar macrophages. B. pertussis creates a toxin that paralyzes the cilia and causes inflammation of the respiratory tract.21 The infection causes excessive secretions of mucus, pus, and even blood. Pertussis begins with a catarrhal phase that may last one to two weeks. The catarrhal phase is indistinguishable from

other respiratory infections, with the patient experiencing runny nose, low-grade fever, and cough. The infection is most contagious at this phase. The second phase of pertussis is known as the paroxysmal phase because it is characterized by paroxysms of coughing—rapid, numerous coughing fits, with or without an inspiratory whoop. This phase may last from one week up to six to 10 weeks. Coughing may last many weeks longer as the illness enters the final, convalescent phase.21 Cough overall improves, but the infected patient remains highly susceptible to other respiratory infections, during which the coughing paroxysms can return. Testing for pertussis is notoriously difficult and will only be detected during the first three weeks of infection, when it might not even yet be suspected. Nasopharyngeal culture is the gold standard, but the incidence of false-negative results increases after two weeks of infection. Polymerase chain reaction amplification is quite sensitive, and can detect illness in the first three weeks of infection. In infants and unvaccinated persons, the test may be effective through four weeks of illness.22 Serologic testing can detect infection that has been present up to eight weeks, but no commercially available test exists. Only the Centers for Disease Control and Prevention and the Massachusetts state public health laboratory have a validated assay for pertussis.23 Clinicians must have a high index of suspicion for pertussis. The CDC has a working definition of pertussis that focuses on the character of the cough: “A cough illness lasting at least two weeks with one of the following: paroxysms of coughing, inspiratory ‘whoop,’ or post-tussive vomiting, without other apparent cause.” Both laboratoryconfirmed cases and probable cases fitting the definition are reportable to the CDC.21 The macrolide antibiotics are the first-line treatment for pertussis. Azithromycin (Zithromax, Zmax), clarithromycin (Biaxin, Prevpac), and erythromycin are all acceptable; sulfa drugs can be used in patients who are allergic to the macrolides. Isolation is recommended for the patient until he or she has completed five days of antibiotics. Consider administration of a course of antibiotics to persons in close contact with the patient within three weeks of exposure. Conclusion

Cough is a physiologic mechanism for clearing the airways, and is the most common chief complaint among persons

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The second, or paroxysmal, phase of pertussis is characterized by rapid, numerous coughing fits, with or without an inspiratory whoop. presenting to health-care providers in the United States. The efficacy of cough depends on its etiology and the biophysical mechanics of the patient, including respiratory muscle strength, ciliary mobility, bronchial compliance, and mucus rheology. In children, as in adults, cough may be a warning sign of disease, and many coughs have characteristic sounds and presentations that can guide clinicians to an appropriate diagnosis and treatment plan. ■

11. Goodman GG, Wojtczak HW, Welliver RC Sr. Respiratory Syncytial Virus: a Frontline Pediatrician’s Guide to Effective Prevention and Treatment. Vindico Medical Education CME Monograph. March 2012March 2013. 12. Mandelberg A, Tal G, Witzling M, et al. Nebulized 3% hypertonic saline solution treatment in hospitalized infants with viral bronchiolitis. Chest. 2003; 123(2):481-487. Available at journal.publications.chestnet.org/data/ journals/chest/21989/481.pdf. 13. Sarrell E, Tal G, Witzling M, et al. Nebulized 3% hypertonic saline solu-

Mr. Wingrove is a physician assistant at Georgia Pediatric Pulmonology Associates in Atlanta and Children’s Healthcare of Atlanta at Scottish Rite.

tion treatment in ambulatory children with viral bronchiolitis decreases symptoms. Chest. 2002;122(6):2015-2020. Available at journal.publications. chestnet.org/data/Journals/CHEST/21985/2015.pdf. 14. Weinberger M. The habit cough syndrome and its variations. Lung.

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for Disease Control and Prevention; 2011: chap 10-1. Available at www.

10. American Academy of Pediatrics. Respiratory syncytial virus. In: Red

cdc.gov/vaccines/pubs/surv-manual/chpt10-pertussis.html.

Book: 2012 Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, Ill.: Pickering LK; 2012.

All electronic documents accessed April 15, 2014.

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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.

Inside the Forum M AY 2 0 1 4

Consultations Interactions between antibiotics and warfarin . . . . . . . . . . . 66 Does itching indicate healing? . . . . . . 66 Is petroleum jelly toxic?. . . . . . . . . . . 67 BMI as a vital sign. . . . . . . . . . . . . . . 67

Clinical Pearls Written reminder of risky sex. . . . . . . 68 Subtle signs of a failing heart . . . . . . . 68 The handyman’s wart treatment. . . . . 68

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 also fax (646) 638-6117, or contact us by e-mail at letters@ 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.

CONSULTATIONS INTERACTIONS BETWEEN ANTIBIOTICS AND WARFARIN When placing a patient on an antibiotic (e.g., azithromycin [Zithromax, Zmax]) that may affect his or her warfarin [Coumadin, Jantoven] use, how is the associated change in warfarin dosing calculated? – SEAN GREEN, MSN, APRN, FNP-BC, Fort Worth, Tex. Macrolide antibiotics have the potential to increase the serum concentration of warfarin, so careful monitoring of therapy is required. Azithromycin may alter the international normalized ratio (INR) response to warfarin, but warfarin should be dosed normally. There is an increased risk of bleeding associated with clarithromycin [Biaxin], so the warfarin dose should be decreased by 15%. INR should also be monitored in patients taking clarithromycin and warfarin concomitantly. To combat the increased risk of bleeding associated with erythromycin, decrease the warfarin dose by 20%. No interactions are associated with dirithromycin and spiramycin, so a normal dose of warfarin can be maintained.—Abimbola Farinde, PharmD, MS (187-1)

DOES ITCHING INDICATE HEALING? I recently received a significant burn that turned intensely pruritic during the healing process. For years, I have advised

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, PharmD, MS,

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

Abby A. Jacobson, PA-C,

Maria Kidner, DNP, FNP-C,

is a physician assistant at Delaware Valley Dermatology Group in Wilmington, Del.

is a nurse practitioner with Cheyenne Cardiology Associates in Cheyenne, Wyo.

66 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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patients that itching is a sign of healing. Is there any science behind this, or is it simply an old wives’ tale? – DOUG COBB, PA, Auburn, Calif. This is one old wives’ tale that is supported by science. The skin is part of the human body’s defense system against infection and invaders. The body is unable to recognize the difference between a clean clinical wound made by a sterile scalpel and the dirty wound of a dog bite. Any injury to the skin is interpreted in an identical manner. During the healing process, the body infiltrates a wound with inflammatory cytokines to clean the area of any foreign body or infection. These pro-inflammatory cytokines produce itch. In many skin diseases, such as atopic dermatitis and psoriasis, the body inappropriately dumps pro-inflammatory cytokines into the skin, thereby causing the sensation of itching. Additionally, a high level of histamine has been found in healing skin and scabs, which we know will create the sensation of itching. During an injury (especially a burn), nerves may have been damaged, creating inappropriate signals that the brain interprets as itch. Oil glands may also be damaged by injury, and dry skin is itchy. This is why it is recommended to keep healing skin clean, covered, and moist with petroleum jelly.—Abby A. Jacobson, PA-C (187-2)

IS PETROLEUM JELLY TOXIC? Many of the patients in my occupational-health clinic are factory workers who often present with dry, cracked hands. This is a concern because of the chemicals these workers use daily. I have recommended applying petroleum jelly and wearing a cotton glove at night. Some patients have voiced concern that the petroleum in the product is toxic. Is there any credence to this claim?—EILEEN NEWTON, ARNP, Everett, Wash.

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.

While I do not give this claim any credence, patients will have to judge things for themselves. I use petroleum jelly on my three young children and myself regularly. If a person is concerned about product safety, I strongly suggest that he or she buy branded Vaseline petroleum jelly. This product goes through a rigorous process of purification and is highly refined, tightly controlled, and widely considered noncarcinogenic. If the patient is still hesitant to use this product or wants a more natural option, consider beeswax, coconut oil, or olive oil. I always suggest a one-week trial on the inner arm to evaluate for allergy or reaction. Apply the product on the same spot every night and if there is no reaction after one week, it should be considered safe to use on the hands. Olive oil can be very pure, and very few people are allergic to it. It is not the most cosmetically elegant solution, but it does work. Most importantly, I foresee no potential cancer or toxic risks on the horizon.—Abby A. Jacobson, PA-C (187-3)

BMI AS A VITAL SIGN Obesity seems to be underdiagnosed in primary care. When evaluating and treating a patient, the vital signs include blood pressure, heart rate, respiration rate, body temperature, oxygen, and pain. If one of these is abnormal, we evaluate and intervene early to prevent long-term complications. To prevent long-term complications of obesity, should BMI [body mass index] be included as one of the vital signs? KRISTINE YEARWOOD, DNP, FNP, El Paso, Tex. This is an excellent recommendation. In some practices, weight and BMI are trended in the electronic medical record and other patient tracking systems. Unfortunately, recent evidence indicates that only 26% of primary-care providers regularly note elevated BMI and then provide counseling and track weight-loss goals as part of routine practice (Am J Health Promot. 2014;28[3]:e67-e80). More importantly, along

Claire O’Connell, MPH, PA-C,

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

Sherril Sego, FNP-C, DNP,

is a primary-care nurse practitioner at the Department of Veterans Affairs Medical Center in Kansas City, Mo.

Julee B.Waldrop, DNP,

is associate professor at the University of Central Florida (UCF), and practices pediatrics at the UCF Health Center.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2014 67

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Advisor Forum with including this “vital sign,” clinicians would need to recognize the elevated BMI, rule out other causes for the weight gain (e.g., thyroid disease and high suspicion for Cushing syndrome), and provide patient interventions that would facilitate weight loss for health. The 2013 obesity guidelines from the American College of Cardiology and the American Heart Association provide a useful treatment algorithm of clinician recommendations for weight management that include measurement of waist circumference and screening for diabetes, dyslipidemia, and hypertension (2013 Nov 12. [Epub ahead of print]; available in Circulation at circ.ahajournals.org/ content/early/2013/11/11/01.cir.0000437739.71477.ee.long, accessed April 15, 2014).—Katherine Pereira, DNP, RN, FNP-BC, ADM-BC, FAANP coordinator, FNP specialty, Duke University School of Nursing, Durham, N.C. (187-4)

“Welcome aboard, and if you have any problems at all, don’t hesitate to shut up.”

CLINICAL PEARLS WRITTEN REMINDER OF RISKY SEX Due to the high prevalence of sexually transmitted diseases (STDs) among adolescents, I incorporate the patient’s lab results into my teaching moment when delivering positive results. Before the patient leaves, I provide a copy of his or her lab results to take home. My hope is that seeing his or her name associated with an STD emphasizes the seriousness of the diagnosis and inspires a change in sexual behaviors.— KASAUNDRA EWING, FNP-BC, Norfolk, Va. (187-5)

THE HANDYMAN’S WART TREATMENT To get rid of a wart, cover the affected area with the silver duct tape and leave it in place for one week. After removing the tape, soak the wart in water, and use a pumice stone or emery board to get rid of the dead skin. Wait one day, reapply the silver duct tape, and repeat the process until the wart is gone.—JOHN DONOHUE, PA-C, Fayetteville, Ga. (187-7) ■

“This is the breakroom, where we watch reruns of classic security footage.”

“Should we take lunch first?”

SUBTLE SIGNS OF A FAILING HEART When patients with heart failure call their primary-care office (instead of their cardiologist) asking for something to help them sleep, this could be a sign of worsening heart failure. Additionally, if they ask for something to help their postnasal drip, a more thorough assessment is needed as this may indicate a cough when they lie down, which could be a sign of worsening heart failure. Often these patients do not see their diseases as chronic, and they miss signs of worsening failure.—SUSAN TAPLIN, FNP, Nashville, Tenn. (187-6)

68 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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PHOENIX

Primary Care Conference & Pharmacology Update October 13-16, 2014

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November 8-11, 2014

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Derm 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 CliniAd.com/10KIbCF. Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues.

A necrotic mass located on the back A 57-year-old man presented with a large, oblong necrotic mass on the left posterior lateral region of his back. The lesion was 35 cm x 16 cm and tender but firm, with an erythematous border. The patient was in no acute distress. WHAT IS YOUR DIAGNOSIS?

• Cutaneous B-cell lymphoma • Dermoid cyst • Lipoma • Epidermal inclusion cyst

● See the full case at CliniAd.com/1hvsVWo.

Progressive generalized blisters A man aged 51 years presented with blisters on his face, scalp, trunk, and groin, which had been progressing for months. He was otherwise healthy and on no medications. ELISA showed autoantibodies to desmoglein 1. WHAT IS YOUR DIAGNOSIS?

• Pemphigus vulgaris • Pemphigus foliaceus • Lupus vulgaris • Impetigo ● See the full case at CliniAd.com/1haED41.

Have you missed any recent Derm Dx cases? Go to CliniAd.com/10KIbCF for a complete archive of past quizzes as well as additional images of last month’s other cases.

Furrowing on the scalp

A brown plaque on the nose

70 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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LEGAL ADVISOR CASE

Comments in chart lead to a lawsuit

BY ANN W. LATNER, JD

Ms. C, 54, sighed to herself when she saw the patient in the waiting room again. As a nurse practitioner working for a family practice, Ms. C both helped the physicians and saw patients of her own. This particular patient was one who came to see Ms. C specifically, and in her private thoughts, Ms. C wished the woman would find another practitioner. The patient, Ms. L, was only in her early 30s, but had more complaints than most patients her age. Ms. L had been in occasionally over the past few years, but it was during the last few months that she had become a bit of a problem. The issue had begun two months earlier, when Ms. L made an appointment to see Ms. C. The patient had fallen at work, and was reporting significant pain in her back and her neck. “I could have killed myself!” Ms. L said to Ms. C. “The floor at work was wet and those lazy janitors didn’t wipe it up fast enough. I fell flat on my back, and the pain has been excruciating ever since.” Ms. C ordered imaging studies, but the results showed nothing out of the ordinary, so Ms. C

A clinician’s opinions about a patient, noted in the patient’s chart, become grounds for charges of defamation.

The issue began when the patient fell at work; she was reporting significant pain in her back and her neck.

advised the patient to rest for a few days and prescribed a small amount of pain-killers to be taken as needed. Within a week, however, Ms. L returned, complaining that the pain wasn’t abating. Ms. C examined her and couldn’t find anything significant, but noted that the patient might still feel some muscle strain or some pain from bruises caused by the fall. Ms. L asked for more painkillers, but Ms. C advised her to try over-the-counter ibuprofen. “I’m filing a workers’ comp claim,” Ms. L announced to Ms C. “The janitors at my job should have been more careful. I haven’t been able to go back to work since the fall because the pain is so bad.” Over the next six weeks, Ms. L returned to see Ms. C at least four times, each time complaining that the pain was unremitting and that she wasn’t improving. “I’ve heard that Percocet Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2014 71

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LEGAL ADVISOR fact, said the court. To be defamatory, a written or spoken communication must be false. Only a statement of fact can be false; a matter of opinion cannot be true or false. Thus, the court found that Ms. C’s opinions that the patient might be drug-seeking or malingering could not be defamatory. The court also noted that Ms. L had signed medical releases before her charts were turned over to anyone. Since she had consented to the release of information, the statements in her chart were considered legally privileged, which negated an essential element of defamation—that the comments be part of an unprivileged communication. Finally, the court stated that no evidence had been presented to prove that any medical practitioners had refused to see Ms. L based on the opinions Ms. C had expressed in the patient’s chart. The court dismissed the case against Ms. C. Protecting yourself

Numerous practitioners have been saved from lawsuits because they took detailed chart notes that could then be used to prove that they had acted appropriately in treating a patient—for example: Yes, a certain screening test had been recommended to a patient who then refused it, or no, the patient had not been suffering from a high fever. Clinicians have to see so many patients that remembering the details of each case would be impossible, making note-taking crucial. This need outweighs the very unlikely circumstance seen in this case, in which a patient sued her clinician for defamation based on notes written in the chart. It’s far more important to take accurate notes, including your opinions, than to leave medical charts incomplete. n Ms. Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, N.Y.

Legal background

The state Supreme Court ultimately agreed with the lower court for various reasons, and dismissed the case on several grounds. First, Ms. C’s notes did not rise to the level of defamation because they were a matter of opinion, not

“It’s the downstairs neighbors again—they say you’re technically proficient, but there’s not enough emotion.”

72 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

[oxycodone and acetaminophen] or Vicodin [hydrocodone and acetaminophen], or maybe Oxycontin [oxycodone], might help my pain,” Ms. L said to Ms. C. “Can you write me a prescription for one of those?” Ms. C put off the patient each time, but did write in Ms. L’s chart that the patient was requesting painkillers by name, and that Ms. C believed the patient to be malingering. At another visit, Ms. L again complained about her pain, her lack of improvement, and her inability to work, and again asked for medication. Ms. C declined to prescribe anything stronger than ibuprofen, and noted in the chart that Ms. L might be a drug-seeker. On this visit, Ms. L dropped off several signed waivers, requesting that her medical chart be shared with her employer and other medical practitioners as part of her workers’ compensation lawsuit. Several months passed with no sign of Ms. L, and then Ms. C received notice that she was being sued by her former patient for defamation. Ms. L was claiming that Ms. C had “intentionally, negligently, and/or recklessly without regard for the truth” expressed to several people that Ms. L was “a drug-seeker or abuser,” who was “committing insurance fraud by pretending to have nonexistent injuries,” and was “only trying to scam money out of workers’ compensation.” The clinician was stunned and immediately went to consult with a defense attorney. “I never said any of those things!” Ms. C told the attorney. “I merely wrote in the chart that she was asking for painkillers and that I believed she was malingering. She had no serious injuries and should have been improving.” The attorney explained to Ms. C that the term “defamation” includes the terms libel and slander. Libel is “false and unprivileged communication by writing…” that causes damage to the person being written about; slander is essentially the same, but the communication is verbal rather than written. “Your former patient is claiming that your notes in the chart indicating that she might be malingering or seeking narcotics caused other medical providers to refuse to see her,” pointed out the attorney. He didn’t believe the patient had a case, and told Ms. C he would file a motion on Ms. C’s behalf to dismiss the case. The district court judge agreed, and dismissed the case. However, the nightmare began again when Ms. L immediately appealed to the Supreme Court of the state.

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CME CE

n LEARNING OBJECTIVES:

For Dermatology Clinic • Identify and diagnose dermatologic conditions and review up-to-date treatment.

For Dermatologic Look-Alikes • Distinguish and properly treat dermatologic conditions with similar presentations. n COMPLETE THE POSTTEST: Page 83

DERMATOLOGY COURSES

n ADDITIONAL CME/CE CREDIT: Page 59

This activity is jointly sponsored by Medical Education Resources (MER) and Haymarket Medical Education (HME). Release Date: May 2014 Expiration Date: May 2015 Estimated time to complete the educational activity: 30 minutes Statement of Need: Undertraining in dermatology for primary-care providers is a common phenomenon. Thus, primary-care providers need additional educational outlets devoted to identifying and treating dermatologic conditions. For clinicians out of training, CME/CE becomes the most accessible route. Target Audience: This activity has been designed to meet the educational needs of primary-care clinicians who treat patients with various dermatologic conditions. Faculty Audrey Chan, MD Baylor College of Medicine, Houston Tiffany L. Shih, MD University of Minnesota, Minneapolis Damjan Jutric The University of Texas School of Dentistry, Houston Kerri Robbins, MD Baylor College of Medicine, Houston Accreditation Statements Physician Credit: This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of MER and HME. MER is accredited by the ACCME to provide continuing medical education for physicians. Credit Designation: MER designates this educational activity for a maximum of 0.5 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Nursing Credit: MER is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Credit Designation: This CE activity provides 0.5 contact hour of continuing nursing education. MER is a provider of continuing nursing education by the California Board of Nursing Registered Nursing, Provider #CEP 12299, for 0.5 contact hour. American Academy of Physician Assistants AAPA accepts certificates of participation for educational activities certified for Category I credit from AOACCME, Prescribed credit from AAFP, and AMA PRA Category 1 Credit™ from organizations accredited by ACCME or a recognized state medical society. Physician assistants may receive a maximum of 0.5 hour of Category I credit for completing this program.

are resolved by MER to ensure all scientific research referred to, reported, or used in a CME/CE activity conforms to the generally accepted standards of experimental design, data collection, and analysis. MER is committed to providing its learners with high-quality CME/CE activities that promote improvements or quality in health care and not a commercial interest. Faculty Disclosures The faculty 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/CE activity: Audrey Chan, MD; Tiffany L. Shih, MD; Damjan Jutric; and Kerri Robbins, MD, have no relevant financial relationships to disclose. Staff/Planners’ 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/CE activity: The following HME planners and managers hereby state the following 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: Delicia Yard, Editor; and Nicole Blazek, Web Editor, have no real or apparent conflicts of interest to report. The MER planners and managers, and Veronda Smith, FNP-BC, 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. Method of Participation: There are no fees for participating in and receiving CME/CE credit for this activity. During the period of May 2014 through May 2015, participants must: 1) read the learning objectives and faculty disclosures; 2) study the educational activity; 3) complete the posttest and submit it online (physicians may register at www.myCME.com); and 4) complete the evaluation form online. A statement of credit will be issued only upon receipt of a completed activity evaluation form and a completed posttest with a score of 70% or better. Disclaimer: The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of MER or HME. The authors have disclosed if there is any discussion of published and/or investigational uses of agents that are not indicated by the FDA in their presentations. The opinions expressed in this educational activity are those of the faculty and do not necessarily represent the views of MER or HME. Before prescribing any medicine, primary references and full prescribing information should be consulted. 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 patients’ conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. The information presented in this activity is not meant to serve as a guideline for patient management.

Accreditor Disclosure of Conflicts of Interest Policy MER ensures balance, independence, objectivity, and scientific rigor in all our educational programs. In accordance with this policy, MER identifies conflicts of interest with its instructors, content managers, and other individuals who are in a position to control the content of an activity. Conflicts

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CME CE

Dermatology Clinic n LEARNING OBJECTIVES: To identify and diagnose dermatologic conditions and review up-to-date treatment. n COMPLETE THE POSTTEST: Page 83

n ADDITIONAL CME/CE: Pages 59, 79

Turn to page 74 for additional information on this month’s CME/CE courses.

CASE #1

Brown macules on a depigmented skin patch AUDREY CHAN, MD

A 4-year-old Hispanic male presents to the dermatology clinic. Although the patient presents for an unrelated dermatology complaint, on physical exam he is noted to have a white forelock, in addition to a depigmented patch with overlying brown macules on the midline abdomen. The physical exam is negative for a broad nasal root or heterochromic irises. The patient is otherwise healthy with no known medical problems. A review of systems is negative for headache or hearing change. Family history is notable for similar findings in the patient’s father and a sibling. What is your diagnosis? Turn to page 76

CASE #2

Vesicular eruption in an ICU patient TIFFANY L. SHIH, MD

A 31-year-old male with no known medical history had been admitted to the surgical intensive-care unit (ICU) service with traumatic brain injury following a motor-vehicle accident. The surgical team grew concerned about a two-day history of vesicles over the man’s trunk and extremities. On admission to the hospital three weeks earlier, the patient had been intubated and sedated, and then underwent a tracheostomy placement due to extensive neurologic damage. No history could be obtained since the patient was responsive only to painful stimuli. Exam revealed clear, superficial vesicles on his proximal upper and lower extremities, neck, chest, back, and abdomen. What is your diagnosis? Turn to page 77 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2014 75

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CME CE

CASE #1

Dermatology Clinic

Piebaldism

Piebaldism is a rare, autosom a l dom i n a nt g eno dermatosis resulting from defective melanoblast migration. The estimated incidence in Caucasians is 1 in 40,000.1 Although piebaldism can occur in any ethnicity, epidemiologic data in other races is lacking. Males and females are equally affected, which is expected in all disorders with autosomal dominant inheritance. Piebaldism results from mutations in the KIT protooncogene, located on chromosome 4q11-12.1 KIT encodes the tyrosine kinase transmembrane receptor found on the surface of melanocytes, which binds steel factor. A functioning KIT receptor is required for the normal development and transport of melanocytes. The phenotype is variable depending on the location or type of mutation. For example, a milder phenotype may be seen when mutations occur in the ligand-binding region, whereas a more severe phenotype may be seen when mutations occur in the tyrosine kinase receptor region of the receptor.2 A variety of mutations have been reported including point mutations, deletions, splice mutations, and insertions in the KIT gene.3,4 This mutation affects the development of melanocytes, both before melanoblast migration from the neural crest and postnatally, preventing melanoblast migration from the dorsally located neural crest cells (neck to posterior end) to the ventral surface of the body (forehead, abdomen, pretibial legs). Recently, a heterozygous deletion of SNAI2 gene has also been reported to cause piebaldism.1 SNAI2 gene also encodes a transcription factor necessary for normal melanocyte development.1 Clinically, piebaldism presents at birth with depigmented patches on the anterior midline body. The most common locations are the central anterior trunk, the mid-extremities, the central forehead, and the midline frontal scalp characterized by the white forelock.1 A white forelock is seen in 80% to 90% of persons with piebaldism, and is triangular or diamond-shaped.1 The skin underlying the forelock is completely amelanotic. The forelock may extend as far posteriorly as the vertex and as far anteriorly as the root of the nose, although extension to the nose has been rarely reported.1 Poliosis (white hairs) of the eyebrows and eyelashes is common.1

A distinctive feature of piebaldism is the presence of normally pigmented and hyperpigmented macules within the depigmented patches.2 These macules may range in diameter from a few millimeters to several centimeters.1 The depigmented areas are irregularly shaped, well-circumscribed, and milk-white in color.1 Both the white forelock and the areas of leukoderma are present at birth and remain static over time. The exceptions to the relatively static nature of these lesions are the rare reports of spontaneous repigmentation, especially after injury.2 The diagnosis of piebaldism is made clinically. However, if a skin biopsy is performed, the most notable finding is the complete absence of melanocytes in the depigmented area.2 The histopathologic findings of the hyperpigmented macules are notable for an increased number of melanosomes in melanocytes and keratinocytes.1 Electron microscopy also demonstrates the absence of melanocytes.1 Gene mutation analysis is available but is not routinely performed as the clinical findings are relatively diagnostic. Although the clinical findings of piebaldism are unique, the differential diagnosis of this condition includes vitiligo, halo nevus, and other genodermatoses with poliosis. Vitiligo is a common, acquired, automimmune condition resulting in depigmented macules and patches. Piebaldism often can be readily distinguished from vitiligo because of the presence of hyperpigmented and normally pig-

A white forelock is seen in 80% to 90% of persons with piebaldism, and is triangular or diamond-shaped. mented macules within areas of leukoderma in piebaldism. However, when vitiligo repigments, it begins from stem cells within the hair follicle, such that round, skin-colored macules develop within the patch of vitiligo in a follicular distribution. Features helpful in distinguishing repigmenting vitiligo from piebaldism are the time of onset, the natural history, and the location of the depigmented lesions. The depigmented patches of piebaldism are always present at birth, whereas vitiligo develops any time from shortly after birth to late adulthood.1 The areas of leukoderma in piebaldism are stable, with no growth or development of new lesions. In contrast, depigmented areas in vitiligo enlarge with time, and it is common for patients to develop new areas of involvement. Lastly, due to the pattern of melanoblast migration in utero, the leukodermic areas

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of piebaldism are restricted to the anterior midline body, most commonly the midline frontal scalp, abdomen, and pre-tibial legs. In contrast, vitiligo has no such restriction and can appear anywhere on the body, with predilection for the face, dorsal hands, nipples, axillae, umbilicus, and the sacral, inguinal, and anogenital regions.1 Rarely, piebaldism presents with only the white forelock. For an isolated circumscribed area of poliosis, the differential diagnosis includes halo nevus, vitiligo, and alopecia areata. The onset at birth and midline frontal location of the white forelock helps distinguish piebaldism from these other acquired conditions. In addition, alopecia areata will be preceded by a circumscribed area of complete hair loss preceding the onset of poliosis. Many other syndromes can present with a circumscribed area of poliosis; however these syndromes have systemic findings, whereas piebaldism is restricted to skin and hair involvement. Like piebaldism, Waardenburg syndrome can also present with a white forelock on the midline frontal scalp. However, patients with Waardenburg syndrome will also present with any combination of the following features: congenital deafness, partial or total heterochromia iridis, medial eyebrow hyperplasia, and broad nasal root.1 Similarly, Vogt-Koyanagi-Harada syndrome, Alezzandrini syndrome, white forelock with osteopathia striata, and white forelock with multiple malformations will present with various ophthalmologic, neurologic, skeletal, and cardiopulmonary findings, which piebaldism lacks. As piebaldism is restricted to the skin and hair, the prognosis is excellent. Patients must be educated regarding good sun protection and sun avoidance to prevent sunburns in affected areas. Interventions are only necessary if patients are distressed by their cosmetic appearance. As no effective therapies exist, self-tanners and camouflage makeup (i.e., Dermablend or Covermark) are first-line treatments.5 There have been reports of autografts of normal skin into amelanotic areas, but this is not a readily available treatment option and requires multiple procedures.1 The patient and his family were already aware of the diagnosis as other family members had the same genetic condition. However, a genetics referral was placed for counseling purposes. Dr. Chan is a third-year dermatology resident at Baylor College of Medicine in Houston. References 1. Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. St. Louis, Mo.: Elsevier-Mosby; 2008:922-923.

2. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, Pa.: Saunders Elsevier; 2011:861-862. 3. Agarwal S, Ojha A. Piebaldism: a brief report and review of the literature. Indian Dermatol Online J. 2012;3(2):144-147. Available at http://www. idoj.in/temp/IndianDermatolOnlineJ32144-7589397_210453.pdf; accessed April 15, 2014. 4. Richards KA, Fukai K, Oiso N, Paller AS. A novel KIT mutation results in piebaldism with progressive depigmentation. J Am Acad Dermatol. 2001;44(2):288–292. 5. Suga, Y, Ikejima A, Matsuba, S, Ogawa H. Medical pearl: DHA application for camouflaging segmental vitiligo and piebald lesions. J Am Acad Dermatol. 2002;47(3):436-438.

CASE #2

Miliaria crystallina

Miliaria crystallina, the mildest form of so-called heat rash, is one of three variants of miliaria. All three variants—miliaria crystallina, miliaria rubra, and miliaria profunda—occur due to obstruction of eccrine sweat glands, most frequently resulting from increased temperature, either exogenous or endogenous. Miliaria has a propensity to occur on the forehead, neck, upper trunk, and any occluded areas. Classically, miliaria occurs in children in warm climates, particularly in the newborn period.1-3 More specifically, miliaria cystallina often present at birth, and its etiology is explained by obstruction of the eccrine sweat duct at the level of the stratum corneum. Its superficial involvement of the epidermis results in the clinical presentation of clear, “dewdrop”-like vesicles in the absence of erythema.1 In contrast, miliaria rubra, often referred to as “prickly heat,” is caused by occlusion of eccrine sweat glands at the level of the mid-epidermis, resulting in pruritic, red papules of 1 mm to 3 mm on the neck and upper trunk. The involved sweat ducts rupture and leak sweat into surrounding tissues, inducing an inflammatory response.1,2 Of note, there is a variant of miliaria rubra called miliaria pustulosa, which is usually sterile on cultures but can become secondarily infected with bacteria. An even rarer variant of miliaria known as miliaria profunda involves the

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Dermatology Clinic

dermal-epidermal junction and presents as non-pruritic white papules of 1 mm to 3 mm on the trunk and proximal extremities. This variant is found more commonly in adults in hot climates, often in coexistence with miliaria rubra.1 Miliaria is a common condition, particularly among newborns in warm climates. Both miliaria crystallina and miliaria rubra are observed in up to 15% of newborns, typically in the setting of excessive warming inside an incubator, overswaddling, fever, or occlusive dressings.1 Miliaria crystallina presents as nonpruritic clear, fragile, 1-mm vesicles. Although the classic patient population consists of neonates younger than age two weeks, miliaria crystallina also can occur among persons in ICUs who are intubated and sedated for many weeks. Often these patients have such endogenous factors as high fevers and such exogenous factors as warm rooms and occlusion with blankets and clothing that contribute to eccrine duct obstruction. Miliaria crystallina is associated with no racial or sex predisposition. Despite the fact that miliaria crystallina also is not associated with any underlying systemic disease, instituting treatment in these patients is still important when large numbers of sweat glands become occluded and nonfunctional, as these patients may lose the ability for thermoregulation, leading to a compensatory hyperhidrosis of the face. These patients may also exhibit axillary and inguinal lymphadenopathy that will resolve with resolution of the miliaria.1,2 Diagnosis of miliaria crystallina, as with the other miliaria variants, usually is quite apparent due to its classic clinical presentation. The superficial-appearing clear vesicles are quite unique to miliaria crystallina. Puncturing a vesicle with a fine needle—an easy and simple diagnostic test— releases trapped clear sweat. A biopsy is neither necessary nor recommended. On pathology, the specimen should demonstrate ductal blockage at the appropriate level, the stratum corneum.1 There typically is no dermal inflammation in miliaria crystallina. While the diagnosis for miliaria crystallina is very unique, the diagnosis for miliaria rubra may be less straightforward. Differential diagnosis in neonates would include erythema toxicum neonatorum, neonatal cephalic pustulosis, candidiasis, and in atypical and rarer cases, other vesiculopustular diseases of the newborn. The differential diagnosis for adults includes folliculitis, candidiasis, and Grover’s disease.1 If a biopsy of miliaria rubra is performed, histology will show sweat duct occlusion at the mid-epidermis or spinous layer with perivascular lymphocytic infiltrates and vasodilation. An eosinophilic cast may be seen in miliaria profunda with occlusion at the deepest level, the dermal-epidermal junction.1,2

As with the other miliaria variants, treatment for miliaria crystallina involves placing the patient in a cool environment—as we recommended for our patient—to decrease sweating. Using a fan and ice packs, avoiding occlusion and heavy blankets, and treating high fevers will resolve the miliaria. Eventually, the obstructed eccrine ducts will shed their occluding keratinous plug, and the patient should sweat normally. The vesicles in miliaria crystallina should resolve very quickly, within approximately one week. Usually, no other treatments are necessary. Keeping the patient from overheating is the mainstay of prevention.1,2 Topical medication such as corticosteroids, antibiotics, and retinoids have been advocated but typically are not recommended for miliaria crystallina. However, these agents may provide symptomatic relief for patients with miliaria rubra and miliaria profunda. Anhydrous lanolin and istotretinoin also have been reported as effective treatments for miliaria profunda.1,2 ■ Dr. Shih is a resident physician at the University of Minnesota in Minneapolis. References 1. Bolognia JL, Jorizzo JL, Schaffer JV, eds. f Dermatology. 3rd ed. Philadelphia, Pa.: Mosby Elsevier; 2012:528-529, 596-597. 2. James WD, Berger TG, Elston D. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, Pa.: Saunders Elsevier; 2011:19-20. 3. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. Philadelphia, Pa.: Mosby Elsevier; 2009:263.

“It’ll never work. You’re a dog person and I’m a cat person.”

CME CE

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CME CE

Dermatologic Look-Alikes n LEARNING OBJECTIVE: To distinguish and properly treat dermatologic conditions with similar presentations. n COMPLETE THE POSTTEST: Page 83

n ADDITIONAL CME/CE: Pages 59, 75

Turn to page 74 for additional information on this month’s CME/CE courses.

Oral hyperpigmentation DAMJAN JUTRIC AND KERRI ROBBINS, MD

CASE #1

CASE #2

A 13-year-old male presented to the dermatology clinic because of brown spots. The lesions were asymptomatic and had been present since early childhood. No prior treatment had been initiated. Physical examination revealed brown macules on the lips and the anogenital region, within the oral cavity, and on bilateral dorsal hands. The patient had no significant medical history and was not taking any medications. Review of systems was positive for abdominal pain. On further questioning, the patient’s mother stated that she had a similar distribution of lentigines since childhood and a history of gastrointestinal and breast cancers.

A 41-year old female presented to the dermatology clinic complaining of brown spots on the lips and within the oral cavity. The lesions, which were asymptomatic, had been present for one year. The patient was currently being seen by a primary-care physician for hypotension as well as complaints of fatigue, nausea, and depression. On physical examination, brown macules were noted on the lips and within the oral cavity. The woman also had diffuse hyperpigmentation of the face, neck, upper chest, and bilateral upper extremities. No family members had similar hyperpigmentation and she denied recent sun exposure or use of tanning products.

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CME CE

CASE #1

Dermatologic Look-Alikes

Peutz-Jeghers syndrome

Peutz-Jeghers syndrome (PJS) is characterized by mucocutaneous lentigines, hamartomatous polyposis, and an increased risk of visceral malignancy. The first documented record of the condition appeared in 1896, when John McHutchinson described a set of identical twins with oral and labial pigmentation who died from intussusception and breast cancer. In 1921, Jan Peutz, a Dutch physician, first described the relationship between mucocutaneous lentigines and intestinal polyps in a Dutch family.1 It wasn’t until 1949 that Harol Jeghers, an American physician, recognized the relationship between the mucocutaneous lentigines and generalized intestinal polyposis.2 In 1954, Andre J. Bruwer introduced the eponym Peutz-Jeghers syndrome.3 PJS is an autosomal dominant disorder that is primarily caused by mutations in the STK11 gene (also known as LKB1) on chromosome 19p13.3, which codes for a serine/threonine kinase. The prevalence is thought to be approximately 1 in 100,000 to 200,000 births. The diagnosis requires the presence of histopathologically confirmed hamartomatous polyps and at least two out of three additional criteria, including mucocutaneous pigmentation, a specific type of gastrointestinal (GI) polyp, and a family history of PJS.

Patients with Peutz-Jeghers syndrome should undergo frequent endoscopic surveillance for removal of polyps. Clinically, 95% of patients with PJS present with light brown to black homogenous pigmented macules, 1 mm to 5 mm in size, which usually develop during childhood. The pigmented macules are normally perioral, periorbital, in the anogenital region, and/or on the ventral aspect of the hands and feet. Pigmentation may also occur in the oral cavity, and these lesions primarily affect the vermilion zone, the labial and buccal mucosa, and the tongue. Fading of the lentigines can occur following puberty, but the oral-buccal mucosal pigmentation tends to be permanent. Patients with PJS are at increased risk of malignancies including GI, pancreatic, breast, uterine, cervical, and

testicular malignancies. The lifetime risk of persons with PJS developing any cancer by age 70 years has been estimated to be 85% to 90%.4,5 A specific type of GI polyp, which may be found throughout the GI tract but is seen most commonly in the small intestine and colon, usually develops in early adolescence among persons with PJS. These polyps may result in abdominal pain, bleeding, obstruction, or intussusception. Persons with PJS as well as any of their relatives who also may be afflicted with the disease should undergo frequent endoscopic surveillance for removal of polyps throughout the GI tract and should be screened for extraintestinal cancers.6 Histologically in PJS, the epidermal basal cell layer shows marked hyperpigmentation, representing increased melanin production. At first glance, it may appear as if the number of melanocytes is also increased. However, DOPA-stained sections have shown that there is no increase in the number of melanocytes. The main diagnosis in the differential is Laugier-Hunziker syndrome. Laugier-Hunziker is a sporadic disorder, with only one familial case described.7 Patients most commonly present with pigmentation that arises on the lips and oral mucosa. The anogenital region and hands are less frequently affected. One distinguishing feature is that approximately half of patients have melanonychia striata of their nails. Another distinguishing feature is that patients tend to present at a mean age of 50 years. The familial history, age at presentation, and presence or absence of melanonychia striata is helpful in distinguishing between the two disorders. Other disorders to be considered in the differential diagnosis include causes of primary adrenocortical insufficiency, such as Addison disease. Patients with Addison disease may develop hyperpigmented macules on the oral mucosa, but the condition is also accompanied by systemic symptoms such as fatigue, weight loss, hypertension, and GI changes. Drug-induced pigmentation, smoker’s melanosis, blue nevus, pigmentation by foreign bodies, melanocytic nevus, oral melanoma, and idiopathic racial or ethnic melanosis should also be considered in the differential diagnosis of oral pigmented lesions. Other disorders associated with multiple lentigines include Bandler syndrome, Cantú, PTEN generelated disorders, centrofacial lentiginosis, inherited patterned lentiginosis, Cronkhite-Canada syndrome, Carney complex, and LEOPARD syndrome. No treatment is necessary for the mucocutaneous lesions unless they appear clinically atypical, at which point a biopsy should be considered to rule out malignancy. Fading of the lentigines may occur with time. Cover-up cosmetics

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may be appropriate if the patient is cosmetically bothered. Another option for treatment includes cryosurgery, or laser therapy with the Nd:YAG or Q-switched alexandrite lasers. Unfortunately, recurrence may occur after treatment. Patients should be encouraged to avoid sun exposure. Due to the increased risk of visceral malignancy among people with PJS, surveillance should begin in childhood because of a tendency for the polyps to cause abdominal pain, bleeding, obstruction, or intussusception. Regular screening for other visceral malignancies should also be routinely performed. Genetic counseling may also be recommended if the patient is planning on having children and/or has a family history of the disorder. The patient in this case was not cosmetically bothered by the mucocuatneous lesions. He was seen by gastroenterology and was found to have the classic polyps of PJS but no evidence of malignancy. He continues to undergo regular screening for gastrointestinal and extraintestinal malignancies.

CASE #2

Addison disease

Addison disease, also known as hypoadrenocorticism, was named after its founder, an English physician by the name of Thomas Addison. He first described the disease in a paper he wrote in 1855, On the Constitutional and Local Effects of Disease of the SupraRenal Capsules.8 Addison disease affects 50 out of every 1 million individuals in the United States. It has no racial predilection. However, females are affected more than males, which is thought to be due to the disease’s autoimmune nature. Typical onset ranges from age 30 years to age 50 years. Addison disease is an insufficiency of the adrenal gland more specifically, the adrenal cortex. The adrenal glands are located on top of the kidneys and are composed of the medulla (inner portion) and cortex (outer portion). The cortex is itself broken up into three different zones: zona glomerulosa, zona fasciculata, and zona reticularis. In combination, these three zones produce approximately 50 different steroid hormones including cortisol, aldosterone, and testosterone. When the body undergoes stress it has a

great need for cortisol, a glucocorticoid produced by zona glomerulosa. Cortisol is considered the stress hormone and raises blood glucose and blood pressure to help the body adapt. However, too much cortisol can also have detrimental effects.

Plasma ACTH levels are elevated in primary Addison disease and suppressed in secondary Addison disease. The production and release of cortisol and other hormones produced by the adrenal gland are controlled by an axis composed of the hypothalamus, the pituitary gland, and the adrenal gland (HPA axis). When an individual undergoes physical stress, the hypothalamus releases corticotropinreleasing hormone (CRH). This hormone stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH then enters the bloodstream and signals the adrenal gland to produce and release its hormones, including cortisol. Once enough cortisol has been released, a negative feedback inhibition causes the pituitary gland to stop releasing ACTH and then informs the hypothalamus to stop releasing CRH. As stated earlier, Addison disease is an insufficiency of the adrenal gland, and the causes may be either primary or secondary. Primary Addison disease is the destruction or dysfunction of 90% of the adrenal gland by autoimmune diseases (most common), infections (such as tuberculosis and deep fungal infections), metastatic tumors, sarcoidosis, hemochromatosis, or amyloidosis.9 Secondary Addison disease is caused by insufficient ACTH release by the pituitary gland. This may occur due to pituitary gland surgery, injury, or exogenous steroid usage. Plasma ACTH levels are elevated in primary Addison disease and suppressed in secondary Addison disease. Patients suffering from primary Addison disease will experience a sinister onset of fatigue, sluggishness, irritability, depression, weakness, and hypotension as a result of decreased levels of adrenal hormones. Oral mucosa changes may be the first presenting sign of the disease and manifest as a diffuse or patchy brown macular pigmentation due to excessive melanin production. Hyperpigmentation may occur anywhere, but most commonly occurs on the vermilion border, ventral tongue, and buccal mucosa. The hyperpigmentation occurs because ACTH and melanocytestimulating hormone (MSH) share a precursor molecule

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Dermatologic Look-Alikes

called proopiomelanocortin (POMC). Thus, high levels of ACTH cause high levels of MSH, which in turn causes melanocytes to overproduce melanin and cause hyperpigmentation. The hyperpigmentation is not just confined to the oral cavity: As time goes on, patients develop a generalized hyperpigmentation of the skin as well, which is classically known as bronzing. Hyperpigmentation is generally more prominent on the sun-exposed skin and at sites of trauma but may also occur on the axillae, perineum, nipples, palms, hair, and nails. Patients also may have such symptoms as GI upset, vomiting, diarrhea, weight loss, and a craving for salt. Histologically, Addison disease reveals increased amounts of melanin in the basilar and upper-spinous-layer keratinocytes. It is important to note that the number of melanocytes is not increased. Also, histologic findings are not sufficient for diagnosis in patients of color, as the findings simulate normal findings in darker-skinned individuals. Oral manifestations of Addison disease may mimic those of Peutz-Jeghers disease and Laugier-Hunziker syndrome. Drug-induced pigmentation, smoker’s melanosis, blue nevus, pigmentation by foreign bodies, melanocytic nevus, oral melanoma, and idiopathic racial or ethnic melanosis should also be considered in the differential diagnosis of oral pigmented lesions. Depending on the localization, diffuse hyperpigmentation may mimic acanthosis nigricans or melasma. The diagnosis of Addison disease is confirmed by an ACTH stimulation test. If cortisol levels are below 20 µg/ml, then the patient has adrenal insufficiency. Plasma ACTH levels will help to differentiate between primary and secondary Addison disease: Plasma ACTH levels above 100 ng/L indicate primary Addison disease. In patients with secondary Addison disease, ACTH levels will be low and hyperpigmentation will not be clinically evident. Treatment includes replacement of the missing adrenal hormones. Dosages of corticosteroids should be increased if the patient is undergoing a stressful event such as dental extractions, pregnancy, or invasive procedures. After replacing the missing adrenal hormones, ACTH levels should normalize and over time, the bronzed skin may return to its natural color. Prognosis is good with hormone replacement therapy and patient compliance. However, if Addison disease is not recognized promptly, death may occur in a relatively short period of time. This patient was found to have primary Addison disease due to autoimmune destruction. She was treated with corticosteroid replacement therapy and the skin pigmentation was improving upon follow-up. ■

Mr. Jutric is a third-year dental student at The University of Texas School of Dentistry in Houston. Dr. Robbins is an instructor in the Department of Dermatology at Baylor College of Medicine in Houston. References 1. Peutz JLA. A very remarkable case of familial polyposis of mucous membrane of intestinal tract and nasopharynx accompanied by peculiar pigmentations of skin and mucous membrane. Nederl Maandschr Geneesk. 1921;10:134-46. Available at www.ncbi.nlm.nih.gov/books/NBK7027/. 2.Jeghers H, McKusick VA, Katz KH. Generalized intestinal polyposis and melanin spots of the oral mucosa, lips, and digits; a syndrome of diagnostic significance. N Engl J Med. 1949;241(25):993-1005. 3. Bruwer A, Bargen JA, Kierland RR. Surface pigmentation and generalized intestinal polyposis; (Peutz-Jeghers syndrome). Proc Staff Meet Mayo Clin. 1954;29(6):168-171. 4. Van Lier MG, Wagner A, Mathus-Vliegen EM, et al. High cancer risk in Peutz-Jeghers syndrome: a systematic review and surveillance recommendations. Am J Gastroenterol. 2010;105(6):1258-1264. 5. Giardiello FM, Trimbath JD. Peutz-Jeghers syndrome and management recommendations. Clin Gastroenterol Hepatol. 2006;4(4):408-415. Available at www.cghjournal.org/article/S1542-3565%2805%2901093-1/fulltext. 6. Stoffel EM, Kastrinos F. Familial colorectal cancer, beyond Lynch syndrome. Clin Gastroenterol Hepatol. [2013 Aug. 17; Epub ahead of print.] 7. Makhoul EN, Ayoub NM, Helou JF, Abadjian GA. Familial Laugier-Hunziker syndrome. J Am Acad Dermatol. 2003;49(2 Suppl Case Reports):S143-145. 8. Addison T. On the Constitutional and Local Effects of Disease of the Suprarenal Capsules. London, UK: Samuel Highley;1855. 9. Napier C, Pearce SH. Autoimmune Addison’s disease. Presse Med. 2012;41(12 P 2):e626-635. All electronic documents accessed April 15, 2014.

“Well, well, well—look who brought a taco to a burrito fight.”

CME CE

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POSTTEST Expiration date: May 2015

Physician Credit This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of Medical Education Resources (MER) and Haymarket Medical. MER is accredited by the ACCME to provide continuing medical education for physicians. Credit Designation Medical Education Resources designates this enduring material for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. American Academy of Physician Assistants AAPA accepts cer tificates of par ticipation for educational activities cer tified for

Category I credit from AOACCME, prescribed credit from AAFP and AMA PRA Category 1 Credit™ from organizations accredited by ACCME or a recognized state medical society. Physician assistants may receive a maximum of 1 hour of Category I credit for completing this program. Nursing Credit Medical Education Resources is accredited as a provider of continuing nursing education by the American Nur ses Credentialing Center’s Commission on Accreditation. This CE activity provides 1 contact hour of continuing nursing education. Medical Education Resources is a provider of continuing nursing education by the California Board of Registered Nursing, Provider #CEP 12299, for 1 contact hour.

CREDITS: 0.5

Feature

Dermatology Clinic

Dermatologic Look-Alikes

page 59

page 75

page 79

1. An 18-month-old child has had a harsh, barky or “seal-like” cough for the past week. What is the most likely etiologic agent? a. Rhinovirus b. Haemophilus influenzae c. Parainfluenza d. Streptococcus pneumoniae

Case #1

1. When do the depigmented lesions of piebaldism develop? a. Present at birth b. During adolescence c. Third or fourth decade d. Late adulthood

1. What feature of Laugier-Hunziker distinguishes it from Peutz-Jeghers syndrome? a. Vermilion zone primarily affected b. A strongly positive family history c. Melanonychia striata of the nails d. Development during childhood

2. Lack of restriction of leukodermic areas can distinguish piebaldism from a. Tinea versicolor b. Albinism c. Halo nevus d. Vitiligo

2. What information should be provided to a patient with Peutz-Jeghers syndrome? a. Lesions should be biopsied once a year. b. Laser therapy can provide definitive treatment. c. Sun exposure may lighten lesions. d. Regular screening for visceral malignancies is recommended.

2. Which group of children should receive prophylaxis during the respiratory syncytial virus (RSV) season? a. Infants born at less than 35 weeks b. Children born with congenital airway abnormalities c. Children younger than age two years with congenital heart disease d. All of the above 3. What is the first-line treatment for acute asthma? a. Salmeterol c. Dexamethasone b. Albuterol d Terbutaline 4. What is the gold standard for pertussis diagnosis? a. Nasopharyngeal culture b. Clinical presentation c. PCR amplification d. Chest x-ray TO TAKE THE POSTTEST please go to CliniAd.com/1megFJz

Case #2 3. What is the clinical appearance of miliaria crystallina? a. Pruritic, red papules 1 mm to 3 mm b. Clear, “dewdrop”-like vesicles in the absence of erythema c. Localized erythema with well-defined margins and satellite lesions d. Nonpruritic white papules on the trunk and proximal extremities 4. What’s effective treatment for miliaria profunda? a. Penicillin c. Istotretinoin b. Fluconazole d. Tetracycline

Case #2 3. What is the most common cause of primary Addison disease? a. Autoimmune disease b. Sarcoidosis c. Metastatic tumors d. Hemochromatosis 4. How is the diagnosis of Addison disease confirmed? a. Serum cortisol concentration b. ACTH stimulation test c. Antiadrenal antibodies d. Insulin-tolerance test

TO TAKE THE POSTTEST please go to CliniAd.com/1km7Yxa

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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 a staff clinician at the VA Hospital in Kansas City, Mo., where she practices adult medicine and women’s health. She also teaches at the nursing schools of the University of Missouri and the University of Kansas.

Activated charcoal

Say the word “charcoal” to almost any American and the immediate mental image will be steaks on a grill. However, say that same word in an emergency department and the image will be drastically different: A squeeze bottle of a black, thick solution; a nasogastric tube, and either a combative patient or an unconscious one will be the scenario. The use of activated charcoal in acute poisoning is an age-old practice dating back as far as as 1500 B.C.1

Background Medicinal activated charcoal is available in many different forms. It is a carbon molecular structure made from a variety of inert materials that have been treated with intense heat and oxygen, making it “activated.”1 This process yields a highly porous particle. It is estimated that a teaspoon of activated charcoal has a surface area of nearly 10,000 square feet.1

Science The utility of activated charcoal in the treatment of acute poisoning and overdose is well-established. When administered orally, the porous particles selectively bind to (absorb) the toxic chemical. This carbon/toxin complex then passes out of the body intact. When given appropriately, activated charcoal absorbs up to 60% of the chemical toxins it encounters. The provider must understand, however, that this complex is unstable and can reverse over time. Consequently,

a cathartic such as sorbitol is frequently coadministered to speed gastric emptying.2,3 Once the absorptive capacity of activated charcoal was established, investigators studied the possibility of using this substance to absorb other undesirable compounds in the body, such as cholesterol. One active control trial compared the efficacy of cholestyramine (Locholest, Prevalite, Questran) and activated charcoal in six patients with known hyperlipidemia.4 After a one-week dietary control, the patients were given three weeks of each treatment on widely separate occasions. Activated charcoal reduced plasma cholesterol levels by an average of 5% more than did the cholestyramine. Since that time, however, more rigorous trials have failed to show any favorable difference between the two therapies. Another area of research for activated charcoal is the management of intestinal flatus. Since the deodorant action of charcoal was already accepted, researchers explored whether the ingestion of activated charcoal, either routinely or with a known gas-inducing meal, would reduce this common

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ALTERNATIVE MEDS UPDATE problem. Small-scale human trials failed to show appreciable reduction in sulfuric intestinal gases.5 Patients with irritable bowel syndrome also complain of bloating and large amounts of gas, but ingestion of activated charcoal has not proven useful in this population.6 Researchers experimenting with charcoal-impregnated undergarments in patients with excess flatus found that the only efficacious design was a brief with a middle layer of charcoal; this garment reduced odor by up to 75%.7 Activated charcoal is also widely used in water purification. For decades, the process of passing water through progressively fine-particle layers of charcoal was known not only to remove particulate matter but also to dissolve contaminants. This knowledge then became part of standardized water purification for medical uses such as hemodialysis.8 The typical hemodialysis patient is exposed to more than 300 liters of water in one week. The water passes through the dialyzer cartridge, which is composed of multiple nonselective membrane fibers. Although this procedure has improved dramatically in the last two to three decades, the purity of the water is imperative, since contaminants can pass directly into the bloodstream. Consequently, the Association for the Advancement of Medical Instrumentation (www.aami.org) established standards for water purity that are also required by the Centers for Medicare & Medicaid Services.9 These approved standards rely heavily on activated charcoal for adequate water purification.

tetracycline (Sumycin), and anticonvulsants are among the medications that can be rendered inactive by binding with charcoal. Routine use in young children is not recommended.

Summary

Activated charcoal did not appreciably reduce sulfuric intestinal gases.

There are several types of medications that can be rendered inactive by binding with charcoal.

Safety, cost, how supplied

The use of activated charcoal is not mainstream medicine. However, activated charcoal is a relatively benign product and certainly one that has withstood the test of time. With its relatively low risk profile, using this substance would be a neutral decision. No well-done clinical trials validate significant health benefits, but the results are not negative. Patients who feel that activated charcoal is helpful should be advised to avoid using it with other medications. n References 1. Activated charcoal. In: Jellin JM, ed. Nautral Medicines Comprehensive Database. Stockton, Calif.: Therapeutic Research Faculty (naturaldatabase.therapeuticresearch.com). 2. Bond GR. The role of activated charcoal and gastric emptying in gastrointestinal decontamination: a state-of-the-art review. Ann. Emerg Med. 2002;39(3):273-286. 3. Isbister GK and Kumar VV. Indications for single-dose activated charcoal administration in acute overdose. Curr Opin Crit Care. 2011;17(4): 351-357. 4. Park GD, Spector R, Kitt TM. Superactivated charcoal versus cholestyramine for cholesterol lowering: a randomized cross-over trial. J Clin Pharmacol. 1988;28(5):416-419. 5. Suarez FL, Furne J, Springfield J, Levitt MD. Failure of activated charcoal to reduce the release of gases produced by the colonic flora. Am J Gastroenterol.1999;94(1):208-212. 6. Whorwell PJ. The problem of gas in irritable bowel syndrome. Am J Gastroenterol. 2000;95(7):1618-1619.Available at www.ibs-care.org/pdfs/ref_085.pdf. 7. Ohge H, Furne JK, Springfield J, et al. Effectiveness of devices purported to reduce flatus odor. Am J Gastroenterol. 2005;100(2):397-400. 8. Azar AT, Ahmad S. Hemodialysis water treatment system. Studies in Computational Intelligence. 2013;404:347-378. 9. Coulliette AD, Arduino MJ. Hemodialysis and water quality. Semin Dial. 2013;26(4):427–438. 10. Mayo Clinic. Charcoal, activated (oral route). Available at www.mayoclinic.org/drugs-supplements/charcoal-activated. All electronic documents accessed April 15, 2014.

Activated charcoal is readily available at health-food stores and in general retail settings. The supplement is usually found as capsules filled with the fine powder. A usual capsule ranges from 500 mg to 600 mg and may be used one or two times daily.10 A bottle of 100 capsules costs about $10. Many natural-based products such as toothpaste also contain activated charcoal for its odor-neutralization action and possible enamel-whitening action. Significant adverse reactions are rare, but users should be advised that their stools will be black. The main consideration is the concomitant consumption of a charcoal supplement and various medications; acetaminophen, oral contraceptives, 86 THE CLINICAL ADVISOR • MAY 2014 • www.ClinicalAdvisor.com

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COMMENTARY Debra Clements Coats, RN, BSN, MSN, FNP-BC, is employed with Matrix Medical Network and with an infectious-disease practice in Greensburg, Pa.

End-of-life talks in primary care The most difficult, ethically driven conversation we have with our patients comes when the word “dying” becomes the focus of the discussion. Where to begin? Do I tell them everything? What if they ask me, “How long do I have to live?” Am I going to take away their hope? These are just a few of the questions that we, as practitioners, agonize over when we have to discuss end-of-life issues. We usually think of such conversations as only taking place in hospitals, but nurse practitioners and physician assistants in primary-care offices are faced with these discussions as well. Primary-care practitioners often have a long-established relationship with their

Knowing what the patient values most is crucial to creating a tailored end-of-life care plan..

patients and have become trusted allies in the patient’s health-care decisions. Having such a relationship with a person who is dying or who has a heightened mortality risk will help us find the best way to broach the topic, identify individuals in the patient’s life who need to be involved in the end-of-life discussion, and work with the patient and family to develop the most appropriate, individualized end-oflife plan of care. The April 2014 issue of the Canadian Medical Association’s CMAJ journal carries a “conversation guide” entitled “Just ask: discussing goals of care with patients in hospital with serious illness,” by John J. You, of McMaster University in Hamilton, Ontario, Canada, and others on behalf of the Canadian Researchers at the End of Life Network (CMAJ. 2014;186[6]:425-432). A press release from the university describing the guide outlined steps that can also be taken in the primary-care setting, such as identifying high-risk patients—a process that begins when treatment options have been exhausted or are few and failing. Another step is that of communicating the prognosis. In my view, this needs to be a faceto-face discussion in the clinician’s office, not in the exam room, with a large block of time set aside for the conversation. Speak in layman’s terms and be straightforward and honest, but also compassionate.

A third measure involves clarifying patient values around the care plan. Ask the patient such open-ended questions as: • “What concerns you most about your illness or end-of-life care?” • “Is faith important to you?” • “Is there still something you want to do?” Determining what the patient values most in his or her end-of-life decisions is crucial to creating a tailored care plan. Be sure to involve substitute decision-makers in the planning process as well—those who might make decisions if the patient cannot. Input from social workers and hospice staff can be invaluable at this juncture. The patient will need to engage in estate planning, make advance directives, create a living will, and register his or her resuscitation orders. The existence of these documents helps to ensure that the patient’s desired end-of-life experience is honored, and makes a difficult situation easier on loved ones. These components of end-of-life discussions are just the tip of the iceberg. Patients will look to you to guide them through the dying process. You as well as your patients may wish to consult end-of-life discussion recommendations offered by the National Library of Medicine (www. nlm.nih.gov), the American Cancer Society (www.cancer.org), and the Family Caregiver Alliance (www.caregiver.org). n

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