May 2016 Clinical Advisor

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

■ CDC: Zika virus update ■ Diabetes drug warning ■ Preventive aspirin therapy FEATURE Improving Health Literacy

An intervention strategy LEGAL ADVISOR

HIPAA Privacy Rule

■ Dermatology Clinic

AN ITCHY RASH ON THE FEET PAGE 75

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■ Featured Course

HYPERTENSION IN THE ELDERLY PAGE 52 Where do you rank in our annual SALARY SURVEY? Turn to page 66 for all the results.

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OSTEOARTHRITIS An X-ray of the knee, showing severe osteoarthritis.

Editor Colby Stong, editor@ClinicalAdvisor.com Senior editor Sandhya George Associate digital content editor Hannah Dellabella Assistant editor Lauren Biscaldi 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; Ann Walsh, PA-C, SCT(ASCP); Kim Zuber, PA-C Production editor Kim Daigneau Group art director, Haymarket Medical Jennifer Dvoretz Production director Ada Figueroa Circulation manager Paul Silver National accounts manager Alison McCauley, 973.224.6414 alison.mccauley @ haymarketmedical.com Publisher Kathleen Hiltz, 201.774.1078 kathleen.hiltz@haymarketmedia.com Editorial director Kathleen Walsh Tulley Senior vice president, digital products and medical magazines Jim Burke, RPh Senior vice president, medical 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.

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EXPERTS If a patient has you stumped, write us and we’ll forward your query to one of our consultants and publish the response in Advisor Forum.You can also use this space to contribute a clinical pearl of your own or comment on another letter.

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

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

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

AVOIDING LABELING PATIENTS AS NONCOMPLIANT Sam Mbugua, MD, wrote about using analogies for education [Advisor Forum, Dec. 2015, p. 54]. I agree that teaching requires visual aids and any other method of teaching and learning that can be used to convey a point of understanding. However, he starts his comment with the word “noncompliance.” Really? I was told in my masters program in the 1980s to never label a patient as noncompliant. My professors said that use of that word only indicates that you do not know why the patient is making the decision that he or she is making.

I work hard to educate patients, friends, and families, but if education, lecturing, and pushing information toward people changed behavior, we would not have any overweight healthcare personnel. All physicians and nurses would be

Advisor F orum

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

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

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

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

Houston. DFA APA, Fallin O’BRin Orange sBeach,

NY 10001 comments .You may Advisor, 114 West 26th to: com. If you contac Street, so by includiare writing in respont us by e-mail at editor 4th Floor, New se to a publish @clinicaladvi Letters are ng the number ed sor. in parent heses at letter, please indicat print the edited for length the and clarity. author e will be accept ’s name with The Clinical end of each item. the letter.

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Write us today.

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OXYGEN IN A PAT THERAPY IENT WIT When treati H EMPHYS setting who ng a patient with emph EMA requires increappears to be hypo ysema in the acute care xic, ased effort to breathe, short of breath, and be very caref ul before

Philip R.

Cohen, MD, is clinical associa te professo of dermat r ology, of Texas MedicaUniversity l Center, Houston.

60 THE CLINICAL

Deborah L. Cross, MPH, ANP-B

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

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SEND TO The Clinical Advisor 114 West 26th Street, 4th floor New York, NY 10001 AdvisorForum_

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Debra August

King, Ph is senior physicia D, PA, at New York-Pren assistant Hospital, New sbyterian York City.

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CONTENTS M AY 2 0 1 6

NEWS AND COMMENT

FEATURES

14 Newsline ■■The CDC issues a Zika virus update for pediatric healthcare providers.

■■Endometriosis is linked to a higher risk for heart disease.

■■The FDA issues a warning for two diabetes drugs that are linked to the risk of heart failure.

■■SSRIs and cardiovascular events— Is there a connection?

■■The USPSTF issues its final recommendations for aspirin therapy for preventing CVD and colorectal cancer.

■■The USPSTF recommends against screening for COPD in adults who are asymptomatic.

■■A Florida bill would allow NPs and PAs to prescribe controlled substances.

■■Survival is unimproved with deferred second defibrillation.

■■Stroke risk is reduced with the DASH diet.

■■Parental caffeine consumption is linked to an elevated risk of early miscarriage.

■■Vaccine refusal is a key factor in measles and pertussis incidence.

24 Conservative treatment options for osteoarthritis A number of treatment options can improve patients’ quality of life.

40 Pesticides and Parkinson’s Is pesticide exposure on the golf course linked to risk of Parkinson’s disease?

Diabetes drugs linked to heart failure 17

58 CME/CE Feature posttest 66 Salary Survey PulsePoint: Results from the 2016 Salary Survey.

Pesticides, Parkinson’s disease, and golf 40

114 ENDO Conference 2016 A roundup of news articles from the annual meeting of the Endocrine Society

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Follow us on Twitter @ClinicalAdvisor

110 Steps for improving health literacy Communicating well with your patients will lead to better provider/patient relationships, better health outcomes, and reduced healthcare disparities.

Continues on page 10

126 Commentary The words that we use and how we use them reflect what we think of ourselves.

MAKING CONTACT

52 CME/CE Adherence and hypertension in the geriatric patient Addressing factors that lead to a lack of adherence to antihypertensive therapy in elderly patients is crucial to improving outcomes.

A guide for improving health literacy 110

Like us on Facebook facebook.com/TheClinicalAdvisor

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Visit us on the web ClinicalAdvisor.com

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CONTENTS DEPARTMENTS

120 Legal Advisor Accessing a relative’s charts. HIPAA’s Privacy Rule can lead to confusion regarding who can access a patient’s medical records.

12

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

75

Dermatology Clinic ■ An itchy rash on the feet ■ Fine wrinkles on the neck, chest, axilla, and back

85

Dermatologic Look-Alikes Erythematous papules and plaques

90

Clinical Challenge An unusual cause of respiratory distress in an infant. A congenital condition is found in an infant with respiratory and gastrointestinal symptoms.

123 Alternative Meds Update Slippery elm. The slimy inner bark from this tree can function as an anti-inflammatory agent or serve as a nutritional substitute.

Zika virus: a clinical overview 107

100 Case Study Managing nephropathy in a patient with type 2 diabetes. An elderly man presents with albuminuria.

107 Stat Consult Zika virus

Legal Advisor: HIPAA’s Privacy Rule 120

ADVISOR FORUM 60

Your Comments ■ Readers weigh in on non-narcotic treatment options for patients with musculoskeletal pain.

■ Passing on full-practice authority

61

Clinical Pearls ■ Obtaining a urine specimen in a child ■ Clozapine use and neutropenia

61

Case Files ■ Salivary duct stone

HOW TO CONTACT US THE CLINIC

F O RU M

E

FEATUR E

Improvin

g Health

An inter vent

Literacy

ion strategy

LEGAL ADV

HIPAA Priva

ISOR

cy Rule

FOR NU R S E P R AC TIT

IONERS

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dvisor.com

CONSER VATIVE TR EATMEN T FOR

OSTEOAR THRITIS An X-ray of the knee showing seve , osteoarthritire s.

■ Dermatolo gy Clinic

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

AN ITCHY THE FEET RASH ON PAGE 75

✶ FREE CE COURSE

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■ Featured

19, NUMB ER 5

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VIEWED

■ CDC: Zika virus update ■ Diabetes drug warning ■ Preventiv e aspirin ther apy

TO SUBMIT A CLINICAL QUESTION FOR PUBLICATION: • www.ClinicalAdvisor.com/AdvisorForum

• Mail it to The Clinical Advisor, 114 W. 26th St., 4th Floor, New York, NY 10001

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HYPERTENSse THE ELDERLION IN Y PAGE 52 Where do you rank in our annual SAL Turn to page ARY SURVEY? 66 for

all the result s.

4/25/16 4:05 PM

EXCLUSIVE TO THE WEB AT

ClinicalAdvisor.com Web Exclusives

Multimedia

ClinicalAdvisor.com/News

Official Blog of The Clinical Advisor

ASCO recommendations aim to increase HPV vaccination rates The American Society of Clinical Oncology has released its recommendations to help improve rates of HPV vaccination worldwide.

ClinicalAdvisor.com/Multimedia

USPSTF issues its final recommendations for aspirin use to prevent CVD, colorectal cancer The USPSTF concluded that a low-dose aspirin regimen can prevent cardiovascular disease and colorectal cancer in adults aged 50 to 59.

FDA issues warning for 2 diabetes drugs linked to risk of heart failure The FDA will add warnings about heart failure risk to the labels of type 2 diabetes medicines containing saxagliptin and alogliptin.

Aspirin for heart attack, stroke, and colon cancer: USPSTF guidelines The USPSTF has found good evidence that aspirin protects against heart attacks, stroke, and colon cancer in certain age groups. Watch it here: ClinicalAdvisor. com/USPSTFAspirinVid

CDC presents Zika virus overview Anne Schuchat, MD, provides a brief overview of signs, symptoms, and preventive measures to protect against the Zika virus. Watch it here: ClinicalAdvisor.com/CDCZikaVid Caffeine consumption in men and women affects miscarriage risk Marc Siegel, MD, discusses results of a new study on the relationship between caffeine consumption and miscarriage risk. Watch it here: ClinicalAdvisor.com/CaffeineMiscarriageVid

The Waiting Room ClinicalAdvisor.com/WaitingRoom Jillian Knowles, MMS, PA-C Conjunctivitis confusion: are we overtreating pink eye?

Not all types of conjunctivitis will respond to antibiotic eye drops. Identifying the type of conjunctivitis that a patient has is the key to identifying the most effective course of action.

Sharon M. O’Brien, MPAS, PA-C Lifestyle changes can reduce risk of restless legs syndrome Patients who are sedentary, obese, or smokers have an increased risk of developing restless legs syndrome.

MAKING CONTACT

Follow us on Twitter @ClinicalAdvisor

Sharon M. O’Brien, MPAS, PA-C Understanding age-related macular degeneration Clinicians should be able to diagnose age-related macular degeneration and distinguish between dry and wet presentations.

Jim Anderson, MPAS, PA-C, DFAAPA, ATC As opioid prescription rates decrease, overdose deaths remain the same: Is this progress?

A national push to decrease opioid prescription rates by focusing on prescription drug abuse has not led to a net decrease in opiate overdose deaths. Has progress been made?

Like us on Facebook facebook.com/TheClinicalAdvisor

Visit us on the web ClinicalAdvisor.com

Go mobile with us mobile.ClinicalAdvisor.com

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Advisor Dx

EXCLUSIVE TO THE WEB

INTERACT WITH YOUR PEERS by viewing the images and offering your diagnosis and comments. To post your answer, obtain more clues, or view similar cases, visit ClinicalAdvisor.com/AdvisorDx. Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues.

Ortho Dx

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TheJopa.org

Journal of Orthopedics for Physician Assistants

A girl who has had more than 30 fractures An 8-year-old girl presents with left ankle pain after “stepping wrong” 2 days previously. The patient appears very small for her age and has a dysmorphic face but is of normal intelligence for her age. She has had more than 30 fractures and several operations before this injury.

WHAT IS CAUSING THESE FRACTURES?

• Hyperparathyroidism • Rickets • Paget disease • Osteogenesis imperfecta ● See the full case at ClinicalAdvisor.com/OrthoDx_May16

Derm Dx A farm worker with a growing lesion A 70-year-old man presents with a 1-month history of an enlarging, irregularly pigmented macule on his forehead.

He has worked on a farm for the past 50 years. He denies any significant medical history. On physical examination, the lesion is found to be non-scaly and smooth.

CAN YOU DIAGNOSE THE CONDITION?

• Pigmented actinic keratosis • Seborrheic keratosis • Lentigo maligna • Solar lentigo ● See the full case at ClinicalAdvisor.com/DermDx_May16

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 13

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Newsline M AY 2 0 1 6

Two diabetes drugs are linked to heart failure page 17

Aspirin therapy for preventing CVD in adults page 18

Parental caffeine consumption and miscarriage risk page 22

PEDIATRIC healthcare providers should be prepared to clinically evaluate, test, and manage infants and children suspected to be infected with Zika virus, according to a report from the CDC published in Pediatrics.

Since early 2015, Aedes aegypti mosquitoes have spread the Flavivirus widely throughout the Americas, including several U.S. territories.

“Local transmission was reported in 31 countries and territories in the Americas as of February 29, 2016, including some U.S. territories,” wrote lead author Mateusz P. Karwowski, MD, MPH, of the CDC. “Based on the distributions of its primary mosquito vector, Aedes aegypti,

and another possible vector, Aedes albopictus, local Zika virus transmission is possible in the continental United States.”

Zika virus is spread primarily via mosquitoes, although sexual transmission has also been documented. Additionally, maternal-fetal transmission during pregnancy, intrapartum transmission, and perinatal transmission have all been reported.

Acute Zika virus infection should be suspected in infants and children who meet the following criteria: • Infants whose mothers traveled to or resided in a Zika-endemic area (http://wwwnc.cdc.gov/ travel/notices) within 2 weeks of delivery; • children who have traveled to

© CDC / CYNTHIA GOLDSMITH

CDC issues Zika virus update for pediatric healthcare providers Symptoms or resided in a Zika-endemic of Zika area within the past 2 weeks; virus include • and patients who have at least fever and 2 of the following symptoms: arthralgia fever, rash, conjunctivitis, or arthralgia. and last Mothers and adolescents who for up to may have had sexual contact with 1 week. an infected partner should also be tested.

Most patients infected with Zika virus are asymptomatic.

When symptoms do present, they generally include maculopapular rash, fever, arthralgia, and nonpurulent conjunctivitis and last for up to 1 week.

Endometriosis is linked to higher risk for heart disease ENDOMETRIOSIS is associated with an increased risk for coronary heart disease (CHD), especially among women aged 40 years or younger, according to a study published March 29 online ahead of print in Circulation: Cardiovascular Quality and Outcomes.

Lead author Fan Mu, ScD, and colleagues studied the association between laparoscopically confirmed endometriosis and subsequent CHD among 116,430 women in the Nurses’ Health Study II (1989-2009), excluding women with a history of heart disease and stroke. A diagnosis of endometriosis was made using surgical examinations in 11,903 women by the end of 20 years of follow-up.

When compared with women without endometriosis, the researchers found that women with endometriosis were 1.52

times more likely to have a myocardial infarction, 1.91 times more likely to have angiographically confirmed angina, 1.35 times more likely to need coronary artery bypass graft surgery or a coronary angioplasty procedure or stent, and 1.62 times more likely to have any combination of these events. These findings were independent of family and reproductive history.

Women aged 40 years or younger were greater than 3 times more likely to have any combination of the end points, and this relative risk decreased as age increased. Of the association between endometriosis and CHD, 42% could be explained by greater frequency of hysterectomy/oophorectomy procedures and earlier age at surgery, the authors said.

14 THE CLINICAL ADVISOR • MAY 2016 • www.ClinicalAdvisor.com

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Newsline TYPE 2 DIABETES medications that include saxagliptin and alogliptin may increase the risk of heart failure, particularly in patients who have heart or kidney disease, according to the FDA, which has announced that new warnings will be added to the drug labels.

“Healthcare professionals should consider discontinuing medications containing saxagliptin and alogliptin in patients who develop heart failure and monitor their diabetes control,” according to the FDA’s statement. “If a patient’s blood sugar level is not well-controlled with his or her current treatment, other diabetes medicines may be required.”

As part of its safety review, the FDA evaluated 2 large clinical trials of patients with heart disease. Both trials found that more patients who received medications

containing saxagliptin or alogliptin were hospitalized for heart failure, compared with patients who received a placebo.

In the saxagliptin trial, 3.5% of patients who received the drug were hospitalized for heart failure, compared with 2.8% of patients who received a placebo. Risk factors included a history of heart failure or kidney impairment.

In the alogliptin trial, 3.9% of patients who received alogliptin were hospitalized for heart failure, compared with 3.3% in the placebo group.

The FDA advises that patients who are taking these medicines should immediately contact their healthcare professionals if they develop signs and symptoms of heart failure, which include: • Unusual shortness of breath during daily activities

© THINKSTOCK

Diabetes drugs linked to heart failure, per FDA

Saxagliptin and alogliptin may increase the risk of heart failure, according to the FDA.

• Trouble breathing when lying down • Tiredness, weakness, or fatigue • Weight gain with swelling in the ankles, feet, legs, or stomach The FDA also recommends that patients should not stop taking their medicine without first talking to their healthcare professionals.

NO EVIDENCE exists to link selective serotonin reuptake inhibitors (SSRIs) to an increased risk of cardiovascular events, including arrhythmia, stroke, or transient ischemic attack, in patients with depression, according to research published in BMJ. Carol Coupland, MSc, PhD, professor of medical statistics in primary care at the University of Nottingham in the U.K., and colleagues conducted a cohort study to assess potential links between SSRI use and myocardial infarction, stroke, or arrhythmia. Participants were between 20 and 64 years of age and were first diagnosed with

SSRIs are not linked to increased risk of CV events, per BMJ report.

depression between January 2000 and July 2011.

The researchers analyzed medical records of 238,963 patients for 5 years. Of those patients, 772 had a myocardial infarction, 1,106 had a stroke or transient ischemic attack, and 1,452 were diagnosed with arrhythmia. In the first year of follow-up, patients treated with SSRIs had a significantly reduced risk of myocardial infarction, and no significant link was found between SSRI use and risk of stroke or arrhythmia; fluoxetine was associated with a significantly reduced risk of myocardial infarction, while lofepramine

was associated with a significantly increased risk. After a 5-year follow-up, the researchers found that treatment with tricyclic antidepressants could be linked to an increased risk of arrhythmia during the first 28 days of treatment.

“This large observational study has found no evidence that selective serotonin reuptake inhibitors are associated with an increased risk of arrhythmia, myocardial infarction, or stroke/transient ischemic attack … but some indication that they are associated with a reduced risk of myocardial infarction and arrhythmia, particularly f luoxetine,” concluded Dr Coupland.

© THINKSTOCK

SSRIs and cardiovascular events—Is there a connection?

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 17

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Newsline

© THINKSTOCK

USPSTF issues final recommendations for aspirin therapy

THE U.S. Preventive Services Task Force (USPSTF) recommends initiation of low-dose aspirin therapy to prevent cardiovascular disease (CVD) and colorectal cancer in adults aged 50 to 59 years, as reported in the Annals of Internal Medicine.

The USPSTF gave this recommendation a B rating, noting that an aspirin regimen should be initiated in adults who have a 10% or

Low-dose aspirin therapy is advised in adults aged 50 to 59 years.

greater 10-year CVD risk, a life expectancy of at least 10 years, and are not at an increased risk for bleeding. The decision to initiate aspirin therapy in adults between 60 and 69 years of age should be made on an individual basis.

Kirsten Bibbins-Domingo, PhD, MD, MAS, professor of medicine and of epidemiology and biostatistics at the University of California, San Francisco, authored the report on behalf of the USPSTF. Dr Bibbins-Domingo noted that potential benefits of aspirin use are prevention of myocardial infarction, stroke, and reduced instances of colorectal cancer, when used long-term. Correlating smallto-moderate harms include possible gastrointestinal bleeding and hemorrhagic stroke. However, the USPSTF has concluded “with moderate certainty that the benefit

of aspirin use for the primary prevention of CVD events, combined with the reduced incidence of colorectal cancer, outweighs the increased risk for bleeding by a moderate amount.”

Before instituting an aspirin regimen, clinicians are advised to perform baseline assessments to determine a patient’s risk for CVD. Risk assessment should include notation of a patient’s age, sex, and ethnicity, as well as total and HDL cholesterol levels, systolic blood pressure, and history of hypertension treatment, diabetes, and smoking. Male sex and old age are considered risk factors for potential GI bleeding.

“The decision about the level of CVD risk at which the potential benefits outweigh the potential harms is an individual one,” wrote Dr Bibbins-Domingo.

SCR EENING for chron ic obstructive pulmonary disease (COPD) in asymptomatic adults is not recommended, according to a recommendation statement from the U.S. Preventive Services Task Force (USPSTF) published in JAMA. Based on the available evidence, the USPSTF determined that early detection of COPD (before a patient develops symptoms) does not change the disease’s course or improve outcomes.

The USPSTF has categorized this as a D recommendation, meaning that there is moderate to high certainty that there is

no net benefit or that the harms outweigh the benefits.

Adults can be screened for COPD through two methods: 1. Risk assessment through a formal prescreening questionnaire; if positive, follow-up diagnostic spirometry testing 2. Screening spirometry administered without a bronchodilator; if positive, follow-up with diagnostic spirometry testing The USPSTF found inadequate evidence that screening asymptomatic adults for COPD via either of these methods benefits health outcomes. The task force also found inadequate evidence

Screening is not required in adults without symptoms, says USPSTF.

regarding the harms of screening, but the lack of benefits may mean that the opportunity cost of screening may be large.

Treatment trials for COPD found that medication decreases the exacerbation of COPD symptoms in patients with mild to moderate COPD. However, none of these trials included asymptomatic patients — even so, the USPSTF states that it is unclear how treatment benefits would apply to patients who do not have any symptoms.

The recommendation is an update to the USPSTF’s 2008 statement.

© THINKSTOCK

USPSTF recommends against screening for COPD

18 THE CLINICAL ADVISOR • MAY 2016 • www.ClinicalAdvisor.com

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Newsline FLORIDA MAY SOON become the latest state to authorize nurse practitioners (NPs) and physician assistants (PAs) to prescribe controlled substances.

Sponsored by Representatives Car y Pig man and Daphne Campbell, House Bill 423 now awaits Governor Rick Scott’s signature. If signed, the law would allow “physician assistants and advanced registered nurse practitioners to prescribe controlled substances under current supervisory standard for PAs and protocols for ARNPs … and creates additional statutory parameters for their controlled substance prescribing,” according to a summary of the bill.

The text of HB 423 goes on to clarify that to retain these privileges, PAs and NPs must complete 3 hours of continuing education on a biennial basis, focused on the “safe and effective prescribing of controlled substances.” In addition,

NPs and PAs would be able to prescribe controlled substances.

these privileges limit prescriptions for Schedule II substances to a 7-day supply, and may not include psychotropic medications for those younger than 18 years old.

Governor Scott’s signature would make Florida the 50th and final state to authorize NPs as controlled substance prescribers; only Kentucky is a holdout for PAs. The Florida Association of Nurse Practitioners and the National Commission on Certification of Physician Assistants estimate that

13,000 NPs and 6,765 PAs practice in Florida, and granting prescribing authority would provide medical access to an expanding population of patients in the state.

“This legislation will help expand the availability of quality medical care by allowing skilled practitioners with advanced medical training to better meet the needs of their patients,” said Florida Senate President Andy Gardiner (R-Orlando) in a press release. “There are many rural communities across our state where physicians are simply not available … After completing years of education of clinical training, PAs and ARNPs have the skills needed to prescribe these medications to the patients they serve.”

“This legislation will help make medical care more readily available while maintaining the high standards of training required to prescribe these controlled substances,” Senator Gardiner concluded.

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Florida bill would allow prescribing for controlled substances

DELAYING a second attempt at defibrillation to allow time for chest compressions, as revisions in the 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend, is not associated with improved survival or better outcomes, according to two studies published April 6 online ahead of print in BMJ. In the first study, lead author Steven M. Bradley, MD, MPH, and colleagues studied the time between the first and second

defibrillation attempts among 2,733 patients undergoing cardiac arrest in 172 U.S. hospitals.

They found that a deferred second defibrillation (more than 1 minute between the first and second defibrillation) was attempted in more than 50% of patients in 2012, which doubled from approximately 25% in 2004, but the deferred defibrillation was not associated with improved survival.

In the second study, senior author Michael W. Donnino, MD, and fellow investigators used data from

Delayed second defibrillation attempt does not lead to better outcomes.

the same registry as the first study for nearly 3,000 patients in cardiac arrest at more than 300 U.S. hospitals. They found that 51% of patients received epinephrine within two minutes after the first defibrillation, and this intervention was associated with decreased odds of survival to hospital discharge and of return of spontaneous circulation and survival to hospital discharge with good functional outcome. The American Heart Association recommends epinephrine after the second defibrillation.

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Survival unimproved with deferred second defibrillation

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Newsline Parental caffeine consumption linked Stroke risk reduced with to elevated risk of early miscarriage Of the 344 couples enrolled, 98 WOMEN who regularly con­ DASH diet pregnancies (28%) ended in mis­ sume more than 2 caffeinated beverages a day leading up to conception are more likely to miscarry a pregnancy, according to research published in Fertility and Sterility.

Germaine M. Buck Louis, PhD, director of the Division of Intramural Population Health Research at the Eunice Kennedy Shriver National Institute of Ch i ld Hea lth and Human Development, and colleagues conducted a prospective cohort study comparing lifestyle factors including cigarette use, caffein­ ated beverage consumption, and multivitamin use in 344 couples with a singleton pregnancy. Each couple was enrolled preconcep­ tion and was followed daily up to 7 weeks postconception.

The association was found in both male and female partners.

carriage. While miscarriage was associated with women 35 years of age and older (hazard ration [HR] 1.96), the researchers also found that caffeine consumption by both men and women was associated with an increased hazard ratio of 1.73 and 1.74, respectively.

Although earlier studies found similar data, Dr Buck Louis and colleagues noted that those studies were not able to rule out whether the pregnancy loss was linked to caffeine consumption or an unhealthy pregnancy.

“Our findings indicate that the male partner matters, too,” said Dr Buck Louis. “Male preconception consumption of caffeinated bever­ ages was just as strongly associated with pregnancy loss as female.”

Vaccine refusal key factor in measles, pertussis risk REFUSAL to receive vaccination is associated with an increased risk for measles and pertussis, according to a report published in JAMA. Lead author Varun K. Phadke, MD, and fellow investigators analyzed published reports of measles outbreaks that have occurred since January 1, 2000, when the United States declared that measles had been eliminated; reports of endemic and epidemic pertussis since January 1, 1977, the lowest point in incidence in the United States; and for studies on disease risk in the context of vaccine delay or exemption.

They included 18 published studies that described 1,416 measles cases (patient age,

2 weeks–84 years); 56.8% of the patients had never been vaccinated against measles.

Of the 970 measles cases with detailed vaccination data, 574 were eligible for the vaccine but chose not to receive it, and 405 (70.6%) of these had nonmedical exemptions. The researchers identified 32 reports of pertussis outbreaks, which included 10,609 individuals (age, 10 days–87 years) with a vaccination status included.

They found that in the 5 largest statewide epidemics, 24% to 45% of those affected were unvaccinated or undervaccinated, but several outbreaks occurred in highly vaccinated populations, suggesting waning immunity instead, the authors said. n

© THINKSTOCK

THE DASH, or Dietary Ap­proach­ es to Stop Hypertension, diet is associated with a reduced risk of ischemic stroke, according to a report in the April issue of Stroke.

Previous findings have found this diet to be associated with lower risk of hypertension, the major risk factor for stroke.

Lead author Susanna C. Larsson, PhD, and fellow investigators fol­ lowed 74,404 men and women (age, 45–83 years) who did not have a history of stroke at baseline and who were enrolled in the Cohort of Swedish Men and the Swedish Mammography Cohort. Using a food-frequency questionnaire, the researchers assessed adherence to the DASH diet with a modi­ fied score based on participants’ consumption of vegetables, fruits, legumes and nuts, whole grains, low-fat dairy, red and processed meat, and sweetened beverages.

During a mean of 11.9 years of follow-up, 3,896 ischemic strokes, 560 intracerebral hemorrhages, and 176 subarachnoid hemorrhag­ es were documented among the study population. The research­ ers found a statistically significant inverse association between modi­ fied DASH diet score and risk of ischemic stroke. Although not statistically significant, an inverse association was also found between the modified DASH diet score and intracerebral hemorrhage. The study findings did not indicate an association between the diet and subarachnoid hemorrhage.

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FEATURE: TASHA LEE, DNP, FNP-BC, ONP-C

Conservative treatment options for osteoarthritis Osteoarthritis is one of the most common problems encountered in primary care, and conservative treatment can improve patients’ quality of life.

© ISM / PHOTOTAKE

R

X-ray of the knee, side view, showing severe osteoarthritis.

outinely referred to as degenerative joint disease, or “wear and tear,” osteoarthritis (OA) is a debilitating condition causing pain and stiffness that significantly limit the lifestyle of more than 27 million individuals in the United States. OA accounts for approximately 25% of primary care visits annually.1 Defined as degeneration of the cartilage and underlying bone within a joint, in addition to bony overgrowth, OA most commonly affects the hips, knees, spine, and hands.2 Advanced age (older than 65 years) is the factor most frequently associated with OA; other contributing factors include genetics, obesity, and trauma.

Symptoms, which range from mild to debilitating, often lead to significant lifestyle limitations as a consequence of pain and decreased function.

According to the Centers for Disease Control and Prevention (CDC),3 80% of patients with OA have some limitation of mobility, while 25% are unable to perform the activities of daily living (ADLs). These statistics underscore that it is essential for primary care providers to be aware of the conservative treatment measures available for OA. Currently recommended conservative treatments are weight loss, physical therapy/exercise, activity modification, drugs, braces/orthotics, and intra-articular injections (Figure 1).4 Each of these measures has proved helpful for some patients, but treatment should be individualized and based on the degree of arthritis and disability and on any comorbidities that the patient may have. Treatment options can be expensive and

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may not elicit desired outcomes; therefore, clinicians must consider cost as well as potential risk/benefit for the patient before initiating treatment. By taking all of these variables into consideration and choosing the best treatment for individual patients, primary care providers can decrease pain and increase function, thus improving patients’ satisfaction and reducing the number of patients who seek nonoperative treatment from a specialist, which is not always available or necessary.

Activity modification

An initial treatment option for OA is activity modification.

More often than not, patients are capable of pointing out specific activities that worsen their pain, such as climbing stairs, squatting and stooping, bending, sitting for long periods of time, heavy lifting, walking long distances, and high-impact exercises. Whereas simply avoiding these is enough for some patients, others may have to modify work level and/or athletic activities. According to the American Academy of Orthopaedic Surgeons (AAOS),5 this may mean switching from high-impact exercises such as running and competitive sports to low-impact exercises such as swimming

and walking. As irrelevant as this change may seem, activity modification has been shown to reduce and/or relieve arthritic pain for many.

Weight loss

Obesity can be a predisposing factor for OA. Studies indicate that approximately 66% of individuals with a diagnosis of OA are overweight or obese.6 Although it is common to see obese patients with arthritic pain, many will state that their joint pain prevents them from exercising and losing weight.

This may be a legitimate statement, but it is the clinician’s responsibility to educate such patients about other methods of losing weight (eg, behavior modification, pharmacologic treatment, weight loss surgery) because a self-discipline or compliance problem is often present.7 Weight loss is advantageous for one’s overall health and has proved to be the most patient-controlled, cost-efficient long-term treatment measure that can be initiated without a provider’s order; furthermore, it can be accomplished at one’s own pace. According to the Framingham Study, if a female patient loses 24.25 kg (11 lb), her risk for OA is decreased by 50%.8 Another study revealed a fourfold reduction in the Discuss total joint replacement for osteoarthritis of the hip, knee, or shoulder if the steps below are unsuccessful.

Consider hyaluronic acid injection for persistent osteoarthritis of the knee.

Consider corticosteroid injection for acute exacerbation of osteoarthritis of the knee.

Consider opioid therapy, but monitor carefully for dependence and abuse.

Add a combination of glucosamine and chondroitin for moderate to severe osteoarthritis of the knee; discontinue if no change after 3 months, but continue if effect is noted.

Start NSAID therapy, beginning with over-the-counter ibuprofen or naproxen. Switch to a different NSAID if the initial choice is not effective. Use generics if possible.

Begin with acetaminophen and continue if effective. Otherwise, step up to NSAID. Encourage regular exercise throughout treatment and encourage weight loss if the patient is overweight or obese. Consider physical therapy referral for supervised exercise (land- or water-based). Consider bracing and splinting.

MILD OSTEOARTHRITIS

MODERATE OSTEOARTHRITIS

NSAID, nonsteroidal anti-inflammatory drug

SEVERE OSTEOARTHRITIS Source: Sinusas K. Osteoarthritis: diagnosis and treatment. Am Fam Physician. 2012;85(1):49-56.

FIGURE 1. Steps in the management of osteoarthritis. www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 25

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OSTEOARTHRITIS

Physical therapy, including manual therapy, aquatic therapy, and strength training, is commonly prescribed for patients with osteoarthritis. amount of weight distributed across the knee joint for each pound lost.9 For example, a patient who loses 10 lb reduces weight across the knee joint by 40 lb, decreasing pain significantly.7 Although weight loss can be challenging, it currently holds a moderate recommendation from the AAOS for patients with symptomatic OA and a body mass index (BMI) of 25 or higher10, and weight loss has been shown to reduce the amount of stress on joints, resulting in decreased pain and improved function.11 Physical therapy and exercise

Physical therapy is commonly prescribed for individuals with OA. Several modalities are available, including manual therapy, aquatic therapy, strength training, electrical stimulation, and balance and proprioception training.12 When considering physical therapy as a potential treatment option, the provider must take several factors into account, including the severity of the patient’s symptoms and the radiographic findings.13 According to Brakke et al,12 patients with mild disease and a score of 6 or greater on the numeric pain scale are more likely to have a positive outcome than are those with advanced OA.

A R T

Continues on page 29

Start low and go slow.

Exercise for 3 to 5 minutes twice daily and increase as tolerated.

Modify activity when arthritis symptoms increase, and stay active.

Decrease the frequency, duration, or intensity of exercise in order to stay active.

Activities should be joint-friendly.

Engage in low-impact exercises like walking, bicycling, water aerobics, and dancing.

Recognize safe places (eg, neighborhood, local park) and safe ways (eg, exercise class) to be active.

Talk to a health professional or certified exercise specialist.

Source: Centers for Disease Control and Convention. Physical activity for arthritis. http://www.cdc.gov/arthritis/basics/physical-activity-overview.html. September 1, 2011.

Last reviewed April 27, 2015. Updated January 7, 2016. Accessed April 5, 2016.

© THINKSTOCK

S M

Therefore, this treatment may be most beneficial early on because it allows patients to improve muscle strength and range of motion. The AAOS has issued a strong recommendation for patients with symptomatic OA of the knee to participate in self-management programs, strength training, low-impact aerobic exercise, and neuromuscular education, and to engage in physical activity consistent with national guidelines.10 Although physical therapy is an effective treatment option for patients with OA, it is not practical for many because of cost, lack of transportation, inconvenience, and other factors.

In such circumstances, a patient may find a self-management program effective. Providers should offer patients exercises to perform at home and encourage other low-impact activities, such as walking, bicycle riding, and swimming, based on their condition and the joints affected. Walking in general has been shown to strengthen muscles and bones, reduce back pain, and lower body weight, decreasing the amount of stress on joints and therefore decreasing pain.14 When providing patients with a home exercise program, the provider should stress that engaging in exercise is a goal

FIGURE 2. SMART exercise for patients with osteoarthritis.

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OSTEOARTHRITIS

Pharmacologic treatments for osteoarthritis include acetaminophen, NSAIDs, topical creams, tramadol hydrochloride, and opiates. to work toward over time and that the extent and duration of the exercises performed can be increased gradually.

Patients may not experience much benefit until they have been exercising consistently as instructed for 6 to 8 weeks, but providers should encourage them to continue because perseverance is likely to result in long-term pain relief.3 According to the CDC,3 the recommendations summarized by the acronym SMART (Figure 2) are good for patients with OA to abide by because some physical activity or exercise is better than none at all.

Pharmacologic treatment

A variety of pharmacologic treatments are currently available for OA, including, but not limited to, acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), topical creams, tramadol hydrochloride, and opiates.15 Acetaminophen tends to be preferred to NSAIDs for arthritic symptoms, especially in older patients, because it has a lower incidence of cardiovascular and gastrointestinal events and is inexpensive, safe, and effective for those with mild arthritic symptoms.15 The current recommendation for patients taking acetaminophen is not to exceed a dosage of 4 g/d in order to avoid hepatotoxicity.16 The Food and Drug Administration (FDA) currently recommends that the quantity of acetaminophen in combination drugs not exceed 325 mg per tablet because of the risk for hepatotoxicity.17 For patients with moderate to severe OA, acetaminophen is often ineffective; therefore, NSAIDs (eg, aspirin, ibuprofen, naproxen, diclofenac, meloxicam, celecoxib) are often prescribed.15 While taking NSAIDs, patients should be educated about the potential risks, including stomach upset, gastrointestinal bleeding, renal dysfunction, and hypertension.15 In patients with a known history of gastrointestinal bleeding, ulcers, renal failure, or poorly controlled hypertension, NSAIDs are not an appropriate treatment option; other medications, such as topical creams and non-opiate or opiate analgesics, may be considered.15 Topical NSAIDs, such as Voltaren Gel 1% (diclofenac sodium topical gel), have been shown to be effective in treating arthritic pain and cause fewer adverse effects than do oral NSAIDS.18 Voltaren Gel 1%, in particular, has been approved by the FDA for the treatment of OA; the currently recommended dosage is 4 g applied to the affected joint four times per day.19 Topical treatments that may be purchased over the counter include capsaicin, Aspercreme,

and Salonpas. Although all medications have known side effects, the topical treatments seem to have less effect on comorbidities, are nonsedating, and are not addictive, yet still provide adequate pain relief.

Another treatment option that may be considered for arthritic pain is the prescription drug tramadol hydrochloride.

Tramadol hydrochloride is a mild opioid agonist currently recommended for treating moderate to severe pain when other pharmacologic measures are not an option or have failed; it has not been linked to gastrointestinal, renal, or cardiovascular complications.20 The literature suggests that tramadol hydrochloride is effective for decreasing pain and improving function in patients with OA.21 The currently recommended dosage is 50 to 100 mg by mouth every 4 to 6 hours as needed for pain (not to exceed 400 mg/d; not to exceed 300 mg/d in persons aged 65 years or older).22 Therefore, when other pharmacologic treatments are not available, tramadol hydrochloride may be considered.

When all other pharmacologic measures have been tried and have failed, or when other treatment options are not feasible, opiates or opioids may be considered, but they are not without risk. Opioid analgesics put patients at increased risk for dependency, falls, and fractures, especially older patients. A recent study determined that even the shortterm use of narcotics for pain secondary to OA is likely to lead to other forms of morbidity and mortality.23 Therefore, before considering opiates for arthritic pain, clinicians need

POLL POSITION

Which of the following is the most effective conservative treatment option for osteoarthritis? n=1,740

■ Pharmacologic treatment ■ Intra-articular injections ■ Braces/orthotics

24.6%

56.03%

19.37%

For more polls, visit ClinicalAdvisor.com/Polls.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 29

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OSTEOARTHRITIS

Orthotic devices are commonly recommended for support, alignment, and the prevention or correction of foot deformities. to take all risk factors into consideration because opiates may ultimately do the patient more harm than good.

Glucosamine and chondroitin

Glucosamine and chondroitin are very popular herbal supplements used in treating arthritis. Glucosamine is a natural substance found in healthy cartilage, primarily in the fluid surrounding the joints. It may be produced in a laboratory or harvested from the shells of shellfish.24 As a dietary supplement, it is believed to have anti-inflammatory properties and assist in cartilage regeneration. Chondroitin is made by the body naturally and helps to retain water in cartilage.24 It too can be made in the laboratory and can also be obtained from the cartilage of other animals, such as pigs, cows, and sharks.24 In many European countries, chondroitin is used as a prescriptive treatment for OA. However, in the United States, it is sold over the counter as a supplement, often in combination with glucosamine. Currently, the AAOS does not recommend glucosamine and chondroitin for the treatment of OA. A review of numerous studies found essentially no evidence that glucosamine and chondroitin, evaluated either alone or in combination, achieves a minimum of clinically important outcomes compared with placebo.25 Chondroitin and glucosamine supplements alone or in combination may not work for everyone with OA. However, patients who take these supplements and who have experienced relief with them should not stop taking them. Both supplements are safe to take on a long-term basis.

Braces and orthotics

Braces and orthotics are often considered for the treatment of OA, but their efficacy may be limited to specific conditions, such as unicompartmental knee arthritis or arthritis of the foot and ankle. To treat OA, universal soft goods, such as wrist splints, neoprene knee sleeves, knee immobilizers, slings, ankle supports, and other devices, are often used to rest and stabilize a joint for several days to relieve pain or to provide compression and “preload” a muscle. Fitting patients adequately with structural braces is often difficult; therefore, custom braces may be used. In particular, for a patient with unicompartmental knee arthritis, a custom brace is helpful in transferring weight from one compartment to the other, relieving pain by approximately 50%.26 However, the AAOS indicates that the evidence for unloader braces is inconclusive

and has issued only a moderate recommendation for lateral shoe wedges in treating OA of the knee.25 Orthotic devices are also often recommended for support, alignment, and the prevention or correction of foot deformities.27 Midfoot arthritis and forefoot arthritis are common conditions affecting many individuals. According to Verhoeven and Vandeputte,28 orthotic devices serve as the mainstay of conservative treatment for these conditions because they evenly distribute load across the foot.

According to the AAOS,29 an assistive device such as an ankle–foot orthosis may improve mobility, and wearing shoe inserts (orthotics) or custom-made shoes with stiff soles and rocker bottoms can help minimize pressure on the foot and decrease pain. In addition, if a deformity is present, a shoe insert may tilt the foot or ankle back straight, relieving pain in the joint.29 Numerous patients begin by using overthe-counter orthotics, but many eventually benefit from custom-molded orthotics because they often provide greater support and routinely have specific modifications based on the condition being treated.30 The one caveat regarding custom orthotic devices is insurance coverage because they tend to be expensive. However, if a patient has a comorbidity, such as diabetes mellitus, that could exacerbate the foot or ankle condition, plans such as Medicare Part B will generally cover therapeutic shoes and/or inserts annually if the patient meets specific criteria.31 Intra-articular injections

Injections are often the mainstay of conservative treatment for OA because they have demonstrated the ability to provide quick and adequate pain relief. Several different types of intra-articular injections are offered, but the two most commonly used are corticosteroid and hyaluronic acid injections.

Corticosteroid injections are currently the only injections approved for essentially every joint. Just as with all other treatment options, results will vary for each patient. A number of patients obtain minimal relief, whereas others experience substantial relief often lasting for several months or even years.

In general, when a corticosteroid is administered, it is often mixed with a local anesthetic, thus providing relief even before the patient leaves the office. However, it may take 24 to 48 hours for the cortisone itself to take effect. Although corticosteroids have proved effective for many patients, they must be used with caution in those with diabetes because they can increase the Continues on page 34

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blood sugar level and cause hyperglycemia. Despite the potential for side effects, as with any other medication, if corticosteroid injections are effective for the patient, they may be repeated safely every 3 to 4 months as needed for pain relief.

Intra-articular injections of the knee joint with hyaluronic acid (viscosupplementation) are currently used by many providers, although they are no longer recommended by the AAOS. Hyaluronic acid is a natural substance in synovial fluid, and its concentration is decreased in the joints of patients with OA.32 In the past, three to five injections were given sequentially, but treatment is currently available as one injection. Some of the formulations include Synvisc-One, Euflexxa, and Orthovisc.

Intra-articular injections are thought to enhance the viscosity of the synovial fluid by increasing its molecular weight and decreasing the amount of inflammatory cytokines and free radicals to reduce arthritic pain, although the exact mechanism is unknown.19 Unfortunately, hyaluronic acid injections do not provide instant analgesic effects, and often several weeks must pass before any benefit is noticed; however, if the injections are effective, the benefits may last for several months.32 The AAOS currently strongly recommends against using hyaluronic acid because it has been shown to be ineffective.25 Although most studies have failed to show superiority of hyaluronic acid injections to placebo, they may be warranted in patients who are not operative candidates or who are averse to surgical treatment.32 The injections are most commonly used for mild to moderate OA when other conservative treatment options have failed, but they may be worth discussing with patients before surgical measures are implemented.

Tasha Lee, DNP, FNP-BC, ONP-C, is a certified family nurse practitioner at Coastal Orthopedics in Conway, S.C. References 1. Leahy M. Changing the paradigm for diagnosing and treating arthritis.

American Academy of Orthopaedic Surgeons. http://www.aaos.org/news/ aaosnow/nov12/clinical6.asp. November 2012.

2. Centers for Disease Control and Prevention. Arthritis basics. Definition. http://www.cdc.gov/arthritis/basics/index.html. September 1, 2011.

Updated May 26, 2015.

3. Centers for Disease Control and Prevention. Arthritis basics. Physical activity for arthritis. http://www.cdc.gov/arthritis/basics/physical-activityoverview.html. September 1, 2011. Updated January 7, 2016.

4. Li CS, Karlsson J, Winemaker M, Sancheti P, Bhandari M. Orthopedic surgeons feel that there is a treatment gap in management of early OA: international survey. Knee Surg Sports Traumatol Arthros.

2014;22(2):363-378.

5. American Academy of Orthopedic Surgeons. Osteoarthritis. OrthoInfo. http://orthoinfo.aaos.org/topic.cfm?topic=A00227. Last reviewed July 2007.

6. Shih M, Hootman JM, Kruger J, Helmick CG. Physical activity in men and women with arthritis, National Health Interview Survey, 2002. Am J Prev Med. 2006;30(5):385-393.

7. Sridhar MS, Jarrett CD, Xerogeanes JW, Labib SA. Obesity and symptomatic osteoarthritis of the knee. J Bone Joint Surg Br. 2012;94(4):433-440.

8. Felson DT, Zhang Y, Hannan MT, et al. Risk factors for incident radiographic knee osteoarthritis in the elderly: the Framingham Study. Arthritis Rheum. 1997;40(4):728-733.

9. Messier SP, Gutekunst DJ, Davis C, Devita P. Weight loss reduces kneejoint loads in overweight and obese older adults with knee osteoarthritis.

Arthritis Rheum. 2005;52(7):2026-2032.

10. American Academy of Orthopaedic Surgeons. Guidelines. Treatment

Conclusion

of osteoarthritis of the knee. http://www.aaos.org/research/guidelines/

Clinicians, particularly in the primary care setting, should have an understanding of the available options for the safe, adequate treatment of patients with OA. When formulating a treatment plan and before administering treatment, the clinician must consider all relevant factors, including the severity of the condition as well as the patient’s comorbidities, financial status, and insurance coverage because each of these variables determines what treatment can be prescribed or recommended. It is also important that clinicians understand that a treatment option that is beneficial for one patient may be ineffective for another. The goals of the treatment of OA are to relieve pain, improve mobility, and maintain or restore quality of life. If or when nonoperative interventions appear to fail to achieve these stated goals, the clinician may consider referral to an appropriate musculoskeletal specialist for surgical evaluation. n

guidelineoaknee.asp. May 18, 2013.

11. American Academy of Orthopedic Surgeons. Arthritis of the knee.

OrthoInfo. http://orthoinfo.aaos.org/topic.cfm?topic=A00212. October 2007. Last reviewed June 2015.

12. Brakke R, Singh J, Sullivan W. Physical therapy in persons with osteoarthritis. PM R. 2012;4(5 Suppl):S53-S58.

13. Fehring TK, Fehring K, Odum SM, Halsey D. Physical therapy mandates

by Medicare administrative contractors: effective or wasteful?

J Arthroplasty. 2013;28(9):1459-1462.

14. Arthritis Foundation. Walking with arthritis. http://www.arthritis.org/ living-with-arthritis/exercise/workouts/walking. 2013.

15. Sinusas K. Osteoarthritis: diagnosis and treatment. Am Fam Physician.

2012;85(1):49-56.

16. US Food and Drug Administration. FDA drug safety communication: Prescription acetaminophen products to be limited to 325 mg per dosage unit; boxed warning will highlight potential for severe liver failure.

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http://www.fda.gov/Drugs/DrugSafety/ucm239821.htm. January 12, 2011.

Updated October 27, 2014.

17. US Food and Drug Administration. FDA drug safety podcast for healthcare professionals: Prescription acetaminophen products to be limited to 325 mg per dosage unit; boxed warning will highlight potential for severe liver failure. http://www.fda.gov/Drugs/DrugSafety/DrugSafetyPodcasts/ ucm240513.htm. Updated August 16, 2013.

18. Peniston JH, Gold MS, Weiman MS, Alwine LK. Long-term tolerability of topical diclofenac sodium 1% gel for osteoarthritis in seniors and patients with comorbidities. Clin Interv Aging. 2012;7:517-523.

19. McCarberg B. Tramadol extended-release in the management of chronic pain. Ther Clin Risk Manag. 2007;3(3):401-410.

20. McPhee SJ, Papadakis M, Rabow MW. Current Medical Diagnosis and Treatment 2012. New York: McGraw-Hill Medical; 2012.

“Look, the new emoji are here.”

21. Van Laar M, Pergolizzi JV Jr, Mellinghoff HU, et al. Pain treatment in arthritis-related pain: beyond NSAIDs. Open Rheumatol J. 2012;6:320-330.

22. Lexicomp mobile application software version 1.12.1. New York, NY: Walters Kluwer; 2013.

23. Rolita L, Spegman A, Tang X, Cronstein BN. Greater number of narcotic analgesic prescriptions for osteoarthritis is associated with falls and fractures in elderly adults. J Am Geriatr Soc. 2013;61(3):335-340.

24. Hess A. Glucosamine and chrondroitin for arthritis. Arthritis Foundation. http://www.arthritis.org/living-with-arthritis/treatments/ natural/supplements-herbs/glucosamine-chondroitin-osteoarthritis.php.

25. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis of the Knee. 2nd ed. Summary of recommendations. http:// www.aaos.org/research/guidelines/OAKSummaryofRecommendations.pdf.

26. Hunter DJ, Lo GH. The management of osteoarthritis: an overview and call to appropriate conservative treatment. Med Clin North Am. 2009;93(1):127-143.

27. American Orthopaedic Foot & Ankle Society. How to use orthotics. http://www.aofas.org/footcaremd/how-to/footwear/Pages/The-Uses-and-

© The New Yorker Collection 2016 from cartoonbank.com. All Rights Reserved.

Abuses-of-Orthotics.aspx. 2013.

28. Verhoeven N, Vandeputte G. Midfoot arthritis: diagnosis and treatment. Foot Ankle Surg. 2012;18(4):255-262.

29. American Academy of Orthopaedic Surgeons. Arthritis of the foot and ankle. OrthoInfo. http://orthoinfo.aaos.org/topic.cfm?topic=A00209. Last reviewed March 2015.

30. Foot orthotics: inexpensive is often best. Mayo Clinic Health Letter.

2012;30(2):6.

31. Centers for Medicare & Medicaid Services. Medicare’s coverage of diabetes supplies & services. http://www.medicare.gov/pubs/pdf/11022.pdf.

Revised September 2013.

32. American Academy of Orthopaedic Surgeons. Viscosupplementation treatment for arthritis. OrthoInfo. http://orthoinfo.aaos.org/topic. cfm?topic=A00217. April 2013. Last reviewed June 2015.

All electronic documents accessed April 5, 2016.

“Miss Muldorf, my plant needs watering.

Send in a lawyer to handle the malpractic charge against the custodial staff.” www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 35

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FEATURE:

THOMAS MASSING, MS, PA-C, FAPACVS

Pesticides and Parkinson’s disease

Increasing evidence has shown a link between pesticide exposure and the risk for Parkinson’s disease. How real is this link on the golf course?

T

hroughout the past 10 years, studies ranging in intensity have suggested a link between pesticide exposure and the development of Parkinson’s disease.1-3 An additional study has found a link between two solvents and Parkinson’s disease.4 This study was cited by Parrish and Gardner5, who suggested a potential risk for Parkinson’s disease by ambient pesticide exposure among those living downwind from a golf course. In 2013, Fields6 published an article that discussed these two reports. The issue has become a source of concern among those who play golf and live near a golf course and may result in patients turning to their primary care clinicians for up-to-date information and opinion.

The following review will reveal the strengths and weaknesses surrounding the issue of pesticides, Parkinson’s disease, and golf and will provide information that a practitioner would need to evaluate past and future studies suggesting such risk to golfers and golf course residents.

© ISTOCK

Background on Parkinson’s disease

How harmful is pesticide exposure from the golf course?

Parkinson’s disease is a disorder of the substantia nigra (basal ganglia) section of the brain.2 Figures 1 and 2 represent a simplified version of normal basal ganglia and dopamine receptors. When neurons within the basal ganglia degenerate, they lose the ability to produce dopamine (dopaminergic neuron degeneration), resulting in abnormalities of movement.

Parkinson’s symptoms develop when these neurons degrade from 550,000 to 100,000.7

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© GWEN SHOCKEY / SCIENCE SOURCE

Figure 3 demonstrates this regression of dopamine levels within the neuron synapse.

The symptoms of Parkinson’s disease are listed in Table 1, and some of the available medications for treatment are included in Table 2. Figure 4 suggests the mechanism of action produced by these medications, which inhibit the oxidative breakdown of dopamine within the neuron. The diagnosis of Parkinson’s is made on the basis of physical and neurologic symptoms, as there are no serologic or diagnostic imaging tests available. The disease is confirmed when 2 of the 3 primary symptoms are present, one of which must be slow movement. Van Den Eeden et al8 estimates that Parkinson’s disease afflicts 17 of every 100,000 persons and is increasing worldwide with the expansion of an aging population. Most individuals afflicted by this disease are able to live without severe disability due to the slow degradation of dopamine-generating neurons and the number of treatment options available. It is the disabling symptoms that are of chief concern.

FIGURE 1. An illustration of dopamine (green) and serotonin (red) pathways in the brain.

Pesticides have long been associated with the development of neurologic disorders. A Medline search using the terms “Parkinson’s” and “pesticides” yielded more than 1500 citations. Animal and human studies have connected the development of Parkinson’s with various groups and classifications of pesticides, which have been implicated in dopaminergic neuron degeneration. According to the CDC,9 the insecticide classes of organochlorine and organophosphorus compounds are thought to be specifically linked to Parkinson’s disease.

Organochlorines are chlorinated hydrocarbons used extensively from 1940 to 1960. Parkinson’ disease symptoms differ from organophosphate poisoning, resulting in acute cholinergic toxicity (SLUDGE/BBB — Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia). According to the Colorado Environmental Pesticide Education Program,10 these two classes were the most frequently banned or severely restricted pesticides. Table 3 lists those pesticides banned or severely restricted in the U.S. The up-to-date list of restricted pesticides can be found in the Environmental Protection Agencies Restricted Use Products report.11 In 2006, Ascherio et al1 found a 70% incidence of Parkinson’s among farm and non-farm workers exposed to pesticides.

Although a diagnosis of Parkinson’s disease was made in these individuals based on movement disorders, pesticide use or exposure was only listed anecdotally by the respondents who did not report a specific pesticide.1 Despite evaluating

© BSIP / SCIENCE SOURCE

The link between pesticides and Parkinson’s disease

FIGURE 2. Dopamine synapse. At the level of the synaptic cleft, transmission of the nerve impulse is made by a neurotransmitter.

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PESTICIDES AND PARKINSON’S DISEASE

NORMAL

PARKINSON’S Reduced dopamine

Transmitting neuron

Dopamine

Dopamine

Synaptic cell

Synaptic cell

Dopamine receptor

Dopamine receptor

Receiving neuron

Receiving neuron

© MONICA SCHROEDER / SCIENCE SOURCE

Transmitting neuron

FIGURE 3. Illustration showing low levels of dopamine in a neuron affected by Parkinson’s disease (right) and normal levels (left).

a cohort of more than 140,000 individuals, Ascherio et al merely reinforced the connection between organochlorine pesticides and Parkinson’s. A specific pesticide link is required to make a connection to the development of Parkinson’s.

Wang et al2 recognized the need to make this connection between specific pesticides used and Parkinson’s disease.

The researchers analyzed individuals working and living in the California Central Valley who were exposed to 3 specific pesticides (ziram, maneb, and paraquat). Contact occurred through air contamination at both the workplace and those residences within 500 meters of pesticide application.2 Wang and colleagues found an 80% increase in Parkinson’s disease development (especially among those younger at onset of symptoms) when exposed to a combination of 2 of the 3 pesticides. The risk was highest when ambient exposure occurred at both the residence and place of work, but it was lower (though not insignificant) among nonworking residents exposed through air contamination at home only. While this lower risk could be used to support a risk to golf course residents, the study further loses strength due to self-reporting. Wang et al also stated that a “derived poundage of active ingredient” could not be translated across pesticide classes equally. This would be needed to establish a connection to dopaminergic neuron toxicity and degradation. This has the effect of decreasing any association among golf course residents and would degrade any epidemiologic connection to golfers exposed to pesticides versus golf course workers.

One year later, Van Maele-Fabry et al3 provided the best attempt at quantification of workplace exposure between pesticides and Parkinson’s through a meta-analysis approach.

The researchers combined 12 prior analyses to increase the statistical power in their study. In addition, they expanded the selection of subjects internationally. The statistical method used evaluated homogeneity (similarities in comparability)2; the researchers also used statistical pooling to reduce publication bias (overstating conclusions). When high heterogeneity (diversity) was found, the evidence proved insufficient to demonstrate a causal relationship between pesticide exposure and Parkinson’s. While the results by Van Maele-Fabry et al showed a statistical increase in the risk of Parkinson’s disease, this increase was limited due to the documentation and diagnostic inconsistencies. Incidentally, Van Maele-Fabry et al also demonstrated a protective factor in cigarette use and caffeine intake. An inference can be made that these attributes are prevalent among golfers and may have provided some protection among older golfers who smoke.

Pesticides, Parkinson’s and golf

According to the previously mentioned studies, practitioners dealing with agricultural workers handling pesticides have reason for concern.1-3 Despite this suggested concern, a North American and European Medline search yields only 3 papers examining the estimated risk of pesticides to golfers. Murphy, Cooper, and Clark published a study evaluating the potential hazards of pesticide exposure via inhalation among golfers.12 The study looked at health risks from dermal exposure to 3 pesticides and extrapolated risk to measured air residues. Due to the suspected inhalation risk, the 3 specific pesticides were banned from golf course application (see Table 3).

Encouraged by this research, Murphy and Haith sought to establish an expanded pesticide list as an inhalation risk to

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golfers.13 These researchers took a broad geographical look at Parkinson’s risk by expanding the study group to 3 sites in the Northeast U.S., including Boston, Philadelphia, and Rochester. In addition, the researchers expanded the pesticides evaluated from their previous 3 to 15. The same study parameters were used in a search for the additional pesticides at risk. Despite a geographically broad and pesticide-specific search, Murphy and Haith’s study was without support for chronic inhalational health risks of current pesticides in use to golfers. The research team based their findings on possible regional variances, such as wind and temperature, in the application of the pesticides evaluated.

One year later, Putnam, Doherty, and Clark14 published a paper on dermal pesticide exposure to golfers. This study looked at 2 pesticides (chlorpyrifos and carbaryl) and 2 methods of exposure (inhalation and dermal). The test subjects were evaluated after walking a simulated 4-hour round of golf 1 hour following full-course pesticide application. Dermal exposure, not inhalation, was determined to be the overriding method of contact post-insecticide application. Despite the short time interval between exposure and application, these dermal doses were found to be 19 to 68 times below the Environmental Protection Agency (EPA) standards.14 The link among pesticides, Parkinson’s disease, and golf was further degraded by 4 factors. First, the exposures were designed to represent a worst-case scenario, as the exposure was early and represented an unlikely pattern for the average, or even professional, golfer to repeat. Second, when pesticides are applied to turf grass, it is not daily and the applications degrade quickly over several days, further decreasing ambient exposure. The same protection was found to apply to

greenskeepers as well. Third, these dermal doses correlate with EPA risk assessment. Last, Putnam et al found that if post-application exposure was delayed an additional hour, further dermal doses were reduced by an additional 30% (an 80% reduction in total dose).14 Putnam et al did note the presence of morning dew, which retards insecticide degradation, and an absence of solar radiation (in overnight application) as providing a lack of protection. Based on these data, Putnam et al suggested that turf grass application be adjusted to “half- or partial-course applications spaced over a day or two.” Putnam et al believed that this provided a best management practice that would further decrease the exposure risk to golfers; however, best management practice standards for pesticide use and application are established by the Occupational Safety and Health Administration (OSHA), as this agency has governmental oversight in this area. Despite having this oversight, as of 2011, U.S. public recording of specific pesticides used on golf courses are not required except in California.15

TABLE 1. Parkinson’s disease symptoms

TABLE 2. Anticholinergic antiparkinsonian drugs

Golf course residency and Parkinson’s

The concern to golf course residents is raised by Fields,6 who recommended that new purchasers of golf course residences consider buying upwind on a golf course. This suggestion is based on a letter to the editor citing chemical solvent exposure and the risk of Parkinson’s disease.5 As already established by Wang et al,2 there was demonstration of low risk to ambient pesticide exposure in the combination of pesticides within an active agricultural region. In 2012, Parrish et al performed a rudimentary, retrospective, randomized study that attempted to provide a connection between ambient pesticide exposure

Slow movement (bradykinesia)—the hallmark

Carbidopa/levodopa (Sinemet) Bromocriptine (Parlodel)

Progressive tremor at rest—usually a single upper extremity

Rotigotine transdermal system (Neupro) Pramipexole (Mirapex)

Muscle rigidity Loss of balance (postural instability) Dementia Unilateral symptoms

Ropinirole (Requip) Benztropine mesylate (Cogentin) Trihexyphenidyl (Artane) Selegiline HCI (Zelapar) Rasagiline (Azilect) Entacapone (Comtan) Tolcapone (Tasmar) Amantadine (Symmetrel)

Control with anti-Parkinson’s medications—medication challenge test (levodopa or a dopamine agonist)

Droxidopa (Northera) Rivastigmine tartrate (Exelon)

Compiled from Chou K. Patient information: Parkinson disease symptoms and diagnosis (beyond the basics). 2013. UpToDate.com

Compiled from the Parkinson’s Disease Foundation. Prescription Medications. 2014.

(Retrieved from http://www.pdf.org/parkinson_prescription_meds.)

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PESTICIDES AND PARKINSON’S DISEASE

TABLE 3. Banned and restricted pesticides U.S. banned pesticides • Aldrin

• EPN

• Benzene hexachloride

• Ethyl hexylene glycol (6-12)

• 2.3.4.5-Bis(2-butylene)tetrahydro- • Fluoroacetamide 2-furaldehyde (Repellent-11) • Hexachlorobenzene • Bromoxynil butyrate • Lead arsenate • Cadmium compounds

• Leptophos

• Calcium arsenate

• Mercurous chloride

• Captafol

• Mercuric chloride

• Carbon tetrachloride

• Mevinphos

• Chloranil

• Mirex

• Chlordane

• Monocrotophos

• Chlordecone (Kepone)

• Nitrofen (TOK)

• Chlordimeform

• OMPA (octamethylpyrophosphoramide

• Chlorinated camphene (Toxaphene) • Chlorobenzilate (chloromethoxypropylmercuricacid)

• Phenylmercury acetate • Phenylmercuric olate

• Copper arsenate

• Potassium 2,4,5-trichlorophenate (2.4.5-TCP)

• Cyhexatin

• Pyriminil (Vacor)

• DBCP

• Safrole

• DDT

• Silvex

• Dieldrin

• Sodium arsenite

• Dinoseb and salts • Di (phenylmercury) dodencenylsuccinate

• TDE • Terpene polychlorinates (Strobane) • Thallium sulfate

• 1,2-dibromoethane ethylene dibromide

• 2,4,5-Trichlorophenoxyacetic acid (2,4,5-T)

• Endrin

• Vinyl chloride

Severely restricted pesticides • Arsenic trioxide

• Lindane

• Carbofuran (granular)

• Pentachlorophenol

• Daminozide/alar

• Sodium arsenate

• Heptachlor

• Tributyltin compounds

and golf course residents.5 This study looked at 26 cases of individuals living with Parkinson’s in a metropolitan area.

Of those Parkinson’s cases, 19 lived within 2 miles of a golf course. From the 19 reported cases, 16 lived downwind of a golf course. Three of the total 26 cases were found to have been exposed to solvents, though they were not among the 19 reported living in the radius of concern. Thus, Parrish and Gardner’s thesis had several shortcomings. First, there was no evidence that any solvents were used on or near the golf courses in their study. Second, Parrish and Gardner’s study was very low in power, analyzing only 19 of 26 cases of individuals living with Parkinson’s disease within 2 miles of a golf course in a metropolitan area. Third, Parrish and Gardner’s conclusion was based only on an empirical connection between the 16 downwind cases.5 According to investopedia.com, the null hypothesis is a proposal used in statistical evaluation that states when there is no difference between study variables or that a single variable is essentially 0 that the study outcome “is presumed to be true until statistical evidence nullifies it for an alternative hypothesis”16 (para. 1). The assumption is that any difference is chance. As the breakdown of these prior studies suggests, the evidence to connect pesticides and Parkinson’s is soft at best. Armed with this information, a practitioner could feel justified in assigning the null hypothesis to the Fields’6 article.

The practitioner would then consider pesticide exposure, golf, and golf course residency as historical information only.

Summary

For the present, there is insufficient evidence to link ambient exposure to pesticides among golfers and the development of Parkinson’s disease. Previously published studies have based their conclusions on flawed case-controlled epidemiologic study methods. Further evaluations are needed to answer this question conclusively. A larger, more controlled evaluation of active pesticides in use is needed to determine conclusively that golfers are at risk of Parkinson’s disease due to frequent pesticide exposure. n Thomas Massing, MS, PA-C, FAPACVS, is a physician assistant at CompHealth in Woodstock, Ga. References 1. Ascherio A, Chen H, Weisskopf MG, et al. Pesticide exposure and risk for Parkinson’s disease. Ann Neurol. 2006;60(2):197-203.

Compiled from the Colorado Environmental Pesticide Education Program. Banned and severely restricted pesticides. 2006.

(Retrieved from http://www.cepep.colostate.edu/Fact %20 Sheets/141BannedPesticides.pdf )

2. Wang A, Costello S, Cockburn M, et al. Parkinson’s disease risk from ambient exposure to pesticides. Eur J Epidemiol. 2011;26:547-55.

Continues on page 48

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PESTICIDES AND PARKINSON’S DISEASE

3. Van Maele-Fabry G, Hoet P, Vilain F, Lison D. Occupational exposure to

10. Colorado Environmental Pesticide Education Program. Banned and

pesticides and Parkinson’s disease: A systematic review and meta-analysis

severely restricted Pesticides. 2006. Retrieved from: http://www.cepep.

of cohort studies. Environ Int. 2012;46:30-43.

colostate.edu/Fact%20Sheets/141BannedPesticides.pdf

4. Goldman S, Quinlan P, Ross W, et al. Solvent exposures and Parkinson

11. Environmental Protection Agency. Restricted use products. 2013.

disease risk in twins. Ann Neurol. 2012;71(6):776-784.

Retrieved from: http://www.epa./opprd001/rup/rupreport.pdf

5. Parrish ML, Gardner RE. Is living downwind of a golf course a risk factor

12. Murphy K, Cooper R, Clark J. Volatile and dislodgeable residues fol-

for parkinsonism? Ann Neurol. 2012;72(6):983-984.

lowing trichlorfon and isazofos application to turfgrass and implications for human exposure. Crop Science. 1996;36:1446-1454.

Retrieved from: http://www.huffingtonpost.com/dr-douglas-fields/golf-

13. Murphy R, Haith D. Inhalation health risk to golfers from turf-

parkinsons_b_2589611.html

grass pesticides at three northeastern U.S. sites. Environ Sci Technol.

7. Pakkenberg B, Møller A, Gundersen H, et al. The absolute number

2007;41(3):1038-1043.

of nerve cells in substantia nigra in normal subjects and in patients with

14. Putnam R, Doherty J, Clark J. Golfer exposure to chlorpyrifos

Parkinson’s disease estimated with an unbiased stereological method.

and carbaryl following application to turfgrass. J Agric Food Chem.

J Neurol Neurosurg Psychiatry. 1991;54(1):30-33.

2008;56(15):6616-6622.

8. Van Den Eeden S, Tanner C, Bernstein A, et al. Incidence of Parkinson’s

15. Arcury-Quandt A, Gentry A, Marin A. Hazardous materials on golf

disease: Variation by age, gender, and race/ethnicity. Am J Epidem.

courses: Experience and knowledge of golf course superintendents

2003;157(11):1015-1022.

and grounds maintenance workers from seven states. Am J Ind Med.

9. Centers for Disease Control and Prevention. Fourth national report on

2001;54(6):474-485.

human exposure to environmental chemicals. 2009. Retrieved from: http://

16. Null hypothesis. Investopedia.com. 2013. Retrieved from: http://www.

www.cdc.gov/exposurereport/pdf/FourthReport.pdf

investopedia.com

© The New Yorker Collection 2016 from cartoonbank.com. All Rights Reserved.

6. Fields D. Golf links to Parkinson’s disease? Huffpost Healthy Living. 2013.

“It’s small, but it’s right on the beach.”

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CME CE

n LEARNING OBJECTIVES After completing the activity, the participant should be better able to: • Discuss the role of targeting adherence issues in the geriatric patient for management of hypertension.

• Identify adherence strategies for the geriatric patients receiving hypertension therapy within the first 3 treatment visits.

• Manage memory loss in geriatric patients with hypertension.

FEATURED COURSE

n COMPLETE THE POSTTEST: Page 58

This activity is provided by Haymarket Medical Education (HME) for physician credit.

This activity is jointly provided by Global Education Group and HME for nursing contact hours.

Release Date: May 15, 2016 Expiration Date: May 15, 2017 Estimated time to complete the educational activity: 30 minutes Statement of Need: Primary care providers need to be aware of recommendations for geriatric patients with hypertension, complications of the aging/geriatric patient, and causes of poor adherence to medical treatment.

Target Audience: This activity has been designed to meet the educational needs of primary care healthcare professionals who will treat geriatric patients with hypertension.

Faculty Michaela Jones, MS, AGPCNP-BC Mount Sinai Hospital, New York, N.Y. Accreditation Statements Physician Credit: HME is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical ­education for physicians.

Credit Designation: HME designates this enduring material for a maximum of 0.5 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Nursing Credit: Global Education Group is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s COA. Credit Designation: This educational activity for 0.5 contact hours (0.10 pharmacotherapy credit) is provided by Global Education Group. Nurses should claim only the credit commensurate with the extent of their participation in the activity.

American Academy of Physician Assistants (AAPA) The AAPA accepts certificates of participation for educational activities certified for AMA PRA Category 1 Credit™ from organizations accredited by ACCME or a recognized state medical society. Physician assistants may receive am ­ aximum of 0.5 hour of Category I credit for completing this program.

Disclosure Policy In accordance with the ACCME Standards for Commercial Support, HME requires that individuals in a position to control the content of an educational activity disclose all relevant financial relationships with any commercial interest. HME resolves all conflicts of interest in an effort to ensure independence, objectivity, balance, and scientific rigor in all its educational programs. Furthermore, HME seeks to verify that 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. HME is ­committed to providing its learners with high-quality CME/ CE activities that promote improvements in health care and not those of a commercial interest.

CME-Feat_Ger-Hyertension_CA0516.indd 52

The faculty reported the following financial relationships with commercial interests whose products or services may be related to the content of this CME activity: Faculty Disclosures

Name of faculty

Reported Financial Relationship

Michaela Jones, MS, AGPCNP-BC

No relevant financial relationships

Staff/Planners’ Disclosures The planners, managers, and reviewers for this program reported the following ­financial relationships with commercial interests whose products or services may be related to the content of this CME activity: HME planners, managers, and reviewers have no relevant financial relationships to disclose.

Global Education Group planners: Ashley Marostica, RN, MSN, Amanda Glazar, PhD, and Andrea Funk have nothing to disclose.

Disclosure of Unlabeled Use: This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the FDA. HME and Global Education Group do not recommend the use of any agent outside of the labeled indications. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings.

Method of Participation: There are no fees for participating in and receiving CME/CE credit for this activity. During the period of February 15, 2016, through February 15, 2017, participants must: 1) read the learning objectives and faculty disclosures; 2) study the educational activity; 3) complete the posttest and submit it online (clinicians 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 HME or Global Education Group. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patient’s conditions and possible contraindications 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.

4/25/16 3:57 PM

CME CE FEATURED COURSE: MICHAELA JONES, MS, AGPCNP-BC

Adherence and hypertension in the geriatric patient Addressing factors that lead to lack of adherence to antihypertensive therapy in elderly patients is crucial to improving outcomes.

H

© THINKSTOCK

ypertension is one of the most common chronic conditions that providers of geriatric care are challenged with managing. As the population gets older, issues associated with aging, such as providing quality medical care, including the management of hypertension, become increasingly difficult to address.

In many cases, poor adherence to a medication regimen is a reason for uncontrolled high blood pressure and a major predictor of nursing home placement in frail geriatric patients.1 Adherence rates in the elderly vary from 26% to 59%.2 Approximately 7.1 million die of complications of uncontrolled hypertension, so managing the problems that lead to poor adherence is a necessity for improving control of hypertension and overall quality of life.

Understanding adherence to treatment is key for primary care providers to effectively treat the elderly patient with hypertension. Factors found to prevent adherence include cognitive degeneration, lack of understanding, depression, complexity of treatment, and cost of treatment. Strategies to increase adherence target these barriers in order to improve cardiovascular health (Figure 1).

This article addresses issues in adherence to treatment in older adults. It provides evidence-based recommendations for interventions that nurse practitioners and physician assistants can use in clinical practice.

Managing hypertension in the elderly is a complicated task.

Management of hypertension in the elderly

Antihypertensive therapy is associated with a decreased incidence of stroke and risk for myocardial infarction

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CME CE

FEATURED COURSE

FIGURE 1. Strategies to increase adherence to antihypertensive therapy in elderly patients.

Confirmed non-adherence to anti-hypertensive therapy

Fill knowledge gaps.

Cognitive impairment

Depression and lack of self-efficacy

Mini mental status exam / patient evaluation

Geriatric Depression Scale

Use memory aids.

Form associations with medication administration.

Consider medications for cognitive health.

Develop trust.

Offer motivational interview.

Provide hope.

Consider SSRIs.

Key: SSRI, selective serotonin reuptake inhibitor.

and heart failure.3 Elderly individuals are already at an increased risk for these conditions; it is therefore particularly important to manage their hypertension effectively and appropriately.

The current guidelines of the Eighth Joint National Committee (JNC 8), released in December 2013, recommend a blood pressure goal below 150/90 mm Hg in all patients aged 60 years or older with uncomplicated hypertension.4 This goal, which is less stringent than the JNC 7 target blood pressure goal, is one of the ways in which providers are attempting to increase adherence and improve outcomes.5 However, barriers to meeting the goal still exist.

Adherence issues and recommendations

Cognitive degeneration. Cognitive degeneration affects much of the geriatric population. Each year, mild cognitive impairment affects more than 6% of Americans aged 70 to 89 years, whereas Alzheimer disease affects more than one-third of Americans aged older than 85 years. The accumulation of amyloid plaque, appearance of neurofibrillary tau tangles, and depletion of acetylcholine are some of the main pathologic changes that occur with the development of Alzheimer disease and cognitive degeneration.

Cognitive degeneration can range from mild disease with some functional dependence (eg, trouble managing finances) to moderate disease with greater dependency on others (eg, frequent inability to drive and some difficulty with bathing and shopping) to severe Alzheimer disease with motor and balance impairment and subsequent dependence on caretakers. The type of memory most commonly affected by cognitive loss is prospective memory—the ability to remember information

pertaining to future events.6 Loss of prospective memory manifests as forgetfulness regarding upcoming appointments, medication regimens, and essentially all future planning involving disease management. Several studies have shown that a decrease in the mini mental state exam (MMSE) score is negatively correlated with adherence.7-10 There are many ways in which cognitive impairment can manifest and therefore, can potentially impact adherence.

Effective blood pressure control does not make individuals “feel” better, and poor control does not make them feel worse. Therefore, patients with little understanding of the significance and consequences of uncontrolled hypertension often do not understand the importance of treatment. Several studies have shown that poor comprehension of treatment and management plans on the part of geriatric patients is a significant barrier to their adherence to medication.10-13 Elderly patients with hypertension and inadequate knowledge of other diseases they may have that are not related to their hypertension are less likely to be compliant.13-15 Tackling cognitive degeneration as an adherence issue in the management of hypertension is particularly challenging because studies have shown that hypertension as well as some other cardiovascular risk factors are strongly correlated with the development of dementia.16 However, several pharmacologic and nonpharmacologic means of addressing cognitive degeneration are available. The provider should consider both when seeking to assess adherence.

Providers must consistently identify and address any misunderstandings or knowledge gaps that a geriatric patient may have regarding a current treatment plan. Counseling the

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Confirmed non-adherence to anti-hypertensive therapy

Consider fixed-dose combination drugs.

Complexity of medication regimen

Cost

Medication reconciliation

Assessment of financial strain

Eliminate unnecessary medications.

Identify one provider to manage therapy.

Use blister packs.

Choose generics over brands.

patient about the medication regimen significantly increases compliance rates, especially when the compliance issue is related to adverse effects or a misguided belief that the therapy is ineffective.15,17 Take the time needed to discuss the diagnosis with the patient and the importance of the treatment plan so that he or she leaves remembering and understanding it.

Memory aids have been shown to increase medication compliance in individuals with any level of cognitive impairment.10 Memory aids are tools and/or techniques used to remind the patient of any certain future task due. External aids are items the patient can touch or handle, therefore providing external sensory information; these include alarms, timers, notebooks, date books, “to-do” lists, calendars, tape recorders, conversation logs, and pillboxes. Allowing a patient to choose the aid with which he or she is most comfortable is also important because self-efficacy improves adherence.10,18 Taking a medication with a daily event, such as a meal, also increases adherence.19 These strategies do not improve cognitive ability but rather serve as ways around the impairment to maintain function and therefore adherence.

Some medications can be used concurrently with antihypertensive drugs to improve cognitive function, in turn improving adherence to the antihypertension medication.

Acetylcholinesterase inhibitors are first-line agents for the treatment of mild to moderate cognitive disease.20 Other medications include N-methyl-D-aspartate (NMDA) receptor antagonists such as memantine and the monoamine oxidase type B inhibitor selegiline.

Depression. Depression is strongly linked to a lack of selfefficacy, especially when it comes to adherence.10,21 Hopelessness

Choose cheaper options for medication plans.

is a key factor in both depression and lack of self-efficacy, which in turn lead a patient to feel less motivated to adhere to therapy.

Depression in the elderly is extremely common; more than 7 million people aged older than 65 years have it. There is a strong correlation between the diagnosis of a chronic condition, disability, and depression.22 Furthermore, the development of depression has been linked to the worsening of disability.23 Studies have shown an increase in mortality from cardiovascular disease among patients who are depressed.24 Although there are benefits to addressing depression that go beyond—and in some ways are more important than— improving adherence to medication, the primary care provider should consider it essential to screen all geriatric patients for depression when medication compliance is a concern. Several effective screening tools for depression are available, including the Geriatric Depression Scale. For those patients who are at risk, taking the time to discuss personal life issues during each visit may be all the therapy they need.

When therapy is not enough, selective serotonin reuptake inhibitors (SSRIs) have been shown to be extremely effective for mitigating depressive symptoms in elderly patients.25 Because depression and lack of self-efficacy go hand in hand, particularly in elderly patients, clinicians can improve self-efficacy in order to guide their patients toward adherence. Primary care providers have always excelled at tailoring regimens to their patients’ lifestyles and needs. Establishing a sense of trust and sharing decision-making regarding a patient’s treatment plan increase the likelihood that the patient will follow through with that plan.10,26 The use of motivational interviewing techniques with a patient works

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CME CE

FEATURED COURSE

Studies show that as the number of daily doses of hypertension medication increases, patient adherence to the regimen increasingly fails. to decrease the patient’s sense of desperation regarding his or her diagnosis. Providing hope for patients is an integral part of assisting them to feel motivated to participate in their plan.

Complexity of the medication regimen. Polypharmacy is the term used to define prescription of multiple drugs across a variety of situations. Polypharmacy can be any of the following: (1) the use of five or more medications or the use of two or more medications to treat the same condition; (2) the use of two or more drugs of the same chemical class; (3) the use of two or more agents with the same or similar pharmacologic actions to treat different conditions; (4) the prescribing of more medication than is clinically indicated; and/or (5) a medical regimen that includes at least one unnecessary medication. Geriatric patients are the most vulnerable when it comes to polypharmacy.27 The average geriatric patient takes between three and five medications daily.28 Two-thirds of community-dwelling people older than age 60 years take four or more medications, and those with chronic diseases may take up to eight or more prescribed medications daily. A small subset of elderly patients who are frail and have multiple comorbidities take an average of nine pills daily.

Hypertension therapy involves the highest number of medications, usually an assortment of drugs of various classes.

Studies provide strong evidence that as the number of daily doses of hypertension medication increases, patient adherence to the regimen increasingly fails.10,19 When investigating

barriers to taking blood pressure medications, clinicians should conduct a medication reconciliation to identify the level of complexity of the medication regimen.

If complexity is found to be a barrier, one of the most important things a clinician can do is to simplify the medication regimen to facilitate adherence. Monotherapy is often inadequate for controlling blood pressure and preventing cardiovascular disease outcomes in elderly patients. When adherence to a treatment plan is a challenge, however, simplifying the regimen should be a goal. The use of fixed-dose combination drugs rather than component-based free-combination therapy has been shown to improve compliance in several cases.17,29 It is recommended that the clinician taper or withdraw one medication at a time.

This is important for diminishing adverse physiologic effects, such as hypotension and syncope, as well as patient confusion.

Patients who have complex plans of care require frequent follow-up visits with a medication reconciliation at each visit. The clinician should perform a periodic review of each patient’s electronic medical records to stay organized and on top of the patient’s personalized antihypertensive therapy.

Because continuity of care helps simplify the management of hypertension, one provider should manage the patient’s hypertension regimen. This helps reduce complications related to communication errors.10,13,18 Blister packs are a relatively new and innovative way of organizing complicated medication regimens. These consist

Case study: A 70-year-old man with hypertension who is having trouble remembering to take his medication A 70-year-old man is referred to your practice for primary care and management of his hypertension. He reports that he feels “overwhelmed” by his high blood pressure regimen and admits that he does not always remember to take each of his medications at the right time.

His vital signs are as follows: weight, 186 lb; height, 58.2 in; body mass index (BMI), 28.0; blood pressure, 168/88 mm Hg; heart rate, 80 beats/min; respiration rate, 16 breaths/min; oral temperature, 98.7˚F. His medications are the following: hydrochlorothiazide, 25 mg; lisinopril, 5 mg; metoprolol, 100 mg; atorvastatin, 20 mg; Colace (docusate sodium), 200 mg; vitamin D3, 2,000 IU. A long list of medications may indicate confusion about polypharmacy and a complex regimen of prescribed therapy.

Other assessments include a review of systems, past medical history, physical examination, mini mental state examination (MMSE), and the Geriatric Depression Scale.

For this patient, simplifying the medication list is an effective way to make it easier for him to follow a prescribed plan. Hydrochlorothiazide and lisinopril are available as a combination drug. Given the number of pills he has to take, the use of blister packs may alleviate his confusion about taking different medications in different containers. Having the patient set an alarm to take his medication at a certain time of the morning can provide an external reminder that helps him to keep on track. Additional cognitive health management and treatment for depression can be provided if necessary.

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Evidence shows that screening for adherence and addressing factors that are leading to a lack of adherence are crucial to improving outcomes. of pre-formed plastic packaging that can contain individual or multiple medications. The purpose of the packs is to help organize medication regimens so that the patient no longer has to organize pills according to when they must be taken throughout the day and week. Blister packs have been found to reduce the risk for noncompliance among consumers significantly.30 If disorganization or cognitive impairment is a potential barrier, the primary care provider can recommend this option and ask the pharmacist to implement blister packs in the patient’s care.

Cost. The cost of medication is a substantial obstacle for the majority of the geriatric population. With the current gaps in today’s health care systems, many geriatric patients find themselves in the “doughnut hole.” With Medicare Part D, insurance pays for medications until a limit of approximately $3,000 is reached, at which time the patient must begin to pay out of pocket.

Because the need for multiple medications to manage hypertension effectively is nearly unavoidable, the maximum Part D benefit is often quickly reached. This may leave patients unable to afford their medications. If they lack funds, elderly patients are more likely to not refill their prescriptions.18 The rates of discontinuation of brand and generic medications do not differ. Therefore, generic medications may achieve similar results in regard to compliance.31 Choosing less expensive regimens, such as diuretics, over more costly medications is recommended when cost is a barrier to a patient’s adherence to treatment. Decreasing the number of medications can decrease confusion; additionally, it can reduce costs and may be especially beneficial for geriatric patients.

foundational ideology of patient-centered practice. Clinicians not only diagnose and manage but also assess how contextual factors can impact the management of care. Assessing these factors on an ongoing basis will improve patient satisfaction and overall quality of life among the geriatric population. n Michaela Jones, AGPCNP-BC, is a DNP candidate at Columbia University and a nurse practitioner at Mount Sinai Hospital Department of Preventative Medicine in Manhattan.

References 1. Lewis A. Non-compliance: a $100 billion problem. The Remington Report.

1997;5(4):14-15.

2. Tangalos EG, Zarowitz BJ. Medication management in the elderly. Ann Longterm Care. 2006;14(8):27-31.

3. Karnes JH, Cooper-DeHoff RM. Antihypertensive medications: benefits of blood pressure lowering and hazards of metabolic effects. Expert Rev Cardiovasc Ther. 2009;7(6):689-702.

4. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults. Report from the panel members appointed to the Eighth Joint National Committee (JNC 8).

JAMA. 2014;311(5):507-520.

5. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Hernandez Cardenache R, Burguera L, Acevedo A, Curiel R, Loewenstein DA. Evaluating different aspects of prospective memory in amnestic and nonamnestic mild cognitive impairment. ISRN Neurol. 2014;2014:805929.

7. Gray SL, Mahoney JE, Blough DK. Medication adherence in elderly patients receiving home health services following hospital discharge. Ann

Conclusion

Pharmacother. 2001;35(5):539-545.

The management of hypertension in the elderly is a complicated task that the health care provider must master.

Poor adherence to medication is a clear contributor to the difficulty. Evidence shows that screening for adherence and addressing any factors that are leading to an individual’s lack of adherence are crucial to improving outcomes. Doing so involves not only understanding hypertension therapy in the context of the geriatric patient but also maintaining close contact with the geriatric patient and consistently assessing for any complications associated with therapy.

Primary care providers play an important role in alleviating the complications that may arise from lack of adherence. The use of individualized treatments that are tailored to the geriatric patient aligns with nurse practitioners’ and physician assistants’

8. Madarshahian F, Hassanabadi M, Koshniat Nikoo M. Cognitive status and foot self care practice in overweight diabetics, engaged in different levels of physical activity. J Diabetes Metab Disord. 2014;13(1):31.

9. Ownby RL, Hertzog C, Crocco E, Duara R. Factors related to medication adherence in memory disorder clinic patients. Aging Ment Health.

2006;10(4):378-385.

10. MacLoughlin EJ, Raehl CL, Treadway AK, et al. Assessing medication adherence in the elderly. Drugs Aging. 2005;22(3):231-255.

11. Pasina L, Brucato AL, Falcone C, et al. Medication non-adherence among elderly patients newly discharged and receiving polypharmacy.

Drugs Aging. 2014;31(4):283-289.

12. Engel KG, Buckley BA, Forth VE, et al. Patient understanding of emergency department discharge instructions: where are knowledge deficits greatest? Acad Emerg Med. 2012;19:1035-1044.

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CME CE

FEATURED COURSE

13. Nelson EC, Stason WB, Neutra RR, Solomon HS, Mcardle PJ. Impact of patient perceptions on compliance with treatment for hypertension.

CME CE

Med Care. 1978;16(11):893-906.

14. Balkrishnan R. Predictors of medication adherence in the elderly. Clin Ther. 1998;20:764-771.

POSTTEST Expiration date: May 15, 2017

15. Morrell RW, Park DC, Poon LW. Effects of labeling techniques on

FEATURED COURSE

memory and comprehension of prescription information in young and old adults. J Gerontol. 1990;45(4):P166-P172.

CREDITS: 0.5

16. Duron E, Hanon O. Vascular risk factors, cognitive decline, and demen-

For more credit information, please turn to p. 52.

tia. Vasc Health Risk Manag. 2008;4(2):363-381.

17. Kellaway GS, McCrae E. The effect of counselling on compliance-failure in patient drug therapy. N Z Med J. 1979;89(631):161-165.

18. Marek KD, Antle L. Medication management of the community dwelling. In: Houghs RG, ed. Patient Safety and Quality: An Evidence-Based Handbook for Nurses. Rockville, MD: Agency for Health Care Research and Quality (US); 2008:chap 18.

19. Bovet P, Burnier M, Madeleine G, et al. Monitoring one-year compliance to antihypertension medication in Seychelles. Bull WHO. 2002;80(1):33-39.

20. Winslow BT, Onysko MK, Stob CM, et al. Treatment of Alzheimer disease. Am Fam Physician. 2011;83(12):1403-1412.

21. Conner M, Norman P. Predicting Health Behaviour: Research and Practice With Social Cognition Models. Buckingham, UK: Open University Press; 1996.

22. Turner J, Kelly B. Emotional dimensions of chronic disease. West J Med. 2000;172(2):124-128.

23. Manalai P, Hamilton RG, Langenberg P, et al. Pollen-specific immunoglobulin E positivity is associated with worsening of depression scores in bipolar disorder patients during high pollen season. Bipolar Disord.

2012;14(1):90-98.

24. Egede LD, Nietert PJ, Zheng D. Depression and all-cause and coronary heart disease mortality among adults with and without diabetes. Diabetes Care. 2005;28(6):1339-1345.

25. Schneider LS. Pharmacologic considerations in the treatment of latelife depression. Am J Geriatr Psychiatr. 1996;28(6):1339-1345.

26. Pawar M. Five tips for generating patient satisfaction and compliance.

Fam Pract Manag. 2005;12(6):44-46.

27. Wooten J, Galavis J. Polypharmacy. Keeping the elderly safe. RN. 2005;68(8):44-50.

28. Williams C. Using medications appropriately in older adults. Am Fam Physician. 2002;66(10):1917-1925.

29. Gupta AK, Arshad S, Poulter NR. Compliance, safety, and effectiveness of fixed-dose combinations of antihypertensive agents: a meta-analysis.

Hypertension. 2010;55(2):399-407.

30. Wong BS, Norman DC. Evaluation of a novel medication aid, the calendar blister-pak, and its effect on drug compliance in a geriatric outpa-

1. According to JNC 8, what is the blood pressure goal in individuals aged older than 60 years? a. 140/80 mm Hg c. 150/80 mm Hg b. 140/90 mm Hg d. 150/90 mm Hg 2. A 68-year-old patient is not taking his blood pressure medications. What is one condition the provider should evaluate when assessing the causes of the patient’s non-adherence? a. Diabetes c. Dementia b. Constipation d. Infection 3. What is NOT a recommendation to improve adherence to antihypertensive therapy of a geriatric patient with cognitive impairment? a. Have the patient keep the medication next to his or her toothbrush. b. Tell the patient to follow a no-salt diet to compensate for missed doses. c. Advise the patient to keep a reminder to take the medication on the refrigerator. d. Have a discussion with the patient about symptoms of high blood pressure that are experienced versus symptoms that are not physically felt.

4. You find that your 66-year-old female patient with a ­history of not taking her blood pressure medication has a Geriatric Depression Scale score indicating the presence of depression. What is an appropriate next step when you discuss adherence with this patient? a. Use motivational interviewing techniques to make the patient feel empowered to take control over her blood pressure. b. Refer the patient for a mental health evaluation. c. Continue to focus on the high blood pressure and add a new medication for tighter control. d. Tell the patient that you are the provider and she needs to listen to you to in order to feel better.

tient clinic. J Am Geriatr Soc. 1987;35(1):21-26.

31. Corrao G, Soranna D, La Vecchia C, et al. Medication persistence and the use of generic and brand-name blood pressure-lowering agents.

J Hypertens. 2014;32(5):1146-1153.

TO TAKE THE POSTTEST please go to: myCME.com/May16CAfeature

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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.

YOUR COMMENTS READERS WEIGH IN ON NON-NARCOTIC TREATMENT OPTIONS FOR PATIENTS WITH MUSCULOSKELETAL PAIN Chronic NSAID use is now one of the most common causes of progressive kidney disease [Advisor Forum, “Non-narcotic analgesics for musculoskeletal pain,” April 2016, p. 51]. As a nephrologist, half of my referrals are because of long-term, standard-dose NSAIDs.—JACK MONCRIEF, MD, Austin, Tex. (211-1) I suggest looking carefully at the literature supporting salsalate as first-line analgesic therapy given: • its endorsement by the American Heart Association as a “first-line” analgesic in 2007 • its effect on metabolism and diabetes—it lowers A1c levels and probably lowers insulin resistance, and it has positive lipid panel effects Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. You may contact us by e-mail at editor@ clinicaladvisor.com. If you are writing in response to a published letter, please indicate so by including the number in parentheses at the end of each item. Letters are edited for length and clarity. The Clinical Advisor’s policy is to print the author’s name with the letter. No anonymous contributions will be accepted.

• its effect on the stomach—ie, does it cause significant GI bleeds; or, can it even be used in patients who have had GI bleeds from other NSAIDs? • its blood level can be monitored (via salicylate levels) • its non-effect on platelet aggregation inhibition • its location in a non–Cox-1 and non–Cox-2 category of NSAIDs —CHARLES BEAUCHAMP, MD, PhD, Ahoskie, N.C. (211-2) I advise patients with musculoskeletal pain to ALTERNATE acetaminophen with an NSAID, thereby producing synergistic pain relief, while reducing the risks of overdosing.—WILLIAM TWEEDDALE, RPA-C, Kingston, N.Y. (211-3)

PASSING ON FULL-PRACTICE AUTHORITY I am writing to support Ms. Pulver’s letter [“No thanks, on full-practice authority,” Advisor Forum, March 2016, p.

46], and to thank her. I also have almost 40 years of physician assistant practice behind me and remember clearly the sales push for oxycontin, the “nonaddicting” wonder drug.

Suboxone, I think, is going to prove to be no different. Our society has always leaned toward the easy fix, but in drug addiction, there isn’t one.

Working now in the emergency room setting, I have cause to often order drug screens. What I consistently see is urine samples that test positive for suboxone, methamphetamine,

OUR CONSULTANTS

Philip R. Cohen, MD,

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

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

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

Abimbola Farinde, PhD, PharmD,

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

Laura A. Foster, CRNP, FNP,

Abby A. Jacobson, MS, PA-C,

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

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

60 THE CLINICAL ADVISOR • MAY 2016 • www.ClinicalAdvisor.com

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cocaine, and opiates, and I rarely see one that tests positive for only suboxone. Suboxone has been sold in many forms, each one changed as it has been noted how easy it is to crush, cook, inject, etc. This is not the history of a safe drug or one that has any place in our practices for helping addicts.

I also agree that we should have full prescribing privileges, the same as MDs and DOs; however, I do not think that anyone should be prescribing suboxone.—BEATRICE BALSAMO, PA-C, MPAS, Ranchos de Taos, N.M. (211-4)

CLINICAL PEARLS OBTAINING A URINE SPECIMEN IN A CHILD When attempting to get a urine specimen from small children (especially great with a male), using a sharpie or a two-sided sticker, place a star or heart on the bottom of the specimen container (outside). Have them try to cover it up with their urine. A challenge becomes a game.—JACQUELINE ANDERSON, MSN, FNP-BC, Santa Rosa, Calif. (211-5) CLOZAPINE USE AND NEUTROPENIA If a patient on clozapine starts having neutropenia (ANC < 2.0), I recommend low-dose lithium to bring his or her ANC back up to > 2.0.—KAREN MILEN, FNP-BC, Chattanooga, Tenn. (211-6)

CASE FILES SALIVARY DUCT STONE A 58-year-old male presents with rapidly increasing pain and tenderness on the right side of his face, centering near the right temporomandibular joint and extending down his

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.

neck. He denies trauma but feels achy all over. He had just tried to use a cough drop, and this caused a sudden, intense burst of pain.

The man’s vital signs indicated a low-grade temperature of 99.8° F. His pain rating was an 8 at rest. The right side of his face was visibly swollen. The area was warm and exquisitely painful to touch, and submandibular and anterior cervical lymph nodes were enlarged. An oral exam showed a swelling near the posterior gum line that was very tender. With the history of increased sharp pain with a cough drop, a preliminary diagnosis of sialolithiasis, or salivary duct stone, was made. These stones are formed by crystallization of certain chemicals in normal saliva but occur often in cases of dehydration or use of medications that cause dry mouth.

Often, these stones are so small that they pass on their own.

When they are large enough to block the duct, the back-up of saliva becomes inflamed, and often a localized infection ensues. Intervention begins with increasing fluid intake and sucking on sour candies or other foods to intentionally increase the flow of saliva in an attempt to “float” out the stone. Application of heat often helps. Another simple technique is to massage the area in a “milking” fashion, applying pressure in the direction of salivary flow to try and force the stone free. In a small percentage of patients, actual surgical intervention is needed, either by making a small slit at the duct or using new micro-endoscopic techniques to snare the stone. Antibiotics are given for the infection.

This patient was not improving after 36 hours and sought relief from his ENT physician, who performed the massage technique with immediate release of a “gush” of foul-tasting saliva. His pain improved rapidly from that point, and he recovered without further incident. (211-7)—SHERRIL SEGO, FNP-C, DNP (See photo at bottom of this page for more information about Dr. Sego.) n

Claire O’Connell, MPH, PA-C,

Katherine Pereira, DNP, FNP,

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

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

Sherril Sego, FNP-C, DNP,

is an independent consultant in Kansas City, Mo.

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READER SURVEY SERIES: LAUREN BISCALDI AND COLBY STONG

PULSEPOINT POINT

SALARYSURVEY

How does your salary compare with that of your peers?

A majority of nurse practitioners (NPs) and physician assistants (PAs) earned a higher income than they did in 2014-2015, according to results from The Clinical Advisor’s 2016 annual salary survey. About 57% of NPs reported that they received a raise this year, while 54% of PAs had a raise.

The average salaries in 2015-2016 for NPs and PAs are:

ALL NPs

$101,989

ALL PAs

$108,743

Family medicine remains top practice area

Family medicine continued to be the top practice area among NPs (24.1%) and PAs (18.8%) this year.

The second most common specialty area for NPs was pediatrics (5.5%), while emergency medicine (8.0%) was the second most common category for PAs. Survey responders are getting younger on average, as the top experience level for NPs and PAs was

How the results were analyzed We asked our readers to provide their current salaries, which included base pay and bonuses, in increments of $5,000. The salaries were then converted to the midpoint within that category (for example, salaries in the $71,000 to $75,000 category were converted to $73,000).

This year, to be more precise with our results, we expanded our salary categories to include increments of $5,000 beginning with $0 to $5,000. And we added categories in $5,000 increments from $150,000 to $200,000.

The findings are based on analysis of 2,139 NPs who responded to the NP survey and 832 PAs who responded to the PA survey.

those having 5 or fewer years experience: 32.1% of NP responders have 5 or fewer years of experience, and 23.9% of PA responders have 5 or fewer years of experience.

The West continues to be the region with the highest salaries for NPs and PAs, and those who work in urban areas continue to make more than their colleagues who work in rural and suburban areas.

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This is the latest installment of Pulse Point, our crowdsourced feature that aims to bring you visual insights on the latest healthcare trends among your clinician peers. If you have a topic that you would like to see covered, please send it to editor@clinicaladvisor.com.

See the complete survey results online at ClinicalAdvisor.com/2016SalarySurvey TABLE 1. Average NP salary by practice area

TABLE 2. Average PA salary by practice area

Practice area

Percent response

Average salary

Practice area

Percent response

Average salary

Family Medicine

24.1% (n=509)

$97,392

Family Medicine

18.8% (n=155)

$96,306

Pediatrics

5.5% (n=117)

$93,562

Emergency Medicine

8.0% (n=66)

$126,364

Adult Medicine

5.2% (n=111)

$101,914

Urgent Care

6.9% (n=57)

$112,237

Primary Care

4.9% (n=104)

$97,404

Orthopedic Surgery

5.8% (n=48)

$125,208

Cardiology

4.5% (n=96)

$103,958

Dermatology

3.4% (n=28)

$133,929

TABLE 3. Average NP salary by experience level

TABLE 4. Average PA salary by experience level

Years of experience

Percent response

Average salary

Years of experience

Percent response

Average salary

≤5

32.1% (n=683)

$98,071

≤5

23.9% (n=199)

$98,153

6-10

16.4% (n=349)

$104,950

6-10

19.5% (n=162)

$108,241

11-15

20.1% (n=427)

$102,512

11-15

21.8% (n=181)

$113,384

16-20

16.2% (n=344)

$106,570

16-20

13.8% (n=115)

$114,065

>20

15.3% (n=325)

$103,054

>20

21.0% (n=175)

$113,214

FIGURE 2. Average PA salary by geographic region

FIGURE 1. Average NP salary by geographic region West

Midwest

Northeast

West

Midwest

Northeast

(n=388) $109,098 average salary

(n=476) $99,979 average salary

(n=448) $102,042 average salary

(n=168) $114,643 average salary

(n=165) $102,045 average salary

(n=204) $106,250 average salary

South

South

(n=827) $99,822 average salary

(n=294) $111,361 average salary

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READER SURVEY SERIES

TABLE 5. Average NP salary by urban, suburban, or rural location

TABLE 6. Average PA salary by urban, suburban, or rural location

Practice setting

Percent response

Average salary

Practice setting

Percent response

Average salary

Rural

25.1% (n=535)

$99,519

Rural

19.4% (n=160)

$107,750

Suburban

36.4% (n=776)

$102,526

Suburban

39.4% (n=325)

$108,423

Urban

38.4% (n=818)

$103,020

Urban

41.1% (n=339)

$109,034

TABLE 7. Average NP salary according to gender

TABLE 8. Average PA salary according to gender

Female

Male

Female

Male

(n=1,937)

(n=168)

(n=555)

(n=258)

$101,008

$115,744

$103,320

$120,543

TABLE 9. Average NP salary according to practice setting

TABLE 10. Average PA salary according to practice setting

Practice setting

Percent response

Average salary

Practice setting

Percent response

Average salary

Clinic – Hospital

22.9% (n=426)

$109,977

Clinic – Hospital

23.5% (n=164)

$109,268

Clinic – Stand Alone

22.2% (n=412)

$97,888

Clinic – Stand Alone

25.4% (n=177)

$105,918

Office Practice

34.8% (n=646)

$94,677

Office Practice

23.4% (n=163)

$102,684

Hospital

14.0% (n=260)

$113,019

Hospital

21.7% (n=151)

$119,884

Walk-in/ Ambulatory Care

6.1% (n=114)

$101,184

Walk-in/ Ambulatory Care

6.0% (n=42)

$102,143

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FIGURE 3. Did you earn more money this year (NPs)?

FIGURE 4. Did you earn more money this year (PAs)?

More

More Less

34%

Same

57%

37%

9%

Same

54%

9%

FIGURE 5. Do you expect to earn more money next year (NPs)?

43%

Less

FIGURE 6. Do you expect to earn more money next year (PAs)?

More

More

Less

Less

Same

54%

43%

Same

52%

5%

3% TABLE 11. Number of patients seen per week (NPs)

TABLE 12. Number of patients seen per week (PAs)

Patients

Percent response

Patients

Percent response

<25

14.7% (n=318)

<25

10.7% (n=89)

26-50

30.4% (n=665)

26-50

24.1% (n=200)

51-75

24.4% (n=526)

51-75

24.7% (n=205)

76-100

19.7% (n=425)

76-100

24.2% (n=201)

101-125

7.3% (n=157)

101-125

10.0% (n=83)

125+

3.5% (n=75)

125+

6.3% (n=52)

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Dermatology Clinic CASE #1

An itchy rash on the feet ANNA GREGOIRE, BS, AND TIFFANY SHIH, MD

A 25-year-old man with no remarkable past medical history presents with an itchy rash on the feet. Symptoms began 2 months ago, starting over the dorsal toes with redness, scaling, and itching. The eruption spread over the dorsum of the feet and progressed to weeping and crusting. He reports recently buying new shoes for work as a chef, which requires 15 hours daily of standing. Due to profuse sweating, his socks become soaked daily. Examination reveals symmetric erythematous plaques over the bilateral dorsum of both feet with fissures, scaling, and lichenification. No blisters or vesicles are present, but there are scattered crusted erosions.

What is your diagnosis? Turn to page 76

CASE #2

Fine wrinkles on the neck, chest, axilla, and back JULIE NGUYEN, BS, AND MAURA HOLCOMB, MD

A 55-year-old black man presents for evaluation of fine wrinkles that had developed over the past year. Physical examination reveals diffuse areas of fine wrinkling that run parallel to lines of cleavage on his neck, chest, axilla, trunk, back, and upper arms bilaterally. The affected skin has normal pigmentation and lacks erythema, induration, and atrophy. Lateral tension obliterates the wrinkling. The patient never notes any inflammation, itching, or pain. There are no signs or symptoms of systemic involvement. He denies sunbathing and denies any history of skin disorders or other significant health problems.

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Dermatology Clinic CASE #1

Shoe dermatitis

Shoe dermatitis represents a form of allergic contact dermatitis (ACD) that varies in frequency and presentation based on environmental factors, such as climate conditions, cultural traditions regarding footwear, and diverse manufacturing techniques.1 As a form of ACD, shoe dermatitis is classified as a delayed type IV hypersensitivity reaction (cell-mediated). The pathogenesis of ACD requires an initial sensitization phase, with exposure to a chemical, which penetrates the skin and elicits a cascade of events. Following sensitization, subsequent exposure leads to antigen presentation to “primed” T cells, causing a release of cytokines and chemotactic factors, triggering the clinical picture of contact dermatitis.2 Shoe dermatitis often starts on the dorsal toes. This initial involvement with the dorsum of the toes and then feet is attributed to greater surface area, thin stratum corneum, and sustained contact with the upper portion of the shoe.3 Often, the eruption presents as erythema, lichenification, and weeping and crusting in severe cases. With extended contact, areas of exposure may become xerotic with more prominent scaling. After resolution, postinflammatory hypoand hyperpigmentation may occur.2 Pruritis, burning, and pain present as the most commonly reported symptoms.3 Secondary bacterial or fungal infections frequently occur. In severe cases, an id reaction may occur, resulting in an eruption on the hands. The distribution is important, often with symmetric involvement and sparing of the toe webs, which have no contact with the offending agent. The distribution shown in this case is classic. Another pattern of shoe dermatitis involves the sole of the foot, with sparing of the instep and flexural creases of the toes. Patients with hyperhidrosis and atopy are at increased risk for development of shoe dermatitis.4 Common offending allergens include rubber accelerators, 2-mercaptobenzothiazole, carbamates, tetramethylthiuram disulfide, potassium dichromate in leather, and adhesives in synthetic materials.1,2 One report also described a case of shoe dermatitis resulting from the allergen colophonium.5 Foam rubber padding in athletic shoes contain diisocyanates, which are thought to be a causative agent. Other possible offenders include cork liners, felt, formaldehyde, dyes, asphalt, dimethyl fumarate, and tar.2 The allergen, in conjunction with the environment within shoes, leads to susceptibility to shoe dermatitis. Moist

environment, chronic venous insufficiency, friction, and heat can exacerbate foot dermatitis. It is more common in patients who wear occlusive footwear, including factory workers and military personnel, to have a higher incidence of shoe dermatitis.3 Patch testing is the gold standard for diagnosis of shoe dermatitis. Patch testing with pieces of various shoe parts may be done by soaking them for 15 minutes in water with application to the back for 72 to 96 hours. It is important to apply patches on disease-free skin, test all footwear, and use materials of at least 1 cm and less than 2 mm in thickness. Gas chromatography, mass spectroscopy, and high-performance liquid chromatography have also been used in cases of shoe dermatitis to identify the offending agent.3 Once the allergen is identified, selection of shoes without the offending substance leads to resolution. This is a difficult process, as most shoes are made in areas without mandatory labeling requirements. Plastic, wooden, or fabric shoes, which contain fewer allergens, are often impractical.3

Patch testing is the gold standard for the diagnosis of shoe dermatitis. It is important to apply patches on disease-free skin and to test all footwear.

Alternative diagnoses to consider with ACD that clinically present similarly include irritant dermatitis, dyshidrosis, psoriasis, insect bite reaction, tinea pedis, lichen planus, juvenile plantar dermatosis, Sézary syndrome, and mycosis fungoides.2,3 Irritant contact dermatitis occurs with rubbing of footwear against the feet or from contact with irritants, including detergents, soaps, cement, or topical medications. The main difference is that irritant contact dermatitis has no immunologic mechanism involved in the response.3 Dyshidrosis, or dyshidrotic eczema, can also present as scaly pink patches, but often is isolated to the palms and occasionally the soles of the feet. Patients often develop blisters or vesicles in ACD and dyshidrosis, which can also be seen in bullous tinea pedis and some exuberant insect bite reactions. Thinner plaques of psoriasis and mycosis fungoides can also look similar but are not limited to the acral surfaces. Therefore, history of new contacts to allergens is essential for diagnosis. If there is concern about an alternative diagnoses, a biopsy should be performed.2,5 ACD, including shoe dermatitis, is usually self-limited after removal of the causative agent; most cases resolve in days to weeks. However, due to a lack of product information, identifying and minimizing contact with the causative agent presents a challenge to treatment. Treatment for specific allergens includes

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chromium-free leather for patients allergic to chromium or switching to new leather shoes every few months. Patients with allergies to components of work boots are advised to wear two pairs of socks or alternate different pairs of boots daily. Those allergic to rubber can replace the insoles with cork composite or felt using a nonrubber cement adhesive. Custom-made shoes represent another option, although additional expense is associated with this option.3 A newer treatment option is the use of barrier socks developed to prevent skin contact with shoe allergens. Hyperhidrosis should also be treated, because a moist environment may exacerbate ACD. Medical treatment options include occasional use of topical and oral corticosteroids, as well as immunosuppressive treatments such as cyclosporine or mycophenolate mofetil.3,4 Secondary bacterial and fungal infections may also require treatment.5 For the patient in our vignette, we asked him to avoid wearing his new shoes, as they were highly suspected to be the cause of the dermatitis. Because severe hyperhidrosis presented a problem at work, we asked him to change into dry socks whenever he soaked through the socks he was wearing and to use aluminum chloride, an antiperspirant, to help with his perfuse sweating. The patient did not have significant superimposed infection such as Staphylococcus colonization or tinea pedis; however, such infections must frequently be treated with vinegar soaks, bleach baths, mupirocin ointment, or antifungal creams. Finally, we prescribed fluocinonide ointment twice daily to quickly reduce the inflammation. Because the skin is thick and often hyperkeratotic in this condition, it requires a strong class I or II topical corticosteroid. The patient improved quickly over the next few weeks and returned with complete resolution.

Anna Gregoire, BS, is a medical student and Tiffany Shih, MD, is a resident physician at the University of Minnesota in Minneapolis.

References 1. Vandebuerie L, Aerts C, Goossens A. Allergic contact dermatitis resulting from multiple colophonium-related allergen sources. Contact Dermatitis. 2014;70(2):117-119.

2. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

3. Matthys E, Zahir A, Ehrlich A. Shoe allergic contact dermatitis.

Dermatitis. 2014;25(4):163-171.

4. James WD, Berger TG, Elston D. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Saunders Elsevier; 2011.

5. Febriana SA, Soebono H, Coenraads PJ, Schuttelaar ML. Contact allergy in Indonesian patients with foot eczema attributed to shoes. J Eur Acad Dermatol Venereol. 2015;29(8):1582-1589.

CASE #2

Mid-dermal elastolysis

Mid-dermal elastolysis (MDE) is a rare acquired elastic tissue disorder that is characterized clinically by well-circumscribed patches and plaques of fine wrinkles and histopathologically by focal loss of elastic fibers in the mid-dermis.1,2 MDE frequently manifests on the trunk and proximal extremities. The clinical appearance of MDE is variable and may include perifollicular papular protrusions and inflammatory skin changes. There is a significant sex predominance observed in MDE; most cases are in white women of reproductive age, and the median age of onset is 34 years.2 MDE is exceedingly rare; fewer than 100 cases have been reported in the literature since its first description in 1977.

MDE is a chronic condition in which the only clinical manifestation is fine wrinkling that gives the skin a prematurely aged appearance. MDE is categorized into types according to the observable skin changes: well-circumscribed patches of fine wrinkles arranged parallel to skin cleavage lines (type I), small soft papular lesions composed of perifollicular protrusions (type II), or persistent reticular erythema with wrinkling (type III).2,3 The most frequently affected sites are the trunk, neck, and proximal aspects of the extremities; the face and hands are notably spared of wrinkling.2,3 Most patients with MDE present with asymptomatic, well-demarcated, symmetrically arranged lesions of fine wrinkling that follow Blaschko lines, a normally invisible pattern that represents pathways of epidermal cell migration during development.1,2 The size of the lesions can vary from a few centimeters in diameter to much larger, diffuse areas that involve the entire back. The affected skin generally lacks pigmentary changes, erythema, scaling, induration, atrophy, and telangiectasia.3,4 Patients typically do not experience any itching, burning, or pain, although some report mild erythema. MDE appears to be a localized cutaneous disorder that has no associated systemic involvement. Once the lesions appear, they remain relatively stable in morphology for life.

Sporadic cases have been reported in which the onset of MDE is preceded or accompanied by an inflammatory dermatosis; for most patients, however, there is no history of skin disorders. Reported associations include urticaria, atopic dermatitis, granuloma annulare, pityriasis rosea, Sweet

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Dermatology Clinic syndrome, phototoxic dermatitis, and guttate psoriasis.2,4 Autoimmune diseases such as Hashimoto thyroiditis, Grave disease, lupus erythematosus, and rheumatoid arthritis have also been described in patients with MDE.4 The pathognomonic feature of MDE is the characteristic histopathologic finding of a complete band-like loss of elastic fibers in the mid-dermis of affected skin, which can be visualized by elastic tissue stains.1,2 MDE is characterized by an absence of inflammatory infiltrate, but a mild perivascular infiltrate is sometimes detected in the dermis.

The elastolysis is localized only to the mid-dermis, with preservation of normal elastic tissue in the superficial papillary dermis, in the reticular dermis, and along adjacent hair follicles.1 The precise pathogenesis of MDE remains unknown, although several mechanisms have been proposed to explain its etiology. Recent data suggest that an altered balance between matrix metalloproteinases (MMPs; mainly MMP-2 and MMP-9) and proteolytic inhibitors results in increased degradation of extracellular matrix proteins and elastic fibers.3 Other possible mechanisms include defects in elastic fiber synthesis, autoimmunity against elastic fibers, and damage to elastic fibers via unregulated release of elastase by inflammatory cells.1 There is no known genetic predisposition for MDE. Ultraviolet light exposure has been suggested as a contributing factor in the development of MDE lesions, because approximately half of patients with MDE report noticing the appearance of fine wrinkles following prolonged sun exposure.3 There is evidence that ultraviolet light induces MMPs, resulting in increased destruction of elastic fibers.

However, MDE does not manifest in a photodistribution, notably sparing the face and dorsum of the hands. In addition, the typical histologic features of ultraviolet-induced damage are not consistently observed in MDE, thereby suggesting that sun exposure may be contributory but not causative of the disease process.

The differential diagnosis of MDE should include closely related dermatologic disorders such as anetoderma, perifollicular elastolysis, Marshall syndrome (postinflammatory elastolysis and cutis laxa), and pseudoxanthoma elasticumlike papillary dermal elastolysis. Anetoderma is a disorder characterized by elastolysis in any part of the dermis and herniation of subcutaneous tissue upon palpation. It is similar to MDE in its distribution on the trunk and proximal extremities, but is characterized by small, soft macules and papules instead of fine wrinkles.1,2 Perifollicular elastolysis is caused by Staphylococcus epidermidis and can be distinguished

from MDE by the selective loss of elastic fibers surrounding hair follicles.1 Marshall syndrome is characterized by an inflammatory phase, consisting of an urticarial eruption with malaise and fever, followed by acute destruction of elastic tissue that results in atrophy and severe disfigurement.1,2 It is distinguished from MDE by its occurrence in children, elastolysis pattern, and face involvement. Pseudoxanthoma elasticum-like papillary dermal elastolysis clinically manifests as yellow nonfollicular cobblestone-appearing papules that may coalesce into large plaques on the neck, flexural forearms, and the axillae.2

No definitive therapy exists for MDE. Current treatment options are empiric and reports of improvement of the lesions are anecdotal.

No definitive therapy exists for MDE. Current treatment options are empiric and reports of improvement of the lesions are anecdotal. Pharmacologic agents such as vitamin E, clofazimine, oral and topical corticosteroids, colchicine, and chloroquine have been used with little to no benefit.4 Topical tretinoin has been reported to improve the appearance of wrinkles, but does not alter the course of the disease.4 For the patient in the vignette, a punch biopsy of the skin revealed classic band-like loss of elastic fibers in the middermis. The patient was not significantly bothered by the appearance of his skin and decided not to treat his MDE. n Julie Nguyen, BS, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston.

References 1. Maari C, Powell J. Anetoderma and other atrophic disorders of the skin. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. Fitzpatrickâ&#x20AC;&#x2122;s Dermatology in General Medicine. 8th ed. New York, NY: McGraw-Hill; 2012:718-723.

2. Gambichler T. Mid-dermal elastolysis revisited. Arch Dermatol Res. 2010;302(2):85-93.

3. Patroi I, Annessi G, Girolomoni G. Mid-dermal elastolysis: a clinical, histologic, and immunohistochemical study of 11 patients. J Am Acad Dermatol. 2003;48(6):846-851.

4. Lewis KG, Bercovitch L, Dill SW, Robinson-Bostom L. Acquired disorders of elastic tissue: Part II. Decreased elastic tissue. J Am Acad Dermatol.

2004;51(2):165-185.

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Dermatologic Look-Alikes Erythematous papules and plaques EMAN BAHRANI, BA, AND RANA MAYS, MD

CASE #1

CASE #2

A 46-year-old white woman presents with a 2-week history of a rash on her back and feet. She denies any associated pain, pruritus, or fever, and her medical history is unremarkable. Her social and family histories are noncontributory. Physical examination is notable for erythematous papules scattered across her back, with some coalescing into plaques. Examination of her dorsal feet showed symmetrical, erythematous to skincolored annular plaques that are 2 to 5 cm in diameter.

The lesions do not exhibit tenderness or scaling. Her hands, nails, scalp, and face are normal.

A 42-year-old white man presents with a 3-month history of rash on his back and chest. He denies having pruritus, but he complains of arthralgias and he has tried topical corticosteroids without experiencing improvement. His medical history is noncontributory.

After a physical examination is conducted, the patient is observed to have multiple nonscaly, annular, pink to violaceous plaques on his back with swelling in the periphery and a flat center. His chest exhibits similar, smaller plaques and scattered pink papules. His scalp, hair, and nails are normal.

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Dermatologic Look-Alikes CASE #1

Granuloma annulare

Granuloma annulare (GA) is a disorder of T cells and macrophages that presents most commonly in patients under age 30 with a femaleto-male ratio of 2:1 in its most common, localized form.1 Generalized GA is more likely to occur in patients of middle age or older and may have increased frequency in men. Another variant, subcutaneous GA, is more common in children.2 Although GA is a relatively common disease, its etiology remains unknown. Various inciting factors proposed in the literature include biologic therapies, various drugs, insect bites, trauma, Bacillus Calmette–Guérin vaccination, and herpes zoster infection.2 Associations of GA with systemic and infectious diseases, such as diabetes mellitus, malignancy, thyroid disease, dyslipidemia, human immunodeficiency virus (HIV), hepatitis B and C, and rheumatoid arthritis, have also been cited.2-6 Based on the Th1 immune cells seen in the lesions, GA has been described a delayed-type hypersensitivity reaction to unknown antigens. This tuberculous-like immune response involves the production of interferon-γ and other cytokines that cause macrophage accumulation in the dermis and connective tissue degradation, such as elastic fiber degeneration and injury. Some studies reported genetic links and familial cases.1,2 GA is a benign, self-limited, and polymorphic cutaneous disease with many variants (localized, generalized, subcutaneous, and perforating). Subtypes of generalized GA include generalized annular, disseminated papular, and atypical generalized GA. The most commonly seen subtype is localized GA, in which annular erythematous or skin-colored papules present on the dorsal hands or feet; it makes up approximately three-quarters of all GA cases.2 Almost two-thirds of GA cases are isolated to the hands and arms, 20% to the legs and feet, 7% to both upper and lower extremities, 5% to the trunk, and 5% to the trunk plus other areas.1 Generalized GA is defined by at least 10 skin lesions present at once or by extensive annular plaques. Disseminated GA presents with a pattern of scattered papules. Atypical generalized GA fits neither the description of annular or disseminated GA. Subcutaneous GA presents most commonly on the lower legs and is also referred to as pseudorheumatoid nodules. Perforating GA papules have a clinically distinct central umbilication or

keratotic plug due to collagen destruction. Rare subtypes include macular or patch type, palmar, photodistributed, and pustular GA. Although most GA lesions are asymptomatic, there are reports of pruritic and painful cases.1,2 GA has a broad differential diagnosis; therefore, skin biopsy is necessary for definitive diagnosis when suspected. The differential includes sarcoidosis, granulomatous mycosis fungoides, necrobiosis lipoidica, interstitial granulomatous dermatitis, tinea, nummular eczema, psoriasis, cutaneous lupus, leprosy, verruca vulgaris, and eruptive xanthomas. Subcutaneous GA can be clinically similar to rheumatoid nodules, sarcoidosis, and infectious processes.1,2 Clinical findings and histology together differentiate GA from the other diseases listed.

Granuloma annulare has a broad differential diagnosis; therefore, skin biopsy is necessary for definitive diagnosis when suspected.

Histologically, palisading granulomas in the dermis with central degeneration of collagen, mucin, and an infiltrate of lymphocytes and histiocytes characterize GA. Mucin distinguishes GA from the other noninfectious granulomatous diseases. Sarcoidosis exhibits noncaseating granulomas without mucin. Necrobiosis lipoidica diffusely involves the dermis with granulomas in parallel layers and plasma cell infiltrates without mucin. Cutaneous lupus classically involves the dermal-epidermal junction with necrotic keratinocytes and no mucin. Lupus erythematosus tumidus, however, demonstrates a lymphocytic infiltrate confined to the dermis and contains mucin, but it does not exhibit the histiocytic infiltrate necessary for a diagnosis of GA. Perforating GA is unique in that it is characterized by collagen being ejected through the epidermis.1,2,7 Management of GA depends on the clinical characteristics.

Localized and asymptomatic disease can be managed with reassurance and clinical observation. Patients with localized GA who are concerned about symptomatic lesions or cosmesis may benefit from first-line high-potency topical corticosteroids or intralesional corticosteroid injections. Topical tacrolimus 1% ointment, cryosurgery, localized psoralen with ultraviolet A light (PUVA) therapy, photodynamic therapy, and various lasers have also shown some success should corticosteroids fail.1,2 Thornsberry and English2 discussed more than 30 successful therapies for nonlocalized GA, but none are evidence-based.

Systemic agents are often necessary for generalized GA. Isotretinoin at 0.5 to 1.0 mg/kg/d is most commonly used

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first. Intravenous use of infliximab, adalimumab, PUVA, cyclosporine, and doxycycline are other therapies that have shown success in case reports or case series. Combination therapies of PUVA with prednisone and isotretinoin with topical pimecrolimus 1% cream have also been effective.1,2,8 Half of all patients have resolution of GA within 2 years and have a 40% recurrence rate. Untreated GA has been documented to persist for several weeks to several decades.1 Given the association with various systemic diseases, a thorough review of systems is recommended, as is encouraging the patient to follow up with his or her primary care provider for any needed screening. Furthermore, therapy must be chosen taking into consideration the patient’s medical history, laboratory results, current medications, and potential for pregnancy given the various adverse side effect profiles and interactions of systemic agents.2 Regarding the patient in the vignette, a punch biopsy of a lesion on her back confirmed the diagnosis of GA. The patient was reassured that her lesions were benign and was prescribed clobetasol propionate 0.05% cream twice daily for 2 weeks on lesions of cosmetic concern. At 1-month follow-up, her lesions exhibited almost complete resolution.

Take-away points: granuloma annulare Clinical presentation

• Localized: annular erythematous or skin-colored papules present on the dorsal hands or feet • Generalized: at least 10 skin lesions present at once or extensive annular plaques • Disseminated: pattern of scattered erythematous papules • Subcutaneous: pseudorheumatoid nodules on lower legs • Perforating: papules have clinically distinct central umbilication or keratotic plug due to collagen destruction

Differential diagnosis

• Sarcoidosis, granulomatous mycosis fungoides, necrobiosis lipoidica, interstitial granulomatous dermatitis, tinea, nummular eczema, psoriasis, cutaneous lupus, leprosy, verruca vulgaris, eruptive xanthomas • Subcutaneous granuloma annulare may resemble rheumatoid nodules, sarcoidosis, infectious process

Diagnosis

• Punch biopsy: palisading granulomas in the dermis with central degeneration of collagen, mucin, and an infiltrate of lymphocytes and histiocytes • Perforating granuloma annulare subtype characterized by collagen being ejected through the epidermis

Management

• Localized and asymptomatic: reassurance, observation • Localized and symptomatic: high-potency topical corticosteroids, intralesional corticosteroid injections, tacrolimus ointment • Generalized: isotretinoin, 0.5-1.0 mg/kg/d • Recalcitrant generalized: infliximab, adalimumab, psoralen and ultraviolet A radiation, cyclosporine, doxycycline*

*These treatments for granuloma annulare are not approved by the FDA.

CASE #2

Lupus erythematosus tumidus

Lupus erythematosus tumidus (LET) is classified as a variant of cutaneous lupus erythematosus (CLE). LET affects men and women and is thought to be underdiagnosed. The mean onset age is in the 30s and 40s, but there are reports of affected children.1,9,10 Cutaneous lesions in lupus erythematosus (LE) are categorized into histopathologically specific and nonspecific subtypes. Acute CLE includes the transient, erythematous malar rash, diffuse alopecia, oral ulcers, plaques, and bullae often associated with systemic LE. Subacute CLE includes the inflammatory, scarring discoid lupus erythematosus (DLE), nonscarring photosensitive CLE, and psoriasiform lesions. LET is considered a form of chronic CLE, along with DLE, lupus panniculitis, and chilblain lupus, which are infrequently seen in systemic LE. A newer classification of intermittent cutaneous LE was proposed for LET in 2004.9 LET typically presents as indurated plaques with a pink or violaceous hue and smooth surface in photodistributed areas, such as the face, upper back, neck, extensor surfaces, and shoulders. LET lesions appear succulent or swollen with well-demarcated borders, and they do not show macroscopic epidermal involvement, such as follicular plugging or scale.

The borders of the plaques may coalesce, leading to a raised periphery and relatively flatter center.9,11-14 Some patients have exhibited erythematous, annular lesions on the cheeks and upper extremities, resembling the annular subtype of subacute CLE, but they do not demonstrate the collarette scale seen in the subacute form.9 LET is further distinguished from other types of CLE by the absence of scarring, follicular plugging, and hyperkeratotic scaling, as is seen in DLE. Epidermal atrophy and postinflammatory hypopigmentation are also not seen in LET.9-14 Several reports have indicated specific triggers for LET, with cases of drug-induced LET following initiation of infliximab and LET in an HIV-positive man following immune reconstitution. It is well established, however, that LET exhibits photosensitivity in the majority of cases and can be reproduced with phototesting.9,11 The diagnosis of LET can only be confirmed with histologic analysis of the lesions by punch biopsy in conjunction with the clinical features. A perivascular and periadnexal lymphocytic infiltrate of T cells (CD4 > CD8) in the superficial and deep

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Dermatologic Look-Alikes Take-away points: lupus erythematosus tumidus Clinical presentation

• Indurated plaques with pink or violaceous hue and smooth surface (classically in photodistributed areas) • Lesions appear succulent or swollen with well-demarcated borders and do not show macroscopic epidermal involvement (eg, follicular plugging or scale) • Borders of the plaques may coalesce, leading to raised periphery and relatively flat center

Differential diagnosis

Jessner lymphocytic infiltration of the skin, granuloma annulare, erythematous plaques of acute lupus erythematosus, cutaneous mucinosis of systemic lupus erythematosus, discoid lupus erythematosus, pseudolymphoma, polymorphous light eruption

corticosteroids and sun protection. Antimalarial agents, such as chloroquine (3.5-4.0 mg/kg/d) and hydroxychloroquine (6.0-6.5 mg/kg/d) have been shown to be effective as well.

Methotrexate (7.5-10.0 mg/wk) and systemic corticosteroids (10-30 mg/d) are options in cases recalcitrant to topical therapies and antimalarial agents.9,12,14 The addition of topical tacrolimus 0.1% cream may lead to complete regression in patients with flares while on the antimalarial agents.14 The patient in the vignette was educated regarding effective sun protection. His lesions resolved completely after 1 week of treatment with oral hydroxychloroquine at 200 mg twice daily. n

Diagnosis

Punch biopsy: perivascular and periadnexal lymphocytic Tcell infiltrate (CD4 > CD8) in superficial and deep dermis with interstitial mucin deposition; no epidermal changes

Eman Bahrani, BA, is a medical student and Rana Mays, MD, is a dermatology resident at Baylor College of Medicine in Houston.

Management

• First-line: sun protection, topical corticosteroids • Second-line: antimalarials (hydroxychloroquine) • Recalcitrant: methotrexate, systemic corticosteroids

References 1. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

dermis with interstitial mucin deposition is frequently seen.9,11,13 In contrast to other types of CLE, the epidermis and dermalepidermal junction show minimal or no change in LET.1,12 The majority of LET cases studied with direct immunofluorescence (DIF) showed a low prevalence of immunoglobulin or complement deposition at the dermal-epidermal junction, also differentiating it from other types of LE.9,12,13 In support of its categorization under CLE, LET is seen in patients with other forms of CLE simultaneously.1,10 Serologically, low-titer antinuclear antibodies may be detectable in a minority of cases.9,12 The differential diagnosis for LET includes Jessner lymphocytic infiltration of the skin (JLIS), granuloma annulare, erythematous plaques of acute LE, cutaneous mucinosis of systemic LE, DLE, pseudolymphoma, and polymorphous light eruption. JLIS bears many similarities to LET. It is an uncommon relapsing disorder with clinical and histologic findings often indistinguishable from LET, presenting with nonscaly red patches on the face, neck, and upper back. Slight differences in DIF between the two conditions have been recorded, but some investigators now regard them as variations of the same disease entity under CLE.9 Granuloma annulare exhibits histiocytes on histology, and DLE and systemic LE lesions have epidermal and dermal-epidermal junction involvement with necrotic keratinocytes. Mucin is absent in pseudolymphoma and polymorphous light eruption.9,11-13 Given the photosensitivity of LET, patients are encouraged to avoid sun exposure and utilize potent physical and chemical barriers from ultraviolet A and B light, such as creams with sun protection factor greater than 50 and photoresistant clothing. First-line therapies include topical

2. Thornsberry LA, English JC 3rd. Etiology, diagnosis, and therapeutic management of granuloma annulare: an update. Am J Clin Dermatol. 2013;14(4):279-290.

3. Maschio M, Marigliano M, Sabbion A, et al. A rare case of granuloma annulare in a 5-year-old child with type 1 diabetes and autoimmune thyroiditis. Am J Dermatopathol. 2013;35(3):385-387.

4. Toro JR, Chu P, Yen TS, LeBoit PE. Granuloma annulare and human immunodeficiency virus infection. Arch Dermatol. 1999;135(11):1341-1346.

5. Wu W, Robinson-Bostom L, Kokkotou E, et al. Dyslipidemia in granuloma annulare: a case-control study. Arch Dermatol. 2012;148(10):1131-1136.

6. Li A, Hogan DJ, Sanusi ID, Smoller BR. Granuloma annulare and malignant neoplasms. Am J Dermatopathol. 2003;25(2):113-116.

7. Günes¸ P, Göktay F, Mansur AT, et al. Collagen-elastic tissue changes and vascular involvement in granuloma annulare: a review of 35 cases. J Cutan Pathol. 2009;36(8):838-844.

8. Mahmood T, Mansouri B, Menter A. Successful treatment of generalized granuloma annulare with adalimumab. Clin Exp Dermatol. 2015;40(5):537-539.

9. Kuhn A, Bein D, Bonsmann G. The 100th anniversary of lupus erythematosus tumidus. Autoimmun Rev. 2009;8(6):441-448.

10. Maize JC Jr, Costner M. Tumid lupus erythematosus: a form of lupus erythematosus. Arch Dermatol. 2010;146(4):451.

11. Alexiades-Armenakas MR, Baldassano M, Bince B, et al. Tumid lupus erythematosus: criteria for classification with immunohistochemical analysis. Arthritis Rheum. 2003;49(4):494-500.

12. Hsu S, Hwang LY, Ruiz H.Tumid lupus erythematosus. Cutis. 2002;69:227-230.

13. Rodriguez-Caruncho C, Bielsa I, Fernández-Figueras MT, et al. Lupus erythematosus tumidus: a clinical and histological study of 25 cases. Lupus.

2015;24(7):751-755.

14. Verma P, Sharma S, Yadav P, et al. Tumid lupus erythematosus: an intriguing dermatopathological connotation treated successfully with topical tacrolimus and hydroxychloroquine combination. Indian J Dermatol. 2014;59(2):210.

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Clinical Challenge An unusual cause of respiratory distress in an infant CHAD R. STOUGH, MPAS, PA-C

A congenital condition is found in an infant with respiratory and gastrointestinal symptoms.

Lily, a 6-week-old infant, presents with diff icult y breathing, grunting, and irritability. The child had no documented fever, and no other family members at home were ill. Her mother reported that Lily made a “clicking” noise while breathing or grunting and that the child’s breathing was heavy and at times labored. The patient had not been vomiting.

CASE

HISTORY

An infant presents with difficulty breathing and grunting.

At birth, Lily had a gestational age of 38 weeks and weighed 7 lb 2 oz. She was delivered by cesarean section. At the initial early-discharge appointment, some minimal scleral icterus, indicating jaundice, was noted, but phototherapy was not needed. The 2-week well-child examination was normal except for dacryocystitis.

At age 4 weeks, weighing 10 lb 8 oz, Lily was brought to the office because she was vomiting while breastfeeding. Ranitidine and reflux precautions were initiated. At age 6 weeks, weighing 12 lb 4 oz, she was seen in the office for “fussiness” and constipation. The dose of ranitidine was increased for the reflux, and intake of prune juice was initiated for the constipation. Within days, the patient was again brought to the office with difficulty breathing and grunting.

PHYSICAL EXAMINATION

© THINKSTOCK

At this latest presentation, Lily’s vital signs were as follows: temperature, 97.8°F; weight, 11 lb 15 oz; pulse rate, 185/min; respiratory rate, 44/min; white blood cell count, 9800/mm3; and SpO2 , 98%. General examination: some irritability and grunting. Skin examination: no rashes. Head, neck, eyes/ears/nose/throat: normal. Chest: no wheezing, clear to auscultation bilaterally. Cardiac examination: no murmurs.

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tenderness, no hepatosplenomegaly, bowel sounds of generalized gurgling, and generalized tympany to percussion.

EVALUATION AND TESTS

© DU CANE MEDICAL IMAGING LTD. / SCIENCE SOURCE

Based on the physical examination findings, the differential diagnosis could include abdominal pain secondary to constipation or gastroesophageal reflux, given the patient’s history, infection, or a respiratory issue with a possible abdominal cause. Lily’s symptoms rapidly became worse later in the day, and she was taken to the hospital for further evaluation and treatment. She was initially seen and admitted for respiratory distress.

Chest radiography showed a possible congenital diaphragmatic hernia (CDH) with bowel in the left side of the chest.

A pediatric surgery consultation was then obtained, and magnetic resonance imaging confirmed the presence of intestine in the left side of the chest. Medical imaging also showed an enlarged heart and a possible horseshoe kidney.

The results of echocardiography and renal ultrasound were normal, except for a small patent foramen ovale noted on the echocardiogram.

TREATMENT The treatment for CDH is surgery. In the operating room, the patient underwent thoracoscopic repair of a left-sided CDH. After surgery to repair the hernia and place the organs in normal position, she was extubated and taken to the post-anesthesia care unit, then to the neonatal intensive care unit in stable condition. By the next day, she was taking Pedialyte and breastfeeding without emesis.

OUTCOME Lily did extremely well following the surgery. After 2 months, chest radiography was repeated, and the results were normal with no evidence of CDH. During this time, she was feeding and growing well, with only minimal vomiting. The patient again underwent chest radiography at approximately age 18 months, and the results were normal. She continues to eat well and gain weight, with no respiratory issues.

DISCUSSION A presentation of CDH at age 6 weeks is later than the typical onset. Most cases of CDH are diagnosed in the perinatal/neonatal period, and most are detected on prenatal

FIGURE 1. Congenital diaphragmatic hernia. Most cases are diagnosed in the perinatal/neonatal period.

ultrasound by a mean gestational age of 24 weeks.1 The reported incidence of CDH varies from 1 in 5000 live births to 1 in 2000 births if stillbirths are included.2 The majority of infants with CDH experience severe respiratory distress within the first hours of life.2 A provider who is treating pediatric patients needs to keep CDH in the differential diagnosis when an infant or child is in respiratory distress but also should be aware that with a delayed onset, nonspecific symptoms may be present, especially gastrointestinal symptoms. The earlier CDH is diagnosed, the better the outcome of surgical intervention.

Chest radiography is usually diagnostic,2 but other medical imaging modalities, such as computed tomography, may be required depending on the individual case.

Late presentation of CDH was once considered rare, but an increasing number of reports now show that CDH is diagnosed in up to 25% of patients after the neonatal period, with a better outcome.3 Many patients present with a wide array of respiratory and gastrointestinal symptoms, but at least 25% are asymptomatic, and the condition is often diagnosed incidentally on chest radiographic images.3

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Clinical Challenge

“I found the old format much more exciting.”

Chad R. Stough, MPAS, PA-C, works as a physician assistant at West Atlanta Pediatrics in Dallas, Georgia.

References 1. Chan HY, Wong CC, Ng F. Late-presenting congenital diaphragmatic hernia: a potentially life threatening case. Hong Kong J Emerg Med. 2009;16(2):102-105.

2. Hartman GE. Congenital diaphragmatic hernia. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed.

Philadelphia, PA: WB Saunders; 2004:1353-1355.

3. Hamid R, Baba AA, Shera AH, et al. Late-presenting congenital diaphragmatic hernia. Afr J Paediatr Surg. 2014;11(2):119-123.

“That’ll be the day!”

© The New Yorker Collection 2016 from cartoonbank.com. All Rights Reserved.

CDH is generally considered to result from defective formation and fusion of the pleuroperitoneal membranes, which provide a potential passage through which abdominal contents can herniate into the thorax.1 The left side is more commonly affected because of earlier closure of the right pleuroperitoneal area and a protective effect of the liver developing in the septum transversum.1 Herniation of a solid organ, such as the liver or spleen, can be a risk factor for misdiagnosis on medical imaging in late-presenting CDH in children because the typical appearance of bowel herniation can be obscured.1 During an acute presentation of CDH, management of the respiratory symptoms is extremely important. Blow-by oxygen or bag masking can lead to gastric and abdominal distension and compression of the lung, so a patient presenting with severe respiratory distress should be intubated and ventilated with low-peak inspiratory pressure to minimize lung injury.1 To stabilize the patient further, a nasogastric tube should be placed and connected to continuous suction to decompress the abdominal contents and decrease respiratory compromise.1 If additional respiratory management is needed, then extracorporeal membrane oxygenation (ECMO) should be considered.

Thoracoscopic or laparoscopic approaches to repair CDH with a late presentation have been described.1 In a study of 20 patients conducted by Hamid et al and published in 2014 in the African Journal of Paediatric Surgery, repair with Vicryl suture material was possible in 19 patients, and only 1 patient required a polypropylene mesh graft for a large defect.3 As mentioned earlier, a thoracoscopic approach was used in the patient in this case to repair a CDH on the left side, which is more commonly affected. As in any patient with a CDH, it is important to diagnose the condition early and repair it as soon as possible. n

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Writers’ Guidelines The Clinical Advisor welcomes submissions from its readers. Writing for us is an opportunity to share your knowledge and experience with your colleagues — and to collect a fee in the bargain! We pay an honorarium for every submission we accept.

We’ll be glad to work with you to develop your ideas into compelling articles. As for length, that depends on which kind of article you submit.

CLINICAL FEATURES update our readers on the latest information about conditions seen in everyday practice. Running approximately 2,500 to 5,000 words, including the references, features can be written either as regular narratives or as a series of questions and answers. Topics should be selected with the busy primary-care clinician in mind; specialists should review specialty topics from the primary-care point of view.

If at all possible, articles should be accompanied by clinical photos.

Charts, tables, and algorithms are also encouraged. Please include your title and affiliation.

CLINICAL CHALLENGE is our popular department comprising histories of difficult cases. Each case is presented as a step-by-step, chronological account, revealing the author’s thought processes along the way. It is divided into sections in this order: the patient presentation; the patient history; the twists and turns eventually leading to a diagnosis; the treatment and outcome; and a discussion of the lessons learned or of the condition in general.

The length should be about 1,500 words, and accompanying images are encouraged. Please include your title and affiliation.

DERMATOLOGY CLINIC is a department that presents photos of actual cases and asks readers to identify the condition. Each case opens with one or two color photos and a 75-to-100-word description of the patient presentation, without giving away the diagnosis.

This is followed by a 750-to-1,000-word summary that includes a fuller description of the ailment, an explanation of how the correct diagnosis was reached, a general review of the condition along with a differential diagnosis, and a description of the patient’s treatment and outcome. Topics must be approved by the editor prior to submission. Please include your title and affiliation.

COMMENTARY is our guest editorial page. It gives you the opportunity to sound off on an issue of importance to your colleagues nationwide. A typical Commentary runs about 600 words in length. Please include your title and affiliation.

To discuss your editorial ideas, contact us by phone at 646.638.6078; by e-mail to editor@ClinicalAdvisor.com; or by mail to The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MAY 2016 95

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Case Study | DIABETES Managing nephropathy in a patient with type 2 diabetes © THINKSTOCK

An elderly man with a long history of type 2 diabetes presents with albuminuria.

JENNIFER A. GRENELL, APRN, CNP

The patient is a 72-year-old nonsmoking man who has a 30-year history of type 2 diabetes. His current therapy consists of insulin glargine 40 units once daily in the morning and insulin lispro 12 units 3 times a day with meals.

He also takes extended-release metformin 2,000 mg/d and reports having 100% adherence to this regimen.

History of present illness

His glycated hemoglobin (HbA1c) has improved from 8.1% 3 months ago to 7.7% at this visit. At the previous visit, his mealtime doses of insulin lispro were adjusted due to hyperglycemia noted prior to noon and evening meals.

He has been on his multiple daily injection program for nearly 3 years. Prior to this, his HbA1c was elevated at 9.2% on neutral protamine hagedorn insulin twice daily and metformin.

Blood glucose monitoring

The patient brings his glucose meter to the visit. A review of the information that was downloaded from his meter indicates that he is using the meter 2 to 3 times per day with no hypoglycemia observed within the previous 3 months. His morning glucose levels average from 93 to 264 mg/dL, with elevated levels occurring if the patient has snacked at bedtime.

There are 2 noon levels of 95 to 104 mg/dL. Pre-evening meal glucose levels average 135 to 258 mg/dL, and bedtime levels average 159 to 195 mg/dL. The elevated levels in the mornings following snacking at bedtime and elevated levels occurring primarily prior to evening meal time are the most concerning data from the meter.

Diet and exercise

The patient reports that he has been making an effort to stay consistent with carbohydrate intake with meals but has been snacking more at bedtime, contributing to the approximate 2-kg weight gain from his previous visit.

His snacks at bedtime consist primarily of carbohydratecontaining foods. He has not been exercising regularly in the last 3 months.

Review of systems

• Eyes: Patient has annual eye exams with no reported retinopathy.

• Cardiac: He underwent coronary artery bypass graft surgery 20 years ago. He reports no issues with chest pain or shortness of breath with activity. He also has a history of atrial fibrillation and angina. He sees a cardiologist regularly.

• Hyperlipidemia: Cholesterol panel is checked at the current visit; low-density lipoprotein cholesterol (LDLC) level is 63 mg/dL. • Hypertension: The patient’s blood pressure is well controlled at 124/72 mm Hg. • Weight: The patient’s weight has increased 2 kg from his previous visit.

• Sleep: The patient reports using a continuous positive airway pressure (CPAP) device daily.

• Renal: Microalbumin is elevated at this time but has improved from 418.3 mg/L 6 months ago to the current level of 324.3 mg/L. Potassium is checked and is within normal limits. Creatinine is 1.2 mg/dL with an estimated glomerular filtration rate of 53 mL/min/1.73m 2.

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• Medications: The patient’s medications include lowdose aspirin, dabigatran, atenolol, atorvastatin 80 mg/d, hydrochlorothiazide, and lisinopril.

QUESTION 1: Which is true regarding diabetic nephropathy?

Answer for Question 2: E. High blood pressure can elevate albuminuria. Albuminuria can be present if patients are ill when testing is performed, if they have a urinary tract infection, during a period of heavy exercise, or if they smoke.

QUESTION 3: All of the following would be important recommendations for this patient to improve his albuminuria, except A. Improved glycemic control B. Ongoing efforts to keep blood pressure under control C. Adherence to a high-protein diet in an effort to lose weight D. Referral to a dietician to review carbohydrateconsistent diet in setting of nephropathy.

A. Assessment of urinary albumin in all patients with type 1 and type 2 diabetes should occur every 5 years.

B. Either an ACE inhibitor or ARB is suggested for the treatment of the non-pregnant patient with modestly elevated urinary albumin excretion (30 to 299 mg/day).

C. Microalbuminuria is the recommended term used for the patient with urinary albumin excretion of 30 to 299 mg/day.

D. None of the above.

Answer for Question 3: C. After detecting the patient’s Answer for Question 1: B. Annual assessment of urinary

albumin is recommended for patients who have had type 1 diabetes for ≥5 years and in all patients with type 2 diabetes.

Either an ACE inhibitor or an ARB is suggested for the treatment of nonpregnant patients with modestly elevated urinary albumin excretion (30 to 299 mg/d) and is recommended for those with urinary albumin excretion >300 mg/d. Per the 2015 American Diabetes Association Standards of Medical Care, the terms “microalbuminuria” (30 to 299 mg/d) and “macroalbuminuria” (>300 mg/d) are no longer the recommended terminology, since albuminuria occurs on a continuum. Albuminuria is defined as a urine albumin-tocreatinine ratio ≥30 mg/g. Consider referral to a nephrologist when there is uncertainty about the etiology of kidney disease, difficult management issues, or advanced kidney disease.

QUESTION 2: Other than poor glucose control, what are known factors that affect albuminuria?

A. High blood pressure B. Periods of illness or infection C. Heavy exercise D. Smoking E. All of the above

albuminuria, improved glycemic control, ongoing efforts at keeping his blood pressure under control, and tactics for eating healthy and losing weight were reviewed. Adherence to a high-protein diet would not be beneficial for this patient.

The patient’s HbA1c of 7.7% was improved from 8.1% at his previous visit but there was still room for improvement.

Recommendations for this patient were to continue insulin glargine 40 units once daily with adjustment to his insulin lispro doses at mealtimes (increasing from 12 units to 14 units with his noon meal) in an effort to maintain a blood sugar goal of 100 to 140 mg/dL. The patient was referred to a diabetes educator to review principles of insulin dose adjustment. He will continue on his current blood pressure regimen, which includes an ACE inhibitor, lisinopril. He was also referred to a dietitian to review a carbohydrate-consistent diet that will assist in weight loss and improve glycemic control. The dietitian can also help the patient to better assess the amounts of protein he is consuming. Several studies suggest that following a lower-protein diet can be beneficial in managing kidney disease. The patient also agreed to work on limiting snacking at bedtime. The patient has a follow-up appointment in 3 months to assess the efficacy of these interventions with repeat HbA1c and fasting glucose evaluation. ■ Ms. Grenell practices at the Mayo Clinic department of endocrinology in Rochester, Minn., specializing in diabetes management.

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Stat Consult

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

Background

Zika virus

BY ALAN DRABKIN, MD

© SINCLAIR STAMMERS / SCIENCE SOURCE

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

Macrophotograph of an Aedes aegypti mosquito, which can transmit Zika virus.

• mosquito-borne flavivirus, lineages include ——African lineage ——Asian lineage (most often found in Americas) • transmission ——primarily by Aedes aegypti mosquito bite ——human-to-vector-to-human transmission occurs during outbreaks ——maternal-fetal ——sexual transmission ——blood or blood products ——no cases of transmission reported during breast feeding (not yet well evaluated) • epidemiology ——virus first isolated in 1947 from a macaque in Zika forest of Uganda ——first human case reported in Nigeria in 1954 ——East African Zika virus likely spread to Southeast Asia around 1945 ——period of stable endemicity in Africa and Southeast Asia persisted in 20th century ——first large-scale outbreak and eastward spread in 2007 on Yap Island, Micronesia ——second major outbreak reported in French Polynesia in 2013-2014 ——major outbreak presently ongoing in the Americas ■■ first reported in Brazil in May 2015 (estimated 500,000 to 1.5 million persons infected) ■■ outbreak now spread to Central and South America and Caribbean, including Puerto Rico.

■■ international spread of Zika virus from Brazil likely to occur due to high volume of tourism and wide distribution of Aedes mosquito vectors ■■ local transmission not yet reported in mainland USA, but infections have been reported among travelers returning to USA from affected areas.

Clinical presentation and course

• about 75% to 80% of infections asymptomatic • symptomatic disease generally mild

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Stat Consult ——common symptoms include fever, rash, arthralgias and conjunctivitis ——symptoms typically arise about 3 to 12 days after exposure and are self-limited, resolving in about 5 to 7 days • severe disease and need for hospitalization uncommon • hemorrhagic fever not yet reported • mortality extremely low in 2015-2016 Zika virus outbreak in Americas Complications

• fetal abnormalities reported in fetuses whose mothers acquired acute Zika virus infection during pregnancy include ——microcephaly ■■ incidence of fetal microcephaly in Brazil »»5.7 cases per 100,000 live births in 2014 »»99.7 cases per 100,000 live births in 2015 ■■ prevalence of microcephaly in infants born to women who resided in regions with active transmission during first trimester of pregnancy 2.8 cases per 10,000 live births, compared with infants born to women living in regions without confirmed Zika virus transmission (0.6 cases per 10,000 live births) during January 2015 and January 2016 ■■ Zika virus RNA detected in placental and fetal tissue of those affected ——other complications ■■ intrauterine growth restriction ■■ fetal death ■■ cerebral calcification or other central nervous system lesions • Guillain-Barre syndrome ——increase in rate during outbreak reported but causal role not confirmed Evaluation

• consider diagnosis of Zika virus infection in patients with both ——acute febrile illness with one or more of: ■■ maculopapular rash ■■ arthralgias ■■ conjunctivitis ——exposure history ■■ residence in or history of travel to area with active transmission within 2 weeks of illness onset ■■ unprotected sexual contact with recent traveler to an area with active transmission

• In USA, suspected cases should be reported to local health departments for coordination of testing, care, and to prevent spread • testing ——for Zika virus ■■ performed by CDC only as no commercially available test »»serum reverse transcriptase-polymerase chain reaction (RT-PCR) »»serum virus-specific IgM and neutralizing antibodies »»CDC IgM Antibody Capture ELISA (Zika MAC-ELISA) approved by FDA for emergency evaluation in selected laboratories in February 2016 »»Culture rarely used ——other testing ■■ CBC, routine chemistries often normal ■■ mild leukopenia, thrombocytopenia, and hepatic transaminitis reported • evaluate any patient with suspected Zika virus infection for ——diseases in which symptoms, mosquito vector, and geographic distribution overlap, including ■■ dengue ■■ chikungunya virus infection ——other conditions ■■ malaria ■■ rubella ■■ measles ■■ parvovirus B19 infection ■■ leptospirosis ■■ influenza ■■ enteroviral illnesses ■■ rickettsial illnesses ■■ acute HIV infection ■■ group A streptococcal infection ■■ other alphavirus infections ACOG »»Ross River virus disease (Australia and Oceania) »»Mayaro virus (South America) »»Barmah forest virus (Australia) »»O’nyong’nyong (Africa) »»Sindbis virus (Africa, Asia, Scandinavia, Russia) »»Semliki Forest virus (Africa) • any pregnant woman with appropriate exposure history and 2 or more symptoms or findings of fetal microcephaly or intracranial calcifications on ultrasound should be tested for Zika virus.

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• recommendations ——CDC interim guidelines for evaluation and management of both pregnant women and infants with suspected Zika virus infections published January 2016 ——ACOG and Society for Maternal-Fetal Medicine practice advisory providing interim guidance for care of obstetric patients and women of reproductive age during a zika virus outbreak are consistent with CDC recommendations Management

• no specific antiviral treatment available • treatment generally supportive such as rest, hydration, and pain and fever control ——aspirin and other NSAIDs should be avoided until dengue can be ruled out to reduce risk of hemorrhage ——febrile pregnant women should be treated with acetaminophen • infected patients should be advised to avoid mosquito exposure during first week of illness to reduce risk of further transmission CDC 2016 Interim Guidelines for follow-up for infants with possible congenital Zika virus infection

• no vaccine or preventive medications currently available • for pregnant women or women trying to become pregnant ——several national health agencies have recommended that women postpone pregnancy during the outbreak and avoid travel to regions with active transmission ——Interim guidelines from CDC ■■ advise pregnant women to avoid travel to elevations <2,000 meters (6,562 feet) in regions with active transmission ■■ for women who reside in areas of active transmission, discuss risks and benefits of timing of pregnancy on an individual basis • men who live in or have traveled to area of active transmission should ——abstain from sexual activity, or ——consistently and correctly use condoms during all sexual activity, particularly with pregnant partners. n For more coverage on Zika virus, please see “CDC issues Zika virus update for pediatric healthcare providers,” on page 14.

CONTEMPORARY

• report to local health departments and monitor • perform hearing screen at age 6 months and follow-up of hearing abnormalities if any hearing loss is detected through newborn hearing screening • evaluate occipitofrontal circumference and developmental characteristics and milestones during first 12 months • consult medical specialists if necessary ——pediatric neurology ——developmental and behavioral pediatrics ——physical and speech therapy CDC interim guidelines for breastfeeding for mothers with Zika virus infection — United States, 2016

• no cases of breastfeeding-associated Zika virus infection reported • breastfeeding encouraged in mothers with Zika virus infection and living in areas with ongoing transmission Prevention

• mosquito avoidance (especially during viremic phase [first week of illness] to prevent local transmission)

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FEATURE: DENISE J. BOWEN, PA-C, MA

Steps for improving health literacy Communicating well with your patients will lead to better provider/patient relationships, better health outcomes, and reduced healthcare disparities.

© THINKSTOCK

M

Communicating well with your patients has significant rewards.

ost practicing primary healthcare providers have had a patient who has had no clue about what you had just explained to him or her. I had an occasion when I had just spent 15 minutes talking to a collegeeducated mother whose child had just been diagnosed with asthma. I carefully explained that I was going to make arrangements to have a nebulizer delivered to her home so that she could start the appropriate treatments. The home health agency later reported to me that she was quite shocked to learn that the medications given to her at the pharmacy were not to be given to her infant by mouth. She apparently was under the impression that the nebulizer was a humidifier. We get so involved in delivering a message that we do not always realize that it was not being understood.

A patient’s ability to read, understand, and apply health-related information plays a huge role in the effectiveness of both oral and written patient education. This concept of health literacy has been recognized as a key contributor to health for many years. In 2003, for the first time, the National Assessment of Adult Literacy (NAAL) measured health literacy among American adults. The results were eye-opening. Only 65% of adults scored at an intermediate or proficient level of health literacy.

Some 14% (30 million) adults scored below the basic level, and another 22% (47 million) scored at only a basic level.1 A systematic review of the literature in 2012 indicated that low health literacy is linked to

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worse health outcomes and poorer use of healthcare services.2 This includes higher rates of readmissions and emergency department use and lower use of preventive care. The authors of the review also concluded that there was emerging evidence that lower health literacy could also partly explain the racial and ethnic disparities in health outcomes The NAAL survey in 2003 indicated that race, ethnicity, and socioeconomic status were risk factors for poor health literacy. About 35% of Hispanic adults, 19% of Black adults, and 43% of adults living below the poverty threshold scored below the basic level in health literacy, compared with 14% of all American adults participating in the survey.1 According to Sylvia Mathews Burwell, Secretary of the U.S. Department of Health and Human Services, “If we want health equity, we need to make health literacy a priority.”

Interventions that address low health literacy may help to reduce these disparities.3 Learning these strategies will help you to communicate effectively with your patients, and they will have better health outcomes. What are some things that you can you do to make sure that your patients understand you?

1. Make sure that you can identify patients with low health literacy. Healthcare providers are notoriously poor at identifying patients with low health literacy.4 In addition, patients with reading problems often do not disclose their illiteracy.5 Some signs that a patient may struggle with literacy include poor compliance with treatments and appointments, confusion about medication, and making excuses for not reading. A great way to check the health literacy skills of a patient is to do a medication review. Ask your patients to explain the purpose of their medications and show you how they are using it.

2. Make sure to use plain language. Using plain, nonmedical language can enhance understanding dramatically. Using the patients’ own terms for their illness and treatments is a good starting point. We often need to be reminded of alternative language for our familiar medical terminology. For example: “pain-killer” instead of “analgesic”; “birth control” instead of “contraception”; “keeping bones strong” instead of “preventing osteoporosis.”

Try giving simple explanations for medical terminology that you do use. Analogies can also be helpful.

Avoid acronyms. Instead of saying, “The tests show that you have had an MI,” say “It looks like you had a heart attack.”

Using plain language for nonmedical words is also useful: “Use” instead of “utilize”; “end” instead of “terminate”; and “try” instead of “attempt.”

3. Learn how to focus the message. Less than half of the information provided during a typical medical encounter

is retained by the patient, even if the patient is proficient in health literacy. Limiting the information by focusing on only 1 to 3 key messages per visit is crucial. Patients who struggle with health literacy will respond more to information that is designed to promote action rather than to detailed explanations and facts. Focusing the key messages on behavior instead will help to motivate and empower the patient. Developing short explanations for common diagnoses and treatments will help you to avoid giving the patient a lecture on pathophysiology and pharmacology.

4. Use the “Teach-Back” method. Reviewing and repeating each point at the end of every visit will help to reinforce the key messages. The “Teach-Back” method is a powerful tool for this and should be used by all health professionals. It is a test of how well the provider has explained the concept in a way that the patient understands. It provides an opportunity to check for understanding and if needed, to re-teach the information. It involves asking the patients to repeat in their own words what they need to know or do, in a nonshaming way.

This method can be as simple as asking, “What are you going to do when you get home?” or “Can you tell me the things that you need to do before the next visit?” or “Show me how you would (…).” This simple method is one of the top 11 most effective safety practices backed by scientific evidence.6 When using the “Teach-Back” method, it is important to use open-ended questions and avoid yes/no questions such as “Do you understand?” or “Do you have any questions?”

TABLE 1. Elements of competence for using teach-back effectively 1. Use a caring tone of voice and attitude.

2. Display comfortable body language, and make eye contact.

3. Use plain language.

4. Ask the patient to explain back, using his or her own words.

5. Use non-shaming, open-ended questions.

6. Avoid asking questions that can be answered with a simple yes or no.

7. Emphasize that the responsibility to explain clearly is on you, the provider.

8. If the patient is not able to teach back correctly, explain again and re-check.

9. Use reader-friendly print materials to support learning.

10. Document use of and patient response to teach-back.

Source: Always use teach-back! Available at: www.teachbacktraining.org

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IMPROVING HEALTH LITERACY

There is a great toolkit available at the “Always Use Teach-back!” website, which can help you to become proficient in this technique: http://www.teachback training.org/ 5. Evaluate the written materials that you are giving your patients. Using written materials to educate our patients can be an efficient way to help patients absorb new information. Unfortunately, they are often inappropriate or given to patients in lieu of providing educational counseling and end up in the trash cans in the waiting room. We need to know how to assess the content and effectiveness of the materials we provide, and we need to make sure that we review the information in the handout with the patient. Patient-friendly educational materials should be written at a 4th to 6th grade level, and the number of messages in the handout should be limited to no more than 2. The Flesch-Kincaid Grade Level and Flesch Reading Ease Score are simple tools available on Word for Windows for testing readability.

Commit yourself to becoming a more effective clinician and making sure that you are communicating well with your patients. The rewards are significant: better provider/patient relationships, better health outcomes, reduced healthcare disparities, and better patient safety. n

Denise J. Bowen, PA-C, MA, is an assistant professor at the Western Michigan University Physician Assistant Program in Kalamazoo, Mich.

“Something’s wrong with the broccoli. Please take it back to the kitchen and have it genetically modified.”

“I’ve been working out for six months, but all my gains have been in cognitive function.”

References 1. White S. Assessing the nation’s health literacy : key concepts and findings of the National Assessment of Adult Literacy (NAAL). Chicago: American Medical Association; 2008.

2. Berkman ND, Sheridan SL, Donahue KE, et al. Low health literacy and health outcomes: an updated systematic review. Ann Intern Med. 2011;155(2)97-107.

3. Bennett IM, Chen J, Soroui JS, White S. The contribution of health literacy to disparities in self-rated health status and preventive health behaviors in older adults. Ann Fam Med. 2009;7(3)204-211. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682976 (Accessed April 16, 2016).

4. Parker RM, Davis TC, Williams MV. Patients with limited health literacy.

In: Bateman WB, Kramer EJ, Glassman KS, eds. Patient and Family Education in Managed Care and Beyond. New York: Springer; 1999: 63–71.

5. Parikh NS, Parker RM, Nurss JR, et al. Shame and health literacy: the unspoken connection. Patient Educ Couns. 1996;27(1):33–39.

6. Agency for Healthcare Research and Quality. Making health care safer: a critical analysis of patient safety practices. Evidence report/technology

© The New Yorker Collection 2016 from cartoonbank.com. All Rights Reserved.

Assessment, no. 43. 2001.

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Conference Roundup ENDO 2016 The Endocrine Society Boston

HYPOTHYROIDISM MAY INCREASE TYPE 2 DIABETES RISK Patients diagnosed with prediabetes have a 40% greater likelihood of developing diabetes if they are also diagnosed with hypothyroidism, researchers reported.

“Low thyroid function is associated with higher risk of developing diabetes, but also the progression from prediabetes to diabetes, and this is even within the normal range of thyroid function,” said Layal Chaker, MD, of Erasmus Medical Center in Rotterdam, Netherlands.“Low thyroid function as represented by higher TSH [thyroid-stimulating hormone] is associated with a 1.2-fold increased risk of diabetes and a 1.4-fold increased risk for progression from prediabetes.”

She added that, during a lifetime, 70% to 75% of people diagnosed with prediabetes will progress to diabetes.

Thyroid hormone is important for metabolism, and thus important in controlling weight and cholesterol metabolism. Therefore, Dr Chaker and her team hypothesized that thyroid hormone could also be important in the development of type 2 diabetes.

To test their hypothesis, the research team evaluated thyroid function, incidence of diabetes, and progression from prediabetes to diabetes. Dr Chaker and colleagues selected 8,452 participants from the Rotterdam Study, a population-based study of adults aged 45 or older that reflects the general population in the Netherlands.

The study population was 58% women and average age was 65 years. On average, TSH and free thyroxine (FT4) were on par with that of the general population (1.91 mIU/L and 1.22 ng/dL, respectively).

Patients with prediabetes have an increased risk of developing diabetes if they also have low thyroid function.

No patient had diabetes at baseline. All participants were tested for blood sugar and thyroid function and were reexamined every 2 to 3 years to check for the development of type 2 diabetes.

Patients with fasting glucose between 6 mmol/L and 7 mmol/L were considered to have prediabetes, and those with a fasting glucose of 7 mmol/L or greater were considered to have diabetes.

During an average follow-up of nearly 8 years, 1,100 participants developed prediabetes and 798 developed diabetes. Higher TSH was linked to increased diabetes risk (hazard ratio [HR]=1.13), even within the reference range of thyroid function (HR=1.24).

In addition, diabetes risk was lower with higher FT4 levels in all (HR=0.96) and in those within the reference range (HR=0.96).

Risk for progression from prediabetes to diabetes was 1.4 times greater for participants in the lowest third of thyroid function levels, compared with those in the highest third.

“We found it surprising that even people whose thyroid function was in the low-normal range had an increased risk of diabetes,” Dr Chaker said. “These findings suggest we should consider screening people with prediabetes for low thyroid function.”

NEW PROCEDURE MAY BE MORE EFFECTIVE THAN GASTRIC BYPASS FOR GLYCEMIC CONTROL IN MILD OBESITY Compared with gastric bypass or clinical treatment, mildly obese patients with type 2 diabetes had greater improvement in glycemic control after undergoing surgery with a new technique, researchers reported.

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PALEO DIET MAY REDUCE FATTY ACID LEVEL LINKED TO INSULIN RESISTANCE Postmenopausal women assigned to a high-protein “Paleolithic-type” diet had greater reductions in fatty acids associated with insulin resistance than women assigned to a low-fat diet.

© THINKSTOCK

Study results showed that 100% of patients with class I obesity and poorly controlled type 2 diabetes who underwent sleeve-IT achieved glycemic control, as defined by an HbA1c of 6.5% or less, compared with 46% of those who underwent gastric bypass and 8% of those treated clinically for diabetes after 1 year of treatment.

Further, diabetes remission, defined as glycemic control without medication, was also achieved by more patients in the sleeve-IT group than in the gastric bypass group (75% vs 30%).

“Although in 2010, the International Diabetes Federation recommended surgery for diabetic patients with mild obesity if clinical treatment is not successful, few related studies on this topic have been published,” said lead study author Ana Priscilla Soggia, MD, an endocrinologist in the division of clinical research at the Hospital Sirio-Libañes in São Paulo. “The first surgical choice is gastric bypass. However, sleeve-IT, a recent technique not yet approved, increases the beneficial effects of traditional surgery, due to intestinal physiological mechanisms, without increasing the risk of side effects.”

In this trial, Dr Soggia and colleagues randomly assigned 42 patients with class I obesity (BMI of 30 to 35) and poorly controlled type 2 diabetes to sleeve-IT surgery (n=12), gastric bypass (n=13), or clinical diabetes treatment (n=12).

Average age was 51 years; 62% were women, and average HbA1c level was 9.3%.

Although more patients achieved glycemic control in the sleeve-IT group, average HbA1c still improved in all 3 groups (sleeve-IT, 5.6%; gastric bypass, 6.9%; clinical treatment, 8%).

Greater weight loss was seen among patients in the sleeveIT and gastric bypass groups. On average, participants in the sleeve-IT group lost 18.6 kg, those in the gastric bypass group lost 22.5 kg, and those who received clinical treatment lost 4.7 kg.

After surgery, drugs to lower glucose, lipid levels, and blood pressure decreased in the sleeve-IT and gastric bypass groups.

Four patients had a serious adverse event, but no deaths or life-threatening complications occurred.

“This recent technique that combines sleeve gastrectomy with ileal transposition was an effective and safe choice for treating patients with mild obesity,” noted Dr Soggia.

Postmenopausal women who adhered to the Paleolithic-type diet had greater reductions in fatty acids associated with insulin resistance.

Women on the Paleolithic-type diet, known as the Paleo diet, had health benefits even though weight loss was similar in both groups, researchers noted.

The diet, which was 30% protein, 30% carbohydrates, and 40% fats, reduced the intake of saturated fatty acids by 19% and increased intake of polyunsaturated fatty acids by 47%.

“A Paleolithic-type diet reduced specific fatty acids in the blood more distinctly than a control diet despite similar weight loss,” said Caroline Blomquist, a doctoral student in the department of public health and clinical medicine at Umeå University in Sweden. “The Paleolithic-type diet may have long-term beneficial effects on obesity-related disorders such as insulin resistance and cardiovascular diseases.”

After menopause, women have an increased risk for abdominal adiposity, which is associated with a reduction in insulin resistance and cardiovascular disease.

Ms. Blomquist said it is of particular interest to find a diet for these women that helps them avoid obesity and metabolic dysregulation.

Seventy obese postmenopausal women (BMI, 32.6) were randomly assigned to either the high-protein Paleolithictype diet or a low-fat diet that included 15% protein, 55% carbohydrates, and 30% fat.

The Paleolithic-type diet was based on lean meat, fish, eggs, nuts, and berries. Additional fat sources included rapeseed, olive oils, and avocado. Dairy products, cereals, added salt, and refined fats and sugar were excluded.

Both diet groups participated in 12 group sessions with a dietitian and kept ongoing records of food intake.

At 24 months, the researchers found that, in the Paleolithictype diet group, intake of saturated fatty acids decreased by 19% and intake of monounsaturated fatty acids and polyunsaturated fatty acids increased by 47%.

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Conference Roundup Ms. Blomquist said that delta-6 and delta-9 desaturase activities decreased significantly more in the Paleolithic-type diet group than in the low-fat diet group after 24 months.

Fatty acids associated with insulin resistance, including 14:0, 16:1, 18:3n-6, and 20:3n-6, all decreased in the Paleolithictype diet group after 24 months.

© VOISIN / PHANIE / SCIENCE SOURCE

STIMULANT USE FOR ADHD MAY LEAD TO LOWER BONE DENSITY IN YOUNG PEOPLE Use of stimulants such as amphetamine and methylphenidate for attention-deficit/hyperactivity disorder (ADHD) may lead to loss of bone mineral content in teenagers and children.

“Children and adolescents using stimulant medications have lower bone density than their peers,” said Alexis Feuer, MD, assistant professor of pediatrics and a pediatric endocrinologist at Weill Cornell Medicine in New York.

Dr Feuer discussed results from a study of nearly 6,500 young people. She cautioned that the findings do not prove that these medications cause lower bone density. Researchers need to collect more data before they can determine what impact, if any, these results might have on the roughly 6 million young people in the United States who are being treated for ADHD, she said.

Young people who took stimulants for longer than 6 months had lower bone density at the spine and hip than those assigned to those medications for less than 6 months.

“Those children taking stimulants for less than 6 months still had lower bone density than nonusers,” she said.

Previous studies have found that stimulants may slow children’s rate of growth in height, and lower bone density could result in increased fracture risk or the development of osteoporosis later in life.

Bone densitometry X-ray of the hip. Young people who use stimulants have lower bone density compared with their peers.

Dr Feuer and colleagues analyzed data collected in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2010. Among 6,489 people aged 8 to 20 years who participated in the survey and had a bone density scan using dual-energy X-ray absorptiometry (DXA), 159 participants used stimulants and 6,330 did not.

Among stimulant users, average bone mineral content was 5.1% lower at the lumbar spine and 5.3% lower at the hip than in nonusers. Bone mineral density (BMD) was 3.9% lower at the spine and 3.7% lower at the hip in stimulant users.

“I firmly believe that moving forward, clinicians caring for children taking stimulants should immediately begin screening them for bone health,” said Dr Feuer, noting that routine imaging with DXA scans is not currently recommended.

“Fortunately, a child’s bone health can be comprehensively screened through careful monitoring of their linear growth and weight gain and by ensuring that these children are engaging in adequate weight-bearing exercise and have sufficient vitamin D levels.”

She also did not recommend discontinuing the use of stimulant medications.

“The decision to take a stimulant medication is not taken lightly by doctors who are prescribing them or parents and families of patients who need them. If a child needs a stimulant medication, they 100% should be taking them,” Dr Feuer noted.

HIGHER AMOUNT OF WEIGHT LOSS MAY INCREASE LIKELIHOOD OF SUSTAINED WEIGHT LOSS A review of medical records from more than 177,000 people showed that those who lost the most weight were also the most likely to keep losing weight after 2 years and the least likely to “cycle” between periods of weight loss and weight gain.

In addition, individuals who lost the least amount of weight were also the most likely to regain at least 50% of the weight they lost.

Researchers reviewed records of adults with a BMI of 30 or greater who had no medical conditions associated with unintentional weight loss and who had at least 4 BMI measurements per year for at least 5 years. Patients were categorized into 4 weight groups based on their amount of weight change during a 6-month period.

The researchers followed participants for 2 years. Weight maintenance during this follow-up period was 23.1% in the modest weight loss group, 14.1% in the moderate weight loss group, and 19.4% in the high weight loss group.

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© THINKSTOCK

“Weight loss maintenance, even in the moderate and high weight loss groups, is very difficult to achieve,” she said.

“Successful and sustained clinically meaningful weight loss requires chronic and effective weight management strategies.”

People who have greater amounts of weight loss are less likely to cycle between periods of weight loss and weight gain.

These data underscore the difficulty of maintaining weight loss, according to Joanna Huang, PharmD, senior manager of health economics and outcome research with Novo Nordisk.

“Focusing on the highest weight loss group, only 20% were able to maintain their initial weight loss after 2 years,” Dr Huang said. “Maintenance of the weight loss is very difficult to achieve.”

For 2 years, however, the high weight loss group was significantly more likely than the other 2 groups to continue losing weight after the first quarter.

The high weight loss group was also less likely to regain the weight lost. About 18.6% of that group regained at least 50% of weight lost, compared with 40.0% of the modest weight loss group and 35.9% of the moderate weight loss group.

“There is an inverse relationship between the amount of weight loss and the amount of patients who regained that initial weight loss,” Dr Huang noted. “Looking at the modest weight loss group, they lost the least amount of weight, but that group had the most people who regained 50% or 75% or even 100% of their weight.”

However, of those in the high weight loss group who did regain the weight, they did so in just 12 months, compared with 14 months in the modest weight loss group and 15.2 months in the moderate weight loss group.

Dr Huang said that people in the high weight loss group were less likely to become “cyclers,” people who did not consistently lose, maintain, or gain weight in each quarter.

Overall, about 60% of the population were classified as cyclers after 2 years, 58.3% in the high weight loss group, 71.5% in the modest weight loss group, and 74.1% in the moderate weight loss group.

LARGE BREAKFAST WITH WHEY PROTEIN BENEFICIAL FOR PATIENTS WITH TYPE 2 DIABETES Adults with type 2 diabetes who start the day with a large breakfast that includes whey protein may be able to lose weight and better manage the disease, said Daniela Jakubowicz, MD, professor of medicine at Tel Aviv University.

In a study conducted by Dr Jakubowicz and colleagues, 48 overweight and obese participants with type 2 diabetes ate the same number of calories over a large breakfast (660 kcal), medium-sized lunch (567 kcal), and small dinner (276 kcal) for 23 months. The researchers assigned participants to 1 of 3 breakfast diets: Primarily whey protein such as whey protein shakes (n=17), other proteins including eggs, soy, or tuna (n=16), or a breakfast high in carbohydrates or starch (n=15). Participants in both protein groups consumed 49 grams of protein at breakfast, compared with 17 grams in the carbohydrate group.

Patients in the whey protein group had greater weight loss at 12 weeks, compared with the other protein and carbohydrate groups (7.6 kg vs 6.1 kg and 3.1 kg, respectively).

Patients in the whey protein group were more satiated and less hungry throughout the day and had lower glucose spikes after meals. Greater reductions in HbA1c were also noted among these patients, with the percent change being 11.5% for the whey protein group vs 7.7% for the other protein group and 4.6% for the carbohydrate group.

In addition, area under the curve (AUC) for overall postprandial glucose (PPG) was 12% lower in the other protein group and 19% lower in the whey protein group, as compared with the carbohydrate group, while AUC for overall insulin was 38% higher in the whey protein group and 27% higher in the other protein group.

Dr Jakubowicz added that the whey protein diet significantly suppresses the hunger hormone ghrelin.

“We can see a significant decrease in body weight in the whey protein diet, compared to the other groups,” she said.

“Also, we can see the significant decrease in HbA1c in the whey breakfast diet. Along the day, the overall postprandial glycemia is significantly lower along the day in comparison to the other diets.”

“Whey protein should be considered an important adjuvant in the management of the type 2 diabetes,” she concluded.

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Conference Roundup while undergoing functional magnetic resonance imaging (fMRI) brain scanning.

“Liraglutide decreased activation in the parietal cortex to these highly desirable food cues,” Dr Farr said. “It is selectively decreasing attention or attractiveness to these high-calorie or high-fat food cues.”

Dr Farr said her team is planning more studies to determine if the results remain consistent at the 3.0-mg liraglutide dose. The researchers also hope to learn if there are individual differences in the brain’s response to liraglutide and whether any compensatory brain activations may arise at higher doses to curb weight loss.

ASTHMA RISK MAY BE ASSOCIATED WITH POLYCYSTIC OVARY SYNDROME AND OBESITY AMONG WOMEN Women with polycystic ovary syndrome (PCOS) or those who are overweight and obese may be more likely to have asthma, suggest data from a large Australian cohort study.

PCOS is common among reproductive-aged women, affecting between 1 in 5 to 1 in 10 women, according to Anju Elizabeth Joham, MBBS, FRACP, an endocrinologist and postdoctoral research fellow at Monash University in Melbourne, Australia.

Although asthma is not understood to be associated with PCOS, one study in Western Australia suggested that asthmarelated hospital admissions were higher in women with PCOS than in those without the condition, she said.

To further investigate the potential link between asthma and PCOS, Dr Joham and colleagues conducted a cross-sectional analysis of data from the Australian Longitudinal Study on

©THINKSTOCK

LIRAGLUTIDE MAY LOWER THE BRAIN’S REWARD RESPONSE TO HIGH-FAT FOODS Brain scans of adult patients with diabetes showed that the drug liraglutide reduced the brain’s reward response associated with highly desirable high-fat, high-calorie foods, researchers reported.

Liraglutide decreased reward activations in the cortex in response to images of highly desirable foods, such as cake, pastries, and fried food, compared with less desirable foods, such as fruits, vegetables, and other low-calorie, low-fat foods, said study co-investigator Olivia Farr, PhD, an instructor in medicine at Beth Israel Deaconess Medical Center and Harvard Medical School in Boston.

She added that these findings could mean that liraglutide makes people pay more attention to what they are eating, particularly calorie-dense foods that are high in fat.

“This decreased activation means that individuals on liraglutide find highly desirable foods less attention-grabbing and less rewarding than they typically would without liraglutide,” Dr Farr. “Thus, this medication may prove to be better for weight loss for people who tend to eat more high-fat food as a reward, such as when they are stressed.

Our study identifies neural targets for more effective weight loss therapeutics in the future.”

Injectable liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that is FDA-approved for the treatment of type 2 diabetes (Victoza, Novo Nordisk). Research suggests that a 1.8-mg dose can induce weight loss in patients who have type 2 diabetes, while a 3.0-mg dose is FDA-approved for weight management in obese and overweight people with at least 1 weight-related comorbidity (Saxenda, Novo Nordisk).

Based on animal studies, Dr Farr and her team hypothesized that liraglutide may work directly in the brain to decrease weight. They assessed 22 human brain tissue samples using immunohistochemistry for the presence of GLP-1 receptors and found evidence, for the first time, that GLP-1 is expressed in human brains.

Further, the investigators found that the hormone is expressed on the cerebral cortex, not just the brainstem and hypothalamus.

The researchers then performed a randomized, placebocontrolled crossover trial involving 18 adults with type 2 diabetes. Participants were assigned to 17 days of increasing doses (0.2 mg to 1.2 mg to 1.8 mg) of liraglutide or placebo. Following a 3-week washout period, the same participants received 17 days of the opposite treatment.

On day 17, participants viewed images of different foods

Women with polycystic ovary syndrome and those who are overweight have an increased risk of developing asthma.

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Women’s Health. The study includes a periodic national survey that has been collecting data on more than 58,000 women of various ages about factors that influence their health.

The researchers assessed the responses of 8,612 randomly selected women from the study on self-reported PCOS and asthma.

Prevalence of PCOS was 5.8% (95% CI, 5.3-6.4) among women aged 28 to 33 years, according to the data. Although the prevalence was low, noted Dr Joham, the fact that the condition was self-reported may have contributed to underreporting.

Among those reporting PCOS, the prevalence of asthma was 15.2% vs 10.6% among those not reporting PCOS. For women reporting asthma, mean BMI was significantly higher in women reporting PCOS vs those not reporting PCOS (BMI, 29.9 vs 27.7).

The proportion of women reporting asthma and type 2 diabetes across healthy weight, overweight, and obese categories was comparable in women with PCOS vs those without the condition.

Results linked PCOS with increased odds of asthma after adjustment for age, BMI, PCOS, and smoking status (odds ratio [OR]=1.34). Similarly, odds of asthma were increased for BMI in the overweight range (OR=1.24) and for BMI in the obese range (OR=1.77).

The study’s strengths included its large size, while its main limitation was the fact that the data were self-reported, noted Dr Joham.

“Overall, our findings were that the prevalence of asthma was higher in women with PCOS. PCOS on its own was associated with a 34% increased risk of asthma, and weight in the overweight and obese range was also associated with asthma,” she said.

“The link could be inflammation,” added Dr Joham.

“However, this is an observational study, and at this stage, we can’t really look at exact causation … so further research is definitely needed in this area, and longitudinal studies would be helpful.”

ESTROGEN THERAPY MAY BOOST MEMORY IN YOUNG ATHLETES WITH AMENORRHEA Six months of estrogen replacement therapy appeared to restore cognitive function in female athletes with amenorrhea, according to researchers.

An estimated 44% of women who exercise experience amenorrhea, or lack of periods. Estrogen deficiency due to amenorrhea may cause forgetfulness and poor concentration,

and some studies have found a positive effect of estrogen replacement on mental processes such as memory, the researchers noted.

“This is the first study, we believe, to assess the impact of estrogen replacement on memory and other cognitive processes in young athletes who lose their periods due to excessive exercise,” Charu Baskaran, MD, the study’s lead investigator and a pediatric endocrinologist at the Massachusetts General Hospital for Children, said. “This information is important because these athletes are in their prime of neurocognitive development.”

Dr Baskaran and her colleagues assigned 29 athletes with amenorrhea aged 14 to 25 to estrogen replacement therapy and compared them with 19 athletes who did not receive estrogen. Athletes in the study either never started their period or stopped having a period for at least 3 months because of too much aerobic physical activity—more than 10 hours a week on average.

Participants were randomly assigned to oral estradiol and progesterone at a dose similar to a birth control pill (n=16), transdermal estradiol at a physiologic replacement dose with cyclic progesterone (n=13), or no estrogen (n=19).

All participants underwent cognitive testing before and after treatment, which included an assessment of their verbal memory and their ability to suppress a response. They were also evaluated for cognitive flexibility, switching back and forth between different tasks. The researchers then evaluated the change between pre- and post-treatment test scores.

Compared with the control group, the estrogen groups had significantly better verbal memory and cognitive flexibility scores compared with their pretreatment scores at 6 months. Even when the researchers controlled for patient age and pretreatment test scores, athletes who received estrogen had greater improvement in immediate recall of words and cognitive flexibility.

Only athletes who received the transdermal estrogen experienced significantly greater improvement in certain cognitive tests.

The estrogen patch is a more physiologic form of estrogen delivery that is not metabolized in the liver like oral estrogen, and that may affect other hormone levels that can affect mental processes, Dr Baskaran said. n

These articles originally appeared on EndocrinologyAdvisor.com

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LEGAL ADVISOR CASE

Accessing a relative’s charts

BY ANN W. LATNER, JD

Ms. D, age 48 years, was a nurse in the neurology department of a large medical center. She had been employed by the medical center for 5 years.

Although divorced, she maintained a close relationship with her ex-husband, Joe, who worked at the same place as a technician in the emergency department. Joe was battling advanced-stage multiple myeloma and was being treated at the medical center where the two worked.

When Joe was diagnosed, he and Ms. D talked about his prognosis, his concerns about the future, and his treatment. He knew that he was facing an uphill battle, and he needed support from Ms. D. “I will be there for you no matter what,” she reassured him. “Whatever you need … I’m here.”

And indeed, over the past year, Ms. D had been extremely involved in Joe’s care. She accompanied him to medical appointments, saw him through hospitalizations and a stem cell transplant, and helped him manage his medication regimen.

To facilitate Ms. D’s involvement in his care, Joe executed a number of documents that would provide Ms. D with the authority to gain access to his medical records. These

© THINKSTOCK

A medical center takes issue with a clinician who uses her employee access to view her ex-husband’s medical records.

HIPAA’s Privacy Rule can lead to confusion regarding who can access a patient’s medical records and for what reasons.

documents included a durable power of attorney, an advanced medical directive, and an authorization form from the medical center itself.

Toward the end of the year, Joe’s condition worsened. The medication he was taking was affecting his ability to understand complex medical issues and he was becoming confused. He was also experiencing weakness, tremors, and impaired vision. Typing and using a computer had become increasingly difficult for him. In desperation, he called Ms. D for help.

He explained that he did not understand the significance of his latest lab results and asked Ms. D if she would look at his records and help him understand them. Ms. D, who had far more medical training than Joe, was happy to help him.

Over the next 3 months, Ms. D used her employee code to access Joe’s records 4 times.

Continues on page 122

Cases presented are based on actual occurrences.

Names of participants and details have been changed.

Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.

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LEGAL ADVISOR The medical center provided each employee with an individual access code to the computer system so that it could monitor what the employees were accessing. Ms. D pulled up Joe’s records and on each occasion, she was able to help explain them to him or answer a question that he had.

A few weeks later, a fellow employee mentioned to Ms. D that she had heard that the medical center was going to be auditing its computer records, and Ms. D did not give it a second thought. When the medical center itself sent a memo advising employees of the audit and stressing the medical center’s strong commitment to patient privacy, the Health Insurance Portability and Accountability Act of 1996 (HIPAA), and HIPAA’s Privacy Rule, Ms. D was not concerned.

The medical center claimed that Ms. D had violated the HIPAA Privacy Rule by accessing records that she had no “legitimate work-related reason” to access. The court disagreed, stating that nothing in HIPAA prevents a patient from appointing someone to act as a representative. According to the court, Joe had every right to his own medical records, and he had every right to appoint Ms. D, as his representative, to view those records. The medical center argued that Ms. D should not have accessed the records directly. However, the court of appeals pointed out that federal law does not forbid direct access, and since proper legal authorization had been given, there was no fault by Ms. D. Ms. D was restored to her position, and the medical center had to pay her back wages for the time when she was out of work.

A patient is always entitled to access his or her own records. A patient is also entitled to appoint a representative to look at his or her records.

Legal background

That changed when she arrived at work the week following the audit. Within 10 minutes of clocking in, Ms. D was summoned to human resources, where several other confusedlooking employees sat quietly in the waiting room. When she was called into the supervisor’s office, she began feeling uneasy, although she knew she had not done anything wrong.

“We take privacy issues very seriously here,” began the supervisor, who then listed the 4 times that Ms. D had accessed Joe’s records. Ms. D immediately began explaining the situation, including the fact that she had Joe’s consent, but the supervisor seemed to be working from a script.

“Is Joe your patient?” the supervisor asked.

“Well, no....” Ms. D said.

“Right,” the supervisor said. “He is not your patient. You accessed his records in violation of our privacy policy and HIPAA, and you had no legitimate work-related reason to access those records.” The supervisor went on to tell Ms. D that her employment with the medical center was terminated and that she would be escorted out of the building.

Ms. D was stunned and furious. She filed a grievance to challenge the medical center’s actions. A hearing was held, during which Joe testified that he had executed every form necessary to give Ms. D authority to look at his records and that she had his full authority to speak with his physicians, obtain his files, and act as his agent. The hearing officer found in Ms. D’s favor and ordered that she be reinstated. The medical center appealed, and the appeal was heard by the court of appeals of the state.

A patient is always entitled to access his or her own records.

Nothing in HIPAA’s Privacy Rule ever affects that. A patient is also entitled to appoint a representative to look at his or her records. In this case, the court of appeals reiterated that HIPAA does not change the fact that one person can act as the authorized representative of another person for purposes of accessing confidential medical information, provided that a power of attorney or other appropriate formal legal document has been properly executed according to state law in the local jurisdiction.

Protecting yourself

There are few things that cause as much confusion as HIPAA. In particular, HIPAA’s Privacy Rule, despite being published 16 years ago, still causes misunderstanding when it comes to who can access patient medical records and for what reasons.

Ms. D did almost everything she could to protect herself from what eventually happened to her. She and her exhusband obtained and executed the proper forms, including the medical center’s own form. The only thing she might have done to better protect herself was to inform her supervisor that she wanted to see the records before she accessed them. The medical center seemed particularly disturbed that she accessed the records on her own, rather than follow the normal policy involved with requesting records.

Be sure to familiarize yourself with the policies of your place of employment. If someone who is not your patient gives you permission to access records, be sure that: 1) he or she has filled out the requisite paperwork giving consent; and 2) you are accessing the records according to your employer’s policy. n Ms. Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, N.Y.

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ALTERNATIVE MEDS UPDATE

What you should know about the herbs and supplements patients use

By Sherril Sego, FNP-C, DNP Ms. Sego is an independent consultant in Kansas City, Mo.

Slippery elm

© 123RF / RAY ANTHONY

The aptly named slippery elm tree, or Ulmus rubra, is a deciduous tree that is native to most of North America, and it was designated as a specific species in 1793 by Gotthilf Muhlenberg, a German American clergyman and botanist from Pennsylvania.1 Slippery elm trees can grow to a height of 65 feet and may have a diameter as large as 20 inches.2 The tree’s distinctive feature is its slimy inner bark. It is this mucilaginous product that functions as a demulcent, or antiinflammatory agent, and it may also serve as a nutritional substitute.1

Background Slippery elm has a laudable history in the United States, beginning with the early settlers. During the American Revolution, soldiers found its paste useful as a salve for healing wounds. The bark and its resultant mucilage not only contain anti-inflammatory agents, but also contain nutrients such as vitamin E and bioflavonoids.3 According to several sources, slippery elm played a role in saving soldiers from starvation during the brutal winter at Valley Forge.3 It was recommended in King’s American dispensatory and was also included in the United States Pharmacopeia from 1820 to 1960.4 The medicinal uses of U rubra have been documented for hundreds of years. The mucilage of this tree bark is a complex polysaccharide that becomes a gel-like substance when mixed with water. Native Americans noted using formulations of the mucilage for wound healing, skin conditions, cough control, and sore throats.5 As pioneers moved into the frontier, folk medicine and Native American healing methods gradually

merged, and slippery elm continues to be used today for a variety of conditions. One unique use for slippery elm was the chewing of slippery elm tablets by baseball pitchers to enhance saliva production for the famous spitball, a practice that was banned in 1920.6

Science Slippery elm’s most popular use is for the treatment of inflammatory conditions of the gastrointestinal tract. The mechanism of action in the upper stomach and esophagus appears to be reflux stimulation of the nerve endings in the lining, which causes increased mucous secretion.7 This increases the protective coating, shielding the stomach and small intestine from excess acidity.8 In one study, slippery elm was found to elicit a similar response in patients with the inflammatory bowel disease ulcerative colitis, when compared with 5-aminosalicylic acid.9 Researchers examined the anti-inflammatory effect of

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ALTERNATIVE MEDS UPDATE slippery elm on colonic cells biopsied from 45 patients with active ulcerative colitis. Findings revealed a nearly equal dose-dependent response in both slippery elm and 5-aminosalicylic acid.9 Slippery elm has also been used successfully for the management of irritable bowel syndrome (IBS). Taken orally as a dry powder, the waterabsorbing capacity of slippery elm draws water into dry stool in the colon and adds bulk to loose and watery stools.10

gastrointestinal complaints. Although its use alone may not be sufficient for serious conditions such as ulcerative colitis, its lack of drug interactions makes it a very attractive add-on therapy when additional symptom management is needed. n References 1. Jellin JM, Gregory PJ, Batz F, Bonakdar R, eds. Natural Medicines Comprehensive Database. http://naturaldata base.therapeuticresearch.com/home.aspx?cs=&s=ND. 2. Cooley JH, Van Sambeek JW. Slippery Elm. http://www.na.fs.

Safety, interactions In addition to allergic reactions, which are always possible, slippery elm can also slow and/or inhibit absorption of other medications and should therefore be taken 2 hours before or after other medications.11 Slippery elm is not recommended for use in infants or small children. There are conflicting data regarding the use of slippery elm during pregnancy, but in the most current information on the oral use of slippery elm, it is considered safe for use in pregnancy. However, folk medicine resources and anecdotal sources describe miscarriages in women inserting small strips of the bark into the cervical os, as the bark absorbed moisture and expanded.12 The US Food and Drug Administration has granted slippery elm a status of generally regarded as safe.13

fed.us/spfo/pubs/silvics_manual/volume_2/ulmus/rubra.htm.

Slippery elm may be beneficial for patients with GI complaints.

Slippery elm may be an attractive add-on therapy when additional symptom management is needed.

How supplied, dose, cost

3. Hanrahan C, Frey R. Slippery Elm. In: Longe JL, ed.

The Gale Encyclopedia of Alternative Medicine. 2nd ed.

Farmington Hills, MI: Thomson Gale; 2005. http://www. encyclopedia.com/doc/1G2-3435100729.html.

4. Anderson MK. Plant Guide: Slippery Elm. US Department of Agriculture Natural Resources Conservation Services. http://www.plants.usda.gov/plantguide/pdf/cs_ulru.pdf.

Updated May 30, 2006.

5. Watts CR, Rousseau B. Slippery elm, its biochemistry, and use as a complementary and alternative treatment for laryngeal irritation. J Invest Biochem. 2012;1(1):17-23.

6. Spitball. Baseball Reference website. http://www.baseballreference.com/bullpen/Spitball. Updated November 28, 2015.

7. Blumenthal M, Busse WR, Goldberg A, et al., eds.

The Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, TX: American Botanical Council;1998:167.

8. Ehrlich SD, ed. Slippery elm. University of Maryland Medical Center website. http://www.umm.edu/altmed/ articles/slippery-elm-000274.htm. Updated July 6, 2014.

9. Langmead L, Dawson C, Hawkins C, et al. Antioxidant

Summary

effects of herbal therapies used by patients with inflammatory bowel disease: an in vitro study. Aliment Pharmacol Ther. 2002;16(2):197-205.

10. Hawrelak JA, Myers SP. Effects of two natural medicine formulations on irritable bowel syndrome symptoms: a pilot study. J Altern Complement Med. 2010;16(10):1065-1071.

11. Skidmore-Roth L. Mosby’s Handbook of Herbs & Natural Supplements. 2nd ed. St. Louis, MO: Mosby Elsevier; 2005.

12. Ehrlich SD, ed. Slippery elm. Penn State Hershey Milton S. Hershey Medical Center website. http://pennstatehershey.adam.com/content.aspx?productId=107&pid=33&g id=000274. July 6, 2014.

13. Das S, Shillington L, Hammett T. Fact sheet no. 17:

Slippery elm appears to be a benign supplement with adequate research to support its use for many

Slippery elm. http://www2.ca.uky.edu/forestryextension/ PDF/slipperyelmbark.pdf. January 2001.

© THINKSTOCK

Slippery elm is available in a variety of forms.

Tablets, powder-filled capsules, lozenges, ground bark for teas, and poultices are found in health food stores. Dose depends, to a large extent, on the intended use. However, for the common capsule formulation, 400 to 500 mg 3 to 4 times daily for up to 8 weeks is considered minimal.11 Capsules should be taken with a full glass of water. For conditions of a chronic nature, such as ulcerative colitis, long-term use will be necessary.

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COMMENTARY Kahlil Demonbreun, DNP, WHNP-BC, ANP-BC, is the women’s health medical director at William ­Jennings Bryant Dorn VA Medical Center, Columbia, S.C., and Julee B. Waldrop, DNP, FAANP, is a professor in the School of Nursing, University of North Carolina at Chapel Hill.

What our words say about ourselves Change is often a slow process, even within a profession. There is still work to be done in how we communicate our self-views. As professionals, we are in a position to effect change with simple awareness of the words that we use.

One example of that awareness relates to use of the term “mid-level provider.” Whereas many of our colleagues recognize the negative connotations of the term and choose not to use it, many more appear to be quite comfortable with it. The largest professional organization for nurse practitioners (NPs), the American Association of Nurse Practitioners, “opposes use of terms such as mid-level provider

The words that we use and how we use them ultimately reflect what we think of ourselves.

in reference to NPs individually or to an aggregate inclusive of NPs” [https://www.aanp.org/ aanpqa2/images/documents/publications/ UseofTerms.pdf]. The organization encourages employers, policy makers, healthcare professionals, and other parties to refer to NPs by their title. The term calls into question the legitimacy of NPs to function as independently licensed.

And if the designation of being “mid-level” is not concerning enough, consider the standard of being last in lists. As an example, one phenomenon related to this professional view of self can be observed quite frequently in the literature when nurse authors include nurses in lists with other providers. Regularly, providers are ordered in lists as “physicians, physician assistants, NPs, and nurses,” with nursing consistently being mentioned last.

From a professional perspective, placing nursing last prompts questions of why we as nurse authors list nursing roles last, especially because “n” comes before “p” in the alphabet. If we do not see ourselves first, why should anyone else?

There is also confusion about use of the word “doctor.” Doctor has long been a popular synonym for physician in the United States.

Unfortunately, despite the fact that many other scholars and professionals earn doctoral degrees, this synonym has been difficult to change. When many different types of healthcare professionals are working to provide the highest quality

of care, this unclear use of the word “doctor” brings more confusion to the roles of healthcare team members. It is very simple and clear to refer to people by their role (eg, NP, physical therapist, physician, etc) in our language and our written words.

In discussing the value of accurate phrasing, Summers [Am Nurse. 2015;47(2):10] highlights the nuances of the words “independent,” “collaboration,” supervision,” and “accountability.” The author indicates that the word “independent” is not def ined by place of employment, business model of practice, or reimbursement mechanisms and is most prone to misinterpretation to mean “in a vacuum” or “alone.” Collaboration is vital to all health care; however, it becomes a barrier when laws, regulations, or institutional guidelines require formal agreements in a biased manner for individual groups of providers. Supervision in NP practice is a misnomer, and the notion that NPs require supervision by physicians or any group of providers is archaic. NPs alone are legally responsible for the care they deliver, and that responsibility cannot be delegated to others.

To effect change, we first must change. It will take all of us (and likely our friends and colleagues) working to change how we communicate about our profession of nursing. The words that we use and how we use them ultimately reflect what we think of ourselves. n

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