September 2016 Clinical Advisor by The Clinical Advisor

THE CLINICAL ADVISOR • SEPTEMBER 2016

A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS

NEWSLINE

■ Kidney stone guideline ■ Chronic pain and cancer ■ Blood pressure/CV events FEATURE Physical Activity and Cancer

Exercise can help lower mortality rate from cancer

SEPTEMBER 2016

| www.ClinicalAdvisor.com

BEST PRACTICES FOR MANAGING

HEAD LICE

Lice are 1 to 3 mm in length and can live for as long as 3 to 4 weeks.

LEGAL ADVISOR

Positive hepatitis B results overlooked for 7 years

■ Feature

CONCUSSION MANAGEMENT PAGE 24

VOLUME 19, NUMBER 9

■ Dermatology Clinic

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You see recovery. Your patients may see OINV. Opioid-Induced Nausea and Vomiting

References: 1. Kalso E, Edwards JE, Moore RA, McQuay HJ. Opioids in chronic non-cancer pain: systematic review of efficacy and safety. Pain. 2004;112(3):372-380. 2. Chang DJ, Desjardins PJ, Bird SR, et al. Comparison of rofecoxib and a multidose oxycodone/acetaminophen regimen for the treatment of acute pain following oral surgery: a randomized controlled trial. Curr Med Res Opin. 2004;20(6):939-949. 3. Daniels S, Casson E, Stegmann JU, et al. A randomized, double-blind, placebo-controlled phase 3 study of the relative efficacy and tolerability of tapentadol IR and oxycodone IR for acute pain. Curr Med Res Opin. 2009;25(6):1551-1561. 4. Park YB, Ha CW, Cho SD, et al. A randomized study to compare the efficacy and safety of extended-release and immediate-release tramadol HCl/acetaminophen in patients with acute pain following total knee replacement. Curr Med Res Opin. 2015;31(1):75-84. 5. Musclow SL, Bowers T, Vo H, Glube M, Nguyen T. Long-acting morphine following hip or knee replacement: a randomized, double-blind, placebo-controlled trial. Pain Res Manag. 2012;17(2):83-88. ©2016 Daiichi Sankyo, Inc. DSNA16102590 06/16

learn more at KnowOINV.com

B:10.75”

S:10”

Is OINV disrupting more recoveries than you realize?

T:10.5”

≈40% of patients receiving opioids experience OINV1-5

Editor Colby Stong, editor@clinicaladvisor.com Senior editor Sandhya George Associate editor Lauren Grygotis 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 275 7th Avenue, 10th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints, contact Wright’s Reprints at 877.652.5295. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Clinical Challenge” are not the actual individuals mentioned in the articles.They appear for illustrative purposes only. The Clinical Advisor ® (USPS 017-546, ISSN 1524-7317), Volume 19, Number 9, is published 12 times a year, monthly, for $75.00 per year in the United States; $85.00 in Canada; $110.00 for all other foreign, in U.S. dollars, by Haymarket Media, Inc., 275 7th Avenue, 10th Floor, New York, NY 10001. Single copy: $20 U.S.; $30 foreign. www.ClinicalAdvisor.com. To order or update your paid subscription, call 800.436.9269. Periodicals postage rate paid at New York, NY, and additional mailing offices. POSTMASTER: Send address change to DMD Data Inc., 10255 W. Higgins Rd, Suite 280, Rosemont, IL 60018. Subscription inquiries: call 800.430.5450 to change your address or make other subscription inquiries. Requests for subscriptions from outside the United States must be accompanied by payment. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2016

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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.

CLINICAL PEARLS

It cannot be beat.—TERRI JORDAN, ARNP, Daytona Beach, Fla. (202-2)

NEUTROPHILS AND LYMPHOCYTES In interpreting a complete blood count with differential, anytime the neutrophils and lymphocytes are numerically close, it is a viral cause; when the neutrophils and lymphocytes are numerically distant, it is a bacterial cause. This is very helpful in determining treatment.—DONNA CARTER, FNP-C, Scottsburg, Ind. (202-1) GENERIC “CAINE” IS EFFECTIVE FOR WOUND CARE For pain relief, most pharmacies offer a “caine” at 2-510%, and basically nothing higher, for between $5 and $30 per tube. I work in wound care and use Walmart’s

INTRA-ARTICULAR INJECTIONS FOR SEVERE OSTEOARTHRITIS Patients with severe osteoarthritis in the knees seem to do better with intra-articular injections if you have them sit up and dangle their legs off the examination table and distract the knee slightly when administering the injection.—ROSEMARY LEDBETTER, PhD, PA, Troy, Ill. (202-3)

YOUR COMMENTS SLIPPED CAPITAL FEMORAL EPIPHYSIS IN OBESE ADOLESCENTS I just read the CME/CE article by Marilou Shreve, DNP, APRN, entitled, “Assessing and treating pediatric obesity” [ June 2015]. I was concerned regarding the oversight of a critical issue in obese adolescents: the increased risk of slipped capital femoral epiphysis (SCFE). This was not addressed in the article. The case study (p. 55) gave incomplete advice regarding the evaluation of an obese adolescent male with knee pain. The most common etiology of the insidious onset of knee pain in children is the hip, due to referred pain from the

Equate brand—vagicaine 20% benzocaine. When using this before debriding a wound, give it three minutes to sedate the nerves, then perform the procedure. I get good results, as patients say. It relieves pain and burning for $1.88.

Advisor F

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.

orum

These are lette and successe rs from practitioners s, observat around the below. We ions, and country who OUR CONSULTANTS pearls with invite you want to shar to participa their colle e their clinic agues. Resp te. al problems onding cons ultants are identified CON SULTAT IONS

TREATM ENT FOR INFECT URINAR ION SGLT2 REC MALE CHI S IN THE UNC Y TRACT IRCUMCI LD FOR DIA EPTOR BLOCKE If a male SED child conti Deborah L. Cross, MPH, CRNP, Laura A.BET Foster,ES CRNP, FNP, Abby A. Jacobson, PA-C, RS Abimbola Farinde, PhD, PharmD, With the nues toassociate ANP-BC, is practices family medicine is a physician assistant is a professor redevprogram adven t ofPrimary circu SGLT2 recep at Delaware Valley urinaryattract director, Gerontology NP elop Program, mcisi Columbia Southern moda litywith Palmetto on be perfo for type tor infecPhysicians Dermatology University of Pennsylvania School blockersGroup University 2 diabe rmed? regarding inCare as a treatm in Wilmington, Del. in Orange Beach, Ala. useCharleston, S.C. tes, is there ent urology is of Nursing, Philadelphia. any evide NATHAN in patients with to protect the is well advise nce or data type 1 diabe GARDNE d tes mellitus?— R, PA-C, continues to to recommend a circum upper tracts, the kidne CPAAPA, ys. develo cision It p recurr•ent 44 THE ADVISOR AUGUST 2015 •on www.ClinicalAdvisor.com Castleton, severaCLINICAL l consideration urinary tract the male child who As it currently stands N.Y. , SGLT2 s that infections. for glycemic impede the receptor blocke There are control in ability to cleansenter into this decisio rs are FDA adults with n. Poor hygien should the e and quell -approved child have e may appro diet and exercise, but with type 2 diabetes phimosis, simpl infection potential. appropriate the in ved conjun FDA for use in patien Moreover, AdvisorForum_CA0815.indd urine 44 9/29/15ction 2:38 PM e cathet culture can ts with type has stated that they ketoacidosi steroid cream be a challenge. erization to obtain s, or those are not may tempo an FAR with severe 1 diabetes, patients with Having a short tion of the rarily solve renal functi diabetic steroid the trial of informINDE, PhD, Pharm these issues tenden , though after for infection D (See bottom on.—ABIMBOL ation about once again.—C cy redevelops, placin cessaA Dr. Farinde.) of this page Milwaukee g (203-2) for more , Wis. (203- OLEEN ROSEN, the child at risk 1) DNP, FNP -C, CLI Philip R. Cohen, MD,

is clinicaltions associate professor , shou ld of dermatology, University a of Texas Medical Center, The focus of Houston.

NICAL

Send us your letter Advisor Forum, The s with questions New York, and comm Clinical Advisor ents to: , 114 clinicaladvisoNY 10001. You may contacWest 26th Street , please indicatr.com. If you are writing in t us by e-mail at 4th Floor, each item. e so by including response editor@ to a the Letters are policy is edited for number in parent published letter, to heses at length and contribution print the author ’s name with clarity. The Clinicathe end of s will be accepted. l Advisor the letter. No anonym ’s ous

Write us today.

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VAGINA L RESULT DISCHARGE AND ING FRO If a female M TAMPON ODOR patient has USE a ask if she uses tamp history of vaginal disch ons. If she the pelvic arge with says “yes,” exam when cond odor, that you woul , do not enter ucting the rotating of d to take a pap smea vagina in the same the specu way r. Instead, the cervix. lum Most retain from side to side start shallow until reach ed tampons ing are lodge d in the fold

Philip R.

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

SEND TO The Clinical Advisor 275 7th Avenue, 10th floor New York, NY 10001

62 THE CLINI

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.

CAL ADVI

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Abimbo la Farinde

, PhD,

is a profess PharmD, or at Columb ia Souther n Univers in Orange ity Beach, Ala.

• www.Clinic

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Laura A.

Foster,

practices familyCRNP, FNP, with Palmett medicine o Primary Care Physicia ns in Charles ton, S.C.

Abby A.

Jacobso

is a physicia n, PA-C, n at Delawa assistant re Dermatology Valley in Wilmington,Group Del.

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CONTENTS SEPTEMBER 2016

NEWS AND COMMENT 18 Newsline ■■A new guideline is published for managing patients with kidney stones. ■■ASCO issues a guideline for managing chronic pain in adults with cancer. ■■ICU care may be overused and may not improve the mortality rate in hospitals. ■■Early interferon beta-1b treatment may be beneficial in patients with multiple sclerosis. ■■A blood pressure level that is lower than currently recommended is beneficial in patients who have type 2 diabetes. ■■The FDA approves a new test for human papillomavirus. ■■Marijuana poisoning cases increase in children in Colorado in the 2 years since the state legalized the drug. ■■Comparing ventilation strategies for preventing bronchopulmonary dysplasia in preterm infants

32 Physical activity’s effect on cancer mortality Exercise may prevent cancer from developing, as well as reduce the risk of death after cancer is diagnosed.

Guideline for managing kidney stones 18

52 CME Feature posttest

DEPARTMENTS 12 Web Roundup A summary of our most recent opinion, news, and multimedia content from ClinicalAdvisor.com

Pediatric marijuana poisoning 22

FEATURES

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61 Dermatology Clinic n Green discoloration of a dishwasher’s fingernail n An asymptomatic lesion with positive Darier sign

Continues on page 10

24 Managing concussion in primary care The incidence of concussion is increasing among children and adults, as is the demand for clinicians who can diagnose and treat both patient groups.

MAKING CONTACT

42 CME Update on the diagnosis and treatment of head lice Best practices for recognizing and managing head lice using a variety of new and existing therapeutic options are reviewed.

Physical activity and cancer mortality 32

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CONTENTS 67

Dermatologic Look-Alikes Papules on the mid-face

Stat Consult Allergic rhinitis

Legal Advisor Missed blood test results. A patient’s positive hepatitis B results were overlooked for 7 years.

Alternative Meds Update Inulin may be beneficial for weight loss, diabetes management, intrahepatic fat reduction, or bowel function management.

DEPARTMENTS cont’d

ADVISOR FORUM 54

Your Comments ■ Suboxone and methadone— our readers weigh in on the pros and cons

“Why can’t you ever relax at parties?”

HOW TO CONTACT US THE CLINIC AL

FEATUR E

Physical Acti vity

and Cancer Exercise can mor tality ratehelp lower from cancer

LEGAL ADV

ISOR

Positive hepa over looked titis B results for 7 year s

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

R 2016

| www.Clin icalA

dvisor.com

BEST PR ACTICES FOR MANA GING

HEAD LIC

Lice are 1 to 3 mm in length and can live for as long as 3 to 4 weeks.

■ Feature

CONCUSS MANAGEMION ENT

19, NUMB ER 9

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

• Mail it to The Clinical Advisor, 275 7th Avenue, 10th Floor, New York, NY 10001

SEPT EMBE

NEWSLIN

■ Kidney ston e guideline ■ Chronic pain ■ Blood pres and cancer sure/CV even ts

PAGE 24

VOLUM E

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BER 2016

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EXCLUSIVE TO THE WEB AT

ClinicalAdvisor.com Web Exclusives

The Waiting Room

ClinicalAdvisor.com/News

Official Blog of The Clinical Advisor ClinicalAdvisor.com/WaitingRoom

Vital sign instability at hospital discharge linked to increased mortality risk Nearly 17% of patients who exhibited 1 unstable vital sign at the time of hospital discharge were readmitted or died within 30 days. FDA approves generic Tamiflu The US Food and Drug Administration approved oseltamivir phosphate, which can be used to prevent flu in patients aged 1 year and older. MRI may be useful in assessing hypovascular hepatic lesions Researchers found significant differences on MRI between malignant and benign hypovascular lesions of the liver.

Jim Anderson, MPAS, PA-C, DFAAPA Implicit biases in the exam room In the last few years, clinicians have overwhelmingly moved to recognize the implicit biases in their practice of medicine. Jillian Knowles, MMS, PA-C How long is long enough? Taking time off after an illness Different illnesses require that patients stay home from school or work for different lengths of time. Sharon M. O’Brien, MPAS, PA-C Increased mortality rates in patients with nocturia Patients who experience nocturia, or frequent urination during the night, may have increased mortality rates.

Multimedia ClinicalAdvisor.com/Multimedia Guideline released for clinicians treating patients with kidney stones The American Urologic Association released a guideline for the surgical management of patients with kidney or ureteral stones. Watch it here: ClinicalAdvisor.com/AUAGuidelineVideo USPSTF releases draft recommendation statement for herpes treatment In a draft recommendation statement, the US Preventive Services Task Force gave a Grade D recommendation for herpes screening in asymptomatic adolescents and adults. Watch it here: ClinicalAdvisor.com/USPSTFHerpesTxVideo

MAKING CONTACT

Lipid management in the era of PCSK9 inhibitors Robert Eckel, MD, discusses his presentation regarding lipid management after the advent of PCSK9 inhibitors at the American Association of Clinical Endocrinologists’ (AACE) 25th Annual Scientific & Clinical Congress. Watch it here: ClinicalAdvisor.com/LipidPCSK9Video Challenges surrounding opioid use among disabled adults Dr Ellen Meara discusses findings from her study, “State legal restrictions and prescription opioid use among disabled adults,” in the New England Journal of Medicine. Watch it here: ClinicalAdvisor.com/OpioidUseVideo

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12 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.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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Journal of Orthopedics for Physician Assistants

Heel pain that worsened after a walking tour A 72-year-old woman presents with left heel pain that was aggravated by a walking tour. The pain seems to be worse at day’s end and is intensified by long walks and stairs. The pain is located at the back of the heel, which is tender to touch at times. The patient has point tenderness at the Achilles insertion site on the calcaneus. WHAT TREATMENT IS RECOMMENDED?

• Calcaneal bone spur excision • Walking boot, oral steroid taper, and physical therapy • Steroid injection into the Achilles insertion • Achilles tendon resection ● See the full case at ClinicalAdvisor.com/OrthoDx_Sept16

Derm Dx Dark spots on the lip A 33-year-old woman requests consultation for dark spots that have been present on her lip for several years. One of the discolorations was biopsied elsewhere and was reported to her as benign. Examination reveals 2 well-demarcated black macules on her lower lip as well as a similar lesion on the buccal mucosa. CAN YOU DIAGNOSE THIS CONDITION?

• Labial macules • Melanoma in situ • Addison disease • Peutz-Jeghers syndrome ● See the full case at ClinicalAdvisor.com/DermDx_Sept16

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

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Newsline S E P T E M B E R 2 016

Guideline for chronic pain in adult cancer page 20

Early treatment of MS boosts clinical outcomes page 21

Legalized pot and pediatric poisoning cases page 22

New guideline published for managing kidney stones

procedures with significant risk of hemorrhage or for patients with suspected anemia, thrombocytopenia, or infection. • Additional contrast imaging may be required in patients with complex stones “if further definition of the collecting system and the ureteral anatomy is needed.” Treatment for Patients With Ureteral or Renal Stones

A GUIDELINE regarding the surgical management of patients with kidney or ureteral stones has been published by the American Urological Association (AUA) and Endourological Society. A summary of the recommendations is as follows: Preoperative Testing

• Patients should undergo a noncontrast CT scan prior to percutaneous nephrolithotomy, and to help clinicians decide the best candidates for shock wave lithotripsy compared to ureteroscopy. • A functional imaging study should be performed if clinicians suspect significant loss of renal function in the kidney. • A urinalysis should be obtained prior to intervention, and a urine culture should be obtained from patients with signs of infection. A complete blood count and platelet count should also be obtained for patients undergoing

The new guideline focuses on kidney, ureteral, and renal stones.

• Patients could consider endoscopic procedures when residual fragments are present to render the stone free. A safety guide wire should be used for endoscopic procedures. Treating Ureteral Stones in Adult Patients

• Clinicians should offer observation to patients with uncomplicated ureteral stones ≤10 mm, and those with distal stones of the same size can take medical expulsive therapy with beta-blockers. Treating Renal Stones in Adult Patients

• Clinicians should offer shock wave lithotripsy or ureteroscopy in patients with a total non-lower pole renal stone burden ≤20 mm. For patients with a stone burden >20 mm, clinicians should offer percutaneous nephrolithotomy as the first-line therapy instead of shock wave lithotripsy. • Clinicians can offer stone treatment for patients with

symptomatic, non-obstructing, caliceal stones without obvious etiology for pain. Active surveillance should be considered for patients with asymptomatic, non-obstructing caliceal stones. Treatment for Pediatric Patients With Ureteral or Renal Stones

Clinicians should observe pediatric patients with uncomplicated ureteral stones ≤10 mm with or without medical expulsive therapy using a-blockers. For pediatric patients with ureteral stones who are unlikely to pass the stones, clinicians should suggest ureteroscopy or shock wave lithotripsy. Pediatric patients with ureteral stones should not receive a stent prior to ureteroscopy. Treatment for Pediatric Patients With Ureteral or Renal Stones

• Clinicians should coordinate pharmacological and surgical intervention with the patient’s obstetrician. • Observation should be used as a first-line therapy for pregnant patients with ureteral stones and well controlled symptoms. Clinicians may offer to ureteroscopy to patients with ureteral stones who fail observation. The complete guideline is available at: https://www.auanet.org/ education/guidelines/surgicalmanagement-of-stones.cfm

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

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Newsline CLINICIANS WHO see patients with chronic pain and a history of cancer as an adult should screen them for pain at every visit, according to the American Society of Clinical Oncology (ASCO) Clinical Practice Guideline published in the Journal of Clinical Oncology. The ASCO authors, led by Judith A. Paice, PhD, RN, a Research Professor in the Division of Hematology/Oncology at Northwestern University Feinberg School of Medicine in Chicago, reviewed 63 studies to come to a consensus on the recommendations. “As a result of extraordinary advancements in diagnosis and treatment, approximately 14 million individuals with a history of cancer (excluding nonmelanomatous skin cancers) are living in the United States,” Dr Paice and

colleagues wrote. “Two thirds of these individuals are surviving ≥5 years after diagnosis.” The author s h igh l ighted the following as their main recommendations: • Clinicians should use a quantitative or semiquantitative tool to screen for pain at each encounter. • If a patient reports new onset of pain, clinicians should evaluate

A quantitative or semiquantitative tool is advised for screening for pain at each clinician visit.

and monitor for recurrent disease, second malignancy, or late-onset effects of treatment. • To relieve pain in patients with no contraindications, clinicians should use systemic nonopioid analgesics, including nonsteroidal anti-inflammatory drugs and acetaminophen, and adjuvant analgesics, including antidepressants such as duloxetine and anticonvulsants such as gabapentin and pregabalin, which have been shown to be effective for neuropathic or chronic pain. The guideline also details the appropriate use of opioids, universal precautions against abuse, addiction, and adverse effects to opioids, and evidence for referral to specialized care or alternative interventions. The complete guideline can be found at www. asco.org/chronic-pain-guideline.

Chronic pain guideline for adults with cancer

INSTITUTIONS that more frequently use ICU care are more likely to perform invasive procedures with no improvement in hospital mortality rates, according to research published in JAMA Internal Medicine. Dong W. Chang, MD, MS, Division of Respiratory and Critical Care Physiology and Medicine, Los Angeles Biomed Research Institute, UCLA Medical Center, and colleagues conducted a retrospective cohort study of 156,842 hospitalizations across 94 acute-care nonfederal

Frequent ICU use may not improve hospital mortality.

hospitals. The researchers studied cases involving diabetic ketoacidosis (DK A), pulmonar y embolism (PE), upper gastrointestinal bleeding (UGIB), and congestive heart failure (CHF) in Washington state and Maryland between 2010 and 2012. ICU admission rates were as follows: • 16.3% to 81.2% for DKA • 5% to 44.2% for PE • 11.5% to 51.2% for UGIB • 3.9% to 48.8% for CHF Invasive procedures and hospitalization costs were greater in

institutions with higher ICU use across all 4 conditions. “Maximizing the value of critical care services requires understanding the relationship between ICU utilization, clinical outcomes, and costs,” noted Dr Chang. “For medical conditions where ICU care is frequently provided, but not only necessary, institutions that utilize ICUs more frequently are more likely to perform invasive procedures and have higher costs, but have no improvement of hospital mortality.”

ICU care overused, may not improve mortality

20 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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EARLY INTERFERON beta1b treatment could improve clinical outcomes in patients with multiple sclerosis (MS) after clinically isolated syndrome (CIS), according to a study published in Neurology. Ludwig Kappos, MD, from the Departments of Medicine, Clinical Research, Biomedicine, and Biomedical Engineering at the University Hospital Basel in Switzerland, and colleagues assessed the outcomes in 278 patients in the BENEFIT (Betaferon/Betaseron in Newly Emerging MS for Initial Treatment) trial. The participants were randomly assigned to receive interferon beta-1b early treatment or placebo, which was considered “delayed treatment.” Patients in the placebo group switched to interferon beta-1b or another treatment after 2 years, or after

conversion to clinically definite multiple sclerosis (CDMS). The patients were reassessed after 11 years of follow-up. “Despite the relatively short delay in treatment initiation in the placebo group, measures reflecting clinical disease activity such as time to CDMS, time to first relapse, and relapse rates, as well as scores on the PASAT, the only neuropsychological test applied from baseline to year 11, still suggest persistent long-term benefits of the earlier treatment,” the authors wrote. After the 11-year follow-up period, patients who received early treatment had a lower risk of CDMS compared with patients in the placebo group. Patients in the early treatment group also had a longer median time to the first relapse (1888 days vs 931 days) and a lower overall annual relapse

Early interferon beta-1b may be beneficial in MS patients

Clinical outcomes may be improved with early treatment in MS patients.

rate (0.21 vs 0.26). Overall, 25 patients converted to secondary progressive MS. The Expanded Disability Status Scale scores were low and stable in both treatment groups (median: 2.0), although the early treatment group had improved Paced Auditory Serial Addition Task-3 total scores. The researchers also noted that employment rates were high, and use of health resources was generally low in both groups.

Lower than recommended BP level is beneficial in type 2 diabetes SYSTOLIC BLOOD pressure lower than 140 mm Hg is associated with a lower risk of cardiovascular events in patients with type 2 diabetes, according to data published in BMJ. Samuel A Eryd, PhD, and colleagues conducted a populationbased cohort study that included 187,106 patients with type 2 diabetes who were registered in the Swedish national diabetes register. The researchers sought to compare cardiovascular risk among individuals with blood pressure levels that meet current recommendations with the risk in individuals with lower blood pressure levels. ”Recent hypertension guidelines have raised the target blood pressure for patients with diabetes from below 130 mm Hg to below 140 mm Hg because of a lack of conclusive randomized studies to support the lower goal, together with observational studies showing a J shaped relation between blood pressure and complications,” the study authors wrote.

The patients were younger than age 75 years and had no previous cardiovascular disease. The investigators used hospital discharge and death registers to obtain data regarding clinical events, including acute myocardial infarction, stroke, cardiovascular disease, coronary heart disease, heart failure, and total mortality. Compared with patients with systolic blood pressure between 130 mm Hg and 139 mm Hg, patients with blood pressure between 110 mm Hg and 119 mm Hg had a significantly lower risk of non-fatal acute myocardial infarction (adjusted hazard ratio [HR]: 0.76) total acute myocardial infarction (HR: 0.85), non-fatal cardiovascular disease (HR: 0.82), total cardiovascular disease (HR: 0.88) and non-fatal coronary heart disease (HR: 0.88). The researchers also noted that there was no indication of a J-shaped association between blood pressure and the clinical events, with the exception of heart failure and total mortality.

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Newsline FDA approves Marijuana poisoning cases increasing hospital was 2.4 years; 25 were marijuana poisonnew HPV test PEDIATRIC girls (40%). The median age of ing cases have increased significantly in Colorado in the 2 years since the state legalized recreational use of the drug, a rate that is also higher than that reported in the rest of the United States, according to research published in JAMA Pediatrics. “Almost half of the patients seen in the children’s hospital in the 2 years after legalization had exposures from recreational marijuana, suggesting that legalization did affect the incidence of exposures,” stated George Sam Wang, MD, from the Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, and colleagues. A total of 81 patients were evaluated at the children’s hospital, and 163 marijuana exposure cases presented to the RPC between January 1, 2009, and December 31, 2015. All children were younger than age 10 years. The median age of children who were admitted to the

Pediatric marijuana poisoning cases increase in Colorado.

children who presented to the RPC was 2 years; 85 were girls (52%). The mean rate of marijuana-related visits to the children’s hospital increased from 1.2 per 100,000 population 2 years prior to legalization to 2.3 per 100,000 population 2 years after legalization. The known marijuana products that were involved in the exposure included 30 infused edibles (48%). The number of annual RPC ped iat r ic m a r iju a n a ca se s increased more than fivefold from 2009 (9) to 2015 (47). Colorado had an average increase in RPC cases of 34% per year, compared with an increase of 19% in the rest of the United States. For 10 exposure cases (9%), the marijuana was not stored in a childresistant container. In 40 cases (34%), poor child supervision or marijuana storage was reported. Edible products were responsible for 51 exposures (52%) among the RPC group.

Preventing bronchopulmonary dysplasia Less invasive surfactant administration (LISA) use in preterm infants is linked to the lowest likelihood of the composite outcome of either death or bronchopulmonary dysplasia (BPD), according to a study in JAMA. Nearly 5600 infants participated across 30 trials. The primary outcome – a composite of death or BPD at 36 weeks postmenstrual age – occurred in 33% of cases (1665 of 4987, including 505 deaths and 1160 cases of BPD). Secondary outcomes – including death,

severe intraventricular hemorrhage, and air leak by discharge – occurred in 6% of air leak cases and 26% of BPD cases. LISA had lower odds of the primary outcome, compared to mechanical ventilation. “Ranking probabilities indicated that LISA was the best strategy with a surface under the cumulative ranking curve of 0.85 to 0.94, but this finding was not robust for death when limited to higher-quality evidence,” concluded Dr Isayama. n

THE FDA HAS approved the Roche cobas HPV Test, the first test for the human papillomavirus (HPV) that can use cervical cells collected in SurePath Preservative Fluid for a Pap test. SurePath Preservative Fluid is 1 of 2 FDA-approved liquid collection fluids commonly used to collect cells for Pap tests. “Healthcare providers have been using samples stored in the SurePath Preservative Fluid with HPV tests for some time now, but there have been concerns about false negative results,” said Alberto Gutierrez, PhD, director of the Off ice of In Vitro Diagnostics and Radiological Health in the FDA’s Center for Devices and Radiological Health. “Now healthcare providers have access to an FDA-approved test and the information they need to use it properly to ensure the most accurate results for their patients.” The Roche cobas HPV Test with SurePath Preservative Fluid is approved to screen women aged 30 years and older for HPV. The test is also approved for women aged 21 years and older who have already had an abnormal Pap test result (borderline cellular cytology). The Roche cobas HPV Test can detect high-risk HPV genotypes 16 and 18. The Roche cobas HPB Test is not approved as a first-line primary HPV screening test and should be used in conjunction with patient screening history and other risk factors.

22 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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FEATURE: SHAUN LYNCH, PA-C, MS, MMSC

Managing concussion in primary care The incidence of concussion is increasing in children and adults, as is the demand for clinicians who can diagnose and treat both patient groups.

Between 1.6 and 3.8 million sports-related concussions occur annually in the U.S.

oncussions, considered a type of mild traumatic brain injury (TBI), are increasing in incidence in both adult and pediatric populations.1,2 Concussions can occur as the result of motor vehicle accidents, falls, occupational accidents, recreational accidents, and assaults. The Centers for Disease Control and Prevention (CDC) estimates that between 1.6 and 3.8 million concussive injuries related to sports occur in the United States annually.3 As the number of emergency department visits for concussionrelated injuries increases, so does the demand for primary care providers competent in the evaluation and management of concussions during both the initial presentation and clinical follow-up. The 4th International Conference on Concussion in Sport, held in 2012, agreed upon the following definition of concussion: “an injury involving a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”4 A concussive head injury can be characterized by the following features: (1) It originates with a direct blow to the head or to another part of the body with transmission of an “impulsive” force to the head; (2) the rapid onset of transient neurologic impairment follows spontaneously; (3) the symptoms largely reflect a functional disturbance rather than a structural injury, with no abnormality seen on standard structural neuroimaging studies; (4) variable clinical symptoms may not include loss of consciousness; and (5) symptom resolution typically follows a sequential course but may be prolonged in a small percentage of cases.4

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TABLE 1. Signs and symptoms of concussion11

Clinical presentation

Because concussion remains a clinical diagnosis, recognition of the typical symptoms and signs (Table 1) is fundamental to initiating management promptly. The hallmark symptoms that a patient typically describes are confusion and amnesia, occasionally with but often without loss of consciousness.5 Symptoms may manifest immediately after the head injury or appear several minutes later.6 The victim usually retains a memory of the traumatic event, but loss of recollection of the events before (retrograde amnesia) and after (anterograde amnesia) the head trauma is frequent. Other early symptoms of concussion include headache, dizziness (vertigo or imbalance), and nausea with or without vomiting.6 Throughout the next several hours or days, the patient may experience cognitive and mood disturbances, photophobia, hyperacusis, or sleep disturbances.7 It is important to note that in many cases, a concussion is not associated with any pertinent examination findings. However, some typical signs may be the following: vacant stare, inability to focus, disorientation, slurred speech, memory deficits, gross observable incoordination, and delayed verbal expression.6 Lastly, posttraumatic seizures typically occur in fewer than 5% of concussion injuries and are more commonly seen in patients with severe TBI.8 In the typical clinical course, a concussion resolves within a short period (7–10 days).4 Diagnosis

It is important that any patient in whom a concussion or a mild TBI is suspected be medically evaluated immediately, whether in a physician’s office or hospital emergency department or on the sideline of an athletic event. Evaluation of an acute injury should include a comprehensive history, determination of the mechanism of injury, mental status testing, and a detailed neurologic assessment. “Red flag” signs and symptoms, such as prolonged loss of consciousness, persistent alterations in mental status, and abnormal findings on a neurologic examination, should prompt urgent neuroimaging and possible neurosurgical consultation.9 Numerous standardized diagnostic tools have been developed to aid in the recognition of concussions and to provide guidance regarding athletes’ return to play. These include the Standardized Assessment of Concussion (SAC), Postconcussion Symptom Scale and Graded Symptom Scale Checklist, Sport Concussion Assessment Tool 3 (SCAT3), Westmead Posttraumatic Amnesia Scale (WPTAS), and Immediate Postconcussion Assessment and Cognitive Testing (ImPACT), to name a few.10 A child SCAT3 has also been developed to assess concussion in patients aged 5 to 12 years. It is believed that children report concussion symptoms differently, so an assessment tool with an age-appropriate

Category

Sign or symptom

Physical

• Headache • Nausea • Vomiting • Balance problems • Dizziness • Visual problems

Cognitive

• Feeling mentally "foggy" • Confusion about recent events • Feeling slowed down • Answering questions slowly • Difficulty concentrating • Repeating questions • Difficulty remembering • Forgetfulness of recent information

Emotional

• Irritability • Sadness • Anxiety

• Increased emotional lability • Nervousness

Sleep-related

• Drowsiness • Difficulty falling asleep

• Sleeping more or less than usual

• Fatigue • Photophobia • Phonophobia • Numbness/tingling • Feeling dazed • Feeling stunned

symptom checklist is required.4 These tools are useful in the sideline assessment of athletes who have potential concussion injuries as well as in the office setting, with serial monitoring used to determine the resolution of symptoms.11 The findings on conventional imaging are almost always normal because concussions are typically a functional and not a structural problem. However, if neuroimaging is being considered, brain computed tomography (CT) is typically the test of choice initially, especially for an acute injury. Magnetic resonance imaging should be considered for patients with persistent symptoms who are at risk for posttraumatic complications, such as headaches, vertigo, seizures, and postconcussion syndrome.12 Neuropsychological testing has been shown to be a useful adjunct, providing clinical value regarding cognitive function. However, testing is best performed and the results interpreted by a neuropsychologist, although there are currently no agreed-upon recommendations for the universal use of neuropsychological testing.4,11 Management

Most patients with a concussive head injury can be managed safely in the outpatient setting. Observation with a responsible caregiver is recommended in the first 24 hours after an injury because of the slight risk for an intracranial complication.13 Admission to the hospital is typically recommended for patients with any of the following: (1) Glasgow Coma Scale score <15, (2) abnormal findings on CT scan, (3) seizures, and (4) abnormal bleeding parameters due to an underlying disorder

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MANAGING CONCUSSION IN PRIMARY CARE

A more conservative return-to-play protocol has been proposed for children and adolescents that includes extended periods without symptoms. or oral anticoagulation.14 A patient with an uncomplicated concussion is typically educated about the need for physical and cognitive rest for at least 24 hours. Certainly, this period can be longer if the patient remains symptomatic or the severity of the symptoms warrants continued rest. Cognitive rest is especially important in children and adolescents and should include abstaining from activities such as playing video games, watching television, working on a computer, using tablets and smart phones, listening to loud music, reading, and engaging in mental exercises requiring focus and concentration in the academic setting.15 This period should be followed by a gradual return to work, school, or physical activity, depending on the patient.4 Again, it is important to note that the majority of patients with concussion-related injuries typically recover spontaneously over several days. Return to play. Because a significant number of concussionrelated injuries occur within the sporting arena, many providers seek guidelines on when to counsel athletes, parents, and coaches about returning to competition. Most experts concur that no athlete should return to play on the day that a concussive injury occurred. This minimizes the risk for complications resulting from a repeated head injury. Moreover, research indicates that athletes at the collegiate and high school level are more likely to have a delayed onset of symptoms and neuropsychological deficits following injury as a result of same-day return to play.4 The current recommendations use a stepwise process and graduated return-to-play protocol as defined in Table 2. Essentially, an athlete should progress to the next level if he or she remains asymptomatic within the current level. Therefore, it takes about 1 week to progress through the full rehabilitation protocol because each step should take approximately 24

hours. However, if any postconcussion symptoms occur during the graduated return-to-play program, the patient should “drop back” to the previous asymptomatic level and attempt progression again after a 24-hour period of rest. Patients who fail to recover or who exhibit persistent concussion-related symptoms should be referred to specialists with experience managing concussions in a multidisciplinary approach. A more conservative return-to-play protocol has been proposed for children and adolescents that includes extended periods without symptoms and/or longer periods of graded exertion. This approach is recommended because of the different physiologic responses of children and adolescents to head trauma and the longer time needed for recovery.4 Participation in schoolrelated extracurricular activities, including athletics, is not usually recommended until the patient has fully resumed school activities.16 Lastly, each return-to-play progression, regardless of the patient’s age, should be individualized, with the final clearance documented by a licensed healthcare provider knowledgeable in the evaluation and management of concussions.11 Pharmacologic therapy. The use of medications in treating concussion is tailored mainly to the management of symptoms. According to the most recent position statement on concussion in sport from the American Medical Society for Sports Medicine, no convincing evidence has been found of the effectiveness of any particular medication in treating the acute symptoms of concussion.11 Acetaminophen is currently recommended in the treatment of postconcussive headaches, with the addition of physical measures such as massage, the application of ice, and rest in a dim, quiet environment. Sleep disturbances should initially be managed with conservative measures, such as sleep hygiene, but medical and/or cognitive therapy or even referral

TABLE 2. Graduated return-to-play protocol4 Rehabilitation stagea

Functional exercise

Objective of stage

1. No activity

Complete physical and cognitive rest until medical clearance

Recovery

2. Light aerobic exercise

Walking, swimming, stationary cycling; <70% MPHR, 15 minutes

Increase in heart rate

3. Sport-specific exercise

Skating or running drills (no head-impact activities); <80% MPRH, 45 minutes

Addition of movement

4. Noncontact training drills

Complex training drills, start of resistance training; <90% MPRH, 60 minutes

Exercise, coordination, and cognitive load

5. Full-contact practice

Normal training activity if symptom-free

Restoration of athlete’s confidence; assessment of functional skills by coaching staff

6. Return to play MPHR, maximum predicted heart rate

Patient must be symptom-free for 24 hours before progressing to next rehabilitation stage.

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Postconcussion syndrome encompasses symptoms including headache, dizziness, neuropsychiatric symptoms, and cognitive impairment. to a sleep specialist should be considered for a patient with protracted symptoms. Stimulants are not currently recommended for treating cognitive symptoms, such as decreased attention. True vertigo and balance dysfunction may be mitigated by meclizine or diazepam, but these drugs should be used judiciously because they can affect cognitive function. There is currently insufficient evidence to determine the effectiveness of vestibular therapy in patients with vertiginous symptoms. Patients who have depressive symptoms should be screened and treatment with medication and/or cognitive therapy should be considered if the symptoms persist beyond 6 to 12 weeks.11 Complications

Second-impact syndrome is a rare but potentially fatal complication leading to diffuse cerebral swelling that can occur after a patient who is still symptomatic from an earlier concussion sustains a second head injury.17 The term postconcussion syndrome encompasses the symptom complex of headache, dizziness, neuropsychiatric symptoms, and cognitive impairment.18 These symptoms can develop in the first few days after a mild TBI but typically resolve within a few weeks to few months. Patients can also exhibit isolated symptoms as sequelae that include posttraumatic headaches and/or posttraumatic vertigo. The incidence of posttraumatic epilepsy is increased 2-fold after mild TBI, with 50% of cases occurring during the first year and 80% within the first 2 years.19 However, prophylactic treatment with anticonvulsants is not currently recommended because it has not been shown to be effective. Chronic traumatic encephalopathy (CTE) has been one of the most publicized potential long-term complications, with increasing reports of dementia occurring in National Football League players who have a history of multiple concussions. CTE is a neurodegenerative disease that is associated with repetitive brain trauma and pathologically characterized by the accumulation of an abnormal tau protein in specific areas of the brain. Patients should be aware of this potential long-term complication of cumulative head trauma, although most experts agree that larger-scale, epidemiologic studies are required to understand the causes and develop prevention strategies.11

POLL POSITION

Which of the following best describes your opinion about sports concussions? n=729

■ I strongly recommend that children and adolescents do not participate in contact sports. ■ I have advised parents of the potential dangers of contact sports.

21.4% 8.9% 69.7%

■ With new protocols in place, it is much safer than before.

For more polls, visit ClinicalAdvisor.com/Polls.

good patient care. It is essential that healthcare providers be able to recognize the symptoms and signs of a concussion, but it is equally important that athletes, coaches, officials, and parents be educated so that patients are properly evaluated. Healthcare providers trained in the evaluation and management of concussion are therefore important in establishing the diagnosis. Standardized diagnostic tools provide a helpful and uniform approach to assessing and following a patient with a concussion. However, further research is needed to determine their accuracy. The mainstay of treatment remains physical and cognitive rest. No athlete with a concussion should be allowed to return to play on the day of the injury or while he or she is symptomatic. Moreover, the decision to return to play should be a medical one, with clearance given by a licensed healthcare provider. A provider with any uncertainty regarding an athlete’s return to play should follow the mantra “when in doubt, sit them out.” ■ Shaun Lynch, PA-C, MS, MMSc, is a physician assistant and an assistant professor in PA studies at Elon University in North Carolina. References 1. Injury prevention & control: traumatic brain injury & concussion. Centers for Disease Control and Prevention website. http://www.cdc.gov/ TraumaticBrainInjury/index.html. Updated February 9, 2016. 2. Marin JR, Weaver MD, Yealy DM, Mannix RC. Trends in visits for trau-

Conclusion

matic brain injury to emergency departments in the United States. JAMA.

Concussions remain a complex and common type of mild TBI evaluated by primary care providers. Diagnosis and management remain challenging because of insufficient scientific evidence to support much of the clinical decision making required for

2014;311(18):1917-1919. 3. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil. 2006;21(5):375-378.

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MANAGING CONCUSSION IN PRIMARY CARE

4. McCrory P, Meeuwisse W, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Clin J Sport Med. 2013;23(2):89-117. 5. Duhaime AC, Beckwith JG, Maerlender AC, et al. Spectrum of acute clinical characteristics of diagnosed concussions in college athletes wearing instrumented helmets: clinical article. J Neurosurg. 2012;117:1092-1099. 6. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology. 1997;48(3):575-580. 7. Cantu RC. Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl Train. 2001;36(3):244-248. 8. Lee ST, Lui TN. Early seizures after mild closed head injury. J Neurosurg. 1992;76(3):435-439. 9. Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology. 1997;48(3):581-585.

“Looks like another case of someone over forty trying to understand Snapchat.”

10. Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24):2250-2257. 11. Harmon KG, Drezner JA, Gammons M, et al. American Medical Society for Sports Medicine position statement: concussion in sport. Br J Sports Med. 2013;47:15-26. 12. Hughes DG, Jackson A, Mason DL, Berry E, Hollis S, Yates DW. Abnormalities on magnetic resonance imaging seen acutely following mild traumatic brain injury: correlation with neuropsychological tests and delayed recovery. Neuroradiology. 2004;46(7):550-558. 13. Lawler KA, Terregino CA. Guidelines for evaluation and education of adult patients with mild traumatic brain injuries in an acute care hospital setting. J Head Trauma Rehabil. 1996;11:18-28. 14. Evans RW. Concussion and mild traumatic brain injury. UpToDate.

“My parents hate it.”

http://www.uptodate.com/contents/concussion-and-mild-traumatic-brain15. Concussion recognition, diagnosis, and acute management. In: Graham R, Rivara FP, Ford MA, Mason Spicer C, eds. Sports-Related Concussions in Youth: Improving the Science, Changing the Culture. Washington, DC: National Academies Press; 2014:99-180. 16. Halstead ME, McAvoy K, Devore CD, et al. Returning to learning following a concussion. Pediatrics. 2013;132:948-957. 17. Wetjen NM, Pichelmann MA, Atkinson JL. Second impact syndrome: concussion and second injury brain complications. J Am Coll Surg. 2010;211(4):553-557. 18. Bazarian JJ, Wong T, Harris M, Leahey N, Mookerjee S, Dombovy M. Epidemiology and predictors of post-concussive syndrome after minor head injury in an emergency population. Brain Inj. 1999;13(3):173-189. 19. Annegers JF, Grabow JD, Groover RV, Laws ER Jr, Elveback LR, Kurland LT. Seizures after head trauma: a population study. Neurology. 1980;30(7 Pt 1):683-689. All electronic documents accessed August 4, 2016.

“Can’t we all just get along?”

injury. Updated April 29, 2015.

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“Are you here for your annual or your perennial?”

“Wait for it …”

“I don’t know—the minute I figured out how to make it self-aware it realized that it was naked, ran, and hid from me.”

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FEATURE: BRADLEY WEILER, PAS-II, AND SANDRA BANAS, MST, PA-C

Physical activity’s effect on cancer mortality Exercise may not only prevent cancer from developing, but it may also reduce the risk of death after cancer is diagnosed.

Exercise may lower the risk of breast, colon, lung, and prostate cancers.

he health benefits of increasing one’s level of physical activity are numerous and well-known. For example, exercise lowers the risks for hypertension, stroke, type 2 diabetes, coronary artery disease,1 and several forms of cancer, including breast and colon cancers.2,3 In addition, it is very likely that the risks for prostate, lung, and endometrial cancers are also affected.4,5 Recent research seems to indicate that exercise not only helps to stave off the development of cancer but also may contribute to reducing the risk for death from cancer. The Centers for Disease Control (CDC), American College of Sports Medicine (ACSM), and American Heart Association (AHA) recommend that everyone expend 9 metabolic equivalent (MET)–hours of energy per week to take advantage of the health benefits of exercise.6 The MET is a unit of measurement used to express the amount of energy one expends while sitting at rest. The greater the amount of physical activity in which one engages, by increasing either the duration or the intensity of the activity, the higher the number of METs expended. The nationally recognized figure of 9 MET-hours per week is equivalent to 150 minutes of moderate-intensity exercise or 75 minutes of vigorous-intensity exercise per week. Brisk walking is an example of moderate-intensity exercise, and running is an example of high-intensity exercise. Several prospective studies have shown that the amount of physical activity in which individuals engage, both before and after specific types of cancer are diagnosed, has an effect on their

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mortality.2-4 These population-based studies had the advantage of being able to recruit large samples and follow the subjects for long periods of time. The greatest risk reductions were demonstrated in breast and colon cancers2,3; however, the same principles may very well also extend to other forms of cancer.5 Evidence

In a 2013 study, after an 11-year follow-up, women who had expended more than 7.5 MET-hours of energy per week prior to their breast cancer diagnosis had a risk for dying of their cancer that was 41.5% lower than the risk of women who expended less than that amount of energy.7 A similar trend was seen in men with colorectal cancer, in whom regular exercise before their diagnosis was associated with a 12% reduction in mortality after 5.5 years; in addition, the chance of death from cancer in those with stage II or III tumors at diagnosis was decreased by 50% if they had previously routinely participated in physical activity.8 Current research indicates that this inverse relationship between exercise and risk for death from specific types of cancer also extends to the period after diagnosis.3,4,9 Three studies conducted between 2005 and 2014 found that women with breast cancer who maintained a level of physical activity at or above the recommendation of 9 MET-hours per week established by the CDC, ACSM, and AHA had a 26% to 67% lower risk for dying from their cancer.2,9,10 In patients with stage III colorectal cancer, researchers observed lower rates of cancer recurrence and death following treatment if the patients engaged in at least 18 MET-hours of exercise per week.3 A similar correlation may exist in prostate cancer; a 35% reduced risk for mortality from prostate cancer was observed in men who exercised for more than 9 MET-hours per week after their diagnosis.4 The manner in which exercise habits change after a diagnosis of breast cancer can also affect prognosis. In one study with a 6-year follow-up, women who maintained or exceeded a level of physical activity of 3 MET-hours per week had a survival rate higher than that of women who remained

Reprinted with permission from: Nevit Dilmen. https://commons.wikimedia.org/wiki/ File:1IGL_Insulin-Like_Growth_Factor_Ii_01.png. Published 2002. Accessed August 10, 2016.

FIGURE 1. Insulin-like growth factor 1.

inactive; this was noted even if the women had been physically inactive before their diagnosis.11 Irwin et al reported that women who decreased their exercise time after a diagnosis of breast cancer were 4 times more likely to die of their cancer than those who maintained or increased their level of physical activity.9 Alternatively, women who increased their activity levels reduced their risk for death by 45%.9 Biological mechanisms

The precise relationship among exercise, the development of cancer, and death is poorly understood. However, 2 biological mechanisms have been suggested as possible contributors to the protective benefits of physical activity; these physiologic mechanisms involve the family of insulin-like growth factors (IGFs) (Figure 1) and the p53 protein (Figure 2).12,13 IGF-1, IGF-2, and the IGF binding proteins (IGFBP-1 through IGFBP-6) are proteins that play a role in cell division.12 IGF-1 has a stimulating effect on cell proliferation, accelerating the advancement of the cell cycle; in addition, IGF-1 has an inhibitory effect on programmed cell death,

p53 Protein Structure Transactivation Transactivation Domain 1 Domain 2

(1 – 43)

(44 – 63)

Proline-rich Region

DNA Binding Domain

(64 – 92)

(102 – 292)

393 NILS

Tetramerization Domain

Regulatory Domain

(320 – 355)

(356 – 393)

Reprinted with permission from: Raiha T. https://commons.wikimedia.org/wiki/File:P53_Schematic.tif. Published April 29, 2014. Accessed August 10, 2016.

FIGURE 2. A schematic of the known protein domains in p53. NLS, nuclear localization signal. www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2016 33

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PHYSICAL ACTIVITY AND CANCER

or apoptosis.12 In patients with cancer, IGF levels tend to be abnormally high. These proteins have been found to overstimulate cell proliferation in various cancer cell lines, including breast, colorectal, prostate, brain, and uterine cancer cell lines, among several others.12 In patients with cancer, IGFBP-1 acts by binding IGF-1, therefore decreasing free levels of IGF-1 in serum; this process interferes with the proliferative effect of IGF-1 while also promoting apoptosis.12 There is scientific evidence that IGFBP-1 levels are lowered in persons with cancer.12 Studies have shown that IGF-1 levels are lower and IGFBP-1 levels are higher in serum taken from subjects who are more physically active.14,15 In addition, when lymph node cancer of the prostate (LNCaP) cell lines are exposed to this serum in vitro, cell proliferation is significantly decreased.16,17 Researchers are still examining the complex relationship between this family of proteins and neoplasia, but their work may provide an early insight into how exercise has an effect on cancer. The protein p53 is also crucial to regulation of the cell cycle. It plays a role in the transcription of numerous genes, which means that p53 is intimately linked to apoptosis, cell growth and arrest, protein translation, and DNA repair.18 Normally, p53 functions by stimulating cell cycle arrest and DNA repair or inducing apoptosis in cells with damaged DNA.18 Loss of this “wild-type function” has been implicated in most cancers.19 It has been demonstrated in an animal model that levels of p53 are significantly higher in subjects that are more physically active and that this protein may play a direct role in slowing the growth of tumor cells.19 Similar results were obtained in another study, in which prostate cancer cell lines were exposed to serum from fasting blood samples collected from men who exercised or who were sedentary; cells exposed to exercise serum exhibited a 27% reduction in growth and a 37% increase in apoptosis in comparison with cells from the same line cultured in serum from the sedentary group.14 Researchers attributed this difference to a 100% increase in p53 in the LNCaP cells exposed to exercise serum.14 Conclusion

The current recommendation that individuals should expend at least 9 MET-hours per week by exercising extends not only to the prevention of cancer but also to the reduction of cancer mortality.1 Although some research has demonstrated that higher levels of activity are required to reduce one’s risk for dying of cancer, the nationally recommended figure was more than enough to make a difference in many instances.5 This seems to indicate that practitioners should urge their patients not only to exercise to stave off the development of chronic

Key take-aways • Physical activity reduces the risk for a variety of ailments, including cancer, and it may also reduce the risk for death after a diagnosis of cancer. • Studies have demonstrated that exercise both before and after a cancer diagnosis reduces cancer-specific mortality. • The ideal level of physical activity is 9 MET-hours per week, which is the equivalent of 150 minutes of moderateintensity exercise or 75 minutes of vigorous-intensity exercise per week. • The biological mechanisms are poorly understood, but the insulin-like growth factor family and p53 protein may play a crucial role in halting cancer growth. • Practitioners should encourage their patients to exercise as much as possible as a supplement to their cancer treatment.

illnesses but also to make every effort to continue being physically active after receiving a diagnosis of a disease such as cancer. Although it may be more difficult for patients undergoing treatment for cancer to expend the energy required to improve their chances of survival, the importance of increasing heart and respiratory rates should not be forgotten. Physical activity should be promoted as a supplement to traditional treatments, such as chemotherapy and radiation, and could be as simple as going outdoors or getting on a treadmill and walking for a half-hour 5 days a week. Many studies have had the advantage of being able to follow patients over long periods; however, the specific length of time that the protective benefits of exercise last remains unclear. Nevertheless, based on the most recent data, patients with cancer may benefit from regular physical activity, which leads to a more favorable prognosis.2-4 n Bradley Weiler, PAS-II, is a physician assistant student, SUNY Upstate Medical University, and Sandra Banas, MST, PA-C, is the founding chairperson and PA program director, SUNY Upstate Medical University, Syracuse, New York. References 1. 2008 physical activity guidelines for Americans. Centers for Disease Control and Prevention website. https://health.gov/paguidelines/guidelines. Published October 2008. Updated August 10, 2016. 2. Bradshaw PT, Ibrahim JG, Khankari N, et al. Post-diagnosis physical activity and survival after breast cancer diagnosis: the Long Island Breast Cancer Study. Breast Cancer Res Treat. 2014;145(3):735-742. Continues on page 37

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PHYSICAL ACTIVITY AND CANCER

3. Meyerhardt JA, Heseltine D, Niedzwiecki D, et al. Impact of physical activity on cancer recurrence and survival in patients with stage III colon cancer: findings from CALGB 89803. J Clin Oncol. 2006;24(22):3535-3541. 4. Kenfield SA, Stampfer MJ, Giovannucci E, Chan JM. Physical activity and survival after prostate cancer diagnosis in the health professionals followup study. J Clin Oncol. 2011;29(6):726-732. 5. World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007. 6. Haskell WL, Lee IM, Pate RR, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc. 2007;39(8):1423-1434. 7. Williams PT. Breast cancer mortality vs exercise and breast size in runners and walkers. PLoS ONE. 2013;8(12):e80616. 8. Haydon AM, Macinnis RJ, English DR, Giles GG. Effect of physical activity and body size on survival after diagnosis with colorectal cancer. Gut. 2006;55(1):62-67.

“Don’t believe everything you see on Shark Week—we’re not all bad.”

9. Irwin ML, Smith AW, McTiernan A, et al. Influence of pre- and postdiagnosis physical activity on mortality in breast cancer survivors: the health, eating, activity, and lifestyle study. J Clin Oncol. 2008;26(24):3958-3964. 10. Holmes MD, Chen WY, Feskanich D, Kroenke CH, Colditz GA. Physical activity and survival after breast cancer diagnosis. JAMA. 2005;293(20):2479-2486. 11. Irwin ML, McTiernan A, Manson JE, et al. Physical activity and survival in postmenopausal women with breast cancer: results from the women’s health initiative. Cancer Prev Res (Phila). 2011;4(4):522-529. 12. Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst. 2000;92(18):1472-1489. 13. Muller PA, Vousden KH. Mutant p53 in cancer: new functions and therapeutic opportunities. Cancer Cell. 2014;25(3):304-317. 14. Leung PS, Aronson WJ, Ngo TH, Golding LA, Barnard RJ. Exercise alters the IGF axis in vivo and increases p53 protein in prostate tumor cells 15. Ngo TH, Barnard RJ, Leung PS, Cohen P, Aronson WJ. Insulin-like growth factor 1 (IGF-1) and IGF binding protein-1 modulate prostate cancer cell growth and apoptosis: possible mediators for the effects of diet and exercise on cancer cell survival. Endocrinology. 2003;144(6):2319-2324. 16. Barnard RJ, Leung PS, Aronson WJ, Cohen P, Golding LA. A mechanism to explain how regular exercise might reduce the risk for clinical prostate cancer. Eur J Cancer Prev. 2007;16(5):415-421. 17. Rundqvist H, Augsten M, Strömberg A, et al. Effect of acute exercise on prostate cancer cell growth. PLoS ONE. 2013;8(7):e67579. 18. Hasty P, Christy BA. p53 as an intervention target for cancer and aging. Pathobiol Aging Age Relat Dis. 2013;3. doi: 10.3402/pba.v3i0.22702 19. Higgins KA, Park D, Lee GY, Curran WJ, Deng X. Exercise-induced lung cancer regression: mechanistic findings from a mouse model. Cancer. 2014;120(21):3302-3310. All electronic documents accessed August 10, 2016.

“I know it’s small and expensive, but wait till you see all the Pokemon.”

in vitro. J Appl Physiol. 2004;96(2):450-454.

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CME CE FEATURED COURSE

n EDUCATIONAL OBJECTIVES After participating in this activity, clinicians should be better able to: • Discuss the etiology and biology of head lice infestation • Identify signs and symptoms of head lice infestation and distinguish between active infestation and other material in hair • Evaluate the effectiveness and risks of various prescription and over-the-counter lice treatment options, particularly newer agents • Counsel parents and patients on proper implementation of various treatments for head lice n COMPLETE THE POST-TEST: Page 52

Release Date: June 29, 2015 Reviewed: August 1, 2016 Expiration Date: September 1, 2017 Estimated Time to Complete: 1 hour Accredited Provider: This program is jointly provided by Haymarket Medical Education (HME) and Postgraduate Institute for Medicine (PIM). Commercial Supporter: There is no commercial support for this activity. Program Description: Head lice infestation (also known as pediculosis) is the infection of the head hair and scalp by the head louse, Pediculus humanus capitis. The condition is common in the United States, particularly among the young; an estimated 14 million individuals are treated for head lice annually, with 6 to 12 million being children. Once infection occurs, the head lice irritate the skin and/or scalp and cause itching. This activity, which consists of a text-based monograph followed by an interactive patient case study scenario, describes the biology of the head louse and provides a review of best practices for the diagnosis and management of head lice. In addition, the safety and clinical success rates for a variety of new and existing therapeutic options are discussed. Intended Audience: Physicians, physician assistants, nurse practitioners, and registered nurses who treat patients with head lice Conflict of Interest 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 to ensure independence, objectivity, balance, and scientific rigor in all its educational programs. Faculty Michael W. Simon, MD, PhD, FAAP Department of Pediatrics University of Kentucky Private Practice Nicholasville, KY CME Reviewer Ruchit Parikh, PharmD Assistant Medical Director Haymarket Medical Education Faculty Dislosure: Dr. Simon has disclosed that he has received fees for non-CME/CE services from Zylera and has conducted contracted research for GlaxoSmithKline, Sanofi, Anacor, Sunovion Pharmaceuticals, Arbor Pharmaceuticals, Abbott, and Astellas Pharma US, Inc. Dr. Nashed has no relevant financial relationships to disclose. Planners’ and Managers’ Disclosures: HME planners and managers have no relevant financial relationships to disclose. The planners and managers reported the following financial relationships or relationships to products or devices they or their spouse/life partner have with commercial interests related to the content of this CME activity:

any financial relationships or relationships to products or devices with any commercial interest related to the content of this activity of any amount during the past 12 months. Accreditation Statement: Haymarket Medical Education is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Designation Statement: Haymarket Medical Education designates this enduring material for a maximum of 1.00 AMA PRA Category 1 CreditTM. Physicians should claim only those credits commensurate with the extent of their participation in the activity. Accreditation Statement: Postgraduate Institute for Medicine is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Designation Statement: This educational activity for 1.00 contact hours is provided by Postgraduate Institute for Medicine. Designated for 0.50 contact hours of pharmacotherapy credit for Advance Practice Registered Nurses. 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. Haymarket Medical Education (HME) and Postgraduate Institute for Medicine (PIM) do not recommend the use of any agent outside of the labeled indications. The opinions expressed in the educational activity are those of the faculty and do not necessarily represent the views of HME or PIM. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings. Disclaimer: Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patient’s conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. Instructions: There are no fees for participating in and receiving CME credit for this activity. During the period June 29, 2015 through September 1, 2017, participants must: 1) read the learning objectives and faculty disclosures; 2) complete the pre-assessment test; 3) study the educational activity; 4) complete all case study questions; 5) complete the post-test and submit it online. A statement of credit will be issued only upon receipt of the above elements and a post-test score of 70% or higher. All components must be completed and submitted online at ClinicalAdvisor.com/Sept16feature. Jointly provided by

The following PIM planners and managers, Trace Hutchison, PharmD, Samantha Mattiucci, PharmD, CHCP, Judi Smelker-Mitchek, RN, BSN, and Jan Schultz, RN, MSN, CHCP, hereby state that they or their spouse/life partner do not have

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CME CE FEATURED COURSE: MICHAEL W. SIMON, MD, PHD, FAAP

Update on the diagnosis and treatment of head lice Best practices for recognizing and managing head lice using a variety of new and existing therapeutic options are reviewed.

ediculosis is an infestation of the head louse, Pediculus humanus capitis. The louse is an arthropod ectoparasite living on the body of its host human. Pediculosis is the most common parasitic infestation in children 3 to 12 years of age.1,2 Incidence is higher in females than in males and no seasonal trends have been observed, although cases may occur more frequently during the school year. The occurrence of head lice infestations is not influenced by hygiene, hair length, or frequency of shampooing or brushing.³ Caregivers and household contacts are at an increased risk of infestation.1

The basics

Head lice infestation

The adult head louse is 1 mm to 3 mm long, the size of a sesame seed. In most cases, it is tan to grayish white in color, although it may be clear and turn reddish brown or black with feeding.1,4 Lice live up to 3 to 4 weeks and, once mature, females lay up to 10 eggs each day and 50 to 150 eggs during their lifetime.5 The eggs cannot survive and hatch at temperatures lower than that found near the scalp, so they attach fi rmly to the base of the hair shaft using a gluelike substance produced by the female.6,7 Viable eggs are gray to white or camouflaged with pigment matching the hair color of the infested individual.1 Empty egg casings are easier to see because they are white and are further out on the hair shaft. Any form attached to the hair shaft may be called a nit, but it may be more accurate to refer www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2016 43

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Head lice are not a health hazard or sign of poor hygiene. It is generally accepted that they do not spread disease or illness.

to nits as the empty egg casing and to eggs as developing, unhatched nymphs. The eggs are incubated by the host’s body heat and hatch in 6 to 9 days, but that can vary between 7 to 12 days depending on environmental temperature.1 Once hatched, the nymph starts to feed and passes through 3 developmental stages called instars; each instar lasts 3 to 5 days, and full maturity is reached in 9 to 15 days.1,6 The nymph looks like the adult, only smaller. Once reaching adulthood, the females may mate and begin to lay viable eggs in 1.5 days. Lice cause intense itching by injecting small amounts of their saliva, which has anticoagulant and vasodilating properties, into the scalp while feeding, producing a sensitivity reaction in the host.1,8 This sensitization may take 2 to 6 weeks to occur with the first infestation but only several hours with any subsequent infestation.9 If left untreated, the cycle may repeat every 3 weeks. Head lice are not a health hazard or sign of poor hygiene. It is generally accepted that they do not spread disease or illness.1,10-12 However, some authors suggest that head lice harbor Bartonella quintana and Rickettsia prowazekii and may serve as a source of trench fever and louse-borne typhus, respectively.13,14 Head lice do cause limited morbidity but will produce a high level of anxiety for parents.1 Scratching may lead to skin infection (impetigo) with Streptococcus or methicillin-resistant Staphylococcus aureus (MRSA) and local swollen lymph nodes (lymphadenopathy).7,15-16

Examination of the hair using a nit comb.

Lice have 6 legs but cannot fly, hop, or jump.1 They spread by head-to-head contact, fomites, and personal items like combs, brushes, hats, and bedding (fomites). Experts are divided regarding which is the most significant mechanism of transmission. For head-to-head contact, it may take 30 seconds to spread from one head to another.17 For personal items, lice don’t survive more than 3 days away from their human host. They are required to feed on their human host several times a day to survive.6 Those found on combs may already be injured or dead.18 Examination and diagnosis

The gold standard for diagnosis of an infestation is detecting live lice.1 Combing was found to be 3.8 times more effective than simple visual inspection.19,20 Visual inspection may miss up to 50% of infestations. Using a magnifying glass may be helpful to visualize the lice.21 Finding eggs is insufficient to make the diagnosis because they may not be viable. The hatched, empty egg casings (nits) may be confused for viable eggs. Adults avoid light and may move quickly. They may be more easily seen if the hair is moistened with water, oil, or conditioner to slow down their movement. Visualization may also be improved in a darkened room with an ultraviolet light (Wood’s lamp).22 Viable eggs and adults may be more readily seen at the nape of the neck or behind the ears, and they will be within 1 cm (a little less than ½ inch) of the scalp on a hair shaft.1,21 Eggs found further out on the hair shaft are most likely not viable unless the environmental temperature is very warm.23 Experience is helpful to avoid confusing dandruff, hair debris, hair casts, hairspray droplets, scabs, and other insects for viable lice eggs.24,25 Examine the hair shaft at the back of the head and neck and behind the ears, starting close to the scalp and working toward the end of the hair. Wet comb the hair with a nit or bug-busting comb with teeth less than 0.3 mm apart. Dry combing may create enough static electricity to physically eject the adult lice more than 1 meter from an infested scalp.26 Nits more than 3 mm to 4 mm out on the hair shaft from the scalp may be empty egg casings or dead eggs.23 However, it is still worthwhile to remove all nits.25 Advise parents and patients that applying a vinegar rinse to the hair may help to loosen nits from their attachment. However, do not use vinegar with permethrin, as vinegar interferes with permethrin due to its residual effect.1 Also tell

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Treatment involves a combination of topical, oral, and physical methods, factoring in the individual's age and size, resistance patterns in the area, and the agent's toxicity. them that other agents such as WD-40, acetone, vodka, or bleach are ineffective in loosening nits. They should recheck the scalp and comb hair daily, cleaning combs frequently. Tell patients to keep their eyes closed with a towel placed over them during any topical application4 and to rinse over a sink—not in the bath or shower because that will increase skin exposure and possibly absorption. If burning and itching occur after application, oral antihistamines and topical steroids may be used. The American Academy of Pediatrics’ (AAP) Red Book recommends examining and treating household and other close contacts if infested.27 Treat bedmates at the same time as the infested individual even if no lice are seen at examination. Head transfer may be through pillowcases, with an incidence of 4%.28 Prophylactic treatment of other noninfested individuals is not needed. Pets do not harbor nor are they carriers of head lice and require no treatment. General precautions would include no sleepovers and no sharing of hats or hair-care items. Parents/patients should wash personal items that have been in contact with the infested person in the 48 hours prior to treatment in hot water (130°F to 150°F) for 5 to 10 minutes and clothing for at least 20 minutes. Dry in a dryer on the hot setting to kill lice and nits, and dispose of debris in the dryer trap.1,4,25 Dry cleaning may also eliminate lice, but freezing is ineffective. Chemical treatments using permethrin 0.5% are available but may be unnecessary.4 Vacuuming furniture, mattresses, pillows, carpets, and car seats to remove infested hair that may have attached viable eggs is a safer alternative; advise parents to discard the sweeper bag. For items that cannot be washed, place in a sealed plastic bag for 2 weeks.4,25 Hatching lice and nymphs at different stages will not survive without feeding.¹ It has never been demonstrated that a No Nit policy—that is, prohibiting affected children from returning until no nits are present—reduces the spread of lice at school.4 Experts are divided on whether head-to-head contact or sharing of hats, combs, or clothing is more significant in spreading head lice.6 Misidentification of nits or eggs not hatched and nit casings may occur, leading to lost school and work days, treatment expenses, and lost wages. Dismissal of affected children from school following the initial diagnosis may be unnecessary because it may take 1 to 2 months for an infestation to become established and the degree of contagiousness in the classroom is low.29

Only 1 in 3 children with nits have live lice.30 Only 18% of children with nits alone developed an active infestation over the next 2-week period. These children could complete the school day; advise their parents to treat afterward. After treatment, the child should be allowed to return to school with the nurse doing periodic checks with a nit comb and informing the parents when retreatment is appropriate. Treatment

Families may rely on pharmacists, school nurses, or other individuals to diagnose head lice and then initiate overthe-counter (OTC) treatment without first consulting their healthcare provider. This could result in inaccurate diagnosis and unnecessary treatment with potentially toxic agents. Advise parents that treatment should never be started without a confirmed diagnosis of head lice. Treatment may involve some combination of topical, oral, and physical methods, factoring in the age and size of the individual, resistance patterns in a geographic area, and toxicity of the agents.1 The standard regimen recommended today is 2 topical applications given 7 days apart. If treatment failure occurs, use a different class of pediculicide for the subsequent treatment.21 Two topical treatments help to reduce the occurrence of resistance and are effective for emerging nymphs. First-line treatment. The AAP recommends OTC permethrin or synergized pyrethrins (pyrethrin with piperonyl butoxide) as first-line options for treatment of head lice. Permethrin (Nix), introduced in 1986, went OTC in 1990. It is the most studied and least toxic agent, and it works by inhibiting sodium influx across a cell membrane, which results in delayed repolarization of cell membrane channels, producing paralysis and death of the lice.¹ It is not ovicidal. Permethrin may be used in individuals as young as 2 months of age. It has pregnancy precaution Category B. Use with caution in those with ragweed allergy because it may trigger asthma symptoms or respiratory difficulties. Be aware that it has a residual effect that is designed to kill emerging nymphs: it adheres to the hair shaft as long as conditioners or silicone-based shampoos are not used.31 It is best to first moisten the hair so it is damp, not wet, then saturate the hair with permethrin. Caregivers should be instructed to leave it on for 10 minutes, rinse, and then towel dry. Lastly, thoroughly nit comb dry hair and wet comb it daily. If live lice are seen 7 or more days after the

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TABLE 1. Comparison of FDA-approved treatments for head lice Treatment agent

Formulation

Age indication

Application method

Length of application

Benzoyl alcohol

5% lotion

≥6 months

Applied to dry hair

10 minutes

Rinsed off, then shampooed

Ivermectin

0.5% lotion

≥6 years

Applied to dry hair

10 minutes

Rinsed off, then shampooed

Lindane

1% shampoo

≥10 years

Applied to dry hair

4 minutes

Rinsed off, then shampooed

Malathion

0.5% lotion

≥6 years

Applied to dry hair

8 to 12 hours

Rinsed off, then shampooed

Permethrin

5% cream or 1% lotion

≥2 months

Applied to damp hair

10 minutes

Rinsed off

Pyrethrin/piperonyl butoxide

Piperonyl butoxide 4%-pyrethrins 0.33% shampoo

≥2 years

Applied to dry hair

10 minutes

Rinsed off, then shampooed

Spinosad

0.9% topical suspension

≥4 years

Applied to dry hair

10 minutes

Rinsed off, then shampooed

Removal method

FDA, US Food and Drug Administration. *Day 1, day 7, then 13-15 days after first application.

initial application, repeat the treatment. The overall success rate may vary between 45% and 80%.32 Side effects include eye irritation and scalp redness and irritation. Pyrethrin/piperonyl butoxide (Rid) is synergized pyrethrin. It contains pyrethrin extract from chrysanthemums and piperonyl butoxide, which reduces the metabolism of pyrethrin by arthropods. It has an action similar to dichlorodiphenyltrichloroethane (DDT). It acts by disrupting the sodium channel current, resulting in delayed repolarization and paralysis of nerves in the exoskeletal muscles that lice use in order to breathe.10 It is neurotoxic for lice but has extremely low toxicity for humans.1 It is ovicidal, but not for newly laid eggs for the first several days, when lice have not yet developed a nervous system. Approximately 20% to 30% of the eggs remain viable after a treatment. In certain studies, up to 75% of adult lice appeared to be eliminated 30 minutes after application; however, in one study, only 53% of adult lice were actually dead 3 hours after treatment.33 Lice may survive more than 1 hour without oxygen. Pyrethrin/piperonyl butoxide has an estimated overall success rate of 10% to 75%. It should be applied only to dry hair and then rinsed after 10 minutes. No residual activity

remains after rinsing. Nit combing should be done after the initial application, and then wet comb daily. Retreatment on day 7 is necessary if there are surviving adults and newly emerging nymphs after the first treatment. Pyrethrin/ piperonyl butoxide is approved for use for patients 2 years of age and older and has pregnancy precaution Category C. Do not use in patients who are allergic to chrysanthemums or ragweed. Newer treatment agents. Newer, safer, and more effective agents have been developed that have different mechanisms of action and require fewer reapplications. However, they are also more expensive.4 The first of these products is benzyl alcohol 5% lotion (Ulesfia). Approved by the US Food and Drug Administration (FDA) in April 2009, it is the first non-neurotoxic topical agent for head lice.¹ Benzyl alcohol stuns the breathing openings (spiracles), keeping them open so that inactive components may enter and clog the respiratory system, leading to suffocation and death of the head louse by asphyxia. It is not ovicidal. This agent is indicated for those 6 months of age and older and has Pregnancy Category B precautions. Those younger than 6 months of age may have increased absorption across the scalp.

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Pregnancy precautions

Pediculicidal / ovicidal?

Success rate

9 days after initial application or in 3 cycles*

Category B

Yes / No

>80%; may achieve 100% with 1 or 2 treatments

7 days after initial application if live lice are seen

Category C

Yes / No

76%

9 to 10 days after initial application

Category C

Yes / Yes

Not reported

7 days after initial application if live lice are seen

Category B

Yes / No

90% to 100%

7 days after initial application if live lice are seen

Category B

Yes / No

45% to 80%

7 days after initial application if live lice are seen

Category C

Yes / Yes

10% to 75%

7 days after initial application if live lice are seen

Category B

Yes / Yes

85%

Retreatment

Enough product should be applied to cover the entire scalp and dry hair. Massage it into the hair and allow to set for 10 minutes before rinsing, then shampoo. Use a nit comb to complete the treatment. The kill rate is greater than 80%, and 100% treatment success may be achieved with 1 or 2 applications.34 Each bottle may cost up to $50, and as many as 6 bottles may be needed per application.4 Side effects may include scalp itching and redness and eye irritation. If nymphs reemerge, either retreat 9 days after the initial application or use 3 cycles: day 1 of treatment, day 7, and then 13 to 15 days after the first application. Spinosad 0.9% topical suspension (Natroba), approved in January of 2011, is both ovicidal and pediculicidal. It interferes with the louse’s nicotinic acetylcholine receptors, resulting in neuronal excitement, involuntary muscle contraction, paralysis, and death of the lice.35 Cross-resistance is unlikely because this mechanism is different from other pediculicides. Its success rate is 85%. Studies have shown it to be effective in patients as young as 6 months of age, but safety has not been evaluated in children younger than 4 years of age. For this reason, it is indicated for those 4 years of age and older. While spinosad itself is not absorbed, one of its vehicle ingredients

(benzyl alcohol) may be absorbed, pass into breast milk, and produce central nervous system (CNS) effects.4 Benzyl alcohol may produce “gasping syndrome,” which can cause CNS depression, metabolic acidosis, and gasping respirations. It is, therefore, not recommended for those younger than 6 months of age, who have a greater risk of systemic absorption due to larger head surface area and increased skin absorption. This agent carries Pregnancy Category B precautions. When applying spinosad, saturate the scalp and then completely coat the hair by working toward the ends. After 10 minutes, rinse the hair and scalp thoroughly and nit comb. Retreat if live lice are seen 7 days after treatment. Since it is ovicidal, nit removal is not necessary, but it may be recommended, especially for early eggs that have not yet developed a nervous system at the time of treatment. Effective treatment for long hair may require an entire bottle at a cost of approximately $210.4 Ivermectin 0.5% lotion (Sklice) was approved by the FDA in February 2012. It binds selectively to glutamategated chloride channels in parasite nerve and muscle cells, increasing their permeability and causing hyperpolarization, paralysis, and death.4 Ivermectin is indicated for treatment of head lice in those 6 years of age and older and has pregnancy precaution Category C. Studies have not evaluated this agent in pregnant women, but it is known that this product may pass through into human breast milk. Ivermectin should be applied to dry hair and the scalp for 10 minutes, then be rinsed off. It has a 76% success rate. Advise parents to have a healthcare provider confirm that infestation is still present before giving a second treatment. Isopropyl myristate rinse (Resultz), is a non-neurotoxic topical pediculicide that dissolves the waxy-shell exoskeleton, resulting in the louse dying from dehydration. The product is applied to dry hair and massaged until the scalp is completely wet. After 10 minutes, the hair should be rinsed with warm water and shampoo. Application should be repeated in 7 to 10 days to kill newly hatched lice from eggs. Isopropyl myristate rinse is flammable, so it should be kept away from open flames or any device that creates heat. The hair should be nit combed between applications to remove nits. It is available only in Canada. Older treatment agents. Malathion 0.5% lotion (Ovide) was reintroduced into the marketplace in 1999 after being removed on 2 previous occasions. It is a weak organophosphate poison that inhibits acetyl cholinesterase activity for head lice, causing respiratory paralysis, and is both ovicidal and pediculicidal.36 The current formulation also

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FEATURED COURSE

contains terpineol dipentene and pine needle oil, both of which are pediculicidal and may delay development of resistance.37 Indicated for use in those 6 years of age and older, this agent should not be used in infants because they have increased scalp absorption. Malathion is classified as pregnancy precaution Category B and is not recommended for breastfeeding women. After the product is applied to dry hair, the hair and lotion should be allowed to dry naturally. A hair dryer, curling iron, flat iron, or other heat-producing device should not be used because malathion is flammable, containing 78% isopropyl alcohol.1,38 Do not smoke near a child being treated. The product may be effective in 20 minutes, but 8 to 12 hours of application is recommended before shampooing and rinsing out.³² Next, a nit comb should be used to remove dead lice and nits. Frequently, a single application is all that is necessary, with a clinical success rate of between 90% and 100%.39 Retreatment should occur after 7 to 10 days if live lice or nits are seen. Side effects may include a burning sensation on the scalp and/or skin and chemical irritation to the eyes. A new, less toxic 0.5% gel formulation of malathion, indicated for those 2 years of age or older, is in development; this version requires only 30 minutes of scalp contact before shampoo and rinse.4 Lindane 1% shampoo (Kwell), on the market since 1951, is both pediculicidal and ovicidal. It is an organophosphate and is a slow killer of lice (and people as well). Lindane works by blocking GABA-gated chloride channels, resulting in hyperstimulation of the nervous system and producing paralysis and death.40 Ovicidal activity is low at between 0% and 50%. It is uncertain whether this agent is teratogenic, but it will cross the placenta, can be detected in breast milk, and is classified as pregnancy precaution Category C. Lindane is absorbed across the skin and is no longer recommended by the AAP’s Red Book and Medical Letter due to its CNS toxicity.41 California has banned its use due to concerns about water supply contamination.1,4 At best, it is now a second-line therapy and should be reserved for those who have failed other treatments, are 11 years of age or older, weigh more than 100 pounds (50 kg), have no seizure disorders, are not taking medicines that lower the seizure threshold, or are HIV positive.4 The product should be left on the hair for 4 minutes then rinsed off, and this regimen should be repeated in 9 to 10 days if live lice are seen. Other treatment options. With the alarming rate of resistance to certain topical products and potential toxicity of others, oral agents may become the next treatment

of choice. Oral ivermectin (Stromectol) has been found to be effective, but it is not currently approved for head lice.1 A single dose of 200 mcg/kg is given, with a second dose 9 to 10 days later. Alternatively, 400 mcg/kg given in a single dose with a repeat dose 1 week later has been shown to eliminate 95% of lice by day 15.42 This agent may cause CNS toxicity and is not recommended for patients who weigh less than 66 pounds (30 kg). A 1% topical preparation is also available and should be applied for only 10 minutes then washed off. However, this formulation is not FDAapproved for treatment of head lice, either.1 Trimethoprim-sulfamethoxazole; cotrimoxazole (Bactrim, Septra, Sulfatrim) was reported in 1978 to be effective for head lice, although it is not FDA-approved for this usage.³ It is given orally at 10 mg/kg/day based on trimethoprim in 2 equally divided doses. Lice feeding on host blood take in the agent, which kills the symbiotic intestinal flora of the lice and either prevents production of vitamin B or has a direct toxic effect on the head lice. The success rate is 93%, and it may be more effective when given with permethrin 1%.43 However, bear in mind that trimethoprim-sulfamethoxazole has the potential to cause a Stevens-Johnson syndrome reaction, making other treatment modalities safer options.1,3 Crotamiton 10% topical lotion (Eurax), a prescription agent used to treat scabies, may be effective for head lice when left on the scalp for 24 hours. However, it has not been evaluated or licensed by the FDA and safety and efficacy have not been established; it is therefore not FDA-approved for treatment of head lice.1 Application on 2 consecutive nights may eradicate lice from adults.44 Permethrin 5% (Elimite) is available by prescription and has also been used for scabies. Although it is not FDA-approved for treatment of head lice, it has been used for head lice infestations that are resistant to other treatments. Lice resistant to permethrin 1% will also be resistant to permethrin 5%.45 Dimethicone lotion (Silicone, LiceMD, and Resultz [available in Canada]) dissolves the waxy exoskeleton of head lice, which leads to drying out and death. It is applied for 2 to 8 hours, with reapplication after 1 week. The reported eradication rate is 69%.46 Topical products like petroleum jelly, mayonnaise, olive oil, tea tree oil, or Cetaphil conditioner may be applied to suffocate the lice.47 These products require 2 to 4 properly timed treatment cycles. Cetaphil cleanser (Nuvo lotion) is used once a week for 3 consecutive weeks.48 Products should be massaged into the scalp and left on overnight, with the patient wearing a shower cap. These products

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Patient case study Read the following patient case scenario and guess the correct answer for each poll question. When you are finished, log your answers and complete the pre-assessment and post-test at ClinicalAdvisor.com/ Sept16feature. Mrs. Smith calls your office 10 minutes before closing time. She tells you that she noticed what she believes may be lice in her 4-year-old son’s hair. She asks you what she should do. You tell her to: a. Start permethrin tonight and come into the office in 1 week for follow-up b. Initiate no treatment tonight, but set up an appointment to examine him in the morning c. Shampoo her son’s head and launder the bed linens d. Avoid allowing any pets to sleep in the same bed with him Mrs. Smith brings Jake and his siblings into the office the following morning for evaluation. You begin by searching Jake’s scalp. Something seems to move quickly to avoid light. To more accurately see whether these are lice, you may: a. Moisten the hair to slow down movement b. E xamine the scalp in a darkened room with an ultraviolet (Wood’s) lamp c. E xamine the nape of the neck or behind the ears and use a magnifying glass

Before the visit concludes, Mrs. Smith asks whether items such as the family car in which they have been traveling as well as the furniture, carpet, and clothes should be cleaned, discarded, or otherwise treated. All of the following responses are correct except: a. S he may vacuum the car seats, furniture, mattresses, pillows, and carpets, then discard the sweeper bag b. Jake’s clothes may be washed in hot water at 130° to 150°F for 20 minutes, then dried in the dryer on the hot setting c. Items not washable may be dry cleaned or sealed in an airtight plastic bag for 14 days d. Personal items such as hairbrushes and hats should be discarded, as lice can survive on these items for several weeks A few days later, Jake’s school nurse contacts you and says she is confused about your care for Jake and his siblings. She asks why you allowed Jake and his brothers to return to school given that they have a No Nit policy in place (students are not permitted to return to school until they are free of nits). You tell the school nurse: a. The No Nit policy has never been shown to reduce the spread of head lice b. The No Nit policy leads to unnecessary lost school and work days c. The degree of contagiousness in the classroom is low

d. All of the above

After confirming the presence of live lice on Jake’s scalp but not on his siblings’, you discuss a treatment plan with Mrs. Smith. While you make arrangements for the necessary prescriptions, Mrs. Smith tells you Jake won’t sleep at night without his teddy bear, so she is hesitant to seal it in a plastic bag for 3 weeks. She asks if she can freeze it overnight to kill the lice. You tell her:

The nurse accepts your response, but tells you she is concerned that the head lice may spread to other children. She says she has requested that the health department disinfect Jake’s classroom, as well as her office since Jake has been seen there. You respond:

a. Freezing is very effective to kill lice and eggs b. The teddy bear may be effectively cleaned by dry cleaning c. Freezing is effective, but it should be frozen for 3 to 5 days before use d. Neither freezing nor dry cleaning is effective

a. Classroom disinfection is highly recommended b. Lice may survive on surfaces, including hats and combs, for up to 2 weeks c. Everyone in the classroom is at risk because head lice are a significant health hazard d. The degree of contagiousness in the classroom is low and disinfecting is unnecessary

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CME CE

FEATURED COURSE

block the spiracles of adults and holes in the eggs that allow air exchange.47 The lice may close their respiratory spiracles—essentially, hold their breath—until the product is washed off, then start to feed. This is called the resurrection effect.33 These products may be difficult to remove from the hair and require daily shampooing; they may also enhance bacterial growth on the scalp. Flammable products like gasoline or kerosene should never be used, nor should products intended for animal use. However, applying hot air or washing or dry cleaning at a temperature of 130°F to 150°F for 20 minutes will kill lice.4,29 The LouseBuster device uses 30 minutes of hot air to desiccate lice and is 95% effective.4 Another study showed that it produces 100% mortality for eggs and 80% mortality for adults. The machine costs $2000 and requires special training and a new applicator tip (costing $11) for each treatment. Electronic combs will electrocute the lice. Some electronic combs have oscillating teeth to remove live lice and nits. Table 1 compares FDA-approved agents discussed above for the treatment of head lice. ■

14. Sasaki T, Poudel SK, Isawa H, et al. First molecular evidence of Bartonella quintana in Pediculus humanus capitis (Phthiraptera: Pediculiae), collected from Nepalese children. J Med Entomol. 2006;43(1):110-112. 15. Mumcuoglu KY, Klaus S, Kafka D, et al. Clinical observations related to head lice infestation. J Am Acad Dermatol. 1991;25(2 pt 1):248-251. 16. Taplin D, Porcelain SL, Meinking TL, et al. Community control of scabies: a model based on use of permethrin cream. Lancet. 1991; 337(8748):1016-1018. 17. Burgess IF. Treatment of head lice. Matern Child Health J. 1996; 6:142-146. 18. Chunge RN, Scott FE, Underwood JE, Zavarella KJ. A pilot study to investigate transmission of headlice. Can J Public Health. 1991;82(3): 207-208. 19. Mumcuoglu KY, Friger M, Ioffe-Uspensky I, et al. Louse comb versus direct visual examination for the diagnosis of head louse infestations. Pediatr Dermatol. 2001;18(1):9-12. 20. Balcioglu C, Burgess IF, Limoncu ME, et al. Plastic detection comb better than visual screening for diagnosis of head louse infestation. Epidemiol Infect. 2008;136(10):1425-1431. 21. Ferri FF. Ferri’s Clinical Advisor. Philadelphia, PA: Elsevier. 22. Guenther LCC, Maguiness S, Austin TW, et al. Pediculosis and pthiriasis (lice infestation). Medscape. http://www.emedicine.com/med/topic1769.

References

htm. Updated February 10, 2015. Accessed June 3, 2015.

1. Frankowski BL, Bocchini JA Jr; Council on School Health and Committee

23. Aronson SS, Shope TR. Managing Infections Diseases in Child Care and

on Infectious Diseases. Head lice. Pediatrics. 2010;126(2):392-403.

Schools: A Quick Reference Guide. 2nd ed. Elk Grove, IL: American Academy

2. Leung AK, Fong JH, Pinto-Rojas A. Pediculosis capitis. J Pediatr Health

of Pediatrics; 2009.

Care. 2005;19(6):369-373.

24. Pollack RJ, Kiszewski AE, Spielman A. Overdiagnosis and consequent

3. Frankowski BL, Weiner LB; Committee on School Health the

mismanagement of head louse infestations in North America. Pediatr Infect

Committee on Infectious Diseases. American Academy of Pediatrics.

Dis J. 2000;19(8):689-693.

Head lice. Pediatrics. 2002; 110(3):638-643.

25. Nutanson I, Steen CJ, Schwartz RA, Janniger CK. Pediculus

4. Eisenhower C, Farrington EA. Advancements in the treatment of head

humanus capitis: an update. Acta Dermatovenerol Alp Pannonica Adriat.

lice in pediatrics. J Ped Health Care. 2012;26(6):451-461; posttest 462-464.

2008;17(4):147-159.

5. Ko CJ, Elston DM. Pediculosis. J Am Acad Dermatol. 2004;50(1):1-12; quiz

26. Burgess IF. Human lice and their management. Adv Parasitol. 1995;

13-14.

36:271-342.

6. van der Wouden JC, Klootwijk T, Le Cleach L, et al. Interventions for

27. Committee on Infectious Diseases; American Academy of Pediatrics;

treating head lice. Cochrane Database Syst Rev. 2011;10:CD009321.

Pickering LK, Baker CJ, Kimberlin DW, Long SS. Head Lice. In: Red Rook.

7. Meinking TL. Infestations. Curr Probl Dermatol. 1999;11:73-118.

2012 Report of the Committee on Infectious Diseases. Elk Grove Village,

8. Weir E. School’s back, and so is the lowly louse. CMAJ. 2001;165(6):814.

IL: American Academy of Pediatrics; 2012: 543-546.

9. Burkhart CG, Burkhart CN. Safety and efficacy of pediculicides for head

28. Speare R, Cahill C, Thomas G. Head lice on pillows, and strategies to

lice. Expert Opin Drug Saf. 2006;5(1):169-179.

make a small risk even less. Int J Dermatol. 2003;42(8):626-629.

10. Elston DM. Drugs used in the treatment of pediculosis. J Drugs Dermatol.

29. Hootman J. Quality improvement projects related to pediculosis man-

2005;4(2):207-211.

agement. J Sch Nurs. 2002;18(2):80-86.

11. Angel TA, Nigro J, Levy ML. Infestations in the pediatric patient. Pediatr

30. Williams LK, Reichert A, Mackenzie WR, et al. Lice, nits, and school

Clin North Am. 2000;47(4):921-935, viii.

policy. Pediatrics. 2001;107(5):1011-1015.

12. Chosidow O. Scabies and pediculosis. Lancet. 2000;355(9206):819-826.

31. Meinking TL, Serrano L, Hard B, et al. Comparative in vitro pediculici-

13. Robinson D, Leo N, Prociv P, Barker SC. Potential role of head lice,

dal efficacy of treatments in a resistant head lice population in the United

Pediculus human capitis, as vectors of Rickettsia prowazekii. Parasitol Res.

States. Arch Dermatol. 2002;138(2):220-224.

2003;90(3):209-211.

32. Meinking TL, Vicaria M, Eyerdam DH, et al. Efficacy of a reduced

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application time of Ovide lotion (0.5% malathion) compared to Nix crème

41. Tenenbein M. Seizures after lindane therapy. J Am Geriatr Soc.

rinse (1% permethrin) for the treatment of head lice. Pediatr Dermatol.

1991;39(4):394-395.

2004;21(6):670-674.

42. Chosidow O, Giraudeau B, Cottrell J, et al. Oral ivermectin versus

33. Meinking TL, Entzel P, Villar ME, et al. Comparative efficacy of treat-

malathion lotion for difficult-to-treat head lice. N Engl J Med. 2010;

ments for pediculosis capitis infestations: update 2000. Arch Dermatol.

362(10):896-905.

2001;137(3):287-292.

43. Hipolito RB, Mallorca FG, Zuniga-Macaraig ZO, et al. Head lice infesta-

34. Meinking TL, Villar ME, Vicaria M, et al. The clinical trials supporting

tion: single drug versus combination therapy with one percent permethrin

benzyl alcohol lotion 5% (Ulesfia): a safe and effective topical treatment for

and trimethoprim/sulfamethoxazole. Pediatrics. 201;107(3):E30.

head lice (pediculosis humanus capitis). Pediatr Dermatol. 2010;27(1):19-24.

44. Burkhart CG, Burkhart CN, Burkhart KM. An assessment of topical

35. McCormack PL. Spinosad: in pediculosis capitis. Am J Clin Dermatol.

and oral prescription and over-the-counter treatments for head lice. J Am

2011;12(5):349-353.

Acad Dermatol. 1998;38(6 pt 1):979-982.

36. Mumcuoglu KY. Effective treatment of head louse with pediculicides.

45. Pollack RJ, Kiszewski A, Armstrong P, et al. Differential permethrin

J Drug Dermatol. 2006;5(5):451-452.

susceptibility of head lice sampled in the United States and Borneo. Arch

37. Dodd CS. Interventions for treating head lice. Cochrane Database Syst

Pediatr Adolesc Med. 1999;153(9):969-973.

Rev. 2001;2:CD001165.

46. Burgess IF, Brown CM, Lee PN. Treatment of head louse infestation

38. Janniger CK, Kuflik AS. Pediculosis capitis. Cutis. 1993;51(6):407-408.

with 4% dimethicone lotion: randomised controlled equivalence trial. BMJ.

39. Meinking TL, Taplin D, Kalter DC, Eberle MC. Comparative effi-

2005;330(7505):1423.

cacy of treatments for pediculosis capitis infestations. Arch Dermatol.

47. Schachner LA. Treatment resistant head lice: alternative therapeutic

1986;122:267-271.

approaches. Pediatr Dermatol. 1997;14(5):409-410.

40. Lebwohl M, Clark L, Levitt J. Therapy for head lice based on life cycle,

48. Roberts RJ, Burgess IF. New head-lice treatments: hope or hype?

resistance, and safety considerations. Pediatrics. 2007;119(5):965-974.

Lancet. 2005;365(9453):8-10.

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POST-TEST

CME CME CE CE

Expiration date: September 1, 2017 Credit Designation: Haymarket Medical Education designates this enduring material for a maximum of 1.00 AMA PRA Category 1 CreditTM. Physicians should claim only those credits commensurate with the extent of their participation in the activity. This educational activity for 1.00 contact hours is provided by Postgraduate Institute for Medicine. Designated for 0.50 contact hours of pharmacotherapy credit for Advance Practice Registered Nurses. A statement of credit will be issued only upon receipt of a completed pre-assessment test, case study questions, activity evaluation form, and post-test with a score of 70% or better. All components must be completed and submitted online at ClinicalAdvisor.com/Sept16feature.

CREDIT: 1.00

| Update on the diagnosis and treatment of head lice

1. The likelihood of head lice infestation is influenced by: a. Hygiene b. Frequency of shampooing or brushing c. Gender d. Hair length

5. The gold standard for diagnosis of lice involves: a. Conducting a visual inspection b. Finding eggs in the hair shaft c. Detecting live lice using combing d. Visualizing the presence of nits

2. After lice inject saliva into the scalp, a sensitivity reaction occurs within _______ of the first infestation. a. 1 to 2 weeks b. 2 to 6 weeks c. 3 to 9 weeks d. 4 to 8 weeks

6. Following diagnosis, which of the following precautions should not be taken? a. Wash personal items that have been in contact with the infested person in the 48 hours prior to treatment b. Avoid sleepovers and sharing of hats or hair-care items c. Vacuum furniture, mattresses, carpets, and car seats to remove infested hair that may have attached viable eggs d. Bring in pets living in the same household as the infected individual for evaluation for head lice

3. Lice can be spread by all of the following means except: a. Flying, hopping, or jumping b. Head-to-head contact c. Fomites d. Personal items (combs, brushes, hats) 4. Mrs. D presents to your office to have her 6-year-old son, Jake, examined for lice. She states that his schoolteacher spotted what she believes to be nits in his hair. At the appointment, the mother asks you to check her 3 other children who live in the same household for lice as well. After examination, you find live lice on Jake’s scalp but not on his siblings’. Your next course for treatment is to: a. Treat Jake and all of his siblings with benzyl alcohol b. Treat Jake and his brother who shares a bed with him with a second-line pediculicide c. Instruct Mrs. D to take their pet dog to the vet to be treated d. Recommend that the children all stay home from school until Jake and his bedmate have been treated for 2 additional cycles

7. After a topical product is applied, all of the following actions should be taken except: a. Rinsing out products over the shower or tub b. Washing the hands thoroughly c. Brushing with a nit comb to remove dead lice and nits d. Considering a different class of pediculicide if the initial agent fails 8. A 10-year-old girl accompanied by her father presents with complaints of an itchy scalp. Upon examination, you visualize eggs and nits along the entire length of hair and adults on the scalp. Which of the following confirms a definite diagnosis of head lice? a. Visualizing either nits or eggs on the hair b. Spotting nits on a pillowcase the father brings in a sealed plastic bag c. Finding live lice on the scalp d. Receiving a note the girl’s father brings from the school nurse, who saw lice on her head

TO TAKE THE POST-TEST please go to: ClinicalAdvisor.com/Sept16feature

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YOUR COMMENTS SUBOXONE AND METHADONE— OUR READERS WEIGH IN ON THE PROS AND CONS I have recently witnessed a rash of individuals either on Suboxone (buprenorphine and naloxone) or methadone requesting phentermine for weight loss. After researching this issue with local law enforcement and drug task force officials, I have found that oftentimes the individuals seeking phentermine in addition to Suboxone or methadone are using the phentermine for enhancement or extension of the “high” associated with Suboxone or methadone. Drug addiction is strong in the rural counties where I work, and I feel that all providers need to be aware of the potential for misuse of these drugs in combination. The pain management clinics that I have spoken to are in agreement that the use of these drugs in combination can be harmful.—DIANE PERRY, FNP-BC, Hohenwald Tenn. (215-1) Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 275 7th Avenue, 10th 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.

Is Suboxone a bad drug? It is literally a lifesaver and lightyears ahead of methadone in terms of safety and usefulness for narcotic addiction. Regarding chronic pain, a meta-analysis in the July 6 JAMA on narcotics for back pain clearly shows that narcotics have absolutely no proven benefits for either functional recovery or pain relief for back pain and should not be used beyond 1 week. Regarding patients who are on Suboxone for multiple years, yes, possibly they can be safely tapered down and off or onto naltrexone implants if they have worked hard on reducing their relapse risk and are continuing to actively work on their recovery. I am a board-certified addiction psychiatrist who has been working with these patients since Suboxone was invented. However, sometimes you have patients afraid to wean and practitioners who only took a weekend course to write Suboxone and are therefore very undertrained. No one gets high injecting Suboxone (Subutex, maybe). Never prescribe more than 16 mg per day (receptors saturated), and never prescribe refills or more than enough for a patient to get to his or her next appointment.—JOSEPH HAAS, MD, Clearwater, Fla. (215-2) I work in an opiate treatment clinic where both methadone and Suboxone are used along with addiction counseling. I have seen people improve and get their lives back, get out of the revolving jail door, and get their families and self-worth back, as well as address other health problems (diabetes,

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.

54 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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hypertension, hepatitis C, skin problems, and dental problems). They are breaking familial patterns in which multiple generations use one or more drugs. I have also dealt with addicts coming into the emergency department without treatment. They suffer. They hurt. We have looked at all sorts of treatment options. Detoxification doesn’t work. Research shows that medication treatment with counseling is effective. What are we measuring as successful treatment? The reality may well be that we will never get those who become addicted to narcotics completely off medication. But, and it sounds trite, do we expect to get diabetics off their medication? We are not treating this and pain management appropriately because we are stuck on political correctness, and we’re afraid of the Drug Enforcement Administration (DEA). And we have too many providers who think they know how to manage pain. A lot of my clients got started because they were over-medicated with pain pills, and then the provider got scared and immediately stopped prescribing. Immediate withdrawal. We need to take a huge step back and look at this problem for what it is, not what it should or shouldn’t be. Then treat it for what it is.—DEBBIE DAVIS, FNP, Spokane, Wash. (215-3) Whose brilliant idea was it to limit the availability of pain-managing opiates? Besides my primary care practice, I have worked in a methadone clinic for the past 30 years. I have seen it go from encountering heroin addiction to prescription medication addiction. Now it’s back to heroin. Not only is it difficult for my primary care patients to get their prescription filled, it has caused them to drive all over trying to find a pharmacy to fill 120 Norco 10/325. These patients have chronic debilitating pain. Help us help these patients. Give us tools (nonopiates) that control pain. Until then, why are too many patients suffering? The use

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.

of Suboxone is limited. I’ve found that if patients use opiates for pain relief, Suboxone does not work. For opiate addiction, it can work well, except for the expense. It is a very good time to be a heroin dealer. Well done DEA! Educate yourself on addiction!—HEATHER PORTER, PA, Lancaster, Calif. (215-4) Suboxone and methadone are 2 good medicines that are not used according to the purpose for which they should be prescribed. They are money-makers to nonphysician owners and few physicians. Methadone is political, and Suboxone is headed in the same direction. Both drugs are supposed to be used for detoxification, but as the money rolls the medicine rolls. Where is the rehabilitation? Public assistance rehabilitation typically involves groups of 15 who are corralled in a room with their addicted peers sleeping next to them, and the ones who are awake are listening to the same lectures that are more than 50 years old! In private rehabilitation, you can lower doses gradually and let the addicted person leave and eventually relapse several times without ever receiving rehabilitation. And this is not to mention the polysubstance abuse that eventually takes over after time. I assume that it is because of the other medications, prescribed by clinicians, that contribute to addiction and/or death in these patients. Well, if the political elite were to come to us who are on the front line, we can tell them what works when treating substance abuse. This is only the tip of the iceberg. I had to get it off my mind after 25 years of treating addiction and knowing the pros and cons. I have many successful cases, but too few because of the restriction on treatment regimens. Remember, there are other medicines that treat addiction and the lack of real rehabilitation.—RAYMOND SANCHEZ, PA, New York, N.Y. (215-5) n

Claire O’Connell, MPH, PA-C,

Katherine Pereira, DNP, FNP,

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

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

Sherril Sego, FNP-C, DNP,

is an independent consultant in Kansas City, Mo.

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Dermatology Clinic CASE #1

Green discoloration of a dishwasher’s fingernail MELINDA LIU, BA, AND MAURA HOLCOMB, MD

An otherwise healthy 60-year-old dishwasher presents with asymptomatic green discoloration of his right middle fingernail over a period of 2 months. The discoloration began from the distal margin. He denies wearing gloves while working and reports a tendency to pick at his nails when nervous. On examination, distal onycholysis and green discoloration are present exclusively on the right middle nail plate starting from the distal edge without signs of paronychia. Dermoscopy reveals pigment localization under the nail plate. What is your diagnosis? Turn to page 62

CASE #2

An asymptomatic lesion with positive Darier sign TIFFANY SHIH, MD

A healthy 12-month-old infant girl presents with a yellowishorange papule on the right upper extremity. Her mother first noticed this lesion approximately 6 months earlier. It has never bled, ulcerated, or formed blisters. The infant does not scratch the lesion. However, when the lesion is rubbed, it appears to swell and turn bright red. On physical examination, there is a soft, oval-shaped, yellowish papule with a peripheral rim of erythema on the right extensor forearm. What is your diagnosis? Turn to page 63 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2016 61

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Dermatology Clinic CASE #1

Pseudomonas nail infection

Green nail syndrome, also known as chloronychia, is caused by secondary Pseudo monas aeruginosa infection in the setting of nail damage and is characterized by green discoloration of the nail plate.1-3 P aeruginosa is an opportunistic gram-negative bacterium that infects the lungs, urinary tract, soft tissues, skin, and nails, in both immunocompetent and immunocompromised patients.4 Although it is not a component of normal skin flora, P aeruginosa is prevalent in soil and water, and it can colonize moist regions of the skin, axillae, anogenital regions, and retroauricular areas.4 The most common predisposing factors for P aeruginosa nail infection are distolateral onycholysis and proximal chronic paronychia.3 Onycholysis refers to separation of the nail plate from the nail bed in the fingers and toes and most commonly Take-away points for chloronychia Clinical presentation

• Green-black pigmentation restricted to 1 to 2 nails, often in the setting of damaged nails due to onycholysis, chronic paronychia, and chronic exposure to wet environments

Differential diagnosis

• Subungal hematoma, nevi, malignant melanoma, infection with other organisms (Aspergillus, Candida, Proteus sp.)

Diagnosis

• Diagnosed clinically and confirmed by gram stain and culture of ungual fragments • Large, flat, oval colonies with characteristic fruity smell that express pyocyanin when cultured on cetrimide agar medium

Management

• Remove detached nail plate and treat nail bed with antiseptic solution (2%–4% thymol in chloroform or 2% sodium hypochlorite solution) • Topical antibiotics (polymyxin B or bacitracin) applied 2 to 4 times daily for 1 to 4 months, or oral antibiotics (ciprofloxacin) for 2 to 3 weeks if topical treatment fails • Minimize trauma to affected digits and avoid water or irritant environments by wearing cotton gloves under rubber gloves during manual work

occurs due to constant local trauma, especially in the elderly.1 Secondary infection of the onycholytic space occurs when the nails are exposed to warm, moist environments.4 Chronic paronychia refers to nail matrix damage producing an irregular and friable nail plate, which is easily colonized.2 Chloronychia is most common in homemakers, barbers, dishwashers, and medical personnel, and it can be considered an occupationally triggered disease.4 Chloronychia is diagnosed clinically and confirmed by gram stain and culture of the exudate and ungual fragments from the affected nail.1,5 Usually, infection is restricted to

Chloronychia is diagnosed clinically and confirmed by gram stain and culture of the exudate and ungual fragments. one or two nails, and it causes a sudden green or brown appearance of the damaged nail.2 In the setting of onycholysis, P aeruginosa colonizes the subungual space, causing discoloration of one side of the nail.2 Dermoscopy reveals green pigment and localization under the nail plate.2 In the setting of chronic paronychia, pigmentation occurs above the nail plate, typically on one side, and may resemble a band to the naked eye.2 Dermoscopy reveals a bright green color that fades to yellow.2 Gram stain of cuttings of the affected nail results in randomly arranged gram-negative rods.4 Cultures on cetrimide agar result in flat, large, oval colonies that produce the blue-green exopigment, pyocyanin, and the characteristic fruity smell due to production of trimethylamine.4,5 Alternatively, clinicians may collect scrapings from under the affected nail and culture for fungus.5 When fungal culture results are negative, patients are treated empirically for P aeruginosa.5 In summary, green or black discoloration of the nail in the setting of nail trauma should raise suspicion for P aeruginosa infection.3 Other conditions that can produce discoloration include subungual hematomas, which are associated with repetitive trauma and present with extreme pain, malignant melanoma, which often presents as a pigment band along the length of the nail plate, and glomus tumors, which present as bluish discolorations under the fingernails and are associated with pain, especially with cold exposure.5 Patients with chloronychia are treated with removal of the detached nail plate, application of a topical antiseptic

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solution, and use of antibiotics. First, the damaged nail plate should be clipped every 2 weeks until the nail plate grows in normally.6 Occasionally, removal of the entire nail may be indicated.5 Second, topical antiseptic solutions, such as 2% to 4% thymol in chloroform, or 2% sodium hypochlorite solution, should be applied twice daily on the exposed nail bed to prevent infection.4,6 Topical therapies, including silver sulfadiazine, ciprofloxacin, gentamicin, polymyxin B, and bacitracin, are initially applied up to four times daily for up to 4 months.4 If topical therapies fail or are not preferred by the patient, oral ciprofloxacin is prescribed for 2 to 3 weeks.4 In addition, patients must be counseled to avoid trauma to the affected digits, including avoiding aggressive cleaning under the nail plate, wet and irritating environments, and nail cosmetics and artificial nails until 3 months after the onycholysis has resolved.6,7 Treatment is important to prevent transmission of P aeruginosa to wounds or surgical sites, which can result in local and systemic complications in immunocompromised invidiuals.3 The patient described in this case was treated with oral ciprofloxacin and topical application of 2% sodium hypochlorite, and he was counseled to wear cotton gloves under rubber gloves during dishwashing responsibilities. Bacterial infection was cured after 6 weeks of therapy. Melinda Liu, BA, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston. References 1. Zaias N, Escovar SX, Zaiac MN. Finger and toenail onycholysis. J Eur Acad Dermatol Venereol. 2015;29(5):848-853. 2. Piraccini BM, Dika E, Fanti PA. Tips for diagnosis and treatment of nail pigmentation with practical algorithm. Dermatol Clin. 2015;33(2): 185-195. 3. Müller S, Ebnöther M, Itin P. Green nail syndrome (Pseudomonas aeruginosa nail infection): two cases successfully treated with topical nadifloxacin, an acne medication. Case Rep Dermatol. 2014;6(2):180-184. 4. Chiriac A, Brzezinski P, Foia L, Marincu I. Chloronychia: green nail syndrome caused by Pseudomonas aeruginosa in elderly persons. Clin Interv Aging. 2015;10:265-267. 5. Barankin B, Levy J. Dermacase. Can you identify this condition? Pseudomonas aeruginosa infection. Can Fam Physician. 2012;58(10): 1103-1104. 6. Iorizzo M. Tips to treat the 5 most common nail disorders: brittle nails, onycholysis, paronychia, psoriasis, onychomycosis. Dermatol Clin. 2015;33(2):175-183. 7. Bae Y, Lee GM, Sim JH, et al. Green nail syndrome treated with the application of tobramycin eye drop. Ann Dermatol. 2014;26(4):514-516.

CASE #2

Solitary mastocytoma

Mastocytosis describes a group of disorders that involve accumulation of mast cells in the skin and, in some cases, other organs of the body. Clinical presentation can occur at any age, from birth to middle age.1-5 The majority of cases, however, occur before age 2 years.3 These lesions are congenital in up to one-quarter of pediatric cases. There is genetic correlation with c-KIT mutations in adult patients with mastocytosis, and similarly activating c-KIT mutations are found in pediatric cases of mastocytosis. Although this condition usually presents sporadically, familial cases are also reported in the literature.3 Mastocytosis is divided into two forms: cutaneous and systemic. Cutaneous mastocytosis can be categorized into four diagnoses: urticaria pigmentosa, solitary mastocytoma, diffuse cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans.4,5 All of these subtypes can present with vesicular or vesicular variants that are suspected to be due to leakage of histamine or some other mast-cell-associated mediator. Cutaneous symptoms occur when these clusters of mast cells degranulate, releasing histamine, prostaglandin D2, heparin, tryptase, chymase, leukotrienes, and other mediators. This subsequently results in clinical signs and symptoms of flushing, blistering, and pruritus.1-2 Solitary mastocytoma is localized to one single lesion that contains a collection of mast cells in the skin.3 A physical examination, involving a Darier sign test, can assist with diagnosing cutaneous mastocytosis. This involves gently rubbing the affected area with a tongue blade or the blunt end of a pen or pencil to induce urtication. Within a few minutes, there should be localized erythema and urticarial wheals. This reaction may persist for 30 minutes to 1 hour and occasionally result in blistering.1-3 Although this does help confirm the diagnosis, it is possible that patients with mastocytosis will have a negative Darier sign test result.3 Mechanical irritation is not the only potential trigger of mast cell degranulation. Other documented triggers include exercise, heat, hot baths and beverages, cold exposure, stress, and exposure to sunlight. These patients should also avoid certain medications, such as aspirin, some narcotics (morphine), dextromethorphan, nonsteroidal anti-inflammatory

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Dermatology Clinic ointment to be used only when symptomatic, and it is to be used short-term. The parents were counseled to return if new lesions appear. Typically, the prognosis for childhood mastocytosis is favorable; symptoms improve before adulthood in approximately 50% of patients.3 n Tiffany Shih, MD, is a resident physician at the University of Minnesota in Minneapolis. References 1. Ramos-e-Silva M, Ribeiro de Castro MC. Myobacterial infections. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:1221-1242. 2. Hansen’s disease. In: James WD, Berger TG, Elston DM, eds. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Saunders Elsevier; 2011:334-344. 3. Cutaneous tumors and tumor syndromes. In: Paller AS, Mancini AJ, eds. Hurwitz Clinical Pediatric Dermatology. 4th ed. Philadelphia, PA: Elsevier Saunders; 2011:206-209. 4. Briley LD, Phillips CM. Cutaneous mastocytosis: a review focusing on the pediatric population. Clin Pediatr (Phila). 2008;47(8):757-761. 5. Bulat V, Mihic´ LL, Situm M, et al. Most common clinical presentations of cutaneous mastocytosis. Acta Clin Croat. 2009; 48(1):59-64.

drugs, amphotericin B, thiamine, and topical polymyxin. Snakebites, bee stings, jellyfish stings, and iodine-containing contrast media may also trigger mast cell degranulation. In some patients, certain foods are also culprits—most common are strawberries, chocolate, tomatoes, citrus, egg white, ethanol, lobster, and crayfish.3 A diagnosis of solitary mastocytoma can often be made based on cutaneous morphology and presence of a Darier sign. However, atypical presentations can be confirmed by skin biopsy, which reveals a collection of mast cells in the dermis.1-3 Special immunohistochemical stains, such as Giemsa, toluidine blue, or tryptase antibodies, can provide further confirmation.1,2 Typically, solitary mastocytoma does not require further workup due to lack of systemic involvement. However, if the patient develops extensive cutaneous involvement or systemic involvement, other laboratory testing is available, including measurement of serum tryptase levels (a protease produced by mast cells) and urinary histamine levels.3 Because these lesions can urticate spontaneously, mastocytosis may be confused with urticaria. However, these lesions are so characteristic, the differential diagnosis is quite narrow. Of note, lesions such as those seen in urticarial pigmentosa will resolve but leave hyperpigmented macules in their place, which is atypical for urticaria. Occasionally, these may be confused with blistering conditions, since they can form overlying vesicles and bullae. Therefore, the differential diagnosis for blisters in children includes bullous arthropod bites, herpes simplex viral infection, bullous impetigo, autoimmune blistering diseases, epidermolysis bullosa, toxic epidermal necrolysis, and linear immunoglobulin A bullous dermatosis.1 Treatment for mastocytosis is primarily for symptom management. Patients should be counseled about the condition and its possible triggers. Typically, solitary mastocytomas do not require any treatment, especially if they are asymptomatic. For more generalized disease, nonsedating antihistamines, such as cetirizine, loratadine, and fexofenadine, are effective initial treatments. If there is severe or diffuse involvement, classic H1 antagonists, such as hydroxyzine and diphenhydramine, with or without H2 antagonists such as cimetidine, ranitidine, or famotidine for flushing and gastrointestinal symptoms, can also be helpful. Mastocytomas can also improve or resolve with a potent topical corticosteroid under occlusion, especially if these lesions are itchy or begin to form vesicles or bullae.1,2 In our case, given the localized involvement and lack of symptoms, the patient was prescribed topical triamcinolone

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Dermatologic Look-Alikes Papules on the mid-face OMAR MERCHANT, BS, AND MAURA HOLCOMB, MD

CASE #1

CASE #2

An 18-year-old African-American woman presents for evaluation and removal of lesions on her face. The patient says that the lesions began to develop years ago and have increased in number. They have been asymptomatic. The patient reports no fever, chills, or weight loss. Her medical history is negative for seizures and cancers. Her family history includes similar asymptomatic lesions on her mother’s nose, nasolabial folds, and scalp. On physical examination, the patient has multiple, 2- to 3-mm round, firm, skin-colored papules on her face, particularly on the malar cheeks and nasal dorsum, as well as on the scalp.

A 54-year-old Hispanic woman presents for an evaluation of lesions that have developed on her face. The asymptomatic lesions began to develop years ago, and they have increased in number and size. The patient reports no fever, chills, or weight loss. Her medical history is negative for shortness of breath, vision changes, seizures, and palpitations. Her family history is noncontributory. On physical examination, the patient has multiple, 5- to 7-mm round, firm, erythematous papules on her face, particularly on the nose. No other lesions were noted.

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Dermatologic Look-Alikes CASE #1

Brooke-Spiegler syndrome

Brooke-Spiegler syndrome is an autosomal dominant disease causing cutaneous adnexal tumors. Patients present with small, skin-colored papules distributed in the head and neck region. Lesions initially present in late childhood or early adulthood and increase in size and number. Girls and women are affected twice as commonly as boys and men.1 These tumors are typically benign cylindromas, trichoepitheliomas, and spiradenomas, but patients can also develop parotid basal cell adenomas, milia, organoid nevi, and basal cell carcinomas.1 Cylindromas and spiradenomas are tumors of the apocrine and eccrine sweat glands, respectively, and trichoepitheliomas are tumors of the hair follicle. Brooke-Spiegler syndrome overlaps clinically with multiple familial trichoepithelioma and familial cylindromatosis, all of which are dominantly inherited disorders that cause benign adnexal tumors, and share a common defect in the CYLD gene. Although multiple familial trichoepithelioma is characterized by trichoepitheliomas and familial cylindromatosis is characterized by cylindromas, Brooke-Spiegler syndrome is characterized by cylindromas, spiradenomas, and trichoepitheliomas, as well as follicular cysts and milia. Considering the rare nature of Brooke-Spiegler syndrome, the incidence and prevalence of the disease is unknown. Although adnexal tumors are typically benign, each class also has a rare but malignant form. It is critical that benign tumors are monitored, as their malignant counterparts have poor outcomes.2 Malignant transformation of cylindromas and spiradenomas into carcinomas and sarcomas can occur as part of Brooke-Spiegler syndrome, whereas trichoepitheliomas can give rise to basal cell carcinomas. In rare cases, cylindromas transform into malignant cylindrocarcinomas, which grow rapidly while discoloring, ulcerating, and bleeding. Special consideration must be given to spiradenomas, due to the potential of malignantly transformed spiradenomas to metastasize.1 Specifically, enlargement, color changes, and pain warrant evaluation for malignant spiradenocarcinoma.2 Additionally, patients with Brooke-Spiegler syndrome can also develop adenocarcinoma of the salivary glands.3 Cylindromas are pink, firm, rubbery tumors predominantly found on the scalp, whereas trichoepitheliomas occur on the nose and upper lips, and in the nasolabial folds. Extensive

development of cylindromas on the scalp are called “turban tumors,” and these are associated with alopecia, or hair loss.1 Histologically, cylindromas are characterized by islands of tumor cells in the dermis that are arranged in close proximity to one another in a “cobble stoning” manner on a background of hyalinized stroma; stain results are positive for periodic acid-Schiff and are type IV collagen reactive.2 Each island has large, central cells with pale nuclei, surrounded by smaller palisading peripheral cells with dark basophilic nuclei. Malignant forms of cylindromas—cylindrocarcinomas—will lose the characteristic jigsaw pattern and island arrangement

Brooke-Spiegler syndrome is an autosomal dominant disease characterized by small, skin-colored papules on the head and neck. with focal necrosis.2 Spiradenomas are multilobular, sharply demarcated growths found in the deep dermis and subcutis, often with a fibrous capsule.2 The lobules are basophilic and have cords of epithelial cells that consist mostly of nuclei and little cytoplasm. Cystic structures may also form in the lobules. Malignant spiradenocarcinomas exhibit increased mitotic rates, necrosis, atypia, and pleomorphism; they also show loss of lobular growth pattern.2 Brooke-Spiegler syndrome, multiple familial trichoepithelioma, and familial cylindromatosis arise from mutations in the CYLD gene on chromosome 16q12-q13, which normally deubiquitinates target proteins and negatively regulates nuclear factor κB (NF-κB) activation. Wild-type CYLD promotes apoptosis through regulation of NF-κB, preventing uncontrolled cellular proliferation. In Brooke-Spiegler syndrome, the mutated CYLD gene is unable to suppress NF-κB activity, which subsequently results in uncontrolled growth and, ultimately, development of adnexal neoplasms. NF-κB is an inducible transcription factor with roles in inflammation and oncogenesis, and activation of NF-κB has been associated with a variety of neoplasms.3,4 The differential diagnosis for numerous firm skin-colored papules on the face should include Cowden syndrome, tuberous sclerosis, Birt-Hogg-Dubé syndrome, Rombo syndrome, and basaloid follicular hamartoma syndrome.5 Benign lesions arising from Brooke-Spiegler syndrome do not need to be treated, except for cosmetic reasons. Treatment of adnexal tumors ranges widely and includes Continues on page 75

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Dermatologic Look-Alikes Neoplasms in Brooke-Spiegler syndrome Basal cell carcinoma

Sarcoma

Carcinoma

Spiradenoma

Cylindroma

Trichoepithelioma

excision, dermabrasion, electrodessication, and cryotherapy, in addition to the use of lasers (CO 2 and argon).1 Erbium:yttrium aluminum garnet (Er:YAG) laser treatment can be used to ablate trichoepitheliomas but should not be performed on cylindromas, as histologic assessment due to malignant potential is necessary. New lesions can arise with ablative treatments, although it is still favorable for cosmetic purposes, due to minimal scarring.1 After counseling the patient about monitoring her lesions, 2 lesions under the nose were electrodessicated for cosmetic reasons. The patient was educated on inheritance pattern and disease course and was advised to schedule biannual skin checks.

CASE #2

Sarcoidosis

Sarcoidosis is a disease affecting multiple organ systems and characterized by the for mation of noncaseating epithelioid granulomas. Although the inciting cause is still unknown, granulomas result from T-cell recognition of antigens by macrophage presentation, triggering a cellular immune response, and lymphocytic and mononuclear phagocytic infiltration.6 Disease progression results in a mass effect, causing dysfunction of surrounding tissue. Prevalence of the disease in the United States ranges from 10:100,000 to 40:100,000. The disease typically presents in the third and fourth decades of life, and it is more common in women.7 Skin manifestations of the disease are present in up to one in every four patients, most frequently at disease onset. Thus, any granulomatous skin lesions without known cause should be evaluated for systemic sarcoidosis. However, the presence or absence of cutaneous disease has not been found to correlate with prognosis or extent of disease.6

Cutaneous sarcoidosis can be present in various forms, including papules, maculopapules, nodules, plaques, subcutaneous nodules, lupus pernio, or infiltrative scars. The most common form is maculopapular.8 Skin lesions are divided into specific (granulomatous) or nonspecific (reactive with no granulomas). Papular sarcoidosis presents most commonly around the eyelids and nasolabial folds, and it typically resolves with minimal scarring. Maculopapular lesions are found on the neck and below, and they are associated with acute organ disease. Plaque sarcoidosis is associated with chronic disease, with lesions found on the face and extensor surfaces of the extremities, back, and buttocks.7 Lupus pernio presents with coalescing chronic indurated lesions on the face, often with telangiectasias and disfigurement. Local spread can damage the upper airway and nasal cavity. Lupus pernio is often resistant to therapy and is temporally associated with organ involvement.7 Other diseases to consider on the differential diagnosis for these lesions include infectious, autoimmune, or foreign-bodyrelated causes. Syphilis, leprosy, and atypical mycobacteria can all present with widespread lesions as well. Autoimmune disorders such as lupus vulgaris, lupus disseminatus faciei, and metastatic Crohn disease can have similar lesions.6 Although no diagnostic test exists for sarcoidosis, biopsy confirmation of lymph nodes, skin, or salivary glands with noncaseating granulomas without foreign bodies, and negative tissue culture results, are necessary to exclude other potential etiologies.6 Angiotensin-converting enzyme levels are elevated in 60% of patients with sarcoidosis, and can aid in diagnosis.9 Sarcoid histology is characterized by distinct, necrosis-free islands of epithelioid cells with giant cells. Epidermal histology in cutaneous lesions shows hyperkeratosis, acanthosis, parakeratosis, and epidermal Âatrophy,

Sarcoidosis affects multiple organ systems and is characterized by the formation of noncaseating epithelioid granulomas. leading to the variety of lesions described. Epidermal atrophy likely results from a reaction to growth of dermal granulomas, as indicated by the presence of a normal zone between the granulomas and the epidermis.10 Once suspected, evaluation of pulmonary, ocular, neurologic, and cardiac systems is warranted. Baseline chest radiographs and pulmonary function test results should be obtained, in addition to an electrocardiogram, echocardiogram, complete

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Dermatologic Look-Alikes serum chemistry panel, urine analysis, complete blood count, and tuberculosis screening.9 Once diagnosis is confirmed, patients undergoing treatment should be seen twice a year; if they do not require treatment, they should be seen once a year. During visits, lesions should be monitored, and systemic symptoms should be evaluated with a focus on respiratory, ocular, and cardiac symptoms. Any abnormal findings warrant further investigation and referral to indicated specialists.6 Treatment of cutaneous sarcoidosis focuses on limiting disfigurement and symptoms. Topical therapy includes high potency corticosteroids, often applied with occlusive dressing.6 Monthly intralesional injections of triamcinolone acetonide (5–10 mg/mL) or chloroquine (50 mg/mL) is also an option. Additionally, procedures such as dermabrasion, excision, and grafting for ulcerative lesions, and plastic surgery for lupus pernio, are available.6 Oral therapies are reserved for large, refractory lesions or generalized eruptions. Prednisone, hydroxychloroquine, chloroquine, allopurinol, methotrexate, thalidomide, isotretinoin, and psoralen plus ultraviolet A (PUVA) therapy have all proven to be effective.6 Systemic corticosteroids are first-line therapies in these cases and should be tapered to the minimal dose necessary for relapse prevention.7 Patients requiring 10 mg of prednisone daily should be considered candidates for corticosteroid-sparing agents. Methotrexate is

frequently given for corticosteroid-resistant lesions. Tumor necrosis factor-α (TNF-α) plays a pivotal role in granuloma formation and has led to the use of targeted therapies such as infliximab, a chimeric monoclonal anti-TNF-α antibody, which has shown efficacy in severe cases.7 A total of 60% of patients with sarcoidosis have spontaneous resolution within 2 to 5 years, and an additional 10% to 20% of cases will resolve with corticosteroids. The disease can also progress to fibrosis, which is irreversible.7 Overall, prognosis of cutaneous manifestations is tied to the degree of systemic disease.6 In our case, this patient was evaluated and oral prednisone was initiated, beginning with 20 mg daily and tapering to 5 mg daily over the course of 1 month. Additionally, baseline chest radiograph, pulmonary function test, complete blood count, and chemistry panel results were obtained. A 1-month follow-up was scheduled to evaluate treatment response and discuss results from laboratory and imaging studies. n Omar Merchant, BS, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston. References 1. Rallan D, Harland CC. Brooke-Spiegler syndrome: treatment with laser ablation. Clin Exp Dermatol. 2005;30(4):355-357. 2. Storm CA, Seykora JT. Cutaneous adnexal neoplasms. Am J Clin Pathol.

Morphologic subtypes of sarcoidosis7

2002;118(suppl):S33-S49. 3. Young AL, Kellermayer R, Szigeti R, et al. CYLD mutations underlie

Lesion

Location

Prognosis

Atrophic/ulcerative

Traumatic wounds

Requires systemic therapy

Erythema nodosum

Shins

Associated with transient, self-limiting disease

4. Blake PW, Toro JR. Update of cylindromatosis gene (CYLD) mutations in

Lupus pernio

Nose and cheeks

Disfiguring lesions, recalcitrant to systemic steroids; indicator of organ damage

in cell signaling. Hum Mutat. 2009;30(7):1025-1036.

Neck, trunk, extremities, and mucous membranes

Acute organ involvement common; favorable prognosis

J Am Acad Dermatol. 2003;49(4):698-705.

Face (eyelids and nasolabial folds)

Favorable; minimal scarring

7. Haimovic A, Sanchez M, Judson MA, Prystowsky S. Sarcoidosis: a com-

Back, buttocks, face, and extensor surfaces of extremities

Associated with chronic disease

Maculopapular

Papular Plaque

Brooke-Spiegler, familial cylindromatosis, and multiple familial trichoepithelioma syndromes. Clin Genet. 2006;70(3):246-249. Brooke-Spiegler syndrome: novel insights into the role of deubiquitination 5. Vincent A, Farley M, Chan E, James WD. Birt-Hogg-Dubé syndrome: a review of the literature and the differential diagnosis of firm facial papules. 6. English JC 3rd, Patel PJ, Greer KE. Sarcoidosis. J Am Acad Dermatol. 2001;44(5):725-743. prehensive review and update for the dermatologist: part I. Cutaneous disease. J Am Acad Dermatol. 2012;66(5):699.e1-699.e18. 8. Mañá J, Marcoval J, Graells J, et al. Cutaneous involvement in sarcoidosis. Relationship to systemic disease. Arch Dermatol. 1997;133(7):882-888.

Scar

Surgical scars, tattoos, Increased incidence of piercings, traumatic wounds systemic disease

Subcutaneous

Upper extremities

Associated with systemic disease

9. Haimovic A, Sanchez M, Judson MA, Prystowsky S. Sarcoidosis: a comprehensive review and update for the dermatologist: part II. Extracutaneous disease. J Am Acad Dermatol. 2012;66(5):719.e1-719.e10. 10. Okamoto H. Epidermal changes in cutaneous lesions of sarcoidosis. Am J Dermatopathol. 1999;21(3):229-233.

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Stat Consult

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

Description

Allergic rhinitis

• presence of more than 1 of nasal congestion, rhinorrhea, sneezing, and itching • 12th most common diagnosis in family physician visits Types

BY ALAN DRABKIN, MD

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

• seasonal allergic rhinitis (SAR, hay fever) ——common aeroallergen triggers in USA include ■■ grasses (timothy, Bermuda) ■■ outdoor mold spores ■■ weeds (ragweed) ■■ trees (birch, oak, maple, mountain cedar) • perennial rhinitis ——common triggers include ■■ dust mite ■■ indoor molds ■■ animal dander ■■ pollen in some climates ■■ occupational allergens • episodic rhinitis (occasional exposure) • mixed rhinitis (presence of both AR and non-AR) affects 44% to 87% of patients with AR Likely risk factors

• family history of atopy • serum IgE > 100 units/mL < age 6 years • higher socioeconomic class • atopy • air pollution • maternal AR and intranasal corticosteroid use during pregnancy Possible risk factors

• smoking • FLG mutation Complications of allergic rhinitis include sinusitis and conjunctivitis.

Factors not associated with increased risk

• infant vaccinations • pet ownership < age 2 years • antibiotic use before age 5 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • SEPTEMBER 2016 77

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Stat Consult • introduction of solid foods before age 4 months • recurrent otitis media

• Social history (SH) ——occupational exposure ——presence of mold and water damage in home

Factors associated with reduced risk

• early and long-term exposure to stables and farm milk Associated conditions

• other atopic disease ——asthma ——atopic dermatitis ——allergic conjunctivitis • nasal polyps • sinusitis • sleep apnea • atherosclerosis • oral allergy syndrome • otitis media with effusion Causes

• aeroallergens Pathogenesis

• biphasic IgE type I allergic inflammatory mediator response to aeroallergens ——immediate response (within minutes of exposure, peaks at 15 to 30 minutes) ■■ release of mediators from mast cells »»preformed (such as histamine, tryptase, chymase, kininogenase, heparin) »»newly formed mediators, such as prostaglandins ——late phase response (starts 4 to 8 hours after exposure, release of cytokines and leukotrienes) History

• Chief concern (CC) ——sneezing, rhinorrhea, nasal congestion ——copious rhinorrhea and sneezing within minutes of exposure to allergen ——nasal congestion (later) • Medication history ——assess response to past medications • Family history (FH) ——assess family history of ■■ atopic disorders ■■ chronic sinus complaints or infections, or recurrent bronchitis

Physical

• HEENT ——nasal findings ■■ pale or bluish boggy nasal mucosa (edematous turbinates covered with thin clear secretion) ■■ nasal airway obstruction ■■ transverse nasal crease (“allergic crease” due to “allergic salute” of hand pushing nose up) ——throat findings ■■ postnasal mucous discharge ■■ tonsillar hypertrophy ■■ cobblestoning (lymphoid hypertrophy of posterior pharynx) ——mouth breathing (nasal obstruction) ——eye exam may show ■■ “allergic shiners” (infraorbital venous congestion) ■■ conjunctival injection and swelling ■■ tearing ■■ Dennie lines on eyelids (Dennie-Morgan folds) ——tympanic membrane dullness ——rarely high arched palate, overbite malocclusion (adenoid facies) Making the diagnosis

• diagnosis usually based on history and exam ——typical history includes ■■ nasal symptoms ■■ seasonal or perennial symptom pattern ■■ identification of precipitating factors such as exposure to dust, pollen, or animal dander ■■ identification of coexisting atopic conditions ——physical findings may be slight or absent • history may elicit enough information to justify presumptive treatment Causes of nonallergic rhinitis

• vasomotor • gustatory • nonallergic rhinitis with eosinophilia syndrome (NARES) • atrophic

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»»dust mite covers for bedding »»humidity control »»high efficiency particulate air (HEPA)

• drug-induced • rhinitis medicamentosa (topical decongestants or cocaine) • infectious • hormonal • pregnancy

vacuuming of carpeting

»»acaricides ■■

hot water

Complications

»»remove carpeting, feather pillows, upholstered

• sinusitis • conjunctivitis • sleep apnea/poor sleep • high arched palate • dental malocclusion • school absenteeism • impaired cognitive functioning

furniture; especially in bedroom

»»keep clothes off bedroom floor »»dust frequently with damp cloth »»ban furred pets from bedroom (or from home) »»use double-bag vacuum bags

• in most children, may persist >10 years • in adults mostly chronic with variable severity Testing

• diagnostic testing ——rarely needed for making initial treatment decisions for most adults ——may be useful for ■■ patients with uncertain diagnosis ■■ perceived need for objective confirmation • testing for specific triggers to confirm diagnosis of AR or aid management decisions ——skin testing ——specific IgE blood testing • other diagnostic tests occasionally needed ——nasal smears for eosinophils ——beta-2 transferrin (sensitive for confirming CSF rhinorrhea) ——sleep study ——pulmonary function test • other testing in children may include ——immune studies ——sweat test ——sinus CT ——nasal endoscopy • allergen avoidance ——dust mite avoidance ■■ clinically effective avoidance includes combination of

pollen allergen avoidance »»keep windows closed »»stay indoors on high-pollen days if highly allergic »»do not dry clothes outside »»shower at bedtime ——reduce indoor fungal exposure (may require removal of moisture sources and replacement of contaminating materials) ——cockroach elimination measures may include ■■ careful sanitation of infested areas ■■ not allowing food to stand open or remain on unwashed dishes or countertops ■■ storage of garbage in tightly sealed containers ■■ use of roach traps ■■ insecticide application by professional exterminator if heavy infestation ——animal avoidance (most effective, but may take 4 to 6 months for home to clear of allergens) ■■

Prognosis

Treatment

other common recommendations include

»»wash pillows and bed sheets regularly in

Medications

• intranasal corticosteroids ——most effective medication class ——more effective than combination of antihistamine and leukotriene antagonist in treatment of seasonal AR ——may be used as-needed (less effective than continuous use) • other medications ——intranasal antihistamines ■■ equal or superior to oral second-generation antihistamine ■■ can be considered first-line treatment ——oral antihistamines (second-generation preferred)

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Stat Consult ——oral and topical decongestants (use with caution in specific clinical situations) ——oral leukotriene receptor antagonists alone, or in combination with antihistamines ——intranasal cromolyn ——anticholinergics (ipratropium or atropine sulfate nasal spray) may reduce rhinorrhea but not other nasal symptoms • other therapies ——nasal saline irrigation (alone or as adjunct) ——butterbur ——acupuncture (limited evidence for prevention or treatment) ——homeopathic preparations ( especially for ocular symptoms) ——herbal medicines with some efficacy for allergic rhinitis include ■■ combination of Cinnamomum zeylanicum, Malpighia glabra, and Bidens pilosa ■■ Astragalus membranaceus ■■ Bu-zhong-yi-qi-tang (a Chinese medicine) • other nasal therapies ——petrolatum application to nares 4 times daily ——rhinophototherapy ——intranasal non-inhaled CO2 • immunotherapy ——subcutaneous (“allergy shots”) ■■ variable reduction of symptoms ■■ consider if specific IgE antibodies to clinically relevant allergens present ■■ fexofenadine pretreatment may prevent severe systemic reactions ——sublingual ■■ FDA-approved therapies include »»Timothy grass pollen allergen extract »»Sweet Vernal, Orchard Perennial Rye, Timothy and Kentucky bluegrass mixed pollens allergen extract »»Short ragweed pollen allergen extract n

KEEP UP-TO-DATE Find clinical reviews of many common conditions by visiting our Stat Consult online library at:

ClinicalAdvisor.com/Stat-Consult

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“Are you married to the name?”

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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 • SEPTEMBER 2016 81

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LEGAL ADVISOR CASE

A patient’s positive hepatitis B results were overlooked for 7 years.

ANN W. LATNER, JD

In the late fall of 2013, when nurse practitioner Ms R, aged 56 years, was notified about a lawsuit involving one of her patients, she was dismayed but not surprised. She had been expecting it since that day this past March when she realized that she had neglected to tell the patient that he had tested positive for hepatitis B … in 2006. Ms R had been working for a veterans’ medical center for more than 20 years. Her duties were varied and included seeing her own patients and going over medical results with patients. Because Ms R had been working at the medical center for so long, some of her patients had been with her for many years. One of these patients was Mr H, a 52-year-old veteran. Mr H had been coming to the medical center since 2002, and he had been seeing Ms R since 2006, which was the first year that she was assigned to go over his test results with him. She did not remember much of that first meeting—it was 7 years ago—but she had noted in the file that she told him his blood test results were normal. She saw the patient again in 2008, 2009, and 2010, but never looked back at the 2006 test

A dispute occurs about whether a patient’s untreated positive hepatitis B status led to his developing liver cancer.

results, which had indicated that the patient had tested positive for hepatitis B. This was not surprising. The medical center was busy and understaffed, and Ms R was responsible for many patients. She rarely had the time to look at old test results unless there was an obvious problem. However, in March 2013, when Mr H returned to the medical center and Ms R was looking through his records, she discovered that the 2006 lab results had information that she had neglected to convey to the patient. Ms R’s heart sank as she looked at the report. Had she noticed it 7 years earlier, she would have ordered followup tests and referred the patient to a specialist. Now, years had passed without treatment and without an appropriate explanation. Mr H was sitting in the exam room, looking at the clinician expectantly. Continues on page 84

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.

82 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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LEGAL ADVISOR “Everything okay?” he asked. “I’m afraid I owe you an apology,” Ms R began. “I realize that you tested positive for hepatitis B in 2006 and that information wasn’t conveyed to you … I should have recommended further testing at that point. I honestly don’t know why I didn’t see this in 2006 … It was a terrible oversight, and I am so very sorry about it.” The patient looked concerned. “What does this mean?” he asked. “What happens now?” Ms R informed Mr H that she would order more tests and provide a referral to a specialist for further treatment, as she should have in 2006 when he first tested positive.

Ms R saw the patient year after year but never looked back at his prior results or went over his prior lab work for 7 years. Unfortunately, lab tests and scans performed in March and April showed that Mr H had a mass in his liver. Further testing revealed the mass to be hepatocellular cancer, which had spread to the patient’s lungs. Mr H was admitted to the hospital and given radiation therapy, but he succumbed to the disease by the summer. By late fall, Mr H’s widow had consulted with a plaintiff’s attorney and had instituted a lawsuit against the medical center, based on Ms R’s treatment of Mr H. When Ms R was notified about the lawsuit, she was unhappy but not surprised. She knew she had made a mistake. The defense attorney representing the medical center spoke to Ms R to get the facts. Ms R was hoping that the case would settle so she could avoid having to testify, but the defense attorney had ideas about challenging the case legally. “I’m going to make a motion asking the court for summary judgment,” the attorney told Ms R. “That means I am asking the court to dismiss the case before it ever goes to trial, because the plaintiff has not introduced any evidence that the liver cancer was caused by the failure to treat the hepatitis B. I am also asking the court to exclude the proposed testimony from their nurse practitioner expert because she has never practiced in this state.” The defense attorney filed the summary judgment motion and challenged the expert witness who was going to testify that Ms R had breached the standard of care by not conveying her patient’s lab results to him. The court considered the motions and ruled that the summary judgment motion was

not appropriate and that the expert, despite never practicing in that particular state, would be allowed to testify as to what Ms R’s standard of care should have been. The case was sent back to the lower court and is pending trial. Legal background

Summary judgment is a decision by a judge, based on a party’s motion, that decides in favor of one party in a lawsuit without having a trial. Summary judgment can only be used in cases where there is no dispute as to the material facts, and the case can be solely decided on just the law. Summary judgment can resolve the entire case, or just certain issues. The party who asks for summary judgment generally does so to avoid the expense and time-sink of a trial, and many cases are resolved prior to trial this way. However, summary judgment is never appropriate when there are disputes as to the material facts of the case. In this case, there was clearly a dispute as to whether the untreated positive hepatitis B status led to Mr H’s liver cancer. This issue could not be determined by the court without a full trial, including medical expert testimony. Therefore, the court properly denied the summary judgment motion and sent the case back for trial. The court also held that an expert witness does not have to practice in the same state in order to be qualified to testify as to the standard of care. “The procedures at issue here are so commonplace that the same standard of care applies locally and nationally,” stated the court. Protecting yourself

Missing the positive hepatitis B result in 2006 was a bad oversight on Ms R’s part, but it was compounded by the fact that she saw the patient year after year and never looked back at his prior results, or went over his prior lab work, until she discovered her error in 2013. Even if she had missed the result the first year, there was no excuse for so much time to go by before she reviewed the patient’s file carefully. Rather than just tell a patient, “Your results are normal,” consider going through all the lab results with the patient. There is a better chance of catching an error of this sort if you are going line by line. Also, compare new lab work with prior results. Had Ms R done this, she would have caught her error long before 7 years had passed. While the end result might not have changed for Mr H, it would have put Ms R in a far better position to defend herself. n Ms Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, N.Y.

84 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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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.

Inulin

High in fiber, inulin is a collective term for a large group of complex carbohydrates that are found in nature, including a wide variety of fruits, vegetables, and herbs. Tasteless and odorless, inulin blends easily with fiber compounds as well as other nutrients. Inulin has been mentioned frequently as a component of nutritional supplements that claim to be weight loss aids. Because of its high physiologic utility, inulin is considered a “functional food” and is on the US Food and Drug Administration’s list of Generally Recognized as Safe products.1 Most inulin is extracted from the chicory root.

Background

Science

Inulin is composed of large numbers of fructose molecules— up to several thousand strung end to end.2 A soluble dietary fiber, inulin is found in more than 36,000 plant species around the world,3,4 but most inulin is extracted from the chicory root. It has no color and no odor, and it has little taste. Inulin exerts substantial prebiotic actions. It has been shown to stimulate growth of the Bifidobacterium species and Lactobacillus species both in vitro and in vivo, likely as a result of the low-level fermentation that occurs in the gut.5,6 Because of this action and its fiber component, inulin is beneficial for the maintenance of gut microflora, for maintenance of blood glucose and lipid homeostasis, and for immunomodulation.5 In addition, inulin has become the gold standard for measuring glomerular fi ltration rate because of its ability to resist enzyme degradation and reabsorption in the renal tubules.7

Inulin has shown promise in weight reduction as a strategy for those with prediabetes. Researchers randomly assigned 44 subjects to either inulin or plain cellulose supplementation8 and monitored them for weight loss as well as intrahepatocellular and intramyocellular fat and glucose levels. Although both groups lost nearly the same amount of weight by week 9, subjects taking inulin continued to lose weight throughout the following 9 weeks. The percentage of body fat reduced was nearly 3 times greater in the inulin group than in the cellulose group at the end of 18 weeks, and intrahepatocellular lipid levels in the inulin group were reduced nearly 5 times the rate found in the cellulose group.8 In another report, the influence of prebiotics and inulin on bowel movements was studied.9 A group of 38 women who underwent intra-abdominal radiation following surgery for gynecologic cancer was randomly assigned to receive either Continues on page 88

86 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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Accreditation Boston University School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Boston University School of Medicine designates this activity for a maximum of 2 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Continuing Nursing Education Provider Unit, Boston University School of Medicine is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. CNE Contact Hours: 2, all of which is pharmacology credit worthy. Disclosure This educational activity is supported by an independent educational grant from the ER/LA Opioid Analgesic REMS Program Companies. Please see http://ce.er-la-opioidrems.com/IwgCEUI/ rems/pdf/List_of_RPC_Companies. pdf for a listing of the member companies. This activity is intended to be fully compliant with the ER/ LA Opioid Analgesic REMS education requirements issued by the US Food & Drug Administration.

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ALTERNATIVE MEDS UPDATE placebo (maltodextrin) or a prebiotic with inulin and fructo-oligosaccharide.9 Patients reported the number of bowel movements per day, the consistency of the bowel movements, and a self-rating of the quality-of-life indicators of insomnia and diarrhea. At the end of the study, which lasted from before beginning radiation therapy to 3 weeks after the last treatment, patients on the prebiotic formulation reported significantly improved scores regarding the number of days of watery stool, compared with the placebo group. The highest scores for quality of life measures were for insomnia and diarrhea in the placebo group but only for insomnia in the treatment group. Inulin has also been shown to enhance calcium absorption in the gut, thereby aiding with bone mineralization.10 However, results of short-term studies have been inconsistent. In one, researchers studied the long-term effect of inulin supplementation on bone mineralization in prepubertal teens. One group received inulin-type fructan supplementation, and the control group received maltodextrin placebo. At the end of one year, the fructan group showed significantly higher bone mineralization than the placebo group.10

Safety, interactions, side effects

The dose can be increased as tolerated over several weeks to a maximum of 20 to 30 grams per day. The cost is variable depending on the form but averages approximately $20 per month’s supply.

Summary

Inulin has shown promise in weight reduction for patients with prediabetes.

Inulin has been shown to enhance calcium absorption in the gut, thereby aiding with bone mineralization.

Not often does a natural food substance come along that is adaptable, palatable, and affordable, and has basically no downside. Whether the need is weight loss, diabetes management, intrahepatic fat reduction, or bowel function management, inulin can be a valuable additive to any current regimen. n References 1. Rulis AM. Agency Response Letter GRAS Notice No. GRN 000118. http://www.fda.gov/Food/ IngredientsPackagingLabeling/GRAS/NoticeInventory/ ucm153932.htm. Published May 5, 2003. 2. Inulin. NutrientsReview.com. http://www.nutrientsreview.com/carbs/soluble-fiber-inulin.html. 2016. 3. Niness KR. Inulin and oligofructose: what are they? J Nutr. 1999;129(7 Suppl): 1402S-1406S. 4. Mensink MA, Frijlink HW, van der Voort Maarschalk K, Hinrichs WL. Inulin, a flexible oligosaccharide. II: Review of its pharmaceutical applications. Carbohydr Polym. 2015;134:418-428. 5. Boeckner LS, Schnepf MI, Tungland BC. Inulin: a review

Because inulin itself is not specifically a single entity, its safety is viewed in the context of the plant containing it. Consequently, allergic reactions to plants with high inulin content are possible but rarely reported. There are no documented interactions. Side effects are dosedependent; the most common side effects are bloating and excessive flatus.

How supplied, dose, cost

of nutritional and health implications. Adv Food Nutr Res. 2001;43:1-63. 6. Schaafsma G, Slavin JL. Significance of inulin fructans in the human diet. Comprehensive Reviews in Food Science and Food Safety. 2015;14(1):37-47. 7. Franck A. Technological functionality of inulin and oligofructose. Br J Nutr. 2002;87(Suppl 2):S287-S291. 8. Guess ND, Dornhorst A, Oliver N, Bell JD, Thomas EL, Frost GS. A randomized controlled trial: the effect of inulin on weight management and ectopic fat in subjects with prediabetes. Nutr Metab (London). 2015;12:36. 9. Garcia-Peris P, Velasco C, Hernandez M, et al. Effect of inulin and fructo-oligosaccharide on the prevention of acute radiation enteritis in patients with gynecological cancer and impact on quality of life: a randomized, double-blind, placebo-controlled trial. Eur J Clin Nutr. 2016;70(2):170-174. 10. Abrams SA, Griffin IJ, Hawthorne KM, et al. A combination of prebiotic short- and long-chain inulin-type fructans enhances calcium absorption and bone mineralization in young adolescents. Am J Clin Nutr. 2005;82(2):471-476.

The food source with the highest inulin content is chicory root. A serving of 3.5 ounces of this plant contains as much as 48 grams of pure inulin. Chicory root is the main source of commercially prepared inulin in the United States. Inulin is often paired with other supplements such as psyllium fiber for constipation relief. To determine individual tolerance to inulin, starting with a low dose of 2 to 3 grams per day is recommended. 88 THE CLINICAL ADVISOR • SEPTEMBER 2016 • www.ClinicalAdvisor.com

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