October 2018 Clinical Advisor

A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS

Community paramedics contribute to effective and efficient healthcare utilization.

PAGE 60

NEWSLINE

■ Meningococcal vaccine ■ Dairy consumption, CVD ■ Otitis media LEGAL ADVISOR

NP faulted for patient care via fax

DERMATOLOGY CLINIC

Red-brown papules on the extremities

FEATURE

Current guidelines for management of low back pain

|

OCTOBER 2018

| www.ClinicalAdvisor.com

CME: CASE CHALLENGE

Psoriasis and Hodgkin’s Lymphoma Approximately 2% to 3% of the global population is affected by psoriasis.

Vice President, content, medical communications, editor Kathleen Walsh Tulley editor@clinicaladvisor.com Associate editor Madeline Morr Assistant editor Rita Aghjayan 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 manager Krassi Varbanov Assistant manager, audience development Ashley Noelle Director of audience insights Paul Silver National accounts manager Alison McCauley, 973.224.6414 alison.mccauley @ haymarketmedical.com Publisher Kathleen Hiltz, 201.774.1078 kathleen.hiltz@haymarketmedia.com General manager, medical communications Jim Burke, RPh President, medical communications Michael Graziani 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.

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Unsure about a diagnosis or treatment?

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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.

OUR CO

NSULTA

PEARLS

NTS

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

AdvisorForum_

CA0915

SOR • SEPTE

MBER 2015

Abimbo la Farinde

, PhD,

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

• www.Clinic

alAdvisor.c

om

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.

.indd 62

9/29/15

2:44 PM

E-MAIL editor@clinicaladvisor.com

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 5

CONTENTS OCTOBER 2018

NEWS AND COMMENT

12 Knowledge about MenB vaccine lacking

12 Newsline ■ Many PCPs Unfamiliar With MenB Vaccine, Disease ■ GU Syndrome of Menopause Consensus Statement ■ Dairy Intake Linked to Reduced CVD, Mortality Risk ■ Short-Course Oral Steroids Ineffective for Otitis Media ■ Discharge Directly From ICU Safe and Cost-Effective ■ Labor Induction May Be Beneficial in Women With Chronic Hypertension ■ Thyroid Dysfunction Not Associated With HIV Status ■ TID, Poor Glycemic Control Linked to Infection 60 Commentary The Community Paramedic Model: Bridging the Healthcare Gap

30 Vaginal foreign body in the ED

FEATURES 23 Current Guidelines for Management of Low Back Pain An estimated 31 million Americans will experience low back pain at some point in their lifetime.

49 Asymptomatic hyperpigmented plaques

30 Clinical Case Challenge: A Zebra in the Emergency Department Many cases of vaginal foreign body are unusual and often difficult to detect.

Continues on page 8

57 NP faulted for negligence for using fax

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CONTENTS OCTOBER 2018

FEATURES (cont’d) Psoriasis and Hodgkin’s Disease This case discusses the relationship between psoriasis, Hodgkin’s lymphoma, and anti-tumor necrosis factor therapy.

THE CLINICAL ADVISOR • SEPTEMBER 2018

CME Case Study: A 49-year-old Woman With

THE CLINICAL ADVISOR • OCTOBER 2018

34

A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS

Community paramedics contribute to effective and efficient healthcare utilization.

PAGE 60

|

Assessment ofOverview current of a growing Psoriasis and Hodgkin’s screening methods US public for health concern Lymphoma predicting diabetes risk Is clinician testimony hearsay?

Approximately NEWSLINE 2% to 3% of the ■ Hydrocodone upscheduling There is room global population for improvement ■ CDC Shigella update is affected of T2Dpreterm GER ■current Managing by psoriasis. screening guidelines.

■ Meningococcal vaccine ■ Dairy consumption, CVD ■ Otitis media DERMATOLOGIC LOOK-ALIKES

Erythematous annular lesions

DERMATOLOGY CLINIC

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

43

Dermatology Clinic ■ Burning acneiform eruptions ■ Red-brown papules on the extremities

FREE CE COURSE

Laparoscopic sleeve gastrectomy

VOLUME 21, NUMBER 9

VOLUME 21, NUMBER 10

10

Current guidelines for management of low back pain

A HIPAA violation threatens a nurse’s career

DERMATOLOGY CLINIC

Red-brown papules on the extremities

FEATURE

These protozoa can multiply rapidly in the brain, liver, and heart.

LEGAL ADVISOR

LEGAL ADVISOR

DEPARTMENTS

audience shares how their practice has changed during that time PAGE 27

LEGAL ADVISOR

NEWSLINE

CME Feature Posttest

| www.ClinicalAdvisor.com

As we celebrate VS FASTING INSULIN CHAGAS HBA1C DISEASE 20 years, our

■ Fidaxomicin for C difficile ■ Pediatric vaccine exemptions

NP faulted for patient care via fax

41

A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS A PEER-REVIEWED | SEPTEMBER FORUM FOR 2018NURSE | www.ClinicalAdvisor.com PRACTITIONERS | AUGUST 2018 OCTOBER 2018 | www.ClinicalAdvisor.com

NEWSLINE CME: CASE CHALLENGE ■ Celiac disease

Hyperpigmented bands across all fingernails

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Precancerous GI mucosal lesions

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Dermatologic Look-Alikes Hyperpigmented plaques

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NEWS ClinicalAdvisor.com/News

USPSTF Updates Guidance for Cervical Cancer Screening

THE WAITING ROOM

Official Blog of The Clinical Advisor ClinicalAdvisor.com/WaitingRoom Sharon M. O’Brien, MPAS, PA-C Assessing the Risks of Using Alcohol as a Sleep Aid Discussing alcohol use with patients is important as alcohol consumption before bedtime is shown to negatively affect sleeping patterns.

Screening was found to detect highgrade precancerous cervical lesions and cervical cancer, thereby reducing cervical cancer incidence and mortality.

Cell-Free DNA Testing for High-Risk Pregnancies For women with pregnancies at high risk for trisomy 21, performing cell-free DNA tests over direct invasive karyotyping procedures did not reduce the risk for miscarriage.

How to Tell Your AntiVaccine Patients the Truth About Vaccines It may be tempting to lecture anti-vaccine patients about why they’re wrong, but you might get further by telling and showing them what can happen when a child gets sick from a preventable disease.

Patient Navigation Associated With Positive Outcomes in HIV Patient navigation may be an effective strategy to enhance engagement and continuation in disease treatment among people with HIV.

CASE STUDY Clinical Advisor.com/CaseStudy Brady Pregerson, MD Elbow and Biceps Pain After a Fall A 72-year-old man presents to the emergency department complaining of elbow and biceps femoris tendon pain. He states he was at home when he had a mechanical fall on the stairs and grabbed the handrail with his right arm while falling to the left. Read the full case here: ClinicalAdvisor.com/CaseElbowBicepsPain

PRACTICE MANAGEMENT ClinicalAdvisor.com/Practice Management Recommendations Issued for Enhancing ICU Diagnostic Safety Recommendations include enhancing recognition of potential errors, increasing teamwork and patient-centeredness in the diagnostic process, providing feedback on the diagnostic process, and expanding the role of health information technology.

MULTIMEDIA ClinicalAdvisor.com/Multimedia Put Your Stamp on the 2019 Salary Survey!

Don’t miss your opportunity to provide your feedback for our 2019 survey!

View the results from this year’s Nurse Practitioner/Physician Assistant Survey, and tell us which topics you’d like to see repeated or omitted from next year’s results. See the results here: ClinicalAdvisor.com/2018SalarySurvey

10 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

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✔ 96% patient satisfaction rate* ✔ #1 GI-recommended laxative for over 10 years Start with MiraLAX for proven relief of occasional constipation. *Survey of 300 consumers, 2017.

Use as directed on product labeling or as directed by your doctor.

Reference: 1. Clinical decision support tools. American Gastroenterological Association website. http://campaigns.gastro.org/algorithms/constipation/index.html. Accessed May 12, 2017.

Bayer, the Bayer Cross, and MiraLAX are trademarks of Bayer. © 2017 Bayer May 2017 68522-PP-MLX-BASE-US-0328

1003669ha_a.indd 1

Doctor recommended, patient approved

6/2/17 10:21 AM

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

Check out some of our latest cases below!

DERM DX

Rash on the Cheek and Scalp A 24-year-old Hispanic man presents for evaluation of an acute-onset rash on his left cheek and scalp. He experienced a slight fever the day prior to the eruption and currently complains of minimal discomfort.

Medical history is significant for atopic dermatitis that developed in early childhood. This condition had recently flared, and the patient received an intramuscular injection of triamcinolone 2 weeks ago.

Examination revealed multiple papulovesicles of the affected area.

CAN YOU DIAGNOSE THIS CONDITION?

• Acne conglobata • Eczema herpeticum

• Eosinophilic folliculitis • Varicella

● See the full case at ClinicalAdvisor.com/DermDx_Oct18

In partnership with

ORTHO DX

TheJopa.org

Journal of Orthopedics for Physician Assistants

Right Ankle Pain Following Sports Injury A 12-year-old girl presents to the office with right ankle pain after an injury sustained 4 days earlier. She was running for a football when her foot slipped on wet grass and she twisted her ankle.

Anteroposterior and lateral radiographs were taken in the emergency department on the day of injury.

WHICH IS THE MOST LIKELY DIAGNOSIS?

• Maisonneuve fracture • Weber C fracture

• Tillaux fracture • Triplane fracture

● See the full case at ClinicalAdvisor.com/OrthoDx_Oct18

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 11

Newsline A SUBSTANTIAL number of p­ rimary care providers are not knowledgeable about serogroup B meningococcal (MenB) disease and vaccine, which may contribute to a lack of vaccine discussions with parents and healthy adolescents, according to a study published in Pediatrics.

A team of researchers from the University of Colorado conducted a national survey among family physicians and pediatricians to evaluate MenB vaccine delivery practices and factors that would sway decisions to recommend or discuss MenB vaccination to patients.

Fifty-one percent of pediatricians and 31% of family physicians reported always or often discussing MenB vaccines during routine visits. The majority of clinicians who reported always or often discussing vaccines also recommended vaccination

to their patients (91%), while 11% of those who rarely or never discussed vaccination recommended the MenB vaccine to patients; 73% and 41% of participating pediatricians and family physicians administer the MenB vaccine in their practices.

The results of the survey suggested that many primary care physicians are unfamiliar with the data required to confidently discuss the pros and cons of MenB vaccination in healthy adolescents. Issues associated with a greater likelihood of vaccine recommendations included MenB disease outbreaks (89%), incidence of disease (62%), efficacy (52%), safety (48%), and duration of MenB protection (39%). In contrast, the Advisory Committee on Immunization Practices decision to categorize the vaccine as Category B instead of Category A

© RAWPIXEL / GETTY IMAGES

Many PCPs Unfamiliar With MenB Vaccine, Disease

Clinicians appear to lack the information needed for a well-informed discus­sion.

decreased the likelihood of vaccine recommendation among physicians (45%).

MenB vaccine discussion was less likely among physicians who were not at all or somewhat aware of the MenB vaccine and those participating in a health maintenance organization (risk ratio, 0.32 and 0.39, respectively) vs those who were more aware of disease outbreaks in their state (risk ratio, 1.25).

GU Syndrome of Menopause Consensus Statement THE INTERNATIONAL Society for the Study of Women’s Sexual Health (ISSWSH) expanded the recommended clinical man­agement of genitourinary syndrome of menopause (GSM) and published the outcomes in Menopause.

Symptoms of vulvovaginal atrophy (VVA) such as vaginal dryness and urinary frequency/urgency have a marked impact on sexual functioning, emotional health, body image, and relationships with peers.

Factors that contribute to an increased risk for these symptoms may include Hispanic ethnicity, obesity, diabetes, depression,

and urinary incontinence.Women with ovarian insufficiency or hypoestrogenic amenorrhea, as well as women prescribed ultralow-dose oral contraceptives were also found to be at risk for symptoms ofVVA. Clinicians should assess menstrual and medication history for women presenting with symptoms of GSM. Signs may include thinning/absent pubic hair, diminished elasticity of vulvar skin, introital narrowing and decreased moisture, and fusion or resorption of the labia minora.A thorough physical examination can differentiate GSM from other conditions of

12 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

the vulva such as lichen sclerosus, lichen planus, or lichen simplex chronicus.

Treatments for GSM should combine both androgenic and estrogenic actions, such as seen with esterified estrogens with methyltestosterone and tibolone, which exerts estrogenic, progestogenic, and androgenic effects. In placebo-controlled clinical trials, daily insertion of dehydroepiandrosterone vaginal ovules decreased vaginal pH, improved the vaginal epithelial maturation index and vaginal epithelial thickness and integrity, and increased vaginal secretions resulting in improvement in dyspareunia.

Dairy Intake Linked to Reduced CVD, Mortality Risk AN INCREASE in dairy consumption is associated with a reduced risk of mortality and major cardiovascular disease (CVD) events, such a stroke, in low- and middle-income countries, according to a study published in The Lancet.

A total of 136,384 participants used food frequency questionnaires to record dairy product intake, including milk, cheese, and yogurt. At a median follow-up of 9.1 years, the investigators reported that 7.7% of participants had either died (n=6796) or had a major CV event (n=5855) defined as noncardiovascular death (n=4796), car­diovascular death (n=2000), myocardial infarction (n=2594), stroke (n=2718), and heart failure (516).

High consumption of total dairy (>2 servings/d), when compared with no intake, was associated with a reduced risk of combined outcome (hazard ratio [HR],

0.84), total mortality (HR, 0.83), noncar­ diovascular mortality (0.86), cardiovascular mortality (0.77), major CVD (0.78), and stroke (0.66). Myocardial infarction results were not significant (HR, 0.89).

High consumption of milk and yogurt (>1 serving/d), when compared with no intake, was associated with reduced risk

lower risks of mortality and cardiovas­ cular disease, particularly stroke,” the authors wrote. “Our study suggests that consumption of dairy products should not be discouraged and perhaps should even be encouraged in low-income and middle-income countries where dairy consumption is low.”

A large, multinational group analysis was conducted to evaluate the association between the consumption of dairy products and mortality and major CVD events. of combined outcome (HR, 0.90 and 08.6, respectively). Cheese consumption was not significantly associated with reduced combined outcome (HR, 0.88), and but­ter consumption was low with no sig­nificant clinical associations (HR, 1.09).

“In conclusion, we observed that high­ er dairy consumption was associated with

In an accompanying commentary, the authors state that “it is not the ultimate seal of approval for recom­mending whole-fat dairy over its low-fat or skimmed counterparts.”They further advise, “Readers should be cautious and should treat this study only as yet another piece of evidence (albeit a large one) in the lit­erature.”

Short-Course Oral Steroids Ineffective for Otitis Media

© ARIEL SKELLEYT / GETTY IMAGES

THE FREQUENCY OF spontaneous resolution is high for children with persistent otitis media with effusion (OME) and hearing loss, suggesting that the use of short-term oral steroids may not significantly improve symptoms, according to a study published in The Lancet.

A group of investigators from the United Kingdom conducted a randomized,

At baseline, hearing was slightly better in children receiving steroid vs placebo.

parallel, double-blinded, placebo-­ controlled study to determine whether the short-term use of oral steroids would improve hearing in persistent pediatric otitis media with effusion and hearing loss.

The primary outcome measured was satisfactory hearing 5 weeks following randomization. Secondary outcomes included the impact of treatment on satisfactory hearing at 6 and 12 months, tympanometric relief of otitis media with effusion, otoscopic results, functional health status, and health-linked quality of life.

Children aged 2 to 8 years with ≥3 months of symptoms associated with otitis media with effusion and bilateral hearing loss were eligible to participate. Participants were randomly assigned to receive either oral steroid (prednisolone) or placebo.

The investigators reported satisfactory hearing in 40% of the steroid-group participants and 33% in the placebo group (absolute difference, 7%). No significant differences were identified with regard to adverse events and quality-of-life measures between the 2 groups.

“The high rate of spontaneous resolution identified in this study will support the evidence base informing discussions about watchful waiting in children with hearing loss associated with otitis media with effusion,” the authors wrote.“Given the findings of some benefit from antibiotics for otitis media with effusion in children, and limited trial evidence for a benefit from oral steroids in combination with antibiotics, a rigorous trial of oral steroids combined with antibiotics might be indicated.”

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 13

Newsline

© BSIP / UIG / GETTY IMAGES

Discharge Directly From ICU Safe and Cost-Effective

Discharging select adult patients from ICU to home is common.

DISCHARGING PATIENTS directly home from an intensive care unit (ICU) compared with discharging patients to home after transfer to a a hospital ward is not associated with increased patient hospital care utilization or mortality, according to a study published in JAMA Internal Medicine.

A group of researchers conducted a population-based, retrospective cohort study to analyze the characteristics, healthcare utilization patterns, and outcomes of ICU patients recovering from critical illnesses.All patients were aged ≥18 years and admitted to medical-surgical ICUs in various hospitals across Canada.

Patients discharged directly from an ICU (n= 922) were compared with patients transferred to a hospital ward after ICU followed by discharge (n=5810).

Data were obtained from 3 Canadian databases; patient factors included demographic variables, comorbidities, ICU admission diagnosis, illness severity upon admission and discharge, interventions received in the ICU, and external support prescribed at discharge. Hospitals included in the study were identified based on teaching status, number of hospital

and ICU beds, number of patients discharged directly home, ICU occupancy, and transfer delay.

The primary outcome was defined as hospital admission within 30 days of discharge. Secondary outcomes included emergency department visits within 30 days and death at 365 days.

More patients were discharged directly home from an ICU at hospitals that were nonteaching and had fewer ICU and hospital beds.These patients were also younger (median age, 47 vs 57 years), less likely to have comorbidities (39% [n=360] vs 65% [n=3774]), less likely to have been admitted to the ICU from the operating or recovery room (11% [n=98] vs 29% [n=1669]), and less acutely ill in the first 24 hours in the ICU (median APACHE II score 15 vs 18) compared with patients discharged home via the hospital ward. Illnesses most frequently seen in ICU patients discharged directly home included overdose (23%; n=208), pneumonia (11%; n=104), and trauma or orthopedic injuries (9%; n=79).

Patients discharged directly home were more likely to leave against medical advice (6%, [n=45] vs 4% [n=31]) and less likely to be prescribed external support services (6% [n=52] vs 16% [n=131]) compared with patients discharged via the hospital ward.

A total of 10% of patients discharged directly home (n = 81) were readmitted to the hospital after 30 days compared with 11% of patients discharged home via the hospital ward (n = 92) (hazard ratio [HR], 0.88). Approximately 25% of patients in both groups had an emergency department visit within 30 days of hospital discharge (HR, 0.94).A total of 4% [n=31] of patients sent directly home vs 4% [n=34] discharged home via hospital ward died within 1 year of discharge (HR, 0.90).

Labor Induction May Be Beneficial in Women With Chronic Hypertension INDUCING LABOR at 38 or 39 weeks of gestation may benefit women with isolated chronic hypertension by preventing severe hypertensive events without increasing the risk of cesarean delivery, according to a study published in Obstetrics & Gynecology. In addition, the study suggests that labor induction at 39 weeks of gestation may be linked with a reduced risk of neonatal respiratory morbidity compared with expectant management.

Expectant mothers who underwent labor induction for chronic hypertention at either 38 or 39 weeks were compared with mothers who were expectantly managed until delivery at 39 or 40 weeks.

Women who were managed expectantly at 38 and 39 weeks were at risk for superimposed preeclampsia (19.2% and 19.0%, respectively) and eclampsia (0.6% and 0.7%, respectively). Later in gestation, more than half of those women underwent induced labor (56.8% and 57.8%, respectively).

Cesarean delivery risks were lower in 38-week induction groups or similar in 39-week induction groups to women who were managed expectantly at the same weeks. For 38 and 39 weeks, the adjusted relative risks were 0.74 and 0.90, respectively.

“Our findings suggest that in women with isolated chronic hypertension, induction of labor at 38 or 39 weeks of gestation may prevent severe hypertensive complications without increasing the risk of cesarean delivery,” the authors concluded.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 17

Newsline Thyroid Dysfunction Not Associated With HIV Status THE PREVALENCE of hyperthyroidism and hypothyroidism is similar in uninfected patients and those with well-treated HIV, suggesting that there is no association between thyroid dysfunction, serum thyroid-stimulating hormone (TSH) concentrations, and HIV status, according to a study published in AIDS. A group of investigators from Denmark conducted a longitudinal group analysis, The Copenhagen Comorbidity in HIV Infection Study (COCOMO; ClinicalTr ials.gov Identifier: NCT02382822), to evaluate the association of non-AIDS morbidities in HIV-positive individuals.

The researchers invited HIV-positive adults (n=826) and uninfected controls (n=2503) to participate in the trial. Blood samples were collected to record glycated hemoglobin values, as well as glucose and serum TSH levels. Statistical analysis was

No associations were identified between HIV and hypo- or hyperthyroidism.

used to study the link between thyroid dysfunction and HIV as well as the link between HIV and serum TSH. The majority of individuals with HIV (95%) had undetectable viral replication.

Of this group, 3.8% (n=31) and 0.8% (n=7) had hypothyroidism or hyperthyroidism, respectively. In the control group, 4.6% (n=114) and 0.8% (n=21)

had hypothyroidism or hyperthyroidism, respectively.

After adjusting for known risk factors, no associations were identified between HIV and hypothyroidism or hyperthyroidism (odds ratio, 0.8 and 1.1, respectively).

“This study is the first ever to evaluate thyroid dysfunction in a large cohort of well-treated [people living with HIV] and uninfected controls in the modern [combination antiretroviral therapy] era,” the authors noted.“We found no association between HIV and thyroid dysfunction. Furthermore, HIV-related variables were not associated with hypothyroidism or hyperthyroidism. Thus, no evidence was found to support increased risk of thyroid dysfunction in well-treated [people living with HIV].”

Disclosure: Please refer to the original article for full disclosure listing.

© CHRISCHRISW / GETTY IMAGES

T1D, Poor Glycemic Control Linked to Infection INFECTION RATES in diabetes mellitus (DM) increase among those with type 1 diabetes (T1D) and those with poor glycemic control, according to a study published in Diabetes Care.

Glycated hemoglobin (HbA1c) measurements of patients from the Clinical Practice Research Datalink were averaged over a 2-year period; after exclusion criteria were applied, 78,964 patients in the T2D group, 4496 in the T1D group, and 1852 with type uncertain were matched with 153,341 controls. Mean follow-up was 4.2 years; HbA1c measurements were excluded if they fell within 2 weeks of the baseline assessment period.

Infection was identified across 18 categories and grouped into 3 main subcategories; these were then grouped into 3 main subcategories: 1) any infection that

resulted in a prescription for an antibiotic, antifungal, or antiviral drug within 2 weeks of the initial diagnosis; 2) any infection leading to a hospital admission; or 3) any infection that resulted in patient death.

The average HbA1c for patients with T1D was higher than for patients withT2D

Rates of infection increased among patients with DM as well as with increasing HbA1c. Associations between infectionrelated hospitalizations and DM were more significant for patients with T1D than for those with T2D, and patients with DM with both good (mean HbA1c, 6%-7%)

Poor glycemic control was associated with increased risk of bone and joint infections, endocardi­tis, tuberculosis, sepsis, pneumonia, skin infec­tions, and candidiasis.

(8.3% vs 7.4%); patients with unknown DM had levels similar to patients with T1D (8.3%). Increasing levels of HbA1c were associated with younger age, longer duration of DM, deprivation (defined as unmet needs caused by a lack of resources), and obesity.

18 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

and poor HbA1c (≥11%) control were at increased risk for hospitalization compared with patients without DM. Overall, 15.7% of infection-related deaths, 16.5% of infection-related hospitalizations, and 6.8% of infections requiring a prescription were attributed to poor glycemic control. ■

Beyond Rx

A S U P P L E M E N T TO T H E C L I N I C A L A DV I S O R

Research-Backed Reasons To Recommend Omega-3s

T

here are many research-based reasons to make you feel good about recommending omega-3s to your patients. EPA and DHA omega-3s are backed by decades of research showcasing their benefits for four areas in particular: heart, brain, eye, and prenatal health. Omega-3s aren’t just beneficial – they’re vitally important for every cell in the body.

55,000

annual cardiometabolic deaths in the US are estimated to be linked to low omega-3 intake.1

Cardiovascular Health 95% of the US population are below cardioprotective levels of omega-3 fatty acids.2

Prenatal/ Infant Health The omega-3 DHA is important for a healthy pregnancy as it's a critical building block of a developing baby's brain, retina, and nervous system.

58%

of early pre-term births could have been prevented with omega-3s according to a 2017 study.5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852674/pdf/nihms946949.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690086/pdf/nutrients-07-05534.pdf http://fatsoflife.com/health-benefits/brain/ 4 https://www.aoa.org/patients-and-public/caring-for-your-vision/diet-and-nutrition/essential-fatty-acids 5 https://www.ncbi.nlm.nih.gov/pubmed/26773247

DHA is the most abundant fatty acid in the human brain.

Brain Health Omega-3s are important for brain health.

Research has shown omega-3s impact cognitive function, memory, symptoms of depression and ADHD, and recovery from traumatic brain injuries.3

88% of Americans believe good vision is vital to overall health.

Omega-3s can play a role.

Eye Health According to the American Optometric Association, research shows EPA and DHA are important for proper visual development and retinal function.4

1 2 3

fatsoflife.com

Content provided by Global Organization for EPA and DHA Omega-3s (GOED), a trade association representing 200 global companies active in the EPA and DHA omega-3 industry.

A SUPPLEMENT TO THE CLINICAL ADVISOR 19

Beyond Rx Cardiovascular Health: How Omega-3s Help the Heart

According to the Centers for Disease Control, about 610,000 people die of heart disease in the United States every year — that’s 1 in every 4 deaths.1 Most Americans (95.7%) are below the cardioprotective levels of EPA and DHA omega-3 fatty acids without even knowing it.2 A 2017 publication reported that low omega-3 intake was estimated to contribute to 54,626 cardiometabolic deaths.3 Similarly, a 2013 meta-analysis of interventional clinical trials found that 22% of disability-adjusted life years lost are attributable to insufficient EPA/ DHA intake, and that every additional 100 mg/d reduces the risk of coronary heart disease death by 5%.4 This research brings omega-3s to the forefront in reducing cardiac death risk.A meta-analysis published in 2017 showed that consumption of EPA and DHA omega-3s reduced the risk of cardiac death by a statistically significant average of 8%.5 The meta-analysis showed even greater — 17% — risk

Almost 55,000 cardiometabolicrelated deaths in the U.S. were estimated to be linked to low omega-3 intake according to a 2017 publication. reduction in groups who had elevated triglycerides or LDL cholesterol. The greatest reduction in cardiac death rates — an almost 30% risk reduction — was observed in trials that utilized dosages of more than 1 g of EPA and DHA per day.

Research also shows that EPA and DHA omega-3s address heart disease risk factors in other ways. They help lower triglycerides and reduce blood

Seafood • Supplements • Fortified foods*

EPHA and DHA Intake: Continuum of Cardioprotection Primary prevention

Secondary prevention

Therapeutic Intervention

Level 2

Level 3 2000-4000 mg EPA+DHA per day

≥ 1000 mg Level 1 250-500 mg EPA+DHA per day^

EPA+DHA per day

Primary prevention recommendation

Patients with documented CHD

Better Brain Health: How Omega-3s Support Cognitive and Mental Health Patients who need to lower triglyceride levels

*Everyone meets their EPA+DHA needs differently ^GOED recommendation is 500mg; WHO & other scientific bodies recommend 250 mg

20 A SUPPLEMENT TO THE CLINICAL ADVISOR

pressure. Twenty-one meta-analyses have demonstrated a 20% to 40% reduction in serum triglycerides with consumption of EPA and DHA omega3s.6 A meta-analysis of 70 randomized controlled trials found statistically significant reductions in systolic and diastolic blood pressure.7 Consider the potential benefits and positive impact omega-3s can play.They can be as effective as lifestyle changes like increasing physical activity, and restricting alcohol or sodium intake.

Research supports additional potential benefits. A study published in Mayo Clinic Proceedings found that EPA and DHA omega-3 consumption may reduce the risk of coronary heart disease (CHD), particularly in higher risk populations — a 16% reduction in those with high triglycerides and a 14% reduction in those with high LDL cholesterol.8 The research also found a non-statistically significant 6% risk reduction among all populations in randomized controlled trials (RCTs) and a statistically significant 18% reduced risk of CHD among prospective cohort studies.These findings are particularly relevant for the management of CHD risk in the general US population because 25% of Americans older than 20 years are estimated to have triglyceride levels of 150 mg/dL or more9 and 27% of Americans between 40 and 74 years have LDL cholesterol levels of 130 mg/dL or more.10

Omega-3s have been shown to benefit the brain’s health in several ways.

Research has shown an impact on cognitive function and memory, symptoms of depression, ADHD, and recovery from traumatic brain injuries.11

Omega-3s are associated with lower risk of cognitive impairment and in a meta-analysis of 21 studies, DHA in particular was associated with lower risk of dementia and Alzheimer disease.12 This is potentially an exciting promise to the massive 80 million baby boomer population getting older.

Research is also promising when it comes to mental health.There is some evidence that those who experience depression may not consume enough EPA and DHA. With major depression becoming one of the most common mental disorders in the United States, research is looking at the role omega-3s play in mood regulation, helping the brain communicate using the neurotransmitters serotonin and dopamine, and reducing inflammation in the brain, which has been linked to depression. Diets deficient in omega-3s are associated with a 50% decrease in the number of dopaminergic neurons, the main source of dopamine. This is not surprising, considering at least 50% of the brain is fat and DHA is the most abundant omega-3 fatty acid in the brain.11

At least 50% of the brain is fat and DHA is the most abundant omega-3 fatty acid in the brain — but it must be replenished regularly.

Omega-3 Daily Intake Recommendations Based on the current body of scientific evidence, GOED has established the following intake recommendations:

500 MG For the general healthy adult population in order to lower the risk of heart disease (CHD)25

700-1000 MG • For pregnancy / lactation: 200 additional mg/day of DHA over recommendation for healthy adults13 • For secondary prevention of CHD: 1000 mg/day EPA+DHA26

>1 G

Higher Intakes are supported for a range of additional health conditions (e.g. blood pressure,27 triglycerides28)

In addition, emerging research is showing that omega-3 supplements may reduce the symptoms associated with ADHD, and in high doses may be beneficial for brain injuries such as TBI, concussion, and post-concussion syndrome.11 Prenatal and Infant Health: Building Better Outcomes for Baby and Mom

The omega-3 DHA is generally known as the most vital omega-3 for pregnancy as it is a critical building block of the brain, retina, and nervous system.

Getting enough omega-3s during pregnancy has been associated with numerous benefits for the child. Proceedings from an Early Nutrition Academy workshop recommend that pregnant women should aim for an additional 200 mg of DHA over and above the intake recommendation for the general adult population, resulting in a total DHA intake of at least 300 mg/day.13 In early 2018, the American Academy of Pediatrics recognized the importance of DHA and ARA to support

brain development in the first 1000 days of life. Indeed, during pregnancy and breastfeeding, the research-backed benefits of DHA include supporting the healthy development of the fetal brain, eye, and nervous system.14 Importantly, research consistently demonstrates a benefit in decreasing the likelihood of early preterm birth and also supports omega-3 intake and healthier birth weight. In one recent meta-analysis, omega-3s were associated with a 58% decrease in the likelihood of early preterm birth.15 There is also some research supporting immune system function and development.16 Seeing the Benefits: How Omega-3s Protect the Eyes

Omega-3s support visual development in infants, but their impact doesn’t end there.The body’s highest concentration of DHA is found in the retina of the eye17 and DHA is an important nutrient for the cells of the eye that control the ability to see under different lighting conditions.18 The American Optometric

A SUPPLEMENT TO THE CLINICAL ADVISOR 21

Beyond Rx Association states that research has shown EPA and DHA are important for proper visual development and retinal function.19 Omega-3s also play a role in dry eye syndrome, which affects an estimated 3.2 million women age 50 and over20 and 1.68 million men age 50 and over.

Research suggests that taking an omega3 fatty acid supplement can reduce symptoms of dry eyes.21 In addition, several studies suggest that higher intakes of omega-3s may decrease risk of age-related macular degeneration (AMD).21 This is particularly important since nearly 2.1 million Americans age 50 and older have late AMD, which can lead to severe vision impairment.22 In 2010, 9.1 million Americans had early AMD.23 By age 80, 1 in 10 Americans has late AMD, which is more common in women than in men.24 â– REFERENCES 1. CDC Wonder Online Database. Underlying Cause of Death 1999-2013. Atlanta, GA: Centers for Disease Control and Prevention. Available at: https:// wonder.cdc.gov/. Accessed September 17, 2018.

2. Murphy RA, Yu EA, Ciappio ED, Mehta S, McBurney MI. Suboptimal plasma long chain n-3 concentrations are common among adults in the United States, NHANES 2003-2004. Nutrients.

2015;7:10282-10289.

3. Micha R, Penalvo JL, Cudhea F, Imamura F, Rehm CD, Mozaffarian D. Association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA. 2017;317(9):912-924.

4. Engell RE, Sanman E, Lim SS, Mozaffarian D. Seafood omega-3 intake and risk of coronary heart disease death: an updated meta-analysis with implications for attributable burden. Lancet. 2013;381:S45.

5. Maki KC, Palacios OM, Bell M, Toth PP. Use of supplemental long-chain omega-3 fatty acids and risk for cardiac death: an updated metaanalysis and review of research gaps. J Clin Lipidol.

2017;11:1152-1160.

6. Cardiovascular studies. Facts of Life website. Available at: http://www.fatsoflife. com/?s=cardiovascular+studies. Accessed September 17, 2018.

7. Miller PE, Van Elswyk M, Alexander DD. Longchain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and blood pressure: a meta-analysis of randomized controlled trials. Am J Hypertens. 2014;27(7):885-896.

8. Alexander DD, Miller PE, Van Elswyk M, Kuratko CN, Bylsma LC. A meta-analysis of randomized controlled trials and prospective cohort studies of eicosapentaenoic and docosahexaenoic long-chain omega-3 fatty acids and coronary heart disease risk.

Mayo Clin Proc.2017;92(1):15-29.

9. Carroll M, Kit B, Lacher D. Trends in elevated triglyceride in adults: United States, 2001-2012. NCHS Data Brief. 2015;(198):198.

10. Kuklina EV, Carroll MD, Shaw KM, Hirsch R. Trends in high LDL cholesterol, cholesterollowering medication use, and dietary saturated-fat intake: United States, 1976-2010. NCHS Data Brief.

2013;(117):1-8.

11. Brain studies. Facts of Life website. Available at: http://www.fatsoflife.com/?s=brain+studies.

Accessed September 17, 2018.

12. Zhang Y, Chen J, Qiu J, Li Y, Wang J, Jiao J. Intakes of fish and polyunsaturated fatty acids and mild-tosevere cognitive impairment risks: a dose-response meta-analysis of 21 cohort studies. Am J Clin Nutr.

2016;103(2):330-340.

13. Koletzko B, Boey CCM, Campoy C, et al. Current information and Asian perspectives on long-chain polyunsaturated fatty acids in pregnancy, lactation, and infancy: systematic review and practice recommendations from an Early Nutrition Academy Workshop. Ann Nutr Metab. 2014;65:49-80.

14. Ramakrishnan U, Stein AD, Parra-Cabrera S, et al. Effects of docosahexaenoic acid supplementation during pregnancy on gestational age and size at birth: randomized, double-blind, placebo-controlled trial in Mexico. Food Nutr Bull. 2010;31:S108–S116.

15. Kar S, Wong M, Rogozinska E, Thangaratinam S. Effects of omega-3 fatty acids in prevention of early preterm delivery: a systematic review and metaanalysis of randomized studies. Eur J Obstet Gynecol Reprod Biol. 2016;198:40-46.

16. Prenatal studies. Facts of Life website. Available at: http://www.fatsoflife.com/?s=prenatal+studies.

Accessed September 17, 2018.

17. Fliesler SJ, Anderson RE. Chemistry and metabolism of lipids in the vertebrate retina. Prog Lipid Res. 1983;22(2):79-131.

18. Grossfield A, Feller SE, Pitman MC. A role for direct interactions in the modulation of rhodopsin by omega-3 polyunsaturated lipids. Proc Natl Acad Sci U S A. 2006;103(13):4888-4893.

22 A SUPPLEMENT TO THE CLINICAL ADVISOR

19. Essential fatty acids. Omega-3: DHA and EPA. American Optometric Association website. Available at: https://www.aoa.org/patients-and-public/caringfor-your-vision/diet-and-nutrition/essential-fatty-acids.

Accessed September 17, 2018.

20. Schaumberg DA, Sullivan DA, Buring JE, Dana MR. Prevalence of dry eye syndrome among US women. Am J Ophthalmol. 2003;136(2): 318-326.

21. Eye studies. Facts of Life website. Available at: http://www.fatsoflife.com/?s=eye+studies. Accessed September 17, 2018.

22. Eye health statistics. American Academy of Ophthalmology website. Available at: https://www. aao.org/newsroom/eye-health-statistics. September 17, 2018.

23. Rein DB, Wittenborn JS, Zhang X, Honeycutt AA, Lesesne SB, Saaddine J; Vision Health CostEffectiveness Study Group. Forecasting age-related macular degeneration through the year 2015: the potential impact of new treatments. Arch Ophthalmol. 2009;127(4):533-540.

24. Age-related macular degeneration (AMD).

National Eye Institute website. Available at: https:// www.nei.nih.gov/eyedata/amd. Accessed September 17, 2018.

25. Report of the sub-committee on recommendations for intake of polyunsaturated fatty acids in health adults. Washington, DC: International Society for the Study of Fatty Acids and Lipids; 2004.

Available at: http://www.issfal/news-links/resources/ publications/PUFAIntakeReccomdFinalReport.pfd 26. Kris-Etherton PM, Harris WS, Appel LJ; for the American Heart Association Nutrition Committee (2002). Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease [published correction appears in Circulation 2003;107:512]. Circulation.

2003;106:2747-2757.

27. Scientific opinion on the substantiation of health claims related to EPA, DHA, DPA and maintenance of normal blood pressure (ID 502), maintenance of normal HDL-cholesterol concentrations (ID 515), maintenance of normal (fasting) blood concentrations of triglycerides (ID 517), maintenance of normal LDL-cholesterol concentrations (ID 528, 698) and maintenance of joints (ID 503, 505, 507, 511, 518, 524, 526, 535, 537) pursuant to Article 13(1) of Regulation (EC) No 1924/2006. EFSA J. 2009;7(9):1263.

28. Eslicks GD, Howe PR, Smith C, Priest R, Bensoussan A. Benefits of fish oil supplementation in hyperlipidemia: a systematic review and metaanalysis. Int J Cardiol. 2009;136(1):4-16.

FEATURE: CHRISTY M. LENAHAN, DNP, MSN, FNP-BC; DEEDRA H. HARRINGTON, DNP, MSN, ACNP-BC

Current Guidelines for the Management of Low Back Pain An estimated 31 million Americans will experience low back pain at some point in their lifetime.

© LAURENTIU IORDACHE / ALAMY STOCK PHOTO

L

A tiered treatment approach provides the most benefit for patients with low back pain.

ow back pain — also called lumbago — is defined as a common, painful condition affecting the lower portion of the spine.1 The prevalence of low back pain is reported to range between 51% and 84%, with most individuals experiencing this condition at some point in their lifetime.2 The economic burden of low back pain in the United States is significant; estimated direct costs are from $20 to $98 billion, with an estimated indirect cost as high as $200 billion annually.3 The Centers for Disease Control and Prevention reports low back pain as the second most common cause of disability, which contributes to the high overall indirect expense associated with the condition.4 The American Chiropractic Association estimates that approximately 31 million Americans will experience low back pain during their lifetime.5 Approximately 90% of all low back pain will resolve within 6 weeks, with more than 80% of cases resolving within 2 weeks.6 Low back pain is usually classified based on symptom duration, anatomical location, potential cause, and presence or absence of radicular symptoms.7 Nonradicular low back pain is pain without associated sensory distribution and nerve root involvement.7 Classification of low back pain is based on the duration of symptoms and is further divided into acute, subacute, and chronic conditions. Acute low back pain, which is pain lasting up to 4 weeks, is usually nonspecific and has no underlying condition as an identified cause. Acute low back

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 23

LOW BACK PAIN MANAGEMENT GUIDELINES

While some pharmacologic treatments will alleviate acute and subacute low back pain, the majority of patients will improve over time. pain is usually self-limited and resolves on its own with nonpharmacologic treatment. Subacute low back pain may persist for 4 to 12 weeks and may require pharmacologic therapy.

Unresolved low back pain, which is pain lasting longer than 12 weeks, is classified as chronic.6,7 Acute/Subacute Low Back Pain

Both nonpharmacologic and pharmacologic therapies are available for the management of acute and subacute low back pain (Table).

Nonpharmacologic Therapy While some pharmacologic treatment modalities have shown small to moderate efficacy in alleviating acute and subacute low back pain, the majority of patients will improve over time.

Thus, current recommendations suggest that clinicians select nonpharmacologic therapies prior to instituting the use of pharmacologic agents.7 Specific nonpharmacologic therapies that have proven efficacious in treating acute and/or subacute low back pain include the use of superficial heat,8 massage,9 acupuncture,10 and spinal manipulation.11 If nonpharmacologic therapies do not improve pain or if a patient desires treatment with pharmacologic agents, there are a few drug categories that have proven efficacy in decreasing pain and improving functional ability.

Pharmacologic Therapy Studies indicate that a majority of pharmacologic treatment modalities currently used for acute and subacute low back pain have shown little to small effect on patients’ pain levels and functional abilities.7 However, 2 categories of

drugs — nonsteroidal anti-inflammatory drugs (NSAIDs) and skeletal muscle relaxants (SMRs) — have demonstrated evidence for improving the quality of life for patients with acute or subacute low back pain.7 Research has demonstrated that when compared with placebo, patients taking NSAIDs demonstrated improvement in pain intensity12 and a small improvement in functional ability.13 No significant changes were identified to indicate that one NSAID was superior to another in head-to-head trials. In similar studies, patients taking SMRs also reported improved pain relief when compared with those taking placebo.14 Chronic Low Back Pain

Nonpharmacologic and pharmacologic therapies have been identified for the management of chronic low back pain (Table).

Nonpharmacologic Therapy In patients with chronic low back pain, the American College of Physicians recommends initial treatment to include nonpharmacologic therapies as the first-line option because they are affiliated with fewer harms to the patient as compared with pharmacologic therapies.7 Several nonpharmacologic therapies have demonstrated improvement in pain intensity and functional ability in patients with chronic low back pain. Moderate-quality evidence supports the use of exercise,15 multidisciplinary rehabilitation,16 acupuncture,17 and mindfulness-based stress reduction18 to assist in decreasing pain associated with chronic back low pain and increasing patient functional abilities.Additional nonpharmacologic therapies recommended in the treatment of chronic low back pain but supported by low-quality evidence include tai-chi,19

TABLE. Nonpharmacologic and pharmacologic treatment for the management of low back pain Nonpharmacologic Therapy

Pharmacologic Therapy

Acute (0-4 weeks) Subacute (4-12 weeks)

• Superficial heat • Massage

• Acupuncture • Spinal manipulation

• Nonsteroidal anti-inflammatory drugs • Skeletal muscle relaxants

Chronic (>1 year)

• Exercise • Multidisciplinary rehabilitation • Acupuncture • Mindfulness-based stress reduction • Tai-chi • Yoga

• Motor control exercises • Progressive relaxation therapy • Electromyography biofeedback • Low-level laser therapy • Cognitive behavioral therapy • Spinal manipulation

• Nonsteroidal anti-inflammatory drugs (first-line) • Tramadol or duloxetine (second-line) • Opioids (only if all previous therapies have failed)

24 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

First-line therapy for chronic low back pain should include NSAIDs, which have been shown to reduce pain and increase functional ability.

POLL POSITION Which nonpharmacologic strategy for the management of chronic low back pain is associated with moderate-quality (vs low-quality) evidence?

■ Yoga

18.01%

■ Spinal manipulation ■ Acupuncture ■ Cognitive behavioral therapy

15.32%

42.47%

24.19%

For more polls, visit ClinicalAdvisor.com/Polls.

yoga,20 motor control exercises,21 progressive relaxation therapy,22 electromyography biofeedback,22 low-level laser therapy,23 cognitive behavioral therapy,22 and spinal manipulation.24

to discuss known risks as well as expected, realistic benefits of opioid treatment (short-term reduction in pain and increase in functional ability) with the patient prior to making the decision to prescribe this treatment for chronic low back pain.28 Conclusion

Low back pain has been found to have a significant economic impact, with substantial direct and indirect healthcare costs.

Providers must first distinguish between acute, subacute, and chronic presentation of low back pain before considering the initiation of treatment modalities. Utilization of a tiered treatment approach with the combination of nonpharmacologic and nonnarcotic pharmacologic therapy has been proven most beneficial for the treatment of a majority of patients with low back pain. Use of opioid therapy should only be considered for patients with chronic low back pain that has not responded to more conservative treatment options and only if the benefits associated with the treatment outweigh the potential risks. ■ Christy McDonald Lenahan DNP, APRN, FNP-BC, ENP-C, CNE, and Deedra Harrington, DNP, MSN,APRN,ACNP-BC, are assistant professors at the University of Louisiana at Lafayette College of Nursing and Allied Health Professions.

References

Pharmacologic Therapy Pharmacologic therapy should only be considered for patients with chronic low back pain if there has been an inadequate response to nonpharmacologic management. Current guidelines suggest clinicians should consider a tiered approach when prescribing pharmacologic therapy, starting with medications that result in the greatest benefit and pose the least possible risk.7 First-line therapy for chronic low back pain should include the use of NSAIDs that have shown efficacy in reducing pain and increasing functional ability.12 Progression to second-line therapy, should the patient not be a candidate for NSAIDs or should treatment with NSAIDs fail, includes consideration of tramadol or duloxetine.25,26 The use of these medications has been associated with decreased pain and increased functional ability in patients with chronic low back pain25,26; however, clinicians should be cautious in light of the risk for abuse associated with tramadol.27 In the setting in which all nonpharmacologic and nonnarcotic pharmacologic efforts have been exhausted and the patient continues to experience chronic low back pain, the clinician may consider the use of opioids.7 It is prudent for the clinician

1. Ben-Yishay A. Understanding low back pain (lumbago). Spine-health. April 25, 2012. Accessed September 9, 2018.

2. Henschke, N, Kamper SJ, Maher CG. The epidemiology and economic consequences of pain. Mayo Clin Proc. 2015;90(1):139-147.

3. Thiese MS, Hegmann KT, Wood EM, et al. Prevalence of low back pain by anatomic location and intensity in an occupational population. BMC Musculoskelet Disord. 2014;15:283.

4. Centers for Disease Control and Prevention. Prevalence and most common causes of disability among adults -- United States, 2005. Morb Mortal Weekly Rep. 2009;58(16):421-426.

5. American Chiropractic Association. Back pain facts and statistics. Accessed September 7, 2018.

6. Papadakis MA, McPhee SJ, Rabow MW (eds). Current Medical Diagnosis & Treatment 2014. New York: McGraw-Hill Medical; 2014.

7. Qaseem A, Wilt TJ, McLean RM, Forciea MA; for the Clinical Guidelines Committee of the American College of Physicians. Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166(7):514-530.

8. French SD, Cameron M, Walker BF, Reggars JW, Esterman AJ. Superficial heat or cold for low back pain. Spine (Phila Pa 1976). 2016;20(31):998-1006.

Continues on page 29

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LOW BACK PAIN MANAGEMENT GUIDELINES

19. Weifen W, Muheremu A, Chaohui C, Wenge L, Lei S. Effectiveness of tai chi

Cochrane Database Syst Rev. 2008;(4):D001929.

practice for non-specific chronic low back pain on retired athletes: a random-

10. Lee JH, Choi TY, Lee MS, Lee H, Shin BC, Lee H. Acupuncture for acute

ized controlled study. J Musculoskelet Pain. 2013;21:37-45.

low back pain: a systematic review. Clin J Pain. 2013;29(2):172-185.

20. Williams K, Abildso C, Steinberg L, et al. Evaluation of the effectiveness

11. von Heymann WJ, Schloemer P, Timm J, Muehlbauer B. Spinal high-velocity

and efficacy of Iyengar yoga therapy on chronic low back pain. Spine (Phila Pa

low amplitude manipulation in acute nonspecific low back pain: a double-

1976). 2009;34:2066-2076.

blinded randomized controlled trial in comparison with diclofenac and pla-

21. Byström MG, Rasmussen-Barr E, Grooten WJ. Motor control exercises

cebo. Spine (Phila Pa 1976). 2013;38(7):540-548.

reduces pain and disability in chronic and recurrent low back pain: a meta-

12. Roelofs PD, Deyo RA, Koes BW, Scholten RJ, van Tulder MW. Non-

analysis. Spine (Phila Pa 1976). 2013;38:E350-E358.

steroidal anti-inflammatory drugs for low back pain. Spine (Phila Pa 1976).

22. Henschke N, Ostelo RW, van Tulder MW, et al. Behavioural treatment for

2008;33(16):1766-1774.

chronic low-back pain. Cochrane Database Syst Rev. 2010:CD002014.

13. Dreiser RL, Marty M, Ionescu E, Gold M, Liu JH. Relief of acute low

23. Basford JR, Sheffield CG, Harmsen WS. Laser therapy: a randomized, con-

back pain with diclofenac-K 12.5 mg tablets: a flexible dose, ibuprofen 200 mg

trolled trial of the effects of low-intensity Nd:YAG laser irradiation on muscu-

and placebo-controlled clinical trial. Int J Clin Pharmacol Ther. 2003;41(9):

loskeletal back pain. Arch Phys Med Rehabil. 1999;80(6):647-652.

375-385.

24. Rubinstein SM, van Middelkoop M, Assendelft WJ, de Boer MR, van

14. van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM. Muscle relaxants

Tulder MW. Spinal manipulative therapy for chronic low-back pain. Cochrane

for non-specific low back pain. Cochrane Database Syst Rev. 2003:CD004252.

Database Syst Rev. 2011;(2):D008112.

15. van Middelkoop M, Rubinstein SM, Verhagen AP, Ostelo RW, Koes BW, van

25. Lee JH, Lee CS; Ultracet ER Study Group. A randomized, double-blind, placebo-

Tulder MW. Exercise therapy for chronic nonspecific low-back pain. Best Pract

controlled, parallel-group study to evaluate the efficacy and safety of the extended-

Res Clin Rheumatol. 2010;24(2):193-204.

release tramadol hydrochloride/acetaminophen fixed-dose combination tablet for

16. Kamper SJ, Apeldoorn AT, Chiarotto A, et al. Multidisciplinary biopsycho-

the treatment of chronic low back pain. Clin Ther. 2013;35(11):1830-1840.

social rehabilitation for chronic low back pain. Cochrane Database Syst Rev.

26. Skljarevski V, Ossanna M, Liu-Seifert H, et al. A double-blind, randomized

2014:CD000963.

trial of duloxetine versus placebo in the management of chronic low back

17. Lam M, Galvin R, Curry P. Effectiveness of acupuncture for non-specific

pain. Eur J Neurol. 2009;16(9):1041-1048.

chronic low back pain: a systematic review and meta-analysis. Spine (Phila Pa

27. Drug Enforcement Administration. Department of Justice. Schedule of

1976). 2013;38(24):2124-138.

controlled substances: placement of tramadol into schedule IV. Final rule. Fed

18. Cherkin DC, Sherman KJ, Balderson BH, et al. Effect of mindfulness-based

Regist. 2014;79(127):37623-27630.

stress reduction vs cognitive behavioral therapy or usual care on back pain

28. Chaparro LE, Furlan AD, Deshpande A, Mailis-Gagnon A, Atlas S, Turk DC.

and functional limitations in adults with chronic low back pain: a randomized

Opioids compared to placebo or other treatments for chronic low-back pain.

clinical trial. JAMA. 2016;315:1240-1249.

Cochrane Database Syst Rev. 2013:CD004959.

© The New Yorker Collection 2018 from cartoonbank.com. All Rights Reserved.

9. Furlan AD, Imamura M, Dryden T, Irvin E. Massage for low-back pain.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 29

FEATURE: PATRICK AYARZAGOITIA, DNP, APRN, FNP-BC

Clinical Case Challenge: A Zebra in the Emergency Department Although frequently encountered in the emergency department, many cases of vaginal foreign body are unusual and often difficult to detect.

© JOSE LUIS PELAEZ INC / GETTY IMAGES

V

The importance of a good history and physical examination should not be ignored.

30 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

aginal foreign body (VFB) is a diagnosis that is often encountered in the emergency department (ED), yet it may be easily misdiagnosed. Several dynamics are present in the ED setting that can contribute to misdiagnosis and delayed treatment. Each year in the United States, there are countless ED visits that result in the diagnosis of VFB; however, the number of cases that were initially missed or misdiagnosed remains unknown. Serious consequences of delayed diagnosis and treatment can include infection, vaginal abrasion, ulceration, perforation, and fistula.1 Many cases are not straightforward and can become zebras in the ED setting: unusual cases that are difficult to detect.

The presentation of VFB can be considered a zebra by many ED clinicians, especially in light of the plethora of more common diagnoses such as candidiasis, bacterial vaginosis, and trichomoniasis.2 Forgotten tampons are one VFB cited frequently in the majority of cases.3 Despite the known educational maxim that touts that clinicians should “focus on the horses — the most common presentations of medical problems — and not the zebras”,4 in the case of VFB, clinicians might fare better by considering the zebra cases and by placing VFB on the top of their differential diagnosis list, especially for patients who return to the ED for the same complaint (also referred to as “bounce-back patients”). Moreover, the importance of a good history and physical examination (including a

pelvic exam) should not be ignored, most particularly in these cases.

The following case study highlights these central points and the necessity of a thorough work-up.

Case Study

The patient, a 33-year-old woman, was seen in a local ED with complaints of increased vaginal discharge, vague abdominal pain, and odor that have persisted for “several days.” Her vital signs were within normal limits. She was a poor historian, as she was unable to remember many details when asked. She stated that she may have had some burning on urination 3 days earlier. She denied any flank pain. She stated that she did not recall when the discharge began, but she reported that the abdominal pain began recently. Her voided urinalysis showed bacteria, scant white blood cells, positive squamous cells, and no nitrites. Her urine pregnancy test was negative.

She was seen by a physician who diagnosed her with a urinary tract infection. The patient was discharged home with a prescription for sulfamethoxazole/trimethoprim double strength (Bactrim®). There was no documentation that a pelvic examination was performed.

After 2 weeks, the patient returned to the ED, at which time she was seen by a physician’s assistant (PA) who noted her chief complaint as vaginal discharge, abdominal pain, and pelvic pain. She stated that she had recently finished “some antibiotics.” Her vital signs were again within normal limits.

Her voided urine showed results similar to those seen at her first encounter.The PA performed a pelvic examination but did not note any obvious abnormalities.The patient was sent for a computed tomographic (CT) scan of the abdomen and pelvis, which was reported as showing nonspecific findings.

Wet prep showed 1+ clue cells, 2+ white blood cells, and 0 yeast.The patient was diagnosed with bacterial vaginitis and pelvic inflammatory disease pending lab results. She was discharged home with a prescription for doxycycline and metronidazole (Flagyl®) after receiving a one-time intramuscularly administered dose of ceftriaxone (Rocephin®) 250 mg in the ED. Four weeks later, the patient returned to the ED complaining of dyspareunia, increased pelvic/abdominal pain, and vaginal discharge. The patient described her pain as unique to her lower abdomen and pelvic area this time. During this encounter, the patient was seen by a nurse practitioner (NP), who documented a more detailed history and a more extensive physical examination, including a pelvic exam. It was noted on examination that the patient had increased tenderness upon palpation and inspection of the vaginal vault. A VFB was seen this time and documented by the NP.The VFB was noted as an almost unrecognizable tampon with malodorous, whitish

discharge. It was removed without incident; there was a trace of bleeding and some mild discomfort to the patient.The patient appeared shocked to learn that there was a retained tampon in her vagina and could not recount previously forgetting to remove her tampon, nor could she recall any incident that would lead her to believe that there was a VFB accounting for her symptoms.

Discussion

While the patient may be unwilling or unable to provide accurate historical details initially, the diagnosis of VFB hinges on thorough details that may come after the initial work-up.

Patients may honestly not remember a retained foreign body and the unique anatomy may not readily alert the patient to the fact that a VFB is present.

The most common symptom in these cases is the production of increased vaginal secretions.3 Unfortunately, increased vaginal secretions and vaginal discharge is a nonspecific symptom of various medical problems and a common gynecologic complaint by women.5 In the case study, a pelvic examination was not performed until the patient returned for a second time to the ED, and then, nothing abnormal was seen by the provider.

This might be attributed to a wide variety of factors including the clinical expertise of the provider, the skill of the provider in performing pelvic exams, the natural course of progression of the foreign body itself, or the fast-paced environment of the ED, which can lead to some providers not being as thorough as possible when faced with multiple patients being treated at the same time and a lobby full of patients waiting to be seen.

Time can be saved by not performing a pelvic exam, especially when VFB is low on the list of possible conditions or when VFB is mistakenly excluded.

In the case study, a CT of the abdomen and pelvis was ordered and obtained; however, this was done to exclude any abdominal pathology.The fact that the VFB was not detected

by CT perhaps illustrates another important point: there is documentation in the literature that magnetic resonance imaging (MRI) is the best modality for the detection of VFBs.5 Nonetheless, since MRIs are frequently difficult to obtain due to cost, they may be discouraged in the ED setting.

In addition, as providers may be required to obtain approval prior to ordering the study, they may not be routinely ordered.

Bedside ultrasound has also been documented in the literature as a good choice for detection of VFB.6 As clinicians, we must remember that a thorough history and physical examination will help us to recognize both the horse and the zebra. Unfortunately, sometimes the historical details only become clearer as the symptoms progress or on subsequent evaluation of bounce-back patients. Hawkins et al7 identified a list of pertinent questions clinicians should

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 31

CLINICAL CASE CHALLENGE

Increased vaginal secretions and discharge are nonspecific symptoms of various medical problems and are a common gynecologic com­plaint. consider when conducting a patient interview, including an obvious question about whether or not the patient uses tampons, which can be easy to forget to ask in clinical practice if VFB is not high on your list of differential diagnoses.

In this case, a zebra was missed due to several factors, most importantly, the initial lack of a thorough history and physical examination. Clinicians must be aware that when this type of bounce-back patient presents to the ED, the zebra diagnosis of VFB must be placed high on the list of potential diagnoses.■

References 1. Amidat A, Taylor A. Unusual presentation of vaginal foreign body.

J Obstet Gynecol. 2010;30(8):873-875.

2. Raphaelidis L. Uncommon vaginitis cases: expect the unexpected.

J Nurse Pract. 2015;11(1):135-138.

3. Nwosu EC, Rao S, Igweike C, Hamed H. Foreign objects of long duration in the adult vagina. J Obstet Gynaecol. 2005;25(7):737-739.

4. Smith CS, Paauw DS. When you hear hoof beats: four principles for separating zebras from horses. J Am Board Fam Pract. 2000;13:424-429.

5. Nanda S, Malhotra V, Yadav S, et al. Foreign body in the vagina mimicking a transverse vaginal septum. J Gynecol Surg. 2014;30(6):386-389.

Patrick Ayarzagoitia, DNP,APRN, FNP-BC, is the CEO, professor, and founder of Education for Advanced Practice, LLC, the mission of which is to provide low-cost, high-quality education for advanced practice providers and students. Dr Ayarzagoita also works in the emergency department for Schumacher Clinical Partners.

6. Sivitz A. Ultrasonography: expanding bedside applications in the pediatric emergency department setting. Contemp Pediatr. 2011;28(4):48-58.

7. Hawkins JW, Roberto-Nichols DM, Stanley-Haney JL (eds). Bacterial vaginosis. In: Guidelines for Nurse Practitioners in Gynecologic Settings, 10th ed.

New York; Springer Publishing Company; 261-262.

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32 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

CME FEATURED COURSE EDUCATIONAL OBJECTIVES At the conclusion of this activity, participants will be able to: • Discuss the comorbidities and complications which make treatment and management decisions more complex • Determine the most appropriate treatment approaches to psoriasis based on individualized patient needs

COMPLETE THE POSTTEST: Page 41

Release Date: June 20, 2018 Expiration Date: June 20, 2019 Estimated Time to Complete: 30 minutes Maximum Credits: 0.50 AMA PRA Category 1 CreditTM Accredited Provider: This activity is jointly provided by A. Webb Roberts Center for Continuing Medical Education (AWRC) and International Psoriasis Council.

Commercial Supporter: This activity is supported by educational grants from Janssen Scientific Affairs, LLC, Lilly, and Sun Pharma.

Partner:This activity is provided in partnership with the International Psoriasis Council.

Program Description: A 49-year-old woman with a history of psoriasis is referred to your office.

She developed psoriasis at the age of 5. After a trial with etanercept to treat her psoriasis, she develops Hodgkin’s disease.This case discusses the relationships among psoriasis, Hodgkin’s lymphoma, and anti-tumor necrosis factor therapy.

Intended Audience: This activity was developed for dermatologists, physicians, physician assistants, nurse practitioners, nurses, pharmacists, and other healthcare providers who treat patients with psoriasis.

Conflict of Interest Disclosure Policy: It is the policy of the A. Webb Roberts Center for Continuing Medical Education of Baylor Scott & White Health, Dallas to inform each speaker of his/her responsibility to disclose to the attendees when products or procedures discussed are off-label, unlabeled, experimental, and/or investigational (not FDA approved) and of any limitations on the information that is presented, such as data that are preliminary or that represent ongoing research, interim analyses, and/or unsupported opinion.

Each speaker reported he/she will notify the audience if/when discussion includes off-label, unlabeled, experimental, and/or investigational (not FDA approved) information or limited use references within the content of his/her presentation.

Faculty Alan Menter, MD Chief of Dermatology Baylor University Medical Center Director, Baylor Psoriasis Research Center Clinical Professor, University of Texas Southwestern Medical Center Dallas,TX Dr. Menter has nothing to disclose.

Accredited Provider Disclosures: The A. Webb Roberts Center for Continuing Medical Education of Baylor Scott and White Health staff involved in the planning and content review of this activity have no relevant financial relationships to disclose.

Publishing Staff Disclosures: Daniel Duch, PhD, has nothing to disclose.

Accreditation Statement: A. Webb Roberts Center for Continuing Medical Education (AWRC) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Designation Statement: A. Webb Roberts Center for Continuing Medical Education (AWRC) designates this enduring material for a maximum of 0.50 AMA PRA Category 1 Credit(s)TM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Disclosure of Unlabeled Use: This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the FDA. AWRC does 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 any organization associated with this activity. 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 in this activity should not be used by clinicians without evaluation of patient conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities.

Non-Endorsement of Products: The A. Webb Roberts Center for Continuing Medical Education of Baylor Scott & White Health, Dallas does not imply either real or implied endorsement of any product, service, or company referred to in this educational activity.

Instructions: There are no fees for participating in and receiving CME credit for this activity. During the period June 20, 2018 through June 20, 2019, participants must: 1) read the learning objectives and faculty disclosures; 2) complete the pre-assessment test; 3) respond to all polling questions online; 4) study the educational activity; and 5) complete the post-test and evaluation form 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/Oct18feature.

If you have any questions relating to the accreditation of this activity, please contact CME@BSWHealth.org.

If you have any questions relating to your certificate or other issues with this activity, please contact myCME. Support@haymarketmedical.com.

Jointly provided by

CME FEATURED COURSE: ALAN MENTER, MD

Case study: A 49-year-old woman with psoriasis and Hodgkin’s disease This case discusses how the comorbidities and complications of psoriasis make treatment and management decisions more complex.

A

49-year-old woman with a history of psoriasis since she was 5 years of age is referred to your office. She initially experienced psoriasis on her legs. She has no history of psoriatic arthritis.

Physical exam

• Height: 5 ft. 3 in,Weight: 179 lbs.; BMI = 31.7 • She has erythematous indurated plaques over the upper extremities, trunk, abdomen, buttocks, bilateral lower extremities and feet • Groin involvement is noted • You find plaques over 50% of body surface area (BSA) • Her scalp has confluent involvement • Her bilateral palms, soles, and 10/10 fingernails clear • Joints: normal – no evident psoriatic arthritis

© BIOPHOTO ASSOCIATES / SCIENCE SOURCE

Past medical history and medications

• PUVA (psoralen and ultraviolet A) × 6 months — Patient experienced some mild relief • Cyclosporine 4mg/kg/day 1997 (3-4 months) — No response Plaque psoriasis is a chronic, relapsing, autoimmune disorder characterized by red skin plaques with a silver scale.

Family history

• The patient’s paternal grandmother, father, 2 daughters have psoriasis • Mother had leukemia • Father had colon cancer

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 35

CME FEATURED COURSE

Psoriasis can have a negative impact on healthrelated quality of life and is linked to several behavioral and systemic comorbidities.

Social history

• Patient is married and lives with her husband • They have 2 daughters • Drinks on holidays • Nonsmoker Discussion: Psoriasis overview

Psoriasis is a chronic systemic, immune-mediated, inflammatory disorder of the skin that affects 2% to 3% of the global population.1,2 Its presentation can vary widely, but is characterized by the common features of erythema, skin thickening, and scaling.1,2 Its most prevalent phenotype is plaque-type, although other less common subtypes may occur.1 There are still no definitive genetic or biochemical markers for psoriasis, and it continues to be diagnosed primarily based on skin manifestations.2 The disease impact on patients is affected not only on the percentage of body surface area of the lesions but also on their location. Involvement of the hands, feet, scalp, and genital areas can have a disproportionate effect on quality of life and disability.2,3 In addition, psoriasis often has a large negative impact on health-related quality of life, and is linked with a number of behavioral and systemic comorbidities in many patients.4 These comorbidities include obesity; cardiovascular disease (CVD); metabolic syndrome; hypertension; diabetes; other immune-related ailments such as Crohn’s disease; liver, kidney and psychiatric disease; and an excess risk of mortality.4-7 Patients with psoriasis are also at greater risk of developing a malignancy.8 Psoriasis patients often suffer from depression, and more frequently smoke and drink alcohol to excess.4 Additionally, in a significant subset of psoriasis patients, the disease process involves progressive damage to the articular joints, leading to arthritis and enthesopathy.9 Treatments of psoriasis can be classified as topical, systemic, or phototherapeutic.Topical therapy alone is indicated in mild psoriasis.10 These include low-potency corticosteroids (betamethasone, desoximetasone), vitamin D analogs (calcipotriol), retinoids, and calcineurin inhibitors (tacrolimus).11-14 However, if the scalp, palms, soles, and genital region are affected, compliance is generally poor because application is difficult. For the scalp and genitalia, creams and ointments are less acceptable to patients than solutions, lotions, and mousse.2,12,15 Phototherapy, including normal sunlight, is also used as adjunctive treatment for mild to moderate psoriasis.13 PUVA—a combination of psoralen (administered either systemically or topically) with controlled UVA light—has been found to inhibit the rapid skin cell hyperplasia in psoriatic skin. Other phototherapy

methods include excimer laser and narrowband UVB exposure.12,13 Because of the skin sensitivity in the genital region, treatment with phototherapy or retinoids is not recommended.2,16 Given the high incidence of disability and discomfort associated with palmoplantar psoriasis, systemic treatment is often considered when there is inadequate response to topical treatments and phototherapy.17,18 These systemic treatment alternatives include nonsteroidal anti-inflammatory drugs (NSAIDs),19 methotrexate (MTX), cyclosporine, acitretin, and TNF-α inhibitors.3,20,21 MTX works well to reduce lesions in patients with severe psoriasis and good liver function, in whom risk of hepatotoxicity due to MTX is minimal.24,25,33 However, MTX does not work on axial disease, and it has not shown effectiveness as monotherapy in preventing radiologic progression of joint deterioration.7,34 The growing knowledge on molecular and cellular processes involved in the pathogenesis of psoriasis has allowed the development of biological therapies, and biosimilar therapies, directed to T-lymphocytes and cytokines, including agents that target TNF-α (adalimumab, etanercept, and infliximab), IL-12/IL-23 (ustekinumab), IL-17A (brodalumab, ixekizumab, and secukinumab), LFA 1-3 (alefacept), and CD 211a (efalizumab).22,23 In addition to these biologic agents, several IL23p19 blockers are being developed for the treatment of plaque psoriasis:24 guselkumab was recently approved for the treatment of patients with moderate-to-severe plaque psoriasis; the approval of tildrakizumab, also targeting IL-23, was approved by the FDA for treatment of moderate-to-severe plaque psoriasis March 2018; and risankizumab is in Phase 3 trials.24 The National Psoriasis Foundation (NPF) recommends that approved biologic agents should be considered first-line treatment in the management of moderate-to-severe plaque psoriasis.25 ■ Case discussion

The patient asks about using a biologic agent for therapy.You discuss the various available options, including efficacy and adverse events, and together decide on a trial with the TNF-α inhibitor, etanercept.

POLLING QUESTION

Is there an increased baseline risk of lymphoma in patients with psoriasis?

a. Yes b. Yes, but only if they have other risk factors c. No

36 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

The increased risk of malignancy in patients with psoriasis may be due to the inflammatory and immunologic consequences of the disease.

Discussion: Psoriasis and malignancy

The correct answer is a. Yes. Patients with psoriasis have a greater prevalence and higher baseline risk of malignancies such as lymphoma,8 nonmelanoma skin cancer,26-28 cutaneous T-cell lymphoma,5 and solid organ cancer.28-30 This may be a manifestation of the inflammatory and immunologic consequences of the disease itself, or it could be secondary to comorbidities, modifiable risk factors (e.g., smoking, alcoholism, dyslipidemia and, obesity—which are generally higher in patients with psoriasis), or the effects of therapies.31,32 Much of what is known about the risk of malignancy in psoriasis comes from analysis of studies that did not adequately account for confounders and relied on data from hospitalized patients, who were more likely to have severe psoriasis and/or different cancer types than other psoriasis patients. Those studies reported substantial increases in the risk of all cancers, lung cancer, and colon cancer among psoriasis patients versus the general population.28,30,33 In contrast, the Iowa Women’s Health Study attempted to address confounders by controlling for age, education level, smoking status, anthropometric characteristics, alcohol intake, physical activity level, reproductive history, use of oral contraceptives, and hormonal therapy.10 That study found that after these adjustments, among solid organ cancers, psoriasis was only associated with colon cancer (hazard ratio [HR] = 1.5 for mild, 1.9 for severe psoriasis), and that smoking was the determining factor.34 Thus, the increased risk of malignancy in patients with psoriasis may be a manifestation of the inflammatory and immunologic consequences of the

disease itself, or it could be secondary to comorbidities, modifiable risk factors (e.g., smoking, alcoholism, dyslipidemia, and obesity, which are generally higher in patients with psoriasis), or the effects of therapies.31,32 Psoriasis has been associated with an increased risk of lymphoma due to its pathophysiology, its treatments, or a combination of these factors.27 It has been reported that this association is strongest for Hodgkin’s lymphoma and cutaneous T-cell lymphoma.27 However, cutaneous T-cell lymphoma is frequently misdiagnosed as psoriasis,35 and therefore this increased incidence of cutaneous T-cell lymphoma in psoriasis is debatable.

POLLING QUESTION:

What is the increased baseline risk of lymphoma in patients with psoriasis?

a. <2-fold b. 2.1 to 3-fold c. 3.1 to 4-fold d. 4.1 to 5-fold Discussion

The correct answer is a. < 2-fold. Overall, studies8,26,27,36 assessing lymphoma risk in patients with psoriasis found persistently increased risks of lymphoma (1.3- to 2-fold increased).

POLLING QUESTION:

Given the patient’s family history of malignancy, should a TNF- α inhibitor be considered for treatment of psoriasis in this patient? (Select the best answer.)

© JAMES CAVALLINI / SCIENCE SOURCE

a. Yes, there is no evidence that TNF-α inhibitors have any effect on malignancies. b. Yes, because short- to intermediate-term treatment with TNF-α inhibitors appears to be safe. c. No, because TNF-α inhibitors, although approved for treatment of psoriasis, have been found to increase the incidence of colon cancer. d. No, any family history of malignancy is a contraindication for the use of biologic agents such as TNF-α inhibitors.

Discussion The cellular origin of Hodgkin’s lymphoma is B-lymphocytes and diagnosis is made by presence of large, multi-nucleated ReedSternberg cells.

The correct answer is b.Yes, because short- to intermediateterm treatment with TNF-α inhibitors appears to be safe.

Elevated levels of TNF-α have been found in both the affected

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 37

CME FEATURED COURSE

It is recommended that the decision to use a TNF antagonist in patients with a history of malignancy, particularly lymphoma, should be carefully considered. skin and serum of patients with psoriasis.These elevated levels indicate the importance of TNF-α in the pathophysiology of psoriasis;3 and the increased levels also have a significant correlation with psoriasis severity as measured by the psoriasis area and severity index (PASI) score.37 Successful treatment of psoriasis with TNF-α inhibitors leads to a decreases numbers of T-cells and a reduction of epidermal hyperplasia in psoriatic skin.38 Short- to intermediate-term treatment with biologics (e.g., up to 7 years39) appears to be very safe with respect to lymphoma risk, especially with TNF-α inhibitors in which their potential risks appear to be well defined.40,41 An analysis of 7 years of the ESPRIT registry, which followed patients treated with psoriasis with adalimumab, found no significant increase in lymphoma compared with controls.39 However, it is recommended that the decision to use TNF antagonist in patients with a history of malignancy, particularly lymphoma, should be carefully considered.3 POLLING QUESTION:

With TNF- α as monotherapy, is there any evidence of increased risk of Hodgkin’s lymphoma?

a. Yes, studies have indicated a 50% increased risk of lymphoma over baseline with TNF-α as monotherapy. b. Yes, studies have indicated a two-fold increased risk of lymphoma over baseline with TNF-α as monotherapy. c. Yes, studies have indicated a three-fold increased risk of lymphoma over baseline with TNF-α as monotherapy. d. No, studies have indicated no significant increased risk of lymphoma over baseline with TNF-α as monotherapy.

Discussion

The correct answer is d. studies have indicated no significant increased risk of lymphoma over baseline with TNF-α as monotherapy. Treatment with TNF-α is not associated with increased malignant risks of overall cancer, lymphoma, or melanoma in psoriasis patients.39,41 In 1 case study, a 59-yearold Caucasian with a history of primary B-cell lymphoma, severe recalcitrant plaque-type psoriasis and psoriatic arthritis, was started on etanercept for treatment of his psoriasis and psoriatic arthritis.42 After treatment, the patient experienced significant global improvement with essentially complete remission of the cutaneous lesions and arthritis, and had no recurrence of his lymphoma or other systemic complications while on etanercept after follow-up for > 3 years.

POLLING QUESTION:

In other autoimmune diseases such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), and inflammatory bowel disease (IBD), are TNF- α inhibitors associated with an increased risk of lymphoma?

a. Yes b. No c. Data is not conclusive Discussion

The correct answer is a.Yes. Anti-TNF medications have been associated with higher rates of malignancy in these other autoimmune diseases compared with the general population.43-45 Studying the link between lymphoma and disease severity in RA is complicated because patients with persistently active disease are at increased risk for lymphoma.46 However, in clinical trials of TNF-α inhibitors with RA and IBD patients, approximately 50% of patients are on systemic, pre-existing therapies, which potentially plays a role in increasing the risk of lymphoma. In addition, disease severity correlates with more intense use of immunosuppressive medications.46 Overall, cancer risk in patients with RA is slightly above that of the general population, with the increased risk likely secondary to an increased risk of lymphomas in those with high disease activity.46 Therefore, anti-TNF agents are contraindicated in patients who have had lymphoproliferative disease within the past 5 years, and in patients with demyelinating disorders.47 ■ Case continues

Etanercept was initiated in 2003 at standard dosing, and it was discontinued after 6 months therapy because the patient was diagnosed with Hodgkin’s lymphoma.The patient was placed on chemotherapy in May of 2004, and her psoriasis cleared.

In 2005, she received radiation and her psoriasis flared. Her Hodgkin’s disease was then in remission.

Discussion

In psoriasis patients,TNF-α inhibitors are used as monotherapy, unlike other autoimmune diseases where they are used in combined with methotrexate (MTX). This may be part of the reason why there has been no increased risk of lymphoma in psoriasis patients when TNF-α inhibitors are used. The treatment of patients with early-stage Hodgkin’s lymphoma is one of the success stories of modern oncology.48 More than 90% of patients with early-stage Hodgkin’s lymphoma survive for more than 5 years after treatment with chemotherapy.48

38 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

In the appropriate patient, the risk-to-benefit profile of psoriasis treatment with respect to lymphoma risk appears to be highly favorable.

■ Case continues

After discussion with the patient, she was placed on MTX therapy in 2005.

When examined in June,2009 with CT scan and liver biopsy, the patient was found to have liver cirrhosis. MTX discontinued in 2009.

that most patients remained free of all treatment emergent cardiovascular events, serious infections, and malignancy.39 Therefore, in the appropriate patient, the risk-to-benefit profile of psoriasis treatment with respect to lymphoma risk appears to be highly favorable.

References

Laboratory tests

1. Gottlieb AB, Greb JE, Goldminz AM. Psoriasis Trends and Practice Gaps.

• Complete blood count (CBC): ——White blood cells (WBC): 3,400 x103/uL (normal= 4,300-10,800) ——Platelets: 65,000/uL (normal= 150,000-400,000) • Comprehensive metabolic panel (CMP): Alkaline phosphatase: 161 IU/L (normal= 25- 150) • Hepatitis panel: normal • Gamma-glutamyl transferase (GGT): 88 iU/L (normal= 0-60)

Dermatol Clin. 2016;34(3):235-242.

2. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: case-based presentations and evidence-based conclusions. J Am Acad Dermatol. 2011;65(1):137-174.

3. Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58(5):826-850.

Discussion

4. Kimball AB, Gladman D, Gelfand JM, et al. National Psoriasis Foundation

The decreased WBC may indicate lymphopenia; platelet levels may increase or decrease with lymphoma; GGT elevated due to liver damage.

clinical consensus on psoriasis comorbidities and recommendations for screening. J Am Acad Dermatol. 2008;58(6):1031-1042.

5. Boehncke WH, Boehncke S. More than skin-deep: the many dimensions of the psoriatic disease. Swiss Med Wkly. 2014;144:w13968.

Summary

6. Yeung H, Takeshita J, Mehta NN, et al. Psoriasis severity and the prevalence

This patient has a longstanding history of psoriasis with a moderate response to multiple traditional systemic antipsoriatic medications. She developed Hodgkin’s disease after she started a trial with etanercept therapy. After the therapy was stopped, and was successfully treated to remission. She began therapy with MTX, but developed liver cirrhosis after 4 years of therapy.

of major medical comorbidity: a population-based study. JAMA dermatology.

2013;149(10):1173-1179.

7. Ogdie A, Haynes K, Troxel AB, et al. Risk of mortality in patients with psoriatic arthritis, rheumatoid arthritis and psoriasis: a longitudinal cohort study.

Ann Rheum Dis. 2014;73(1):149-153.

8. Margolis D, Bilker W, Hennessy S, Vittorio C, Santanna J, Strom BL. The risk of malignancy associated with psoriasis. Arch Dermatol. 2001;137(6):778-783.

9. Gelfand JM, Gladman DD, Mease PJ, et al. Epidemiology of psoriatic arthritis

Discussion

in the population of the United States. J Am Acad Dermatol. 2005;53(4):573.

Psoriasis has been associated with an increased risk of lymphoma, especially Hodgkin’s disease. It has been postulated that anti-TNF drugs might increase lymphoma risk in RA, where the rate of lymphoma is slightly increased as it is in psoriasis. An increased rate of lymphoma has also been reported in ankylosing spondylitis following 6 months of etanercept treatment.49 However, examination of psoriasis patients having up to 7 years of treatment with biologics appears to be very safe with respect to lymphoma risk.39 This study (ESPRIT) is an ongoing 10-year international prospective observational registry that is evaluating the long-term safety and effectiveness of adalimumab in routine clinical practice for adult patients with chronic plaque psoriasis.39 Examination of the registry after 7 years found

10. Gisondi P, Del Giglio M, Girolomoni G. Treatment Approaches to Moderate to Severe Psoriasis. Int J Mol Sci. 2017;18(11).

11. Kircik LH, Kumar S. Scalp psoriasis. Journal of drugs in dermatology : JDD. 2010;9(8 Suppl ODAC Conf Pt 2):s101-105.

12. Crowley J. Scalp psoriasis: an overview of the disease and available therapies. Journal of drugs in dermatology : JDD. 2010;9(8):912-918.

13. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy. J Am Acad Dermatol. 2010;62(1):114-135.

14. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad Dermatol. 2009;60(4):643-659.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 39

CME FEATURED COURSE

15. Zivkovich AH, Feldman SR. Are ointments better than other vehicles for

33. Hannuksela-Svahn A, Pukkala E, Laara E, Poikolainen K, Karvonen J.

corticosteroid treatment of psoriasis? Journal of drugs in dermatology : JDD.

Psoriasis, its treatment, and cancer in a cohort of Finnish patients. J Invest

2009;8(6):570-572.

Dermatol. 2000;114(3):587-590.

16. Meeuwis KA, de Hullu JA, Massuger LF, van de Kerkhof PC, van Rossum

34. Prizment AE, Alonso A, Folsom AR, et al. Association between psoriasis

MM. Genital psoriasis: A systematic literature review on this hidden skin

and incident cancer: the Iowa’s Women’s Health Study. Cancer Causes Control.

disease. Acta Derm Venereol. 2011;91(1):5-11.

2011;22(7):1003-1010.

17. Farley E, Masrour S, McKey J, Menter A. Palmoplantar psoriasis: a pheno-

35. Guitart J, Martinez-Escala ME, Subtil A, et al. Primary cutaneous aggres-

typical and clinical review with introduction of a new quality-of-life assess-

sive epidermotropic cytotoxic T-cell lymphomas: reappraisal of a provisional

ment tool. J Am Acad Dermatol. 2009;60(6):1024-1031.

entity in the 2016 WHO classification of cutaneous lymphomas. Mod Pathol.

18. Bulai Livideanu C, Lahfa M, Mazereeuw-Hautier J, Paul C. Efficacy of

2017;30(5):761-772.

ustekinumab in palmoplantar psoriasis. Dermatology. 2010;221(4):321-323.

36. Gelfand JM, Berlin J, Van Voorhees A, Margolis DJ. Lymphoma rates are

19. Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for the man-

low but increased in patients with psoriasis: results from a population-based

agement of psoriasis and psoriatic arthritis: Section 2. Psoriatic arthritis: over-

cohort study in the United Kingdom. Arch Dermatol. 2003;139(11):1425-1429.

view and guidelines of care for treatment with an emphasis on the biologics.

37. Mussi A, Bonifati C, Carducci M, et al. Serum TNF-alpha levels correlate

J Am Acad Dermatol. 2008;58(5):851-864.

with disease severity and are reduced by effective therapy in plaque-type

20. Ash Z, Gaujoux-Viala C, Gossec L, et al. A systematic literature review of

psoriasis. J Biol Regul Homeost Agents. 1997;11(3):115-118.

drug therapies for the treatment of psoriatic arthritis: current evidence and

38. Zaba LC, Cardinale I, Gilleaudeau P, et al. Amelioration of epidermal

meta-analysis informing the EULAR recommendations for the management

hyperplasia by TNF inhibition is associated with reduced Th17 responses.

of psoriatic arthritis. Ann Rheum Dis. 2012;71(3):319-326.

J Exp Med. 2007;204(13):3183-3194.

21. Heydendael VM, Spuls PI, Opmeer BC, et al. Methotrexate versus

39. Menter A, Thaci D, Wu JJ, et al. Long-Term Safety and Effectiveness of

cyclosporine in moderate-to-severe chronic plaque psoriasis. N Engl J Med.

Adalimumab for Moderate to Severe Psoriasis: Results from 7-Year Interim

2003;349(7):658-665.

Analysis of the ESPRIT Registry. Dermatology and therapy. 2017.

22. Vide J, Magina S. Moderate to severe psoriasis treatment challenges

40. Dommasch E, Gelfand JM. Is there truly a risk of lymphoma from biologic

through the era of biological drugs. An Bras Dermatol. 2017;92(5):668-674.

therapies? Dermatol Ther. 2009;22(5):418-430.

23. Ronholt K, Iversen L. Old and New Biological Therapies for Psoriasis.

41. Dommasch ED, Abuabara K, Shin DB, Nguyen J, Troxel AB, Gelfand JM.

Int J Mol Sci. 2017;18(11).

The risk of infection and malignancy with tumor necrosis factor antagonists

24. Tonini A, Gualtieri B, Panduri S, Romanelli M, Chiricozzi A. A new class of

in adults with psoriatic disease: a systematic review and meta-analysis of ran-

biologic agents facing the therapeutic paradigm in psoriasis: anti-IL-23 agents.

domized controlled trials. J Am Acad Dermatol. 2011;64(6):1035-1050.

Expert Opin Biol Ther. 2017:1-14.

42. Chong BF, Wong HK.Treatment of psoriasis with etanercept in a patient with

25. Hsu S, Papp KA, Lebwohl MG, et al. Consensus guidelines for the manage-

a history of primary B-cell lymphoma. Clin Exp Dermatol. 2009;34(5):e11-13.

ment of plaque psoriasis. Arch Dermatol. 2012;148(1):95-102.

43. Askling J, Baecklund E, Granath F, et al. Anti-tumour necrosis factor

26. Brauchli YB, Jick SS, Miret M, Meier CR. Psoriasis and risk of incident can-

therapy in rheumatoid arthritis and risk of malignant lymphomas: relative

cer: an inception cohort study with a nested case-control analysis. J Invest

risks and time trends in the Swedish Biologics Register. Ann Rheum Dis.

Dermatol. 2009;129(11):2604-2612.

2009;68(5):648-653.

27. Gelfand JM, Shin DB, Neimann AL, Wang X, Margolis DJ, Troxel

44. Hellgren K, Baecklund E, Backlin C, Sundstrom C, Smedby KE, Askling

AB. The risk of lymphoma in patients with psoriasis. J Invest Dermatol.

J. Rheumatoid Arthritis and Risk of Malignant Lymphoma: Is the Risk Still

2006;126(10):2194-2201.

Increased? Arthritis & rheumatology (Hoboken, NJ). 2017;69(4):700-708.

28. Ji J, Shu X, Sundquist K, Sundquist J, Hemminki K. Cancer risk in hos-

45. Chen Y, Friedman M, Liu G, Deodhar A, Chu CQ. Do tumor necrosis

pitalised psoriasis patients: a follow-up study in Sweden. Br J Cancer.

factor inhibitors increase cancer risk in patients with chronic immune-

2009;100(9):1499-1502.

mediated inflammatory disorders? Cytokine. 2016;in press.

29. Anderson LA, Gadalla S, Morton LM, et al. Population-based study of

46. Wilton KM, Matteson EL. Malignancy Incidence, Management, and

autoimmune conditions and the risk of specific lymphoid malignancies. Int J

Prevention in Patients with Rheumatoid Arthritis. Rheumatology and therapy.

Cancer. 2009;125(2):398-405.

2017;4(2):333-347.

30. Boffetta P, Gridley G, Lindelof B. Cancer risk in a population-based

47. Saag KG,Teng GG, Patkar NM, et al. American College of Rheumatology 2008

cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol.

recommendations for the use of nonbiologic and biologic disease-modifying

2001;117(6):1531-1537.

antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum. 2008;59(6):762-784.

31. Bernatsky S, Ramsey-Goldman R, Clarke A. Malignancy and autoimmunity.

48. Armitage JO. Early-stage Hodgkin’s lymphoma. N Engl J Med.

Curr Opin Rheumatol. 2006;18(2):129-134.

2010;363(7):653-662.

32. de Visser KE, Eichten A, Coussens LM. Paradoxical roles of the immune

49. Aksu K, Donmez A, Ertan Y, et al. Hodgkin’s lymphoma following treatment

system during cancer development. Nat Rev Cancer. 2006;6(1):24-37.

with etanercept in ankylosing spondylitis. Rheumatol Int. 2007;28(2):185-187.

40 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

CME

POSTTEST Expiration date: June 20, 2019

A statement of credit will be issued only upon receipt of a completed preassessment test, activity evaluation form, and posttest with a score of 70% or higher. All components must be completed and submitted online at ClinicalAdvisor.com/Oct18feature.

CREDITS: 0.50 | Case study challenge: A 49-year-old woman with psoriasis and Hodgkin’s disease

1. What is the increased risk of lymphoma in patients with psoriasis? d. 3.1 to 4-fold a. No increased risk e. 4.1 to 5-fold b. < 2-fold c. 2.1 to 3-fold 2. A patient is referred to you with a severe case of plaque psoriasis that has not been well-controlled. His family history includes a father with prostate cancer, a mother with leukemia, and a sister with colon cancer. Should treatment with a tumor necrosis factor (TNF) inhibitor be considered for this patient? c. Only if he does not drink a. Yes alcohol or smoke b. No 3. Which of the following statements is TRUE regarding TNF inhibitors as monotherapy when treating psoriasis? a. Studies have indicated a decreased risk of lymphoma over baseline with TNF-α as monotherapy. b. Studies have indicated a 50% increased risk of lymphoma over baseline with TNF-α as monotherapy. c. Studies have indicated a two-fold increased risk of lymphoma over baseline with TNF-α as monotherapy. d. Studies have indicated a three-fold increased risk of lymphoma over baseline with TNF-α as monotherapy. e. Studies have indicated no significant increased risk of lymphoma over baseline with TNF-α as monotherapy.

4. The ESPRIT study is an ongoing 10-year international prospective observational registry evaluating the long-term safety and effectiveness of adalimumab in routine clinical practice for adult patients with chronic plaque psoriasis.

Which of the following statements is true regarding their findings? a. There were small treatment-emergent cardiovascular risks, but no treatment-emergent increased risks for serious infections or malignancies. b. There was a small treatment-emergent risk of serious infections, but no treatment-emergent increased cardiovascular risks or malignancies. c. There was a small treatment-emergent risk of malignancies, but no treatment-emergent increased cardiovascular risks or risks of serious infections. d. There were no treatment-emergent risks of serious infections, increased cardiovascular risks, or malignancies. e. There were small treatment-emergent risks of serious infections, increased cardiovascular risk, and malignancies.

5. Which of the following are common comorbidities of psoriasis? a. Obesity d. Colon cancer b. Cardiovascular disease e. All of the above c. Diabetes f. Only a, b and c

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Dermatology Clinic CASE #1

Burning, Acneiform Eruption KATIE ARMSTRONG, PA-S; ALICIA ELAM, PHARMD

A 24-year-old white female graduate student presents with erythematous, papulopustular patches of skin in a muzzle-like distribution surrounding the mouth, chin, and glabellar region.

The lesions are tender to palpation, associated with a stinging and burning sensation, and are aggravated by exfoliating facial washes.Two-year treatment history includes a variety of topical antibiotics, azelaic acid cream, retinoid agents, benzoyl peroxide preparations, topical corticosteroids, and oral tetracycline for cyclic recurrences of outbreaks.These treatment methods were previously successful with complete resolution of each outbreak; however, at present the lesions are persisting despite treatment.

What is your diagnosis? Turn to page 44

CASE #2

Red-Brown Papules on the Extremities JUNRU YAN, BA; JOAN FERNANDEZ, BS; CHRISTOPHER RIZK, MD

An 8-year-old male child is brought to the clinic for the third time in 4 months presenting with red-brown papules with an overlying mica-like scale on the ventral side of his arms and legs. His medical and family histories are otherwise unremarkable. His mother states that when the macules and papules go away, the skin where the lesions were previously located is typically lighter than before.

What is your diagnosis? Turn to page 45 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 43

Dermatology Clinic CASE #1

Perioral Dermatitis and Candida Species

Perioral dermatitis, an acneiform eruption, is often referred to as periorificial dermatitis and rosacea-like dermatitis. It is a relatively common chronic inflammatory papulopustular dermatitis of the skin affecting the perioral region with occasional spreading to the perinasal and periocular areas.1 Perioral dermatitis is characteristically diagnosed in young to middle-aged women (ages 20 to 45 years) and is relatively uncommonly found in children.1,2 It typically manifests as a circumoral eruption of grouped scaly erythematous papules and pustules measuring 1 to 2 mm in diameter sparing the vermilion border.3 Accompanying symptoms of stinging, burning, and tenderness are often mild but can be aggravating. Although the diagnosis of perioral dermatitis appears to be uncomplicated, it is often misdiagnosed and treated inappropriately due to presenting similarly to other facial acneiform and inflammatory eruptions.4 The condition was first described by Frumess and Lewis in 1957 as a cyclic dermatitis and given the name “lightsensitive seborroeid.”2,5 The etiology of perioral dermatitis remains an enigma; however, the use of topical steroids on the face often precedes the appearance of the disease.1,2 Other common causes of perioral dermatitis include fluorinated toothpaste, cosmetics, emotional stress, hormonal factors (eg, oral contraceptives), and ultraviolet radiation.2 Microbiologic factors such as fusiform spirilla bacteria, Demodex folliculorum, Candida species, and other fungi have been implicated as causative factors in perioral dermatitis.2,6 The pathophysiology of topical steroids being the culprit in inducing perioral dermatitis is common as it leads to an overgrowth of yeast, bacteria, and other organisms in the hair follicle due to local immune suppression and impairment in the skin barrier.1,3 Confirmatory diagnosis of perioral dermatitis following topical steroid use involves clinical history of a cyclical pattern or rebound phenomenon, and clinical presentation of predominantly pustules and papules on an erythematous base localized in the circumoral region is usually enough to establish the diagnosis.1 The histopathology of perioral dermatitis from biopsied specimens consists of sebaceous hyperplasia, epidermal edema, and perifollicular and perivascular lymphocytic infiltration; this histologic appearance is similar to that of rosacea.2 Direct examination of skin scrapings and cultures can reveal the

growth of the causative organism, such as Candida and other fungi showing yeast and pseudohyphae.6,7 Skin barrier dysfunction can be assessed by conducting specific immunoglobulin E testing against numerous aeroallergens and prick testing.1 Other papulopustular facial eruptions present in a similar fashion as perioral dermatitis, but slight differences in clinical history or clinical presentation can elicit an accurate diagnosis and thus appropriate treatment. Rosacea, a type of facial acneiform eruption, is histologically similar to perioral dermatitis and affects the central face. Patients often present with a history of flushing, telangiectasias, rhinophyma, and a lack of comedones.4

Perioral dermatitis is often misdiagnosed due to presenting similarly to other facial eruptions.

Seborrheic dermatitis is predominantly retroauricular and is linked to overgrowth of Pityrosporum yeast. History will plausibly include dandruff and scaling of the scalp, eyebrows, and nasolabial region.1,4 Acne vulgaris, a common culprit in the misdiagnosis of perioral dermatitis, involves the presence of comedones, which is a major distinguishing feature in comparison to perioral dermatitis and other facial acneiform eruptions.6 Facial, chest, and back lesions can develop, but they will often lack the symptoms of itching, burning, and stinging usually experienced with perioral dermatitis. In contrast, perioral dermatitis is strictly localized to the face and characteristically spares the vermilion border. The pathophysiology of acne vulgaris is commonly referred to as “clogged pore” due to the inflammation and obstruction of pilosebaceous follicles, creating a microcomedo in areas where sebaceous glands are more prominent. Acne lesions are commonly treated with both physical and chemical exfoliators such as salicylic acid, which can worsen or irritate perioral dermatitis.

Other differential diagnoses include allergic contact dermatitis, contact dermatitis, facial demodicosis, folliculitis, nevus comedonicus, and drug-induced acneiform eruptions.3,4 The primary goal and first step in management of perioral dermatitis is referred to as “zero therapy,” meaning the discontinuation of all topical pharmacotherapies and abandonment of abrasives, moisturizers, and all other possible irritants.1 Initial worsening of symptoms is presumed with the removal of topical corticosteroid use. Initial treatment options for perioral dermatitis include systemic antibiotics

44 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

such as tetracycline, minocycline, or doxycycline for a period of 3 to 4 months for effective resolution, while other studies suggest that topical metronidazole cream should be considered initially.1-3 Topical treatments include anti-acne drugs such as benzoyl peroxide, adapalene, and azelaic acid. A combination of a systemic antibiotic with either a topical antibiotic such as clindamycin, metronidazole, or erythromycin or a topical anti-acne drug is commonly recommended.2,3 Severe cases can be treated with isotretinoin or topical immunomodulatory creams (eg, tracrolimus or pimecrolimus).1 The evaluation of coexisting perioral dermatitis and Candida species is a poorly explored topic with exiguous evidencebased reviews, but research has shown that microbiologic factors, including Candida and other fungi, have demonstrated culpability as a causative factor.1,6,7 Due to lack of evidence, topical antifungal agents have not been considered as treatment options for perioral dermatitis, although a few studies have shown patients’ cultured skin scrapings to reveal Candida albicans with rapid and complete resolution upon exposure to antifungal agents.7 For the patient in this case, her perioral dermatitis had previously been controlled with a combination of systemic and topical antibiotic therapies and retinoid agents. After several cyclical recurrences, she began to notice resistance in her typical treatment regimen. Several frustrating months went by with adjustments of both topical and systemic therapies with no resolution of symptoms. She was prescribed and recommended various treatment options including continuing the current pharmacotherapy regimen, initiating isotretinoin, or possibly considering an antifungal agent in the event the organism involved is of Candida species.

One month later, the patient returned to the clinic with remarkable improvement after the use of an over-the-counter topical antifungal, clotrimazole cream. At follow-up, after a 3-month period of applying clotrimazole topical cream, the patient remained asymptomatic and lesion free, and she was advised to continue using the cream as needed. Even though it is not well documented, the use of a topical antifungal agent proved to be effective therapy in the treatment of perioral dermatitis for the patient in our case.

Katie Armstrong is a physician assistant student at Augusta University in Georgia, and Alicia Elam, PharmD, is an associate professor and associate admissions director in the Physician Assistant Department at Augusta University.

References 1. Lipozencic J, Hadzavdic SL. Perioral dermatitis. Clin Dermatol. 2014;32(1);125-130.

2. Lipozencic J, Ljubojevic S. Perioral dermatitis. Clin Dermatol. 2011;29(2);157-161.

3. Tilton EE, Bavola C, Helms SE. Rash around the mouth: what is it? J Am Acad Dermatol. 2015;146(5);337-340.

4. Dessinioti C, Antoniou C, Katsambas A. Acneiform eruptions. Clin Dermatol.

2014;32(1);24-34.

5. Kuflik JH, Janniger CK, Piela ZC. Perioral dermatitis: an acneiform eruption.

Cutis. 2001;67(1);21-22.

6. Massone C, Propst E, Kopera D. Rosacealike dermatitis with Candida albicans infection. Arch Dermatol. 2006;142(7):927-947.

7. Bradford, Linwood G, Montes, Leopoldo F. Perioral dermatitis and Candida albicans. Arch Dermatol. 1972;105;892-895.

CASE #2

PLC and PLEVA

Pityriasis lichenoides (PL) is a benign, self-limited inflammatory cutaneous condition.

Historically, defining PL has been quite challenging as it was at one time confused as a form of parapsoriasis.1 Over time, however, the disorder has been better characterized and is now described along a spectrum, ranging from the more chronic form, pityriasis lichenoides chronica (PLC), to the more acute-phase disorder, pityriasis lichenoides et varioliformis acuta (PLEVA), also known as Mucha-Habermann disease.2 The terms acute and chronic used in this context do not refer to the onset or duration of the disease itself but to the characteristics of the lesions present on the affected individual.3 PLEVA and PLC are viewed as 2 diseases on a spectrum rather than 2 separate entities.

Both PLC and PLEVA are rare disorders; therefore, the exact prevalence, incidence, and risk factors have not been well documented. Although the disorders appear to occur more frequently in children and young adults, they have the potential to occur at any age. Studies have shown a slight male predominance among children with PL, but this gender predominance has not been observed in the general population of individuals with PL.2 The pathogenesis of PL has yet to be clearly described.

Some research has suggested that there may be associations with an aberrant immune response to bacterial, viral, or protozoal infections that lead to the development of the disease.4 More recent studies pose the hypothesis that PL is a lymphoproliferative disorder, existing at the benign end of the spectrum with lymphocytic malignancy.5,6

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 45

Dermatology Clinic In both PLC and PLEVA, patients tend to experience waves of eruptions of papules, with multiple relapsing and remitting cycles before spontaneous resolution occurs.The entire duration of symptoms can range from weeks to years, with the median duration of disease in PLEVA and PLC lasting approximately 18 and 20 months, respectively.7 The development of PLC typically occurs gradually and results in erythematous papules that have a reddish-brown hue and a micaceous scale in the center. These eruptions occur most commonly on the trunk, buttocks, and proximal portions of the extremities and, unlike PLEVA, spontaneously flatten and regress over a period of weeks. Aside from the lesions, patients with PLC are usually otherwise asymptomatic. After resolution of the papules, patients are commonly left behind with hypopigmented macules in the areas where the lesions previously existed.8 In contrast to PLC, PLEVA begins as an acute eruption of erythematous papules and macules measuring approximately 2 to 3 mm in diameter that quickly develop into papules with progressively thickening scales. These lesions, like in PLC, often occur on the trunk and proximal areas of the extremities; however, unlike in PLC, they can also display a generalized eruption pattern.2 Associated burning and pruritus occur more commonly in patients with PLEVA, whereas those with PLC generally lack symptoms outside of the lesions themselves.

Disorders that may be considered in the differential diagnosis for PLEVA include varicella, disseminated herpes simplex virus (HSV), arthropod bites, Gianotti-Crosti syndrome, and Langerhans cell histiocytosis.Varicella and disseminated HSV may be differentiated from PLEVA using polymerase chain reaction or direct fluorescence antibody testing. Arthropod bites rarely have necrotic findings and a thorough patient history is useful for diagnosis. Gianotti-Crosti syndrome and Langerhans cell histiocytosis can both be differentiated using information obtained from a skin biopsy.9 Disorders that may be considered in the differential diagnosis for PLC include lymphomatoid papulosis (LyP), pityriasis rosea, guttate psoriasis, lichen planus, secondary syphilis, and hypopigmented mycosis fungoides. LyP, unlike PLC, heals with scarring. Pityriasis rosea has a shorter resolution time frame.

Guttate psoriasis is usually preceded by a streptococcal infection. Lichen planus is often accompanied by pruritus and may also be present on the mouth, genitals, and nails. Secondary syphilis often involves the palms and soles, and serologic studies can confirm the diagnosis. Hypopigmented mycosis fungoides can be successfully differentiated via skin biopsy.10 The diagnosis of PLC and PLEVA can be made clinically, as PLEVA is typically characterized by the eruption of acute, crusting, hemorrhagic papules, whereas PLC is characterized

by red-brown papules with a micaceous scale covering.2 However, if the diagnosis is uncertain, punch biopsy followed by histologic examination of the tissue can confirm the diagnosis.7 Histologic findings characteristic of PLC include focal parakeratosis, spongiosis, band-like (lichenoid) lymphohistiocytic infiltrate in the superficial dermis, and superficial vessel dilation with no invasion of the vessel wall by inflammatory cells.2 The histologic characteristics seen in PLEVA include a more severe, diffuse parakeratosis, spongiosis, focal necrotic keratinocytes, vacuolar alteration of the basal layer, dense wedge-shaped lymphohistiocytic infiltrates into the deep reticular dermis, and engorgement of blood vessels

PLC and PLEVA are benign, self-limiting conditions that can be managed with observation and close follow-up. in the papillary dermis with extravasation of erythrocytes and lymphocytes.2 Immunohistochemical stains can also be used for the diagnosis of PLEVA, which would show a predominance of CD8+ T lymphocytes and an absence of CD30+ cells in the inflammatory infiltrate. This staining can be particularly useful for differentiating PLEVA from the clinically similar LyP. Both PLC and PLEVA are benign, self-limiting conditions that can be managed with observation and close follow-up.

Pharmacologic treatment is not required; however, patients concerned with the cosmetic disfiguration associated with the lesions frequently desire treatment. In these cases, the first-line regimen includes topical corticosteroids in combination with oral antibiotics. Topical corticosteroids, such as triamcinolone (0.1% cream), have been shown to hasten lesion clearance in some patients.11 Oral antibiotics, most commonly tetracycline in adults and erythromycin in children, are often prescribed to be used in conjunction with the topical steroids.7,12 Second-line therapies include narrowband ultraviolet B (UVB) phototherapy, broadband UVB, psoralen plus UVA (PUVA), and methotrexate.13 In this case, the clinical picture and skin biopsy were both consistent with PL.Treatment was initiated with topical corticosteroids and oral antibiotics (erythromycin).The patient responded well to therapy, with near complete resolution of his lesions. ■ JunruYan, BA, is a medical student; Joan Fernandez, BS, is a medical student; and Christopher Rizk, MD, is a dermatology resident at Baylor College of Medicine in Houston,Texas.

46 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

Continues on page 48

References

lichenoides in childhood: a retrospective review of 124 patients. J Am Acad

1. Wile UJ. Discussion of case presented by Dr. Ormsby. Arch Dermatol

Dermatol. 2007;56:205-210.

Syph. 1926;13:690.

8. Rogers M. Pityriasis lichenoides and lymphomatoid papulosis. Semin

2. Fernandes NF, Rozdeba PJ, Schwartz RA, Kihiczak G, Lambert WC.

Dermatol. 1992;11:73-79.

Pityriasis lichenoides et varioliformis acuta: a disease spectrum. Int J

9. Treat J.R Pityriasis lichenoides et varioliformis acuta. UpToDate.

Dermatol. 2010;49:257-261.

https://www.uptodate.com/contents/pityriasis-lichenoides-et-varioliformis-

3. Bowers S, Warshaw EM. Pityriasis lichenoides and its subtypes. J Am Acad

acuta-pleva. Updated August 8, 2017. Accessed September 11, 2018.

Dermatol. 2006;55(4):557-572.

10. Musiek, A Pityriasis lichenoides chronica. UpToDate.

4. Clayton R, Haffenden G, Du Vivier A, Burton J, Mowbray J. Pityriasis

https://www.uptodate.com/contents/pityriasis-lichenoides-chronica.

lichenoides - an immune complex disease. Br J Dermatol. 1977;97:629-634.

Updated August 24, 2018. Accessed September 11, 2018.

5. Magro C, Crowson AN, Kovatich A, Burns F. Pityriasis lichenoides: a clonal

11. Wahie S, Hiscutt E, Natarajan S, Taylor A. Pityriasis lichenoides: the differ-

T-cell lymphoproliferative disorder. Hum Pathol. 2002;33:788-795.

ences between children and adults. Br J Dermatol. 2007;157(5):941-945.

6. Fortson JS, Schroeter AL, Esterly NB. Cutaneous T-cell lymphoma

12. Piamphongsant T. Tetracycline for the treatment of pityriasis lichenoides.

(parapsoriasis en plaque): an association with pityriasis lichenoides et vario-

Br J Dermatol. 1974;91(3):319-322.

liformis acuta (Mucha-Haberman disease) in young children. Arch Dermatol.

13. Aydogan K, Saricaoglu H, Turan H. Narrowband UVB (311 nm, TL01)

1990;126:1449-53.

phototherapy for pityriasis lichenoides. Photodermatol Photoimmunol

7. Ersoy-Evans S, Greco MF, Mancini AJ, Subasi N, Paller AS. Pityriasis

Photomed. 2008;24(3):128-133.

“We can’t all go as Elsa from Frozen.”

48 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

© The New Yorker Collection 2018 from cartoonbank.com. All Rights Reserved.

Dermatology Clinic

Dermatologic Look-Alikes Hyperpigmented Plaques JAY PATEL, BS; JOAN FERNANDEZ, BS; CHRISTOPHER RIZK, MD

CASE #1

CASE #2

A 17-year-old female patient presents to the clinic with hyperpigmented plaques on her neck and upper trunk.

They have been present for several weeks, and both the patient and her mother report that rigorous scrubbing with soap and water does not remove the plaques. The lesions are neither painful nor pruritic, and the patient does not seem to be bothered by them. However, she thinks they are unsightly. The patient reports no other symptoms and is otherwise healthy.

A 26-year-old man presents to the clinic with a rash that began 1 year ago as small brown papules on his neck that slowly grouped and spread to his chest. He denies other symptoms or family history of similar-appearing rashes. Previous treatment with antifungal therapy did not improve the rash. Routine blood work at his last primary care appointment did not reveal any abnormalities. Shave biopsy revealed epidermal hyperkeratosis, papillomatosis, and acanthosis.

Continues on page 54

www.ClinicalAdvisor.com â&#x20AC;˘ THE CLINICAL ADVISOR â&#x20AC;˘ OCTOBER 2018 49

Dermatologic Look-Alikes CASE #1

Terra Firma-Forme Dermatosis

Terra firma-forme dermatosis (TFFD), or Duncan disease, was first described in 1987 by W. Christopher Duncan, MD.1 It is an asymptomatic condition characterized by dirt-like, hyperpigmented plaques most commonly distributed on the neck, axilla, and trunk.1 These plaques are resistant to regular washing, often leading to the clinical presentation described as “dirt” that cannot be cleaned off.1 It most frequently occurs in children and adolescents with good hygiene habits.2 There are no known predisposing risk factors,TFFD is neither lifethreatening nor contagious, and currently a pathogenic cause has not been identified.2 Although primarily a cosmetic concern, there is a high potential for unnecessary diagnostic testing and therapeutic procedures such as biopsies and blood work.3 Therefore, it is important to note that the hyperpigmented plaques in TFFD are easily distinguishable from other conditions as they can easily be rubbed off with 70% isopropyl alcohol.1 TFFD appears as light-to-dark brown, slightly elevated hyperpigmented plaques that are frequently described as “dirt like”.1-5 Patients or their parents will commonly report that the plaques are resistant to rigorous washing and scrubbing.2 These lesions can present anywhere on the body, most commonly occurring on the neck, axilla, trunk, face, scalp, and ankles.2 Currently, there is no consensus regarding the existence of predisposing risk factors. However, individual case reports have indicated emollients and sun exposure as potential causative agents. These finding are controversial as conflicting case reports have found this not to be true, describing lesions that can occur on non-sun-exposed regions of the trunk.3,6 TFFD affects both sexes equally, and with most patients being young adults and children, lesions are often first noticed by parents.3 The precise cause of TFFD has yet to be elucidated. Some case reports indicate Malassezia furfur spores in the basal layer as the causative agent; however, malassezia can be found in any hyperkeratotic skin lesion as part of the normal flora and is not always a pathogenic organism.7 Most often, cultures from the hyperpigmented lesions are negative for bacterial and fungal species and reveal only normal flora, indicating a noninfectious cause.3 Histologically, thick keratin globules can be found throughout the stratum corneum as well as increased melanin in compact hyperkeratotic areas.1 Additionally, areas of abundant melanin pigment with areas of anucleated keratin may also be observed.1,3,4 These changes suggest incomplete keratin development since

both large amounts of melanin and desmosomal attachments are retained.This failure in development then leads to the hyperkeratosis and hyperpigmentation that results in the development of the characteristic lesions seen on presentation.1,3,4 The differential diagnosis for TFFD includes a variety of dermatologic diseases, all of which are characterized by hyperpigmented plaques. These include pityriasis versicolor, acanthosis nigricans, epidermolytic hyperkeratosis, idiopathic deciduous skin, dermatosis neglecta, seborrheic keratosis, and confluent and reticulated papillomatosis.1,3 The ability to remove the hyperpigmented lesions with soap and water suggests a diagnosis of dermatosis neglecta rather than TFFD.5,8 Most of the other diseases in which hyperpigmented plaques can be found have individual diagnostic criteria, some of which include: positive cultures or fungal stains (pityriasis versicolor, seborrheic keratosis), the presence of systemic disease associated with insulin resistance (acanthosis nigricans), or the presence of one or more clinical criteria (confluent and reticulated papillomatosis). However, TFFD is uniquely identified and diagnosed by the ability to resolve the skin lesions through the application of 70% alcohol to the affected area.

The diagnostic and treatment modalities for TFFD are the same: the application of 70% alcohol to the affected area with subsequent removal of the hyperpigmented plaque from the patient’s skin both confirms the diagnosis as well as treats the condition.Although most cases can be resolved by gentle application of the alcohol solution, some may require more vigorous rubbing.9 Because there have not been any identified predisposing risk factors, no changes in daily hygiene habits or cutaneous exposures are required. Recurrences are rare, but patients may choose to prophylax against the development of further lesions by wiping previously affected skin with 70% alcohol.3 Other less common treatment methods that have been reported include topical antifungal agents, topical steroids, and urea cream.7 How these treatments clear skin affected by TFFD is unclear. For sensitive skin for which 70% alcohol may be irritating, salicylic acid alcohol has been reported as an alternative.The efficacious nature of this intervention is likely due to the combination of the alcohol with the keratolytic feature of the salicylic acid.7 Overall, it is important to remember that the lesions of TFFD appear as hyperpigmented plaques that occur most commonly in the axilla, neck, and trunk. These lesions often present in childhood and can easily be removed with the application of a 70% alcohol solution.TFFD should always be considered in patients presenting with new-onset hyperpigmented plaques to avoid unnecessary diagnostic procedures for a disease for which the treatment is simple, quick, and effective.

The patient in this case was suspected of having TFFD given the characteristic appearance and location of the lesions, as

54 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

well as the fact that they had failed to subside with soap and water scrubs. The diagnosis was confirmed after resolution of the lesions upon rubbing the affected areas with 70% isopropyl alcohol pads.

CASE #2

Confluent and Reticulated Papillomatosis

Confluent and reticulated papillomatosis (CRP) was first described in 1927 by Gougerot and Carteaud.10 It is a largely asymptomatic skin condition that manifests as multiple brown, hyperpigmented papules that can coalesce to form plaques.11 These papules and plaques exhibit epidermal changes, hyperkeratosis, and atrophy.11 The plaques may be pruritic in some individuals, but overall CRP is limited to the skin with no systemic involvement.11 CRP most commonly involves the upper trunk, axilla, and neck.

CRP can occur in any patient, but it has a higher predominance in white and adolescent individuals with a slight predilection for males over females.12 Proposed risk factors for CRP include some endocrinopathies, particularly obesity and diabetes. Careful evaluation must occur in these patients, especially those with diabetes, as CRP may be confused for insulin resistance-associated acanthosis nigricans.13 Exposure to ultraviolet light, as well as a diagnosis of amyloidosis have also been proposed as being associated with the diagnosis of CRP; however, neither of these associations has been validated in the literature.14,15 Although many associated conditions have been proposed, the majority of patients diagnosed with CRP are healthy and lack any comorbid conditions.11 The pathogenesis of CRP involves disordered keratinization.

Histologically, this can be identified by the presence of undulating basket-weave hyperkeratosis, papillomatosis, and focal acanthosis.11 Evaluation of the lesions by electron microscopy is also consistent with altered keratinocyte differentiation, showing disrupted cellular architecture and proliferation of lamellar granules (Odland bodies).11 Ultrastructure studies have also shown increased melanosomes within the hyperkeratotic stratum corneum.11 The etiology of these pathogenic skin changes resulting in CRP was originally thought to be due to an abnormal response to infection by the fungus Malassezia furfur. However, case reports have not consistently detected this species within the lesions in patients diagnosed with CRP.Additionally, antifungal therapy has been unsuccessful in treating the lesions associated with CRP. Currently, the most convincing etiology of CRP

is now thought to be bacterial. In 2005, a novel actinomycete resembling Rhodococcus was identified in a patient with CRP, and more recently Dietzia papillomatosis was identified using a polyphasic taxonomic approach.16,17 The latter species is now the main infectious cause implicated in CRP development.16,17 The differential diagnosis for CRP includes other hyperpigmented, hyperkeratotic skin disorders such as terra firma-forme dermatosis, acanthosis nigricans, Dowling-Degos disease, GalliGalli disease, and dyskeratosis congenita.11 CRP can be differentiated from TFFD through the use of 70% alcohol, which in this case would not remove the plaque.11 Acanthosis nigricans affects body-fold regions and is diagnosed clinically with a history of insulin resistance. Dowling-Degos and Galli-Galli are both autosomal-dominant genetic disorders resulting in progressive hyperkeratosis. Dyskeratosis congenita is a rare x-linked recessive disorder characterized by systemic abnormalities including dystrophic nails, oral mucosa leukoplakia, and overall shortened lifespans. Identification of the unique features of these diseases with similar presentations can assist in elucidating one from the other.

The diagnosis of CRP is made clinically, with histopathologic assessment used as an important tool to exclude other diseases.

Shave biopsies will reveal many of the pathogenic features of CRP including hyperkeratosis, papillomatosis, focal acanthosis, and increased basal melanin pigmentation. Dermoscopic features include brownish pigmentation with overlying white scales.18 The location of the lesions, most commonly on the upper trunk and neck, can also be used as a tool for diagnosis.

Additionally, negative fungal cultures, resistance to antifungal treatment, or a positive response to minocycline treatment all support the diagnosis of CRP.12 Treatment for CRP primarily consists of oral antibiotics.The first-line regimen includes minocycline 50 mg taken orally twice a day for 6 weeks.19 An alternative antibiotic regimen that may be used is azithromycin 500 mg orally once daily for 1 week or 500 mg 3 times a week for 3 weeks.11 Both of these antibiotic schedules have been shown to result in complete clearance of the lesions with no recurrence for up to 6 months after completing treatment.20 In addition to antibiotic therapy, topical retinoids may be used.These agents reduce keratinocyte proliferation and are most appropriate when the lesions are limited to areas of the body that the patient can easily reach in order to apply the retinoid. Lastly, systemic retinoids may be used in recalcitrant cases. However, given the relatively safe profile of minocycline and azithromycin, systemic retinoids are reserved for patients who do not respond to these oral antibiotics.11,12 Overall, CRP is an uncommon but treatable keratinizing disorder that primarily affects adolescents. It presents as hyperpigmented papules and plaques most commonly located in the axilla and on the trunk. The diagnosis is predominantly

www.ClinicalAdvisor.com â&#x20AC;˘ THE CLINICAL ADVISOR â&#x20AC;˘ OCTOBER 2018 55

Dermatologic Look-Alikes TABLE 1.Terra Firma-Forme Dermatosis vs Confluent and Reticulated Papillomatosis Terra firma-forme dermatosis2-5,7-9

Confluent and reticulated papillomatosis12-15, 17-19

Dermatologic presentation

Dirt-like hyperpigmented hyperkeratotic papules and plaques

Hyperpigmented hyperkeratotic papules and plaques

Most common location

Neck, axilla, trunk

Neck, axilla, trunk

Age group

Adolescent and young adult

Adolescent and young adult

Histology

Lamellar hyperkeratosis, whorled orthokeratosis

Basket-weave hyperkeratosis, papillomatosis, focal acanthosis, increased basal melanin pigmentation

Diagnosis

Clears with 70% alcohol wipe

Scaly brown macules and patches with involvement of the upper trunk and axilla; negative fungal stains; responsive to oral antibiotics

Treatment

70% alcohol wipe

Oral antibiotics (minocycline or azithromycin)

Recurrence

Rare

Rare

clinical; once diagnosed, treatment with oral antibiotics often results in complete resolution of the lesions.

In the case presented here, the histologic findings and lack of response to antifungal treatment were consistent with CRP. The patient was prescribed oral minocycline and the lesions began to fade, with complete resolution achieved in 6 weeks. ■

[TFFD]: a rare presentation. Indian Dermatol Online J. 2015;6(6):458-459.

10. Gougerot H, Carteaud A. Papillomatose pigmentée innominée [Unclassified pigmented papillomatosis]. Bull Société Fr Dermatol Syphiligr. 1927;(34):712-719.

11. Lim JH-L,Tey HL, Chong W-S. Confluent and reticulated papillomatosis: diagnostic and treatment challenges. Clin Cosmet Investig Dermatol. 2016;9:217-223.

12. Davis MDP, Weenig RH, Camilleri MJ. Confluent and reticulate papillomatosis (Gougerot–Carteaud syndrome): a minocycline‐responsive dermatosis

Jay Patel, BS, is a medical student; Joan Fernandez, BS, is a medical student; and Christopher Rizk, MD, is a dermatology resident at Baylor College of Medicine, in Houston,Texas

without evidence for yeast in pathogenesis. A study of 39 patients and a proposal of diagnostic criteria. Br J Dermatol. 2005;154(2):287-293.

13. Hirokawa M, Matsumoto M, Iizuka H. Confluent and reticulated papillomatosis: a case with concurrent acanthosis nigricans associated with obesity and

References

insulin resistance. Dermatology. 1994;188(2):148-151.

1. Duncan WC, Tschen JA, Knox JM. Terra firma-forme dermatosis. Arch

14. Vassileva S, Pramatarov K, Popova L. Ultraviolet light-induced confluent

Dermatol. 1987;123(5):567-569.

and reticulated papillomatosis. J Am Acad Dermatol. 1989;21(2 Pt 2):413-414.

2. Ashique KT, Kaliyadan F, Goyal T.Terra firma‐forme dermatosis: report of a series

15. Groh V, Schnyder UW. [Nosology of confluent and reticulated papillo-

of 11 cases and a brief review of the literature. Int J Dermatol. 2015;55(7):769-774.

matosis (Gougerot-Carteaud)]. Hautarzt Z Dermatol Venerol Verwandte Geb.

3. Aslan NÇ, Güler Ş, Demirci K, Isiyel E. Features of terra firma-forme derma-

1983;34(2):81-86.

tosis. Ann Fam Med. 2018;16(1):52-54.

16. Natarajan S, Milne D, Jones AL, Goodfellow M, Perry J, Koerner RJ. Dietzia

4. Greywal T, Cohen PR. Terra firma-forme dermatosis: a report of ten indi-

strain X: a newly described Actinomycete isolated from confluent and reticu-

viduals with Duncan’s dirty dermatosis and literature review. Dermatol Pract

lated papillomatosis. Br J Dermatol. 2005;153(4):825-827.

Concept. 2015;5(3):29-33.

17. Jones AL, Koerner RJ, Natarajan S, Perry JD, Goodfellow M. Dietzia papil-

5. Moon J, Kim M-W, Yoon H-S, Cho S, Park H. A case of terra firma-forme

lomatosis sp. nov., a novel actinomycete isolated from the skin of an immuno-

dermatosis: differentiation from other dirty-appearing diseases. Ann Dermatol.

competent patient with confluent and reticulated papillomatosis. Int J Syst Evol

2016;28(3):413-415.

Microbiol. 2008;58(Pt 1):68-72.

6. Erkek E, Sahin S, Çetin ED, Sezer E. Terra firma-forme dermatosis. Indian J

18. Bernardes Filho F, Quaresma MV, Rezende FC, Kac BK, Nery JA da C, Azulay-

Dermatol Venereol Leprol. 2012;78(3):358.

Abulafia L. Confluent and reticulate papillomatosis of Gougerot-Carteaud and

7. Chun SW, Lee SY, Kim JB, Choi HM, Ro BI, Cho HK. A case of terra firma-

obesity: dermoscopic findings. An Bras Dermatol. 2014;89(3):507-509.

forme dermatosis treated with salicylic acid alcohol peeling. Ann Dermatol.

19. Montemarano AD, Hengge M, Sau P,Welch M. Confluent and reticulated papil-

2017;29(1):83-85.

lomatosis: response to minocycline. J Am Acad Dermatol. 1996;34(2 Pt 1):253-256.

8. Errichetti E, Stinco G. Dermoscopy in terra firma-forme dermatosis and

20. Jang HS, Oh CK, Cha JH, Cho SH, Kwon KS. Six cases of confluent and

dermatosis neglecta. Int J Dermatol. 2017;56(12):1481-1483.

reticulated papillomatosis alleviated by various antibiotics. J Am Acad Dermatol.

9. Panchal K, Bhalla N, Salunke P, Jerajani H. Extensive terra firma forme dermatosis

2001;44(4):652-655.

56 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

LEGAL ADVISOR CASE

© ROBERT LLEWELLYN / GETTY IMAGES

NP Faulted for Patient Care via Fax Use of a fax machine and lack of a timely response resulted in the demise of a patient.

BY ANN W. LATNER, JD

This month we look at the case of a nurse practitioner (NP) who spent years trying to get the courts to overturn a Board of Nursing decision placing her on 3 years of probation based on a finding of gross negligence.

Ms B, aged 56, was an NP with close to 30 years of healthcare experience in a variety of settings.

For the past 2 years she had been working for a medical group, under the supervision of her collaborating physician, Dr G. The medical group provided care for residents in assisted living facilities.The work provided a great deal of flexibility, which Ms B enjoyed. She worked from a home office and provided care onsite at the facilities as needed.

One of her patients, Mr H, was an 82-year-old man living in a facility for patients with dementia.

Ms B had been working with this facility since she started with the medical group, and she and the staff at the facility primarily communicated via fax, which Ms B had in her home office.

At 6 PM on March 23rd, the facility sent a fax to Ms B stating that Mr. H appeared to be in distress and asking whether a urinalysis was needed.

A more than 6-hour delay in assessment of the patient was determined to fall below the standard of care.

Ms B was at dinner with friends and did not see the fax until the following morning.

On March 24th, Ms B responded to the fax with a phone call and spoke to the wellness nurse, who reported that Mr H’s vital signs were stable, he was walking around, and he did not have abdominal distension. Ms B filled out a lab request for a urinalysis and faxed it to the facility.

At 2 PM that same day, the wellness nurse faxed Ms B reporting that Mr H had experienced 2 episodes of “chocolate-colored” diarrhea and that the urine sample had been obtained and sent to the lab. Ms B did not respond.At 4:30 PM, Ms B received a second fax from the facility, this one marked “URGENT.”The fax stated that in the last 2 hours Mr H had urinated on the carpet while screaming in pain.According to the faxed message, “He isVERY uncomfortable and when urinating, screams loudly. Please advise as soon as possible.”

Cases presented are based on actual occurrences.

Names of participants and details have been changed.

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

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • OCTOBER 2018 57

LEGAL ADVISOR Four hours later, at 8:30 PM, Ms B arrived at the facility and examined the patient. After the exam, she called a pharmacy that was able to deliver antibiotics so that the patient could be started on them as soon as possible.The patient began taking the antibiotics at 3 AM on March 25th.

Later that same morning, at 10 AM, Ms B received another fax from the facility, reporting that Mr H had lost his balance and fallen on the floor. The faxed message read that he was sweating, had no balance, and had been placed on 1-on-1 care. Ms B faxed a reply, instructing that the patient’s condition should continue to be monitored. She also prescribed a narcotic pain reliever for the patient.

Two days later, on March 27th, Ms B received a call from the wellness nurse advising her that Mr H had vomited a “chocolate-like” substance after lunch.The nurse advised that he had ingested chocolate pudding with his medications that afternoon. Ms B replied that the medications might be causing an upset stomach and she advised that the patient be given Gatorade and acidophilus.That evening the patient fell again.

The next morning, Mr H was vomiting blood. Paramedics were called, and he was transported to the hospital where he was diagnosed as suffering from acute renal failure and septic shock. He died in the hospital the following day.

The Board of Nursing deemed the NP negligent in her care of the patient and put her on 3 years of probation.

Although his family declined to file a medical malpractice suit against Ms B, they did report her to the state Board of Nursing.

The Board held an administrative hearing, at which time an expert in NP practice testified that Ms B had departed from the standard of care required in this case in various ways. First, according to the expert, Ms B should have responded immediately to the initial fax on the evening of March 23rd. Due to the patient’s age, opined the expert, the right response would have been to order a urinalysis and begin treatment with a standard antibiotic while waiting for the culture to be completed.The expert went on to fault the NP for not assessing the patient herself the following morning and for not referring the patient to a provider who would immediately assess his condition.

The expert believed that the report of “chocolate-colored diarrhea” indicated that the patient had possible gastrointestinal bleeding. Ms B should have gone to see the patient immediately after receiving that fax at 2 PM, said the expert.

Her delay in not assessing the patient until 8:30 that night

fell below the standard of care. She could have satisfied her duty to the patient by ordering the facility to take him to the emergency department, opined the expert.

Similarly, after the report that the patient was sweating and had lost his balance, Ms B should have asked the facility to call an ambulance for the patient, said the expert.

There was conflicting testimony about whether Ms B had consulted with her supervising physician, but there were no notes in the file indicating that she had. Ms B introduced her own expert, who testified that Ms B’s handling of the situation fell within the standard of care; however, the expert also stated that Ms B should have been checking her fax machine more frequently and should have seen the first fax before a whole night had passed.

The Board issued a decision finding Ms B grossly negligent in her care of the patient and put her on 3 years of probation.

Legal Background

Ms B was extremely upset about the Board’s decision. Probation meant that she could not continue to work at her current job and could no longer work out of her home office. She filed a request for reconsideration, but it was denied. She then filed a petition in trial court seeking a writ directing the Board to set aside its decision.The trial court denied her petition. Finally, she appealed to the Court of Appeals.That court upheld the trial court’s decision and affirmed the order of the Board of Nursing. The court found that Ms B’s treatment fell below the acceptable standard of care.

Protecting Yourself

The court was critical of Ms B’s method of communication – fax – and felt that she had not acted in a responsive enough manner after being alerted to symptoms that should cause alarm.

Faxes can get lost, jammed in the machine, or can go unread or unnoticed. If something important needs to be communicated, one should pick up a phone and make a call. Even an email might have been preferable in this case because Ms B might have gotten it the night of March 23rd and responded promptly.

In addition, although Ms B testified that she called her consulting physician for advice, there was no evidence of the communication, and the physician did not remember the conversation.Without a notation that it happened, it may as well not have – at least legally.

Be responsive, take action when needed, and document everything.

Finally, there were several instances when Ms B could simply have advised the facility to take Mr H to the hospital. That call, made in a timely manner, would have met the standard of care required for the appropriate management of this case. ■ Ms Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, NY.

58 THE CLINICAL ADVISOR • OCTOBER 2018 • www.ClinicalAdvisor.com

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COMMENTARY Cody Hoff, PA-C, family practice and emergency medicine, Deckerville Community Hospital, Michigan

The Community Paramedic Model: Bridging the Healthcare Gap When a patient walks out of the clinic doors or leaves the emergency department (ED), their care doesn’t stop there. Follow-up appointments are scheduled, referrals to specialists have been made, and medications are often prescribed. It is uncertain, however, if the patient will make it to those appointments. Do they have resources for travel, and if so, are they going to remember the appointment? Will a minor condition or exacerbation cause them a return visit to the ED? Are they taking the medications as prescribed? These are questions that practitioners often don’t get the answers to unless patients make it back for that follow-up appointment, or they may never get the answers at all.

Community paramedics can assist HCPs in both primary care and emergency settings.

These problems often create a healthcare gap for patients, which lead to a decrease in care efficacy.

The community paramedic model includes our emergency medical service colleagues providing a new usable tool to bridge this healthcare gap. The idea of the community paramedic is still in its infancy, meaning many providers are unsure what a community paramedic is.

Community paramedics are first trained within the standard paramedic education model. Then, licensed paramedics can go through further program-dependent training to work as a community paramedic. California, for example, has developed a statewide curriculum that is contracted with the UCLA Center for Prehospital Care.The pilot program curriculum, including both lecture and clinical components, will then be taught at various other sites.Topics include chronic management of heart failure, proper medication management, and hearthealthy diet organization. Effective implementation works toward the goal of decreasing unnecessary hospital readmissions and improving overall care.1 To properly utilize the community paramedic, it is important to understand their role.Across the

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country, the scope of practice of the community paramedic varies based upon local medical direction. According to a report on the community paramedicine model of care by Kizer et al,2 community paramedics can transport patients to facilities outside the ED when appropriate; determine if a patient needs transport to an ED after proper prehospital treatment; tailor care to frequent users of the 911 system in the form of primary care and social services; provide and facilitate proper follow-up care for discharged patients; provide support for patients with chronic conditions such as diabetes, asthma, and heart failure; and partner with primary care providers to deliver preventive care in underserved urban and rural areas. This facilitation of care is used to guide patients to the most effective method of healthcare given their current condition.

Community paramedics are also able to assist healthcare providers in both the primary care and emergency medicine specialties. In primary care, providers see patients during all 3 of the phases of care in which community paramedics can successfully be utilized. A patient with heart failure is one

In recognition of 20 years of providing information designed to improve clinical practice, Clinical Advisor acknowledges the role of the community paramedic in promoting health care and optimizing patient outcomes.

example that commonly needs care in all 3 facets: preventive care including medication and diet management, the actual heart failure exacerbation event, and then post-event care in the form of discharge care facilitation. Community paramedic assistance helps ED providers ensure proper follow-up care is obtained, while also decreasing repeat ED visits due to poor follow-up compliance.

MedStar, a not-for-profit agency out of Dallas, Texas, is an example of a new program enjoying success. They saw an opportunity to work with their local hospital systems to decrease ED visits and improve overall care.At the time the program was started, 21 frequent users of the 911 system equated 2100 ambulance hours and approximately $150,000 in healthcare expense the previous year.

Identifying and targeting those patients with the new community paramedic program cut patients’ usage by 57%. This also evolved into chronic care management by the community paramedic between healthcare visits, creating better followup compliance and overall efficacy.3 MedStar is only one example, but as the community paramedic model continues to grow, providers across the nation will be able to turn to these programs to improve overall patient care. Community paramedics provide vital services in the form of preventive care in underserved areas, triage of acute

calls, and facilitation of follow-up care, as necessary.

Community paramedic utilization provides one more tool to help bridge the healthcare gap and answer those often unanswered questions. ■ Cody Hoff, PA-C, graduated from Drexel University with a Masters of Health Sciences - Physician Assistant degree and is now NCCPA certified and working in family practice and emergency medicine for Deckerville Community Hospital in Michigan. He is also licensed as an EMT-B and previously worked in pre-hospital medicine, which sparked his interest in the community paramedic model during his schooling References 1. Erich J. (2014, September 4). Community paramedic curriculum. EMSWorld.com. August 4, 2014. Available at: http://www.emsworld.com/article/11610552/communityparamedic-curriculum. Accessed September 17, 2018.

2. Kizer K, Moulin A, Shore K. Community paramedicine: a promising model for integrating emergency and primary care. August 1, 2012. Available at: http://www.naemt.org/ Files/MobileIntegratedHC/UC%20Davis%20Community%20 Paramedicine%20Report.pdf. Accessed September 17, 2018.

3. Berry J. Community Health Programs Create New Niche for EMS. July 25, 2012. Available at: https://www.jems.com/ articles/print/volume-37/issue-8/2020vision/community-healthprograms-create-new-nic.html. Accessed September 17, 2018.

Community paramedics are trained within the standard paramedic ­education model and then complete programdependent training with a goal of decreasing unnecessary hospital ­readmissions and improving overall ­patient care.

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