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Stenosis of the blood vessels resulting from atherosclerosis.
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CONTENTS MARCH 2018
NEWS AND COMMENT
24 Reducing risk factors for coronary artery disease Primary prevention efforts such as exercise, weight control, cessation of smoking, and alcohol intake can greatly affect the development of CAD.
Newsline ■■The 2018 Recommended
Immunization Schedule for Children and Adolescents Aged 18 Years or Younger from the Advisory Committee on Immunization Practices ■■The ACIP has released its 2018 Recommended Immunization Schedule for Adults Aged 19 Years or Older. ■■The American Heart Association and American Stroke Association have released updated clinical guidelines for the early management of acute ischemic stroke, which opens up the treatment window to 24 hours in some patients. ■■Gastric bypass vs sleeve gastrectomy in morbidly obese patients. A study compares weight loss at 5 years after the two surgical procedures. ■■Serum caffeine and downstream metabolites may be biomarkers for early Parkinson disease ■■Women who were previously diagnosed with gestational diabetes mellitus have an extremely elevated risk of developing type 2 diabetes and more frequent occurrences of hypertension and ischemic heart disease. ■■Glucocorticoid therapy is ineffective for septic shock. Continuous hydrocortisone infusion does not reduce mortality rates in patients with septic shock on mechanical ventilation systems.
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CME/CE Smoking cessation:
CME/CE Feature posttest
Guidelines for acute ischemic stroke 18
Practical tools for busy clinicians A collaborative treatment plan that emphasizes behavior change strategies and appropriate clinical options can help motivate persistent smokers.
Web Roundup A summary of our most recent opinion, news, and multimedia content from ClinicalAdvisor.com
Dermatology Clinic n Hairless plaque on a woman’s forearm n An itchy rash on a man’s hand
An itchy rash on a man’s hand 49
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Your Comments ■ Cutaneous leishmaniasis: a potential treatment option
My Most Memorable Patient ■ A patient with a bone marrow transplant shows how short and precious life is
Case Files ■ Fever, chills, and nausea after beginning long-acting reversible contraception
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ClinicalAdvisor.com Web Exclusives
ACA has led to reduced cost burden for lowest to middle income households The Affordable Care Act is associated with moderate reductions in the cost burden for the lowest-, low-, and middle-income households, and a repeal or substantial reversal of the ACA would especially harm poor and low-income Americans.
Pediatrician recommended tips to prevent flu in children These tips, recommended by pediatrician Shilpa Patel, MD, include keeping children home from school if they develop flu-like symptoms and monitoring your child’s reaction to a fever. Watch the video here: ClinicalAdvisor.com/ PediatricFluPrevention
Herpes zoster subunit vaccine more effective, less expensive than live attenuated herpes zoster vaccine At a proposed price of $280 per series, the herpes zoster subunit vaccine is more effective and less expensive than the live attenuated herpes zoster vaccine at all ages.
Case Study in Urgent Care ClinicalAdvisor.com/CaseStudy Brady Pregerson, MD Diarrhea and rash A 60-year-old man with a history of gastroesophageal reflux disease (GERD) presents to the emergency department with 2 to 3 days of fever, non-bloody diarrhea, and a worsening non-pruritic rash. Read the full case at: ClinicalAdvisor.com/
Depressive symptoms may increase mortality risk in patients undergoing aortic valve replacement In patients undergoing transcatheter or surgical aortic valve replacement, about 1 in 3 had depressive symptoms at baseline and a higher risk of short-term and midterm mortality.
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Long-term memory enhanced by electrical stimulation of the amygdala Researchers sought to determine if the amygdala could improve declarative memory without stimulating any emotional response.
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Cerebral palsy, epilepsy risk linked with lower Apgar score Epilepsy and cerebral palsy risks are inversely related to 5- and 10-minute Apgar scores in singlet newborns born at term.
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Tafari Mbadiwe, MD, JD The CVS/Aetna merger and the future of primary care In a new partnership, CVS and Aetna are hoping to maximize profits, not consumer savings, although they claim to care deeply about the prices of pharmaceuticals.
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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.
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Arthritis of the knee A 58-year-old woman presents with left knee pain for several months. She had a left knee arthroscopic lateral meniscectomy 10 years ago. Bilateral knee anteroposterior radiograph taken 5 years ago showed moderate lateral joint line osteoarthritis. Repeat anteroposterior radiograph shows that her arthritis has progressed significantly in the lateral compartment of the left knee. WHICH IS MOST LINKED WITH ARTHRITIS?
• The amount of meniscal tissue removed • Obesity • Female gender • Genetic predisposition • Advanced age ● See the full case at ClinicalAdvisor.com/OrthoDx_March18
Derm Dx A rash on the cheek and forehead A 43-year-old Hispanic man complains of a rash affecting his right cheek and forehead. The eruption was first noted 3 weeks ago and is asymptomatic. He has had 2 similarly appearing episodes within the past 3 years, which resolved following oral prednisone. CAN YOU DIAGNOSE THIS CONDITION?
• Fixed drug eruption • Polymorphous light eruption • Jessner lymphocytic infiltrate • Discoid lupus ● See the full case at ClinicalAdvisor.com/DermDx_March18
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 13
Newsline M A R C H 2 018
Acute ischemic stroke: updated clinical guidelines page 18
Comparing weight loss surgery options page 18
Gestational diabetes and T2D risk page 20
THE ACIP has published its 2018 Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. Updated changes include the following: • The maximum ages for the first and last doses in the rotavirus vaccination series have been included • Information on the inactivated poliovirus vaccine was updated to clarify the catch-up recommendations for children 4 years of age and older • A reference for use of live vaccines in patients with HIV has been added
In addition, the footnotes were updated to include the following: • Hepatitis B vaccine (HepB): includes information regarding timing of the birth dose for <2,000 g infants born to hepatitis B virus surface antigen (HBsAg)-negative mothers • H. influenzae MenHibrix has been removed because the vaccine is no longer commercially available, and all remaining doses have expired. • Poliovirus vaccine: includes updated guidance for persons who received oral poliovirus vaccine as part of their vaccination series.
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2018 recommended immunization schedule for children, adolescents The ACIP has made revisions to its poliovirus, influenza, and MMR vaccine schedules.
• Inf luenza vaccine: updated to indicate that live attenuated influenza vaccine (LAIV) should not be used during the 2017–2018 influenza season. • MMR vaccine: updated to include guidance regarding the use of a third dose of mumps virus-containing vaccine during a mumps outbreak. uFor more information about the updated immunization schedule, visit the CDC’s website.
ACIP issues 2018 recommended immunization schedule for adults THE ACIP has released the 2018 Recommended Immunization Schedule for Adults Aged 19 Years or Older. Major changes in the schedule include new recommendations on the use of recombinant zoster vaccine (RZV) for adults aged ≥50 years, and the use of an additional dose of the measles, mumps, and rubella (MMR) vaccine in a mumps outbreak setting. With the October 2017 approval of Shingrix, the ACIP recommends the use of: • RZV among immunocompetent adults aged ≥50 years for the prevention of herpes zoster and related complications • RZV among adults aged ≥50 years who previously received the zoster vaccine live (ZVL; Zostavax) • RZV or ZVL for adults aged ≥60 years (RZV preferred) There is currently no ACIP recommendation on the use of RZV among pregnant women or immunocompromised adults
(eg, HIV infection). In adults with chronic conditions, RZV should routinely be used. Recommendations on MMR vaccination now include use of a third dose of a mumps virus-containing vaccine in certain individuals during a mumps outbreak. Adults identified by a public health authority as being at increased risk and who have received ≤2 doses of mumps virus–containing vaccine or whose mumps vaccination status is unknown should receive 1 dose of MMR. Adults with no immunity to mumps are recommended to receive 1 dose of MMR for mumps prevention. Students in postsecondary institutions, international travelers, or household contacts of immunocomuFor more information promised persons should about the updated receive 2 doses of MMR at immunization schedule, least 28 days apart. visit the CDC’s website.
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 17
Newsline Acute ischemic stroke: updated clinical guidelines
The stroke treatment window has been expanded to 24 hours in select patients.
local, regional, and state agencies to create triage paradigms and protocols to facilitate the rapid identification and assessment of patients with stroke or suspected stroke. • The statement regarding the formation of regional systems for stroke care has been reworded from the previous guidelines. “This is significant in that
it provides definite language encouraging collaboration between EMS, hospitals, and regional governments to form efficient stroke networks—a positive move by the AHA/ ASA in that the language is highly supportive of the formation of integrated systems for the triage and treatment of stroke patients,” according to Dr Favate. • “A major point of debate pertains to an item about bypassing a primary stroke center to transport the patient to a comprehensive stroke center offering mechanical thrombectomy,” said Dr Favate. While this is new in the guidelines, the authors concluded that further research is needed before a definitive recommendation can be made.
Gastric bypass vs sleeve gastrectomy in obese patients NO STATISTICALLY significant difference in weight loss at 5 years was observed in comparing laparoscopic sleeve gastrectomy vs laparoscopic Roux-en-Y gastric bypass in morbidly obese patients though both resulted in sustained weight loss, according to two studies published in JAMA. In one study, participants were randomized to undergo laparoscopic sleeve gastrectomy (107 patients) or laparoscopic Rouxen-Y gastric bypass (110 patients). Among the 217 patients (mean age, 45.5 years; 72% women; mean BMI, 43.9) 205 (94.5%) completed the trial. Excess BMI loss
was not significantly different at 5 years: sleeve gastrectomy, 61.1%, vs Roux-en-Y gastric bypass, 68.3%. Gastric reflux remission was observed more frequently after Roux-en-Y gastric bypass (60.4%) than after sleeve gastrectomy (25.0%). Gastric reflux worsened more often after sleeve gastrectomy (31.8%) than after Roux-en-Y gastric bypass (6.3%). In the second study, investigators enrolled 240 morbidly obese patients to examine the clinical equivalence of laparoscopic sleeve gastrectomy (121 patients) with laparoscopic Roux-en-Y gastric bypass (119 patients).
18 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
The two surgical options resulted in sustained weight loss for patients.
Among 240 patients randomized (mean age, 48 years; mean baseline BMI, 45.9; 69.6% women), 80.4% completed the 5-year follow-up. The estimated mean percentage excess weight loss at 5 years was 49% after sleeve gastrectomy and 57% after gastric bypass and did not meet criteria for equivalence. No statistically significant difference in quality of life between groups and no treatment-related mortality were observed. At 5 years, the overall morbidity rate was 19% (n = 23) for sleeve gastrectomy and 26% (n = 31) for gastric bypass.
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THE AMERICAN Heart Asso ciation and American Stroke Association (AHA/ASA) have released updated clinical guidelines for the early management of acute ischemic stroke, as published in Stroke and presented at the 2018 International Stroke Conference. William J. Powers, MD, FAHA, chair of the writing group, noted 2 especially significant changes: The window of time to perform thrombectomy has been increased from 6 hours to up to 24 hours for carefully selected patients; and because of several revisions, a greater number of patients may now be eligible for alteplase. Albert Favate, MD, highlighted other notable points from the guidelines in an interview. • Emergency medical services (EMS) leaders should coordinate with medical experts and
SERUM CAFFEINE and downstream metabolites may be indicative biomarkers for early Parkinson disease, according to a study published in Neurology. Researchers evaluated 31 healthy individuals (18 women) and 108 patients with Parkinson disease and without dementia (50 women). Controls were either spouses of patients or patients with asymptomatic brain ischemia. The concentrations of caffeine were evaluated as 60 mg per cup of coffee, 30 mg per cup of tea, and 20 mg per cup of green tea. None of the participating members had a history of cancer or aspiration pneumonia. Additionally, 51 healthy participants (82 total controls, 26 additional women) and 67 Parkinson disease patients (176 total, 34 additional women) were monitored genetically for any mutations in caffeine-affiliated genes. Serum caffeine and 9 of the 11 associated downstream metabolites were found to be at lower levels in patients with Parkinson disease than the controls. The top 3 closest downstream metabolites, theophylline, theobromine, and paraxanthine, were found in significantly lower concentrations in Parkinson disease patients. “Considering disease severity differences between patients with Parkinson disease with and without motor fluctuations, lower levels of caffeine in patients with Parkinson disease may result in greater disease progression,” reported the authors.
Gestational diabetes increases T2D, heart disease, and hypertension risk WOMEN previously diagnosed with gestational diabetes mellitus have an extremely elevated risk of developing type 2 diabetes (T2D) and more frequent occurrences of hypertension and ischemic heart disease (IHD), according to a study published in PLoS Medicine. A total of 9118 women diagnosed with gestational diabetes mellitus were randomly matched in age and time of pregnancy to 37,281 women without gestational diabetes mellitus (control). T2D was more common in women with gestational diabetes mellitus than in those without (incidence rate ratio [IRR], 21.96) after an age, smoking, and body mass index (BMI) adjustment. In addition, women diagnosed with gestational diabetes mellitus had a greater risk of hypertension (IRR, 1.85). Women with
Women with gestational diabetes have a higher risk of T2D.
gestational diabetes mellitus had incidence rate ratios of 2.78 and 0.95 for IHD and cerebrovascular disease. Of the women who were diagnosed with gestational diabetes mellitus, 58% were screened in their initial year postpartum for T2D in primary care. The population of women screened after this time decreased dramatically (40% at 2 years; 24% at 3 years postpartum). Cardiovascular risk factor screening rates were low for both groups of women. “Results showed that women diagnosed with gestational diabetes mellitus were significantly more likely to develop type 2 diabetes, hypertension, and IHD at a relatively young age compared with women without a previous diagnosis of gestational diabetes mellitus,” reported the authors.
Glucocorticoid ineffective for septic shock CONTINUOUS hydrocortisone infusion does not reduce mortality rates in patients with septic shock on mechanical ventilation systems, according to a study published in the New England Journal of Medicine. Investigators randomly grouped 3800 septic shock patients on mechanical ventilators to be administered either 200 mg of hydrocortisone per day or a placebo. The randomized treatment lasted for either 7 days, until death, or until patients were discharged from the intensive care unit (ICU), whichever was first. By day 90,511 patients taking hydrocortisone (27.9%) and 526 (28.8%) taking the placebo died (odds ratio, 0.95). The
20 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
investigators noticed a quicker shock resolve (hazard ratio, 1.32), decreased length of time on initial mechanical ventilation (HR, 1.13), and fewer blood transfusions in patients receiving hydrocortisone (OR, 0.82) compared with patients taking the placebo. Rates of mortality at 28 days, shock relapse, and renal-replacement therapy were not statistically significant between the two treatment groups. Results were also insignificant for the number of days that patients were alive and out of the ICU or hospital, mechanical ventilation recurrence, and occurrence of new-onset bacterial or fungal infections between the two patient groups. n
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Parkinson disease and caffeine level
A quick review of common conditions, using the best global evidence
Intimate partner violence ALAN DRABKIN, MD
Dr Drabkin is a senior clinical writer for DynaMed (www.ebscohost. com/dynamed), a database of comprehensive updated summaries covering more than 3,200 clinical topics, and assistant clinical professor of population medicine at Harvard Medical School.
• Intimate partner violence (IPV) is physical, sexual, or psychological harm perpetrated by a current or former intimate partner, such as a spouse, cohabitating partner, or dating relationship. Who is most affected
• Women are more affected than men (often with male perpetrator). • Women and men in all types of relationships may be affected regardless of race, sexual orientation, or economic status. Incidence/prevalence in US
• 1.5 million women and 834,700 men report rape and/or physical assault by an intimate partner annually • 30% to 33% lifetime prevalence of IPV reported among female psychiatric patients Likely risk factors
• victim-related risk factors ——preexisting mental health and/or substance abuse ——history of traumatic events, such as ■■ sexual abuse in childhood ■■ prior IPV ■■ war-related trauma ——unmarried status ——family history of abuse • perpetrator-related risk factors ——men with exposure to parental violence or who have experienced physical abuse during childhood ——preteen alcohol use • exposure to political violence
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Screening questions and resources
• Start with generalized statement, such as “many people experience problems at home or in their relationships that can affect their health, so I have started to ask all my patients about any issues at home.” • ask about ——current violence www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 21
Stat Consult Have you been hit, kicked, punched, or otherwise hurt by an intimate partner within the past year, and if so, by whom? ■■ Do you feel safe in your current relationship? ■■ Is someone from a previous relationship making you feel unsafe now? ■■ Is anyone forcing you to do something sexual that you do not want to do? ■■ Is anyone in the community following or harassing you? ——history of violence ■■ Have you ever been in a relationship in which you were frightened or hurt by your partner? ■■ Did anyone ever physically hurt you, force you to do something sexual, or hurt you psychologically (such as telling you that you were worthless or unwanted) when you were a child? ■■ As an adult, have you ever been physically hurt or forced to do something sexual you did not want to do? ——aggressive behavior in partner such as ■■ jealousy ■■ exhibiting controlling behavior ■■ anger with patient or children ■■ controlling conversations ■■ canceling appointments for patient or insisting on being present during appointments with patient • screening questionnaires include ——Hurt, Insult, Threaten, and Scream (HITS) ——Woman Abuse Screening Tool (WAST) and WASTshort form (WAST-SF) ——Partner Violence Screen (PVS) ——Humiliation, Afraid, Rape, Kick (HARK) ■■
Efficacy of screening
• Screening instruments might accurately identify IPV toward women. • HITS reported to have 88% sensitivity and 97% specificity for identification of male victims of IPV. • Screening for IPV in healthcare setting may improve identification in women but does not appear to reduce recurrence. History
• Ask about current assault, including (WHO strong recommendation, indirect evidence) ——type of assault ——when the assault took place ——risk of pregnancy ——risk for HIV infection and other sexually transmitted infections
——mental health status • ask about general signs and symptoms of distress, including ——fatigue ——headache ——gastrointestinal symptoms ——cardiac symptoms ——pelvic pain ——sexual dysfunction ——chronic pain ——description of frequent or vague symptoms ——substance abuse ——anxiety or depression ——PTSD ——missed appointments ——social isolation • repeated injury, delay in seeking care, or reported etiology inconsistent with injury findings may each be signs associated with violence Physical
• Perform complete physical exam (including genitalia) to assess for injuries in patients with suspected IPV (WHO strong recommendation, indirect evidence) • specific signs of violence may include ——multiple injury sites ——contusions, abrasions, or minor lacerations of ■■ head/neck and facial area (most common) ■■ torso ■■ abdominal area ■■ genital area ■■ anal area ——burns ——fractures ——sprains ——injury during pregnancy General management strategies
• if patient denies IPV ——provide education about effects of IPV (including effects on children in household) ——express availability to discuss any concerns about IPV in future visits • If patient confirms IPV, SOS-DoC intervention may help guide clinician response. ——S: offer support and assess safety ——O: discuss options, including safety planning and follow-up ——S: validate patient’s strengths ——Do: document observations, assessment, and plans
22 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
— C: offer continuity • Mandatory reporting laws vary by state, mechanism of reporting, and patient age. Counseling
• Mental health care provided by clinician with good understanding of violence against women recommended for women with preexisting diagnosis or partner violencerelated mental disorder who are experiencing IPV (WHO strong recommendation, indirect evidence) • CBT for men who physically abuse their female partners might not reduce continued violence • Counseling intervention in primary care setting may not improve quality of life in women with history of IPV Medications
• Addition of fluoxetine to behavioral and self-help programs may reduce perpetration of IPV in patients with depression and history of alcohol-associated violence
anxiety violence toward peers ■ attempted suicide ■ drug and/or alcohol abuse ■ running away from home ■ risky sexual behaviors ■ increased likelihood of committing sexual assault — increased mortality and morbidity • HIV infection ■ ■
• mortality — About 39% of global homicides with female victim may be committed by intimate partner. — One in 5 women killed by an intimate partner are reported to receive emergency care in previous year for injuries infl icted by same partner. • Dating violence during middle or high school is associated with increased risk of young adult intimate partner victimization.
Consultation and referral
• Refer patients exposed to IPV to community-based treatment and advocacy programs. Follow-up
• Offer follow-up appointment and assess barriers to follow-up. Complications
• in women with history of IPV — gynecologic, gastrointestinal, urinary, musculoskeletal, and neurologic symptoms — sexually transmitted infections — chronic pain — elective abortions — poor pregnancy outcomes — increased risk for obesity and hypertension • psychological complications include — PTSD — depression — suicide attempts — misuse of alcohol and/or drugs — eating disorders • children exposed to household with IPV may have increased risk for negative outcomes that can persist into adulthood, including — child abuse (up to 50% of households with IPV) — behavioral and physical health problems, such as ■ depression
• Cognitive behavioral and empowerment-based interventions may reduce domestic violence during pregnancy. • Educational or skills-based interventions for preventing relationship and dating violence may not be effective in adolescents and young adults. • Insufficient evidence to evaluate advocacy interventions for women experiencing IPV
Case Study Library Check out all of our case studies in obesity, diabetes, and other important topics in primary care — along with our clinical challenges — by visiting us at: ClinicalAdvisor.com/Case-Study
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 23
FEATURE: KELSEY ONDER, CRNP
Reducing risk factors for coronary artery disease Primary prevention efforts such as exercise, weight control, cessation of smoking, and alcohol intake can greatly affect the development of CAD.
© SPL RM IMAGES / SCIENCE SOURCE
Colored angiogram of the coronary arteries showing extensive stenosis.
24 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
ardiovascular disease (CVD), which encompasses coronary artery disease (CAD), stroke, and peripheral artery disease, is a significant global health burden, affecting men and women. CVD is the leading cause of death worldwide, accounting for more than 17.3 million deaths per year, a rate that is expected to increase to more than 23.6 million by 2030.1 The mortality rate of CVD is higher than the rate of all cancers combined and represents about 31% of global deaths.1 About 801,000 people in the US died from heart disease, stroke, and other cardiovascular diseases in 2013, and about 2,200 Americans die each day from these diseases, one every 40 seconds.1 CAD is the most common type of CVD, accounting for 370,000 annual deaths and 1 in 7 deaths in the US.1 About 17.5 million Americans have CAD.2 CAD is characterized by accumulation of atherosclerotic plaques in the coronary arteries that progressively narrow the arterial lumen, resulting in impaired blood flow to the myocardium. The reduction of blood flow depends on the severity of arterial narrowing and may result in symptoms. A myocardial infarction is often the result of CAD due to the blockage of coronary arteries and rupture of atherosclerotic plaques. According to the CDC,3 735,000 Americans have a myocardial infarction annually, with 525,000 being first-time myocardial infarctions and 210,000 involving people who have previously had a myocardial infarction. Patients with CAD may
be asymptomatic or present with angina or shortness of breath. Angina is typically classified based on the Canadian Cardiovascular Society grading system (Table 1). Patients presenting with an acute myocardial infarction present with angina, shortness of breath, nausea, vomiting, dizziness, diaphoresis, pallor, and pain that radiates to the upper extremity or jaw. A health and economic burden
CAD not only has a significant impact on morbidity and mortality in the US but also a significant financial impact regarding management of the disease. Hospital use expenditures related to managing and treating CAD in the US exceed $100 billion per year, and expenditures for all US adults older than age 55 with CAD exceed $60 billion per year, according to the Center for Financing, Access, and Cost Trends’ Agency for Healthcare Research and Quality’s Medical Expenditure Panel Survey 2010 and analysis by Frost and Sullivan.4 Management of CAD encompasses combined efforts with lifestyle/behavioral changes, pharmacologic management, and revascularization procedures such as percutaneous coronary intervention (PCI) and coronary artery bypass graft (CABG). PCI has become a first-line procedure in the management of CAD in the US. The procedure is performed 600,000 times annually in the US at a cost of more than $12 billion.5
Development of obesity contributes to hypertension, dyslipidemia, and insulin resistance, which eventually leads to diabetes mellitus and development of metabolic syndrome. Healthcare providers should encourage patients to have an ideal BMI between 19 and 25. Patients who consume heavy amounts of alcohol have high rates of morbidity and mortality associated with CVD. Small amounts of daily alcohol consumption regardless of type of alcoholic beverage have been shown to decrease the rates of morbidity and mortality associated with CVD. Dyslipidemia significantly contributes to the development of CAD and should be treated according to the National Cholesterol Education Program (NCEP) recommendations. Continues on page 30
TABLE 1. Canadian Cardiovascular Society grading of angina pectoris Grade
Ordinary physical activity does not cause angina, such as walking and climbing stairs. Angina with strenuous, rapid, or prolonged exertion at work or recreation
Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, or in cold or wind, under emotional stress, or only during the few hours after awakening. Walking more than 2 blocks on the level and climbing more than 1 flight of ordinary stairs at a normal pace and in normal conditions
Marked limitation of ordinary physical activity. Walking 1 or 2 blocks on the level and climbing 1 flight of stairs in normal conditions and at normal pace
Inability to carry out any physical activity without discomfort; angina may be present at rest. There are four subgroups in CCS Grade 4. Groups A to D:
Considering the morbidity, mortality, and economic impact of CAD, healthcare providers must make a strong effort to effectively treat patients and help control the overall disease burden. The cornerstone in the treatment of CAD is prevention of the disease by reducing risk factors and addressing them along the course of treatment. Risk factors associated with CAD include dyslipidemia, hypertension, diabetes mellitus, weight, smoking, diet, exercise, and alcohol consumption. Lifestyle modification to reduce the risk of CAD includes smoking cessation, exercise, weight control, and alcohol consumption. Tobacco use induces endothelial dysfunction, reduces coronary vasoreactivity, increases circulatory carbon monoxide levels, impairs functional status, and increases blood pressure.6 Educating patients on health risks associated with tobacco use and offering tobacco cessation have been shown to lessen the risk of disease development. Regular physical activity provides cardiovascular benefits and should be recommended for patients in a program of at least 30 minutes of physical activity per day. Weight control to prevent obesity is a strong avoidable cause of CAD.
A. Admitted to hospital, becomes relatively asymptomatic with aggressive medical therapy, and may be managed on an outpatient basis B. Admitted to hospital, continues to have angina despite aggressive medical therapy and cannot be safely discharged home, but does not require IV nitroglycerin C. Admitted to hospital, and maximal medical therapy, including IV nitroglycerin, fails to control symptoms D. Patient in shock Modified from Campeau L. Grading of angina pectoris. Circulation. 1976;54:522–523. Available at: www.ccs.ca
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REDUCING RISK FACTORS FOR CORONARY ARTERY DISEASE
Which of the following is the strongest risk factor for coronary artery disease? 8.27% 22.24%
■ Age ■ Family history ■ Smoking
■ High blood pressure
For more polls, visit ClinicalAdvisor.com/Polls.
Reduction of LDL with statin therapy has been associated with the greatest outcomes. Control of hypertension is an essential factor in reducing risk of CAD. Control of blood pressure reduces myocardial oxygen consumption and reduces angina, and it also lowers the incidence of cardiovascular disease.6 Optimal blood pressure management is about <140 mm Hg systolic and < 90 mm Hg diastolic, with goals slightly different in patients with a chronic disease such as chronic kidney disease and diabetes mellitus. Blood pressure control should be promoted through use of antihypertensive and nonpharmacologic measures such as weight reduction, reduced sodium intake, exercise, and avoidance of alcohol. Glycemic control in patients with diabetes continues to be an important risk factor in the development of both macrovascular and microvascular complications. According to the American Diabetes Association,7 optimal glucose control should include a hemoglobin A1c of 7% or lower to prevent the development of CAD and reduce the risk of cardiovascular events. Revascularization procedures
Aside from primary prevention measures and reducing risk factors, the primary treatment for CAD entails revascularization procedures such as PCI and CABG. The procedures work by producing revascularization to the heart by opening blocked vessels as with PCI or bypassing blocked vessels as with CABG. Neither PCI nor CABG is performed without risk, and neither offers a permanent fix to CAD, as patients still have to live with the burden of the primary disease and
are at risk for myocardial infarction, restenosis, and death associated with the procedures. Percutaneous coronary artery intervention is more effective than medical therapy in relieving angina, but it confers no greater survival benefit.6 Healthcare providers must educate patients that postprocedure care still includes management of risk factors, aggressive statin therapy, and antiplatelet therapy to reduce the risk of restenosis at the intervention site. CABG produces better survival rates than does medical therapy in selected circumstances and is recommended for symptomatic patients with left main coronary artery disease, 3-vessel CAD, or 2-vessel CAD marked by stenosis of the proximal left anterior descending artery.6 CABG is an effective procedure for management of CAD; however, benefits of the procedure begin to decline at about 10 years postprocedure, and the procedure still does not stop the progression of atherosclerosis. Healthcare providers must inform patients that after surgery aggressive treatment of the underlying CAD along with treatment of risk factors is essential to stop the progression of CAD in the future. Conclusion
Overall, CVD continues to pose a significant health burden not only in the United States but worldwide and accounts for the leading cause of global deaths. CAD is the leading form of CVD and accounts for substantial amounts of morbidity, mortality, and expenditure of healthcare dollars. Healthcare providers must work with patients to decrease the disease burden in the US. Primary prevention efforts such as exercise, weight control, cessation of smoking, and alcohol intake can greatly affect the development of CAD. Healthcare providers must also assess risk factors in patients and treat such factors as hypertension, diabetes, and dyslipidemia according to medical standards to prevent and accelerate CAD in patients. Alleviation of symptoms associated with the disease is done via PCI and CABG; however, these procedures do not cure or lessen the burden of the disease. Healthcare providers should emphasize primary prevention and aggressively assess and treat arising risk factors to reduce the disease burden. ■ Kelsey Onder, CRNP, is a family nurse practitioner in Johnstown, Pa. References 1. Writing Group Members, Mozaffarian D, Benjamin EJ, et al. Heart disease and stroke statistics—2016 update: a report from the American Heart Association. Circulation. 2016;133:e38-e360. doi: 10.1161/ CIR.0000000000000350
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2. Kempf J, Buysman E, Brixner D. Health resource utilization and direct costs associated with angina for patients with coronary artery disease in a US managed care setting. Am Health Drug Benefits. 2011;4:353-361. Available at: http://carlow.idm.oclc.org/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=rzh&AN=104635673&site=eho st-live&scope=site 3. CDC. Heart disease facts. November 28, 2017. Available at: http:// www.cdc.gov/heartdisease/facts.htm 4. Frost & Sullivan. Coronary heart disease and the cost effectiveness of omega-3 and b vitamin dietary supplementation. 2013. Available at: https://www.crnusa.org/sites/default/files/pdfs-hccs/03-CRNFSHCCSCHD%2BOmega-3sandBVitamins-SP.pdf 5. Behnke LM, Solis A, Shulman SA, Skoufalos A. A targeted approach to reducing overutilization: use of percutaneous coronary intervention in stable coronary artery disease. Popul Health Manag. 2013;16:164-168. doi: 10.1089/pop.2012.0019 6. Rimmerman CM. Coronary artery disease. Cleveland Clinic, Center for Continuing Education. February 2013. Available at: http://www. clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/ coronary-artery-disease/ 7. American Diabetes Association. A1C and eAG. Updated September 29, 2014. Available at: http://www.diabetes.org/living-with-diabetes/
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Top, bottom: © Harley Schwadron, 2018. Middle: © The New Yorker Collection 2018 from cartoonbank.com. All Rights Reserved.
CME CE FEATURED COURSE
■ EDUCATIONAL OBJECTIVES At the conclusion of this activity, participants should be better able to: • Identify the key role of NPs and PAs in facilitating smoking cessation through behavior change strategies • Describe specific skills to effectively motivate and engage, or re-engage, persistent smokers in a collaborative smoking cessation treatment plan • Assess patients’ readiness to quit and stage of change utilizing evidence-based tools • Select the appropriate pharmacotherapeutic and nicotine replacement options for smoking cessation • Develop an individualized behaviorally based smoking cessation treatment plan and appropriate pharmacotherapeutic and nicotine replacement options for patients who desire to quit smoking • Demonstrate how you used screening, risk assessment, and use of behavioral strategies to enlist patients’ commitment to quit smoking
■ COMPLETE THE POSTTEST: Page 44
Release Date: November 2, 2017
Accredited Provider Disclosures
Expiration Date: November 2, 2018
Pam Jenkins, MS, NP Program Director and Lead Nurse Planner Nurse Practitioner Healthcare Foundation Pleasanton, CA Ms. Jenkins discloses no conflicts of interest.
Estimated Time to Complete: 2 hours Accredited Provider: This activity is jointly provided by the Nurse Practitioner Healthcare Foundation and Integrated Learning Partners, LLC., in collaboration with Consultants in Medical Education. Commercial Supporter: This activity is supported by an educational grant from GlaxoSmithKline. Program Description: This program is designed to increase the skills, motivation, and confidence of NPs and PAs to address smoking cessation with their challenging, non-adherent patients as well as patients who continue to smoke despite the efforts of their healthcare providers or in spite of the patient’s repeated expressed commitments to quit. Best practices for clinical treatments for smoking cessation among challenging persistent smokers will be presented, along with concrete behavioral counselling tips, references, and evidence-based resource materials. The goal of this program is to motivate and re-energize healthcare providers to treat and counsel smoking cessation more effectively and efficiently, especially to those patients who persist in smoking. Intended Audience: Nurse practitioners, physician assistants, and registered nurses Conflict of Interest Disclosure Policy: NPHF has implemented a process to identify and resolve conflicts of interest that may exist which might affect the independence and fair balance of an educational activity. All planning committee members, authors and speakers were required to disclose relevant financial relationships with any commercial interest providing support for this program. There were no potential or real conflicts of interest disclosed. Faculty Sean M. Hayes, PsyD Clinical Psychologist Healthcare Behavioral Change Strategist Montreal, Canada Dr. Hayes discloses no conflicts of interest. Jennifer Marjama, PA-C Certified Physician Assistant Physical Medicine and Rehabilitation Southeastern Integrated Medical Chiefland, FL Ms. Marjama discloses no conflicts of interest. Marjorie Wells, PhD, FNP Project Director Tobacco Free Nurses UCLA School of Nursing Los Angeles, CA Dr. Wells discloses no conflicts of interest.
Phyllis Zimmer, MN, FNP, FAANP, FAAN President and Nurse Planner Nurse Practitioner Healthcare Foundation Bellevue, WA Ms. Zimmer discloses no conflicts of interest. Partner Disclosures: All partner organizations reported no conflicts of interest. Accreditation Statement: The Nurse Practitioner Healthcare Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Designation Statement: This activity provides 2.00 contact hours and 0.50 hours of pharmacology credit. Accreditation Statement: This program has been reviewed and is approved for a maximum of 2.00 AAPA Category 1 CME credits by the AAPA Review Panel. PAs should claim only those hours actually spent participating in the CME activity. Instructions: There are no fees for participating in and receiving CME/ CE credit for this activity. During the period November 2, 2017, through November 2, 2018, participants must: 1) read the learning objectives and faculty disclosures; 2) complete the pre-assessment test; 3) study the educational activity, including listening to the audio clips throughout the online version of the activity; and 4) complete the posttest 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/Mar18feature. If you have any questions relating to the accreditation of this activity, please contact Pam Jenkins, MS, NP, of NPHF at pamjw@ nphealthcarefoundation.org or 925-461-1102. If you have any questions relating to your certificate or other issues with the activity, please contact myCME.Support@haymarketmedical.com.
Jointly provided by
In collaboration with
CME CE FEATURED COURSE: SEAN M. HAYES, PSYD; JENNIFER MARJAMA, PA-C; MARJORIE WELLS, PHD, FNP
Smoking cessation: Practical tools for busy clinicians A collaborative treatment plan that emphasizes behavior change strategies and appropriate clinical options can help motivate persistent smokers.
© FUNNYANGEL / SHUTTERSTOCK
Successful smoking cessation depends on a patient’s access to many resources.
ne of the largest public health threats the world has ever seen, tobacco use is responsible for the deaths of an estimated 7 million people worldwide annually.1 Data suggest that around 1 in every 5 deaths annually in the United States is caused by tobacco smoking, and the death rate among smokers is roughly 3 times that of people who have never smoked.2 In 2005, the World Health Organization’s Framework Convention on Tobacco Control (WHO FCTC) laid out comprehensive policies for the worldwide control of tobacco use, one of which is the provision of smoking cessation programs in each FCTC member country. Despite the demonstrated effectiveness of smoking cessation programs,3 almost 10 years after ratification of the FCTC only 24 of the 195 FCTC member states had complete policies offering cessation programs, covering only an estimated 15% of the world population.4 In the United States, substantial progress has been made toward all the WHO’s recommended tobacco control policies,4 but states still only spend on average 2% of the funds they receive from tobacco taxes and legal settlements on cessation and control programs. This is substantially less than the level recommended by the Centers for Disease Control (CDC), which varies for each state based on its income from tobacco tax revenue and legal settlements.5,6 In 2014, a report from the Surgeon General indicated that almost 7 out of every 10 adult smokers want to quit,7 suggesting that current
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demand for smoking cessation support may outweigh the supply of state-funded tobacco cessation programs. An important opportunity therefore exists for care teams, including those providing primary care to patients, to make up that shortfall in providing assistance and support to their patients who express a desire to quit smoking. Impact of nicotine use: toxicity, dependence, and adverse health
The nicotine contained within tobacco has been regarded as both toxic and addicting since the Surgeon General’s 1988 report on the health consequences of smoking.8 Toxicity caused by nicotine is dependent on several factors, including route of exposure, dose, dose duration and frequency, and nicotine formulation. Nicotine in inhaled tobacco smoke is rapidly absorbed into the bloodstream due to the large surface area of the alveoli and small airways and the solubility of nicotine in the lungs’ epithelial layer fluid coating, which has a physiological pH that facilitates absorption. Nicotine from oral tobacco products is absorbed more gradually across the oral mucosa but more rapidly in the small intestine. Nicotine accumulates in the liver, kidneys, spleen, lungs, and brain as well as in gastric juice and saliva, breast milk, skeletal muscle, fetal serum, and amniotic fluid; estimates suggest that it takes 10 to 20 seconds for nicotine from a cigarette puff to reach the brain.7 The development of tolerance with repeated exposure is relatively rapid.9,10 Nicotine dependence (tobacco use disorder)11 is characterized by persistence of a drug-taking behavior and emergence of withdrawal symptoms upon abrupt cessation of nicotine administration. Nicotine binds directly to nicotinic acetylcholine receptors in the brain; these are ligand-gated ion channels whose activation results in widespread release of multiple neurotransmitters throughout the brain.12 Chief among these is the neurotransmitter dopamine. The ventral tegmental area (VTA) of the brain, a focal initiation point of the mesolimbic (reward) pathway, consists of dopaminergic neurons. These cells respond when stimuli indicative of a reward are present, such as opioids or nicotine. The VTA supports learning and sensitization development, and these neurons project and release dopamine into both the prefrontal cortex and the nucleus accumbens.13 The prefrontal cortex in the forebrain is important for the integration of information that contributes to whether any relevant behavior will be elicited. It appears to be the area in which motivation originates and the relevance of stimuli is determined.14 The final critical areas involved in the reward pathway are the nucleus accumbens and arcuate
nucleus. These regions consist mainly of endorphin- and gamma-aminobutyric acid-secreting (GABAergic) neurons associated with acquiring and eliciting conditioned behaviors and involved in the increased tolerance to nicotine as addiction progresses.15 Nicotine dependence develops as a neurobiologic adaptation to long-term nicotine exposure. The trajectory of dependence varies among individuals, but the transition from experimental use to regular smoking can occur with as few as 100 cigarettes.7 It is worth noting, however, that all forms of nicotine delivery do not present equal risk in establishing or maintaining dependence. In particular, nicotine replacement therapies (NRTs) are designed to minimize dependence risk. These products carry a low risk of establishing and maintaining dependence and are generally easier to discontinue than tobacco products.16 The adverse health consequences of smoking are well established (Figure 1). Among the causes of mortality in smokers, the leading 3 are lung cancer, ischemic heart disease, and chronic obstructive pulmonary disease (COPD).17 The critical issue for primary care providers is that all these diseases are chronic and long-term, causing a substantial economic and care burden on the care team and health system, and causing the patient substantial distress and significant quality-of-life consequences. Additionally, the secondary smoke consequences for nonsmoking family members are considerable. One significant example is the link between smoking and type 2 diabetes (T2DM). The causal relationship between smoking and T2DM is well established; smokers have significantly higher HbA1c than nonsmokers18 and have almost a 40% greater risk of T2DM than nonsmokers.19 The American Diabetes Association and the European Association for the Study of Diabetes recommend smoking cessation as an integral component of the management of diabetes.20 Insulin resistance is increased in smokers, likely via increased inflammation and oxidative stress.21-23 Given the additional evidence linking smoking with both obesity24 and cardiovascular disease, the impact of which appears exacerbated in smokers with T2DM,25 smoking represents an important modifiable risk factor for T2DM and cardiovascular health that can be addressed in primary care. Promoting motivation for change in nicotine use
Nicotine dependence is a chronic disease that often requires multiple quit attempts (on average 7 to 9 quitting efforts) before sustained smoking cessation is achieved 26; around half of smokers reportedly make at least 1 attempt to quit
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FIGURE 1. Health consequences causally linked to smoking7
Stroke Blindness, cataracts, age-related macular degeneration Congenital defects-maternal smoking: orofacial clefts
Periodontitis Aortic aneurysm, early abdominal aortic atherosclerosis in young adults Coronary heart disease
Esophagus Trachea, bronchus, and lung
Pneumonia Atherosclerotic peripheral vascular disease Chronic obstructive pulmonary disease, tuberculosis, asthma, and other respiratory effects
Acute myeloid leukemia Liver Stomach
Diabetes Obesity Reproductive effects in women (including reduced fertility) Hip fractures
Pancreas Kidney and ureter
Male sexual function-erectile dysfunction
Rheumatoid arthritis Immune function Overall diminished health
each year.6 Thus, repeated interventions by clinicians and patients to both attain and maintain abstinence are crucial. However, this can be challenging; only approximately 7% succeed for any length of time (data based on patient’s last cigarette more than 6 months ago), and less than 1 in 3 patients use pharmacotherapeutics or counseling when they attempt to quit.27 Given these statistics, it is easy to understand why both care team members and patients are clinically disengaged or reluctant to discuss the subject during every office visit. On a more positive note, in 2015 almost 60% of people in the United States who had ever smoked had quit, and in the decade 2005 to 2015, the percentage of people who smoke had dropped significantly across all ethnic groups.27,28 Primary care clinicians should understand that abstinence from nicotine is feasible, and a combination of
pharmacologic treatment and counseling support is widely accepted as being most beneficial to help patients.29-31 Primary care providers must be able to critically assess each patient’s cognitive, emotional, and behavioral readiness to initiate quitting smoking and tailor their discussions and intervention plan with each patient accordingly. People only change voluntarily and follow a distinct cognitivebehavioral sequencing32,33: • They become aware that they need to change • They become interested in or concerned about the need for change • They become convinced that change is in their best interests or will benefit them more than cost them • They organize a plan of action that they are committed to implementing
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In 2015 almost 60% of people in the US who had ever smoked had quit, and from 2005-2015, the percentage of people who smoke had decreased significantly. • They take the actions that are necessary to make and sustain the change By correctly assessing the stage of readiness to change, clinicians will be able to see their nicotine-dependent patients not as unmotivated or nonadherent, but as patients who have either a) not shifted in their cognitive-emotional awareness and insight to the need to change or b) are not ready or do not know how to engage in behaviors that others perceive as helpful. Many patients have tried to quit, but given their history believe that they cannot succeed and have rationalized their continuance of smoking. The evidence-based stages of behavioral change through which individuals progress is a good framework for clinicians to utilize in practice (Figure 2). A key initial step in this process is to ensure that patients are being asked about tobacco use at every office visit, practice-wide, to build awareness of the dangers and ultimately enhance cognitive dissonance. Cognitive dissonance refers to a situation involving conflicting attitudes, beliefs, or behaviors that, in turn, create feelings of discomfort and imbalance.35 By consistently and nonjudgmentally building awareness of the risks with a patient who persists in smoking, the patient’s smoking behaviors become increasingly dissonant with the understanding that smoking is dangerous for his or her health, and ultimately the patient will be motivated to reduce this state. However, data from a 2005–2008 survey of outpatient office visits indicated that fewer than two-thirds of patients were screened for tobacco use.36 Consistently and systematically asking about any form or any amount of tobacco use should be part of every visit, as ”social smokers” who only smoke on rare occasions may feel it is acceptable not to identify themselves as smokers. Similarly, users of e-cigarettes, hookahs, or smokeless tobacco products may not realize the combinatorial impact on their dependence; 40% of tobacco users use more than 1 product, incorrectly perceiving noncigarette products as less risky than cigarettes.37 Three suggested questions are useful in assessing whether a cigarette smoker has clinically meaningful dependence. This is a practical application of the Fagerström Test for Nicotine Dependence (FTND)38,39: A. How many cigarettes per day do you smoke? B. When do you smoke your first cigarette of the day? C. What is the longest period of time between cigarettes before you crave another?
An approximate guide is that if the first cigarette is smoked within 30 minutes of awakening and the patient smokes more than 10 cigarettes per day, he or she is likely to be tobacco dependent. A contributing factor is the age at which the patient first started smoking; the younger the patient started, the more likely he or she is to be tobacco dependent as an adult.38 Clinicians should use their own judgment when including other tobacco products in this assessment; cigarettes are specifically designed for maximal effectiveness of nicotine intake, and other products are considered to contribute less to tobacco dependence overall when assessed head to head.40 Once nicotine dependence is established, it is important for the clinician to assess patients’ readiness (or motivation) to change their behavior. Identifying the individual patient’s stage of change, particularly precontemplators (those who are not ready to quit) and contemplators (ready to quit), helps direct clinicians in their tasks. In the Stages of Change model,41 therapeutic interventions, whether pharmacologic or otherwise, are not offered to FIGURE 2. Adult readiness to change behavior: stages of change32-34
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Recent estimates using a longitudinal cohort of smokers suggested that it can take anywhere from 6 to 30 attempts before abstinence is successfully attained. precontemplators, as they are not ready to begin the quitting process. In contrast, an alternative approach is to proactively offer treatment, either pharmacologic or psychosocial, in the same way as would be offered for any other chronic disease. Using that approach, clinicians can continue to: • Reinforce the dangers of not quitting; • Emphasize the positive results of quitting to enhance cognitive dissonance; • Support the potential for success (counter the history of failed attempts) with pharmacologic or psychosocial therapies, and reminders of how effective these are in helping people quit; and • Utilize the placebo effect generated by the simple act of initiating an intervention. Neither approach has been shown to be more effective in randomized trials,42 and it is therefore critical for clinicians to select an approach that they believe in to maximize success with patients. For tobacco users who are identified as ready to attempt to quit, clinicians should discuss the following plan, which takes the patient from contemplation through preparation and action: • Assess any prior attempts to quit, what the degree of success was, the challenges/obstacles experienced, and use that knowledge to inform recommendations. • Anticipate any barriers to quitting and proactively set measures to help the patient avoid or overcome them. • Work with the patient to identify negative reinforcement factors in the patient’s daily life and develop a concrete action plan to address these. The presence of a spouse or family member who smokes at home or a colleague at work who invites the patient for “smoke breaks” is a powerful environmental trigger to relapse and can adversely impact the patient’s ability to progress with dose tapering or maintain abstinence after cessation. • Attain concordance with the patient on a quit date and identify whether the patient would benefit from a gradual taper or abrupt cessation on that date. NRT and delivery devices with adjustable doses such as some e-cigarette brands may assist with this process. • Discuss with the patient the use of appropriate pharmacotherapy and counseling approaches. • Facilitate the patient’s access to support and resources. • Arrange a follow-up with the patient after the quit date. This helps boost motivation and allows the clinician
to identify any unforeseen barriers, such as withdrawal symptoms or adverse effects of pharmacotherapy. For tobacco users who are identified as not yet ready to quit, the task of the clinician at this juncture is to continue to raise doubts in the patient’s mind, thereby building cognitive dissonance—focus on the risks of continuing to use tobacco products (cost, inconvenience, and health consequences) and the benefits of abstinence. Individualizing the message will be very helpful, such as using personal health risk, risk of secondhand smoking to family members and/or children, or family history if the patient had relatives who smoked and suffered serious health consequences. Motivational interviewing can be an effective tool for precontemplators and is feasible even within the time constraints of a primary care visit. Patient-identified barriers to abstinence
Clinicians must be aware that many patients with addictive disorders are often reluctant to accept their illness as real.43 The adverse effects of smoking are experienced a long way down the road. Patients with addictive disorders, with or without comorbid psychiatric illness, may be particularly prone to minimizing the seriousness of their problems and may adhere to intervention regimens erratically as a result. It is important to identify patients who are precontemplators who may not understand, or are actively in denial of, the long-term consequences of smoking and continue to reinforce the risks they are taking and the benefits of cessation. Symptoms of nicotine withdrawal following reduction in use pose a major potential barrier to abstinence. The cravings for a cigarette, along with the knowledge that a cigarette can ease the symptoms of withdrawal, often drive the patient to return to tobacco use. Recent estimates using a longitudinal cohort of smokers suggested that it can take anywhere from 6 to 30 attempts before abstinence is successfully attained.26 Withdrawal symptoms typically peak within the first 3 days of cessation and subside over the next 3 to 4 weeks. Documented symptoms include increased appetite and weight gain, changes in mood (dysphoria or depression), insomnia, irritability, anxiety, difficulty concentrating, and restlessness.11 Withdrawal should be a significant part of any discussion with patients who are getting ready to initiate a quit plan to effectively manage expectations as well as provide a starting point for pharmacologic therapy consideration. All of the first-line pharmacotherapies, as well as NRT, alleviate withdrawal symptoms.
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In motivational interviewing, clinicians use strategic questioning and empathic listening to help patients resolve their ambivalence about behavior change. A final key issue among patients is a very rational fear and/or historical experience of failure. The feeling of frustration or of being a “failure” because he or she cannot quit can often influence a patient’s future quit attempts. Patients who relapse often had inadequate psychosocial or counseling support as part of their cessation plan and/or experienced strong withdrawal symptoms, weight gain, or mood symptoms.3 Intensification of structured behavioral counseling can be beneficial, particularly as an estimated two-thirds of patients report wanting to try again within 30 days.44 Another discussion around pharmacotherapy is also recommended, particularly if an agent was perceived as helpful in a prior quit attempt. Clinicians should remind patients that most smokers require multiple attempts to attain and maintain successful abstinence.45 Above all, ongoing motivation is key. Identification of the appropriate clinician strategy pertinent to each patient’s stage of change can be helpful to provide motivation, as change is gradual and may require a structured, step-wise approach for many patients. Practical aspects and techniques for motivating patients to change
Motivational interviewing (MI) can be an effective tool for patients who feel they are not yet ready to quit. In MI, clinicians use strategic questioning and empathic listening to help patients resolve their ambivalence about behavior change to initiate quitting and enhance cognitive dissonance regarding the risks of continuing to smoke. MI works by building motivation and confidence, and the clinician strives to resolve any patient ambivalence about the necessary change. The overall goal is to help patients understand the discrepancy between where they are and where they want to be and amplify that discrepancy to motivate patients to make the change.46 In primary care, where office visits are time-constrained, the use of a 3-question Brief Action Plan can be helpful.47 The 3 core questions ask what the patient’s desired goals are, evaluate his or her confidence about making that change, and then request a follow-up to check on the outcomes. Key to MI is the use of questions that allow patients to affirm their goals and state the changes they want to make; effective MI gets the patient to drive change (self-efficacy). Meta-analyses have demonstrated a small increase in smoking cessation rates with MI versus care as usual;
it is particularly effective when delivered over multiple sessions, each under 20 minutes, making it a feasible approach for use in primary care.48 The structured model of 5 R’s can be helpful for clinicians to use with their patients: • Relevance – MI is most effective if the patient identifies personally relevant information. • Risks – The patient should identify his/her personal negative consequences of tobacco use. • Rewards – The patient should be encouraged to identify potential benefits of quitting smoking. • Roadblocks – The patient can be invited to identify barriers to abstinence or negative reinforcements and suggest mechanisms to overcome them. • Repetition – It is critical to repeat the approach at every intervention. The 5 A’s: A simple algorithm for structuring care visits
A useful mnemonic for a structured approach to smoking cessation that can be implemented at each clinic visit with the patient by one of the primary care team members is the 5 A’s3: • Ask patients about smoking, • Advise all smokers to quit, • Assess their readiness to quit, • Assist them with their smoking cessation effort, and • Arrange for follow-up visits or contact. Central to this approach is the concept of a practice-wide system for querying and documenting tobacco use for each patient at each office visit, regardless of which individual clinician is seeing the patient each time. This practice-wide approach ensures that: 1) the patient is approached systematically by all members of the primary care team, 2) a unified message is communicated about the need to quit, and 3) the primary care team, not a single team member, is held accountable for successful patient outcomes. The Centers for Medicare and Medicaid Services (CMS) Meaningful Use Core Measures include documentation of smoking status for all patients over the age of 13.49 Checkboxes in the electronic health record for patients can be used to document smoking status, whether the patient has been referred for counseling, whether pharmacologic therapy has been prescribed, and other data the team wants to document for each office visit.
38 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
Behavioral therapy techniques may be used by clinicians to identify and avoid triggers and manage situations in which a patient may feel tempted to smoke. Evidence-based behavioral therapy techniques can be used by clinicians in a primary care setting. • Cognitive behavioral therapy (CBT): Cognition influences emotions and behavioral processes. CBT works to help patients change negative behaviors and incorporate healthy lifestyle changes into their tobacco cessation plan.50 Interventions include self-monitoring and stress management, relaxation exercises, and coping skills development. CBT is more effective in motivated patients due to the self-observation and self-management at its core. Developing coping skills to manage withdrawal is an area that can be discussed in primary care; examples of coping skills include plans to minimize time spent in the company of smokers, chewing gum or eating small healthy snacks, exercise plans, and distraction techniques such as knitting.51 • Classical conditioning: Addictive behaviors can become associated with other activities, such as smoking while in a bar or restaurant or watching sports games. Repeated pairing can cause patients to feel a craving for cigarettes simply by being in the aforementioned environments. The goal with classical conditioning is to identify and extinguish these cues. If a patient repeatedly bought cigarettes at the gas station while filling up the car on the way to work, for example, he or she could have a family member call at the appropriate time with a reminder not to buy cigarettes or could take the car to the gas station at a different time. • Operant conditioning: Reinforcement and consequences are the basis of much addiction-specific behavioral therapy. When patients use tobacco as a reward or to experience a pleasurable feeling to temporarily mitigate the effects of stress, it becomes more likely that they will use it repetitively. Working through the negative consequences of patients’ actions is the basis of operant conditioning and can help motivate them toward cessation; suggesting alternative rewards or coping skills to mitigate stress can also be beneficial. These techniques may be used by clinicians to identify and avoid triggers and manage situations where the patient may feel tempted to smoke. Both individual and group therapy techniques are effective.3,52 The advantage of group therapy is that it provides a support network that is mutually dependent; positive reinforcement is crucial in successful behavior change and should be a role of the clinician during office visits.
Referrals and smoking cessation resources
Although primary care providers may use individual and group CBT techniques to increase their effectiveness in providing smoking cessation care, successful cessation relies on the patient having access to as many resources and as much information as possible, so he/she is prepared for what to expect and how to overcome challenges. Numerous telephone, web-based, and smartphone app resources are available to assist patients in their smoking cessation efforts. Success may also be enhanced with more in-depth structured psychotherapy; referral to a psychologist, psychiatric nurse practitioner, or counselor will be necessary for this level of smoking cessation support. How pharmacotherapeutics facilitate the change process
All Food and Drug Administration (FDA)-approved agents for aiding in smoking cessation work by alleviating the withdrawal symptoms commonly encountered by smokers after cessation, thereby facilitating the change process by removing a significant barrier. Figure 3 lists some of the considerations for use of the current FDA-approved medications for tobacco and nicotine cessation that are considered to be first-line therapies.53 Patient preference is generally considered to be the driving factor for decision-making among first-line therapies. The goal of NRT is to allow a smoker to receive nicotine in a nontobacco form, permitting a gradual nicotine taper after cessation and thereby alleviating some of the withdrawal symptoms and facilitating the cessation process. Differences in bioavailability between products allow for combination therapy, which is considered safe and effective; for example, a slow-onset, long-acting patch to control baseline withdrawal symptoms can be supplemented with short-acting lozenges, gums, or the prescription nasal spray or oral inhaler to curb immediate cravings.54,55 The transdermal long-acting patch (available over the counter in the United States) is generally considered the best product for baseline withdrawal symptom control; it has the lowest adherence concerns of any NRT and provides a slow pattern of regular nicotine levels that provide relief over 24 hours. Clinicians should advise patients that the patch can take several hours to reach maximal delivery dose, and the patient has no control over the dose, so combination therapy with rapid-onset NRT on an as-needed basis is considered helpful.
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 39
The dosing schedule for the patch is critical, and clinicians should consider the following approach: Starting on the quit date, patients who smoke more than 10 cigarettes a day (half-pack) should use the highest dosage of the nicotine patch (21 mg/d) for 6 weeks, followed by 14 mg/d for 2 weeks, and finish with 7 mg/d for 2 weeks. Smokers who weigh <100 lb or smoke 10 or fewer cigarettes per day should begin with the 14-mg/d patch for 6 weeks, followed by 7 mg/d for two weeks. This 8- to 10-week dosing strategy is fairly standard; however, 2 clinical studies have suggested that a 24-week taper down may be more effective for abstinence rates at the 24-week mark.56,57 Clinicians should
work with their patients on an individualized approach, as some patients may not desire the additional cost burden of a longer period on NRT. Smokers might also worry that they will remain dependent on nicotine if they use NRT. Clinicians should advise patients that this is a very rare occurrence.58 Gums and lozenges are the most commonly used shortacting NRTs and both are available over the counter. Clinicians should advise patients that there are different techniques associated with correct use of these products and, while both product types appear similarly efficacious, patients should avoid changing between products
FIGURE 3. Considerations for clinical use of FDA-approved pharmacotherapy for smoking cessation53 1 Pregnant smokers should be encouraged to quit without medication based on insufficient evidence of effectiveness and theoretical concerns with safety. Pregnant smokers should be offered counseling interventions that exceed minimal advice to quit.3 1 1
40 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
2 Wholesale acquisition cost obtained from Red Book Online. Thomson Reuters, December 2016
MAO, monoamine oxidase; OTC, over-thecounter, Rx, prescription product.
For complete prescribing information and a comprehensive listing of warnings and precautions, please refer to the manufacturers’ package inserts.
to minimize risk of incorrect use. The lozenge should not be chewed; it dissolves in the mouth. By contrast, the gum should be chewed with correct technique; chewing too fast will release nicotine too quickly and it will be swallowed instead of absorbed across the buccal mucosa. The so-called “chew and park” technique is recommended; patients should chew the gum until the nicotine flavor is detected, then “park” the gum in their cheek to allow absorption. When the taste disappears, the patient should repeat; after around 30 minutes the gum can be discarded. Clinicians should advise patients to avoid leaving transdermal patches on overnight. Abstinence rates are reportedly the same for 24-hour dosing versus removal of the patch overnight,59 and leaving the patch on overnight increases the rates of adverse events such as insomnia and hypnagogic hallucinations.54 The prescription nasal spray and oral inhaler may provide additional assistance as they partially mimic the physical use of a cigarette, more so for the oral inhaler. The nasal spray is probably the fastest system for nicotine delivery into the bloodstream, peaking about 10 minutes following delivery of the aqueous spray.60 They are also likely the most burdensome (2 uses of the nasal spray per hour) and public of the delivery devices, and some patients may feel embarrassment over using them. Patients may erroneously believe that the use of other nicotine delivery methods—such as snuff, hookahs/water pipes, chewing or packet tobacco, or e-cigarettes—may be safer than smoking cigarettes, and that these approaches can be used as aids in cessation. Some e-cigarette brands allow dose adjustment and therefore could be used to aid cessation, but this has yet to be established in formal trial settings. Clinicians should discuss tobacco options with their patients, as intake of nicotine and other toxins present in tobacco by any means is still adversely affecting their health. Varenicline is a nicotinic acetylcholine receptor partial agonist, which is effective in smoking cessation and works via a similar overall approach to NRT. Instead of low-dose nicotine alleviating withdrawal symptoms, varenicline partially stimulates the receptor bound by nicotine for a similar end result.61 It has also been theorized that, because varenicline binds the receptor with very high affinity, it may prevent nicotine from binding the receptor and thereby reduce some of the reward feelings induced.62 This allows the clinician to have the patient start varenicline 1 week before quitting cigarettes. This may also be helpful for patients who are ambivalent about quitting but are willing to try reducing their nicotine intake. Clinical trial data indicate that not only may a longer lead-in time of varenicline be beneficial
as part of the treatment plan for some patients, allowing them to reduce nicotine intake prior to cessation,63 but also that in patients who do not wish to quit immediately, but instead reduce dose and aim for cessation in the following 3 months, varenicline use can improve abstinence rates.64 Sustained-release bupropion is the second non-NRT agent approved by the FDA for smoking cessation. More commonly encountered in primary care practice as an antidepressant, bupropion is a norepinephrine and dopamine reuptake inhibitor. Its mechanism of efficacy in smoking cessation is unclear; the prevailing idea is that because the reward neurotransmitter dopamine persists in synaptic clefts due to reuptake being abrogated, the reward feelings are sustained longer and withdrawal symptoms are blunted. Effectively bupropion may be working downstream of varenicline and NRTs to achieve the same result. One headto-head study of varenicline and bupropion indicated that varenicline is more effective at promoting abstinence,65 but clinicians must select therapy based on patient preference and other considerations. For example, bupropion may be a more suitable choice in patients with pre-existing depression, as it may help mood symptoms; bupropion may also be a better selection for patients concerned about weight gain following cessation, as bupropion helps mitigate this.66 Clinicians should create an environment where the patient feels comfortable discussing issues with taking medicines as prescribed. NRTs other than the transdermal patch must be taken routinely and patients may require some help in remembering, so reminder notes, calendars, alarms, pill boxes, and smartphone apps all can be effective in improving adherence, which will help improve the behavior change toward abstinence. ■ This is an abridged version. To view the full article, which includes smoking cessation resources, please visit ClinicalAdvisor.com/ Mar18feature. References 1. World Health Organization. Tobacco Fact Sheet. Geneva, Switzerland: World Health Organization; 2017. 2. Jha P, Ramasundarahettige C, Landsman V, et al. 21st century hazards of smoking and benefits of cessation in the United States. N Engl J Med. 2013;368:341-350. 3. Fiore MC, Jaén CR, Baker TB, et al. Treating tobacco use and dependence: 2008 update US Public Health Service Clinical Practice Guideline executive summary. Respir Care. 2008;53(9):1217-1222. 4. World Health Organization. WHO Report on the Global Tobacco Epidemic. Geneva, Switzerland: World Health Organization; 2015.
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www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 43
POSTTEST Expiration date: November 2, 2018
A statement of credit will be issued only upon receipt of a completed pre-assessment test, activity evaluation form, and posttest with a score of 70% or higher. All components must be completed and submitted online at ClinicalAdvisor.com/Mar18feature. CREDITS: 2.00 | Smoking cessation: Practical tools for busy clinicians
1. The increased mortality rate conferred by smoking is estimated to be how much? a. There is no increase in c. 3-fold increase mortality due to smoking. d. 50-fold increase b. 1.5-fold increase
6. Telephone, texting, and Web-based counseling and resources have shown no benefit in assisting patients to overcome challenges and successfully quit smoking. a. True b. False
2. Which of the following statements about nicotine dependence is false? a. Nicotine dependence develops as a neurobiologic adaptation to long-term nicotine exposure. b. Nicotine dependence is characterized by emergence of withdrawal symptoms upon abrupt cessation of nicotine administration. c. Nicotine dependence requires a substantial length of time smoking and at least 20 cigarettes per day to develop. d. Nicotine dependence develops via repeated stimulation of the dopaminergic reward pathway in the brain.
7. Which of these is not an FDA-approved NRT delivery method? a. Lozenge b. Intravenous injection c. Patch d. Inhaled
3. Which of the following statements about smoking cessation is false? a. Around half of smokers make at least one attempt to quit per year. b. Roughly 50% of patients succeed in quitting for any length of time. c. Multiple quit attempts (7-9 on average) are often required before sustained abstinence is achieved. d. Less than 1 in 3 patients use pharmacotherapeutics to assist in smoking cessation. 4. Which of the following question(s) is/are useful in assessing an individual’s smoking habits? a. How many cigarettes per day do you smoke? b. When do you smoke your first cigarette of the day? c. When do you smoke most heavily during the day? d. What is the longest period of time between cigarettes before you crave another? e. All of the above 5. Which of the following is NOT one of the 5 A’s? a. Ask patients about smoking b. Advise all smokers to quit c. Assess their readiness to quit d. All of the above are from the 5 A’s e. None of the above are from the 5 A’s
8. Which of the following is an FDA-approved pharmacotherapeutic to aid in smoking cessation? a. Acamprosate b. Topiramate c. Lamotrigine d. Varenicline 9. The “stages of change” approach includes which of the following key concepts? a. Behavior change occurs along a continuum b. Targeted and tailored messages have impact on those who change behavior AND those who don’t c. Can impact on all patients–and predict future change d. All of the above 10. According to the Stages of Change model, a therapeutic plan of care for the CONTEMPLATOR might include which of the following: A. Reinforcement of the dangers of not quitting B. Pharmacologic therapy C. Identification of barriers to quitting, and setting measures to help the patient overcome them D. Establish a quit date, and tell the patient to stop all cigarettes as of that day E. Refer the patient for behavioral counseling a. b. c. d.
A and B A, B, C, and D A, B, C, and E All of the above
TO TAKE THE POSTTEST please go to: ClinicalAdvisor.com/Mar18feature
44 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
Advisor Forum These are letters from practitioners around the country who want to share their clinical problems and successes, observations, and pearls with their colleagues. Responding consultants are identified below. We invite you to participate.
YOUR COMMENTS CUTANEOUS LEISHMANIASIS: A POTENTIAL TREATMENT OPTION Kudos to the cutaneous leishmaniasis case [Derm Clinics, Jan. 2018, p. 51). This is a disease that will affect clinicians in the southwest US and eventually the entire country as climate warming progresses. Currently, very few providers can make the correct diagnosis, and counter to the authors’ recommendation to refer the patient to a leishmaniasis expert, these experts are extremely numbered. There are treatments, but the process is complicated. The most effective treatment differs depending on the strain of leishmania contracted. One treatment option is amphotericin B, used originally to treat systemic fungal infections. It is also effective against mucosal leishmaniasis, but the treatment is not pleasant. It is often called “amphoterrible.” Kidney functions must be closely monitored and treatment stopped if kidney function drops below 40%. Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 275 7th Avenue, 10th Floor, New York, NY 10001.You may contact us by e-mail at firstname.lastname@example.org. 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.
The authors chose not to discuss mucosal leishmaniasis in detail, which involves the parasites migrating to the mucosal tissues of the mouth and nose. Although they are often referred to as flesh-eating, the parasites do not consume tissue. Rather, the body has a profound immune response, eventually deforming and destroying the nose and mouth. There is no “cure.” This is a chronic infection, and we have yet to find a vaccination that works any better than the body’s own natural responses.—RICHARD E. HARBIN, MSN, MEd, CPNP, ARNP, Redondo Beach, Calif. (233-1)
MY MOST MEMORABLE PATIENT A PATIENT WITH A BONE MARROW TRANSPLANT SHOWS HOW SHORT AND PRECIOUS LIFE IS During my 3rd year in nursing school for my bachelor’s degree in nursing, I was enrolled as a nurse extern at Memorial Sloan Kettering Cancer Center in New York City in the summer of 1993. This 9-week experience allowed us to shadow the nurses. I was assigned to the 6th floor, which specialized in bone marrow transplants, lymphoma, and gastrointestinal cancers. It was so heartbreaking to see people on isolation who were post a bone marrow transplant, as it was so touch and go. One incredible patient who was very ill after his bone marrow transplant was a gem for me. He was a wealthy,
Philip R. Cohen, MD,
is clinical associate professor of dermatology, University of Texas Medical Center, Houston.
Deborah L. Cross, MPH, CRNP, ANP-BC, is associate program
director, Gerontology NP Program, University of Pennsylvania School of Nursing, Philadelphia.
Abimbola Farinde, PhD, PharmD,
is a professor at Columbia Southern University in Orange Beach, Ala.
46 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
Laura A. Foster, CRNP, FNP,
Abby A. Jacobson, MS, PA-C,
practices family medicine with Palmetto Primary Care Physicians in Charleston, S.C.
is an assistant professor at Thomas Jefferson University and a dermatology PA at Family Dermatology of Reading, Pa.
midlife executive in a private room with the oddity of a video phone to see and talk to his family and children from out of state. His room was decorated with family photos, a golf-putting strip, golf clubs, inspirational movie posters, fake plants, a lava lamp, and wonderful stereo equiptment with dance music always pumping from it. Donning reverse isolation gowns, a mask, and booties for the nurses was such an ordeal to prep as we came in to hang IV meds or change his PICC line dressings, and there he was, wearing shorts and an Aloha shirt and usually flip-flops, clicking or swaying to the beat of music but always lying in bed. He usually engaged us politely in conversation, but some nurses were experts in getting him to open up during our brief encounters. After my third week of working with him, learning and feeling my way as a novice nurse and following protocols to the T, I looked forward to the brief encounters, as his room was a haven of life compared with the other rooms outside his walls, especially the silence of the other patients. He asked me about my plans for the coming weekend, and I mentioned that I may go to the Jimmy Buffet concert in Long Island. Then I said it was also an issue of cost on a student’s budget. He got up slowly and walked over to his phone and asked how many tickets I wanted as he would call Ticketmaster and order tickets for me right then and there. I was shocked and embarrassed to see him get up and stand, and I hemmed and hawed about it. I felt horrible for mentioning it, as he was a big fan of Jimmy Buffet. He came over to me, with his hands gripping my gowned shoulders, and stressed to never put off anything you wanted to do in life. He candidly said that he now understood how precious and short life is and how we put off the little things, which are the most important things. And we regret doing so much before our time is up. I will never forget the intent of his teaching as he knew the prognosis was grim for him.
Debra August King, PhD, PA,
is senior physician assistant at New York-Presbyterian Hospital, New York City.
Mary Newberry, CNM, MSN,
provides well-woman gynecologic care as a midwife with Prima Medical Group, Greenbrae, Calif.
I told him that I would try to go, and I did make it to the parking lot of the concert to hear most of it. Close enough was good enough. He did not survive past my externship, and quickly his room was turned over to another person. I still feel his presence when I hear Jimmy Buffet.—VALERIE ARMSTRONG, NP, Jacksonville, Fla. (233-2)
CASE FILES FEVER, CHILLS, AND NAUSEA AFTER BEGINNING LONG-ACTING REVERSIBLE CONTRACEPTION Contributed by Sherril Sego, FNP-C, DNP A 26-year-old woman, para 3, gravida 5, with 2 miscarriages, developed a rapid onset of fever, chills, nausea, vomiting, and severe pelvic pain, as well as heavy vaginal bleeding not associated with her normal menses. During presentation to the emergency department, she was found to have a white blood cell count of 18,000 with a left shift, urinalysis positive for leukocytes and nitrites. Abdominal CT scan was negative for any abscess or appendiceal signs. Her most recent miscarriage was 4 months prior, after which she had a progestin-eluting LARC inserted. Oral antibiotics were prescribed, and she was released to home. After 5 days, however, her symptoms were not improved and she saw her gynecologist, who immediately recommended removal of the LARC device and also changed the antibiotic. The patient began to rapidly improve. The gynecologist believed that the etiology of this unusual presentation of PID was due to retained tissue after the last miscarriage (in spite of a D&C) and the progestin LARC, which inhibited natural endometrial sloughing. (233-3) n
Claire O’Connell, MPH, PA-C,
an associate professor at the Rutgers University Physician Assistant Program, Piscataway, N.J.
Katherine Pereira, DNP, FNP,
is assistant professor, Duke University School of Nursing, Durham, N.C.
Sherril Sego, FNP-C, DNP,
is an independent consultant in Kansas City, Mo.
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 47
Writers’ Guidelines The Clinical Advisor welcomes submissions from its readers. Writing for us is an opportunity to share your knowledge and experience with your colleagues — and to collect a fee in the bargain! We pay an honorarium for every submission we accept. We’ll be glad to work with you to develop your ideas into compelling articles. As for length, that depends on which kind of article you submit. CLINICAL FEATURES update our readers on the latest information about conditions seen in everyday practice. Running approximately 2,500 to 5,000 words, including the references, features can be written either as regular narratives or as a series of questions and answers. Topics should be selected with the busy primary-care clinician in mind; specialists should review specialty topics from the primary-care point of view. If at all possible, articles should be accompanied by clinical photos. Charts, tables, and algorithms are also encouraged. Please include your title and affiliation. CLINICAL CHALLENGE is our popular department comprising histories of difficult cases. Each case is presented as a step-by-step, chronological account, revealing the author’s thought processes along the way. It is divided into sections in this order: the patient presentation; the patient history; the twists and turns eventually leading to a diagnosis; the treatment and outcome; and a discussion of the lessons learned or of the condition in general. The length should be about 1,500 words, and accompanying images are encouraged. Please include your title and affiliation. Dermatology Clinic CASE #1
Fingernail dystrophy in a young child SIMO HUANG, BS, CHRISTOPHER RIZK, MD
The patient is a 12-year-old Hispanic girl who presents with a 6-month history of nail dystrophy involving all of her fingernails. On examination, all 10 of her fingernails exhibit longitudinal ridging, pitting, fragility, thinning, and distal notching. The patient’s mother is very concerned about the cosmesis of her daughter’s nails. The patient has no systemic symptoms. On review of systems, the patient’s mother noted that her daughter has started to develop circular patches of hair loss that appear to resolve on their own. The patient has no relevant social or family history and does not take any medications. What is your diagnosis? Turn to page 54
Headache, malaise, and a rash ZACHARY SOLOMON, BS, DAVID RIZK, BA, CONNIE WANG, MD
A 42-year-old man presents with a four-day history of experiencing headache, malaise, and stabbing right-sided headache. Two days after his initial symptoms appeared, he developed a rash over the area of pain. He reports that he went hiking through the Texas hill country prior to becoming ill. The patient is otherwise in good health and has an unremarkable medical history. Physical examination reveals unilateral erythematous, thin, raised plaques over the right forehead. In addition, he has no relevant social or family history. What is your diagnosis? Turn to page 55 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • DECEMBER 2017 53
DERMATOLOGY CLINIC is a department that presents photos of actual cases and asks readers to identify the condition. Each case opens with one or two color photos and a 75-to-100-word description of the patient presentation, without giving away the diagnosis. This is followed by a 750-to-1,000-word summary that includes a fuller description of the ailment, an explanation of how the correct diagnosis was reached, a general review of the condition along with a differential diagnosis, and a description of the patient’s treatment and outcome. Topics must be approved by the editor prior to submission. Please include your title and affiliation. COMMENTARY is our guest editorial page. It gives you the opportunity to sound off on an issue of importance to your colleagues nationwide. A typical Commentary runs about 600 words in length. Please include your title and affiliation. To discuss your editorial ideas, contact us by phone at 646.638.6078; by e-mail to editor@ClinicalAdvisor.com; or by mail to The Clinical Advisor, 275 7th Avenue, 10th Floor, New York, NY 10001.
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Dermatology Clinic CASE #1
Hairless plaque on a woman’s forearm TALIA JAYNE NOORILY, BS, DAVID RIZK, BA, CONNIE WANG, MD
The patient is a 46-year-old woman who presents at your primary care office for an examination with a single lesion that appears on her left arm. During the examination, it is revealed that the patient has a large sclerotic, indurated, hyperpigmented, anhidrotic, and hairless plaque on the right dorsal forearm. The patient states that these lesions had previously been slightly pink for several months before they had turned brown in color and had become “hard.” The patient has type 2 diabetes, but she has no other medical problems. In addition, she has no relevant social or family history. What is your diagnosis? Turn to page 50
An itchy rash on a man’s hand MICHELLE VY, JULIA R. NUNLEY, MD
A 37-year-old man without a significant past medical history presents to the dermatology clinic with an itchy rash on his right hand that he has had for about 4 months. He had tried numerous over-the-counter hand creams and hydrocortisone cream with no improvement. Additional questioning revealed a 1-year-history of dry, itchy feet. As a construction worker, he wears occlusive, steel-toed work boots and often wears gloves. He is also right-handed. Examination of his hands reveals a normal left hand and a scaly right palm. Diffuse, fine, dry white scale was present on the plantar aspect of both feet. What is your diagnosis? Turn to page 59 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 49
Dermatology Clinic CASE #1
Morphea is a rare cutaneous inflammatory disease characterized by asymmetric sclerotic plaques.1 It progresses to scar-like sclerosis of the skin, primarily the dermis and subcutaneous fat, and sometimes extends to underlying muscle and bone. It can present in childhood or later in life and is more common in women than in men. The pathogenesis of morphea involves autoimmune mechanisms, and it is clinically distinct from scleroderma.2 Different subtypes of morphea include plaque-type morphea (also known as localized scleroderma), linear morphea, and generalized morphea.1 Morphea was first described in detail by Thomas Addison in 1854; he called it “Alibert’s keloid syndrome.” In 1930, O’Leary and Nomland distinguished morphea from scleroderma.1 There is still a demand for more research regarding the pathogenesis, classification, and treatment of morphea. Information about the epidemiology of morphea is also scarce. A study conducted at the Mayo Clinic identified and followed 82 cases of morphea in Olmsted County between 1960 and 1993. The study concluded that the incidence was 2.7 per 100,000 and increasing by approximately 3.6% per year. The prevalence of morphea at 80 years of age was estimated at 0.2%. The highest prevalence is in Caucasian women.3 The average age of adult presentation is mid-40s, and most cases are plaque-type. In children, 90% of cases present between ages 2 and 14 years, with linear morphea being the most common variant.2 Half of patients with morphea exhibit disease resolution in 3.8 years. Plaque-type morphea yields the briefest active disease duration; the deep and linear types have longer durations with more frequent systemic involvements, including arthralgia and uveitis. Patients with morphea have a normal life expectancy, further distinguishing it from scleroderma. However, there is greater morbidity associated with the linear type.3 Morphea is an inflammatory process leading to imbalanced production and destruction of collagen. The pathogenesis is complex and uncertain. The most widely accepted theory is that the development of morphea is multifactorial, requiring inherent autoimmunity and an environmental trigger. The disease might also be associated with an embryologic origin such as genetic mosaicism or microchimerism.2,4
The initiating event, likely a local trigger in the skin, causes vascular injury. The vascular injury may be secondary to hypoxia, trauma, infection (Borrelia burgdorferi and CMV have been implicated), oxidative stress, or anti-endothelial cell autoantibodies.5 Researchers believe that after the triggering event, morphea follows a pathway similar to that of scleroderma. The damaged vessels release pro-inflammatory signals that recruit lymphocytes. Recruited T-cells secrete pro-fibrotic cytokines, including IL-4, IL-6, and TGF-beta; the latter increases collagen production and decreases protease production. This process causes skin fibrosis.2 The diagnosis of morphea is based on clinical presentation, which varies with type. Plaque-type morphea first presents in the active inflammatory stage with edematous, erythematous, or dusky violaceous plaques, usually on the trunk. As the lesions mature, they appear as violaceous rings with a white sclerotic center. The plaques usually have a diameter between 2 and 15 cm. Most often, there are multiple asymmetric plaques, but cases with one single lesion also exist. Individual lesions may stay the same size or grow in diameter over time. Disappearance of the violaceous ring marks the resolution of the active stage; at this point the sclerotic plaques become hyperpigmented, anhidrotic, and hairless.1
The average age of adult presentation is the mid-40s. In children, 90% of cases present between ages 2 and 14 years. Linear morphea (the most common type in children) first appears as plaque-type morphea, but then extends in a linear fashion, eventually becoming scar-like. This type of morphea tends to be more severe and has higher morbidity than plaque type. The sclerosis may involve underlying fascia, muscles, tendons, and even bone. When linear morphea extends across a joint, it can result in immobilization. Linear morphea of the forehead and scalp is known as the en coup de sabre type. This type often involves deeper structures and, rarely, can extend to the meninges and brain-causing seizures, focal neurologic deficits, and headaches.6 Parry-Romberg syndrome, a severe form of linear morphea, leads to facial atrophy along the trigeminal nerve distribution. Unlike the plaque-type, linear morphea usually does not regress.1
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Generalized morphea is defined as 4 or more morphea plaques involving more than one body site. This category also includes plaque-type morphea that expands rapidly and occupies the trunk in such a way as to limit chest expansion, causing progressive dyspnea. Generalized morphea has the highest rate of extracutaneous manifestations, including arthralgia and fatigue. Other variants of morphea include nodular, bullous, guttate, and atrophoderma of Pasini and Pierini.1 In the early stages of morphea, histology shows a perivascular infiltrate of lymphocytes with few plasma cells and eosinophils in the reticular dermis. Hyalinization and thickening of collagen bundles may also be observed. In later stages, the lymphocytic infiltrate vanishes and the hyalinized collagen bundles appear very crowded. Capillaries wane in number, eccrine glands and hair follicles become atrophic, and collagen expands into the subcutaneous tissues.1,2 Patients with morphea often have serum autoantibodies, including antinuclear antibody, anti-ssDNA, antihistone, anti-topoisomerase II, and antiphospholipid antibody. Cytokines that activate lymphocytes, specifically IL-2, IL-4, and IL-6, may also be significantly elevated. Autoantibodies and elevated cytokines are more strongly associated with linear and generalized morphea than plaque-type morphea.7 Scleroderma (systemic sclerosis) is the number one item on the differential diagnosis for morphea. The two can often be distinguished clinically by the absence in morphea of Raynaud’s phenomenon, nail fold capillary changes, sclerodactyly, and internal organ involvement. Morpheaform plaques must also be differentiated from lichen sclerosus, injection-site sclerosis (from vitamin K, B12, or steroid injections), lipodermatosclerosis, porphyria, eosinophilic fasciitis, chronic graft-versus-host disease, sclerosing congenital melanocytic nevus, or reactions from systemic medications (bleomycin, taxanes, valproic acid, and penicillamine). Morphea can be distinguished based on the clinical picture and histology.1 The treatment plan for morphea depends on the specific type and severity. Current therapies include topical medication, systemic immunosuppressive therapy, and phototherapy. Therapeutics are more effective during the active stage of morphea. In cases of uncomplicated plaque-type morphea, topical corticosteroids or topical tacrolimus may be prescribed, although most important is close observation and monitoring of the plaques.8 Phototherapy (PUVA and UVA1) can also be used as a treatment for morphea. The radiation increases collagenase expression and reduces inflammation in the dermis. The long-term efficacy of phototherapy has
not been demonstrated, but some studies showed regression and softening of morphea plaques.9 In severe cases of morphea (such as linear morphea), or cases that do not respond to topical therapy, systemic therapies may be used. Methotrexate is a mainstay of treatment, usually combined with systemic corticosteroids; multiple retrospective studies have demonstrated their efficacy in treating morphea. In cases of linear morphea with associated debilitation or deformity, physical therapy and plastic surgery may also be considered.10 The patient in this vignette was diagnosed with plaque type morphea. She was prescribed a potent topical corticosteroid (clobetasol 0.05% ointment) to use twice a day. After several months of use, she noted the lesion had become lighter (closer to her normal skin tone) and much softer. She plans to continue using the topical steroid. Talia Jayne Noorily is a medical student at the Baylor College of Medicine, David Rizk is a medical student at the University of South Alabama, and Connie Wang, MD, is a dermatology resident at the Baylor College of Medicine in Houston. References 1 1. Rocken M, Ghoreschi K. Morphea and lichen sclerosus. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:657-670. 2 . Fett N, Werth VP. Update on morphea: Part I. Epidemiology, clinical presentation, and pathogenesis. J Am Acad Dematol. 2011;64:217-228. 3 . Peterson LS, Nelson AM, Sue WP, et al. The epidemiology of morphea (localized scleroderma) in Olmsted County 1960-1993. J Rheumatol. 1997;24:73-80. 4 . Saracino AM, Denton CP, Orteu CH. The molecular pathogenesis of morphoea: from genetics to future treatment targets. Br J Dermatol. 2017;177:34-46. 5. Sartori-Valinotti JC, Tollefson MC, Reed AM. Updates on morphea: role of vascular injury and advances in treatment. Autoimmune Dis. 2013:2013;467808. 6 . Pinho J et al. Localized scleroderma en coup de sabre in the Neurology Clinic. Mult Scler Relat Disord. 2016;8:96-98. 7 . Taehara K, Sato S. Localized scleroderma is an autoimmune disorder. Rheumatol. 2005;44:274-279. 8 . Fett N. Morphea: Evidence-based recommendations for treatment. Ind J Dermatol Venereol Leprol. 2012;78:135-141. 9 . Hassani J, Feldman SR. Phototherapy in scleroderma. Dermatol Ther (Heidelb). 2016;6:519–553. 10 . Careta MF, Romiti R. Localized scleroderma: clinical spectrum and therapeutic update. An Bras Dermatol. 2015;90:62-73. Continues on page 59
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Dermatology Clinic CASE #2
Two feet–one hand disease
Microscopic examination of skin scrapings from his hand and one foot, using a potassium hydroxide (KOH) preparation, demonstrated branching hyphae, confirming the suspected diagnosis of two feet–one hand (2F1H) disease. Two feet–one hand disease is a superficial fungal infection that simultaneously affects both feet (bilateral tinea pedis) and one hand (unilateral tinea manuum); curiously, the other hand is uniformly spared. As with most superficial fungal infections affecting nonmucosal surfaces, the culprit organism is a dermatophyte. Although various genre of dermatophytes cause different skin conditions, the most common dermatophyte to cause 2F1H is a Trichophyton (T), specifically T rubrum.1 Molecular studies, when performed, have demonstrated that strains of T rubrum isolated from the hand and feet are identical.2 The initial infection is usually tinea pedis; tinea manuum tends to develop subsequently. The lifetime risk in the general population for any type of dermatophytosis is 10% to 20%.3 Some patients may have a genetic predisposition for infection with T rubrum,4 and others have a significant comorbidity such as diabetes mellitus or an immune-suppressed state that predisposes them to fungal infections in general.5 However, 2F1H tends to be more common in Caucasian men independent of these known predisposing conditions.5 Although there is no significant relationship between handedness and the development of tinea in the dominant hand, 2H1F is more likely to develop in persons who have occupations that require frequent use of their hands.5 Coexistence of toenail dermatophytosis may be a predisposing factor for 2F1H. In a prospective study by Szepietowski et al, 42.8% of patients with toenail onychomycosis had a concomitant fungal skin infection, with tinea pedis being the most common at 33.8%.6 Although toenail onychomycosis can be caused by a variety of pathogenic fungi, dermatophytes are the most common cause, with the single most common pathogen being T rubrum.7 In this scenario, one typically finds the affected toenail(s) to have thickening of the distal aspect of the nail plate, which is typically soft and more brittle, overlying a collection of subungal debris.
The diagnosis of 2F1H is often suspected given the unusual clinical presentation. However, confirmatory tests are needed. An easy, in-clinic test is the microscopic evaluation of skin scrapings of scale from the feet and the affected hand using the standard KOH preparation. Properly done, and with a skilled eye, one will see the classic branching hyphae of the dermatophyte culprit in each specimen. If this technique is not available, or negative, a culture of the scrapings should be done. The culture should be specific for a dermatophyte in this particular clinical scenario; exactly how this is ordered varies in practice.
Two feet–one hand disease simultaneously affects both feet and one hand, while the patient’s other hand is uniformly spared. Several clinical entities may mimic 2F1H and should be considered in the differential diagnosis; some of these include keratolysis exfoliativa, dyshidrotic eczema, an id reaction, and palmar plantar pustulosis. However, careful evaluation and appropriate testing will subsequently be diagnostic. Keratolysis exfoliativa is an idiopathic disorder of patchy peeling of the palms, soles, or both, most commonly associated with hyperhidrosis, and more common in summer. Fungal studies will be negative. Dyshidrotic eczema typically presents with pruritic vesicles/bullae on the palms, sides of fingers, and/or soles; scaling and redness are associated with rupture of the vesicles. Outbreaks are episodic and may last for several weeks. Dyshidrotic eczema tends to be associated with contact irritants or allergens, not fungal infections, and many patients are atopic. 8 An id reaction, otherwise referred to as an auto-eczematous reaction, is an acute, immunologically mediated skin reaction to a variety of cutaneous stimuli including inflammatory and infectious disorders. The eruption may be generalized or localized to the hands, mimicking dyshidrotic eczema. When associated with a dermatophyte infection, most commonly tinea pedis, the condition is referred to as a dermatophytid. Dermatophytids typically affect both hands, not just one; although studies from the feet will demonstrate fungi, those from the hands will not. The treatment in this setting is to treat the coexistent tinea pedis. As the name would suggest, palmoplantar pustulosis (PPP) is a chronic condition affecting the palms and soles.
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Michelle Vy is a 4th-year medical student, and Julia Nunley, MD, is a professor of dermatology and program director of dermatology at the Medical College of Virginia Hospitals of Virginia Commonwealth University in Richmond. References 1. Seeburger J, Scher RK. Long-term remission of two feet-one hand syndrome. Cutis. 1998;61:149-151.
2. Zaias N, Tosti A, Rebell G, Morelli R, Bardazzi F, Bieley H. Autosomal dominant pattern of distal subungual onychomycosis caused by Trichophyton rubrum. J Am Acad Dermatol. 1996;34(2 Pt 1):302-304. 3. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea faciei, tinea manuum, and tinea pedis. J Am Acad Dermatol. 1996;34 (2 Pt 1):282–286. 4. Korting HC, Tietz HJ, Brautigam M, Mayser P, Rapatz G, Paul C. One week terbinafine 1% cream (Lamisil) once daily is effective in the treatment of interdigital tinea pedis: a vehicle controlled study. LASINT-06 Study Group. Med Mycol. 2001;39:335-340. 5. Daniel CR, Gupta AK, Daniel MP, Daniel CM. Two feet-one hand syndrome: a retrospective multicenter survey. Int. J. Dermatol. 2008;36:658-660. 6. Szepietowski JC, Reich A, Garlowska E, Kulig M, Baran E. Factors influencing coexistence of toenail onychomycosis with tinea pedis and other dermatomycoses: a survey of 2761 patients. Arch Dermatol. 2006;142:1279-1284. 7. Scher RK, Tavakkol A, Sigurgeirsson B, et al. Onychomycosis: diagnosis and definition of cure. J Am Acad Dermatol. 2007;56:939-944. 8. Wollina U. Pompholyx: a review of clinical features, differential diagnosis, and management. Am J Clin Dermatol. 2010;11:305-314. 9. Korting HC, Kiencke P, Nelles S, Rychlik R. Comparable efficacy and safety of various topical formulations of terbinafine in tinea pedis irrespective of the treatment regimen: results of meta-analysis. Am J Clin Dermatol. 2007;8:357-364.
“Your pot o’ gold is doing nothing for you sitting at the end of the rainbow. At the very least, you should put it in a no-risk interest-bearing account.”
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© The New Yorker Collection 2018 from cartoonbank.com. All Rights Reserved.
Patients develop small sterile pustules and plaques; pruritus is a common symptom, and if the plaques fissure they may be painful. Clinically, it may be difficult to distinguish PPP from dyshidrotic eczema or a dermatophyte id. However, unlike either of these conditions, PPP is not associated with atopy or tinea. Although PPP may be idiopathic, it is often considered a variant of psoriasis; it is more common in women and in those who smoke. Evaluation should include an assessment for other signs/symptoms of psoriasis including nail changes and arthritis. For many patients with 2F1H, topical antifungal therapy is adequate therapy. Patients should be advised to use the topical antifungal until the condition is fully resolved, which may take several weeks. The antifungal cream should be applied between the toes, as well as all over the palms and soles. As azoles are fungistatic, an allyamine may be more effective since it is fungicidal.9 Concomitant use of a topical keratolytic containing lactic acid or urea may be synergistic as it dissolves the keratin necessary for dermatophyte sustenance. Systemic treatment should be considered only when topical therapy fails, or when there is a proven co-existent nail infection that warrants treatment. Itraconazole, fluconazole, and terbinafine are the most commonly prescribed oral antifungals for dermatophyte infections. Treatment courses vary and range from 1 week to 3 months, dictated by skinonly, or concomitant skin and nail infection. The decision to use an oral antifungal agent should not be taken lightly since a patient’s comorbidities and use of other medications may heighten adverse drug reactions. Recurrence of 2F1H is common, especially in the setting of onychomycosis. Patients should be advised that routine use of antifungal therapy on their feet is needed to prevent/ manage tinea pedis and prevent the redevelopment of hand involvement once cleared. The rash on our patient resolved after 3 weeks of using topical terbinafine and topical lactic acid cream twice daily. He continues to apply terbinafine to his feet to prevent recurrence. n
Dermatologic Look-Alikes Multiple erythematous plaques JESSICA TRAN, BA, EMMA WEISS, BA, CHRISTOPHER RIZK, MD
A 54-year-old Caucasian man presents for examination with a 2-year history of multiple, well-defined, erythematous plaques with fine scale on his abdomen and groin. The patient states that these lesions are very itchy and have significantly increased in size during the past several months. He has not tried any topical medications for the lesions. His medications include a daily multivitamin and fish oil, and he has no other significant medical history.
A 28-year-old Hispanic man presents with a 2-week history of multiple erythematous lesions on his right leg. The lesions are pruritic, scaly, and approximately 2 centimeters in diameter. The patient has noticed a slight increase in size of the lesions during the past week. He tried an OTC corticosteroid cream, but the lesions became larger and more inflamed. He spent the past year working in Costa Rica and recently returned. He is otherwise healthy and has no other medical problems.
Continues on page 64
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Dermatologic Look-Alikes CASE #1
Mycosis fungoides (MF), also known as Alibert-Bazin syndrome, was first documented in 1806 by the French dermatologist Jean-Louis Alibert, who described multiple lesions with a mushroom-like appearance.1 The name “mycosis fungoides” is a misnomer, as it implies a fungal etiology; however, MF is the most common form of primary cutaneous T-cell lymphoma.2 There are more than 20 identified variants of MF, each possessing distinct clinical and/or histopathologic features of classic MF.6 However, only 3 variants (folliculotropic, pagetoid reticulosis, and granulomatous slack skin) were included in the 2016 World Health Organization update on the classification of cutaneous lymphomas.6 MF most commonly affects adults, with a median age of diagnosis between 55 and 60 years of age.3 However, MF has also been reported in children and adolescents.3 Incidence rates are significantly more prevalent in men compared with women (1.9:1) and tend to affect African Americans more than Caucasians (1.5:1).9 Despite extensive research on the causative agents of MF, no definitive cause has been found.7 The pathogenesis of MF is thought to be a result of persistent antigen stimulation, which results in atypical clonal T-cell proliferation and excessive helper-memory T-cell accumulation.2,3,7 It is hypothesized that keratinocytes play a role in initiation of the skin lesions seen in mycosis fungoides.7 Injury to keratinocytes results in the release of cytokines and chemokines and downstream T-cell migration to the area of damage. T-cells then proliferate and accumulate in areas of the epidermis.7 Another theory proposed by Talpur et al (2008) suggests that certain bacteria, such as Staphylococcus aureus, contain enterotoxins that function as superantigens.8 These enterotoxins stimulate T-cell clonal expansion and can drive a cutaneous T-cell lymphoma such as MF.8 MF is an indolent disorder with an unpredictable, slow progression over years to decades.4,5 Classically, MF has 3 stages: patch, plaque, and tumor.5 The clinical presentation of MF is variable; patients may remain in the patch stage without progression, advance linearly through the stages, or present with all 3 stages of the disorder concurrently.6 The patch stage of MF typically presents as well-defined, irregular, erythematous patches commonly localized to the
buttocks, breasts, groin, and other sun-protected areas.3 These lesions are often pruritic, with secondary scale and evidence of dyspigmentation. 3,7 Poikiloderma, telangiectasia, and atrophy are often defining features of earlystage MF.10 MF advances to the plaque stage when lesions become larger, more discernible, and infiltrated; further progression to nodules and tumors results in a diagnosis of the tumor stage.12 The most common presentation seen concurrently is that of patches and plaques.13 It is rare for MF to immediately present with only tumors, without preceding or concomitant patches or plaques.5 An early diagnosis of MF is often challenging due to its highly variable presentation and nonspecific clinical and histologic aspects.10 Various skin biopsies taken from patients on the same day, from different regions of the body, have shown distinct histologic aspects.11 Therefore, a combination
It is rare for patients with MF to immediately present with only tumors, without preceding or concomitant patches or plaques. of clinical, histologic, molecular, and immunopathologic criteria should be considered.10 Skin biopsies most often demonstrate with an accumulation of helper T-cells (CD3+, CD4+, and CD45RO+) and a loss of CD7 antigen.14 Under microscopy, early-stage patches show atypical, band-like lymphocytic infiltrates in the basal layer of the epidermis (stratum basale), with markedly indented and sometimes hyperchromatic nuclei.5,6 In the plaque stage, epidermotropism becomes more pronounced and lymphocytes can aggregate to form Pautrier microabscesses; in the tumor stage, epidermotropism is diminished and replaced with larger, more diffuse dermal infiltrates.5 Molecular studies, such as polymerase chain reaction, can confirm the diagnosis of MF if dominant T-cell clones are identified within the skin.10 Dominant T-cell clones can be recognized through the detection of alpha-beta or gamma-delta gene rearrangements of the T-cell receptor.3 Clonality is seen in roughly half of patients in the patch stage and in the majority of patients in each of the plaque and tumor stages.3 The differential diagnosis of MF includes nummular eczema, tinea corporis, small plaque parapsoriasis, plaque psoriasis, lichen simplex chronicus, dimorphous leprosy, vitiligo, pityriasis rosea, and pityriasis lichenoides.3,10,12,15
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Due to the variable presentation of MF, a detailed physical examination, skin biopsies, serology, immunohistochemistry, and other analyses should be used to rule out or confirm these well-defined skin disorders.7,12 The treatment of MF is based on the tumor-nodemetastasis-blood (TNMB) clinical staging system.4 MF is generally considered to be an incurable disease, but treatment regimens can afford patients with early-stage MF more than 12 years of survival.4 Depending on the stage of MF, first-line therapy can include: topical corticosteroids (class III-IV), UV phototherapy (systemic or topical psoralen and ultraviolet A [PUVA]), and local radiotherapy (>30 Gy).16 In more advanced clinical stages, MF can spread to the lymph nodes, visceral organs, or blood, often resulting in a poor prognosis with less than 5 years of survival.4 Treatment options for advanced clinical stages include a combination of PUVA with interferon-alpha, topical retinoids (bexarotene), chlorambucil, corticosteroids, or local radiotherapy (>30 Gy).16 However, even aggressive chemotherapy treatment has not been shown to improve the prognosis of patients with advanced-stage MF.17 The patient in this vignette was biopsied and diagnosed with plaque-stage MF. The patient was started on phototherapy to which he responded. The patient is currently doing well and is being maintained on phototherapy treatments.
Fungal (tinea) infections are estimated to affect more than 20% to 25% of the world’s population and are classically named according to their clinical localization.18 Tinea corporis, also referred to as ringworm, includes all dermatophyte infections of the glabrous skin, excluding the scalp, beard, groin, hands, and feet.19 The term “tinea” refers to any type of fungal infection, while the term “corporis” comes from the Latin word meaning “body.”19 The dominant species of dermatophytes that cause tinea corporis include: Trichophyton rubrum, Microsporum canis, and Trichophyton tonsurans.18 There are 3 sources of infection by dermatophytes: humans (anthropophilic), animals
(zoophilic), and soil (geophilic); all 3 types can infect humans via direct or indirect contact.21 Dermatophytes particularly thrive in warm and humid conditions; therefore, fungal infections are commonly seen in tropical climates.18 Individuals who sweat excessively, wear tight-fitting clothing, are exposed to infected animals, or participate in contact sports have an increased risk of contracting tinea corporis.18,20 Tinea corporis more commonly affects children than adults, and is more frequently found in communities of lower social, economic, or educational status.18
Tinea corporis may present as single lesions or multiple lesions ranging from 1 to 5 centimeters in size. Dermatophytes, such as those causing tinea corporis, are able to adhere to the epithelial tissue of the host using mannan glycoproteins.22 Dermatophytes are able to further infect the host by invading the stratum corneum (further proliferating within the epidermis) and degrading the cytokeratin using keratinase, cysteine dioxygenase, and a sulfite efflux pump.22 Dermatophytes are typically unable to colonize tissue layers below the stratum corneum or organs of an immunocompetent host and therefore generally will not advance past a cutaneous infection.23 Tinea corporis typically presents as an erythematous, ring-shaped, scaly, pruritic patch with a raised leading edge and a clear center.19 Tinea corporis may present as single lesions or multiple lesions ranging from 1 to 5 centimeters in size.19 Lesions progress outward from the borders, and multiple lesions may join together to form larger lesions.24 Tinea corporis typically presents in exposed areas of the skin, such as the arms, legs, and abdomen.18 In addition to observing a patient’s physical presentation and obtaining a thorough history, a microscopic observation and fungal culture should be performed to establish a diagnosis.25 The primary methods of diagnosis of tinea corporis include: clinical inspection, microscopic examination of skin scrapings (with a 5% to 20% potassium hydroxide solution [KOH]), and fungal culture on a suitable medium.24 A light scraping of the lesion should be placed on a microscope slide, after which a potassium hydroxide solution should be added.19 The potassium hydroxide solution dissolves squamous cells, leaving behind any fungi.19 A positive
www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • MARCH 2018 65
Dermatologic Look-Alikes TABLE 1. Mycosis fungoides versus tinea corporis Mycosis fungoides (Primary cutaneous T-cell lymphoma)
Tinea corporis (Fungal infection)
• Well-defined, irregular, erythematous lesions of the skin, often pruritic, and somewhat scaly with slight dyspigmentation • Lesions can progress to larger, more discernible plaques and to nodules and tumors
• Erythematous, ring-shaped, scaly, pruritic patch with a raised leading edge and a clear center • Single lesions or multiple lesions ranging from 1 to 5 centimeters in size
• Buttocks, breasts, groin, and other sun-protected areas
• Exposed areas of the skin, such as the arms, legs, and abdomen
• Found commonly in children and adults —— Median age of diagnosis: 55 to 60 years old • More prevalent in males compared with females • More prevalent in blacks compared with whites
• More commonly affects children • High-risk factors: —— Warm and humid conditions —— Excessive sweating —— Wearing of tight-fitting clothing —— Exposure to infected animals —— Participation in contact sports
• Unclear; thought to be caused by persistent antigen stimulation
• Dermatophyte invasion
• Accumulation of helper T-cells (CD3+, CD4+, and CD45RO+) and loss of CD7 antigen • Atypical, band-like lymphocytic infiltrates in the basal layer of the epidermis, with markedly indented and sometimes hyperchromatic nuclei • Varying levels of epidermotropism based on stage of disorder
• Dermatophyte invasion of stratum corneum • Degradation of cytokeratin • Visible hyphae and mycelia (septate, tube-like structures)
• Physical examination and history • Skin biopsy • Polymerase chain reaction testing
• Physical examination and history • Microscopy of skin scrapings with potassium hydroxide (KOH) preparation • Fungal culture • Periodic acid-Schiff stain for atypical cases
• Topical corticosteroids (class III-IV) • UV phototherapy (systemic or topical PUVA) • Topical retinoids • Interferon-alpha • Chemotherapy • Local radiotherapy (>30 Gy)
• Topical antifungals (azoles, allylamines, benzylamines, hydroxypyridones) • Systemic treatment for immunocompromised patients, those with severe cases, or those who did not respond to topical creams
skin biopsy should reveal fungal elements such as hyphae and mycelia (septate, tube-like structures).24 For atypical or incessant lesions, microscopic examination with periodic acid-Schiff stain may be indicated.19 Fungal cultures are more sensitive than the potassium hydroxide preparation.19 A culture can be prepared by sampling the affected area using a moist cotton applicator, which is then applied to a suitable medium such as Sabouraud’s dextrose agar.19 Positive fungal cultures incubated at room temperature should grow evidence of fungal elements within 2 weeks.20
Clinical examination of tinea corporis can often be misdiagnosed due to its similar appearance to other skin disorders.19 The persistence or worsening of a dermal infection despite the use of a topical steroid cream should raise suspicion of a dermatophyte infection.19 The differential diagnosis of tinea corporis includes annular psoriasis, atopic dermatitis, mycosis fungoides, erythema multiforme, granuloma annulare, lupus erythematosus, nummular eczema, pityriasis rosea herald patch, and seborrheic dermatitis.19 Due to the number of disorders that can mimic tinea corporis, microscopy with
66 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
Continues on page 68
Dermatologic Look-Alikes potassium hydroxide preparation, along with a fungal culture, can be used to confirm a diagnosis of tinea corporis.19,20 Tinewa corporis is typically treated with topical antifungal creams, including the azoles (itraconazole, ketoconazole, sulconazole, oxiconazole, miconazole, clotrimazole, econazole), allylamines (naftifine, terbinafine), benzylamines (butenafine), and hydroxypyridones (ciclopirox olamine).20 Due to shorter treatment times, fungicidal drugs such as allylamines and benzylamines may be favored against fungistatic drugs such as azoles.26 Additionally, since patients often discontinue treatment early, when the disorder appears to be healed, tinea corporis is less likely to recur when a fungicidal drug is used.26 A response to topical creams can typically be seen following 2 weeks of treatment, and continuation of treatment for 1 week following infection clearance is recommended.24 Additionally, systemic treatment may be indicated for patients who are immunocompromised, have extensive disease, or did not respond to topical creams.19 A KOH prep was performed on the patient in the previous vignette. Fungal elements were visualized and the patient was prescribed topical terbinafine 1% cream. The patient’s rash resolved within 3 weeks. n
8. Talpur R, Bassett R, Duvic M. Prevalence and treatment of Staphylococcus aureus colonization in patients with mycosis fungoides and Sézary syndrome. Br J Dermatol. 2008;159:105-112. 9. Criscione VD, Weinstock MA. Incidence of cutaneous T-cell lymphoma in the United States, 1973-2002. Arch Dermatol. 2007;143:854-859. 10. Pimpinelli N, Olsen EA, Santucci M, et al. Defining early mycosis fungoides. J Am Acad Dermatol. 2005;53:1053-1063. 11. Massone C, Kodama K, Kerl H, Cerroni L. Histopathologic features of early (patch) lesions of mycosis fungoides: a morphologic study on 745 biopsy specimens from 427 patients. Am J Surg Pathol. 2005;29:550-560. 12. Wollenberg A, Eames T. Skin diseases following a Christmas tree pattern. Clin Dermatol. 2011;29:189-194. 13. Cho-Vega, JH, Tschen JA, Duvic M, Vega F. Early-stage mycosis fungoides variants: case-based review. Ann Diagn Pathol. 2010;14:369-385. 14. Nikolaou VA, Papadavid E, Katsambas A, et al. Clinical characteristics and course of CD8+ cytotoxic variant of mycosis fungoides: a case series of seven patients. Br J Dermatology. 2009;161:826–830. 15. Yamashita T, Abbade LP, Marques MEA, Marques SA. Mycosis fungoides and Sézary syndrome: clinical, histopathological and immunohistochemical review and update. An Bras Dermatol. 2012;87:817-830. 16. Dugas-Breit S, Schulze HJ, and Hallermann C. New and established treatment options for mycosis fungoides and Sézary syndrome—an update. J Dtsch Dermatol Ges. 2014;12:561–569.
Jessica Tran is a medical student, Emma Weiss is a medical student, and Christopher Rizk, MD, is a dermatology resident at the Baylor College of Medicine in Houston.
17. Kaye FJ, Bunn PA Jr, Steinberg SM et al. A randomized trial comparing combination electron-beam radiation and chemotherapy with topical therapy in the initial treatment of mycosis fungoides. N Engl J Med. 1989;321:1784–1790.
18. Havlickova B, Czaika VA, Friedrich M. Mycoses: Epidemiological trends
1. Karamanou M, Psaltopoulou T, Tsoucalas G, Androutsos G. Baron
in skin mycoses worldwide. Mycoses. 2008;51(suppl 4):2-15.
Jean-Louis Alibert (1768-1837) and the first description of mycosis
19. Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and management of
fungoides. J BUON. 2014;19:585-588.
tinea infections. Am Fam Physician. 2014;90:702-710.
2. Yawalkar N, Ferenczi K, Jones DA, et al. Profound loss of T-cell
20. Gupta AK, Chaudhry M, Elewski B. Tinea corporis, tinea cruris, tinea
receptor repertoire complexity in cutaneous T-cell lymphoma. Blood.
nigra, and piedra. Dermatol Clin. 2003;21:395-400.
21. Segal E, Frenkel M. Dermatophyte infections in environmental contexts.
3. Jawed SI, Myskowski PL, Horwitz S, Moskowitz A, Querfeld C.
Res Microbiol, 2015;166:564-569.
Primary cutaneous T-cell lymphoma (mycosis fungoides and Sézary
22. Nenoff P, Krüger C, Ginter-Hanselmayer G, Tietz HJ. Mycology—an
syndrome): part I. Diagnosis: clinical and histopathologic features
update. Part 1: Dermatomycoses: causative agents, epidemiology and
and new molecular and biologic markers. J Am Acad Dermatol.
pathogenesis. J Dtsch Dermatol Ges. 2014;12:188–210.
23. Surendran K, Bhat RM, Boloor R, Nandakishore B, Sukumar D.
4. Mazzeo E, Rubino L, Buglione M, et al. The current management of
A clinical and mycological study of dermatophytic infections. Indian J
mycosis fungoides and Sézary syndrome and the role of radiotherapy:
Principles and indications. Rep Pract Oncol Radiother. 2014;19:77-91.
24. Kaushik N, Pujalte GG, Reese ST. Superficial fungal infections. Prim
5. Willemze R, Jaffe ES, Burg G, et al. WHO-EORTC classification for
Care. 2015;42: 501-516.
cutaneous lymphomas. Blood. 2005;105:3768-3785.
25. Van Zuuren EJ, Fedorowicz Z, El-Gohary M. Evidence-based topical
6. Muñoz-González H, Molina-Ruiz AM, Requena L. Clinicopathologic
treatments for tinea cruris and tinea corporis: a summary of a Cochrane
variants of micosis fungoides. Actas Dermosifiliogr. 2017;108:192-208.
systematic review. Br J Dermatol, 2015;172:616–641.
7. Girardi M, Heald PW, Wilson LD. The pathogenesis of mycosis
26. Kyle AA, Dahl MV. Topical therapy for fungal infections. Am J Clin
fungoides. N Engl J Med. 2004;350:1978-1988.
68 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
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LEGAL ADVISOR CASE
A patient is mistakenly told that he is dying BY ANN W. LATNER, JD
Mr R was a military veteran who received his health care from a Veterans Affairs (VA) facility. By January 2010, he had fallen on difficult times and had to apply for food stamps. The county agency told Mr R that before he could qualify for food stamps, the agency would have to verify his veteran disability status. The agency contacted Ms G, a nurse practitioner working in the VA facility where Mr R went for his medical care. Ms G pulled the records, which indicated that Mr R was HIV positive and he was aware of his diagnosis. After looking at the records, Ms G erroneously concluded that Mr R should have been diagnosed with AIDS, something he had never been told or diagnosed with previously. She noted the new diagnosis on the patient records and then faxed the records to the county agency administering the food stamps. The agency relayed the AIDS diagnosis to Mr R, and told him that he only had a few months to live. Mr R was understandably shocked and immediately began calling the VA for clarification. For several days, no one returned his phone calls. During that time, Mr R, believing his life was
© FSTOP123 / GETTY
A clinician shares a patient’s incorrect diagnosis with another government agency. A VA clinician erroneously concludes that a patient should have been diagnosed with AIDS, something he had never been told or diagnosed with.
70 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
going to end in a few months, became extremely depressed and distressed. Eventually someone from the VA returned his call and told him that the AIDS diagnosis was incorrect. A month after the incorrect diagnosis was made, Mr R received a corrected letter of diagnosis removing the AIDS diagnosis from his medical record. That same month, in 2010, Mr R filed a claim with the VA, regarding its disclosure of his entire medical record without his consent, including the incorrect diagnosis. During the next several months, whenever the patient called to follow up on the claim, he was informed that the VA was backlogged with claims, but that it had received his claim and was working on it. This went on for years. The patient continued to check on his claim, and the VA continued to tell him that it was overwhelmed and had not yet been able to review it. Continues on page 72
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.
A patient’s medical records should never be shared with others without the express written consent of the patient. Legal background
According to the Department of Justice, the Privacy Act of 1974 establishes “a code of fair information practices that governs the collection, maintenance, use, and dissemination of information about individuals that is maintained in systems of records by federal agencies.” Specifically, the Privacy Act prohibits the disclosure of a record of an individual without the written consent of that individual. However, the Privacy Act also requires that a plaintiff sue within 2 years of the date on which the cause of action arises—which generally equates to when the plaintiff had reason to know about it. In its written decision, the court noted that Mr R was aware of the privacy violation in January 2010, but did not file a lawsuit until 2017, and thus his suit falls outside the Privacy Act’s 2-year statute of limitations. Therefore, the court dismissed the Privacy Act claims. However, the court noted that Mr R might be able to amend his complaint and argue that he was entitled to more time by establishing that: 1) he had been pursuing his rights diligently; and 2) that some extraordinary circumstances stood in his way. The FTCA waives the United States’ sovereign immunity for tort actions and allows federal courts to have jurisdiction over suits arising from the negligence of government employees, such as Ms G. But there are many exceptions to
this act, and the court will lack jurisdiction over the matter if the claim falls within one of these exceptions. In this case, the court noted that the tort claim was based on the negligent misrepresentation and documentation by Ms G that Mr R had AIDS. Misrepresentation, however, is one of the exceptions to the act, meaning that Mr R’s claim under the FTCA failed. The court did note, however, that Mr R could reframe his claim as one for medical malpractice based on the false AIDS diagnosis, which would avoid the misrepresentation exception. Thus, Mr R’s Privacy Act claims were dismissed, and the plaintiff was given leave to file an amended complaint if he wished to assert medical malpractice. Protecting yourself
Although Ms G was not personally sued in this case, she made numerous mistakes that could easily have resulted in a direct lawsuit in other circumstances. She made an arbitrary change to the patient’s diagnosis without even seeing the patient, entered it into the file, and never discussed it with the patient. And then she shared all of his medical records with the agency governing the food stamps. This information was far beyond the scope of what the agency was asking for (confirmation of his disabled veteran status) and was provided without the patient’s written consent. A patient’s privacy must be protected at all times. Never share a patient’s medical records without the express written consent of the patient. n Ms Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, N.Y.
72 THE CLINICAL ADVISOR • MARCH 2018 • www.ClinicalAdvisor.com
© The New Yorker Collection 2018 from cartoonbank.com. All Rights Reserved.
In 2015, five years after the incident, Mr R was notified that his claim had been lost or misplaced and he was asked to resubmit it, which he did immediately. A year later, the VA finally made a determination and denied his claim, saying that it was time-barred. However, the VA’s privacy officer concluded that Mr R had not given written consent for release of his medical records in January 2010 and that a breach of privacy had indeed occurred. Frustrated and angry, in late 2017, Mr R filed a federal lawsuit against the United States (as the party responsible for the VA health system) alleging violations of the federal Privacy Act of 1974 and the Federal Tort Claims Act (FTCA). The VA made a motion to dismiss the Privacy Act violations on the basis that the statute of limitations had already expired and Mr R was too late to file the claim. The VA also asked that the FTCA claim be dismissed.
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Identifying Appropriate Pain Management Options for Patients With Osteoarthritis Contributor: Christopher M. Chappel, MD | Medical Director, Chappel Group | Kissimmee, FL
27 million It is estimated that
Americans are living with osteoarthritis (OA).
Acetaminophen and oral nonsteroidal antiinflammatory drugs (NSAIDs) are among the pharmacologic therapies recommended for initial management of pain associated with OA.2,3
A stepwise approach helps ensure that patients receive the appropriate analgesic for their OA pain.5,6
of people with OA
use opioids to manage pain associated with OA.4 The Osteoarthritis Research Society International recommends that weak opioids be considered where other pharmacological agents have been ineffective or are contraindicated.3
A Stepwise Approach to the Management of Pain Associated With OA
Assess Patient Profile
• Identify current medications (including over-the-counter medications, herbals, and supplements) and coexisting medical conditions.
Develop Pain Management Plan
• Educate patients on pain management options. • Incorporate nonpharmacologic measures, such as physical therapy, assistive devices (eg, canes, walkers), or braces, as appropriate.2 • Consider options such as acetaminophen or NSAIDs.2 – Utilize information obtained in Step 1 to help identify an appropriate choice.
Introduce Nonopioid Pharmacologic Agents
The maximum dose of acetaminophen that a healthcare provider (HCP) can recommend for adults is 4000 mg/24 hours.
It is recommended that NSAIDs be given at the lowest effective dose for the shortest period of time.7
Assess Opioid Options for Appropriate Patients
• Start with weak opioids before escalating to stronger opioid options.5,6 • Consider use of acetaminophen or other over-the-counter analgesics to help manage breakthrough pain.8
Evaluate for Specialty Referral
• Consider referral to an orthopedic specialist or rheumatologist for further treatment options, such as surgery.
GetReliefResponsibly.com has more information for HCPs and patients. References: 1. Centers for Disease Control and Prevention. Osteoarthritis. http://www.cdc.gov/arthritis/basics/osteoarthritis.htm. Updated May 16, 2014. Accessed October 20, 2015. 2. Hochberg MC, Altman RD, April KT, et al. American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken). 2012;64(4):465-474. 3. Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage. 2008;16(2):137-162. 4. Gore M, Tai KS, Sadosky A, Leslie D, Stacey BR. Clinical comorbidities, treatment patterns, and direct medical costs of patients with osteoarthritis in usual care: a retrospective claims database analysis. J Med Econ. 2011;14(4):497-507. 5. World Health Organization. WHO’s pain ladder for adults. http://www.who.int/cancer/palliative/painladder/en/. Accessed June 22, 2016. 6. Vargas-Schaffer G. Is the WHO analgesic ladder still valid? Twenty-four years of experience. Can Fam Physician. 2010;56(6):514-517. 7. US Food and Drug Administration. Medication guide for nonsteroidal anti-inflammatory drugs (NSAIDs). http://www.fda.gov/downloads/Drugs/DrugSafety/UCM387559.pdf. Revised May 2016. Accessed June 21, 2016. 8. Chou R, Fanciullo GJ, Fine PG, et al. Clinical guidelines for the use of chronic opioid therapy in chronic noncancer pain. J Pain. 2009;10(2):113-130. © Johnson & Johnson Consumer Inc. 2016
Published on Mar 1, 2018