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Social Media Posts Used in Lawsuit Against an NP FEATURE

Geriatric Polypharmacy: When and How to Deprescribe Medications



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Education, Screening, and Treatment Reduce Toll of Osteoporosis in Women One of the first signs of bone loss is fragility fractures.


Older Woman With Fatigue and Fluctuating Bilateral Ptosis


Verrucous Lesion on Upper Arm



Social Media Posts Used in Lawsuit Against an NP FEATURE

Geriatric Polypharmacy: When and How to Deprescribe Medications



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Education, Screening, and Treatment Reduce Toll of Osteoporosis in Women One of the first signs of bone loss is fragility fractures.


Older Woman With Fatigue and Fluctuating Bilateral Ptosis


Verrucous Lesion on Upper Arm


NEWS ClinicalAdvisor.com/News

CLINICAL CHALLENGE ClinicalAdvisor.com/CaseStudy

Can SARS-CoV-2 Infection Accelerate the Onset of an Autoimmune Disease?

Brady Pregerson, MD Pain in the Right Lower Abdomen A 22-year-old woman presents with pain in her right lower quadrant that has been getting progressively worse over the past 18 hours. The patient is very thin and is experiencing nausea along with the pain. She denies experiencing vomiting, diarrhea, vaginal discharge, fever, dysuria, missed menses, or other symptoms. See the full case at: ClinicalAdvisor.com/CaseNov20

Case report of a healthy man with a family history of ankylosing spondylitis who developed arthritis and myalgia after testing positive for COVID-19.

Pandemic Adds to Increased Isolation, Loneliness in Elderly When asked to compare feelings of isolation before and after the pandemic, 48% of participants said they felt more isolated after March 2020, 44% felt the same level of isolation, and 8% felt less isolated.

Alopecia Areata Tied to Autoimmune, Metabolic Disorder in Children Study finds children with alopecia areata are more likely to have atopic dermatitis, vitiligo, psoriasis, and metabolic disorders than the general pediatric population.

AHA Issues Statement on Drug-Induced Arrhythmias The American Heart Association reviews medications that may cause or exacerbate arrhythmias, monitoring strategies, prevention and risk reduction methods, and treatment options.

Slowing the Spread of Congenital Syphilis: Guidance for Clinicians The rapid syphilis serologic test may be a useful tool for clinicians in areas of limited resources and laboratory capabilities, especially in settings where patients are frequently lost to follow-up.

LEGISLATIVE UPDATE ClinicalAdvisor.com/MyPractice Inside the Debate Over Rehabilitation Services: What NPs and PAs Need to Know Although the CMS had proposed a rule to allow nonphysician providers the ability to conduct the same services as physicians, more than 120 medical organizations opposed the ruling; it ultimately passed with limitations.

FEATURE ClinicalAdvisor.com/Features Danielle Kruger, PA-C, MS Ed; Jordan Elisabeth Fierek, PA-C Care for the Cold: Assessment and Treatment of Accidental Hypothermia The neuroprotective effects of hypothermia, and the treatments currently available for rewarming, give patients an excellent chance of neurologically intact survival despite prolonged cardiac arrest times.

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Education, Screening, and Treatment Reduce Toll of Osteoporosis in Women The risk for fractures among women is greater than the cumulative risk for stroke, heart attacks, and breast cancer.


Geriatric Polypharmacy: When and How to Deprescribe Medications Patients taking more than 5 medications are at increased risk for falls, hospitalizations, and mortality.


Clinical Challenge: Older Woman With Fatigue and Fluctuating Bilateral Ptosis The cardinal feature of myasthenia gravis is fluctuating skeletal muscle weakness that often presents with true muscle fatigue.

11 Deprescribing medications in older adults

23 Unusual location for skin lesion

27 Social media posts are not “private.”


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


Dermatology Clinic ■ Brown-Black Plaque on Ball of Foot ■ Verrucous Lesion on Upper Arm


Legal Advisor Social Media Posts Used in Lawsuit Against a Nurse Practitioner

All correspondence to: The Clinical Advisor 275 7th Avenue, 10th Floor, New York, NY 10001 For advertising sales, call 201.774.1078. For reprints/licensing requests, contact Customer Service at custserv@haymarketmedia.com. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Features” are not the actual individuals mentioned in the articles.They appear for illustrative purposes only. The Clinical Advisor® (USPS 017-546, ISSN 15247317), Volume 23, Number 9. Published 10 times a year, by Haymarket Media, Inc., 275 7th Avenue, 10th Floor, New York, NY 10001. For Advertising Sales & Editorial, call 646.638.6000 (M–F, 9am–5pm, ET). The Clinical Advisor is available on a paid subscription basis at the following annual rates: $75 USA, $85 Canada, $110 for all other foreign, in U.S. dollars, Single copy price: USA $20, Foreign $30. To order or update a paid subscription visit our website at www.ClinicalAdvisor.com or call 800.436.9269. Periodicals postage rate paid at New York, NY, and additional mailing offices. Postmaster: Send changes of address to The Clinical Advisor, c/o Direct Medical Data, 10255 W. Higgins Rd., Suite 280, Rosemont, IL 60018. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2020

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Education, Screening, and Treatment Reduce Toll of Osteoporosis in Women In the United States, less than one-quarter of women eligible for bone mineral density testing are screened, leaving many women at risk for fractures.


steoporosis is a prevalent disease worldwide, with 1 in 3 women and 1 in 5 men older than 50 years at risk for an osteoporotic fracture.1,2 For women, the risk for osteoporotic fractures is greater than the cumulative risk for stroke, heart attacks, and breast cancer combined.3 Having a fracture places a patient at much higher risk for sustaining additional fractures. In the United States, the direct costs associated with osteoporosis treatment rose 118%, from $28.1 billion in 1998-2000 to $73.6 billion in 2012-2014, with the costs distributed between ambulatory care, inpatient care, and prescription drugs.4 The conundrum for primary care practitioners is how to screen women appropriately to detect younger postmenopausal women who may not meet the known criteria for osteoporosis screening. (See Case Study, page 8.)


Risk Factors for Osteoporosis

One in 3 women older than 50 years are at risk for an osteoporotic fracture.

4 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com

In addition to the well-known risk factors for osteoporosis, new studies show there are novel risk factors that can be ascertained with thorough history and physical examination.5,6 Primary care providers can counsel women about risk factors and how to avoid the development of osteopenia and osteoporosis (Table 1). Age of menarche, dietary habits, and laboratory values of calcium, parathyroid hormone, and vitamin D are important diagnostic considerations. For example, moderate (>720 mL) to frequent (>1180 mL) daily consumption of soft drinks

right-hand column like this one does at the top

has been associated with the development of osteoporosis in women.5,6 In addition, Shieh et al reported that high levels of follicle-stimulating hormone (FSH) may be an independent predictor of ongoing or imminent bone loss during the perimenopausal and menopausal phases.7 Shieh et al also found that high levels of FSH and low levels of estradiol were associated with loss of bone mineral density (BMD) at both the lumbar spine and femoral neck in perimenopausal women.7 Late menarche has been associated with lower BMD in later life as well.8 Normal Bone Physiology

Osteoporosis occurs when bone loss (resorption) outpaces the growth of new bone (formation), making the bones more prone to fracture.The structure of bone consists of a tubular shape, with a strong outer shell (cortical layer) surrounding the spongier bone in the core (trabecular layer).2 Peak bone mass occurs in early adulthood, usually late 20s or early 30s.2 As aging occurs, the minerals on the inside of the cortical bone are resorbed, and trabecular bone is lost, causing a widening of the bone cavity.2 Although bones may be getting thicker, they are not becoming denser. On a cellular level, 2 cell types — osteoclasts and osteoblasts — are responsible for resorption and growth of bone. Osteoclasts break down bone by lowering the pH of their microenvironment,2 causing the bone material to dissolve. Osteoblasts then lay down new bone, which is a longer process; thus, any increase in remodeling activity leads to loss of bone. Multiple hormones are implicated in bone health: parathyroid hormone, testosterone, and estrogen, with the latter having the most direct effect on bone cells.When women enter perimenopause, bones become less dense because of the withdrawal of larger amounts of estrogen, predisposing them to fractures.7

all women older than 50 years of age for VCFs with a 2-view spine radiograph.9 If a compression fracture is noted, the National Osteoporosis Foundation recommends repeat testing at regular intervals to confirm that further fractures are not occurring, regardless of whether the patient is receiving preventive drug therapy. Patients with untreated osteoporosis who experience a VCF have a 50% chance of having another within 3 years.11 All postmenopausal women older than 50 years of age should be screened initially for osteoporosis with the Fracture Risk Assessment (FRAX) tool to determine the need for BMD measurement.The FRAX tool uses risk factors such as age, weight, TABLE 1. Risk Factors for Developing Osteoporosis Modifiable Risks

Fixed Risks

Smoking status


Use of alcohol


Low body mass

White or Asian ethnicity

Poor nutrition; excess intake of protein, phosphorus, sodium, and/or caffeine

Parent history of hip fracture

Vitamin D deficiency

Previous fracture

Eating disorders

Rheumatoid arthritis

Insufficient exercise

Late menarche8

Low dietary intake of calcium

Elevated FSH levels in perimenopause7

Frequent falls Bone-damaging medications (eg, steroids)

Diagnostic Screening and Testing

In most patients, the first sign of osteoporosis is a fragility fracture of the hip, wrist, or spine.2 Silent vertebral compression fractures (VCFs), which are often painless, can be the first indication of BMD loss (Table 2).2,9-11 VCFs often are discovered when the curvature of the spine becomes noticeable. In the United States, an estimated 1.5 million VCFs occur annually, the vast majority of which do not attract clinical attention.12 Patients withVCFs have a 15% greater risk for death compared to those without VCFs.12 VCFs are imaged using a standard spine radiograph; although they can be found anywhere in the spinal column, they most commonly are found in the mid-thoracic (T7-T8) and thoracolumbar vertebrae (T12-L1).9 Per the National Osteoporosis Foundation, radiography is warranted if there is documented height loss, new back pain, postural changes, or a deformity on a chest radiograph.11 However, Cai et al recommend screening

FSH, follicle-stimulating hormone

TABLE 2. Signs and Symptoms of Vertebral Compression Fractures2 Pain in thoracic spine Pain in back and chest muscles Stomach pain Difficulty breathing Loss of height Kyphosis

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2020 5

right-hand column like this one does at the top


gender, smoking history, alcohol use, and previous fracture history to evaluate a patient’s risk for sustaining an osteoporotic-related fracture in the next 10 years.11,13 The United States Preventive Services Task Force recommends using a FRAX score (10-year fracture risk) of 9.3% as a cutoff to prompt further screening to assess BMD in women aged 50 to 64 years.13 Bone density is best measured with dual-energy x-ray absorptiometry (DXA) of the hip and spine.12 The BMD results are expressed as a T-score that reflects standard deviations (SDs) from a young, healthy norm, usually female.14 A T-score of -2.5 or lower (SDs from the normal) is considered positive for osteoporosis (Table 3).11 DXA is the preferred method for confirming a diagnosis, predicting future fracture risk, and monitoring of patients; if DXA screening is unavailable, calcaneal quantitative ultrasound is useful for screening.10 The National Osteoporosis Foundation recommends the following indications for BMD testing: age >65 years for TABLE 3. Definition of Osteoporosis Based on Bone Mineral Density11 DXA Scores Normal

≤1 SD of the mean level for a young-adult reference population

T-score, –1.0 and higher

Low Bone Mass (Osteopenia)

1-2.49 SD below that of the mean level for a young-adult reference population

T-score, –1.0 to –2.49


≥2.5 SD below that of the mean level for a young-adult reference population

T-score, –2.5 and lower

Severe Osteoporosis

≥2.5 SD below that of the mean level for a young-adult reference population

T-score, –2.5 and lower with ≥1 fracture

DXA, dual-energy x-ray absorptiometry; SD, standard deviation

TABLE 4. When to Prescribe Medical Therapy11 T-score, –1.0 to –2.5 with either: • ≥3% FRAX-calculated 10-year probability of hip fracture OR • ≥20% FRAX-calculated 10-year probability of major osteoporosisrelated fracture A hip fracture or vertebral fracture regardless of T-score T-score –2.5 or lower at femoral neck or spine, after excluding secondary causes

women and 70 years for men, regardless of clinical risk factors for fracture; fracture at or after age 50 years; and a diagnosis of rheumatoid arthritis or use of drugs associated with low bone mass or bone loss (eg, glucocorticoids) in adults.11 A clinician also should consider testing if a person complains of back pain, height loss of more than 0.5 inches in 1 year, total height loss of 1.5 inches from original height, or a radiograph demonstrating a break or bone loss in the spine.11 Despite the availability of testing, less than one-quarter of women eligible for BMD testing are screened; the adherence rate is 21.2% among women aged 50 to 64 years, 26.5% among women aged 65 to 79 years, and 12.8% among women older than 80 years.15 Even among those who are privately insured, fewer than 1 in 4 women older than 65 years undergo screening for primary prevention of osteoporosis.15 Treatment of Osteoporosis

Early Prevention The cornerstone of osteoporosis prevention and treatment remains patient education and long-lasting lifestyle habits. Early intervention and healthy lifestyle education should occur well before the menopausal transition.Women of all ages need to be informed about the importance of daily exercise, moderate sun exposure, adequate calcium and vitamin D intake, as well as limited alcohol and soft drink consumption to promote healthy bones later in life.5,6 All postmenopausal women should be getting 1200 mg/d of calcium, primarily from food sources, and 800 to 1000 IU/d of vitamin D.11 Encouraging patients of all ages to engage in weight-bearing exercise and balance, strength, and endurance training is vital to reduce the risk for falls and associated fractures. Regular walking as exercise has been shown to reduce hip fracture by 30%.16 Regular weight-bearing exercises such as Pilates and tai chi have been associated with a decrease in falls due to bone loss as well as improvement in BMD, flexibility, balance, posture, and overall health.17 A healthy diet, high in fruits and vegetables, whole grains, poultry, fish, nuts and legumes, and low-fat dairy products, has been shown to be associated with improved bone health and reduced fracture rates.18 When to Prescribe Medications For women with osteopenia, practitioners must decide whether to prescribe bisphosphonate treatment, balancing the benefits and harms.Women with osteopenia who are younger than 65 years and those who are older than 65 years and have mild osteopenia (T-scores between –1.0 and –1.5) will benefit less from medical therapy than older women with osteopenia (T-scores < –2.0).14 Only 10% of women with mild osteopenia develop

6 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com

Continues on page 8


osteoporosis within 15 years, and 10% of women with advanced osteopenia (T-score –2.0 to –2.49) develop osteoporosis within 1 year.14 The decision to treat osteopenia should consider a patient’s DXA scores, age, family history, and whether or not they have sustained a fragility fracture. Calculating a FRAX score for all postmenopausal women older than 50 years of age is the first step in determining risk stratification, possible DXA scanning, and the need for medical therapy (Table 4).11 Treatment should be patient centered, with practitioners and patients setting reasonable mutual goals. All medications should be given only after a thorough workup to identify any secondary causes of bone loss. Secondary causes of osteoporosis are numerous and include hypogonadal states; genetic, endocrine, hematologic, rheumatologic, and autoimmune diseases; and musculoskeletal risk factors.11 Bisphosphonates

Bisphosphonates remain the first-line treatment for most men and women who are at high risk for hip and vertebral fractures.19 There are a number of commercially available bisphosphonates on the market: alendronate, alendronate/cholecalciferol, ibandronate, risedronate, and zoledronic acid.They are available as oral medications (effervescent tablets, tablets, or solution) or injections.19 The antiresorptive effects of a bisphosphonate are maintained in the bone for years after a patient stops taking the drug.20 After 3 to 5 years of therapy, a drug holiday should be considered, with close follow-up of BMD. Other Antiresorptive Therapies

Other treatments include hormone replacement therapy (estrogens), selective estrogen receptor modulators, calcitonin, and monoclonal antibodies. Denosumab, which binds to the receptor activator of nuclear factor κ-B ligand (RANKL inhibitor), prevents osteoclast formation and is recommended as initial treatment for postmenopausal women with a high fracture risk.21 The medication is delivered by a subcutaneous injection every 6 months. Once the patient stops using the medication, a rise in bone turnover and a decline in BMD occurs; therefore, to preserve bone density gains, another antiresorptive should be started immediately when denosumab is discontinued.11 Two parathyroid analogs (teriparatide and abaloparatide) are also on the market. These agents are recommended for postmenopausal women with osteoporosis (without cardiovascular risk factors) who are at very high risk for fractures. The duration of use should not exceed 2 years, since safety and efficacy of the agents for greater than 2 years has not yet been established.19,21 Delivered by daily subcutaneous injection, these drugs regulate bone metabolism and internal calcium absorption.19 When parathyroid analog treatment is completed, other antiresorptive therapy should be initiated.


Atypical Presentation of Osteoporosis A 56-year-old White woman presents for her annual screenings. She is in excellent health and does not take any medications (weight, 59.9 kg; BMI 20; menses cessation, age 52). She reports engaging in regular daily exercise, plays golf, and sees a trainer to guide a weightlifting regimen. She requests a dual-energy x-ray absorptiometry (DXA) scan. She has requested this screening in previous years but was told she was either too young or not at high risk. The patient denies smoking, alcohol use, a history of autoimmune disease, a family history of osteoporosis, glucocorticoid use, or previous fragility fracture (a fracture of the wrist, arm, pelvis, or femur sustained while standing). The patient reports that her menarche was late (age 16) and that she only developed regular menses after the birth of her first child at age 26. As an 18-year-old, she dieted and lost 33 lb from her 5’8” frame, reaching 108 lb. In her early 20s, she regained some weight, reaching approximately 125 lb. Her laboratory findings from her late 40s, although always normal in other areas, demonstrate very high follicle-stimulating hormone levels and menopausal levels of estrogen while she was still menstruating. The DXA scan is performed and yields a T-score of –4.2 for the lumbar spine and –2.6 for the left femoral neck. She is given the diagnosis of severe osteoporosis. Vertebral radiographs show the patient has no vertebral compression fractures, indicating that with prompt medical therapy she likely will be able to avoid future fragility fractures.

Similarly, the newest anabolic agent, romosozumab-aqqg, a sclerostin inhibitor, is administered subcutaneously monthly for 12 doses, during which time bone formation is increased and to a lesser extent bone resorption is decreased. Denosumab should be administered after completing the 12-dose regimen of romosozumab-aqqg if osteoporosis treatment is still warranted.22 If women are unable to take bisphosphonates and denosumab, alternative therapy includes selective estrogen receptor modulators, such as raloxifene or bazedoxifene.19 Raloxifene is approved for both prevention and treatment of osteoporosis in postmenopausal women and bazedoxifene is approved for prevention.11 Women must be at low risk for deep vein thrombosis to be prescribed these agents. An added benefit of raloxifene or bazedoxifene is reducing the incidence of invasive breast cancer, which may be helpful in determining the appropriate patient population for use of these agents.21

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7. Shieh A, Greendale GA, Cauley JA, Karvonen-Gutierrez C, Crandall CJ,


Karlamangla AS. Estradiol and follicle-stimulating hormone as predictors of onset of menopause transition-related bone loss in pre- and perimenopausal

Which of the following is not a criterion for prescribing medical therapy for a person with osteoporosis? 7.63% ■ Hip fracture regardless of T-score ■ Vertebral fracture regardless of T-score ■ T-score –1.0 or greater

women. J Bone Miner Res. 2019;34(12):2246-2253. 8. Elhakeem A, Frysz M, Tilling K, Tobias JH, Lawlor DA. Association between age at puberty and bone accrual from 10 to 25 years of age. JAMA Netw Open. 2019;2(8);e198918. 9. Cai S, Yu H, Li Y, et al. Bone mineral density measurement combined with vertebral fracture assessment increases diagnosis of osteoporosis in post-


menopausal women. Skeletal Radiol. 2020;49(2):273-280. 20.34%


■ T-score –2.5 or lower, after excluding secondary causes

10. deVilliers TJ. Should women be screened for osteoporosis at midlife? Climacteric. 2018;21(3):239-242. 11. National Osteoporosis Foundation. Healthcare professionals toolkit. https://www.bonesource.org/healthcare-professionals-toolkit 2019. Accessed September 27, 2020.

For more polls, visit ClinicalAdvisor.com/Polls.

12. Alexandru D, So W. Evaluation and management of vertebral compression fracture. Perm J. 2012;16(4):46-51. 13. United States Preventive Services Task Force. Final recommendation statement: osteoporosis to prevent fractures: screening. June 26, 2018. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/

Patient Education

For patients who have already had aVCF or have osteopenia/ osteoporosis, adequate monitoring, treatment, and follow-up must occur. Education and regular exercise programs aimed at reducing falls improve patient self-efficacy with respect to osteoporosis and fall risk and may lower rates of osteoporosis-related fractures.23 Encouraging patients to engage in healthy bone lifestyle habits also has positive ramifications for overall health. ■

osteoporosis-screening. Accessed October 9, 2020. 14. Qaseem A, Forciea MA, McLean RM, Denberg TD, Clinical Guidelines Committee of the American College of Physicians. Treatment of low bone density or osteoporosis to prevent fractures in men and women: A clinical practice guideline update from the American College of Physicians. Ann Intern Med. 2017;166(11):818-839. 15. Gillespie CW, Morin PE. Trends and disparities in osteoporosis screening among women in the United States, 2008-2014. Am J Med. 2017;130(3):306-316.

Karen D. French, DNP, FNP-C, RN, is clinical director of the Family Nurse Practitioner Programs at Azusa Pacific University, in Azusa, California.

in White women. Study of Osteoporotic Fractures Research Group. N Engl J


mineral density, physical performance and quality of life of women with post-

16. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture Med. 1995;332(12):767-773. 17. Angin E, Erden Z, Can F. The effects of clinical Pilates exercises on bone

1. Akesson K, Marsh D, Mitchell PJ, et al. Capture the fracture: a best

menopausal osteoporosis. J Back Musculoskelet Rehabil. 2015;28(4):849-858.

practice framework and global campaign to break the fragility fracture

18. Movassagh EZ, Vatanparast H. Current evidence on the association of

cycle. Osteoporosis Int. 2013;24(8):2135-2152.

dietary patterns and bone health: a scoping review. Adv Nutr. 2017;8(1):1-16.

2. International Osteoporosis Foundation. What is osteoporosis? IOF

19. Eastell R, Rosen CJ, Black DM, Cheung AM, Murad MH, Shoback D.

website. https://www.osteoporosis.foundation. Accessed October 7, 2020.

Pharmacological management of osteoporosis in postmenopausal women:

3. Singer A, Exuzides A, Spangler L, et al. Burden of illness for osteoporotic

an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab.

fractures compared with other serious diseases among postmenopausal


women in the United States. Mayo Clin Proc. 2015; 90(1):53-62.

20. Epocrates. Osteoporosis. https://online.epocrates.com/results?query=

4. Wright N. The burden of osteoporosis in the United States - a US bone

Osteoporosis. Accessed October 7, 2020.

and joint initiative report. American Society for Bone and Mineral Research

21. Langdahl B. Management of endocrine disease: treatment breaks in long-

annual meeting. September 22, 2019. Abstract 1079.

term management of osteoporosis. Eur J Endocrinol. 2019;180(1):R29-R35.

5. Hammad LF, Benajiba N. Lifestyle factors influencing bone health in young

22. Evenity [package insert]. Thousand Oaks, CA: Amgen; 2020.

adult women in Saudi Arabia. Afr Health Sci. 2017;17(2):524-531.

23. Park KS, Yoo JI, Kim HY, Jang S, Park Y, Ha YC. Education and exercise

6. Fung TT, Arasaratnam MH, Grodstein F, et al. Soda consumption and

program improves osteoporosis knowledge and changes calcium and

risk of hip fractures in postmenopausal women in the Nurses’ Health Study.

vitamin D dietary intake in community dwelling elderly. BMC Public Health.

Am J Clin Nutr. 2014;100(3):953-958.


10 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com


Geriatric Polypharmacy: When and How to Deprescribe Medications Polypharmacy decreases productivity for health care providers, reduces quality of care, and increases the risk for medication errors.



Polypharmacy is defined as taking 5 or more medications.

he number of Americans over the age of 65 years is increasing. According to the Census Bureau, people older than 65 years will outnumber those younger than 5 years sometime in 2020. By 2050, the number of people older than 65 years will be double the number younger than 5 years.1 With an aging population comes an increase in comorbidities and polypharmacy, defined as taking 5 or more medications.2,3 Polypharmacy can include appropriate pharmacology, in which medicine usage is evidence based, as well as use of potentially inappropriate medications (PIMs) that do not have an evidence-based indication, have the potential to interact with other medications the patient is taking, are continued beyond therapeutic benefit, or are given in place of less expensive options.4,5 Polypharmacy can result in many negative outcomes for patients and the health care system. For patients, these may include adverse drug events (ADEs), falls, and hospitalizations as well as decreased quality of life and increased nonadherence, cost, and mortality.6 Reducing pill burden can increase adherence and improve disease processes.7 The effects of polypharmacy on the health care system include decreases in health care provider productivity and quality of care and increases in medication errors.8 Scott et al define deprescribing as the systematic process of identifying and discontinuing drugs Continues on page 14

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2020 11


that pose more harm than good within the context of an individual patient’s care goals, current level of functioning, life expectancy, and preferences.9 As gatekeepers, primary care providers play a vital role in patient care and are positioned to implement the deprescribing process. Deprescribing Tools

Tools available to assist in deprescribing include the Beers Criteria® for Potentially Inappropriate Medication Use in Older Adults,10 STOPP (Screening Tool of Older Persons’ Prescriptions)/START (Screening Tool to Alert to Right Treatment),11 and the Medication Appropriateness Index (MAI).12 The Beers Criteria were developed by the American Geriatrics Society (AGS) and are updated every 3 years.10 The criteria consist of 5 categories: • PIM in older adults independent of diagnosis • PIM to avoid in older adults due to drug-drug or drugdisease interactions that may aggravate the disease process • Medications to be used with substantial caution in older adults • Medication combinations that may lead to adverse drugdrug interactions • Medications that should be avoided or require dosing adjustments based on renal function4 Beers Criteria are useful in a variety of settings, are succinct, and use a powerful grading methodology. Drawbacks include a failure to identify all potentially inappropriate prescribing and to predict overprescribing and underprescribing.12 STOPP lists drugs according to physiologic systems and provides examples of situations in which drugs are inappropriately prescribed and should be discontinued. START, which is designed to be used in conjunction with STOPP, has 34 criteria and is organized according to physiologic systems. It also includes categories pertaining to analgesic agents, anticholinergic agents, and medications that induce falls. STOPP/ START is beneficial in the clinical setting.12 The MAI includes 10 questions about a drug related to indication, effectiveness, correct dosage, correct directions, practical directions, drug-drug interactions, drug-disease interactions, unnecessary duplication, correct duration, and whether the drug is the least expensive option.A calculator is used to measure risk (https://globalrph.com/medcalcs/medication-appropriatenessindex-calculator/).The MAI is more patient centered and works well in a clinic setting; however, it can be very time consuming, especially when a patient is taking multiple medications.13 These tools should not be substituted for clinical reasoning, available information, and individualized patient care. Changes to medications should be made using an interdisciplinary approach, including consultation with a pharmacist and with the patient. No single tool has been proven to be more effective than another.

CASE STUDY Elderly Woman at Risk of Falling An 83-year-old woman comes to the clinic for a review of her medication regimens. She has a history of coronary artery disease, type 2 diabetes, hypertension, hyperlipidemia, atrial fibrillation, chronic lymphocytic leukemia, breast cancer, hypothyroidism, osteoarthritis, fibromyalgia, and a stroke that left residual weakness in her right leg and hand. The patient lives at home with her 88-year-old husband, who is her primary caregiver. Since her stroke 2 years ago, the patient has an aide come into the home to help her with showering and dressing. She is ambulatory with a walker but recently has been having falls. Her surgical history includes stent placement to treat her coronary artery disease, hysterectomy, cholecystectomy, bilateral mastectomies to treat her breast cancer, colon resection for intestinal obstruction, hernia repair after the colon resection, right total knee replacement, left total hip replacement, and open reduction and internal fixation of a fractured left wrist. She was hospitalized with the flu approximately 3 months ago, at which time her dose of amiodarone was increased. Although her atrial fibrillation was well controlled before hospitalization and has since been well controlled, the amiodarone dose was never decreased. The patient’s vital signs include blood pressure 122/78 mm Hg, pulse rate 76 beats/min, and respiration rate 20 breaths/min. She is 63" tall, weighs 66.7 kg, with a body mass index of 26 (overweight). Physical examination is unremarkable except for the presence of bilateral lower extremity edema. She reports that she is allergic to sulfa drugs; adverse events related to previous medications include a dry cough from lisinopril and muscle aches from statins. Her diabetes is well controlled with a glycated hemoglobin A1C of 7.0%; glomerular filtration rate is 74 mL/min; and thyroid hormone level is within normal range (4.25 mU/L). The table highlights the multiple medications the patient was taking at the time of her clinic visit and the medication reconciliation process the provider undertook to deprescribe and optimize the patient’s medication regimen. The patient was seen again after 3 months. Her atrial fibrillation remained well controlled. Her blood pressure remained normal at 126/82 mm Hg and hemoglobin A1C remained stable (7.0%). She stated that she had not fallen since the last visit. Medication reconciliation was done again to determine whether further dosage adjustments were needed.

14 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com

TABLE. Case Study Medication Reconciliation Drug

Indication/ Diagnosis

Potential For Reduction Considerations for Reductions or Discontinuation

Medications After Reconciliation

Aspirin 81 mg daily



Increased risk for GI bleed in those older than 75 y, especially those taking anticoagulants. CAD prevention benefit at age 83 is small. Diltiazem and venlafaxine may enhance antiplatelet effect.1 Patient is also at high risk for falls. Recommend stopping aspirin. Strong recommendation.2


Metformin 1000 mg twice daily



Not a high-risk medication. HbA1C well controlled at 7.0%. Recommend continuing this medication.

Metformin 1000 mg twice daily

Glipizide XL 20 mg once daily



Sulfonylureas pose a high risk for hypoglycemia. HbA1C is 7.0%. At 83 years, the patient does not need tight glucose control.3 Patient is on highest recommended dosage. Recommend decreasing to 10 mg daily.

Glipizide XL 10 mg once daily

Pioglitazone 30 mg once daily



Recommend keeping pioglitazone, decreasing glipizide (noted above), and monitoring HbA1C .

Pioglitazone 30 mg once daily

Metoprolol XL 100 mg daily

AF, hypertension


Metoprolol needed for heart rate and blood pressure control. Patient is tolerating. Recommend monitoring blood pressure and heart rate.

Metoprolol XL 100 mg daily

Diltiazem ER 120 mg daily



Recommend continuing to control AF. Recommend monitoring heart rate and blood pressure.

Diltiazem ER 120 mg daily

Amiodarone 200 mg twice daily



Effective for maintaining sinus rhythm but has toxicities. First-line treatment for people with heart failure, but patient has normal ejection fraction. Diltiazem enhances bradycardic effect of amiodarone. Amiodarone decreases levels of levothyroxine and enhances effects of beta-blockers.1 Decrease to 100 mg daily (a typical therapeutic dose). Consider switching to another antiarrhythmic agent at next visit. Strong recommendation.2 Recommend monitoring heart rate.

Amiodarone 100 mg once daily

Digoxin 0.125 mg every other day



Digoxin is not a first-line recommendation in treatment of AF, and diltiazem and metoprolol can enhance bradycardic effects.1 Patient is on a very low dose. Recommend continuing current dosage. Recommend monitoring heart rate.

Digoxin 0.125 mg every other day

Dabigatran 150 mg twice daily

AF, stroke prevention


Patient had a stroke when this drug was stopped previously. Patient and family are adamant that she continue this drug.

Dabigatran 150 mg twice daily

Levothyroxine 150 μg daily

Hypothyroidism No

This drug is needed and will be continued.

Levothyroxine 150 μg daily

Cyclobenzaprine 10 mg at bedtime



Muscle relaxants are not recommended for fibromyalgia. Patient is on an SNRI, which will help the fibromyalgia. This drug can cause dizziness and can be habit forming.1 Recommend discontinuing this medication. Strong recommendation.2


Naproxen sodium 500 mg twice daily



This drug can enhance the hypoglycemic effects of a sulfonylurea and should not be taken with an anticoagulant because of increased risk for GI bleed.1 Recommend acetaminophen in place of NSAID. Strong recommendation.2

Substitute with acetaminophen as needed

Venlafaxine 150 mg daily



Patient has been taking this medication for a long time. She is tolerating it well and adamant that she wants to continue.

Venlafaxine 150 mg daily

AF, atrial fibrillation; CAD, coronary artery disease; GI, gastrointestinal; NSAID, nonsteroidal anti-inflammatory drugs; SNRI, serotonin-norepinephrine reuptake Inhibitor; T2D, type 2 diabetes 1. Lexicomp. Wolters Kluwer website. https://www.wolterskluwercdi.com/lexicomp-online/. Accessed September 20, 2020. 2. 2019 American Geriatrics Society Beers Criteria® Update Expert Panel. American Geriatrics Society 2019 updated AGS Beers Criteria® for Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc. 2019;67(4):674-694. 3. Garber A, Handelsman Y, Grunberger G, et al. Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm — 2020 executive summary. Endocr Pract. 2020;26(1):107-139.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2020 15


Deprescribing is necessary in a health care environment where patients are managed by multiple providers and take multiple medications. In a 2018 Cochrane review, Rankin et al surmised that no tool could evaluate all facets of polypharmacy and that it was not clear whether interventions provided to improve appropriate polypharmacy, such as pharmaceutical care,“resulted in clinically significant improvement.”14 The authors concluded that interventions directed at inappropriate pharmacology, such as medication reconciliation, resulted in improvement but the results were based on only 2 studies with bias limitations.14 How to Approach Deprescribing

The American Board of Internal Medicine began the Choosing Wisely Campaign to encourage communication between patients and their health care providers and enable patients to choose health care that is evidence based, does not include unnecessary testing, and does not endanger the patient.15 The AGS and American Society of Health-System Pharmacists both participated in the development of the Choosing Wisely Campaign, which addresses polypharmacy.When considering deprescribing, it is important to gather a full history, obtain an accurate list of all prescription and over-the-counter medications, and ascertain the indication for each medication (See Case Study). Providers must determine the medications that meet criteria for deprescribing.These include duplicate medications, medications with a potential for drug-drug interactions, and drugs causing ADEs.To ascertain the merit of continuing certain medications, providers should consider the complexity of the regimen, the pill burden, the life expectancy of the patient (with risk calculators), and whether the medications are cost effective.9,16 Lastly, providers should discuss the goals of treatment with the patient or caregiver and determine a treatment plan with patient input.9 Many drugs may need to be tapered slowly to prevent withdrawal consequences; thus, patients need to be monitored closely after deprescribing. Duerden et al recommend discontinuation of 1 drug at a time to monitor for withdrawal symptoms, with tapering when possible.17 Providers must develop a clear follow-up plan and assure patients that they will be followed closely and monitored for any adverse effects from discontinuing the medication.18

opposing the original prescribing provider.18 Clinicians also may be reluctant to discontinue a drug prescribed by another provider21 or to discontinue medications because of pressure from family and other caregivers.20 In addition, deprescribing is a complex process. Strict adherence to evidence-based guidelines for treatment may lead providers to focus on disease processes without assessing a patient’s comorbid conditions.22 Discontinuation of a drug may affect pharmacokinetics and pharmacodynamics of another drug or may induce withdrawal symptoms.18 Clinic schedules are extremely tight, and a provider may be seeing patients with multiple issues, leaving little time to discuss medication reconciliation and deprescribing.18,19 Using the available tools can assist providers with decision making and ease the time burden related to geriatric polypharmacy. Deprescribing is necessary in a health care environment in which patients are managed by multiple providers and take multiple medications. Primary care providers are in a perfect position to spearhead the deprescribing process. ■ Lynda Jarrell, DNP,APRN, FNP-BC, CNE, is a clinical assistant professor at the University of Texas at Arlington College of Nursing and Health Innovation. References 1. He W, Goodkind D, Kowal P. US Census Bureau. An Aging World: 2015: International Population Reports. US Government Publishing Office; Published March 2016. https://www.census.gov/content/dam/Census/library/ publications/2016/demo/p95-16-1.pdf. 2. Masnoon N, Shakib S, Kalisch-Ellett L, Caughey GE. What is polypharmacy? A systemic review of definitions. BMC Geriatrics. 2017;17(1):230. 3. Zarowitz BJ, Stebelsky LA, Muma BK, Romain TM, Peterson EL. Reduction of high-risk polypharmacy drug combinations in patients in a managed care setting. Pharmacotherapy. 2005;25(11):1636-1645. 4. Bala SS, Chen TF, Nishtala, PS. Reducing potentially inappropriate medications in older adults: a way forward. Can J Aging. 2019;38(4):419-433. 5. Hill-Taylor B, Sketris I, Hayden J, Byrne S, O’Sullivan D, Christie R. Application of the STOPP/START criteria: a systematic review of the prevalence of potentially inappropriate prescribing in older adults, and evidence of clinical, human-

Barriers to Deprescribing

istic and economic impact. J Clin Pharm Ther. 2013;38(5):360-372.

Fragmented care is common in elderly patients, with many patients seeing multiple specialists. These patients are prone to polypharmacy because no single provider is tasked with overseeing medication safety.19,20 Patients also may be hesitant to discontinue medications, particularly those they have taken for a long time, fearing exacerbation of their disease or

6. Reeve E, Thompson W, Farrell B. Deprescribing: a narrative review of the evidence and practical recommendations for recognizing opportunities and taking action. Eur J Intern Med. 2017;38:3-11. 7. Farrell B, Merkley VF, Ingar N. Reducing pill burden and helping with medication awareness to improve adherence. Can Pharm J. 2013;146(5):262-269.

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Continues on page 18


8. Halli-Tierney AD, Scarbrough C, Carroll D. Polypharmacy: evaluating risks

15. American Board of Internal Medicine. Choosing Wisely. An initiative

and deprescribing. Am Fam Physician. 2019;100(1):32-38.

of the ABIM Foundation. https://www.choosingwisely.org/. Accessed

9. Scott IA, Hilmer SN, Reeve E, et al. Reducing inappropriate polypharmacy:

September 29, 2020.

the process of deprescribing. JAMA Intern Med. 2015;175(5):827-834.

16. Liu LM. Deprescribing: an approach to reduce polypharmacy in nursing

10. 2019 American Geriatrics Society Beers Criteria® Update Expert

home residents. J Nurse Pract. 2014;10(2):136-138.

Panel. American Geriatrics Society 2019 updated AGS Beers Criteria® for

17. Duerden M, Payne R. Medicines management: the importance of when to

Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc.

stop. Prescriber. 2015;26(8):24-26.


18. Endsley S. Deprescribing unnecessary medications: a four-part process.

11. O’Mahony D, O’Sullivan D, Bryne S, O’Connor MN, Ryan C, Gallager P.

Fam Pract Manag. 2018;25(3):28-32.

STOPP/START criteria for potentially inappropriate prescribing in older

19. Reeve E, Hendrix I, Shakib S, Roberts M, Wiese M. Patient barriers to and

people: version 2. Age Aging. 2015;44(2):213-218.

enablers of deprescribing: a systematic review. Drugs Aging. 2013;30(10):793-807.

12. Curtin D, Gallagher PF, O’Mahony D. Explicit criteria as clinical tools to

20. Anderson K, Stowasser D, Freeman C, Scott I. Prescriber barriers and

minimize inappropriate medication use and its consequences. Ther Adv

enablers to minimising potentially inappropriate medications in adults: a

Drug Saf. 2019;10:2042098619829431.

systematic review and thematic synthesis. BMJ Open. 2014;4(12):e006544.

13. Samsa GP, Hanlon JT, Schmader KE. A summated score for the Medication

21. Corsonello A, Onder G, Abbatecola AM, Guffanti EE, Gareri P, Lattanzio F.

Appropriateness Index: development and assessment of clinimetric properties

Explicit criteria for potentially inappropriate medications to reduce the risk

including content validity. J Clin Epidemiol. 1994;47(8):891-896.

of adverse drug reactions in elderly people: from Beers to STOPP/START

14. Rankin A, Cadogan CA, Patterson SM, et al. Interventions to improve

criteria. Drug Saf. 2012;35(suppl 1):21-28.

the appropriate use of polypharmacy for older people. Cochrane Database

22. Dowden A. Deprescribing: reducing inappropriate polypharmacy.

Syst Rev. 2018;9(9):CD008165.

Prescriber. 2017;28(2):45-49.

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Clinical Challenge: Older Woman With Fatigue and Fluctuating Bilateral Ptosis Fluctuating bilateral ptosis, binocular diplopia, and fatigue without pupillary abnormalities raise the clinical index of suspicion for myasthenia gravis.


The main feature of myasthenia gravis is fluctuating skeletal muscle weakness.


70-year-old woman presents to the primary care clinic reporting increasing fatigue over the past 6 months that is more severe in the evenings. Along with fatigue, the patient reports fluctuating bilateral ptosis with vertical binocular diplopia that began 4 months before the visit. Episodes of bilateral ptosis and binocular diplopia lasting 1 to 4 weeks alternate with symptomfree intervals of 3 to 4 weeks. Ptosis is asymmetric and more severe in the left eye. The patient denies muscle weakness (other than ocular weakness), weight loss, fevers, vision loss, dysarthria, headaches, dyspnea, dysphagia, dizziness, and gait disturbances. Her medical history includes macular degeneration, managed with antioxidants and zinc, and hypertension, controlled with metoprolol and losartan. She denies drug allergies and alcohol or drug use. On physical examination, the patient’s vital signs are within normal limits. Extraocular movements show bilateral superior and medial rectus weakness. A sustained upward gaze increases the ptosis bilaterally. Pupils appear equal and reactive to light. Neurologic exam, evaluating cranial nerves, sensation, and reflexes, shows no abnormalities. The patient’s fluctuating bilateral ptosis, binocular diplopia, fatigue, and an absence of pupillary abnormalities raises the clinical index of suspicion for myasthenia gravis (MG). Serologic testing for acetylcholine receptor (AChR) antibodies is positive. A computed tomography (CT) scan of the brain rules out intracranial neoplasm.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2020 19


The most serious complications of MG occur in later stages of the disease with increasing respiratory muscle weakness. Myasthenia Gravis

Myasthenia gravis is an autoimmune disease that causes postsynaptic neuromuscular junction dysfunction via an antibodymediated, T-cell–dependent process. Autoantibodies attack and reduce the number of functioning AChRs and muscle-specific receptor tyrosine kinase (MuSK) receptors.1 Myasthenia gravis is an uncommon disorder with a worldwide prevalence of 70 to 320 per million people. The age of disease onset has a bimodal distribution, with the first peak in the second and third decade, primarily in women, and the later peak between the sixth and eighth decade, primarily in men. Although rare, MG is the most common neuromuscular transmission disorder.2,3 The cardinal feature of MG is fluctuating skeletal muscle weakness that often presents with true muscle fatigue. The fatigue is a declining contractile muscle force specified to particular muscle groups.2 Symptoms of ocular weakness include ptosis and diplopia.4 A sustained upward gaze increases ptosis, in what is called “the curtain sign.” Binocular diplopia is caused by extraocular muscle weakness. Double vision can occur horizontally or vertically, and the pupil always is spared. Bulbar symptoms of MG include dysarthria, dysphagia, and fatigable chewing. Weakened oropharyngeal muscles may prevent the ability of the patient to hold the jaw in a closed position. Changes in speech include a nasal tone or decreased volume. Dysphagia, linked with solids and liquids, increases the risk for aspiration, dehydration, and malnutrition.5 Facial, neck, and limb muscles frequently are affected in patients with MG. Facial muscle weakness can cause patients to appear expressionless. Neck flexor and extensor muscles can weaken, causing a “dropped head.”6 Both upper and lower extremities are affected proximally, with the greatest weakness typically in the upper extremities.Weakness in wrist and finger extensors and foot dorsiflexors also can be present.6 The most serious complications of MG occur in later stages of the disease, with increasing respiratory muscle weakness. Dyspnea and shortness of breath can present spontaneously during the active disease phase or when aggravated by physical activity, illness, infection, surgery, medications, or immunosuppressive tapering. Respiratory insufficiency and impending respiratory failure signal a myasthenic crisis. Crises can be precipitated by events that exacerbate symptoms, such as infection, surgery, or pregnancy.7 Weakness in respiratory and oropharyngeal muscles results in dyspnea, which causes a suffocating or drowning sensation, and dysphagia. Other signs include hypophonia, accessory muscle breathing, and paradoxical abdominal breathing.The patient will have a low vital capacity and need intubation.7

Preventing myasthenic crisis is vital to avoid mechanical ventilation; once it becomes necessary, it often is challenging to wean the patient off the ventilator. In addition, MG crises increase the risk for various infections, such as pneumonia, bronchitis, urinary tract infection, Clostridioides difficile colitis, bacteremia, and sepsis. Vascular complications such as deep vein thrombosis, heart failure, acute myocardial infarction, and cardiac arrest can result.7 Muscle weakness worsens with muscle use and improves with rest. Sensations and reflexes throughout the body remain unaffected. As the disease progresses, symptoms become increasingly severe, widespread, and frequent. Symptom progression peaks within a few years of symptom onset.8 Diagnostic Testing

If a patient presents with symptoms suggestive of MG, tests are available to support the diagnosis.9 The ice pack test is a simple, safe, and cost-effective bedside test to start the diagnostic process for determining whether patients with ptosis have MG, but it lacks specificity and cannot confirm the diagnosis.10 Ice packs are placed on the eyelids, causing increased neuromuscular transmission due to lower muscle temperatures. After 2 minutes, the ice packs are removed; an improvement in ptosis indicates a diagnosis of MG.9-11 Serologic testing for anti-AChR or anti-MuSK antibodies provides reliable diagnostic confirmation with up to 99% specificity.12 Laboratory confirmation of AChR antibodies can include binding, blocking, and modulating assays, but the binding assay is the most sensitive and specific for MG. Titer levels solely indicate disease presence; they do not correlate with disease severity. A negative antibody result does not rule out MG.12 Electrophysiologic studies provide confirmation of MG.9 An electrode is placed over the muscle endplate, stimulating the motor nerve.The stimulation is repeated while measuring the compound muscle action potential amplitude (CMAP). If MG is present, a progressive CMAP decline may occur with repeated stimulation.9 In patients without MG, CMAP values should not change. Single fiber electromyography (SFEMG) is highly sensitive for MG (95%).9 However, SFEMG is more complicated and less available than other electrophysiologic studies. SFEMG records action potentials of 2 muscle fibers innervated by the same motor axon via needle electrodes. The variation in the time interval between the 2 action potenial responses is termed the neuromuscular jitter. In MG, the neuromuscular jitter interval is increased compared with patients without MG.9

20 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com

Continues on page 22


Early Diagnosis Is Vital

Diagnosing MG is challenging; the diagnosis often is missed, delaying treatment and patient education. An early diagnosis is vital to improve patient prognosis and lower the risk for myasthenic crises.13 With advances in diagnosis and treatment, MG is no longer a guarantee of disability and mortality.Therapy is highly individualized. Treatment plans are built around 4 treatment categories: symptomatic, chronic immunomodulating, rapid immunomodulating, and surgical.14 • Symptomatic treatment can be achieved with oral acetylcholinesterase inhibitors.15 Pyridostigmine is the most commonly used anticholinesterase. Symptoms lessen as the degradation of acetylcholine in the neuromuscular junction is slowed or stopped. This medication has a greater effect on limb and bulbar symptoms than ocular symptoms. Pyridostigmine dose is titrated to avoid cholinergic side effects, especially gastrointestinal effects.14 • Chronic immunomodulating treatments include corticosteroids and other immunotherapies that interfere with T- and B-cell production.15 Prednisone is first-line therapy for shorter-term immunosuppression. For long-term immunosuppression, azathioprine is the first choice, typically combined with low-dose corticosteroids. These medications lessen the autoimmune reaction and decrease attack on AChRs.16 • Rapid immunomodulating MG usually is treated with shortterm plasmapheresis; IV immune globulin (IVIG) is used for emergent therapy. These treatments have a faster onset of action of mere days but a shorter duration of action that only lasts for 3 to 6 weeks.17 These typically are reserved for myasthenic crisis, bridge therapy when initiating chronic immunomodulators, or as an addition to chronic treatment in refractory MG. Plasmapheresis removes AChR antibodies from circulation. IVIG provides normal antibodies that modify the immune system temporarily.18 • Surgical treatment involves a thymectomy. Patients with thymomas benefit from the removal of the thymus, and research shows possible benefit for nonthymomatous MG.18 Thymectomy can reduce the immune reaction, relieve disease symptoms and progression, lessen the need for immunosuppression, and decrease hospitalizations. Surgery typically is limited to patients younger than 60 years.18

chewing, diplopia, and ptosis that all fluctuate and worsen with increased activity throughout the day. She sleeps more than 12 hours each night without improvement in fatigue. The patient has undergone additional plasmapheresis and IVIG treatments, with minor symptom improvement. ■ Lauren Blessing, PA-C, is a certified Physician Assistant at Northwest Georgia Oncology Centers in Atlanta. Sara Haddow Liebel, MSA, PA-C, recently retired as an associate professor in the Physician Assistant Department at Augusta University, Georgia. References 1. Hoch W, McConville J, Helms S, Newsom-Davis J, Melms A, Vincent A. Auto-antibodies to the receptor tyrosine kinase MuSK in patients with myasthenia gravis without acetylcholine receptor antibodies. Nat Med. 2001;7(3):365-368. 2. Gilhus NE. Myasthenia gravis. N Engl J Med. 2016;375(26):2570-2581. 3. Nicolle MW. Myasthenia gravis and Lambert-Eaton myasthenic syndrome. Continuum (Minneap Minn). 2016;22(6, Muscle and Neuromuscular Junction Disorders):1978-2005. 4. Nair AG, Patil-Chhablani P, Venkatramani DV, Gandhi RA. Ocular myasthenia gravis: a review. Indian J Ophthalmol. 2014;62(10):985-991. 5. Pal S, Sanyal D. Jaw muscle weakness: a differential indicator of neuromuscular weakness—preliminary observations. Muscle Nerve. 2011;43(6):807-811. 6. Sih M, Soliven B, Mathenia N, Jacobsen J, Rezania K. Head-drop: a frequent feature of late-onset myasthenia gravis. Muscle Nerve. 2017;56(3):441-444. 7. Wendell LC, Levine JM. Myasthenic crisis. Neurohospitalist. 2011;1(1):16-22. 8. Grob D, Brunner N, Namba T, Pagala M. Lifetime course of myasthenia gravis. Muscle Nerve. 2008;37(2):141-149. 9. Benatar M. A systematic review of diagnostic studies in myasthenia gravis. Neuromuscul Disord. 2006;16(7):459-467. 10. Golnik KC, Pena R, Lee AG, Eggenberger ER. An ice test for the diagnosis of myasthenia gravis. Ophthalmology. 1999;106(7):1282-1286. 11. Larner AJ. The place of the ice pack test in the diagnosis of myasthenia gravis. Int J Clin Pract. 2004;58(9):887-888. 12. Deymeer F, Gungor-Tuncer O, Yilmaz V, et al. Clinical comparison of antiMuSK- vs anti-AChR-positive and seronegative myasthenia gravis. Neurology. 2007;68(8):609-611. 13. Mao ZF, Mo XA, Qin C, Lai YR, Olde Hartman TC. Course and prognosis of myasthenia gravis: a systematic review. Eur J Neurol. 2010;17(7):913-921. 14. Silvestri NJ, Wolfe GI. Myasthenia gravis. Semin Neurol. 2012;32(3):215-226. 15. Díaz-Manera J, Rojas García R, Illa I. Treatment strategies for myasthenia

Outcome of Case

gravis: an update. Expert Opin Pharmacother. 2012;13(13):1873-1883.

After the patient’s diagnosis of MG, she began treatment with pyridostigmine; azathioprine was added later, along with periodic tapers of prednisone. She was not a surgical candidate due to her advanced age. After the patient underwent a hysterectomy, her symptoms drastically increased. She now has weakness in her proximal limb muscles, dysphagia, dyspnea, dysarthria, weakness with

16. Arsura E, Brunner NG, Namba T, Grob D. High-dose intravenous methylprednisolone in myasthenia gravis. Arch Neurol. 1985;42(12):1149-1153. 17. Dau PC, Lindstrom JM, Cassel CK, Denys EH, Shev EE, Spitler LE. Plasmapheresis and immunosuppressive drug therapy in myasthenia gravis. N Engl J Med. 1977;297(21):1134-1140. 18. Evoli A, Meacci E. An update on thymectomy in myasthenia gravis. Expert Rev Neurother. 2019;19(9):823-833.

22 THE CLINICAL ADVISOR • NOVEMBER 2020 • www.ClinicalAdvisor.com

Dermatology Clinic CASE #1

Brown-Black Plaque on Ball of Foot ANDREW FISCHER, MD

A 70-year-old White man presents to the dermatology clinic for evaluation of a recent foot injury.The patient is a veteran who lives alone. He states that he hit his foot at home and noticed blood on the floor; because of a previous injury, he was unable to view his sole. On physical examination, a large (several cm), irregularly shaped plaque is seen on the mid-anterior volar foot (ball of the foot). The lesion is brown and black, with central red discoloration and overlying yellow-white scale. Multiple punch biopsies are performed of the lesion. What is your diagnosis? Turn to page 24


Verrucous Lesion on Upper Arm ANDREW FISCHER, MD

A 35-year-old construction worker presents to the dermatology clinic with a well-circumscribed, verrucous plaque on his left upper arm. He notes that he recently relocated to Texas from Ohio for work. The lesion has been present for a few months, but recently has increased in size and become painful. He reports that a cough preceded his skin lesion, but otherwise he has no relevant medical history. On physical examination, a large verrucous and ulcerating lesion with pustules is seen. On palpation, a purulent discharge is expressed. A punch biopsy finds hyperplasia of the epidermis. What is your diagnosis? Turn to page 25 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2020 23

Dermatology Clinic CASE #1

Acral Lentiginous Melanoma

Acral lentiginous melanoma (ALM) is an uncommon type of cutaneous melanoma that occurs on the acral surfaces (palm, sole, or nail unit), with the sole being the most common location.1 In 1976 Reed first reported on ALM, describing it as the fourth distinct subtype of cutaneous melanoma, along with superficial spreading, nodular, and lentigo maligna melanomas.2 Arrington et al helped further characterize ALM and first documented its poor overall prognosis a year later.3 ALM accounts for approximately 2% to 3% of all cutaneous melanomas and affects men and women equally.1 Although the overall incidence of ALM is low (2.0 per million patientyears), it represents the most common type of melanoma diagnosed in darker-skinned individuals, including those of African, Asian, and Hispanic descent.1 Data suggest that ALM is disproportionately represented in dark-skinned individuals because they develop fewer cutaneous melanomas overall, particularly the types linked to chronic sun exposure.1 ALM tends to present in those aged 50 to 60 years and older, which is in line with most cutaneous melanomas.1 Recent, larger studies have attributed the poor prognosis of ALM to delayed diagnosis resulting in more advanced disease stage at presentation.1,4 These studies have shown that the independent prognostic risk factors (ulceration, tumor thickness, and tumor spread) are consistent with those detailed in the American Joint Committee on Cancer (AJCC) staging system, supporting the speculation that the decreased overall survival associated with ALM likely is due to delayed diagnosis, not because the melanoma acts more aggressively.5 A delay in diagnosis may occur because the patient may not realize the lesion is there (they may be unable to examine the bottom of their foot, as was the case in this patient) or they may not recognize the lesion as concerning. In addition, it can be difficult to perform a biopsy on the acral surfaces. In 1 study, physicians (mostly nondermatologists) clinically misdiagnosed 20% of melanomas on the palms and soles, leading to a delay in diagnosis of 12 months.6 Chronic sun exposure does not seem to be a risk factor for the development of ALM, as is the case for other types of melanoma.7 In fact, most of the typical risk factors for

cutaneous melanoma — sun exposure, fair skin, family or personal history of melanoma, and multiple melanocytic nevi — do not seem to apply to this subtype.7 It has been proposed that long-term mechanical trauma may be a risk factor because ALM most commonly is found on the foot, a highly traumatized site. Although the exact pathogenesis of ALM remains uncertain, whole-genome sequencing has revealed mutated genes including BRAF, NRAS, NF1, and KIT.8,9 The overall mutation burden, however, is less than that associated with other types of melanoma.8 Aside from the location, ALM presents similarly to other types of melanoma; pigmented lesions with asymmetry, color variation, and irregular borders that grow and change over time. Raised areas, ulceration, and bleeding are signs of more advanced lesions.7 However, ALM may demonstrate unique dermoscopic findings, including a parallel ridge pattern or irregular diffuse pigmentation.7 For this reason, dermoscopy has been used widely as an adjunctive tool for the diagnosis of ALM. It can be helpful particularly in identifying early lesions and in differentiating ALM from acral nevi, traumatic lesions, tinea nigra, warts, and calluses, all of which should be included in the differential diagnosis.7

The poor prognosis of ALM is due to a delayed diagnosis, not the aggressive nature of the condition. Biopsy is an invaluable tool for diagnosing ALM; there should be a low threshold for performing biopsy if the clinical suspicion for ALM is high. Dermatopathologists use multiple architectural and cytologic features to make the diagnosis. Biopsy of the acral surfaces presents its own challenges. In general, it is best to provide the dermatopathologist with a biopsy of the entire lesion if ALM (or any melanoma) is suspected.This affords the dermatopathologist the opportunity to evaluate the architectural as well as cytologic features of the lesion. A partial incisional biopsy may be acceptable if removal of the entire lesion is not feasible. However, for very large lesions, multiple biopsies may be obtained. When providing the dermatopathologist with a partial biopsy of a larger lesion, it is very important to communicate this information to them, along with clinical details about the lesion (history of change, size, dermoscopic features, etc). Workup and treatment of ALM primarily is based on the AJCC tumor, node, metastasis (TNM) staging system, which

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accounts for tumor characteristics, lymph node involvement, and presence or absence of distant metastases.5 The American Academy of Dermatology also has published guidelines for the treatment of primary cutaneous melanoma.10 Tumor thickness, expressed as the Breslow thickness (mm), is arguably the most important variable because it directly correlates with prognosis.Typically, an excision of the primary site is performed, and consultation with a surgeon familiar with working on the acral surfaces should be considered. If the tumor is particularly thick, sentinel lymph node biopsy should be considered for staging the melanoma. Adjuvant treatments often are added for the management of metastatic lesions.5,8 In the case presented, multiple punch biopsies were performed, with evaluation confirming the diagnosis of ALM. On further workup, the patient was found to have metastatic disease; he was started on adjuvant treatment but later succumbed to the disease. References 1. Huang K, Fan J, Misra S. Acral lentiginous melanoma: incidence and survival in the United States, 2006-2015, an analysis of the SEER Registry. J Surg Res. 2020;251:329-339. 2. Reed RJ. New Concepts in Surgical Pathology of the Skin. Wiley; 1976;89-90. 3. Arrington JH 3rd, Reed RJ, Ichinose H, Krementz ET. Plantar lentiginous melanoma: a distinctive variant of human cutaneous malignant melanoma. Am J Surg Pathol. 1977;1(2):131-143. 4. Teramoto Y, Keim U, Gesierich A, et al. Acral lentiginous melanoma: a skin cancer with unfavourable prognostic features. A study of the German Central Malignant Melanoma Registry (CMMR) in 2050 patients. Br J Dermatol. 2018;178(2):443-451. 5. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer Staging Manual. 8th ed. Springer; 2017:563. 6. Metzger S, Ellwanger U, Stroebel W, Schiebel U, Rassner G, Fierlbeck G. Extent and consequences of physician delay in the diagnosis of acral melanoma. Melanoma Res. 1998;8(2):181-186. 7. Darmawan CC, Jo G, Montenegro SE, et al. Early detection of acral melanoma: a review of clinical, dermoscopic, histopathologic, and molecular characteristics. J Am Acad Dermatol. 2019;81(3):805-812. 8. Hayward NK, Wilmott JS, Waddell N, et al. Whole-genome landscapes of major melanoma subtypes. Nature. 2017;545(7653):175–180. 9. Doma V, Barbai T, Beleaua MA, Kovalszky I, Rásó E, Tímár J. KIT mutation incidence and pattern of melanoma in Central Europe. Pathol Oncol Res. 2020;26(1):17-22. 10. Swetter SM, Tsao H, Bichakjian CK, et al. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2018;80(1):208-250.



Blastomycosis is a systemic infection caused by the dimorphic fungus Blastomyces dermatitidis, which is endemic to North America, specifically the Mississippi and Ohio River Valley regions (although it is not restricted solely to North America).1 It previously was known as Gilchrist’s disease, after Thomas Casper Gilchrist, who first described the disease in 1894 but who originally attributed the cause to a protozoan.2 Gilchrist, along with a collaborator, later identified the responsible organism as the fungus B dermatitidis.3 Soil is an important reservoir for the fungus, and infection usually is acquired through airborne inhalation of the conidia. As such, those who work outside, such as construction workers, are at high risk of acquiring the illness. All ages and genders are at risk; however, some series have reported a higher incidence in men.4 This is thought to be because men are more likely to participate in activities or occupations that put them at higher risk for exposure to B dermatitidis, such as hunting, fishing, construction, or forestry work, and not because they are inherently more susceptible to the organism.4 Following inhalation of the conidia, the lungs are the first site of infection; the resulting pulmonary disease may range from being asymptomatic to severe and frank pneumonia, with cough, fever, sputum production, chest pain, and pulmonary infiltrates/ consolidations seen on imaging.4,5 Pulmonary disease may clear spontaneously or progress and secondarily disseminate, leading to extrapulmonary disease in the skin and bones, most commonly, or the genitourinary tract and central nervous system, uncommonly.5 The skin is the most common site of extrapulmonary spread, which is reported in up to 40% to 80% of cases.4 A cutaneous lesion often leads to the diagnosis, especially in cases in which pulmonary symptoms are relatively mild. Primary cutaneous blastomycosis from direct inoculation of the skin is uncommon; therefore, a thorough search for systemic disease should be undertaken in all patients with cutaneous lesions.4 A well-demarcated verrucous plaque with central ulceration, scale-crust, and pustules is a common cutaneous presentation of blastomycosis.5,6 Advanced cases with large central ulceration may mimic pyoderma gangrenosum. Lesions may begin as well-circumscribed nonpainful papules, nodules, or plaques that become verrucous and/or ulcerate, at which time they may become painful. Patients may have 1 to several lesions, which tend to be on sun-exposed sites.4

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Dermatology Clinic Biopsy with identification of the fungus and corroborating culture results is the preferred method to diagnose skin disease.5 A punch biopsy should be performed from a pustule or from the thick, verrucous edge of the lesion (avoiding the ulcerated areas). On histopathology, there typically is pseudoepitheliomatous hyperplasia (thickening of the epidermis and adnexal structures), neutrophilic inflammation (forming microabscesses), and granulomatous inflammation (composed of histiocytes and giant cells).6 In tissue, B dermatitidis exists as round yeast forms that are approximately 8 to 15 microns in diameter and have thick, double-contoured walls.4 They may be found in the neutrophilic microabscesses or within giant cells and characteristically bud from 1 to another with a broad base.

Conditions that mimic blastomycosis include cutaneous infections, inflammatory dermatoses, and neoplasms. The size, thick wall, and budding pattern are helpful features in differentiating blastomycosis from other fungal infections. The fungal forms can be highlighted with periodic acid-Schiff or Grocott methenamine silver staining on formalin-fixed, paraffin-embedded tissue section.4 Additionally, broad-based budding yeast can be identified quickly in the office by collecting a sample from the purulent discharge, placing it directly onto a microscope slide, and covering it with 10% or 20% potassium hydroxide.4 Skin or pus can be cultured for species identification, but these results may take a few weeks to finalize. If available, polymerase chain reaction–based assays are useful and may yield results more quickly.4 Conditions that should be considered in the differential diagnosis of blastomycosis include cutaneous infections, inflammatory dermatoses, and neoplasms. Cutaneous infections from other dimorphic fungi (such as chromomycosis or histoplasmosis), nocardia, mycobacteria (including atypical mycobacteria and tuberculosis), and bacteria may present like blastomycosis. One study used the terminology “blastomycosis-like pyoderma,” for the clinical appearance of a large verrucous plaque studded with multiple pustules appearing like cutaneous blastomycosis.4 Typically, this is in reference to a chronic, vegetating bacterial infection, most commonly Staphylococcus aureus. Pyoderma gangrenosum is an inflammatory dermatosis that may mimic advanced cases of blastomycosis.6 Halogenoderma may be considered with corroborating historical information.

Squamous cell carcinoma and basal cell carcinoma should be considered in the differential diagnosis as well. Although there may be clinical and histopathologic overlap, a biopsy that identifies the typical yeast forms will help differentiate cutaneous blastomycosis from these entities. Culture results will solidify the diagnosis.4 Blastomycosis almost always requires systemic antifungal therapy, and the Infectious Diseases Society of America has published clinical guidelines for treatment.7 Mild to moderate disease is treated with a prolonged course of itraconazole for 6 to 12 months.When the infection is severe, progressive, or disseminated, or if the patient is immunocompromised, amphotericin B is given first, for 1 to 2 weeks, to gain control, then itraconazole is given for 6 to 12 months. Fluconazole, ketoconazole, and voriconazole can be used as alternatives to itraconazole, but they are less effective and have greater potential to cause adverse outcomes.7 In the case presented, a punch biopsy of the lesion showed hyperplasia of the epidermis, with dermal inflammation containing numerous neutrophils (forming microabscesses) as well as histiocytes and giant cells. Scattered, round-thick walled forms approximately 8 to 15 microns in diameter were seen in the microabscesses and in some giant cells. Some of these forms were broadly connected to one another. The patient also had evidence of pulmonary disease on imaging. Given the progressive course, he was started on amphotericin B in the hospital and transitioned to itraconazole with complete clearance of the lesions over the next several months. ■ Andrew Fischer, MD, is a board certified dermatologist at Elite Dermatology in Houston,Texas. References 1. Centers for Disease Control and Prevention. Fungal diseases. Blastomycosis. CDC website. Accessed September 29, 2020. https://www.cdc.gov/fungal/ diseases/blastomycosis/index.html 2. Gilchrist TC. Protozoan dermatitis. J Cutan Gen Dis. 1894;12:496-499. 3. Gilchrist TC, Stokes WR. A case of pseudo-lupus vulgaris caused by blastomyces. J Exp Med. 1898;3(1):53-78. 4. Saccente M, Woods GL. Clinical and laboratory update on blastomycosis. Clin Microbiol Rev. 2010;23(2):367-381. 5. Kauffman C. Infectious diseases. Blastomyces dermatitidis. Infectious Disease Advisor website. Accessed October 4, 2020. https://www.infectiousdiseaseadvisor.com/ home/decision-support-in-medicine/infectious-diseases/blastomyces-dermatitidis/ 6. Scuderi S, O’Brien B, Robertson I, Weedon D. Heterogeneity of blastomycosislike pyoderma: a selection of cases from the last 35 years. Australas J Dermatol. 2017;58(2):139-141. 7. Chapman SW, Dismukes WE, Proia LA, et al. Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America. Clin Infect Dis. 2008;46(12):1801-1812.

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Social Media Posts Used in Lawsuit


A 5-year-old boy, patient B, was brought to the emergency department (ED) by his parents. His symptoms included headache, sore throat, vomiting, fatigue, and abdominal pain. He was examined and diagnosed with streptococcal pharyngitis, prescribed an antibiotic, and d­ ischarged from the ED within an hour of arrival (6:00 PM). After the family returned home, patient B’s condition worsened; he was vomiting and couldn’t keep down the medicine. By 2:00 AM, patient B’s mother was concerned enough to take him to another hospital ED. At the ED, patient B was not triaged as urgent, despite his mother’s telling the staff that the boy had a sudden onset of symptoms including headache, nausea, vomiting, lethargy, weakness, dizziness, balance issues, slurred speech, and photophobia. She also told the staff that he had been to another hospital earlier that day. Two hours after arrival in the ED, patient B was seen by Ms C, a nurse practitioner. In her notes, Ms C charted that patient B “presents with sore throat for unknown time … was seen at other hospital this evening 6 PM. DX [diagnosed] strep.


The court rules that some social media posts by a nurse practitioner are acceptable as evidence. The plaintiffs argued that a nurse practitioner’s social media posts show a reckless, unprofessional attitude.

PT sent home and then mom states he has been vomiting every hour and not able to keep meds down.The onset was unknown.The course/duration is constant.” Ms C did not check with the other hospital, perform a neurologic examination, or order any imaging. She did, however, admit the child. At approximately 5:00 AM, patient B was seen by 2 family practice residents, neither of whom performed a neurologic assessment or ordered a computed tomography (CT) scan of the child’s head. Although one resident mentioned that a neurologic examination should be done, the exam was deferred as the child was sleeping. At 10:00 AM, about 8 hours after he had arrived at the hospital, the child suffered a stroke. A code blue was called, and subsequent examination showed a mass on the brain. The stroke left the child paralyzed, with neurologic damage and other permanent injuries. Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.

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LEGAL ADVISOR Patient B’s parents hired a plaintiff ’s attorney and sued everyone involved — the first hospital, the second hospital, and the treating nurse practitioner and physicians. In the complaint against Ms C, the plaintiffs alleged that patient B “suffered a catastrophic and medically-preventable stroke that left him with right-side paralysis, neurologic damage, and other debilitating physical injuries that permanently changed his and his parents’ lives.” They alleged that although Ms C admitted patient B for observation, she “failed to chart that he suffered from debilitating headache, inability to walk, severe lethargy, weakness, dizziness, slurred speech, photophobia, inability to answer basic questions, and severe imbalance.” They also alleged that the symptoms were a clear indication that a neurologic assessment and CT scan of the head were needed, and that Ms C was negligent.

Patient B was seen by 2 residents, neither of whom performed a neurologic assessment or ordered a CT scan. In their suit, the plaintiffs claimed that the defendants were both negligent and committed misconduct and requested that they be allowed to seek punitive damages as well as compensatory ones. Claiming punitive damages meant that Ms C’s reckless and careless attitude, not simply a lapse in judgment, was a factor in the child’s outcome.As part of their complaint, the plaintiffs included social media postings by Ms C. The online postings consisted of cartoons, jokes, and dark satire that referenced topics such as job frustrations, job duties (including patient charting), interactions with patients, disdain for children, and drinking. The plaintiffs contended that Ms C’s posts were “a direct reflection of her unprofessional attitude, complete lack of training and qualifications, and her inability to be a patient advocate” and that Ms C’s “attitude toward her profession, her job, her patients, and children are a display of and explanation for her wanton and willful failures” toward the child. Through her defense attorney, Ms C made a motion to strike the social media posts, claiming they were primarily designed to scandalize her, harm her general reputation, and spectacularize the case to the public. Legal Background

The task here “is to parse what sections are pertinent or material to the claims in the case and what sections are simply scandalous,” wrote the court in its decision.The court noted that the

plaintiffs are “not permitted to include unnecessary, scandalous, and unduly prejudicial information” in a complaint. Ultimately, the court decided that some of the social media posts were acceptable for use in the complaint and some were not. The court accepted the social media posts that it considered material or pertinent to the complaint, including memes about refusal or inability to fill out medical charts and memes about patient complaints. The court rejected social media posts it believed were included only to embarrass Ms C, such as posts about job dissatisfaction, memes about children, and posts about drinking.The case is proceeding with some of the social media posts included in the complaint, although the judge noted that the trial judge will decide specifically what the jury will be allowed to see. Protecting Yourself

Do not kid yourself into believing that your social media profiles are private or limited.When you post something on a public platform, even if you weren’t intending for the entire public to see it, it is still in the public domain. The plaintiffs in this case, while seeking punitive as well as compensatory damages, are clearly planning to use the social media posts as evidence of what they believe to be Ms C’s reckless and careless disregard for patients. It would be wise to think twice before posting anything related to your work, your patients, or your workplace on an online platform. ■ Ann W. Latner, JD, a former criminal defense attorney, is a freelance medical writer in Port Washington, New York.

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