Page 1



Delayed Diagnosis of Meningitis in Teenager



Unexplained Tachycardia in 24-Year-Old Woman


Itchy, Scaly Patches Salary Survey Results of the 2021 NP & PA Salary Survey See page 36


Triple-Negative Invasive Ductal Carcinoma in 34-Year-Old Woman An estimated 281,550 new cases of breast cancer are expected in the US.



Director Nikki Kean Medical editor Kristin Della Volpe


Production editor Kim Daigneau Group creative director Jennifer Dvoretz Senior production manager Krassi Varbanov Account executive Michael Delaney, 551.206.5334 Publisher Kathleen Hiltz, 201.774.1078 Vice president, content, medical communications Kathleen Walsh Tulley Chief commercial officer Jim Burke, RPh President, medical communications Michael Graziani Chairman & CEO, Haymarket Media, Inc. Lee Maniscalco All correspondence to: The Clinical Advisor 275 7th Avenue, 10th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints/licensing requests, contact Customer Service at 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 1524-7317), Volume 24, Number 5. Published 6 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 or call 800.436.9269. Periodicals postage rate paid at NewYork, 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 © 2021

Breast cancer remains the second most common cancer among women in the United States. In 2018, 254,744 new cases of female breast cancer were reported and 42,465 women died of this disease, according to the Centers for Disease Control and Prevention. Health disparities in the diagnosis and treatment of breast cancer are especially pronounced, with Black and Hispanic women dying from the disease at higher rates than White women. In 2018, the number of newly diagnosed breast cancers among Black women was 29,661 (age-adjusted incidence of 121.2 per 100,000) compared with 207,932 (127.5 per 100,000) newly diagnosed breast cancer among White women; 6541 Black women died (26.8 per 100,000 women) of their disease compared with 32,275 (19.2 per 100,000) White women. The authors of our cover story describe a case of a Hispanic woman who felt a lump in her breast, had a mammogram, and was told to follow up if anything changed. The medical history confirms she had no further mammograms and was seen 5 years later (by a different clinician) when she started experiencing skin changes (areolar skin thickening and nipple retraction) on her breast. At the time of her diagnosis, she had stage III triple-negative breast cancer (page 27). The 5-year survival rate for patients with regional triple-negative breast cancer is 65%, compared with an approximately 90% survival rate for localized triple-negative disease and other breast cancer types. With biannual or annual mammograms, this type of cancer can be caught earlier in high-risk patients. Because breast cancer occurs at a younger age in Black women, some investigators are recommending that Black women begin screening mammography at age 40. Delaying screening mammography for women of color places them at a disadvantage, especially because Black women are more likely to present with triple-negative and ERBB2positive subtypes. We hope this article helps elucidate recent research in this area and provides a resource for improving breast cancer outcomes in women of color. Nikki Kean, Director The Clinical Advisor



Breast Cancer Awareness

Assistant editor Jeanelle Jacobs


FEATURES 18 Clinical Challenge: Unexplained Tachycardia in 24-Year-Old Woman The patient experienced random short bursts of chest pain starting 2 weeks before the emergency department visit.

27 An aggressive type of breast cancer

7 Triple-Negative Invasive Ductal Carcinoma 2 in 34-Year-Old Woman Triple-negative breast cancer comprises 10% to 15% of breast cancers in the United States. 36 2021 Salary Survey See how your salary compares to your colleagues and how the COVID-19 pandemic has affected earnings.

36 Clinicians earnings during the pandemic


From the Director Health disparaties; Black and Hispanic women are dying from breast cancer at higher rates than White women


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


Dermatologic Look-Alikes Itchy, Scaly Patches


Legal Advisor Delayed Diagnosis of Meningitis in Teenager

41 Itchy lichenified patch on knee

47 Case of meningitis goes to court

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NPs and PAs: VA Pushes for National Standards of Practice

Brady Pregerson, MD Shoulder Pain After Motorcycle Accident A 45-year-old man presents to the emergency department with left shoulder pain after a motorcycle accident. He denies any neck, back, chest, or abdominal pain or other complaints and notes that he wore a helmet and full leather gear when his motorcycle was sideswiped and lost control. See the full case at: Case_September_October21

Proposed standards would allow VA advanced practice practitioners to provide patient care to the full extent of their education, training, and experience regardless of state laws.

Severity of ChemotherapyInduced Nausea Examined Researchers used a latent variable modeling and patient-centered analytic approach to identify cancer patients at greatest risk for severe chemotherapy-induced nausea.

Nurses’ Work Schedules Should Allow Sufficient Recovery Between Shifts Occupational fatigue from hectic and nonstandard work schedules not only impacts health and well-being but also affects patient safety and the hospital organization as a whole, recent findings show.

RSV and HPIV Increase Hospitalization Risk in HIV-Exposed Infants Respiratory syncytial virus and human parainfluenza infections are linked to increased hospitalization rates among HIV-exposed, HIV-uninfected infants.


Official Blog of The Clinical Advisor Jim Anderson, MPAS, PA-C, DFAAPA Racism as a Chronic Disease The issue of how to view the impact of institutional and individual racism on the health of Black, Indigenous, and people of color has gained increased attention, including exploring new and novel ways to think about racism and health.


Healthy Plant-Based Diet Linked to Lower Risk for Elevated PSA Consuming a diet rich in healthy plantbased food is associated with a reduced likelihood of having an elevated prostatespecific antigen level.


Lisa Gay, MSN, RN, FNP-BC, CLCP 5 Best Practices for Medical Documentation Expert discusses common mistakes made in medical documentation, including failing to update prepopulated or copied notes from a previous visit, documenting communication outside visits, and writing down future plans.



Advisor Dx Interact with your peers by viewing the images and offering your diagnosis and comments. To post your answer, obtain more clues, or view similar cases, visit Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues. Check out some of our latest cases below!


Skin Lesions on Arms and Shoulders A 14-year-old adolescent is referred for evaluation of skin growths. First noted approximately 8 months ago, they have rapidly increased in number. All sites are asymptomatic and palpation does not elicit tenderness. No other family members are similarly affected and there is no family history of genodermatoses. Examination reveals a multitude of firm, flesh-colored to slightly erythematous papules and nodules affecting his upper arms, shoulders, and upper trunk. CAN YOU DIAGNOSE THIS CASE?

• Neurofibromatosis • Steatocystoma multiplex

• Spontaneous keloids • Leiomyomas

● See the full case at


In partnership with

Journal of Orthopedics for Physician Assistants

Lateral Knee Pain A 22-year-old man presents with right lateral knee pain that has been present for the last month. He is an avid runner and usually runs 4 to 5 miles every few days. The patient notes that the knee pain started to increase and he is now unable to run more than a mile. Coronal magnetic resonance imaging shows mild inflammation of the iliotibial band bursa at the lateral knee. WHICH PHYSICAL TEST WOULD BE POSITIVE IN THIS PATIENT?

• Lachman test • McMurray test

• Pivot shift test • Ober test

● See the full case at • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 13


Clinical Challenge: Unexplained Tachycardia in 24-Year-Old Woman The patient experienced random short bursts of chest pain and felt that she was going to pass out, starting 2 weeks before ED visit.



The wide variety of symptoms often masks diagnosis of POTS.

24-year-old woman presents to the clinic for follow-up after an emergency department (ED) visit for chest pain and lightheadedness. The patient, a student at a local university, reports that she was studying at the library with a friend when she suddenly felt her heart begin to race and felt “like she was going to pass out.” She says that the chest pain and lightheadedness began 30 minutes before her near-syncope. The patient experienced random short bursts of chest pain starting 2 weeks before the ED visit. However, she describes her current pain as constant (not short bursts), located on the left side of her chest, and so severe (sharp and stabbing pain) that it makes it difficult for her to catch her breath while speaking. The earlier episodes (short bursts of chest pain) seem to have been aggravated by stress or after transitioning from a sitting to a standing position.The patient has not tried anything to alleviate her symptoms. During the ED visit, the patient rated her chest pain as 7 on a scale of 1 to 10, with 1 being very little pain and 10 being the worst pain she has felt in her life. The patient was admitted for chest pain, palpitations (racing, skipped beats), dizziness, and shortness of breath. However, at the clinic visit, the patient denies having experienced any chest pain, dizziness, palpitations, chills, night sweats, fatigue, or weight changes. She also denies chest tightness, edema, decreased endurance, cough, or dyspnea. Continues on page 20



Clinic Examination

The patient is taking an oral contraceptive containing norgestimate and ethinyl estradiol (0.25 mg and 35 mg, respectively). She denies taking any over-the-counter medications or herbal supplements. She reports an allergy to penicillin that causes her to break out in a rash. The patient underwent cholecystectomy in January 2014 and had no surgical complications. She denies any other chronic illnesses. She is up to date on all immunizations and has regular annual screening examinations. She denies tobacco, alcohol, and illicit drug use. The patient states she exercises 3 times a week and eats a balanced diet. The patient has a family history of sudden cardiac death: her older brother passed away when he was 17 years old. She also has a family history of asthma (father and 3 brothers) as well as type 2 diabetes (maternal grandparents). She denies any other family history of chronic illness. On presentation, the patient appears well and is alert and oriented ×4. She appears to be in acute distress but is well nourished and has no body or breath odors. She is 172.72 cm tall (68 in) and weighs 68.2 kg, with a BMI of 22.8.Vital signs are shown in Table 1 and are remarkable for an increase in heart rate of nearly 30 bpm when she transitions from supine to standing. Physical Examination

Review of skin/hair/nails shows that the tips of the fingers and nail beds are cyanotic, with a 4-second capillary refill time. Cardiac examination shows sinus tachycardia but no other abnormalities. No abnormalities are found on respiratory assessment or examination of extremities. The diagnostic and treatment plan for the patient’s chest pain and lightheadedness/hypovolemia are shown in Table 2. Discussion

Postural orthostatic tachycardia syndrome (POTS) is a disorder characterized by the following 3 factors1,2: 1. Increase in heart rate of ≥30 beats per minute (or ≥40 bmp in patients aged 12-19 years) when moving from the supine to standing position; standing heart rate often is >120 beats per minute 2. Symptoms of lightheadedness, palpitations, tremor, generalized weakness, blurred vision, exercise intolerance, and fatigue 3. Absence of orthostatic hypotension The prevalence of POTS is approximately 0.2% to 1% in developed countries; it is most common among premenopausal White women, with the majority of patients presenting between the ages of 15 and 25 years.2,3 More than 75% of patients with POTS are women.2,3 The syndrome is common in patients with chronic fatigue syndrome, anxiety, somatic hypervigilance, and autoimmune disorders.2,3

TABLE 1.Vital Signs Temperature, °F


Heart rate (supine), bpm


Blood pressure, mmHg


Respiratory rate, bpm


Pulse oximetry, %


Orthostatic vitals Blood pressure, mmHg


Heart rate (standing), bpm


TABLE 2. Diagnostic and Treatment Plan Chest Pain Diagnostic

ECG, stress ECG, chest radiograph, event monitor for 30 d

Laboratory tests

CBC, BMP, thyrotropin, urine pregnancy


Atenolol 25 mg orally once daily


Discuss the importance of taking atenolol as directed and not abruptly stopping beta-blockers; set up sessions with physical therapist to begin exercise training

Lightheadedness and Hypovolemia Diagnostic

Orthostatic vital signs


Normal saline 1000 mL IV bolus


Discuss importance of high-salt diet and other strategies to avoid hypovolemic episodes

BMP, basic metabolic panel; CBC, complete blood cell count; ECG, electrocardiogram; IV, intravenous

Patients with POTS present with varying symptoms, which commonly are abrupt and insidious in onset; however, some patients may experience symptoms of POTS after a viral illness, pregnancy, trauma, or surgery.2 In addition to the symptoms already mentioned, patients with POTS may experience migraine headaches, brain fog, sweating, insomnia, edema when standing, acrocyanosis, anxiety, nausea, abdominal cramps, early satiety, bloating, constipation, and diarrhea.2,3 Patients with POTS may faint, but presyncope is a more common symptom.3 Symptoms may be exacerbated by dehydration, heat, alcohol, and exercise.2 The symptoms of POTS may be cyclic in nature, with some women experiencing a worsening of symptoms during


Continues on page 22


certain stages of their menstrual cycle associated with weight and fluid changes, and other patients experiencing a cycle of POTS symptoms lasting several days followed by a similar number of days with no or minimal symptoms.4

excessive heart rate response to orthostatic stress in POTS is not caused by anxiety and is a physiologic response that maintains arterial pressure during venous pooling.4,9 Diagnosis of POTS

Etiology of POTS

Various pathophysiologic mechanisms have been described in patients with POTS, including peripheral autonomic denervation, hypovolemia, hyperadrenergic stimulation, cardiovascular deconditioning, and anxiety/hypervigilance.2,3 It is unclear which of these abnormalities are primary and causative and which are secondary.These various etiologies have led to the categorization of POTS into subtypes: neuropathic, hypovolemic, and hyperadrenergic.The various mechanisms underlying POTS may overlap, complicating diagnosis.2 Neuropathic POTS occurs in approximately 50% of cases and is associated with distal autonomic denervation, most commonly in the feet and toes.2 In this subtype, impaired sympathetic tone results in reduced venoconstriction, causing blood to pool in the lower extremities rather than return to the heart when a patient is standing.2 This decreased blood flow to the heart results in orthostasis and tachycardia.2 Hypovolemia plays a large role in the symptomatic presentation in up to 70% of patients with POTS.2 The exact cause of hypovolemia is unknown but may be related to low plasmin renin activity and aldosterone levels.2 Laboratory findings in patients with POTS has led some investigators to suggest that a renal disorder (eg, renal denervation) may play a primary role in the etiology of POTS.5 In addition, Fu et al found that cardiac size/mass and blood volume were markedly decreased in patients with POTS compared with healthy sedentary patients without POTS.6 The researchers concluded that deconditioning (ie, cardiac atrophy and hypovolemia) is a cause of POTS.6 The hyperadrenergic subtype, which occurs in up to 50% to 60% of patients with POTS, is caused by elevated levels of epinephrine and norepinephrine (≥600 pg/mL) in the blood when a patient is standing.2,3 Unlike neuropathic POTS, in which the patient’s blood pressure decreases and heart rate increases on standing, patients with hyperadrenergic POTS have an increase in both systolic blood pressure and heart rate on standing.2 Patients with this subtype tend to have sympathetic activation symptoms, including palpitations, anxiety, tachycardia, and tremor.2,3 Baroreflex transfer is impaired in all patients with POTS, further decreasing blood pressure when a patient switches from a supine to an upright position.7 Secondary POTS may be caused by underlying conditions such as diabetes, lupus, and alcoholism, as well as chemotherapy.8 Although anxiety, panic disorder, and somatic vigilance are common in patients with POTS, research suggests that the

Because POTS shares overlapping symptoms with serious medical illnesses, especially cardiac diseases, a thorough history, physical examination, and 12-lead electrocardiogram are essential to the differential diagnosis of this condition.2 Evaluation should focus on excluding cardiovascular causes, such as structural heart defects and tachyarrhythmias, as well as endocrine dysfunction.3 Select patients may benefit from the following tests2: • 24-hour Holter monitoring • Transthoracic echocardiogram • Exercise stress test • Autonomic testing • Thyroid function test and complete blood cell count • Tilt-table testing and/or standing test Diagnosis can be aided through a standing test, which requires a patient to transition from a seated to a standing position. During the 30-minute test, the patient’s heart rate and blood pressure are measured to evaluate the body’s response to the change in position.5 Unlike orthostatic hypotension, patients with POTS will not have a decrease in blood pressure when transitioning from a seated to standing position.A head-up tilt test also is helpful in the diagnostic workup of POTS because it allows for monitoring vital signs over a longer period than the standing test.2 Treatment Options

There is no single definitive treatment for POTS, and a combination of approaches often is needed.2 Nonpharmacologic treatment approaches should be used first (Table 3, page 24).2 The American College of Cardiology recommends a regular, structured, and progressive exercise program for POTS that includes aerobic reconditioning and resistance training for the thighs.2 Research by Fu et al found that exercise training increased left ventricular mass and blood volume and decreased upright heart rate in patients with POTS; 10 out of 19 patients in this study no longer met the criteria for POTS after training, and all patients showed improved quality of life.6 Consumption of up to 2 to 4 L of water and 10 to 12 g of sodium daily also may be considered.2 Avoidance of caffeine, alcohol, prolonged heat, and use of norepinephrine transport inhibitors may be helpful.2,3 If nonpharmacologic strategies are not effective, patients with short-term clinical decompensations can be treated with an acute intravenous infusion of up to 2 L of saline.2 Treatment with fludrocortisone, pyridostigmine, midodrine, or low-dose


Continues on page 24


TABLE 3. Guideline-Recommended POTS Treatments2 Nonpharmacologic Treatments Exercise program Increased water and salt intake Compression clothing Pharmacotherapy ≥2 L IV saline infusion Fludrocortisone or pyridostigmine Midodrine or low-dose propranolol Clonidine or methyldopa (for patients with prominent hyperadrenergic features) IV, intravenous

With adherence to exercise recommendations, diet modification, and medication regimens, patients with POTS can reduce or eliminate symptoms and improve their quality of life. Pharmacologic treatment should not be the sole therapy for patients with POTS. Clinicians should stress the importance of exercise and increased salt intake along with medications for symptom relief when counseling patients with POTS.To aid in treatment adherence and optimize outcomes, a strong patient/provider relationship is essential. ■ Laura Gillen, PA-C, works with the Augusta University Medical Center plastic surgery team in Augusta,Georgia;Tyger Meade Clayton, MPA, PA-C, works in urgent care and occupational medicine and is assistant professor in the PA Department at Augusta University. References 1. Shen W-K, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2017;70(5):e39-e110. 2. Sheldon RS, Grubb BP 2nd, Olshansky B, et al. 2015 Heart Rhythm Society

propranolol may be considered.2 For patients with prominent hyperadrenergic features, clonidine or methyldopa may be used.2 Results of a double-blind trial comparing propranolol to exercise in 19 patients with POTS found that both propranolol treatment and exercise training lowered standing heart rate, but only exercise was linked with an increase in plasma aldosterone to renin ratio. In addition, exercise, but not propranolol treatment, was associated with improvements in quality of life.10 In patients with hyperadrenergic POTS, the use of betablockers significantly decreased patients’ norepinephrine blood levels on standing.11 Patients initiating therapy with beta-blockers should be started on low doses and then slowly titrated until symptom relief is achieved because higher doses are not as well tolerated. Patient education on the need for a trial-and-error approach to find an effective treatment for symptomatic relief is important.

expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12(6):e41-63. 3. Zhao S, Tran VH. Postural orthostatic tachycardia syndrome. In: StatPearls. StatPearls Publishing; 2021 Jan. Updated August 15, 2020. Accessed August 14, 2021. 4. Low PA, Sandroni P, Joyner M, Shen W-K. Postural tachycardia syndrome (POTS). J Cardiovasc Electrophysiol. 2009;20(3):352-358. 5. Raj SR, Biaggioni I, Yamhure PC, et al. Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome. Circulation. 2005;111(13):1574-1582. 6. Fu Q, Vangundy TB, Galbreath MM, et al. Cardiac origins of the postural orthostatic tachycardia syndrome. J Am Coll Cardiol. 2010;55(25):2858-2868. 7. Raj SR. Postural tachycardia syndrome (POTS). Circulation. 2013;127(23): 2336-2342. 8. Kizilbash SJ, Ahrens SP, Bruce BK, et al. Adolescent fatigue, POTS, and recovery: a guide for clinicians. Curr Probl Pediatr Adolesc Health Care. 2014;44(5):108-133.


9. Masuki S, Eisenach JH, Johnson CP, et al. Excessive heart rate response to

This condition may negatively affect quality of life; patients may avoid certain activities that caused tachycardic and hypovolemic episodes, such as sports or other physically strenuous activities, or delay activities because of persistent fatigue. However, POTS is a manageable disease that often improves over time with proper treatment.2 In a follow-up study of 54 patients with POTS, the majority of patients (n=39; 70%) experienced symptom improvement at 1 year; 17 patients (30%) experienced worsening of symptoms.12

orthostatic stress in postural tachycardia syndrome is not caused by anxiety. J Appl Physiol (1985). 2007;102(3):896-903. 10. Fu Q, Vangundy TB, Shibata S, Auchus RJ, Williams GH, Levine BD. Exercise training versus propranolol in the treatment of the postural orthostatic tachycardia syndrome. Hypertension. 2011;58(2):167-75. 11. Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic tachycardia syndrome: the Mayo clinic experience. Mayo Clin Proc. 2007;82(3):308-313. 12. Kimpinski K, Figueroa JJ, Singer W, et al. A prospective, 1-year follow-up study of postural tachycardia syndrome. Mayo Clin Proc. 2012;87(8):746-752.


Dermatology Clinic CASE


A 6-year-old girl presents with a 1-year history of a waxing and waning rash on her limbs and face.The rash starts as red scaly bumps that fade over several weeks leaving smooth white spots. Every few months, the patient gets several new red bumps.The rash is not itchy or painful. Her parents have tried topical steroid creams that did not help clear the rash. Examination reveals scattered erythematous scaly papules on both legs and several hypopigmented macules on her legs, arms, and face.


Pityriasis Lichenoides Chronica

Pityriasis lichenoides (PL) describes a spectrum of acute and chronic dermatoses that includes pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC).1,2 The chronic form, PLC, is characterized by scaly red to brown papules that resolve spontaneously and recur frequently.1,2 In 1894, the chronic and acute forms of PL were first described by Jadassohn and Neisser, respectively, in separate case reports.3-5 The term pityriasis lichenoides chronica was first used in 1899 by Juliusberg.3,6 The acute form of PL was distinguished from PLC in 1916 by Mucha7 and was named pityriasis lichenoides et varioliformis acuta in 1925 by Habermann.3,7 The prevalence of PL in the general population is estimated to be 0.05%.1 It is slightly more common in men and occurs more frequently in late childhood or early adulthood, but can occur at any age.3 Pityriasis lichenoides has been reported across many ethnic groups and geographic locations with no racial predilection.1,3,8 The PLC subtype occurs more frequently than PLEVA and tends to affect children.1,3,8 One study found that Black patients were more likely to develop PLC and White patients were more likely to develop PLEVA.9

Although the exact etiology and pathogenesis of PL are not understood fully, 3 theories predominate.8 The first theory is that PL is an inflammatory reaction to an antigenic agent. Infections and drugs have been linked to cases of PL.3,8 An infectious etiology is supported by several characteristics of PL such as familial outbreaks, young age of onset, and acute eruptions. Infectious PL cases have been linked to Toxoplasma gondii, Epstein-Barr virus, and HIV.3 The second theory is that PL is a lymphoproliferative disorder.This theory is supported by reported cases of PLC progressing to mycosis fungoides.8 The third major etiologic theory states that PL is an immune-complex–mediated hypersensitivity vasculitis.3,8 Studies have found immunoglobin deposits in biopsies of PL lesions and circulating immune complexes in some patients with PL.8 PLC typically presents with gradually developing lesions on the proximal extremities and trunk.The lesions are small, erythematous or brown, and have centrally attached fine parakeratotic scales.2,8 When removed, these scales may leave a shiny brown or pink macule.8 The lesions generally do not scar but leave areas of hyper- or hypopigmentation. Patients with PLC may experience periods of remission between outbreaks.1,2 • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 • 25

Dermatology Clinic The distribution of lesions can predict the disease course; peripheral PLC lesions can take years to fade, whereas a generalized rash tends to resolve more quickly.2 Compared with PLEVA, PLC has a more indolent course and lacks epidermal necrosis. The lesions also can present concurrently with PLEVA lesions or after PLEVA lesions subside.3,8 Fever and pruritus rarely occur in PL.8 The histopathology of PL shows epidermal parakeratosis, dermal edema, necrotic keratinocytes, lichenoid inflammation, and perivascular lymphohistiocytic inflammatory infiltrate. In PLC, the lymphocytic perivascular infiltrate tends to be sparse, superficial, and dominated by CD4+ T cells.8 Rarer histologic findings in PLC include hemorrhage, spongiosis, neutrophilic infiltrate, epidermal vesicle formation, dyskeratosis, and basilar vacuolar changes.2,8

Severe PL cases may warrant use of methotrexate, cyclosporine, dapsone, or acitretin.8 The patient in this case had a punch biopsy of a lesion on the lower extremity that confirmed a diagnosis of PLC. She is being treated with a 3-month course of erythromycin, which she is tolerating well. ■ References 1. Jung F, Sibbald C, Bohdanowicz M, Ingram JR, Piguet V. Systematic review of the efficacies and adverse effects of treatments for pityriasis lichenoides. Br J Dermatol. 2020;183(6):1026-1032. 2. Khachemoune A, Blyumin ML. Pityriasis lichenoides: pathophysiology, classification, and treatment. Am J Clin Dermatol. 2007;8(1):29-36. 3. Bowers S, Warshaw EM. Pityriasis lichenoides and its subtypes. J Am Acad Dermatol. 2006;55(4):557-572; quiz 573-576.

Compared with PLEVA, pityriasis lichenoides chronica has a more indolent course and lacks epidermal necrosis.

4. Jadassohn J. Ube rein eingenartiges psoriasiformes und lichenoides exanthem. Verh Dtsch Dermatol Ges. 1894;4:524-529. 5. Neisser A. Zur Frage der lichenoiden eruptionen. Verh Dtsch Dermatol Ges. 1894;4:495-499. 6. Juliusberg F. Uber die pityriasis lichenoides chronica (psoriasiform exanthem). Arch Dermatol Syphilol. 1899;50:359-374. 7. Mucha V. Uber einen der parakeratosis variegata (Unna) bzw. Pityriasis

The condition is diagnosed by clinical presentation correlated with histologic findings.3,8 A full workup may be needed to exclude other diagnoses. Depending on clinical presentation, complete blood cell count and serologic tests for T gondii, herpes simplex virus, HIV, Epstein-Barr virus, and cytomegalovirus may be useful.8 One condition that can be confused with PLC and PLEVA is lymphomatoid papulosis.3 This disease, however, will show different histologic findings than PL and, unlike PL, it is characterized by overexpression of CD30+ atypical T cells.3,8 The differential diagnosis should also include lichen planus, guttate psoriasis, pityriasis rosea, secondary syphilis, and viral or drug exanthems.3,8 These conditions usually can be differentiated from PL via clinical and histologic findings.3,8 Laboratory tests such as venereal disease research laboratory test, immunopathologic evaluation, antistreptolysin O titers, and throat cultures can assist in differential diagnosis.3 Although some cases of PL spontaneously resolve over several weeks, other cases persist for years. The condition is relatively benign, but treatment for PLC may be pursued because of cosmetic concerns and for symptomatic relief.1,8 Oral antibiotics such as azithromycin, erythromycin, and tetracycline are considered first-line treatments. Antibiotic doses must be tapered gradually to prevent recurrence.Topical corticosteroids may be used in conjunction with antibiotics to offer symptomatic relief of pruritus and inflammation.8 Phototherapy with narrowband UV-B has shown success.1,8

lichenoides chronica (Neisser-Juliusberg) nahestehenden eigentumlichen Fall. Arch Dermatol Syph. 1916;123:586-592. 8. Moy A, Sun J, Ma S, Seminario-Vidal L. Lymphomatoid papulosis and other lymphoma-like diseases. Dermatol Clin. 2019;37(4):471-482. 9. Zang JB, Coates SJ, Huang J, Vonderheid EC, Cohen BA. Pityriasis lichenoides: long-term follow-up study. Pediatr Dermatol. 2018;35(2): 213-219.

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:



Triple-Negative Invasive Ductal Carcinoma in 34-Year-Old Woman Triple-negative breast cancer comprises 10% to 15% of breast cancers, mostly in women who are premenopausal, Black, and BRCA1 positive.

Invasive ductal carcinomas are the most common type of triple-negative cancers.


34-year-old Hispanic woman with no significant medical or surgical history presents to the surgical oncology clinic with a 5-year history of feeling a lump in her left breast and skin changes that have worsened over the past 6 months. The patient states that she detected the lump in her left breast 5 years ago. At the time, she had a mammogram that indicated dense breast tissue but was otherwise negative for suspicious findings. She was advised to monitor the lump in her left breast and to seek medical evaluation immediately if there were any changes. Six months ago, she noticed areolar skin thickening and nipple retraction in her left breast, which prompted her to seek further evaluation. The patient started menarche at age 13, was on oral contraceptives for approximately 2 years, and is a nonsmoker. A 12-point review of systems is negative except for the presenting symptoms.


Physical Examination

The patient is well-nourished, well-groomed, alert and oriented ×3, and appears to be in no acute distress. She is 167.64 cm (66 in) tall and weighs 73.2 kg with a BMI of 24.2. Her vital signs are unremarkable: heart rate, 70 beats per minute; blood pressure, 118/72 mmHg; temperature, 98.2 °F; respirations, 16 breaths per minute; and oxygen saturation as measured by pulse oximetry, 99% on room air. Her breasts are examined in sitting and supine positions. The left breast is fuller and sits slightly • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 27


higher than the right. Left nipple retraction with significant periareolar skin thickening is noted. A large, 8-cm, mobile palpable mass occupies the entire upper outer quadrant and central left breast. A palpable left axillary lymph node, measuring approximately 1.5 cm, is present. There is no discrete mass palpable in the right breast, and no palpable right axillary nodes are found. Physical examination is negative for cervical, supraclavicular, and infraclavicular lymphadenopathy bilaterally. Her cardiopulmonary, musculoskeletal, and neurologic examinations are unremarkable.

FIGURE 2. Left. Long-view axis via ultrasound indicating a conglomerate of masses in the left breast at the 12-o’clock position. The masses measure approximately 5.0 cm × 3.3 cm × 1.8 cm and are located 6.0 cm away from the nipple of the left breast. Right. Blood flow to the mass in the left breast.

FIGURE 3. Left. Long-view axis via ultrasound indicating suspicious node involving the left axilla at level 1. The node measures 2.1 cm × 1.5 cm × 0.9 cm. Right. Transverse view axis via ultrasound indicating a suspicious node involving the left axilla at level 1.

Diagnostic Workup

A bilateral diagnostic mammogram is ordered instead of a screening mammogram because the patient has abnormal clinical findings. This imaging indicates a 2.0-cm irregular mass 9.0 cm away from the nipple at the 1-o’clock region associated with fine pleomorphic calcifications in the left breast (Figure 1). The total suspicious area of volume on mammography measures approximately 6.0 cm × 5.0 cm × 4.4 cm and is associated with skin thickening. A 1.0-cm oval mass with circumscribed margins and associated course calcifications is found in the subareolar region of the right breast. A bilateral breast ultrasound indicates a conglomerate of masses measuring approximately 5.0 cm × 3.3 cm × 1.8 cm located 6.0 cm away from the nipple of the left breast (Figure 2). Several other smaller masses and areas of ductal dilatation extending from these masses to the base of the nipple are found. In total, the measurable disease on ultrasound was approximately 7.0 cm. Associated left nipple flattening and skin thickening measuring 0.5 cm are noted. On the right side, ultrasound reveals a mass measuring 1.0 cm × 0.9 cm × 0.9 cm most consistent with a fibroadenoma. A second, smaller mass, measuring 0.8 cm × 0.7 cm × 0.4 cm, also likely represents a fibroadenoma. These findings correlate to the oval circumscribed mass in the right breast on mammogram. Four suspicious-appearing nodes involving the left axillary levels 1 and 2 are found, the largest of which measures 2.1 cm × 1.5 cm × 0.9 cm (Figure 3). No axillary level 3, internal mammary, or supraclavicular adenopathy are found. Pathology results from an ultrasound-guided core biopsy of the left breast at the 12-o’clock position with marker clip placement indicate invasive ductal carcinoma that is histologic grade 3, estrogen receptor-negative, progesterone receptor-negative, ERBB2 (formerly HER2)-negative, and Ki67 54%, with several foci of lymph vascular invasion. An ultrasound-guided, fine-needle aspiration with clip placement of the 2.1-cm left axillary lymph node indicates metastatic adenocarcinoma consistent with primary breast carcinoma.



FIGURE 1. Left. Cranial caudal diagnostic mammogram image of the left breast indicating a 2.0-cm irregular mass located 9.0 cm away from the nipple at the 1-o’clock region that is associated with pleomorphic calcifications. Right. Lateral medial diagnostic mammogram image of the left breast indicating an irregular mass associated with pleomorphic calcifications.

A bone scan of the whole body and CT of the chest, abdo­ men, and pelvis with contrast is performed before chemo­ therapy to rule out distant disease. These studies show no evidence of metastases. Although the patient does not have a family history of breast cancer, genetic testing was indicated per National Comprehensive Cancer Network guidelines because she is younger than 60 years with triple-negative disease. Genetic testing results are negative. Oncofertility consultation is offered because the patient is of childbearing age and chemotherapy may induce ovarian failure.The patient declined this consultation. To address psychosocial support, the patient meets with a social worker and is referred to support groups during her treatment. She also has a nurse navigator to educate her on the various teams involved in her care and what to expect at each appointment.The nurse navigator remains available as a resource for the patient during and after treatment. Treatment Course

Treatment options such as chemotherapy, radiation, and surgical intervention are discussed with the patient. Based on her clinical stage of cT3cN1cM0 and triple-negative profile, chemotherapy is initiated before surgical interven­ tion. Port placement is recommended for the patient before treatment with doxorubicin and cyclophosphamide for 4 cycles every 3 weeks followed by paclitaxel for 4 cycles, with 3 weekly treatments per cycle. The following laboratory evaluations are performed before each cycle of chemotherapy treatment: complete blood cell count with differential, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total bilirubin.

A cold cap is ordered for the patient to decrease risk for hair loss. Cold caps are recommended to wear approximately 1 hour before the infusion, during the infusion, and at least 3 hours after the infusion for each treatment cycle. Ondansetron 8 mg, prochlorperazine 10 mg, and dexamethasone 4 mg as needed are prescribed to manage nausea during treatment. Approximately 4 weeks after completion of chemotherapy, the patient undergoes a left modified radical mastectomy to remove the entire left breast and level 1 and 2 axillary nodes in the same surgery as 2 separate specimens. Magnetic seed localized excision is performed as part of the complete axil­ lary dissection to ensure removal of the biopsy-proven and clipped left axillary lymph node. The pathology results from the left breast mastectomy show rare atypical cells consistent with focal residual carcinoma cells in the background of extensive treatment effects. No lymphovascular invasion is identified. Usual ductal hyper­ plasia, fibroadenomatous change, stromal fibrosis, and focal microcalcifications are noted. The margins are clear, with distance from closest margin greater than 10 mm anteriorly and superiorly (Figure 4). Pathology of the left axillary lymph node with 1 magnetic seed indicates metastatic carcinoma with a metastatic focus of 3 mm without extranodal extension. Level 1 left axillary dis­ section contents indicate metastatic carcinoma with treatment effects in 2 of 21 lymph nodes, with the largest metastatic focus measuring 1.8 mm without extranodal extension. Left axillary dissection of level 2 nodes indicates metastatic carcinoma in 1 of 3 lymph nodes, with metastatic focus measuring 0.7 mm without extranodal extension. Postmastectomy radiation is recommended for this patient to decrease the risk for disease recurrence in the setting of Continues on page 34

FIGURE 4. Pathology specimen obtained after a total left breast mastectomy showing clear margins, with distance from closest margin greater than 10 mm on the superior and anterior sides. All clips are located within the specimen. • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 29

Evoke Giant



in theStrategy United States inn/a 2021.1 Triple-negative breast cancer Giant Creative 49737 Carcinoma dn Triple-Negative Invasive Ductal

has an incidence of 13.2 per 100,000 women and accounts 09/07/21 1,2 for approximately 10% to 15% of all breast cancers. This PMSxxxx PMSxxxx PMSxxxx PMSxxxx 9:45 am advanced node-positive disease. The patient starts physi- subtype is more common in patients who are premenopausal, cal therapy on postoperative day 14 to improve her range Black, and have BRCA1 gene mutations.2,3 Invasive ductal of motion, which decreased because of surgery, and allow carcinoma is the most common phenotype of triple-negative her to initiate radiation therapy within 4 to 6 weeks. The breast cancer, accounting for 14.6% of patients with triplepatient is scheduled for simulation to prepare for radiation negative disease.2 treatment of 50 gray in 25 fractions to the chest wall and Treatment decisions in this case were based on NCCN regional lymphatics followed by 10 gray boosts to the chest and MD Anderson Cancer Center guidelines.4,5 The first wall. The patient is asked to stop taking vitamin C during step was to determine whether the patient had invasive vs radiation treatment because that can decrease the effectiveness noninvasive cancer. In this case, because the patient had of radiation therapy. It is recommended that the patient start cancer cells present in lymph nodes and invasive disease on capecitabine for 6 cycles during radiation therapy to further left breast biopsy, the invasive protocol was followed. Based reduce her recurrence risk. on the treatment guidelines for stage III, triple-negative disease, it was recommended that the patient consider neoadjuvant chemotherapy followed by total mastectomy with Discussion Triple-negative breast cancer is an aggressive type of breast axillary lymph node surgery. This differs from the protocol cancer that is negative for estrogen, progesterone, and ERBB2 for earlier stage, hormone-positive tumors, for which neoadreceptors, making targeted therapy difficult. An estimated juvant chemotherapy is not considered. Because the patient 281,550 new cases of female breast cancer and an estimated had stage III disease with 4 or more involved lymph nodes, 43,600 deaths because of female breast cancer are expected her treatment team also recommended postmastectomy continued from page 29



For surveillance, the patient should have a clinical breast exam every 3 to 6 months for 5 years, then annually after year 5. radiation therapy focused on the chest wall and regional lymphatics. Because the patient was estrogen and progesterone receptor-negative, endocrine therapy to decrease these hormones in the body to reduce the risk for recurrence or spread of disease was not indicated.The patient also was not a candidate for targeted ERBB2 therapy because she was ERBB2-negative. The patient received a cold cap during treatment, which is associated with a significant reduction in alopecia among patients receiving chemotherapy with a taxane, anthracycline, or both.6 Cold caps work by narrowing the blood vessels beneath the skin to reduce the effect of chemotherapy drugs near the hair follicles. For surveillance, the patient should have a clinical breast exam every 3 to 6 months for 5 years, then annually after year 5.7 Because the patient had a total mastectomy on the left side, she does not need mammography of her left breast but should continue annual right breast screening mammography. The patient did not undergo immediate breast reconstruction because of the need for radiation after mastectomy. If she desires reconstruction in the future, she can be referred to a reconstructive surgeon to discuss options. Reconstructive surgery should not take place any sooner than 6 to 12 months after completion of radiation to allow the tissues time to heal.1


Triple-negative breast cancer is the most aggressive breast cancer phenotype. It is considered aggressive because the tumor grows and spreads quickly and is more likely to recur after treatment. Targeted therapy options for this type of malignancy are limited. The 5-year survival rate for patients with regional triple-negative breast cancer (has spread outside the breast to nearby structures or lymph nodes) is 65%, compared with approximately 90% survival rate for localized triple-negative disease and other breast cancer types.3,8 Patients must be monitored closely for side effects while receiving chemotherapy and radiation therapy and followed closely for recurrence and metastasis. ■ Sunayana Chopra Pydah, PA-C, MBA, MHA, MPAM, works in the Department of Pediatrics at Santa Clara Valley Medical Center in San Jose, California; Erin Hernandez, PA-C, works in the Department of Surgical Oncology at MD Anderson Cancer Center in Houston, Texas, and has over 13 years of experience in treating patients with breast cancer; and Melissa Shaffron, MPAS, PA-C, works in emergency and urgent care medicine. She serves as the associate program director and director of clinical education for the University of Lynchburg School of PA Medicine in Virginia. References 1. National Cancer Institute. Surveillance, Epidemiology, and End Results Program. Cancer stat facts: female breast cancer. Accessed August 22, 2021.


2. Plasilova ML, Hayse B, Killelea BK, Horowitz NR, Chagpar AB, Lannin DR. Features of triple-negative breast cancer: analysis of 38,813 cases from the national cancer database. Medicine (Baltimore). 2016;95(35):e4614.

What percentage of breast cancer cases are triple negative?

3. Howard FM, Olopade OI. Epidemiology of triple-negative breast cancer: a review. Cancer J. 2021;27(1):8-16. 4. National Comprehensive Cancer Network. Breast cancer (version 6.2021). August 16, 2021. Accessed August 22, 2021. 4.03% 0.81%

■ 5% to 10% ■ 10% to 15% ■ 20% to 25%

professionals/physician_gls/pdf/breast.pdf 5. MD Anderson Cancer Center. Breast cancer—invasive stage I-III. Accessed August 22, 2021.



documents/for-physicians/algorithms/cancer-treatment/ca-treatment-breastinvasive-web-algorithm.pdf 6. Nangia J, Wang T, Osborne C, et al. Effect of a scalp cooling device on

■ Greater than 25%

alopecia in women undergoing chemotherapy for breast cancer: the SCALP randomized clinical trial. JAMA. 2017;317(6):596-605. 7. Smith TJ. Breast cancer surveillance guidelines. J Oncol Pract. 2013; 9(1): 65-67.

For more polls, visit

8. American Cancer Society. Triple-negative breast cancer. Accessed August 22, 2021. • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 35


Are you being fairly compensated? and earned an average of $108,488. Urgent care and internal medicine/family medicine/ primary care medicine were the 2 most common areas of practice for PAs (8.1% and 7.6%, respectively) and were linked to average salaries of $116,500 and $102,727, respectively. The gender wage gap still persists among PAs. Male PAs (118) reported earning an average of $127,139 compared with $113,236 for women (224), $102,500 for nonbinary (2), and $72,000 for transgender (19) PAs. Salaries among transgender NPs also fell well below their male and female counterparts ($92,500 vs $113,818 and $112,883, respectively). Most NP and PA respondents reported working in the South (35.3% and 29.5%, respectively), and providers in this area reported making average salaries of $106,643 and $111,235, respectively. Similar to the findings from the 2020 survey, both NPs and PAs in the West reported making the highest average salaries ($128,781 and $130,255, respectively). Most NPs worked in urban areas (36.7%) followed by suburban areas (32.5%). For PAs, the percentage of clinicians working in suburban and urban work locations was virtually tied (37.6% and 37.3%, respectively). Similar percentages of NP and PA respondents reported feeling “satisfied” or “very satisfied” with their compensation (51% of NPs and 54% of PAs). However, respondents who reported feeling “very satisfied” earned the highest average salaries ($122,455 for NPs and $141,852 for PAs).



See how your salary compares with those of your peers as reported in the 2021 NP/PA SALARY SURVEY

Throughout our 23-year history, The Clinical Advisor has strived to highlight the successes and accomplishments of nurse practitioners (NPs) and PAs. The COVID-19 pandemic allowed clinicians to practice at the top of their education and clinical training and our survey results reflect the impact the pandemic had on income and job satisfaction. For clinicians considering a career in a new location, specialty, or practice area but are unsure how the change may impact compensation, especially during the pandemic, the results of the 2021 NP/PA Salary Survey may help navigate these areas of uncertainty. Similar to results from previous years, most of the NPs and PAs who responded to the 2021 survey reported earning a higher salary this year compared with last year (47% and 44%, respectively). However, similar numbers of respondents in both fields reported earning the same salary as last year (33% of NPs and 32% of PAs). When asked how the COVID-19 pandemic affected their income, 21% of NPs and 27% of PAs reported earning less income last year because of the pandemic, while 19% of NPs and 15% of PAs reported earning more income. The average earned salary was similar between NPs and PAs. This year, the reported average salary for NPs was $112,979 and average salary for PAs was $116,373. Most NPs who indicated a practice area worked in internal medicine/family medicine/primary care medicine (13.7%)

See the complete survey results online at

TABLE 1. Average NP salary by profession

TABLE 2. Average PA salary by profession



Average salary

Average hourly rate



Average salary

Average hourly rate

Nurse Practitioner




Physician Assistant




TABLE 3. Average NP salary by practice area

TABLE 4. Average PA salary by practice area

Practice area


Average salary

Practice area


Average salary

Internal medicine/ Family medicine/ Primary care

13.7% (n=167)


Urgent care

8.1% (n=32)


Internal medicine/Family medicine/Primary care

Adult medicine

5.9% (n=72)


7.6% (n=30)



5.8% (n=71)


Emergency medicine

6.6% (n=26)



5.5% (n=67)


Orthopedic surgery

5.6% (n=22)



5.5% (n=67)


Adult medicine

4.6% (n=18)


Ambulatory care

4.5% (n=55)


General surgery

4.3% (n=17)


Geriatric medicine

4.0% (n=49)



3.6% (n=14)



55.1% (n=671)



59.7% (n=235)


TABLE 5. Average NP salary by highest degree obtained

TABLE 6. Average PA salary by highest degree obtained



Average salary



Average salary


78.9% (n=962)



66.5% (n=262)



15.8% (n=192)



5.6% (n=22)



1.5% (n=18)


Certificate of Completion

20.1% (n=79)


TABLE 7. Average NP salary according to gender

TABLE 8. Average PA salary according to gender



Average salary



Average salary


80.6% (n=982)



56.9% (n=224)



14.3% (n=174)



29.9% (n=118)



0.2% (n=2)



0.5% (n=2)



1.2% (n=14)



4.8% (n=19)


FIGURE 1. Do you work at multiple locations (NPs)?

43.2% (n=526)

53.0% (n=646)

FIGURE 2. Do you work at multiple locations (PAs)? Yes No

40.6% (n=160)

51.5% (n=203)



FIGURE 3. Average NP salary by geographic region West 15.8% (n=193) $128,781 average salary

Midwest 20.7% (n=252) $107,215 average salary

Northeast 24.4% (n=297) $118,114 average salary

FIGURE 4. Average PA salary by geographic region West 17.8% (n=70) $130,255 average salary

Midwest 22.8% (n=90) $109,142 average salary

Northeast 22.1% (n=87) $119,869 average salary

South 35.3% (n=430) $106,643 average salary

FIGURE 5. Did you earn more this year (NPs)?

South 29.5% (n=116) $111,235 average salary

FIGURE 6. Did you earn more this year (PAs)?




















No response


FIGURE 7. Do you expect to earn more next year (NPs)?


No response


FIGURE 8. Do you expect to earn more next year (PAs)?














No response

TABLE 9. Average NP salary by experience level


(n= 193)





Same Less No response


TABLE 10. Average PA salary by experience level

Experience in years


Average salary

Experience in years


Average salary


31.3% (n=382)



26.9% (n=106)



23.8% (n=290)



16.5% (n=65)



16.1% (n=196)



14.2% (n=56)



7.4% (n=90)



11.4% (n=45)



17.6% (n=214)



23.1% (n=91)



See the complete survey results online at

TABLE 11. Average NP salary according to practice setting

TABLE 12. Average PA salary according to practice setting

Practice setting


Average salary

Practice setting


Average salary

Clinic – Hospital

20.7% (n=252)


Clinic - Stand-alone

21.8% (n=86)


Clinic – Stand-alone

18.1% (n=220)


Clinic - Hospital

20.0% (n=79)


Office practice

14.0% (n=170)



16.2% (n=64)



12.6% (n=154)


Office practice

10.4% (n=41)



2.5% (n=30)


Walk-in/ambulatory care

3.6% (n=14)


Walk-in/Ambulatory care

4.4% (n=53)



1.8% (n=7)



27.9% (n=340)



20.5% (n=79)


TABLE 13. Number of patients seen per week (NPs)

TABLE 14. Number of patients seen per week (PAs)

Patients per week


Patients per week



18.5% (n=225)


12.2% (n=48)


32.0% (n=390)


25.9% (n=102)


26.3% (n=320)


25.4% (n=100)


12.6% (n=153)


18.0% (n=71)


4.2% (n=51)


5.3% (n=21)


2.7% (n=33)


5.3% (n=21)

TABLE 15. How satisfied are you with your compensation (NPs)?

TABLE 16. How satisfied are you with your compensation (PAs)?



Average Salary



Average Salary

Very satisfied

19.6% (n=239)


Very satisfied

17.5% (n=69)



31.8% (n=387)



36.0% (n=142)



20.5% (n=250)



19.8% (n=78)



17.3% (n=211)



14.5% (n=57)


Very dissatisfied

4.7% (n=57)


Very dissatisfied

1.5% (n=6)


FIGURE 9. Has COVID-19 affected your income (NPs)?






FIGURE 10. Has COVID-19 affected your income (PAs)?





Yes, increased Yes, decreased No No response

(n= 57)

10.7% (n=42)

Yes, increased





Yes, decreased No No response • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 39


TABLE 17. Hours per week worked (NPs)

TABLE 18. Hours per week worked (PAs)

Hours per week


Hours per week



6.4% (n=78)


3.0% (n=12)


8.1% (n=99)


4.6% (n=18)


44.5% (n=543)


40.6% (n=160)


29.5% (n=359)


32.2% (n=127)


5.2% (n=63)


8.1% (n=32)


1.2% (n=14)


2.3% (n=9)


1.3% (n=16)


1.3% (n=5)

TABLE 19. Average NP salary by location

TABLE 20. Average PA salary by location



Average salary



Average salary


27.0% (n=329)



17.3% (n=68)



32.5% (n=396)



37.6% (n=148)



36.7% (n=447)



37.3% (n=147)


TABLE 21. How satisfied are you with your job (NPs)?

TABLE 22. How satisfied are you with your job (PAs)?



Average Salary



Average Salary

Very satisfied

26.2% (n=319)


Very satisfied

19.3% (n=76)



42.7% (n=520)



46.4% (n=183)



15.8% (n=193)



14.2% (n=56)



7.9% (n=96)



7.4% (n=29)


Very dissatisfied

1.3% (n=16)


Very dissatisfied

2.0% (n=8)


FIGURE 11. Do you receive reimbursements for CME (NPs)?

73.1% (n=891)

26.9% (n=328)


69.1% (n=842)

70.3% (n=277)


FIGURE 13. Do you receive reimbursements for tuition (NPs)?

30.9% (n=377)

FIGURE 12. Do you receive reimbursements for CME (PAs)?

Yes No

29.7% (n=117)

Yes No

FIGURE 14. Do you receive reimbursements for tuition (PAs)?

20.3% (n=80)


79.7% (n=314)

Yes No

Dermatologic Look-Alikes Itchy, Scaly Patches TARA L. BRAUN, MD; CHRISTOPHER RIZK, MD



A 53-year-old man presents with a 5-year history of an itchy, scaly spot on his leg. He has treated it with overthe-counter creams and ointments, which temporarily relieved the itching and reduced the scaling, but the lesion has never gone away. He has no other personal or family history of skin conditions. His medical history includes type 2 diabetes and depression. On physical examination, a hyperpigmented lichenified patch with overlying white scale is seen on the left superior knee.

A 45-year-old healthy man presents with a 6-month history of a red, scaly rash.The rash started on his lower back and has been spreading. He tried topical corticosteroids, which helped but did not clear the rash. He has some associated morning stiffness in his hands that improves with activity. His paternal uncle has a similar skin condition. On examination, well-demarcated erythematous plaques with silvery scale are noted on the patient’s lower back, elbows, knees, genitals, and scalp. • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 41

Dermatologic Look-Alikes CASE #1

Lichen Simplex Chronicus

Lichen simplex chronicus (LSC), also referred to as circumscribed neurodermatitis, is a condition characterized by an “itch-scratch” cycle in which patients repeatedly scratch affected areas, resulting in skin thickening.1,2 Vidal coined the term lichen simplex chronicus in 1886 and Brocq expanded the description of the condition in 1891.3 The condition is estimated to affect 12% of the population, with a peak incidence among adults 30 to 50 years of age.4 It is approximately 2 times more common in women.4 The incidence of LSC is reported to be higher among people of Asian descent.2 The disorder is linked to other conditions including eczema, hay fever, asthma, and anxiety disorders.5,6 Psychological factors such as stress, anxiety, depression, and obsessive-compulsive disorder are thought to trigger LSC.2,4 The thickening of the skin in LSC arises because of to repeated scratching and rubbing of a pruritic area, which may begin to itch spontaneously or secondary to an underlying condition.The cause of pruritus may be a medical condition such as obstructive biliary disease or chronic renal disease, or a skin condition such as eczema, allergic contact dermatitis, insect bites, psoriasis, or xerosis.3,4,7 Pruritus in LSC also has been linked to nerve regrowth because of repeated mechanical trauma from scratching.3 Psychological factors also may be related to pruritus and scratching may serve as a way to relieve emotional stress and tension; however, the resultant plaques tend to lead to more stress and itching.3,4 The pruritus in LSC may be so intense that it disturbs sleep.5 A patient can have a single or multiple LSC plaques that appear well-circumscribed and lichenified and may have associated scale.The lesions also can have excoriations from excessive scratching.2,4,5 Both hyper- and hypopigmentation may occur, although brown or dusky violaceous hyperpigmentation is more common. Pigment changes can be more significant in patients with darker skin tones.2 Plaques may occur anywhere on the body but are more common in areas that are easy to reach, such as the head, the sides and nape of the neck, extensor surfaces of the arms and lower legs, ankle flexures, genitals (vulva, scrotum), anus, and inner thighs.2,4 Histopathologic findings in LSC include epidermal hyperplasia with acanthosis, dermal fibrosis, and vertically streaked collagen bundles.2 Orthokeratotic hyperkeratosis, regular elongation of rete ridges, hypergranulosis, and perivascular

infiltrate of lymphocytes or macrophages also may be observed in addition to eosinophils in the superficial dermis.1,4 Histologic features can be more difficult to interpret if LSC is superimposed on areas of skin affected by other diseases, such as psoriasis. In these cases, the patient may present with histologic and clinical findings of both conditions.2 Diagnosis of LSC is based on clinical features.2 Clinical evaluation includes a history and physical examination, symptoms reported by the patient, and dermoscopic evaluation. Additional testing is necessary only to rule out other diagnoses or to investigate for underlying systemic disease.2,4 When an underlying condition is suspected, appropriate tests include a complete blood cell count, metabolic panel, kidney and liver function tests, and thyroid function tests.3 Psoriasis, lichen planus, contact dermatitis, mycosis fungoides, and tinea corporis are disorders that mimic LSC. These conditions often can be differentiated from LSC by distribution and morphology, but additional tests occasionally are needed.2 Patch testing can help exclude contact dermatitis and biopsies can help differentiate LSC from mycosis fungoides and psoriasis. In cases with genital involvement, potassium hydroxide preparation or fungal cultures may aid the differentiation from candidiasis and tinea infections.4

The thickening of the skin in lichen simplex chronicus is because of repeated scratching and rubbing of a pruritic area. In general, treatment of LSC can be difficult and relapses are frequent.2 To treat LSC, a practitioner first should consider whether an underlying condition may be the cause of the patient’s pruritus.5 In the absence of an underlying condition, it is necessary to break the itch-scratch cycle.5 Patients are counseled to resist scratching and apply a cold pack or ice to help soothe the area.2 Simple measures to minimize skin irritation include avoidance of excessive washing, harsh soaps, and rough clothing. Topical corticosteroids of moderate or high potency are first-line treatments and can be administered under occlusion.2-5 Topical emollients also may be used.4 For nocturnal pruritus, a sedating antihistamine such as hydroxyzine may prove helpful in some patients.2,5 For cases with a psychological etiology, reduction of stress and anxiety through lifestyle modification, psychotherapy, and/or medication may be effective.2,4 In more persistent cases, corticosteroid or botulinum toxin injections can be considered.2,4 Especially severe cases may warrant surgical removal of localized lesions.4


For the patient in this case, the condition was diagnosed clinically. The patient was counseled extensively about the itch-scratch cycle and the importance of avoiding further scratching and trauma to the area. He was prescribed potent topical corticosteroids. Over several months, the patient’s lesion became thinner and less itchy.



Psoriasis is an immunemediated chronic disorder affecting the skin and joints. Psoriasis likely was described first in Corpus Hippocraticum by Hippocrates, who used the terms psora and lepra to describe a condition later recognized as psoriasis.8-10 In the first century AD, Celsus described 40 dermatoses, one of which was a form of impetigo later interpreted by Willan to be a type of psoriasis.10 In 1809,Willan defined 2 psoriasiform diseases, lepra Graecorum and psora leprosa; in 1841, von Hebra determined these were the same disease.10 Psoriasis affects 2% of the population in North America and Europe and is less prevalent among individuals of Japanese descent.8,11 Patients may develop psoriasis at any age and the prevalence increases steadily between early childhood and adulthood (0.12% at 1 year of age to 1% to 2% at 18 years).8,11 Age at presentation has 2 peaks; at 15 to 20 years and 55 to 60 years.11 Psoriasis is more likely to be severe in men than in women. Factors hypothesized to impact psoriasis prevalence include ethnicity, sun exposure, and climate.8 Two genes have been associated with psoriasis: HLA-Cw6, which is linked to guttate psoriasis, and CARD14; both mutations may result in improved response to tumor necrosis factor (TNF) inhibitors.12,13 Psoriasis can arise in predisposed individuals after exposure to a trigger such as trauma (Koebner phenomenon), certain medications, or infections.15 Streptococcal infections have been identified as a risk factor for guttate psoriasis, which classically presents on the trunk of children and adolescents after an infection and is self-limited, resolving in 3 to 4 months.16 Infections with Staphylococcus aureus, Helicobacter pylori, Candida, Malassezia, papillomaviruses, and retroviruses are potential risk factors. HIV can exacerbate existing cases or cause new-onset disease; as immune function declines, HIV is associated with more

severe psoriasis.12 Psoriasis can arise as an adverse effect of lithium. TNF inhibitor therapy, paradoxically, can trigger psoriasis.12 Obesity, diabetes mellitus, dyslipidemia, hypertension, and stress have been documented as intrinsic risk factors for psoriasis.14 Patients with psoriasis are at a greater risk for metabolic syndrome, psoriatic arthritis, anxiety, depression, cardiovascular disorders, Crohn disease, lymphoma, and nonalcoholic fatty liver disease.8 Generally, psoriasis is considered to be a disorder of the immune system. Crosstalk between the adaptive and innate immune systems and relationships between dendritic cells, macrophages, cytokines, and T cells result in psoriatic pathology.8,15 When activated, these immune cells will produce inflammatory mediators such as interleukin 12 (IL-12), IL-17, IL-23, and TNF-α.15 TNF-α, in turn, induces production of adhesion molecules and secondary mediators, leading to joint and skin disease in patients with psoriasis.8,15

Patients may develop psoriasis at any age and the prevalence increases steadily between early childhood and adulthood. The most common form of psoriasis is psoriasis vulgaris, also known as plaque psoriasis. It is characterized by red or salmon-pink plaques with overlying silver or white scale.15,16 If psoriatic plaques are scratched, they may reveal tiny bleeding spots (Auspitz sign).15 These lesions can be thin or thick, small or large, and they tend to be most active at the edges. Psoriatic plaques usually are symmetrical and appear most frequently on extensor surfaces of the knees and elbows, scalp, umbilicus, and lumbosacral region.16 Psoriasis also may present as inverse psoriasis, in which patients experience well-demarcated, erythematous areas without scaling in the flexural folds.17 Pustular psoriasis exists in both generalized and localized forms, with the acute generalized form being especially severe, resulting in fever, sterile pustules, and potentially life-threatening systemic toxicity. Localized pustular psoriasis, which presents on the hands and feet, can be associated with plaque psoriasis. Erythrodermic psoriasis is relatively rare, comprising less than 2% of psoriasis cases.This type of psoriasis can affect the entire surface of the skin and may be accompanied by chills, hypothermia, dehydration, and even sepsis.17 Psoriatic arthritis, characterized by joint pain, stiffness, and swelling, is present in approximately 25% to 30% of patients with psoriasis.15 • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 43

Dermatologic Look-Alikes TABLE. Lichen Simplex Chonicus vs Psoriasis Lichen Simplex Chonicus1-7


Dermatologic presentation

• Circumscribed, pruritic, lichenified plaques • Scale • Excoriation • Hypo- or hyperpigmentation

• Well-demarcated erythematous or salmon-pink plaques • Silver or white scale

Characteristic location

• Head and neck • Genitals • Arms • Lower legs • Ankle flexures • Inner thighs

• Extensor surfaces of elbows and knees • Scalp • Umbilicus • Lumbosacral region


• Adults aged 30-50 years • 2 times more common in women

• 2 age peaks: 15-20 years, 55-60 years • More severe in men

Potential risk factors

• Eczema, hay fever, asthma • Psychiatric disorders

• HLA-Cw6, CARD14 gene mutations • Infections, medications, trauma, comorbid conditions


• Repeated scratching of a pruritic area • Itch-scratch cycle • Nerve proliferation • Linked to emotional stress

• Immune mediated • Prominent involvement of T-cells and cytokines (IL-12, IL-17, IL-23, and TNF-α)


• Epidermal hyperplasia with acanthosis • Dermal fibrosis • Streaked collagen bundles

• Parakeratosis, loss of granular layer, elongation of rete ridges, micropustules of Kogoj, and Munro microabscesses • Prominent dermal blood vessels • Leukocytic infiltrate


• Clinical history and physical

• Clinical history and physical


• Break the itch-scratch cycle • Topical corticosteroids • Topical emollients • Antihistamines • Reduction of stress

• Topical corticosteroids • Vitamin D derivatives • Calcineurin inhibitors • UV light therapy • Systemic therapy • Biologics

IL, interleukin; TNF, tumor necrosis factor; UV, ultraviolet

Histopathology of psoriasis is characterized by 3 main features: hyperplasia of the epidermis, prominent dermal blood vessels, and dermal inflammatory leukocytic infiltrate.16 Epidermal changes include parakeratosis, loss of the granular cell layer, regular elongation of the rete ridges, micropustules of Kagoj, and Munro microabscesses.16 Although laboratory abnormalities in psoriasis generally are nonspecific and not required for diagnosis, serum uric acid, C-reactive protein, sedimentation rate, and serum immunoglobulin A all may be increased.10 Diagnosis usually is made based on characteristic clinical features.10

Potential conditions to consider in the differential diagnosis of psoriasis include eczema, mycosis fungoides, lichen planus, pityriasis rosea, tinea infections, seborrheic dermatitis, syphilis, pityriasis lichenoides et varioliformis, candidiasis, Paget disease, and squamous cell carcinoma in situ.10,11,17 Psoriasis generally can be differentiated from other disorders based on clinical findings and patient history, but biopsy may be needed to confirm the diagnosis.10 In addition, the specific type of psoriasis must be distinguished from other types.17 Treatment of psoriasis is aimed at reducing symptoms and disease control. The majority of patients (70% to 80%) will


require only topical medications to control their condition.8,9 For mild disease, the first-line treatment is topical corticosteroids.15 Vitamin D derivatives are another option, often combined with topical corticosteroids.8 Tazarotene and calcineurin inhibitors, such as pimecrolimus and tacrolimus, also have shown success. Widespread psoriasis may warrant ultraviolet (UV) light therapy, and more severe disease may require systemic therapies such as acitretin, apremilast, cyclosporine, or methotrexate.8,15 Biologic agents are a more recent development for treatment of psoriasis and typically are used when patients fail topical treatment, light therapy, and conventional systemic medications, or when these treatments are poorly tolerated or contraindicated. Biologic agents are targeted immunomodulators that block cytokines involved in psoriasis pathogenesis including TNF-α, IL-12, IL-23, and IL-17.8 The patient in this case was diagnosed with psoriasis that was resistant to topical treatments.After the patient was counseled about his treatment options, he was started on biologic treatment for his psoriasis and psoriatic arthritis.The patient is tolerating his treatment well and has experienced near-clearance of his psoriasis and improvement in his joint symptoms. ■

LA, Katz S, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. McGraw-Hill Professional; 2003. 4. Charifa A, Badri T, Harris BW. Lichen simplex chronicus. In: StatPearls. StatPearls Publishing; 2021. Accessed August 17, 2021. http://www.ncbi.nlm. 5. Ringel NE, Iglesia C. Common benign chronic vulvar disorders. Am Fam Physician. 2020;102(9):550-557. 6. Liao YH, Lin CC,Tsai PP, Shen WC, Sung FC, Kao CH. Increased risk of lichen simplex chronicus in people with anxiety disorder: a nationwide populationbased retrospective cohort study. Br J Dermatol. 2014;170(4):890-894. 7. Lichon V, Khachemoune A. Lichen simplex chronicus. Dermatol Nurs. 2007;19(3):276. 8. Boehncke WH, Schön MP. Psoriasis. Lancet. 2015;386(9997):983-994. 9. Furue M, Kadono T. Psoriasis: behind the scenes. J Dermatol. 2016;43(1):4-8. 10. Christophers E, Mrowietz U. Chapter 42: Psoriasis. In: Freedberg IM, Eisen AZ, Wolff K, Austen FK, Goldsmith LA, Katz S, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. McGraw-Hill Professional; 2003. 11. Langley RGB, Krueger GG, Griffiths CEM. Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18-23; discussion ii24-25. 12. Lee EB, Wu KK, Lee MP, Bhutani T, Wu JJ. Psoriasis risk factors and triggers. Cutis. 2018;102(5S):18-20.

Tara L. Braun, MD, is a resident in the Department of Dermatology at Baylor College of Medicine in Houston,Texas; Christopher Rizk, MD, is a dermatologist at Elite Dermatology in Houston,Texas.

13. Coto-Segura P, González-Fernández D, Batalla A, et al. Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. Br J Dermatol. 2016;175(1):134-141. 14. Kamiya K, Kishimoto M, Sugai J, Komine M, Ohtsuki M. Risk factors for the


development of psoriasis. Int J Mol Sci. 2019;20(18):4347.

1. Lotti T, Buggiani G, Prignano F. Prurigo nodularis and lichen simplex

15. Schleicher SM. Psoriasis: pathogenesis, assessment, and therapeutic update.

chronicus. Dermatol Ther. 2008;21(1):42-46.

Clin Podiatr Med Surg. 2016;33(3):355-366.

2. Prajapati V, Barankin B. Dermacase. Lichen simplex chronicus. Can Fam

16. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis.

Physician. 2008;54(10):1391-1393.

Lancet. 2007;370(9583):263-271.

3. Soter N. Chapter 23: Nummular eczema and lichen simplex chronicus/

17. Oji V, Luger TA. The skin in psoriasis: assessment and challenges. Clin Exp

prurigo nodularis. In: Freedberg IM, Eisen AZ, Wolff K, Austen FK, Goldsmith

Rheumatol. 2015;33(5 Suppl 93):S14-S19.

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Delayed Dx of Meningitis in Teenager Is physician-owner of medical clinic vicariously liable for not supervising a PA student? ANN W. LATNER, JD

Mr A was a university student enrolled in a PA program. As part of his studies, he was assigned to work in a medical clinic owned by Dr V. During his regular workday at the clinic, Mr A was supervised by Dr V or Ms F, the clinic’s on-staff PA. Miss K, a 17-year-old adolescent came into the clinic with complaints of intermittent headaches and a “hot” forehead that had been present for 2 or 3 days and managed with ibuprofen. In the examination room, Mr A introduced himself to the patient and her mother as a PA student and advised them that he was on a clinical rotation. He told them that he would be taking a history and performing a physical examination, with their permission. He then would present the information to his “preceptor or supervising physician,” who would then perform an independent examination and develop a plan for the patient. The patient and her mother agreed that Mr. A could proceed. In his chart notes, Mr A wrote that the patient had experienced “throbbing, lateral-frontal headaches 15 times a day.” Each episode would last 15 to 30 seconds. Miss K denied having weakness,

The plaintiff attorney presents the argument of respondeat superior, which holds that an employer can be vicariously liable for the acts of an employee.

paresthesia, fever, chills, weight loss, shortness of breath, neck or back pain, chest pain, nausea, or vomiting. He noted that the patient has type 2 diabetes. Palpation of the head and neck did not elicit tenderness and the patient’s neck exhibited full range of motion. Her lungs were clear. The patient was not in acute distress. Mr A noted a fast heartbeat and possibly a diastolic murmur. Mr A did not make a diagnosis and instead went to discuss the case with the supervising PA, Ms F. The clinicians discussed life-threatening illnesses that needed to be ruled out, including stroke, brain tumor, aneurysm, brain hemorrhage, and meningitis.After that, Ms F evaluated the patient, who again denied having any nausea, vomiting, or vision problems. Ms F noted that the patient was not distressed, and that her eyes, ears, nose, throat, and neck examinations were normal. Neurologic examination showed no abnormalities. 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. • THE CLINICAL ADVISOR • SEPTEMBER/OCTOBER 2021 47

LEGAL ADVISOR Ms F checked the patient’s heart and determined that she had a benign venous murmur rather than a diastolic murmur. The chart note was revised, with diastolic murmur changed to venous murmur and “tension headache secondary to stress” added. The patient was told to take acetaminophen as needed and to return to the clinic in a week if the headaches worsened or became constant or she developed nausea, vomiting, photophobia, body aches, or neck pain.

Fifteen days after the clinic visit, the patient complained to her mother about light sensitivity for the first time. The patient reported feeling better for the next 2 weeks with occasional headaches, which were treated with acetaminophen. Fifteen days after the clinic visit, the patient complained to her mother about light sensitivity for the first time. Two days later she had a fever and her headache worsened. The next day she began seeing double and her mother took her to the emergency department (ED). The ED physician conducted physical and neurologic examinations, both of which were normal. The physician was about to perform a lumbar puncture when the patient’s pupils dilated and she began having convulsions. It was later determined that she had coccidioidal meningitis. She suffered numerous strokes that caused permanent brain damage and left her paralyzed from the waist down. Legal Background

The patient’s mother hired a plaintiff ’s attorney and sued the original clinic, Dr V, and Ms F. [She also sued other defendants who settled.] The plaintiff alleged that Ms F had negligently failed to diagnose and treat the patient’s coccidioidal meningitis and that Dr V and the clinic were vicariously liable. The plaintiff also alleged that Dr V and his clinic were directly liable for their failure to supervise Mr A. The case went to a jury trial. Both sides had medical experts testify. The defense experts commended the PA student’s chart notes, calling them thorough.They believed that the patient’s diagnosis and treatment were appropriate given the facts that existed at the time. The plaintiff ’s experts stated that the physician should have conducted an examination, not the PA, and that the patient should have been sent to the hospital. The plaintiff also attempted to introduce expert testimony stating that the standard of care for medical practitioners required Dr V to supervise PA students directly, rather than have another PA

provide supervision, but the medical experts were unable to testify as to the legal requirements of student PA supervision. The jury found no negligence in the treatment of the patient by Ms F or the student PA and, thus, found no liability. The plaintiff appealed arguing the common law doctrine of respondeat superior, which holds that an employer can be vicariously liable for the acts of an employee. The appellate court disagreed and noted that since the jury had returned a verdict that Ms F was not negligent in the diagnosis or treatment of the patient, neither Dr V nor the clinic could be held vicariously liable for medical malpractice. The appellate court also would not entertain the plaintiff ’s claim of ordinary negligence, noting that there was only 1 cause of action for negligence, and it was based on an allegation of misdiagnosis. A general negligence cause of action would be redundant, noted the court. The appellate court affirmed the decision of the lower court and found the clinicians not liable. Protecting Yourself

In this case, the student PA did a comprehensive job examining the patient. Working together, the student and the clinic’s PA ruled out life-threatening conditions based on the patient’s symptoms. Was their diagnosis wrong? Yes. Was it based on solid facts at the time? Also yes. The reasonable diagnosis was made based on the patient’s condition and symptoms, which changed 2 weeks later. At her original clinic visit, the patient did not demonstrate light sensitivity, neck pain, nausea, or other symptoms that might have been indicative of meningitis. The diagnosis made was reasonable under the circumstances, and neither Ms F nor the student was found to have acted negligently in the treatment of the patient; thus, their employers could not be vicariously negligent. ■ Ann W. Latner, JD, a former criminal defense attorney, is a freelance medical writer in Port Washington, New York.

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