Triple-Negative Invasive Ductal Carcinoma in 34-Year-Old Woman

Dermatologic Look-Alikes

TABLE. Lichen Simplex Chonicus vs Psoriasis

Lichen Simplex Chonicus1-7

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

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

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

Potential risk factors

Etiology • 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)

Histology • 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

Diagnosis

Treatment • 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

Psoriasis8-17

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

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

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

• Clinical history and physical

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. ■

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.

References

1. Lotti T, Buggiani G, Prignano F. Prurigo nodularis and lichen simplex chronicus. Dermatol Ther. 2008;21(1):42-46. 2. Prajapati V, Barankin B. Dermacase. Lichen simplex chronicus. Can Fam Physician. 2008;54(10):1391-1393. 3. Soter N. Chapter 23: Nummular eczema and lichen simplex chronicus/ prurigo nodularis. 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. 4. Charifa A, Badri T, Harris BW. Lichen simplex chronicus. In: StatPearls. StatPearls Publishing; 2021. Accessed August 17, 2021. http://www.ncbi.nlm. nih.gov/books/NBK499991/ 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. 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. 15. Schleicher SM. Psoriasis: pathogenesis, assessment, and therapeutic update. Clin Podiatr Med Surg. 2016;33(3):355-366. 16. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;370(9583):263-271. 17. Oji V, Luger TA. The skin in psoriasis: assessment and challenges. Clin Exp Rheumatol. 2015;33(5 Suppl 93):S14-S19.

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LEGAL ADVISOR

CASE

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, 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.

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

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.

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.

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. ■

Fifteen days after the clinic visit, the patient complained to her mother about light sensitivity for the first time.

Ann W. Latner, JD, a former criminal defense attorney, is a freelance medical writer in Port Washington, New York.

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