Week 50: Dermatology Part 2

Measles (rubeola) is caused by a paramyxovirus and spread by respiratory contact. Measles begins with a prodrome of fever, coryza, cough, and conjunctivitis for several days followed by the development of a morbilliform rash. The rash starts with erythematous maculopapular lesions a few millimeters in diameter which become confluent. The rash typically starts on the face and spreads to the extremities. White spots on the buccal mucosa, known as Koplik spots, are pathognomonic for measles. Complications include otitis media, pneumonia, myocarditis, pericarditis, and encephalitis. Treatment is supportive. Choice A) is less specific than choice B). Choice C) is suggestive of roseola. Choice D) is more suggestive of hand foot & mouth disease

This patient presents with pityriasis rosea and should be treated symptomatically with antihistamines as the condition is self-limiting. Pityriasis rosea presents as scaly, salmon colored, oval papules or plaques 1 – 2 cm in diameter on the trunk and proximal extremities. It usually presents in children and young adults. Classically, the diffuse rash is preceded by a herald patch 1 week prior. This lesion is larger (2-5 cm in diameter) than the others that form. Patients may also initially have fever, malaise or lymphadenopathy prior to the appearance of a rash but this is rare. The diffuse form of the rash has a Christmas tree-like distribution following the cleavage lines of the skin. Pityriasis rosea is a self-limiting disease but may take 8-12 weeks to completely resolve. The causative agent is unknown although a virus is suspected (HHV 7). There is no specific treatment for the disease and so care should be directed at relieving symptoms, most commonly itching, with antihistamines.

Erythema nodosum is a condition in which patients develop painful red/violet nodules deep under the skin. It develops as a result of an inflammatory reaction between the dermis and adjacent adipose tissue. It is thought to be a delayed hypersensitivity reaction to various infections, drugs or systemic disease. Most commonly the lesions develop over the anterior tibia but can appear anywhere on the body. Before the development of the rash, the patient often complains of fever and arthralgias, particularly of the ankles. There are multiple diseases or infections associated with erythema nodosum, the most common of which is Streptococcal infections. Others include: tuberculosis, sarcoidosis, cocciodiomycosis, histoplasmosis, ulcerative colitis, enteritis, pregnancy, Yersenia enterocolitica, and Chlamydia. The disease is treated symptomatically (NSAIDs, elevation, stockings) and is typically self-limited.

Henoch-Schönlein purpura (HSP) is a small vessel vasculitis caused by the deposition of immune complexes in blood vessels. In approximately half of cases, it is preceded by an upper respiratory infection. It is also induced by vancomycin, cefuroxime and ACE inhibitors. HSP is characterized by palpable purpura as well as gastrointestinal and renal symptoms. The disease almost always occurs under the age of 20, and children under the age of 5 are more frequently affected. Classically symptoms appear 1-2 weeks after and upper respiratory infection. The triad of signs and symptoms is: purpura, arthralgias and abdominal pain. The purpura typically affect dependent regions of the body and therefore are seen on the legs and buttocks. Patients develop colicky abdominal pain and may even get hematochezia due to the gastrointestinal vasculitis. Rarely, enteroenteral intussusception occurs. Renal manifestations include glomerulonephritis presenting with hematuria, red cell casts and azotemia. Treatment is supportive.

The patient in the question stem has erythema multiforme, characterized by target lesions on the extremities, usually the palms and soles. It is most common in the 20-40 age group, and most cases are due to HSV infections. While drugs/medications can cause EM, it is more rare, but consider it in patients on the “SHNAP” drugs (Sulfa, Hypoglycemics, NSAIDs, AEDs, Penicillins). Treatment is largely supportive, though systemic steroids can be considered if the rash is diffuse or involves oral mucosa.

This patient is exhibiting symptoms and physical exam findings consistent with bullous pemphigoid. Bullous pemphigoid is a chronic bullous disease that involves IgG autoantibodies against the basement membrane (subepidermal). It is the most common bullous disease and is classically seen in adults over the age of 60 years. It may be caused by repeated skin trauma and presence of other inflammatory skin conditions such as psoriasis; however, it is often idiopathic. Signs and symptoms include a pruritic rash that evolves into tender, tense bullae occurring most often over the legs, forearms, and axilla. Mucosal involvement is uncommon. Nikolsky sign is negative. Diagnosis is made by needle biopsy to discriminate from pemphigus vulgaris; however, it may be differentiated clinically based on the differences between the two as pemphigus vulgaris includes oral involvement, flaccid bullae, and a positive Nikolsky sign while bullous pemphigoid does not. Management includes wound care, steroids, tetracycline, dapsone, and immunomodulators such as azathioprine, cyclosporine, and methotrexate. This disease process often improves and relapses spontaneously. Mortality, though rare, is most commonly caused by sepsis. Overall, bullous pemphigoid has a relatively good prognosis when compared to pemphigus vulgaris.

Burn center admission (A) would be appropriate if this patient were suffering from Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN); however, there is no evidence of recent infection or medication use and no description of sloughing skin. Additionally, Nikolsky sign is positive in SJS and TEN. Clindamycin (B) would be appropriate for necrotizing fasciitis, which may exhibit blistering but is also characterized by pain out of proportion to exam findings, crepitus, and gas in the tissues. These patients also tend to be febrile and have abnormal vital signs. Vancomycin (D) would be appropriate for inpatient treatment of cellulitis. This would be warranted if he had vital sign abnormalities or had failed outpatient treatment for cellulitis. Vancomycin should be reserved for instances for MRSA treatment.

The well-demarcated erythematous plaques and papules with silvery white scales are characteristic of psoriasis. Removal of the scale typically reveals pinpoint-bleeding areas referred to as the Auspitz sign. There is a hereditary predilection for the condition and often begins in the 2nd or 3rd decade of life.

Lesions tend to be symmetric and most commonly found on the trunk, scalp, nails (A), and extensor surfaces (C). Systemic steroids (D) should be avoided due to the risk of developing rebound or induction of pustular psoriasis.

The correct answer is topical corticosteroid and moisturizer. This patient’s presentation is most suggestive of atopic dermatitis, particularly due to his history of asthma and the involvement of the flexor surfaces. Treatment is geared towards reducing inflammation using topical steroids, as well as hydration of the skin. Atopic dermatitis in general has three age groups: infantile from infancy to two years, childhood from two to 12 years old, and adult stage for those older than 12. The infantile stage typically presnts on the extensor surfaces and cheeks and scalp and occasionally can have serous exudates. The childhood and adult stage typically involves flexor areas. Lesions are more typically lichenified due to the intense pruritus.

Stevens-Johnson syndrome is an autoimmune type IV hypersensitivity reaction that affects the skin and mucous membranes. Stevens-Johnson syndrome exists on a continuum with toxic epidermal necrolysis where Stevens-Johnson syndrome is defined as less than 10% total body surface area (TBSA) affected, while toxic epidermal necrolysis involves greater than 30% TBSA. The rash occurs most often on the trunk and is classically described as macular and target-like with two zones of color: purpuric at the core with surrounding erythema. However, the rash can also be vesicular, bullous, and necrotic. Ruptured bullae and desquamation place the patient at risk for secondary infection, which is the leading cause of death. Stevens-Johnson syndrome can also affect the renal, hepatic, and pulmonary organ systems. Mucosal involvement is often present as well, affecting the genitals, mouth, and eyes. Up to half of all patients will have eye involvement and early ophthalmologic consultation is necessary for patients with ocular symptoms. Risk factors include antibiotics (e.g., penicillins and sulfonamides), anticonvulsants (e.g., carbamazepine and phenytoin), and infection (e.g. upper respiratory infections). Treatment consists of stopping the offending agent and supportive care. These patients are often best cared for at burn centers.

This patient has classic contact dermatitis, and in this case the patient likely has an allergy to a metal contained in a belt-buckle or jean button. Patient’s will not always know they have an allergy to a particular substance, so be aware of anybody with a rash in areas of common contact with jewelry (e.g. ears/neck/wrist). It also commonly occurs on the hands of people who frequently wear gloves (healthcare workers/food service workers). Avoidance of the source agent, protection of involved skin, and treatment of inflammation is the treatment of choice for contact dermatitis. Because contact dermatitis is defined as patterns of skin reaction resulting from topical contact with external agents it is reasonable to begin management with measures that minimize continued or recurrent exposure to the known or suspected causative agent. The agent may be an irritant (such as solvents, caustics, and detergents) or an allergen (such as nickel in jewelry, soaps, cosmetics, rubber compounds, latex, and poison ivy, oak, or sumac). The cause may be readily identifiable via a detailed history and physical examination or may require eventual skin testing. Contact dermatitis may develop from brief but intense or repetitive low levels of exposure. Avoidance of continued or recurrent exposure may include measures such as substituting a different brand or type of a topical agent, avoiding the location of exposure, or even changing occupation. Protection of involved skin may include wearing gloves or clothing or use of a barrier cream when exposure is possible. The other initial component is treatment of inflammation. Oral antihistamines may be effective for control of itching, low to moderate potency topical steroids can be used on erythematous areas, and cool compresses with aluminum acetate solutions can be used on oozing or vesiculated skin to treat inflammation. Steroid use can sometimes be delayed until patient follow-up to ascertain whether avoidance and protective measures alone have been adequate.