Chapter 7. Dermatology

Clinical Features

Urticaria, or hives, are pruritic raised erythematous superficial skin wheals that arise in response to histamine, leukotrienes, prostaglandins, and other substances released by stimulated mast cells. Lesions develop and resolve quickly; individual lesions should resolve in < 24 hours. Urticaria is often associated with hypersensitivity reactions, including anaphylaxis. Symptoms are characterized as acute if they occur daily for < 6 weeks, and chronic if they occur for longer. Triggers can include allergic reactions to drugs, foods, insect stings, and rarely aeroallergens. Urticaria can also be caused by physical stimuli including cold, heat or exercise (cholinergic), pressure, vibration, and sun exposure. Infections including hepatitis, EBV, helminthes, and fungi have been associated with urticaria. Patients with collagen vascular diseases often develop urticaria. Differential diagnosis includes mastocytosis/urticaria pigmentosa, erythema multiforme, bullous skin disorders, or dermatitis herpetiformis. Obtaining a detailed history can help find an etiology. Urticaria that has been occurring for < 6 weeks usually does not require any laboratory workup. Laboratory tests may be done as indicated for chronic urticaria. Helminth infections would be associated with very high eosinophilia.

Emergency Department Treatment and Disposition

Attempt to identify the trigger based on a thorough history. Advise patients to discontinue or avoid the offending agent, if known. The main form of treatment includes H1 blockers (eg, diphenhydramine) given intravenously (IV) or orally. Second-generation antihistamines (eg, cetirizine) can be used once or twice a day until symptoms resolve. H2 blockers (eg, cimetidine, ranitidine) may be combined with H1 blockers. For patients with severe urticaria, interventions may include epinephrine given subcutaneously, corticosteroids given IV as hydrocortisone or methylprednisolone, or oral prednisone given first bolus followed by once-daily dose. Suspected anaphylaxis should be treated accordingly. Patients should be educated and sent home with injectable epinephrine. Urticaria can be very frustrating for the patient, and referral to an allergist can often help with management and investigation for the trigger.

Pearls

1. Urticaria is characterized by erythematosus, edematous lesions that are pruritic and evanescent.

2. If the lesions last longer than 24 hours, leave a mark, or are painful rather than pruritic, refer the patient for skin biopsy to rule out urticarial vasculitis.

3. The underlying cause for chronic urticaria is rarely found.

The authors acknowledge the special contributions of Binita R. Shah, MD, to prior edition.

Clinical Features

Angioedema is a swelling of the deeper dermal subcutaneous tissue. Commonly affected areas include the extremities and face, specifically lips and tongue. Airway involvement may occur and is life-threatening. It is often painful rather than pruritic. Angioedema occurs secondary to release of various mediators including histamine, leukotrienes, and prostaglandins from stimulated mast cells or abnormalities in the complement or arachidonic acid pathways. Angioedema, like urticaria is often associated with hypersensitivity reactions, including anaphylaxis. Chronic angioedema describes symptoms that last longer than 6 weeks. Triggers may include allergic reactions to drugs, foods, and insect stings. Certain medications including ACE inhibitors often cause a non–IgE-mediated reaction manifesting as angioedema. Hereditary angioedema presents as spontaneous recurrent attacks of angioedema often triggered by trauma. There are 3 genetic types, the most common is inherited in an autosomal dominant fashion; however, many patients have spontaneous mutations. This disorder is characterized by abnormal levels or function of C1 esterase inhibitor. Patients often present with initial attacks around puberty and many have isolated visceral angioedema that mimics an acute abdomen. Patients often report episodes of swelling worsening over a period of 12 to 24 hours, usually with resolution within 3 to 5 days. The swelling may migrate to different areas. The edema is usually unresponsive to antihistamines. Attacks are usually periodic and are commonly followed by weeks of remission. Laboratory screening is accomplished by obtaining a C4 level that is low during attacks. Further testing with C1 esterase inhibitor level or functional C1 esterase inhibitor assays can be used for confirmatory diagnosis if initial C4 screen is low.

Emergency Department Treatment and Disposition

Anaphylaxis should be treated emergently. For hereditary angioedema, treatment includes supportive care and pain management. Patients presenting with breathing difficulty due to laryngeal swelling may need elective intubation. Epinephrine or corticosteroids may help some patients. Refer the patient to an allergist for continuity of care and management. Long-term treatments include synthetic androgen steroids, for example, danazol and stanozolol, which may be considered in older children after careful consideration of the side effects.

Pearls

1. Patients with hereditary angioedema usually do not develop urticaria.

2. Family history is important when considering hereditary angioedema.

3. Children with hereditary angioedema may present with severe abdominal pain mimicking acute abdomen and often undergo unnecessary abdominal surgeries.

Clinical Summary

Serum sickness is an immune complex–meditated type III hypersensitivity reaction, produced by exposure to a variety of agents. It is characterized by fever, joint involvement, skin rash, lymphadenopathy, splenomegaly, arthralgia, and proteinuria. The classic serum sickness is rarely seen nowadays and can be caused by blood products (eg, human γ-globulin) and animal-derived serum (eg, antitoxins for treatment of spider and snake envenomations [eg, Crotalidae antivenin], antitoxins for clostridial intoxication [eg, botulism, gas gangrene], and antirabies serum). Diagnosis is suspected based on history of an exposure to a foreign antigen.

Serum sickness–like reaction is a drug reaction that can be seen 1 to 3 weeks, after exposure to the etiologic agent. The mechanism of this reaction is not well understood. The most commonly associated medication in children is cefaclor. Other medications have been implicated, including penicillins, cephalosporins, sulfa drugs, minocycline, propranolol, bupropion, and griseofulvin. Cutaneous morphology can be urticarial, morbiliform, or erythema multiforme-like. Other features are joint swellings, arthralgia, fever, and lymphadenopathy. Unlike classic serum sickness, frank arthritis, hepatic, renal and CNS involvement are rarely seen. Skin biopsy is not necessary to make the diagnosis. Differential diagnosis includes urticaria, erythema multiforme, vasculitis, and drug reactions.

Emergency Department Treatment and Disposition

The majority of serum sickness–like reactions are self-limited and resolve in 2 to 3 weeks without sequelae in most cases. Patients can be managed by discontinuation of the offending agent (if still receiving it), antihistamines, and nonsteroidal anti-inflammatory drugs as indicated. A short course of systemic corticosteroids may be used in severe cases of arthralgias and myalgias.

Pearls

1. Drugs are the most common cause of serum sickness–like reaction especially the cephalosporin Cefaclor.

2. Typical cutaneous reactions seen in serum sickness–like reactions are urticarial, morbilliform, or erythema multiforme–like eruptions.

Clinical Summary

Erythema multiforme (EM) is an acute hypersensitivity reaction that occurs in response to various etiologic agents such as infections (especially Herpes simplex 1 & 2) and rarely drugs. It is self-limited but potentially recurring. Herpes simplex virus is the most common cause; others include mycoplasma, parapoxvirus, and histoplasma. EM is classified into minor and major types, which can be distinguished by the presence or absence of mucosal lesions. EM minor has no or mild mucosal involvement versus EM major, which has severe involvement of one mucosal surface. The classic EM lesion is a target “iris” lesion characterized by 3 zones. The innermost zone consists of dusky purpura, hemorrhagic crust, or blistering; the middle zone, the largest, is pale pink and edematous, whereas the outermost zone is composed of a ring of erythema. Occasionally, atypical targetoid (composed of 2 zones only) papular lesions can be present. The classic distribution of EM lesions is extremities (especially elbow, knees, wrists, and hands), palms and soles, with few truncal lesions. The skin lesions are symmetrically distributed and tend to be fixed for more than 5 days.

Systemic symptoms are mild or absent. Active herpes simplex lesions or a past history of herpes may be positive. Differential diagnosis of EM includes urticaria (lesions not target-like and transient), urticaria multiforme, drug eruptions, subacute lupus erythematosus, and vasculitis. If diagnosis is unclear, dermatology consult followed by skin biopsy is indicated.

Emergency Department Treatment and Disposition

No specific therapy is required for EM minor, which is a self-limited disorder. Acyclovir may be given if active herpes simplex lesions are present. Antihistamines, antipyretics, topical steroids (eg, desonide cream bid) can be given for symptomatic relief. Typical patients with EM minor are usually not severely ill and can be managed as outpatients with follow-up with a primary care provider. Systemic steroids may be considered for severe cases of EM major (eg, prednisone 1-2 mg/kg/d divided once or twice daily for 5-14 days). Prophylactic oral acyclovir can be used for recurrent HSV-induced EM. Prompt treatment of HSV infections in such patients will prevent EM.

Pearls

1. EM is a separate entity from Stevens-Johnson syndrome and toxic epidermal necrolysis (TEN). EM does not progress to Stevens-Johnson syndrome or TEN.

2. EM is referred to as multiforme because the morphology of lesions is so variable.

3. EM lesions are fixed unlike urticaria, and EM lesions may expand, but they remain on the same body part for 4 to 7 days.

4. Target or “iris” (with 3 concentric zones) lesions are pathognomonic of EM; however, not all patients with EM will have such lesions. Some of these lesions may be targetoid (with 2 zones) or papular lesions.

5. EM lesions are distributed mainly on the extremities including palms and soles with either none or only one mucosal surface involvement.

6. Patients with HSV-associated EM may develop target lesions on the lips associated with lip necrosis that can mimic Stevens-Johnson syndrome.

Clinical Summary

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are part of a spectrum of hypersensitivity disorders with similar etiologies (most commonly drugs) and can be severe and life-threatening. SJS is the milder form and TEN more severe. In SJS, skin and at least 2 mucosal surfaces are involved. SJS has severe mucosal surface involvement as compared to TEN, whereas epidermal detachment is much more in TEN. Depending on area of epidermal denudation, a 3-grade classification has been proposed: SJS (<10% body surface area [BSA]), overlap SJS-TEN (10%-30% BSA), and TEN (>30% BSA). The most commonly implicated drugs are NSAIDS, antibiotics (penicillins, sulphonamides), and antiepileptics (phenytoin, carbamazepine).

The incubation period is usually 1 to 21 days and prodromal symptoms and mucosal surface involvement may occur before rash and epidermal detachment begins. Clinical features include fever, malaise, upper respiratory tract symptoms, skin pain, and mucocutaneous lesions. The cutaneous lesions are targetoid with dusky purpura, truncal and central in distribution, and with a tendency to coalesce. There may be areas of epidermal detachment and a positive Nikolsky sign. Mucosal surfaces of the eyes, oral cavity, and upper gastrointestinal tract, respiratory tract, and genitals may show blisters, hemorrhagic crusts, painful erosions, and ulcerations.

Diagnosis is usually made clinically. Leukocytosis, elevated ESR, and liver enzyme abnormalities may be present. Frozen-section biopsy of the skin may be performed for confirmation of the diagnosis. Hematoxylin-eosin (H&E) staining of the frozen section of the exfoliating skin will show a full-thickness epidermal necrosis.

Complications include secondary bacterial infection, fluid and electrolyte imbalances, and scarring and strictures of the skin and mucosal surfaces. Ocular sequelae include symblepharon, corneal ulceration, and blindness. The course is protracted over 3 to 6 weeks with a mortality rate ranging from 1% to 5% for SJS and 15% to 35% for TEN.

Emergency Department Treatment and Disposition

Hospitalize all patients with suspected diagnosis of SJS or TEN preferably to a burn unit or ICU. Discontinue all drugs introduced within the past month, and do not introduce drugs of a similar class unless the risk of abrupt discontinuation is too high. For example, phenobarbital, carbamazepine, and phenytoin share a common metabolic pathway (cytochrome P450) and may induce a cross-reaction; thus, all 3 drugs are contraindicated after SJS/TEN resulting from any one of them. Obtain urgent dermatology, ophthalmology, urology, and ENT consultations. Supportive care includes management of fluid and electrolytes, pain, thermoregulation, nutritional support, and meticulous skin care (gentle saline soaks and petrolatum gauze to provide barrier over denuded areas). Do not use silver sulfadiazine in patients with sulfonamide-induced SJS or TEN. Provide reverse isolation to prevent secondary bacterial infection. Prophylactic use of systemic antibiotics is not recommended. Systemic corticosteroid use is controversial (risk of increased morbidity and mortality; hence routine use is discouraged). The current and newly recommended therapy is IV IG given as 1 g/kg/d daily for 3 days. It helps to reduce development of new blisters and helps to arrest the progression of the disease. (IV IG should be free of any IgA to prevent hypersensitivity reaction in IgA-deficient individuals.)

Pearls

1. Most common etiology for SJS and TEN are drugs, while most common etiology for EM is herpes simplex virus.

2. In children, SJS is more commonly seen than TEN. Incidence of TEN is more common in human immunodeficiency virus (HIV) patients.

3. Differential diagnosis of TEN includes staphylococcal scalded skin syndrome (SSSS). TEN is full-thickness epidermal necrosis and denudation, whereas SSSS is a superficial peeling of skin (within the epidermis, below the stratum corneum). Hence, complications are much more grave and severe in TEN.

4. Both SJS and TEN are potentially life-threatening diseases because of multisystem involvement.

Clinical Summary

Drug-induced hypersensitivity syndrome (DIHS) is a subset of adverse drug eruptions, which occur 1 to 21 days after starting a new medication, whereas it takes only a few days for the reaction to occur following second exposure to the same class of medication. The most commonly implicated drugs are antibiotics (penicillins, sulfonamides), antiepileptics (phenytoin), NSAIDS, antihypertensives, and anti-HIV medications, though any drug can cause an adverse reaction. Cross-reactivity is common among different drugs of same class of medications. Drug reactions are more common in HIV-positive individuals. Exanthematous (maculopapular or urticarial) reaction is seen most commonly, and has a widespread, bilateral and symmetric distribution that may involve the palms and soles. Fever, malaise, and mild mucosal surface involvement may be the presenting symptoms. In a variant known as drug reaction with eosinophilia and systemic symptoms (DRESS), the exanthematous drug rash is associated with fever, facial edema, and involvement of at least one internal organ (liver commonest) with eosinophilia. The incubation period of DRESS is usually 2 to 6 weeks and it takes weeks to subside, even after drug withdrawal. Another variant is acute generalized exanthematous pustulosis (AGEP), which is an acute eruption characterized by multiple tiny pustules that heal in 4 to 10 days with desquamation. This is considered an adverse eruption to medications or vaccine administration. The closest clinical differential diagnosis is a viral exanthem. Eosinophilia is more common in drug eruption than viral exanthems.

Emergency Department Treatment and Disposition

The diagnosis is clinical, and a detailed current and previous drug history with time charting is mandatory to pinpoint the offending drug. If clinical suspicion of an adverse drug reaction is high, discontinue the suspected offending drug. Laboratory tests include CBC, liver enzymes, and urinalysis. Hospitalize children with severe skin findings, evidence of systemic involvement, or inability to maintain hydration (eg, during erythrodermic phase). A dermatology consultation would assist in such decisions. Biopsy of the skin reveals a dense infiltrate of the papillary dermis, which is composed mostly of lymphocytes and occasionally of eosinophils. Treatment is mostly supportive and includes skin care (eg, topical steroids to alleviate symptoms), prevention of infection, and treatment of any complications. Oral or IV steroids are sometimes used in patients with severe systemic involvement and in DRESS, to prevent complications.

Pearls

1. DIHS is often misdiagnosed as a viral infection. Prompt recognition and discontinuation of the drug is of the utmost importance in preventing or minimizing the severity and duration of internal organ involvement.

2. AGEP is an acute exanthematous drug eruption, characterized by fever, multiple sterile pustules that subside spontaneously with desquamation. In children, it occurs following a viral exanthem, vaccine administration, or rarely drugs.

Clinical Summary

Henoch-Schönlein purpura (HSP) is a small vessel vasculitis characterized by palpable purpura, arthritis, gastrointestinal (abdominal pain), and renal manifestations (glomerulonephritis) and seen in children age 2 to 11 years. About 50% of patients have preceding respiratory infection; mainly group A beta hemolytic streptococcal infection. Other implicated pathogens include hepatitis B virus, adenovirus, mycoplasma, herpes simplex virus, parvovirus, and HIV. Certain foods, drugs, exposure to cold weather, and insect bites are other predisposing factors. Palpable purpura on lower extremities bilaterally is the presenting sign, and new lesions may develop in crops. This may be associated with fever, joint swelling and arthralgia, abdominal pain, bloody stools, and hematuria.

Diagnosis is clinical. CBC may show leukocytosis, thrombocytosis, and anemia. ESR may be elevated and serum complement levels depressed. Antistreptolysin antibodies are positive in about 50% of cases. Perform urinalysis (may show gross or microscopic hematuria, proteinuria, white blood cells, and casts), and stool guaiac to screen for renal and gastrointestinal involvement. Use ultrasound to evaluate for intussusception and Doppler flow studies to evaluate scrotal problems. In doubtful cases, skin biopsy helps to confirm leukocytoclastic vasculitis.

Complications include bowel obstruction or perforation, intussusceptions, nephrotic syndrome, azotemia, oliguria, chronic glomerulonephritis, hypertensive encephalopathy, central nervous system (seizures, coma, paresis), and acute scrotum (mimicking acute testicular torsion).

Emergency Department Treatment and Disposition

There is no specific treatment. The majority of cases are self-limiting, and symptoms resolve in a few weeks without permanent residua. Supportive, symptom-directed treatment includes bed rest, bland diet, and NSAIDs for relief of arthritis and fever. Elevation of the scrotum helps scrotal edema. Hospitalize any patient presenting with complications (eg, hypertension, oliguria, intestinal obstruction, or gastrointestinal bleeding). Remove the offending antigen, if identified (eg, drugs). Treat the infection if identified (eg, group A B-hemolytic streptococcus). Systemic corticosteroids are indicated for systemic involvement such as severe arthritis, renal involvement, gastrointestinal tract complications, and acute scrotum or CNS complications. Corticosteroid therapy does not prevent recurrences, which are usually seen in up to 50% of cases within the first few months (milder and more common in patients with nephritis). Long-term morbidity and mortality is attributed almost exclusively to renal disease. Serial urinalyses and follow-up of renal functions are recommended, if the initial tests show any abnormalities.

Pearls

1. HSP is the most common cause of nonthrombocytopenic purpura.

2. The classic finding is palpable purpura seen most prominently on the lower extremities.

3. Long-term morbidity and mortality is attributed almost exclusively to renal involvement.

4. Arthritis or gastrointestinal symptoms may precede the appearance of rash by up to 2 weeks.

5. Testicular involvement occurs in up to 35% of patients, and acute scrotal swelling may present prior to purpura and can mimic acute testicular torsion or incarcerated inguinal hernia.

Clinical Summary

Seborrheic dermatitis is an inflammatory disorder commonly seen in infancy and adolescence. Affected areas include the scalp, face, retroauricular areas, mid-chest, axillae, groins, and other intertriginous areas where sebaceous glands are prominent. It is characterized by an erythematous, greasy scaly scalp (cradle cap). Lesions may be present in the diaper area including folds (which is spared in atopic dermatitis). Petaloid erythematous noneczematous scaly oval plaques may be present on the trunk, back, and flexures. Secondary monilial infection (due to colonization with Candida albicans) and secondary bacterial infections are common, especially in the diaper area. Peak occurrence in infancy is at 3 months of age and usually starts to resolve around 8 to 12 months of age. Differential diagnosis includes atopic dermatitis, Langerhans cell histiocytosis, and immunodeficiency disorders. Overlap of atopic dermatitis and seborrheic dermatitis is quite common in infants. Lack of response to topical steroids in suspected atopic dermatitis in an infant should raise the suspicion of seborrheic dermatitis.

Emergency Department Treatment and Disposition

For infants, minor amounts of scale are easily removed by frequent shampooing with products containing sulfur, salicylic acid (eg, Sebulex shampoo), or ketoconazole shampoo. Warm mineral or olive oil compresses followed by washing several hours later and lifting off the scale with a fine-toothed comb may be helpful for scales that are dense, thick, and adherent. For older children and adolescents, antiseborrheic shampoos containing selenium sulfide (eg, Selsun blue), zinc pyrithione (eg, Head & Shoulders), coal tar (eg, Neutrogena T/Gel), or ketoconazole (eg, Nizoral) can be used intermittently (eg, 2-3 times per week). Instruct the patient/parent to lather the shampoo and let it sit on the scalp for 5 to 10 minutes before rinsing. If there is evidence of inflammation, application of a topical low- to mid-potency corticosteroid solution to the scalp and cream to nonhairy inflamed areas, is indicated. Caution patients that topical steroids should not be used as maintenance therapy. Topical antifungal agents are also effective.

Pearls

1. Seborrheic dermatitis is the most common rash in the first few months of life.

2. Suspect coexisting atopic dermatitis when lesions are weeping and associated with pruritus.

3. With pronounced localized scaling, seborrheic dermatitis may resemble psoriasis.

4. Seborrheic dermatitis is one of the most common cutaneous manifestations of AIDS in older children and adolescents, and onset usually occurs before AIDS symptoms.

5. Seborrheic dermatitis is a self-limiting disorder and does not cause permanent or scarring alopecia of the scalp.

Clinical Summary

Allergic contact dermatitis results from exposure to a topical allergen by a sensitized individual. Percutaneous absorption of an allergen leads to specific T lymphocytes carrying the immune memory to recognize the antigen as a foreign material. Re-exposure to the same allergen results in proliferation of sensitized T lymphocytes that release inflammatory mediators, leading to a localized eczematous dermatitis. The most common contact allergens include plants (eg, urushiol in poison ivy, poison sumac, poison oak), nickel (eg, jewelry, metal wrist band, snap buttons of trouser jeans), shoe materials (eg, rubber and leather [potassium dichromate used for tanning leather]), thimerosal (a preservative in eye drops and vaccines), fragrances, cosmetics, and topical medications (eg, preparations containing neomycin). Allergic contact dermatitis is seen in children and first exposure to an allergen may occur as early as in infancy.

Diagnosis is based on distribution and morphology of the lesions (eczematous, vesiculation, oozing, and in chronic lesions lichenification) and history of exposure. Sharp demarcation between normal and affected skin, with linearity, suggests allergic contact diagnosis. A patch test, done by a dermatologist (if etiology not apparent), can help with a diagnosis. A positive test shows erythema and papules confined to the test site.

Emergency Department Treatment and Disposition

Once allergic contact dermatitis has been diagnosed, identification and elimination of the allergen (eg, removal of nickel jewelry), and avoidance of further exposure is necessary. Antihistamines are used (eg, hydroxyzine) to control the pruritus. Avoid use of topical diphenhydramine, as it is a sensitizer (with prolonged use, the patient may develop sensitization). Topical high- or mid-potency corticosteroid cream applied twice a day for 2 to 3 weeks, with avoidance of allergen, treats the condition. Rarely, systemic steroids may be needed (eg, in cases caused by poison ivy, prednisone 1-2 mg/kg/d tapered over 2 to 3 weeks, helps to control the acute inflammation). For poison ivy, if possible provide/show a picture of the offending plant for patients and family members so they can avoid further exposure. When outdoors, advise using a barrier cream (eg, Ivy Shield), which blocks the resin from touching the skin and washing the exposed area immediately, if accidental exposure occurs. Recurrences are common if the suspected allergen is not eliminated completely; thus all the ingredients (even in the minutest of proportions) in the suspected allergen should be avoided.

Pearls

1. Diagnosis is based on the history of exposure and the pattern of the rash (eg, a symmetrical erythematous rash on both ear lobes in a patient wearing nickel earrings).

2. One of the most common contact allergens in chidren is urushiol, the sensitizing antigen found in poison ivy.

3. A thorough history is the most important step in management and includes inquiring about animal exposure. Poison ivy dermatitis can result from touching an animal exposed to the plant.

4. Autosensitization dermatitis (Id eruption) occurs as acute papulovesicular pruritic symmetric eruptions on the trunk, forearms, extensor surfaces, and rarely on the face and is a hypersensitive reaction to acute dermatitis and bacterial or fungal infections.

5. Koebner phenomenon (isomorphic phenomenon), in which trauma elicits similar lesions, is also seen in an Id eruption. The diagnosis is clinical and treatment of the primary dermatitis is crucial. Open wet compresses, antihistamines, and topical steroids may also help.

Clinical Summary

Atopic dermatitis (AD) is an eczematous dermatitis manifested as a result of persistent inflammation of the skin. It is often associated with allergic diseases like asthma and allergic rhinitis and manifests as acute, subacute, and chronic dermatitis. Diagnosis is based on classic morphology and distribution of dermatitis depending on the age group. The infantile phase is from 2 months to 2 years, characterized by severe pruritus, oozing, vesiculation, eczematous papules, plaques seen on the face, scalp, extensors of extremities, and trunk. During infancy, the sparing of groin and diaper area helps to differentiate infantile atopic dermatitis from seborrheic dermatitis. The childhood phase lasts from 2 years of age to puberty and is characterized by dry scaly, lichenified pruritic plaques, seen on the antecubital fossae, popliteal fossae, periorbital and perioral areas, wrists, hands, and feet. The adult phase begins at puberty and continues into adulthood and is characterized by chronic pruritic lichenified plaques present on the flexors, neck, face, trunk, hands, and feet. Nummular eczema is a variant of AD characterized by discoid, well-circumscribed, annular plaques, commonly seen on the extremities. Associated features of AD include pityriasis alba, periorbital darkening, ichthyosis vulgaris, white dermographism, keratosis pilaris, and hyperlinear palms. Elevated serum IgE with peripheral eosinophilia may be seen. Secondary bacterial and viral infections are common.

Emergency Department Treatment and Disposition

The majority of patients with AD are treated as outpatients. Management consists of establishing realistic parental expectations that AD is a chronic disorder that involves remissions and exacerbations. Goals of therapy are to control the flare-ups, prevent secondary infections, and keep the skin barrier function intact by constant moisturizing. Advise patient to avoid trigger factors like hot water, heat, allergens like dust mites, pollens, molds, foods like eggs and peanuts, materials like wool and fur, exposures to animals (eg, dogs, cats) or items filled with feathers or down (eg, pillows), stress, and infections (eg, Staphylococcus aureus, herpes simplex, dermatophytes). Advice on constant and regular care of the dry and xerotic skin includes daily moisturizing, brief baths or showers in lukewarm water lasting not more than 5 to 10 minutes, use of a mild unscented soap or liquid gentle skin cleanser (eg, Dove fragrance-free soap, Aveeno), patting (don’t rub) the skin dry, leaving some moisture. Moisturizers (eg, Vaseline, Aquaphor) are applied all over the skin, as soon as the child gets out of the bath or shower to trap moisture in the skin. Moisturizers should be applied to the entire body 2 to 3 times a day. Mid- to high-potency topical steroids are used for body areas (except groin, face, axillae). Mild topical steroids are used for face, groins, and axillae but not more than 2 to 3 weeks at a stretch. Topical antibacterial agents (eg, mupirocin) can be used if there is any evidence of excoriations or open wounds. If the infection is severe, oral antibiotics for 7 to 10 days can be used. Topical immunomodulators like pimecrolimus 1% or tacrolimus 0.03% or 0.1% ointment can be used as steroid-sparing agents. Antihistamine (eg, hydroxyzine) is used for control of the severe itch that causes the rash. Patient should be referred to a primary care physician or dermatologist for ongoing care.

Pearls

1. Atopic dermatitis is the “itch that rashes.” Pruritus, xerosis, and eczema are prominent features of AD.

2. Hospitalization is indicated for eczema herpeticum, generalized erythroderma, severe AD with compromised skin barrier causing failure to thrive or severe flare-ups unresponsive to conventional treatment.

3. Moisturizers form the mainstay of therapy. Topical steroids, antibacterials, and avoidance of trigger factors are the other pillars of the therapy.

Clinical Summary

Eczema herpeticum (EH) is a disseminated cutaneous herpes simplex virus (HSV) infection superimposed on a preexisting active skin condition. A likely cause is the impaired skin barrier in active atopic dermatitis, which allows viral particles to incubate and proliferate quickly, leading to severe dissemination. EH is most commonly caused by HSV-1, and less commonly by HSV-2. Though most commonly seen in patients with atopic dermatitis, it can also occur with other primary dermatologic disorders (eg, seborrheic dermatitis, irritant contact dermatitis, pemphigus, burns, ichthyosis vulgaris, skin grafts). A history of contact with a family member with recurrent oral/facial HSV infection is often found. Clinically, monomorphous vesicles, pustules, and erosions may be seen on a preexisting dermatitis. There may be multiple punctate erosions, some coalescing to form larger polycyclic erosions. EH is more commonly seen on the face, neck, and chest areas and can lead to fatality in infants and young children, if not treated promptly. The diagnosis is usually clinical but can be confirmed by direct fluorescent antibody assays, Tzanck smear, viral culture, and viral DNA polymerase chain reaction for HSV. Complications include secondary bacterial infection (Streptococcus pyogenes and S aureus), keratoconjunctivitis, viremia, and scarring.

Emergency Department Treatment and Disposition

High index of suspicion for EH in patients presenting with a history of “worsening” atopic dermatitis is an important step necessitating DFA or Tzanck smear (DFA preferred over Tzanck because of superior sensitivity, rapid turnover) and viral culture, if diagnosis is uncertain. Dermatology consultation will be valuable in such cases. Ophthalmology consultation is mandatory for involvement of or near the eyes. Hospitalization of infants and young children with EH is indicated in severe cases to prevent complications with prompt administration of IV acyclovir till lesions crust over. Maintaining hydration and skin care are also important. Bland emollients may be applied to the affected areas. Mild cases of EH can be managed as outpatients with acyclovir given orally with a very close follow-up by a primary care physician or a dermatologist. Antistaphylococcal antibiotics should be given along with acyclovir either IV (severe EH requiring hospitalization) or oral or topical mupirocin may be used with early localized mild cases not requiring hospitalization.

Pearls

1. “Punched out” erosions superimposed on a preexisting active dermatitis-like atopic dermatitis are important clues.

2. Suspect EH when infected-appearing eczema does not respond to appropriate antibiotic therapy; this may indicate HSV infection.

3. Appropriate acyclovir dosing and skin care is key to prompt recovery from EH.

Clinical Summary

Psoriasis is a chronic polygenic skin disorder characterized by well-circumscribed, erythematous plaques with an overlying silvery-white scale affecting about 2% of the general population. The most common clinical variant is plaque psoriasis. Patients often experience a waxing and waning course. Precipitating factors include minor trauma (Koebner phenomenon) infection, stress, and drugs. In the severe form of generalized pustular psoriasis, patients are often ill-appearing with fever, generalized erythema, and pustules. Onset is acute and most patients have an antecedent nonpustular psoriasis or a genetic predisposition. Episodes may be precipitated by pregnancy, medications (ie, coal tar, lithium), hypocalcemia, or withdrawal of both topical and systemic steroids. Relapses are common.

Diagnosis is usually clinical and skin biopsy confirms the diagnosis. Complications include generalized exfoliative dermatitis (erythroderma) and psoriatic arthritis. Differential diagnosis includes nummular eczema, tinea corporis, pityriasis rosea, pityriasis rubra pilaris, contact dermatitis, lichen simplex chronicus, Reiter syndrome, psoriasiform drug eruptions, and other conditions of the scalp including seborrheic dermatitis, tinea capitis, and atopic dermatitis.

Emergency Department Treatment and Disposition

Admit patients with severe forms (eg, generalized pustular psoriasis, a serious and at times a fatal disease). Educate parents about the chronic nature of the condition and relapses and remissions. The goal of therapy is to control flare-ups. Advise patients on gentle skin care including lukewarm brief baths (with bath oil or coal tar), gentle soaps, avoiding trauma or scratching the lesions, and use of emollients for skin hydration (eg, Vaseline, petrolatum, mineral oil). For thick scalp lesions, use shampoo 2 or 3 times per week (coal tar, selenium sulfide, or zinc pyrithione). Sunlight exposure helps psoriasis; however, patients should be cautioned to avoid sunburn as this may aggravate their condition. Consider topical corticosteroids creams for management of acute flairs. Low-potency steroid creams may be used on the face and groin (not more than 2 weeks) and medium-potency steroid creams on other body parts (not more than 2 weeks). High-potency steroid creams (not for more than 2 weeks) are reserved for older children and adolescents with severely affected areas. Consider antibiotics (eg, penicillin, cephalexin) when a pharyngitis or perianal cellulitis is suspected as precipitating a guttate flare (see Figure 7-51) and obtain cultures for confirmation. Refer all patients to dermatology. Other therapeutic options in refractory cases include topical vitamin D analogue creams or retinoids, phototherapy, or oral therapies that include, retinoids, methotrexate, or cyclosporine. Biologic agents (ie, etanercept, infliximab) are the newest class of medications being used for treatment.

Pearls

1. Koebner phenomenon (new lesions at the site of trauma) is an important feature of psoriasis.

2. Psoriasis may be seen as early as the first months of life. Diaper area is commonly involved.

3. Pinpoint bleeding where scale is removed (Auspitz sign) is highly characteristic.

4. Involvement of nails is also an important feature and includes nail pitting, oil spots, subungual hyperkeratosis, and onycholysis (detachment of the distal nail plate).

Clinical Summary

Guttate psoriasis is a variant characterized by an abrupt onset of profuse oval or round “guttate” or drop-like lesions, most commonly following group A β-hemolytic streptococcal infections (ie, streptococcal pharyngitis, perianal streptococcal dermatitis, otitis, or sinusitis). Streptococcal pharyngitis or a viral URI precedes the eruption of guttate psoriasis by 1 to 3 weeks.

Emergency Department Treatment and Disposition

Laboratory tests should include a throat culture and serological titer (eg, antistreptolysin O titer) to confirm streptococcal infection, and if infection is confirmed, give antibiotics. The drug of choice is penicillin. Erythromycin or clindamycin are good alternatives for penicillin allergy. Refer the patient to a dermatologist for ongoing care. Guttate psoriasis may resolve spontaneously in a few weeks or months, especially with antibiotic therapy. Tonsillectomy or monthly injections of benzathine penicillin may be helpful if flares are precipitated by recurrent streptococcal infections. Exposure to sunlight and broadband or narrowband UVB phototherapy also helps in resolution of lesions. For persistent lesions, the same therapy as that for psoriasis is recommended.

Pearls

1. Guttate psoriasis is a variant seen more commonly in children and adolescents and may herald the development of generalized plaque psoriasis.

2. Guttate psoriasis is characterized by an abrupt onset of drop-like lesions, mainly on the trunk, buttocks, hips, and proximal extremities.

Clinical Summary

Pityriasis rosea (PR) is a benign eruption of unknown etiology (presumed viral) with a distinct presentation of a solitary “herald patch” lesion followed by an exanthema. About 50% of cases occur before age 20 with highest incidence among adolescents. It is rare in children aged < 5 years. It is commonly seen during the fall, winter, and spring. About 5% of patients have a prodrome of fever, malaise, arthralgia, and pharyngitis preceding the PR eruption (usually seen with florid PR). Atypical clinical variants of PR are seen in about 25% of cases and include

1. Papular PR (especially in African American children)

2. PR with intensely irritated or inflamed edematous lesions

3. “Inverse form of PR,” which includes lesions limited to face, scalp, distal extremities, groin, and axillae

4. PR with vesicular, pustular, urticarial, or hemorrhagic (purpuric) or large annular erythema multiforme-like lesions

5. PR with oral lesions.

The diagnosis is made clinically and rarely a skin biopsy (to exclude other diseases) may be required for atypical cases. Recurrences of PR are rare (about 2% of cases).

Emergency Department Treatment and Disposition

Most patients are asymptomatic and do not need any specific treatment except reassurance about the benign nature and the total duration of the eruption (about 6-8 weeks). Patients are NOT contagious and do not need any isolation. Symptomatic relief from pruritus can be treated by soothing nonprescription lotions like calamine, menthol, or pramoxine. Lukewarm colloidal oatmeal bath (not hot, as this may intensify itching) may be soothing. Nonfluorinated topical corticosteroids (eg, hydrocortisone lotion 1% or 2%) and antihistamines may be given for more intense pruritus, especially at night when pruritus is more troublesome. A rare patient with extensive disease with intense itching may respond to a short course of oral prednisone (dose: 0.5-1 mg/kg/d given orally for 7 days). This is rarely indicated in children and is best reserved for patients with intractable pruritus with severe disease. Refer such patients to a dermatologist. Direct sun exposure may hasten the resolution of individual lesions; however, burning should be avoided as this may exacerbate the rash. Alternatively, ultraviolet B (UVB) administered in 5 consecutive daily erythemogenic exposures, results in decreased pruritus and hastens the involution of lesions. Therapy is most beneficial within the first week of eruption and is rarely indicated in children.

Pearls

1. PR is a self-limiting eruption lasting about 6 to 8 weeks and is characterized by pink oval papules or plaques with a collarette of scale affecting the trunk and proximal extremities.

2. Lesions run parallel to the lines of skin cleavage, forming a “Christmas tree” appearance on the back.

3. A herald patch is seen in 70% of cases and heralds the onset of PR; however, its absence does not preclude the diagnosis of PR.

4. Secondary syphilis may be indistinguishable from PR, especially if the herald patch is absent; obtain serology for syphilis in all sexually active patients presenting with a rash of PR.

Clinical Summary

Granuloma annulare (GA) is a granulomatous skin disorder of unknown etiology occurring in any age group. Multiple associations have been hypothesized including postvaccination (injectables), trauma, insect bites, and sun exposure. A historic association with diabetes has most recently been refuted. The classic and subcutaneous types are common in children. The characteristic morphology is a nonscaly indurated annular plaque with a papular border and central clearing. In the classic type, multiple or solitary painless lesions may be seen distributed over the wrists and dorsum of hands and feet but can involve any part of the body. In subcutaneous GA, patients present with multiple or solitary deep nodules (similar distribution as classic form). The differential diagnosis includes tinea corporis and dermal processes such as sarcoidosis. The subcutaneous type may often be confused with rheumatoid nodules or other tumors. The diagnosis is clinical but can be confirmed on biopsy. The histopathology shows palisading granulomas in the dermis with mucin and necrobiotic degenerated collagen.

Emergency Department Treatment and Disposition

GA is a benign chronic condition and usually followed by a dermatologist. It is known to resolve spontaneously in several months to years. Treatment is mainly in form of topical moderate to high potency steroids or injectable steroids (expected to work better).

Pearls

1. GA can be confused with tinea corporis because of its annular configuration and raised papular border. However, unlike tinea corporis, GA lacks superficial scale.

2. GA sometimes resolves spontaneously after a biopsy.

Clinical Summary

Scabies is a contagious skin infestation caused by the female mite Sarcoptes scabiei subsp. hominis. The mite tunnels into the upper layer of the skin, produces a burrow, and deposits 1 to 4 eggs daily for 15 to 30 days. The larvae hatch in a few days causing intense itching. Only 10% of the eggs develop into adult mites. An infested person has an average of 12 mites on the skin. Signs and symptoms are a result of delayed hypersensitivity cell-mediated immune response to the proteins of the parasite. Nodules are a granulomatous response to the dead mite antigens and feces. The incubation period is 2 to 6 weeks in persons without previous exposure. With a previous infestation, symptoms may develop in 1 to 4 days after re-exposure. Scabies affects persons from all socioeconomic levels without regard to age, sex, or standards of personal hygiene; however, it is more common in crowded living quarters and nursing homes. Dogs and cats may be infested by nearly identical organisms (S scabiei subsp. canis) and sometimes may serve as a source for human infestation.

The diagnosis is clinical based on distribution of lesions, intense pruritus, and a history of affected family members. A light microscopic examination of a skin scraping from a burrow or unexcoriated lesion can be done with a no. 15 surgical blade and may demonstrate a mite, egg, or feces. A negative scraping does not rule out scabies. Complications include secondary infection (S aureus or S pyogenes). Scabies incognito is undiagnosed scabies resulting from the use of topical steroids.

Emergency Department Treatment and Disposition

Untreated scabies can last for months or years. When treating a patient for scabies, it is important to treat all the patient’s contacts. The preferred treatment is permethrin 5% cream, which should be applied from the neck down including intertriginous and genital areas, the intergluteal cleft, and under trimmed nails. Because scabies can affect the head, scalp, and neck in infants and young children, treatment of the entire head, neck, and body in this age group is required. The areas around the eyes and mouth should be avoided. The medication should be left on overnight (about 8 hours) and then washed off. Patients should be instructed to change all the clothes and bed sheets the following morning and the treatment should be repeated 1 week later for optimal results. Side effects include mild, transient burning, stinging, redness, and rash. An alternative treatment for school-aged children, adolescents, and adults includes γ-benzene hexachloride (lindane 1%) cream or lotion. Patients should be cautioned that improper use may lead to a significant systemic absorption, resulting in neurotoxicity. Because of the potential neurotoxicity, lindane should not be used in children younger than age 5 years, premature infants, patients with crusted lesions, children with a prior history of seizure disorders, malnourished children (lindane seeks fat; lack of fat in a malnourished patient may lead to toxicity), children with severe excoriations or inflamed or traumatized skin, children with chronic and preexisting dermatosis, or in women who are pregnant or breastfeeding. Other alternative therapies include sulfur (5%-10% precipitated sulfur in petrolatum), crotamiton cream and oral ivermectin. Advise patients to wash all clothing, towels, and bed linens that have touched the skin (normal washing machine cycle using hot water and a high heat dryer). Educate patients that itching may continue for days to weeks (3-4 weeks), nodules can persist for weeks to months after effective treatment and continued application of medication is unnecessary and worsens itching by causing irritation (overtreatment must be avoided). Children may return to school or childcare after completing treatment. Consider topical or systemic antibiotic therapy, if secondary bacterial infection is suspected. Refer patients to their primary care physician to reexamine for treatment failures in 1 and 4 weeks. Advise isolation of patients with crusted or Norwegian scabies as they carry a high mite load with increased risk of spreading the infection. Several or sequential courses of topical permethrin or γ-benzene hexachloride may be necessary. A single dose of oral ivermectin may also be used.

Pearls

1. Scabies is an intensely pruritic, erythematous, generalized papular eruption.

2. The presence of a similar rash in other family members is an important clue.

3. Interdigital web lesions are less commonly seen in children.

4. Young infants may have hyperpigmented nodular lesions, especially along the axillary line.

5. Use of bland lubricants or oral antihistamines and topical corticosteroids can help relieve itch.

6. Treatment failures are usually due to failure to treat all the contacts (exposed individuals) simultaneously.

Clinical Summary

Tinea versicolor is a common superficial skin infection caused by the dimorphic fungus Malassezia furfur whose yeast forms are called Pityrosporum ovale and Pityrosporum orbicular. The organism is part of the normal skin flora and appears in highest numbers in areas with increased sebaceous gland activity. Predisposing factors include malnutrition, burns, immunosuppressive or corticosteroid therapy, Cushing syndrome, and pregnancy. Excess heat and humidity and oily skin or application of oils (eg, cocoa butter, bath oil) on children leads to yeast overgrowth. The yeast is transmitted by personal contact during periods of scaling. Fungal elements may also be retained in frequently worn garments that are in contact with the skin. While tinea versicolor is more common in adolescents and young adults (years of higher sebaceous gland activity), it may occur in prepubertal children and infants. The diagnosis is made clinically. It is characterized by multiple small, circular macules of various colors (white, pink, or brown) with scales. Lesions are typically reddish-brown in light-skinned patients but can be either hypopigmented (off-white to white) or hyperpigmented (brown) in dark-skinned individuals. Distribution of lesions is highly characteristic. The upper chest is the most common site of involvement. The back, shoulder, and neck are often affected. The forehead may be involved in children. Lesions are usually asymptomatic; however, mild pruritus may be present. Wood lamp examination may demonstrate yellow-green fluorescence. Scraping the lesions lightly with a surgical blade followed by potassium hydroxide (KOH) examination may show numerous short, rod-shaped hyphae mixed with round spores in grapelike clusters (“chopped spaghetti-and-meatballs” appearance).

Emergency Department Treatment and Disposition

Various topical treatment options include selenium sulfide 2.5% lotion or shampoo. This should to be applied over affected areas and washed off after 10 to 15 minutes daily for 1 week followed by monthly applications for 3 months. Antifungal agents (eg, miconazole, clotrimazole, ketoconazole) may also be applied to the entire affected area 1 to 2 times a day for 2 to 4 weeks. For extensive disease, oral therapy may be offered. Ketoconazole (dose: 200 mg once daily for 5 days and refraining from bathing for at least 12 hours after treatment allows the medication to accumulate in the skin) or itraconazole (dose: 200 mg once daily for 5 days) can be used. Alternatively, a single-dose therapy with ketoconazole (400 mg) or fluconazole (300 mg) weekly for 2 weeks may be taken and followed by sweat-producing exercise and again refraining from bathing about 12 hours allowing excretion of the medication onto the skin. Recurrence rates of tinea versicolor vary from 15% to 60%. Monthly prophylaxis with 50% propylene glycol in water, selenium shampoo, or azole creams can help prevent recurrences.

Pearls

1. Lesions may be a variety of colors including pink, tan, or white (hypopigmented).

2. The rash begins insidiously and spreads over months to years.

3. Recurrence is high and considered the rule rather than the exception.

4. Advise patients to exercise ½ hour after taking the oral medication so that the medication may enter the sweat glands for optimal localized treatment.

5. Warn patients that pigmentary changes may take months to resolve even though the treatment was successful.

Clinical Summary

Tinea capitis is a highly contagious fungal scalp infection transmitted by humans and animals. Tinea capitis is more common among African American children than among other racial groups and occurs most commonly in areas of poverty and crowded living conditions. Preschool children (3-7 years) are most commonly affected; however, it is increasingly being recognized in adults, infants, and neonates. Infection may be transmitted by sharing combs, brushes, blankets, telephones, hats, pillowcases, and barber’s shears. Asymptomatic classmates or household members also spread the infection (spores are shed in air in the vicinity of the patient). Thus, tinea of the scalp may be contagious by direct contact or from contaminated fomites. Hair loss occurs because hyphae grow within the shaft, rendering it fragile, so that the hair strands break off 1 to 2 mm above the scalp. Diagnosis is clinical; however, KOH preparation of a diseased hair or fungal culture on dermatophyte test media may aid in diagnosis. Bacterial culture should be included to exclude superinfection in kerion. Complications of tinea capitis include lymphadenitis, bacterial pyoderma, permanent scarring alopecia in severe untreated cases, tinea corporis, and secondary bacterial infection.

Emergency Department Treatment and Disposition

Topical antifungal agents are ineffective and systemic therapy is required. Griseofulvin is first-line treatment at 20 to 25 mg/kg/d once or twice daily. Advise patients to take the medication with milk or a fatty meal and to continue treatment for 6 weeks or 2 weeks after clinical resolution of inflammation (overall duration may vary from 6 to 12 weeks). Laboratory monitoring is usually not necessary in a healthy child. Refractory cases may due to drug resistance, poor compliance, or reinfection. Newer antifungals that may be used include itraconazole, fluconazole, or terbinafine. Laboratory monitoring may be necessary when using these medications. Prednisone therapy can dramatically resolve severe inflammation of a kerion. Typical dosing is 1 mg/kg/d for 1 to 2 weeks to calm the inflammation. If bacterial superinfection in suspected, add oral antibiotics (eg, cephalexin) for the first week of treatment. Recommend antifungal shampoo (eg, selenium sulfide 2.5% or ketoconazole 2%) as adjunct therapy 2 to 3 times and per week. Refer patients to their primary care physician for reexamination in 4 weeks. The patient can attend school once treatment is started. Advise patients to use their own towels, hairbrush, comb, and hats and not to share such items with others. Trichophyton tonsurans lesions may occur outside of the scalp in patients, their families, and their close friends. These lesions serve as a reservoir for reinfection. Advise evaluation of all siblings or close contacts in the family.

Pearls

1. Diffuse, patchy, or discrete alopecia, scalp scaling, scalp pruritus, and lymphadenopathy (postauricular or occipital) are characteristic findings.

2. “Black-dot” appearance of affected areas represents hairs broken off at surface of scalp.

3. Clinical variants include noninflammatory, inflammatory (kerion), seborrheic, and pustular types.

4. Kerion is characterized by an indurated, boggy, painful scalp and represents the patient’s immune response as suggested by a positive skin test to Trichophyton antigen.

5. Id reaction characterized by an acute generalized papulovesicular eruption may be seen, and is commonly misdiagnosed as griseofulvin allergic reaction as the rash frequently coincides with the start of griseofulvin treatment.

Clinical Summary

Tinea corporis is a dermatophyte infection of the body involving the face (excluding the beard area in men), trunk (excluding the groin), or extremities (excluding palms and soles). As the name ringworm implies, it is an annular lesion that spreads peripherally with an active papulovesicular border and central clearing. Tinea corporis is seen in all age groups and may be present concurrently with tinea capitis. It is most commonly seen in warm climates. Infection is transmitted by infected scales from skin lesions of an infected person or from contact with infected scales or hairs deposited on environmental surfaces. Microsporum canis infections are usually acquired from infected pets (especially kittens and puppies). The diagnosis of tinea corporis is made clinically and no tests are required. Direct microscopic examination with KOH preparation or skin scrapings from the scales of the advancing border inoculated on fungal culture (eg, dermatophyte test media) may aid in diagnosis. The differential diagnosis includes other annular plaques, including nummular eczema, pityriasis rosea (herald patch), granuloma annulare, contact dermatitis, psoriasis, seborrhea, tinea versicolor, systemic lupus erythematosus, and erythema chronicum migrans.

Emergency Department Treatment and Disposition

Topical antifungals are effective for treatment. They should be applied twice daily for 10 to 14 days (or until lesions clear) and should be applied at least 2 cm beyond the advancing edge of the skin lesion. Treatment should be continued for 1 more week after clearing to ensure clinical cure. Examples of topical antifungals include the imidazoles (clotrimazole, miconazole, ketoconazole, econazole), allylamines (terbinafine and naftifine), and naphthiomates (tolnaftate). For extensive tinea corporis or if hair-bearing areas are involved, consider griseofulvin given orally with fatty food (dose: 15–20 mg/kg/d for 2–4 week).

Pearls

1. Tinea corporis consists of annular plaques with an active, scaly, raised advancing border, and central clearing.

2. Tinea corporis does not fluoresce with Wood lamp.

3. Tinea incognito is a variant of tinea corporis seen after topical corticosteroid use (when mistaken for nummular eczema). Local immunosuppression causes a loss of characteristic clinical features such as scale and erythema and may make the diagnosis of tinea difficult.

4. Majocchi granuloma, most commonly caused by Trichophyton rubrum, is a deep-seeded granulomatous response to dermatophyte infection often due to trauma or use of potent topical steroids.

Clinical Summary

Tinea cruris is a fungal infection of the groin and upper thigh commonly seen in adolescents, young adults, and athletes and is rarely seen in children. Men are affected much more frequently than women. Predisposing factors include concomitant tinea pedis, obesity, a warm humid environment, sweating, and tight (exercise outfits) or wet clothing (bathing suits). The characteristic lesion of tinea cruris is a well-demarcated, erythematous plaque with an active scaly papulovesicular border and central clearing. Infection usually begins in the crural folds and advances to the thigh forming half-moon-shaped plaques that may extend to the buttock and gluteal cleft. Unlike candidal infection, tinea rarely involves the scrotum or penis. The diagnosis is made clinically. When unsure, diagnosis can be made under direct microscopic examination with KOH preparation from the scales of the advancing border demonstrating hyphae, budding yeasts, or arthrospores. Skin scrapings from the affected area and inoculated on fungal culture (eg, dermatophyte test media) can help identify the specific dermatophyte. The differential diagnosis includes intertrigo, candida, erythrasma, psoriasis, seborrheic dermatitis, or allergic contact dermatitis.

Emergency Department Treatment and Disposition

Topical antifungal therapy with econazole cream twice daily for 2 to 4 weeks is considered first-line for the treatment of tinea cruris. The use of topical steroids or antifungal preparations combined with high-potency topical steroids should be avoided in the groin as this may quickly lead to skin atrophy or other steroid-related changes. For severe cases, consider use of a short course of griseofulvin. Advise patients to wear loose-fitting underwear. Antifungal powder can be applied daily to help prevent reinfection. If present, tinea pedis should be treated and patients should be instructed to put on socks first before their underwear in order to avoid carrying the fungal elements from the infected feet up to the groin area.

Pearls

1. Tinea cruris and tinea pedis are commonly seen together in the same patient.

2. Typically, tinea pedis precedes the groin infection (because of spread of infection from the infected feet to the groin).

3. Erythrasma and candidiasis may coexist with tinea cruris.

Clinical Summary

Tinea pedis is a fungal infection of the feet common in adolescents and uncommon in young children. Infection is acquired by contact with skin scales containing fungi or with fungi in damp areas (eg, swimming pools, locker room floors, communal baths, nail salons). Infection in one family member tends to spread throughout the household and communicability persists as long as the infection is present. Once infection is established, the individual becomes a carrier and is more susceptible to recurrences. Predisposing factors include hot, humid weather (summer months), and occlusive footwear. Interdigital infection is almost always present and is characterized by foul odor, pruritis, dry, and fissuring web spaces with white scaling and maceration. Fissuring of the plantar foot surface may be seen. Chronic infection is characterized by diffuse scaling of both soles and occasionally one hand. Infection may be associated with a hypersensitivity id reaction (erythematous papulovesicular eruption on legs and trunk, and arms). Secondary infection may occur, as macerated skin serves as portal of entry for bacteria. The diagnosis is made clinically. If unsure, a potassium hydroxide wet mount may demonstrate fungal elements, which can help differentiate tinea pedis from other conditions. Skin scrapings inoculated on fungal culture (eg, dermatophyte test media) helps in confirming the diagnosis. The differential diagnosis includes contact or shoe dermatitis, atopic dermatitis, juvenile plantar dermatosis, dyshidrotic eczema, and candida infection.

Emergency Department Treatment and Disposition

Tinea pedis runs a chronic course with frequent exacerbations occurring with hot, humid weather, and exercise. General instructions for treatment and to prevent recurrences include good foot hygiene. Advise patients to keep feet cool and dry (especially between the toes), apply absorbent antifungal foot powder daily to help prevent moisture, avoid occlusive footwear (shoes that promote warmth and sweating encouraging fungal growth), use wider shoes (reduces sweating and irritation), use cotton socks instead of nylon or other fabrics (interferes with dissipation of moisture), change wet socks as soon as possible, and dry the groin area before drying feet to avoid inoculating fungal scales into the groin. Topical antifungal preparations are the treatment of choice for tinea pedis. For example, miconazole, haloprogin, clotrimazole, or terbinafine applied bid, or econazole, ketoconazole, or naftifine applied once a day for 2 to 3 weeks are generally effective. For hyperkeratotic diffuse involvement of the soles, oral treatment may be necessary. Terbinafine given orally for 2 to 6 weeks or griseofulvin given orally for 6 to 8 weeks are generally well tolerated but should be avoided or used with caution in patients with liver disease. Acute vesicular tinea pedis, a rare acute inflammatory form of tinea pedis, should be treated with griseofulvin given orally for 6 to 8 weeks. Burow solution–soaked wet compresses applied for 30 minutes several times a day may provide symptomatic relief. Topical antifungal agents can be used once macerated tissue is dried. If secondary bacterial infection is present, antibiotics should be given. Treatment of id reaction includes wet dressings and low-potency topical steroids (rarely, a short course of prednisone therapy). It is important to inquire about other family members with a similar rash and recommend treatment of all infected family members. Advise patients with active infection to avoid swimming pools in order to prevent spread of the infection. Treat tinea cruris simultaneously, if present. Consider and treat toenail involvement when treating tinea pedis as toenail infection can serve as a reservoir for the reinfection of the rest of the foot.

Pearls

1. Tinea pedis is the most common fungal infection in adolescents and adults.

2. Tinea pedis is uncommon in children and should not be confused with eczema or contact or shoe dermatitis. Nonetheless, tinea pedis should be considered in the differential diagnosis of foot dermatitis in children particularly when other household members are affected.

3. Tinea pedis commonly occurs in association with tinea cruris and tinea unguium.

4. Interdigital scaling and fissuring particularly between the third, fourth, and fifth toes is a clue to diagnosis.

5. “Moccasin-type” or “dry-type” tinea refers to diffuse hyperkeratosis of the soles seen with chronic infection.

6. Look for 2 feet and 1 hand involvement.

Clinical Summary

Fungal infection of the nails is called tinea unguium or onychomycosis. It can be due to Trichophyton species, Epidermophyton floccosum or nondermatophyte species such as Candida albicans. Although uncommon, it may be seen in healthy children whose parents have tinea pedis or unguium. Nail infection may occur simultaneously with hand or foot tinea, or may occur as an isolated phenomenon. Trauma predisposes to infection. Toenails are more commonly affected than fingernails and there are 4 patterns of nail infection seen:

1. Distal subungual onychomycosis (infection starting with the free edge of the nail and extending proximally)

2. Proximal subungual onychomycosis (infection starting through the proximal nail fold, and extending to the nail plate from below)

3. White superficial onychomycosis (diffuse or speckled white discoloration of nail surface)

4. Candidal onychomycosis (seen in chronic mucocutaneous candidiasis or AIDS)

Fungi are found in the nail plate and in the cornified cells of the nail bed. With clinical suspicion, direct microscopic examination of nail clippings or debris in KOH preparation can help in diagnosis. Nail clippings or crumbling debris from under several nails and from different parts of the infected nail can be collected using a curet. Inoculation of these materials on DTM (dermatophyte test media) or Sabouraud media will identify the causative dermatophyte. A periodic acid–Schiff stain of an infected nail clipping will show hyphae. The differential diagnosis of tinea unguium includes nail psoriasis, eczema, trauma, leukonychia (white spots or bands on nail), habitual picking of proximal nail fold, and pachyonychia congenita.

Emergency Department Treatment and Disposition

Topical antifungal creams and lotions do not penetrate the nail plate and are therefore not effective except for controlling inflammation at the nail folds. In general, patients will need systemic antifungal therapy. Long-term oral therapy is often followed by reinfection when the oral medication is discontinued. Prolonged use of a topical antifungal agent after clinical response to an oral agent may prevent nail reinfection. Oral antifungal agents that are used for treating onychomycosis include fluconazole, itraconazole, or terbinafine. Other modalities that help in resolution of the infection include mechanical reduction of the infected nail plate with a nail clipper with pliers-type handles (removal of hard, thick debris). Nonsurgical avulsion of symptomatic dystrophic nails with a urea compound may be helpful. Finally, surgical removal of painful or extremely infected nails (eg, great toenail) may be necessary.

Pearls

1. Tinea unguium results in nails that are opaque, thickened, crumbled, and cracked.

2. It typically affects toenails more than fingernails.

3. Infected nails often coexist with normal-appearing nails.

Clinical Summary

Warts are epithelial tumors of the skin and mucous membranes caused by infection with human papilloma viruses (HPVs). HPVs causing nongenital warts are distinct from HPVs causing anogenital infections. Nongenital warts include the common skin wart (verruca vulgaris), flat warts (verruca plana), plantar wart (verruca plantaris), periungual warts, and threadlike (filiform) wart. Mucous membrane warts include anogenital (condylomata acuminata), oral, nasal, or conjunctival warts and laryngeal papillomatosis. Warts spread from direct contact or by autoinoculation. The incubation period is estimated to range from 1 month to several years. Warts are commonly seen in school-age children (except condyloma acuminata), and young adults. Transmission of laryngeal papillomas occurs through aspiration of infectious secretions during passage through an infected birth canal. Special attention should be given to genital warts in children as these may occur after inoculation during birth through an infected birth canal, as a result of sexual abuse, or from incidental spread from cutaneous warts. Local trauma promotes infection with the virus; thus warts are more common on hands, fingers, elbows, and plantar surfaces. Other predisposing underlying conditions for developing warts include infection with HIV, lymphomas, and immunosuppressive therapy.

Diagnosis is clinical; HPV cannot be cultured and rarely a biopsy is indicated when a diagnosis is in doubt. Differential diagnosis includes molluscum contagiosum, condyloma lata, skin tags, calluses and corns, lichen planus, lichen nitidus, and squamous cell carcinoma.

Emergency Department Treatment and Disposition

The natural course is highly variable, with about two-thirds resolving spontaneously within 2 years, whereas others may last years or a lifetime. Therapy is decided based on the duration, location, and severity of the warts. Conservative management with watchful waiting may be considered. Educate parents/patients that several treatment sessions are usually required before a cure is achieved. Treatment options for warts that do not resolve spontaneously rely on chemical or physical destruction of the infected epithelium. These include topical application of salicylic acid, as solution, patches, or plasters (eg, Duofilm, Compound W, Mediplast, Occlusal-HP), tretinoin gel or cream (flat warts), and topical imiquimod. Duct tape, alone or in combination with imiquimod or salicylic acid can be very effective. Patients should be advised to soak the wart in warm water for 5 minutes before application of medication to remove loose, dry, skin and allow the medication to penetrate more effectively. Therapy may be required for up to 12 weeks. Patients with warts on the face, periungual warts, large plantar warts, or warts resistant to conservative therapy should be referred to a dermatologist for other therapeutic considerations (eg, cryotherapy or electrodesiccation or curettage).

Pearls

1. Cutaneous warts are benign infections and self-limiting in a majority of cases.

2. Common warts occur most frequently in children and adolescents. Anogenital warts are most common in young sexually active patients.

3. Genital warts are the most common viral sexually transmitted disease in the United States.

4. Warts will often resolve spontaneously without treatment and watchful waiting may be done in asymptomatic patients (about two-thirds disappear spontaneously within 2 years); however, failure to treat incurs a risk of spread to other sites.

Clinical Summary

Molluscum contagiosum is a viral skin infection caused by the poxvirus molluscum contagiosum, and characterized by 2- to 5-mm discrete pearly white papules with central umbilication. The face, eyelids, neck, axillae, trunk, and thigh are the most common sites and occurrence is most common in children between the ages of 3 and 16 years. Swimming pools and communal bathing may be predisposing conditions. Humans are the only known source of the virus, which is spread by direct contact or from autoinoculation via fomites (eg, towels). Predisposing conditions include atopic dermatitis, HIV infection, and other immunodeficiency states including leukemia. Unilateral conjunctivitis may develop with lesions located on or near the eyelids. Rarely, lesions may appear on the conjunctiva or cornea.

Diagnosis is usually made clinically. If in doubt, Wright or Giemsa staining of a crushed papule shows characteristic intracytoplasmic inclusions. Skin biopsy reveals epithelial cells with large intracytoplasmic inclusions (molluscum bodies). A central white core seen on magnification can aid diagnosis. Differential diagnosis includes nevi, acne, milia, warts, or herpes simplex.

Emergency Department Treatment and Disposition

Molluscum contagiosum is a self-limited disease, with an average duration of lesions lasting about 6 to 9 months. Lesions can however persist for years, can spread to distant sites, and may be transmitted to others. In young children and in lesions involving sensitive areas (ie, around the eye), a wait-and-see approach should be encouraged. Enlarging or spreading lesions and genital lesions should be definitively treated to prevent spread through sexual contact. Treatment depends on the number and size of lesions, age of the patient, and availability of treatment methods. Mechanical removal of the central core of each lesion with a needle, a sharp curette, or a comedo extractor (lesions involute faster after they are irritated) is often quite effective. Small papules can be removed with a curette with or without local anesthesia (EMLA cream applied 30-60 minutes before treatment effectively prevents pain of curettage). This technique however should not be used in cosmetically significant areas as scar tissue may form. Topical treatment options include tincture of iodine, salicylic acid (applied each day with or without tape occlusion), tretinoin gel or cream (applied once or twice daily to individual small lesions), or cantharidin (applied to each lesion without occlusion and washed off after 2-6 hours). It is important to warn parents that these treatments cause irritation and may lead to blistering. Topical treatments should be applied with a Q-tip to prevent irritation of the surrounding unaffected skin and may require several weeks before results are seen. Patient can alternatively be referred to a dermatologist for other therapeutic modalities that include manual curettage of large lesions, cryotherapy with liquid nitrogen, electrocautery, or carbon dioxide laser therapy. Finally, patients should be advised to avoid shared baths and towels until the infection is clear.

Pearls

1. Molluscum lesions are benign and self-limited. Lesions can regress spontaneously; treatment may prevent autoinoculation and spread to other persons.

2. Molluscum lesions may be associated with other venereal diseases.

3. Molluscum lesions are often misdiagnosed as warts or herpes simplex virus lesions.

4. Genital molluscum contagiosum in children may be a manifestation of sexual abuse and should be investigated.

5. Although umbilication of molluscum papules is characteristic, early lesions may not show this feature.

Clinical Summary

Acropustulosis of infancy is a recurrent, self-limited condition of young children and infants. Most cases begin in infants less than 10 months old and may recur for weeks to years. It is rarely seen in children more than 3 years old. Acropustulosis typically affects the acral surfaces—mostly palms and soles and particularly the lateral surfaces of the hands and feet. Pustules may rarely extend to the wrists, ankles, and dorsal surfaces of the hands and feet. Lesions present as erythematous macules and papules and progress to vesicles and pustules over a period of 7 to 10 days. The rash is often intensely pruritic and children often appear uncomfortable. Most cases resolve after 2 to 3 weeks but recurrence is common and may occur as frequently as every few weeks to months. The etiology is unknown though association with preceding scabies has been reported. Diagnosis is clinical. A smear of the vesicle contents reveals neutrophils and may include eosinophils. Acropustulosis is self-limited and resolves usually by the time the child reaches 2 to 3 years of age. No long-term sequelae associated with this condition are known. Differential diagnosis includes other pustular and papulovesicular eruptions of infancy including pustular psoriasis, cutaneous candidiasis, dyshidrotic eczema, herpes infection, erythema toxicum neonatorum, transient neonatal pustular melanosis, and scabies infection.

Emergency Department Treatment and Disposition

Treatment is symptomatic for relief of itching. High-potency steroids are very effective and can be used safely in limited areas for short periods of time. Oral antihistamines such as diphenhydramine and hydroxyzine may also be helpful. Antibiotics should be considered if bacterial superinfection is suspected.

Pearl

1. Recurrent crops of lesions are considered the hallmark of this condition.

Clinical Summary

Erythema toxicum neonatorum (ETN) is a benign skin eruption of unknown etiology seen in the first few days of life in full term neonates. The characteristic morphology consists of erythematous macules, papules, and pustules that develop between birth and 10 days of life and heal spontaneously within few weeks (about 2 weeks). The face, trunk, back, and extremities are typical sites usually sparing the palms and soles. There is no mucosal involvement nor any systemic complications or internal organ involvement. It may often coexist with another benign neonatal skin eruption called transient neonatal pustular melanosis (TNPM; see Figure 7-113). The pustules in TNPM are sterile and need to be differentiated from other pustulosis of neonates, like impetigo, candidiasis and herpes infections. The diagnosis of ETN is clinical, and dermatology consultation may be indicated to differentiate this benign disorder from other neonatal pustulosis. Biopsy is rarely indicated; the best diagnostic test is a Wright stain or Tzanck smear from a pustule, which shows presence of multiple eosinophils. Peripheral eosinophilia may be present.

Emergency Department Treatment and Disposition

Recognition and prompt diagnosis of this eruption is the most important step in the management. No treatment is needed except reassurance to the family as this is a benign, self-limited disorder. Aggressive diagnostic workup including unnecessary use of antibiotics can be avoided. Wright stain or Tzanck smear is the key to diagnosis. Dermatology consultation may be called if the diagnosis is unclear and if indicated, bacterial, fungal, and viral cultures can be sent to exclude other infectious neonatal pustular conditions.

Pearls

1. ETN does not cause any “toxicity” as the name suggests and the neonates are otherwise completely asymptomatic.

2. Skin lesions are pale or ivory-colored papules surrounded by blotchy erythema resembling flea bites.

3. It is not seen in the premature newborns. It occurs in full-term newborns and seen more commonly as the gestational age of the neonate increases.

Clinical Summary

Epidermolysis bullosa (EB) is a group of inherited (autosomal dominant or recessive) blistering disorders that occurs in 1 in every 50,000 births. Presentation can range from mild to life-threatening. Blistering often occurs in areas of trauma or friction. There are 3 major forms of EB: simplex, junctional, and dystrophic (classified based on the level of cleavage in the skin). EB simplex is the most common form. Blisters develop within the epidermis and generally do not lead to scarring. In junctional EB, cleavage occurs at the dermal-epidermal junction. In dystrophic EB, cleavage occurs within the dermis. Both these forms of EB tend to be more severe and often lead to scarring. Aside from blistering of the skin, patients may experience internal involvement, including the gastrointestinal and genitourinary tracts as well as ocular involvement. Esophageal, tracheal, and anal strictures may occur along with retinal neovascularization. Patients may suffer from chronic malabsorption. Pyloric atresia is associated with one variant of junctional EB. Internal involvement (ie, strictures, pyloric atresia) should be considered in all patients presenting with dysphagia and/or dyspnea. Diagnosis is made by specialized immunofluorescence mapping to determine the level of skin cleavage and the presence of specific antibodies. Prognosis depends on the severity of disease. In patients with the most severe disease, death may occur as early as the first 2 years of life. Secondary infection with sepsis and failure to thrive are the most common causes of death in patients with EB.

Emergency Department Treatment and Disposition

Refer the patient to a dermatologist for ongoing care that is palliative and supportive. Parents should be educated on trauma avoidance. Recommendations include wearing clothing inside out to prevent pressure from seams. Soft fabrics such as cotton are encouraged. Mittens may be helpful particularly in young babies to prevent self-inflicted trauma. Young children and toddlers should be encouraged to wear soft, well-fitting shoes. Wound care should include the use of specialized nonstick dressings like Mepitel (distributed by Mölnlycke Health Care) and Hollister Woundcare. Wounds can be extremely painful and proper pain management should always be employed. Tense bullae may be evacuated using a sterile needle to relieve pressure. Antibiotic ointment should be reserved for cases of suspected infection in order to prevent bacterial resistance. If secondary infection of wounds is suspected, antibiotics should be considered. Patients with failure to thrive will need nutritional supplementation. The Dystrophic Epidermolysis Bullosa Research Association (DEBRA) is an important and comprehensive resource for both patients and physicians (www.debra.org).

Pearls

1. EB refers to a group of genetic mechanobullous disorders.

2. Blistering of EB can be mistakenly attributed to inflicted burn injuries.

3. Though genetically acquired, bullae, in some milder forms, may not appear until adulthood.

4. Prevention of trauma and infection are the mainstays of treatment.

Clinical Summary

Infantile hemangioma (IH) or its precursor (erythematous, telangiectatic, or hypopigmented patch) may be seen in 2% of neonates and in up to 10% of Caucasian babies within the first year of life. Although IHs occur in all races, they are most common in white skin. Risk factors include female sex, prematurity, low birth weight, advanced maternal age, and multiple gestation pregnancy. Traditionally, IH have been classified as superficial, deep, or mixed, with the majority located on the head and neck. Most IH are localized or focal lesions. The less common segmental type are plaque-like and regionally distributed with a higher risk of complications and associated anomalies such as seen in PHACES (posterior fossa malformations, hemangiomas of the face, arterial anomalies, eye abnormalities, and sternal clefting) or PELVIS (perineal hemangiomas, external anogenital defects, lipomeningomyelocele or spinal dysraphism, vesicourinary tract defects, imperforate anus, and skin tag) syndromes. The life cycle of IH involves proliferation, plateau, and involution—with 80% of maximum size reached by 3 months of age. The majority of lesions are first noted at 2 to 3 weeks of age. Clinically, involution is indicated by a color change from bright red to pink or grey, and softening. The vast majority can be diagnosed based on history and physical examination. Differential diagnosis includes other vascular lesions such as Kaposiform hemangioendotheliomas and tufted angiomas. Deep hemangiomas may present as nodules with a bluish hue with or without overlying telangiectasias. Their differential includes congenital soft tissue tumors such as fibrosarcoma, rhabdomyosarcoma, and neuroblastoma.