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A 3-year-old female with rash, open sore on abdomen
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A 3-year-old previously healthy African-American female with a past medical history of eczema presented to the ED with a rash. The rash reportedly started as a small open sore on the abdomen 2 weeks prior. There was no drainage, and the rash was very itchy.
During the next week, the rash spread over the abdominal area. The rash was described as a red, raised area that became dry and hyper pigmented, and the superficial crust sloughed off. No vesicles or bullae were noted. The rash continued to worsen and gradually spread to upper arms and legs. Pruritus persisted and the child became uncomfortable and complained of pain with touching of lesions on the day before admission. The parents reported no fever, and the child’s appetite remained normal. She had some decreased activity secondary to discomfort, but no symptoms of mucosal involvement.
On physical exam, she was well appearing, afebrile and well hydrated. She appeared to be uncomfortable but had no pain at rest. She complained of pain when skin lesions were examined. Skin showed extensive confluent erythematous macules with superficial erosions interspersed with thin, dark crusts on the anterior abdomen, neck, bilateral thighs, arms, elbow creases and axillae. Crusts were not honey colored. Minimal serous but no purulent discharge was noted. There was scattered involvement of legs, forearms, back and face, but no involvement of genital area, inguinal areas, perianal area, buttocks, palms, soles and scalp, as seen in Figure 1.
 Figure 1. There was scattered involvement of legs, forearms, back and face, but no involvement of genital area, inguinal areas, perianal area, buttocks, palms, soles and scalp. Images: Pittalwala R
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A couple of small vesicular areas on the legs were noted transiently on admission, but there was no mucosal involvement. No erythroderma, bullae, pustules or target lesions were noted. White blood cell count was 7,300 cells/mcL; Blood and wound cultures, and wound viral herpes simplex virus (HSV) polymerase chain reaction (PCR) were sent on admission.
She was admitted and started on IV clindamycin for presumed secondary staphylococcal infection of eczema. IV vancomycin was added in view of extent of skin involvement and concern for resistant staphylococcal infection pending wound culture sensitivity results. Other differential diagnoses considered were Steven-Johnson syndrome, toxic epidermal necrolysis and staphylococcal scalded skin syndrome. These were ruled out based on the clinical picture. A skin care regimen with topical petrolatum jelly (Vaseline) and wet to dry dressings was followed.
She required occasional morphine doses for skin care and diphenhydramine for pruritus. She was given IV fluids and had good oral intake. She remained afebrile and well appearing throughout. The lesions gradually became less erythematous and dry, and gradually the erythema resolved. There was diffuse scaling and flaking, taken on day 2 of admission.
What is the most likely etiology?
Wound culture results showed methicillin-susceptible Staphylococcus aureus (MSSA) with intermediate sensitivity to clindamycin, at which time IV clindamycin was discontinued. Wound HSV PCR was negative, and topical steroids were added to the skin care regimen. She was discharged on day 4 on oral trimethoprim-sulfamethoxazole and skin care with topical emollients and topical steroids.
Atopic dermatitis is a chronic inflammatory skin disease that causes dry, itchy skin. It affects about 15% to 20% of children. Typically, it begins in infancy, between ages 2 to 6 months, and follows a remitting and relapsing course. This condition can worsen and cause intractable pruritus, soreness, infection and sleep disturbance. As the child gets older, the rash may become more localized.
Most children outgrow eczema before school age. Although there is no cure, the disease has less impact on daily living and quality of life for the patient and family if treated and managed well. Avoiding environmental aggravators, keeping skin moist and twice daily use of emollient or moisturizing products are the mainstay of treatment. Flares are treated with topical steroids, other topical anti-inflammatory medications and wet dressings.
A secondary bacterial, viral or fungal infection can develop in patients with eczema. Bacterial infection is a common complication, and 90% of patients with eczema are colonized with staphylococcal organisms. The progression from colonization to infection often is associated with a flare of the eczema. More erythema is noted when the infection begins, then the affected areas become crusted or have serous drainage. It should be suspected if there is crusting, weeping, erythema, cracks, frank pus or multiple excoriations and increased itch.
The usual organism is S. aureus. Treatment of secondary infection is oral or IV antibiotics based on severity of illness and local sensitivities. Increase in methicillin-resistant S. aureus makes treatment of secondary infection of eczema with these organisms challenging. Restoration of the skin barrier with emollient, wet dressings and steroids is also important. For children with repeated cutaneous infections, adding 2 teaspoons of household bleach per gallon of bath water can help reduce the incidence of such infections.
References:
- Paller AS. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. 3rd edition. Philadelphia, Pa.: Saunders; 2005.
- Medscape reference: Pediatric atopic dermatitis.
Rashida Pittalwala, MD, is a pediatric hospitalist at The Children’s Hospital of Philadelphia Care Network at Virtua in Voorhees, N.J. Prameela Dibba, MD, is a family medicine resident at Virtua Health in Voorhees, N.J.