Infant’s disseminated rash is twice misdiagnosed

December 1, 2016

A frustrated mother carries her 2-month-old son into the office for evaluation of a diffuse bright red rash with dramatic hypopigmentation. Scalp, neck, axillary, and diaper areas are involved.

THE CASE

A frustrated mother carries her 2-month-old son into the office for evaluation of a diffuse, bright red rash with dramatic hypopigmentation. Scalp, neck, axillary, and diaper areas are involved. The baby is not itchy and rests comfortably on the examination table. He was seen at an urgent care center 1 month ago where he was diagnosed with candidiasis and started on nystatin, which hasn’t helped. He was subsequently seen in the emergency department (ED) where he was started on hydrocortisone for eczema. 

NEXT: What's the diagnosis?

 

DERMCASE diagnosis: Infantile seborrheic dermatitis

Presentation and epidemiology

Seborrheic dermatitis (SD) is a chronic inflammatory skin disorder with a predilection for body areas rich in sebaceous glands, such as the scalp, face, upper chest, axilla, and groin.1,2 Less commonly, the rash may become generalized.3 Typical lesions are well-circumscribed, symmetrical, pink-to-red patches with greasy scales and often postinflammatory hypopigmentation, particularly in dark pigmented infants.4,5

Epidemiological estimates vary because of absence of validated criteria for diagnosis, but generally it is considered to be one of the most common dermatologic conditions, especially the infantile variant, with an incidence anywhere from 42% to 70% in newborns during the first 3 months of life.2,6 The most common presentation of infantile seborrheic dermatitis (ISD) is cradle cap, in which a newborn presents with thick white or yellow greasy scales overlying erythematous patches on the scalp.1,3,7 Although typically only the scalp is involved, ISD can be more extensive, especially favoring the intertriginous areas.4

More: Patch testing in atopic dermatitis

Pathophysiology

The exact pathogenesis of SD is unclear, but is most likely multifactorial, with genetic predisposition to aberrant epidermal barrier function, increased sebaceous gland activity secondary to sex hormones, abnormal host immune response to commensal skin malassezia colonization, emotional stress, and nutrition all hypothesized as possible causative factors.2,6,8

NEXT: Differential diagnosis

 

Differential diagnosis

The diagnosis of ISD is usually clinical and is based on history and physical exam.1 However, when the eruption in disseminated as in this baby's case, the differential is broad and should include:

·      Psoriasis. Psoriasis and SD favor similar locations and both are common in the diaper area. However, the lesions in psoriasis are thicker and more sharply demarcated, and present with indurated plaques with slivery scales that favor extensor surfaces of the elbows or knees and demonstrate koebnerization.2,3,5 Nail involvement also tips the balance toward psoriasis.5 However, in infantile psoriasis, the skin eruption often begins with a persistent, recalcitrant dermatitis before it disseminates, which makes it difficult to distinguish from ISD especially early in the course.

·      Tinea corporis. Ringworm is a dermatophytosis characterized by well-demarcated annular erythematous pruritic patches with central clearing and an active advancing border.3,5

·      Tinea capitis. When ISD presents in the scalp, it is differentiated from tinea capitis by the absence of hair loss. Tinea capitis typically manifests as scaly patches of hair loss that may be indistinguishable from seborrheic dermatitis early in the course. When these findings are present particularly with reactive occipital lymph nodes, microscopic examination of a potassium hydroxide preparation from the scalp, if possible, and a fungal culture should be performed.

·      Irritant contact dermatitis. When ISD presents in the diaper area, it is differentiated from diaper dermatitis by early involvement of the creases. Contact dermatitis is most prominent on convex surfaces and spares the relatively protected genitocrural folds.3,8

·      Atopic dermatitis (AD): The chief mimic of SD in infancy is AD. Infantile seborrheic dermatitis presents earlier, usually within the first month of life, whereas infantile atopic dermatitis (IAD) is typically seen after 3 months of age.7 However, AD may erupt within the first few weeks and overlap with SD. Compared with children with ISD, children with IAD usually develop more impressive scaling, and have a positive family history of atopy. Classic IAD lesions are erythematous excoriated patches and plaques on the face or on the extensor surfaces of the limbs, while scalp, axillary, anterior neck, or diaper involvement are quintessentially SD.9 Although AD lesions may appear unimpressive, they are extremely pruritic, and the infant is miserable and chronically rubbing exposed surfaces against the parents’ chest. On the contrary, seborrheic lesions may appear scary, but the baby is usually asymptomatic.

It is important for pediatricians to be able to distinguish these 2 very common eczematous disorders because the prognosis and treatment are quite different. In AD, management consists primarily of avoiding triggers, keeping the skin moisturized and covered with protective clothing, and using topical steroids to decrease inflammation.3 However, SD is managed differently, with therapy being tailored to body site. Cradle cap will often resolve without treatment, so therapy is conservative, usually emollients to loosen the scales, followed by hair brushing, scalp massage, and baby shampoo. For more refractory cradle cap, over-the-counter ketoconazole and other antiseborrheic shampoos may be used carefully.1 For ISD of the face and body, topical hydrocortisone or ketoconazole used twice daily for 2 weeks is often effective.4

Next: Common pediatric disorders in skin of color

Infantile seborrheic dermatitis has a good prognosis, with most children achieving spontaneous resolution within a year.7 On the contrary, IAD usually persists, but many children improve before kindergarten, and practitioners should set realistic expectations early and focus the family on maintenance regimens.

Patient outcome

In summary, diagnosing ISD can be challenging. The patient’s rash was initially misdiagnosed with candidiasis at an urgent care center and then with atopic dermatitis at the ED. The nystatin was discontinued. Ketoconazole 2% shampoo was prescribed to be used daily on the scalp and on the body as a wash. Hydrocortisone 2.5% ointment was also prescribed to be applied twice daily to affected areas, and the scalp scaling and disseminated inflammatory lesions improved dramatically within a week.

 

REFERENCES

1. Clark GW, Pope SM, Jaboori KA. Diagnosis and treatment of seborrheic dermatitis. Am Fam Physician. 2015;91(3):185-190.

2. Borda LJ, Wikramanayake TC. Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol. 2015;3(2). December 2015. Epub ahead of print.

3. Cohen BA, Davis HW, Gehris RP. Dermatology. In: Zitelli BJ, McIntire SC, Nowalk AJ. Zitelli and Davis’ Atlas of Pediatric Physical Diagnosis. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:299-368.

4. Poindexter GB, Burkhart CN, Morrell DS. Therapies for pediatric seborrheic dermatitis. Pediatr Ann. 2009;38(6):333-338.

5. Siegfried EC, Hebert AA. Diagnosis of atopic dermatitis: mimics, overlaps, and complications. J Clin Med. 2015;4(5):884-917.

6. Naldi L, Rebora A. Clinical practice. Seborrheic dermatitis. N Engl J Med. 2009;360(4):387-396.

7. Elish D, Silverberg NB. Infantile seborrheic dermatitis. Cutis. 2006;77(5):297-300.

8. Dickey BZ, Chiu YE. Eczematous disorders. In: Kliegman RM, Stanton BF, St. Geme JW III, Schor NF. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: Elsevier; 2015:3150.e1-3155.e1.

9. Weidinger S, Novak N. Atopic dermatitis. Lancet. 2016;387(10023):1109-1122.

Ms Abubucker is a fourth-year medical student at Johns Hopkins University School of Medicine, Baltimore, Maryland. Dr Cohen, section editor for Dermcase, is professor of Pediatrics and Dermatology, Johns Hopkins University School of Medicine, Baltimore. The author and section editor have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article. Vignettes are based on real cases that have been modified to allow the author and editor to focus on key teaching points. Images also may be edited or substituted for teaching purposes.