HISTORY
Chief complaint: itchy blisters after burn to the right wrist.
A 40-year-old woman presented to the clinic for evaluation of a pruritic rash on her right wrist after initial assessment via telemedicine. She reported the rash began roughly 2 weeks after a linear thermal burn to the area. She had applied bacitracin zinc/neomycin sulfate/polymyxin B sulfate ointment and Vaseline to the rash and thought it was healing well. However, several days before the initial encounter, blisters developed around the burn site. There was no warmth or swelling in the affected area.
Prior treatment: triple antibiotic ointment and Vaseline. She was taking no medications and has no known allergies.
Prior biopsy: none.
Skin history: benign.
No other significant laboratory/study findings.
TELEDERMATOLOGY IMAGING READER REPORT1
There is one image provided with this consult (Figure 1). A patch of coalescent, weeping vesicles and bullae 1-18 mm were present in a 10 x 8 cm area on the right wrist surrounding a linear scar created by the initial burn.
Image Quality Assessment
Fully satisfactory.
INTERPRETATION OF IMAGES
Lesions
The finding of pruritic, coalescing, weeping vesicles and bullae localized to an area where a common allergen was applied is typically seen in severe allergic contact dermatitis (ACD).
RECOMMENDATION
Skin Care Recommendations
Clobetasol 0.05% ointment twice daily and as needed for pruritus was prescribed. Vaseline was continued, but the triple antibiotic ointment was discontinued and added to her allergy list because both bacitracin zinc and neomycin sulfate are common allergens.
Other
An alternative to a topical steroid would be a calcineurin inhibitor (pimecrolimus) or a phosphodiesterase inhibitor (crisaborole); however, a potent topical steroid would be preferable in severe ACD.
Medication Recommendations
The patient was prescribed prednisone taper of 40 mg daily for 5 days, 20 mg daily for 5 days, and 10 mg daily for 7 days.
Future Recommendations
The possible use of patch testing to specifically identify the exact allergen, which has caused this reaction, and thus avoid using it or any potential cross-reactors in the future has been discussed.
RECOMMENDED FOLLOW-UP
Return to the dermatology clinic in person if symptoms fail to improve or if the patient is interested in pursuing patch testing.
CLINICAL PEARL
ACD is a Type IV delayed hypersensitivity reaction mediated by T-cells (Mowad et al., 2016). The pruritic rash is produced at the site of contact (Krasteva et al., 1999; Rashid & Shim, 2016). Acute lesions consist of erythematous, pruritic macules, papules, and plaques, sometimes showing vesicles and/or bulla. Linearity is produced if the antigen streaked onto the skin (Krasteva et al., 1999; Rashid & Shim, 2016). Agents such as metals, glues, plastics, rubber, fragrances, preservatives, topical antibiotics or corticosteroids, and hair product chemicals are common allergens (Wentworth et al., 2014). The diagnosis is based on clinical features, a history of allergic exposure(s), and lack of recurrence after avoidance of suspected allergen(s). Although generally not necessary, if a biopsy is performed, an acute spongiotic dermatitis with eosinophils is found (Rashid & Shim, 2016). Patch testing may be required to identify allergens implicated in contact allergy (Mowad et al., 2016). Not only does patch testing confirm the diagnosis of ACD, it also can differentiate ACD from other eczematous dermatitides. In this case, neomycin would be the most likely relevant allergen, with bacitracin next and polymyxin B only very rarely causing ACD. Although an oral prednisone taper is beneficial in severe ACD, this would need to be used cautiously in conjunction with careful glucose monitoring in patients with diabetes mellitus.
REFERENCES