A 28-year-old man presents with suspected recurrent right forearm cellulitis. The patient has had four episodes of pruritic, edematous, erythematous plaques on the arms and neck over the past three months. Each episode lasted for seven to ten days and was in a different location. He has been treated successfully with antibiotics, but this episode has developed while on clindamycin. He has a history of HIV managed with daily emtricitabine, tenofovir, and rilpivirine. His recent CD4 count was 1204 cells/cmm with an undetectable viral load. On admission he was afebrile with normal vitals. On his right forearm and inner upper arm were several warm erythematous slightly edematous plaques (Figure 1a). Laboratory analysis was significant for a white blood cell count of 15.2 K/uL with 80.4% neutrophils and 5 % eosinophils. As the patient’s rash did not improve on antibiotics dermatology was consulted and performed a biopsy. Histopathology revealed perivascular and interstitial infiltrate with numerous eosinophils and neutrophils, and prominent superficial papillary dermal edema suggesting a diagnosis of Wells syndrome (eosinophilic cellulitis) (Figure 1b). The patient was successfully treated with anti-histamines and topical corticosteroids.
Discussion:
Eosinophilic cellulitis, also known as Wells’ syndrome, was first described in 1971 by Dr. Wells as a recurrent granulomatous dermatitis with eosinophilia. This rare cutaneous condition lacks systemic involvement, does not respond to anti-biotics, requires a high degree of clinical suspicion to diagnose, and presents with peripheral eosinophilia in only about fifty percent of cases. Cutaneous findings appear cellulitic and most typically present with erythematous plaques preceded by pruritis, but blisters, bullae, or nodules may also be seen. Resolution of the lesions occurs in two to eight weeks and may result in hyperpigmentation and skin atrophy resembling morphea. Acute histology reveals tissue edema and a dermal eosinophilic infiltration in a perivascular pattern, while subacute to chronic histology reveals the classic “flame figures” composed of bundles of collagen coated with eosinophils. A literature review of 32 cases of idiopathic eosinophilic cellulitis in 2012 concluded that oral steroids achieved the highest rate of resolution and were 92% effective. In these patients, oral prednisone was typically given 2mg/kg for one week then tapered over two to three weeks. Topical steroids and oral anti-histamines were less effective. As recurrence occurs in up to half of cases, treatment of the underlying associated condition (if determined) is imperative, and alternate day low dose prednisone may be indicated.
Conclusions:
When a physician is challenged with a case of cellulitis that does not respond to conventional antibiotic therapy, non-infectious etiologies must be considered. After a thorough history, physical, and diagnostic workup has been completed, skin biopsy with histopathology, culture, and direct immunofluorescence may be the only diagnostic option left to secure a diagnosis. This case exemplifies the importance that a Hospitalist may play in securing an accurate diagnosis by employing careful history taking and avoiding premature closure along with anchoring bias when patients are admitted to the hospital with an incorrect leading diagnosis.