Hidradenitis suppurativa (HS) is a common chronic inflammatory skin disease characterized by purulent subcutaneous nodules, papules, abscesses, and fistula tracts that lead to scarring and fibrosis. Lesions develop primarily in the axilla, groin, and other intertriginous and hair-bearing areas.
The natural history of the disease is characterized by periods of disease flare, followed by periods of disease quiescence. Patients might have weeks or months of low disease activity but frequently develop multiple exacerbating episodes over the course of weeks or months. The condition primarily presents in adolescent and peripubescent years, continuing throughout adulthood. Some evidence suggests a bimodal disease distribution, with a second peak of incidence in middle-aged adults. Women and men are affected equally; however, the disease can be phenotypically different in men and women.
Patients frequently present in emergency and inpatient settings for evaluation because of the pain and severity of HS flares as well as associated systemic symptoms. Inpatient and emergency department (ED) care are unique opportunities for dermatologic hospitalist and dermatologic consultative services to educate other physicians about the condition and initiate aggressive treatments that are frequently necessary to control HS flares. This article aims to address best methods for treating HS in these settings.
Pathophysiology
Although the exact pathophysiology of the condition is unknown, HS is thought to begin with follicular occlusion with downstream inflammation mediating neutrophilic activity and scarring. Hyperplasia of the infundibular epithelium is observed on histology, and the resulting occlusion, contained keratin, and follicular rupture initiate robust downstream inflammation.1,2 Follicular occlusion might be initially androgen mediated3 or might occur in combination with friction4 and genetic or acquired factors involving Notch signaling. Although HS characteristically presents in areas of high apocrine density, apocrine glands are not thought to be the primary mediator of disease activity.5 IL-17, IL-23, tumor necrosis factor α, and IL-1β are implicated in the pathogenesis of HS, but it is unknown if these cytokines are the driving pathologic factor in HS or if they are merely secondary sequelae.6
Demographics and Prevalence in Hospitalized Patients
Although increasing treatment availability has brought more attention to HS, true prevalence is unknown. A prevalence of 1% has been reported in many European countries.7 Global prevalence has been more difficult to determine, with variable data suggesting a prevalence of 0.03% to 8%, depending on the population included.8 Most patients studied in a US-based claims database were aged 30 to 64 years, and the overall prevalence was 0.05%.9 Despite prevalence similar to psoriasis, utilization of high-cost emergency and inpatient admissions is notably higher among patients with HS. Recent claims data suggest that HS patients utilize the ED at a rate 3 times higher than psoriasis patients and are admitted as inpatients at a rate 5 times higher.10 Similar data suggest an associated increased cost of care for patients with HS vs other conditions, such as psoriasis, due to frequent ED and inpatient stays.11 Although HS frequently presents in the inpatient and emergency settings, there is little literature on best methods for managing patients in these settings.