Pyoderma gangrenosum demographics, treatments, and outcomes: an analysis of 2,273 cases
Pyoderma gangrenosum is a rare, neutrophil-mediated, auto-inflammatory dermatosis. This condition has clinical features analogous to infectious processes and must be quickly diagnosed to be properly treated. The purpose of this study was to characterise relevant clinical features associated with pyoderma gangrenosum based on a large inpatient cohort.
The National Inpatient Sample (US) was used to identify patients with the diagnosis of pyoderma gangrenosum using ICD-9 diagnosis code 686.01, during the years 2008–2010. Data was collected on demographics, associated diagnoses, treatments and outcomes. Data analysis was performed using SAS 9.3 software.
A total of 2,273 adult patients were identified with pyoderma gangrenosum. Mean age was 56 years; 66.4% were female; 71.1% were Caucasian. Pyoderma gangrenosum was the primary diagnosis in 22.6% of patients, followed by cellulitis (9.4%), inflammatory bowel disease (IBD) (6.9%), wound/ulcer (5.4%), sepsis (4.7%), and postoperative infection/complication (2.7%). The most common procedures performed were wound debridement (5.3%), skin biopsy (5.1%), esophagogastroduodenoscopy (2%), large bowel biopsy (1.9%), and incision and drainage (1.1%). A total of 74 patients (3.2%) died during hospitalisation.
Pyoderma gangrenosum is a serious skin condition, frequently associated with systemic disease, and often confused with other skin pathergies. Pyoderma gangrenosum should be considered when evaluating patients with ulcers, wounds, and post-operative complications. A high index of suspicion is necessary for early and accurate diagnosis and prompt treatment.
Pyoderma gangrenosum (PG) is a rare, auto-inflammatory skin condition characterised by pustules that progress to sterile, ulcerative cutaneous lesions. Most eruptions are spontaneous and occur in association with hematologic, rheumatologic, or gastrointestinal disease. However, lesions also develop at traumatic and surgical sites.1 PG was first described in 1916 by Louis Brocq in five patients with necrotic, rapidly-progressive ulcers with a cliff-like ridge at the border.2 The term ‘pyoderma gangrenosum’ was coined by Brusting et al. in 1930, who believed the condition to be a form of cutaneous gangrene caused by disseminated streptococcal infection.3 Though still poorly understood, the aetiology of PG is currently hypothesised to be autoinflammatory, rather than infectious.4
Diagnosis of PG can be difficult because its presentation is similar to other infectious and inflammatory processes, including wound infection, hidradenitis suppurativa, cutaneous malignancy, antiphospholipid syndrome, Bechet's disease, ecthyma gangrenosum, leukocytoclastic vasculitis, and Sweet's syndrome.5,6,7 PG can progress rapidly, does not respond to antibiotic therapy, and is exacerbated by surgical debridement. Prompt diagnosis is critical to avoid serious morbidity.8
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