This patient has peristomal pyoderma gangrenosum (PG), and a topical potent glucocorticoid, such as clobetasol, is the preferred treatment. PG is an autoimmune ulcerative process that may occur idiopathically or in conjunction with an underlying disease; the most common disease association is inflammatory bowel disease (IBD). This patient has IBD and had recent surgery; 20% to 30% of patients with PG may exhibit “pathergy” or induction of lesions in response to trauma, such as surgery. Peristomal PG is a common manifestation, and early recognition is essential to avoid expansion, thereby limiting ostomy appliance adherence and devastating patients' quality of life. PG ulcers are typically painful, may rapidly expand, and are often exudative. When appropriate therapy is instituted, the lesions often dry out and become less painful over 1 to 2 weeks. Even when the PG inflammation is controlled, patients are left with a large ulcer that must then heal, and local care is critical. PG is treated with glucocorticoids (oral, topical, or intralesional), cyclosporine, or infliximab (a tumor necrosis factor α inhibitor) as first-line therapy for most patients. Active IBD should be treated as well.

Replacing the ostomy to the opposite side would entail major surgery, which, in the setting of active PG, could worsen the problem and may lead to PG at the new site. Removing the ostomy would not address the PG ulcer.

Rituximab is not indicated for PG, as rituximab targets CD20+ cells (B cells), which have little role in the pathogenesis of PG.

Because of the nature of the disease, PG lesions should not be debrided. PG lesions will worsen after debridement. It is not uncommon for PG to be diagnosed after repeated, unsuccessful debridements for a presumed infection result in dramatic worsening of the initial ulcer. Regardless, there is no necrotic tissue here to debride.