Case Presentation: A 48-year old woman with a history or ulcerative colitis, on immunotherapy, presented for evaluation of a two-week history of progressive right forearm pain and new-onset hematochezia with right-sided abdominal pain. On admission, she was afebrile and tachycardic, with a severely tender right forearm but no visible erythema or wounds. Laboratory findings were notable for WBC of 10.8 × 10³/µL, CRP of 178 mg/L, CK of 17 U/L. Enteropathogenic E. coli was positive on stool PCR testing. MRI revealed a 2.6 × 5.6 cm intramuscular abscess in the right forearm with surrounding reactive myositis. She was continued on broad-spectrum antibiotics while awaiting multiple abscess cultures and surgical pathology results obtained by plastic surgery during incision and drainage (I&D). Despite treatment, her right forearm pain worsened, and further CT imaging demonstrated a recurrent 2.0 × 1.6 × 5.0 cm fluid collection, prompting a repeat I&D. Abdominal CT revealed long-segment wall thickening with mucosal hyperenhancement and inflammation extending from the splenic flexure to the rectosigmoid colon. Given multiple negative cultures, recurrent sterile abscesses, and evidence of active ulcerative colitis, the decision was made to continue antibiotics and initiate intravenous methylprednisolone 60 mg daily for aseptic abscess syndrome (AAS). Following corticosteroid initiation, the patient experienced a marked improvement in forearm pain without further recurrence of abscess, hematochezia, and inflammatory markers. Calprotectin returned elevated (>3000 µg/g), and surgical pathology revealed fibrinopurulent debris without granuloma formation, supporting the AAS diagnosis. She was discharged home on prednisone 40 mg daily with a 5 mg weekly taper over eight weeks and completed a 14-day oral antibiotic course. Of note, the patient had reoccurrence of right forearm fluid collection one week prior to completing steroid taper.
Discussion: AAS is a rare extraintestinal manifestation of ulcerative colitis, characterized by deep abscess-like fluid collections in the absence of identifiable pathogens. Fewer than 100 cases have been reported, with most involving the spleen (52%), liver (35%), and lungs (23%), and less frequently the muscle, bone, or joint (13%). Intramuscular AAS is clinically indistinguishable from infectious abscesses or pyoderma gangrenosum (PG), often necessitating antimicrobial therapy and surgical drainage. AAS should be suspected when cultures remain negative, imaging reveals recurrent sterile collections, or symptoms persist despite antibiotics, and particularly in patients with IBD. Corticosteroids are the cornerstone of AAS management, with most patients experiencing a rapid and dramatic improvement after initiation. Immunosuppressive or biologic agents are often required, particularly tumor necrosis factor (TNF) inhibitors. Surgery, while sometimes necessary for diagnostic purposes, should ideally be avoided once infection has been excluded, as recurrence after surgical intervention alone is nearly universal. Relapse remains a major challenge, occurring in roughly 40–60% of patients. Colchicine has been suggested to have a protective role against relapse, although supporting data are limited.
Conclusions: Prompt recognition of AAS is critical to distinguish it from infectious etiologies and guide appropriate immunosuppressive therapy to avoid unnecessary surgical intervention and antibiotic use.