A challenging diagnosis: case report of extensive pyoderma gangrenosum at multiple sites
A 51-year-old female initially presented with infected abdominal, thigh, and sacral ulcers. Her ulcers developed as a result of poor self-care and hygiene. Her past medical history included type 2 diabetes, hypertension, hypercholesterolemia, and back pain. Physical examination revealed an abdominal ulcer measuring 4 cm × 2 cm in the right iliac fossa with surrounding erythema, a small ulcer on her left thigh (1 cm × 1 cm), and two sacral ulcers (7 cm × 3 cm and 4.5 cm × 2 cm, respectively). Ulcer cultures revealed skin flora. Although she did not have any systemic features of infection, blood investigations on admission showed an elevated white cell count of 14.9×109/L (reference interval, 4.0×09−11.0×109/L) and C-reactive protein of 120 mg/L (reference interval, 0–10 mg/L). She was subsequently commenced on 2 g of empirical intravenous flucloxacillin four times daily.\nIn the next few weeks, all her wounds worsened despite wound dressings and antibiotics. Her abdominal and thigh ulcers had increased in size. The size of her two sacral ulcers remained the same but had increased wound necrosis. One month after admission, her abdominal ulcer measured 21 cm × 7 cm, and the thigh ulcer was 4 cm × 1 cm. In view of this, surgical excisions of the necrotic areas were performed. Vacuum-assisted closure dressings were applied to the anterior abdomen and sacrum.\nThree days later, the patient underwent a routine vacuum-assisted closure dressing change. It was noted that her wounds had worsened rapidly since the last debridement. The once healthy wound edges had become necrotic. Further debridement was performed. Excised tissues sent off for microscopy and culture grew methicillin-sensitive Staphylococcus aureus and Enterobacter aerogenes. Intravenous tazocin (4.5g 8 hourly) was added for suspected postoperative wound infection.\nThe patient’s wounds continued to deteriorate with antibiotics and further debridements. After the third debridement, the abdominal ulcer had increased to a size of 32 cm × 11 cm, and the two sacral ulcers became a huge sacral defect extending into the perianal region ( and ). Cultures of subsequently debrided tissue were negative for bacteria and fungi. Repeated histological sections of sacral and abdominal tissues revealed neutrophilic infiltrates extending into deep dermis and no evidence of malignancy ( and ). Antinuclear antibodies, extractable nuclear antigens, rheumatoid factor, and anti-neutrophil cytoplasmic antibodies were all negative. A diagnosis of PG was made, and our patient was commenced on 50 mg of prednisolone daily. After 1 week, her wounds showed slow improvement, with resolution of necrotic wound edges and formation of granulation tissue. Two weeks later, she developed steroid-induced hyperglycemia, and 500 mg twice daily of mycophenolate mofetil was added as a steroid sparing agent. Her prednisolone dose was gradually tapered by 5 mg every 2 weeks, and the dose of mycophenolate mofetil increased to 1 g twice daily. Four months after admission, the patient underwent successful split skin grafts and primary closure to her abdominal and sacral ulcers while on immunosuppressive therapy ( and ). At 3-month follow-up, there was no recurrence of the disease.