Cerebral Septic Emboli: A Unique Complication of Clostridium septicum-Induced Myonecrosis.

Abstract

Nontraumatic clostridial myonecrosis infections are predominantly caused by Clostridium septicum. Most patients have an underlying gastrointestinal malignancy. This case presents a rare association of spontaneous clostridial myonecrosis preceding cerebral septic emboli with underlying invasive colorectal adenocarcinoma. A 60-year-old male with a history of hypertension, diabetes, and a family history of colon cancer presented to the emergency room with worsening left-sided chest pain radiating to his left shoulder. Extensive workup revealed elevated D-dimer, troponin, C-reactive protein, white blood cell count, and creatinine phosphokinase. Due to his clinical signs, symptoms, elevated white count, and further decompensation, he was started on antibiotics for sepsis. Physical exam revealed left upper extremity (LUE) crepitus consistent with imaging of innumerable soft tissue gas collections along the LUE. Incision, drainage, and myomectomy were performed due to concerns of myositis and necrotizing infection. Muscle biopsy revealed myonecrosis, and subsequent samples were positive for C. septicum. Postoperative pressor support and several sessions of surgical debridement were required. He continued to deteriorate and developed left-sided paralysis. Computed tomography head revealed several white matter infarcts indicative of septic emboli. The patient slowly recovered neurologically after switching to central nervous system-penetrating antibiotics. Months later, a colonoscopy revealed cecal adenocarcinoma. This case features a unique course of spontaneous C. septicum infection. There are high mortality rates, and previous studies report an association with colorectal malignancies. Therefore, preventative and diagnostic evaluations are imperative with a confirmed C. septicum infection. To our knowledge, this is the first case reported of cerebral septic emboli secondary to spontaneous myonecrosis with C. septicum, highlighting a unique burden of emboli-induced neurological deficits.