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Washington University Experience | VASCULAR | Infarct - Spinal Cord | 2A0 Case 2 History
Case 2 History ---- The patient is a 61 year old man with a past medical history of inflammatory bowel disease, thought initially to be ulcerative colitis but with a discontinuous pattern which is more consistent with Crohn’s disease, perforated diverticulitis s/p partial colectomy, coronary artery disease, dyslipidemia, hypertension, and a six-week history of C. difficile colitis being treated with metronidazole. He was admitted on 6/30 with a one-week history of headache, progressive confusion and aphasia. He was febrile but alert, oriented, and ambulatory with a non-focal neurologic exam. The next morning he was somnolent, unarousable, and only responsive to painful stimuli. A head CT and brain MRI revealed massive cerebral hemorrhages in the right and left middle cerebral artery distribution with edema and minimal midline shift. In the ICU he was empirically started on acyclovir for presumed herpes simplex encephalitis. Over the next two days he developed left-sided motor deficits which progressed to an absence of spontaneous or reactive movement, seizure activity on EEG, and fixed and dilated pupils. On 7/3 he was extubated, made comfort care only, and shortly thereafter developed respiratory failure and died. ---- At autopsy, brain weight was 1520 grams with numerous large and small hemorrhagic infarcts, likely resulting from multiple thromboemboli. The superior sagittal sinus was free of thrombi. Multiple thromboemboli were also noted in the systemic circulation (and lungs) but no embolic source was identified. The anatomic cause of death was bilateral cerebral hemorrhages with septic emboli, secondary to multifocal active colitis. While GMS and gram stains of the brain sections were negative for fungal or bacterial organisms; however, the multifocal nature of the emboli associated in some vessels with necrotizing vasculitis and numerous PMNs suggests septic emboli; however, these lesions are accompanied by more numerous thromboemboli in which the vascular walls are intact, as well as many thrombi involving small veins which also have participated. Also, it is possible that emboli may have been secondarily infected due to septicemia resulting from ulceration of the colonic mucosa.
