Table of Contents
Washington University Experience | VASCULAR | Infarct - Embolic | 3A0 Case 3 History
Case 3 History ---- The patient was a 64-year-old man with a history of coronary artery disease s/p drug eluting stent, hypertension, diabetes mellitus, medication non-compliance and stroke x 2 with residua of cognitive impairment and right hemiparesis. He presented to the BJH ER on 12/9 unresponsive, hypotensive to 85/54, hyperglycemic (1,470 on BMP) and hypothermic to 33.6. His family had seen him in his usual state 8 hours prior to presentation to the ER. Workup there showed troponin elevation (1.87), diabetic ketoacidosis, acute renal failure, a leukocytosis (15.1K) and hyperkalemia (6.9). Head CT in the ER revealed old bilateral lacunar infarcts in the right basal ganglia, left internal capsule and periventricular white matter changes consistent with microvascular disease. He remained unresponsive. He was placed on broad spectrum antibiotics for sepsis and received insulin. Blood cultures subsequently grew Proteus mirabilis. He had a persistent leukocytosis which peaked at 18.7K, anemia with Hgb of 8.1, hypernatremia with a peak sodium of 161 which was subsequently slowly corrected, resolving acute renal failure, persistent hyperglycemia with value of 374 at last check on 12/17, and a troponin elevation peaking at 6.1. Throughout the remainder of his hospitalization he remained unresponsive to any form of stimulation. A brain MRI on 12/15 revealed widespread patchy T1 and T2 signal abnormalities involving grey and white matter of the bilateral cerebral hemispheres, cerebellum, midbrain, and pons. Neurology consult had been following the patient throughout the majority of his hospital stay and thought his persistent encephalopathy had a poor prognosis. The family decided on comfort care and he passed. ---- At autopsy numerous CNS infarcts involving cerebral hemispheres, deep gray nuclei, cerebellum and brainstem were of varying ages. Some cortical infarcts exhibit large numbers of PMNs and fragments of nuclei, a “dirty” appearance consistent with bacterial involvement. Septic infarcts, likely embolic (no source identified) in origin, particularly involved occipital lobe and cerebellum (bacteria identified) and leptomeningitis, patchy, in continuity with septic infarcts. A clinical history of hypertension, diabetes and coronary artery disease in conjunction with post-mortem findings of cerebral atherosclerosis and marked arteriolosclerosis suggests that microvasculopathy as well as thromboemboli contributed to his neuropathologic picture as well as loss of perfusion resulting in watershed infarction.
