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Washington University Experience | VASCULAR | Cardiac Arrest Encephalopathy | 2A0 Case 2 History
Case 2 History
The patient is an 83 year old woman with past medical history significant for coronary artery disease (s/p coronary artery bypass graft), hypercholesterolemia, and degenerative joint disease who was admitted on 3/14 for surgical repair of a left humeral fracture resulting from a fall on snow on 3/12. On exam she was noted to have a Glascow Coma Scale of 15 with motor strength and sensation intact. She was discharged home and instructed to follow up with Orthopedics in two days. On 3/14, prior to the surgical procedure, no gross neurological deficits were noted by Orthopedics. The patient underwent an open reduction and internal fixation. She tolerated the procedure without complication and postoperatively at 16:40 was reportedly awake, oriented, conversant, and pain free as noted by Anesthesia. The patient had documented stable vital signs at 18:00. At 2000 she was found pulseless. She was resuscitated and transferred to the Surgical ICU comatose and on pressors. Initial laboratories were notable for anemia with a hematocrit of 20 and acidemia with a pH of 7.04. Neurologic consultation on 3/15 revealed no evidence of brainstem function. After discussion with family regarding the dismal prognosis, support was withdrawn and the patient expired on 3/15. ---- At autopsy, the weight of the unfixed brain was 1390g and the appearance of edema. Coronal sections of the cerebral hemispheres revealed hints of laminar necrosis which was confirmed histologically in frontal, parietal, temporal, and occipital neocortices. Microscopic examination of the deep grey structures, including the basal ganglia and thalamus showed patchy eosinophilic neuronal necrosis and small foci of hemorrhage with early margination of neutrophils in several vessels. Not only do both thalami show small hemorrhages and eosinophilic neuronal necrosis, but bilateral lateral geniculate nuclei also show similar changes. There is evidence of eosinophilic neuronal necrosis in both hippocampi involving CA1-4 regions. Sections of the midbrain show patchy eosinophilic neuronal necrosis with small areas of hemorrhage and early infarction involving the periventricular grey matter and several of the periventricular nuclei in a bilateral, symmetrical fashion. Areas of the dorsal pons and medulla showed similar changes. Eosinophilic neuronal necrosis is specifically noted within the olives as well as pontine nuclei. Microscopic examination of the cerebellum shows patchy eosinophilic neuronal necrosis of the Purkinje cells as well as the neurons in the dentate nucleus. Silver stains were performed on areas of neocortex as well as the hippocampus. These show moderate numbers of neuritic plaques and scattered neurofibrillary tangles accompanied by patchy amyloid angiopathy confirmed with Thioflavin-S stain. These are constituents of Alzheimer Disease Neuropathologic Change suggesting a possible dementing component; however, there was no clinical history of dementia in this patient
