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Washington University Experience | VASCULAR | Infarct - Spinal Cord | 10A0 Case 10 History
Case 10 History ---- The decedent was a 33-year-old woman diagnosed with severe obstructive sleep apnea in July of 2006 and was started on CPAP. On April 11, she presented to an outside hospital Emergency Department with intractable shortness of breath for 1 week. According to nursing accounts, the decedent was awake but weak and lethargic upon presentation, and she was found to be dyspneic and hypoxic. The patient was subsequently found unresponsive after pulse oximetry alarms were activated. At that point, cardiopulmonary resuscitation was started, after emergent intubation. The resuscitation lasted for approximately 30 min, when the patient was found in ventricular fibrillation. She converted into a perfusing rhythm after defibrillation and was subsequently admitted to the ICU on a ventilator. The initial set of cardiac isoenzymes were unremarkable. D-dimer was elevated at 2180. Chest x-rays revealed bibasilar infiltrates, possibly pneumonia, atelectasis or edema with cardiomegaly and concern for pericardial effusion. Arterial blood gases done after intubation revealed a pH of 7.16, PCO2 of 93 and PO2 of 323. Repeat arterial blood gas showed PO2:FiO2 ranging from 184 mmHg to 277 mmHg, suggestive of acute lung injury/acute respiratory distress syndrome (ARDS). Head CT showed faint hyperdensities along the basal cisterns, interhemispheric falx and tentorial leaflets, which was thought to possibly represent subarachnoid hemorrhage. Loss of gray-white differentiation, effacement of sulci, lateral features and basal cisterns also raised concern for diffuse cerebral edema and possible uncal herniation. The decedent was started on a hypothermia protocol and transferred to BJH for further care. Blood pressure on arrival was 240/115. Upon arrival, the decedent was examined and determined to be dead by neurological criteria. The family was present upon declaration of death on 4/12. ---- Autopsy demonstrated a 550 g heart (normal=250-300 g), with biventricular hypertrophy. Histologic examination of the CNS showed widespread eosinophilic neuronal necrosis in the cerebral cortex, hippocampus, thalamus, cerebellum and brain stem, consistent with global hypoxic-ischemic brain injury. There were also hemorrhages in the spinal cord, consistent with infarction-reperfusion injury.
