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Washington University Experience | VASCULAR | Small Vessel Disease | 10A0 Case 10 History
Case 10 History ---- The patient was a 48 year old woman with past medical history of obesity, hypertension, hypothyroidism, diabetes mellitus type 2, and multiple abdominal surgeries including a recent laparoscopic incisional hernia repair at an OSH on March 18. The next day she required emergent exploratory laparotomy for a perforated colon and sepsis. She had a prolonged period of hypotension and anemia following the second surgery. She was ventilated and heavily sedated for four weeks post-surgery. Neurologic consultation at the OSH revealed negative carotid Dopplers and echocardiogram, “encephalopathic” EEG, and MRI with diffuse atrophy and diffuse white matter lesions located in periventricular regions and cerebellum. Upon transfer to BJH, she opened her eyes spontaneously and grimaced but did not have any other response. She was treated for a right lower lobe pneumonia and urinary tract infection. MRI showed multiple lesions in periventricular white matter, basal ganglia, and right middle cerebral peduncle thought consistent with anoxic/hypoxic injury. Neurologically she did not show any improvement. Her course was complicated by fevers, hypertension, and tachycardia. She was found without spontaneous respirations, pulses, or pupillary response on May 9. ---- At autopsy the weight of the unfixed brain was 1400g. The grossly identified lesions within the cerebral white matter and corpus callosum microscopically correspond to areas of tissue injury/destruction ranging from patchy white matter rarefaction with concomitant reactive gliosis to overt infarct with accumulation of foamy macrophages. Many of these areas are vasocentric, the associated vessel frequently showing arteriolosclerotic changes with marked wall thickening. Luxol fast blue/PAS and Bielschowsky silver stains confirm the destructive not demyelinative nature of these lesions. A similar area of neuropil rarefaction with concomitant gliosis is identified within the thalamus, though the remainder of grey matter structures including the cortex and hippocampus appear uninvolved by this process. All sectors of the hippocampus contain a full complement of pyramidal neurons. The predominantly white matter pattern of ischemic injury in this patient is somewhat unusual, but is likely a manifestation of the patient's episode of sepsis, hypotension, and anemia superimposed on a state of widespread arteriolosclerosis. There was no evidence of fat embolism, microthrombi or embolic material. Since all the infarcts appear of similar age (i.e. subacute), it supports either a single global hypoxic/ischemic episode or multiple episodes occurring within a relatively short time interval.
