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Washington University Experience | VASCULAR | Small Vessel Disease | 2A0 Case 2 History
Case 2 History ---- The patient was a 56-year-old woman with a past medical history significant for migraine headaches; hepatitis C and non-alcoholic steatohepatitis, Addison's disease, chronic anticoagulation for DVT prevention, coronary artery disease and hypertension. She presented to an OSH with a new, sudden onset headache and confusion. On exam, her blood pressure was 216/136 with a heart rate of 110. A head CT showed intraventricular hemorrhage involving the right lateral, third, and fourth ventricles in addition to the aqueduct. Cerebral angiogram showed no vascular malformation or aneurysm. Suddenly she developed acute deterioration of her mental status, becoming unresponsive, apneic, and had fixed pupils. An emergent cerebral angiogram showed patchy loss of staining of the distal parenchyma bilaterally consistent with ischemic infarction. An emergent EEG showed generalized slowing indicative of diffuse cerebral dysfunction and a repeat head CT showed stable ventricular hemorrhages as well as decreased gray and white matter differentiation concerning for brain edema. She died 3 days after admission. ---- At autopsy the weight of the unfixed brain was 1310g. A large hemorrhage originated in the right basal ganglia with intraparenchymal and intraventricular extension. Patchy foci of discoloration, softening and petechial hemorrhages were consistent with infarcts involving the cortical ACA/MCA and MCA/PCA vascular watershed territories. Thickened hyalinized vessels were demonstrated in the cerebral hemispheric white matter, deep gray nuclei, and thalamus likely reflecting chronic hypertension. Extensive hypoxia-ischemia ranging from selective neuronal necrosis to frank infarction, involved cerebral hemispheres, basal ganglia and thalamus, brainstem and cerebellum, with cerebral watershed exaggeration as well as marked cerebral edema. The exaggeration in the posterior cerebral artery territory in both occipital lobes is often seen in uncal herniation with PCA compression, although only uncal grooving was noted in the absence of Duret hemorrhages.
