Table of Contents
Washington University Experience | VASCULAR | Small Vessel Disease | 12A0 Case 12 History
Case 12 History ---- The decedent was an 88 year old man with a past medical history significant for atrial fibrillation for 2 years (rate controlled without anticoagulation due to history of falls), hypertension, severe aortic stenosis, benign prostatic hypertrophy, degenerative joint disease, L3 burst fracture 2 years prior to death, elbow bursitis fracture, and gastroesophageal reflux disease. His surgical history includes appendectomy and bilateral phacoemulsification. He was a former smoker. At baseline, he was conversant and was able to do some activities of daily life. He had several hospitalizations for falls and syncope/near-syncope. On 7/27, the decedent presented to BJH with altered mental status and right sided weakness. Per nursing home staff, he was at baseline the night before but on morning rounds was found to be incontinent, have slurred speech, leaning to the right, had right sided weakness (upper and lower extremities), and was oriented x 0-1 (usually x 2). In the ED, head CT showed a subacute infarct in the left parietal lobe and chronic lacunar infarcts in the left lentiform nucleus, right pons, and right cerebellum. Laboratories were significant for mild anemia (Hgb 12.2 g/dL), negative Troponin I (<0.03 ng/mL), and INR of 1.2. Tissue-type plasminogen activator was not given due to time interval ineligibility. He was transferred to the Neurosurgery/Neurology ICU ventilator-dependent respiratory failure. He was also found to have forced gaze deviation to the right. MRI on 07/29 showed multiple areas of diffusion restriction and T2/FLAIR hyperintensity, with the largest involving the left parietal lobe, and smaller foci involving the right occipital lobe, lateral to the right thalamus, within both cerebral peduncles and midbrain, and in the pons, medulla and cerebellar hemispheres; clinically these were thought to represent subacute embolic infarcts. Also noted were an old lacunar infarct in the left caudate tail and bilateral periventricular white matter FLAIR hyperintensities, consistent with chronic small vessel disease. MR angiography showed occlusion of the left vertebral artery (just proximal to the basilar artery) and of the left carotid artery; distal flow to the left carotid and left middle cerebral artery was reconstituted from the right anterior circulation via the circle of Willis and by retrograde flow from the large left ophthalmic artery. His hospital course was also complicated by methicillin susceptible Staphylococcus aureus tracheitis that was treated with cefazolin. Due to the patient’s poor prognosis, palliative care was discussed with his family and on 8/8, the decision to withdraw care was made: patient was extubated, and expired. ---- At autopsy the unfixed brain weighed 1270g. There were numerous large and small subacute infarcts in the left occipital lobe, the white matter of the right cerebellar hemisphere, and the midbrain. Although it was thought consistent with embolic origin, a source and definitive emboli was not identified. There was extensive, diffuse atherosclerosis, arteriosclerosis and arteriolosclerosis, with cerebral amyloid angiopathy and Alzheimer disease (A2, B2, C?, intermediate) neuropathologic change. The aorta showed ulcerated atheromatous plaques.
