65 years, Female, prior CVA who initially presented with HHS c/b AKI and AMS. Her AKI and HHS improved however as she was being set up for discharge she had an acute hypoxemic event requiring intubation, likely in the setting of an aspiration event. There is an area of high DWI signal in the left lateral aspect of the medulla with associated low ADC signal and mildly increased T2/FLAIR signal indicating acute infarct. Additional areas of diffusion restriction are present in the right occipital lobe, right frontal lobe white matter, and posterior limb of the left internal capsule. There is asymmetric heterogeneous T1 shortening in the left basal ganglia, which could reflect asymmetric mineralization or minimal blood products from subacute to chronic infarct. There appears to be volume loss in the right caudate nucleus with susceptibility artifact indicating old hemorrhagic infarct. Chronic lacunar infarct in the left paramedian pons is also noted. No intracranial mass or significant mass-effect. Mild prominence of the ventricles and sulci are compatible with generalized cerebral volume loss. There is no evidence of hydrocephalus. Several foci of T2/FLAIR hyperintensity are seen in the bilateral subcortical and periventricular white matter, which are nonspecific, but compatible with background of mild chronic small vessel ischemic changes. Major intracranial vascular flow-voids are preserved. Sella and orbits are grossly within normal limits. There is mild mucosal thickening in scattered ethmoid air cells and moderate mucosal thickening in the right sphenoid sinus. Secretions are noted filling the posterior nasal cavity and nasopharynx. A moderate amount of fluid signal is present in bilateral mastoid air cells. Orogastric and endotracheal tubes are partially visualized.
Multiple small acute, subacute, and chronic supra and infratentorial infarcts as detailed above. In particular acute infarcts involve the left lateral medulla as well as bilateral cerebral hemispheres. 