Progressive Neurodegeneration From Anoxic Injury Following Perioperative Cardiac Arrest

Severe hypoxic-ischemic brain injury following cardiac arrest can result in persistent and evolving neurologic, cognitive, and visual impairment, with later clinical decline that may be difficult to distinguish from superimposed neurodegenerative disease. A prolonged and evolving pattern of neurologic, cognitive, and visual impairment is documented in a woman throughout her 70s and 80s who survived a perioperative cardiac arrest requiring an extended resuscitation interval. Her recovery was complicated by Anton syndrome, prosopagnosia, gait apraxia, chronic microvascular disease with progressive atrophy, intermittent episodes of delirium during superimposed infections, and later neuroimaging findings suggestive of Alzheimer-type degeneration. This case illustrates the dynamic trajectory of severe anoxic encephalopathy, the challenge of differentiating delayed post-hypoxic injury from superimposed neurodegenerative disease, and the need for sustained multidisciplinary care extending well beyond the initial insult. Serial cognitive assessments over nearly a decade further demonstrate the patient's initial severe impairment, subsequent partial cognitive recovery, and later persistent moderate impairment, while the evolution of the neuroimaging raises the important question of whether the changes found represented chronic post-anoxic injury, Alzheimer's disease, or a combination of both.