CORONARY ARTERY bypass grafting (CABG) is one of the most common major surgical procedures performed in the United States, resulting in the relief of angina and an improved quality of life. With improvements in surgical and cardiopulmonary bypass techniques, the rates of mortality and cardiac morbidity have decreased with time, and neurologic complications now represent one of the greatest challenges to the procedure. Several forms of cerebral injury or dysfunction may occur after CABG. Clinically recognized cerebral infarction occurs in 2% to 6% of patients1- 3 and is presumably due to macroemboli arising from the cardiac chambers or cardiopulmonary bypass circuit or from atheromatous debris within the aortic arch. A shower of small embolic particles combined with decreased washout from cerebral hypoperfusion can produce a clustering of ischemic lesions in a watershed distribution.4 Postoperative encephalopathy or delirium occurs in a larger proportion of patients than cerebral infarction and is often transient. A wide variety of factors may contribute to delirium, including adverse effects of anesthesia, infection, hypotension, stroke, seizures, metabolic disturbances, and underlying dementia. Finally, there appears to be a group of patients with more subtle postoperative cognitive dysfunction, as detected by a decline in neuropsychological testing scores from baseline. In many patients these deficits improve by 6 months, but in some patients, longer-term cognitive dysfunction is seen 1 or 5 years later.2,5 The cause of cognitive decline in this latter group is the subject of much debate; it may represent the effect of age in patients with underlying neurological disease, or it may be the result of a subtle brain injury at the time of bypass surgery.
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