Detection of brain injury perioperatively can be a difficult task as it ranges from the very subtle to grossly apparent. Brain injury following cardiopulmonary bypass (CBP) remains a common and serious complication that is often misdiagnosed.1,2 The American College of Cardiology/American Heart Association guidelines for coronary artery bypass graft (CABG) surgery divide postoperative neurologic deficits into two categories.3 Type 1 deficits include major focal neurologic events, stupor and coma. Type 2 deficits describe more global cognitive deficits such as deterioration in intellectual function, memory, and confusion without evidence of focal injury. Type 1 deficits are usually caused by identifiable sources of cerebral hypoxia due to intraoperative hypoperfusion or embolic phenomena. In contrast, the etiology of type 2 deficits is unclear and likely multifactorial; where factors such as hypoxia, time on CPB, age, type of procedure, preoperative creatinine levels, and perioperative inflam-matory response have been implicated in its pathophysiology.4 While physical examination and neuroimaging modalities have proven valuable for the detection and treatment of acute focal brain damage postoperatively, mild and diffuse injuries such as-neurocognitive decline (NCD) seen in type 2 deficits would benefit from improvements in the early diagnosis and identification of these patients. Neuropsycho-logical tests, the current gold standard for detecting NCD, are complex and difficult to use routinely in the postoperative-setting. Identifying biochemical surrogate markers for brain dysfunction would greatly assist in the diag - nosis and timely treatments of patients with this complication.
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