Biochemical markers of brain injury

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.