Embolic Stroke Syndrome Underlies Encephalopathy and Coma Following Cardiac Surgery

In the April 2001 issue of the ARCHIVES, Wityk et al¹ reported that most patients with clinical neurological deficits, and particularly encephalopathy, who were referred for brain imaging after cardiopulmonary bypass procedures sustained acute multifocal embolic cerebral infarction, evidenced on diffusion-weighted and perfusion-weighted brain magnetic resonance imaging (MRI) scans. The importance of this finding is strengthened by examining the parallels to findings from earlier MRI neuroimaging investigations.^{2 - 3}

We reported a detailed review of neuroradiological evidence in patients who became symptomatic after open- and closed-chamber heart surgery. Most patients with global deficits including encephalopathy and coma shared the same mechanism of brain injury as those with focal hemispheric signs: namely, acute multifocal ischemic infarction.² At least 78% of our patients with lesions detectable by T2-weighted MRI and computed tomography (CT) exhibited neuroradiological features consistent with an embolic etiology. These lesions were distributed across multiple cerebrovascular territories such as bilateral hemispheres or anterior, anterior and posterior, or posterior circulations in individual patients, exactly as reported by Wityk et al.¹ Our previous impression that an overall lesion detection rate of only 60% in symptomatic patients was likely due to the incomplete sensitivity of MRI and CT technology available at that time for acute cerebral infarction is now borne out in the article by Wityk and colleagues. The embolic etiology of encephalopathy, the broad multiterritorial distribution of infarctions, and the high frequency of macroscopic lesions in symptomatic patients are 3 prominent parallels between these 2 studies.

Our study also demonstrated that the frequency of ischemic injury in specific brain regions among symptomatic patients was distributed in descending order: occipital, 61%; parietal, 61%; frontal, 50%; cerebellar, 44%; temporal, 28%; thalamus, 22%; brainstem, 22%; and basal ganglia, 17%. Notably, hemorrhagic transformation occurred at the zones of infarction in 33% of patients: cortical petechial hemorrhage in 22% and severe intraparenchymal hemorrhage and hematoma in 11%. Finally, we noted that in patients with perioperative cerebral infarction and preexisting brain parenchymal injury (small-vessel disease, old infarct, or cerebral atrophy), encephalopathy and coma manifested 3 times more often than focal signs.²

The cumulative neuroimaging and clinical correlation evidence^{1 - 2} demonstrates that in the setting of cardiac surgery, global and focal neurological deficits are poles along a continuum of possible stroke manifestations. This realization has immediate clinical applications for guiding postoperative stroke surveillance in the intensive care unit. A formal neurological evaluation and opinion, with early recourse to neuroimaging whenever feasible, should be obtained to diagnose or rule out cerebral infarction and hemorrhage in all patients with unexplained post–cardiopulmonary bypass encephalopathy or coma. These neuroimaging studies also indicate that the methods for clinical research on stroke risk factors should be changed. Traditional approaches emphasizing focal neurological deficits for identifying and weighting stroke risk factors can and should be modified to consolidate global and focal deficits.³

Neuroimaging evidence of a multifocal embolic stroke syndrome in patients who are symptomatic after undergoing cardiac surgery naturally leads to the question of whether some asymptomatic patients might be sustaining occult cerebral infarctions. The prospective study by Steinberg et al⁴ of a series of patients undergoing aortic or mitral valve surgery provides insight into this issue; comparisons between preoperative and postoperative brain MRI scans revealed new perioperative ischemic brain lesions in 58% of their postoperatively asymptomatic patients. The occurrence of cerebral infarctions in "silent" brain regions (although a potential cause of personality changes, disabling visual field defects, decrements in neuropsychological test profiles, and other effects not readily discerned on routine clinical neurological examinations) is logically consistent with the distributed nature of embolic stroke syndrome in cardiac surgery. Cumulative neuroimaging and clinical correlation investigations now provide a base of evidence that embolic cerebral infarction dominates the etiopathogenesis of symptomatic (and possibly asymptomatic) neuroinjury in cardiac surgery and that the specific clinical neurological signs of such injury (global vs focal) will vary from patient to patient according to strategic lesions, burden and distribution of acute injury, and relative integrity of the preoperative cerebral substrate.