Stroke is better characterized with respect to risk factors. Although studies differ somewhat as to all the risk factors, certain patient characteristics consistently correlate with an increased risk for cardiac surgery–associated neurologic injury. In a study of 2108 patients from 24 centers in a study conducted by the Multicenter Study of Perioperative Ischemia, incidence of adverse cerebral outcome after CABG surgery was determined and the risk factors analyzed.² Two types of adverse cerebral outcomes were defined. Type I included nonfatal stroke, transient ischemic attack (TIA), stupor or coma at time of discharge, and death caused by stroke or hypoxic encephalopathy. Type II included new deterioration in intellectual function, confusion, agitation, disorientation, and memory deficit without evidence of focal injury. A total of 129 (6.1%) of the 2108 patients had an adverse cerebral outcome in the perioperative period. Type I outcomes occurred in 66 (3.1%) of 2108 patients, with type II outcomes occurring in 63 (3.0%) of 2108 patients. Stepwise logistic regression analysis identified eight independent predictors of type I outcomes and seven independent predictors of type II outcomes (Table 23-1).

Table 23-1 Risk Factors for Adverse Cerebral Outcomes after Cardiac Surgery

Risk Factor	Type I Outcomes	Type II Outcomes
Proximal aortic atherosclerosis	4.52 [2.52 to 8.09]^*
History of neurologic disease	3.19 [1.65 to 6.15]
Use of IABP	2.60 [1.21 to 5.58]
Diabetes mellitus	2.59 [1.46 to 4.60]
History of hypertension	2.31 [1.20 to 4.47]
History of pulmonary disease	2.09 [1.14 to 3.85]	2.37 [1.34 to 4.18]
History of unstable angina	1.83 [1.03 to 3.27]
Age (per additional decade)	1.75 [1.27 to 2.43]	2.20 [1.60 to 3.02]
Admission systolic BP > 180 mm Hg		3.47 [1.41 to 8.55]
History of excessive alcohol intake		2.64 [1.27 to 5.47]
History of CABG		2.18 [1.14 to 4.17]
Arrhythmia on day of surgery		1.97 [1.12 to 3.46]
Antihypertensive therapy		1.78 [1.02 to 3.10]

BP = blood pressure; CABG = coronary artery bypass graft surgery; IABP = intra-aortic balloon pump.

* Adjusted odds ratio [95% confidence intervals] for type I and type II cerebral outcomes associated with selected risk factors from the Multicenter Study of Perioperative Ischemia.

From Arrowsmith JE, Grocott HP, Reves JG, et al: Central nervous system complications of cardiac surgery. Br J Anaesth 84:378, 2000.

Of all the factors in the Multicenter Study of Perioperative Ischemia analysis, age appears to be the most overwhelmingly robust predictor of stroke and of neurocognitive dysfunction after cardiac surgery. Age has a greater impact on neurologic outcome than it does on perioperative myocardial infarction or low cardiac output states after cardiac surgery (Fig. 23-1).

Figure 23-1 The relative effect of age on the predicted probability of neurologic and cardiac morbidity after cardiac surgery.

(From Tuman KJ, McCarthy RJ, Najafi H, et al: Differential effects of advanced age on neurologic and cardiac risks of coronary artery operations. J Thorac Cardiovasc Surg 104:1510, 1992.)

Atheromatous disease of the ascending, arch, and descending thoracic aorta has been consistently implicated as a risk factor for stroke in cardiac surgical patients. The increased use of transesophageal echocardiography (TEE) and epiaortic ultrasonography has added new dimensions to the detection of aortic atheromatous disease and the understanding of its relation to stroke risk. These imaging modalities have allowed the diagnosis of atheromatous disease to be made in a more sensitive and detailed manner, contributing greatly to the information regarding potential stroke risk. Studies have consistently reported higher stroke rates for patients with increasing atheromatous aortic involvement (particularly the ascending and arch segments). This relationship is outlined in Figure 23-2.

Figure 23-2 Stroke rate 1 week after cardiac surgery as a function of atheroma severity. Atheroma was graded by transesophageal echocardiography as follows: I, normal; II, intimal thickening; III, plaque < 5 mm thick; IV, plaque > 5 mm thick; V, any plaque with a mobile segment.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Hartman GS, Yao FS, Bruefach M 3rd, et al: Severity of aortic atheromatous disease diagnosed by transesophageal echocardiography predicts stroke and other outcomes associated with coronary artery surgery: A prospective study. Anesth Analg 83:701, 1996.)

Cause of Perioperative Central Nervous System Injury

Because central nervous system dysfunction represents a wide range of injuries, differentiating the individual causes of these different types of injuries becomes somewhat difficult (Box 23-1). They are frequently grouped together and superficially discussed as representing different severities on a continuum of similar injury. This likely misrepresents the different causes of these injuries. The following section addresses stroke and cognitive injury (Table 23-2).

BOX 23-1 Causes of Central Nervous System Complications after Cardiopulmonary Bypass

• Cerebral emboli

• Global hypoperfusion

• Inflammation

• Cerebral edema

• Cerebral hyperthermia

Table 23-2 Causes of Cognitive Dysfunction after Cardiac Surgery

Cause	Possible Settings
Cerebral microemboli	Generated during cardiopulmonary bypass (CPB); mobilization of atheromatous material or entrainment of air from the operative field; gas injections into the venous reservoir of the CPB apparatus
Global cerebral hypoperfusion	Hypotension, occlusion by an atheromatous embolus leading to stroke
Inflammation (systemic and cerebral)	Injurious effects of CPB, such as blood interacting with the foreign surfaces of pump-oxygenator; upregulation of proinflammatory cyclooxygenase mRNA
Cerebral hyperthermia	Hypothermia during CPB; hyperthermia during and after cardiac surgery, such as aggressive rewarming
Cerebral edema	Edema from global cerebral hypoperfusion or from hyponatremia; increased cerebral venous pressure from cannula misplacement
Blood-brain barrier dysfunction	Diffuse cerebral inflammation; ischemia from cerebral microembolization or increased intracranial pressure
Pharmacologic influences	Anesthetic-related cognitive damage; necrosis of neonatal brains; proteomic changes
Genetic influences	Effects of single nucleotide polymorphisms on risk for Alzheimer’s disease or for acute coronary syndromes and other thrombotic disorders

Neuroprotective Strategies

Emboli Reduction

The aortic cannula may be very important to reduce cerebral emboli production. Placement of the cannula into an area of the aorta with a large atheroma burden may cause the direct generation of emboli from the “sandblasting” of atherosclerotic material in the aorta. The use of a distal aortic cannula, where the tip of the cannula lies beyond the origin of the cerebral vessels has also been found to reduce emboli load.

Blood that is returned from the surgical field though the use of the cardiotomy suction may significantly contribute to the particulate load in the CPB circuit and subsequently in the brain. The use of cell-salvage devices to process shed blood before returning it to the venous reservoir may minimize the amount of particulate- or lipid-laden material that contributes to embolization.

Management of Aortic Atherosclerosis

A combination of epiaortic scanning and atheroma avoidance techniques (with respect to cannulation, clamping, and vein graft anastomosis placement) have been used to attempt to reduce neurocognitive deficits.⁴ The incidence of cognitive decline may be lower in patients who had an avoidance technique guided by epiaortic scanning compared with no epiaortic scanning. It is an area that requires more investigation. One of the difficulties in interpreting studies that have evaluated atheroma avoidance strategies is the absence of any form of blinding of the investigators. For the most part, a strategy is chosen based on the presence of known atheroma, and the results of these patients are compared with historical controls. Multiple techniques can be used to minimize atheromatous material liberated from the aortic wall from getting into the cerebral circulation. These range from optimizing placement of the aortic cannula in the aorta to an area relatively devoid of plaque to the use of specialized cannulas that reduce the sandblasting of the aortic wall. Alternative aortic cannulas and using different locations possess the ability to decrease embolization of atheromatous plaque. The avoidance of partial occlusion clamping for proximal vein graft anastomosis using a single-step automated anastomotic device and the use of alternatives to cross-clamping all possess the ability to mitigate injury due to embolization.