Neuropsychologic Deficits and Stroke


The brain is the effector organ for all behavior, innate and learned. It is the monarch of blood flow and will shut down all other vascular systems to preserve its own supply. Conversely, dysfunction in other organs can adversely affect brain function. It monitors other organ systems and is acutely sensitive and responsive to both the external and internal environment. Thus, even small injuries to the brain may produce symptomatic, functional losses that would not be detectable or important in other organs. Regional hypoperfusion, edema, microemboli, circulating cytotoxins, or subtle changes in blood glucose, insulin, or calcium may result in changes in cognitive function, ranging from subtle to profound. A small 2-mm infarct may cause a disruption of behavioral patterns. Physiologic and physical function changes can pass unnoticed, be accepted and dismissed, or profoundly compromise the patient's quality of life. Move the lesion half a centimeter, and the same volume lesion may result in a catastrophic stroke. Thus the brain is the most sensitive organ exposed to damage by cardiopulmonary bypass (CPB) and cardiac surgery and also the organ that, with the heart, is most important to protect.

Assessment

Routine assessment of neurologic injury, which occurs in the setting of cardiac surgery, is not done for most patients because of the priority of the cardiac lesion and because of costs in time and money. General neurologic examinations by members of the surgical team or individuals lacking specialized training are not adequate to rule out subtle neurologic injuries, and this is the principal reason that the incidence of stroke, neurologic, or neuropsychologic injury varies widely in the surgical literature.

For studies designed to assess or reduce neurologic injury in the setting of cardiac surgery, nonroutine preoperative and postoperative tests are required. These special tests include a complete neurologic examination by a neurologist or a well-trained surrogate. To improve accuracy, a single neurologist should conduct all serial examinations. A standardized protocol of examination should be followed, with uniform reporting of results. The basic, structured examination includes a mental state examination; cranial nerve, motor, sensory, and cerebellar examinations; and examination of gait, station, deep tendon, and primitive reflexes.

The most obvious neurologic abnormalities are paresis; loss of vital brain functions such as speech, vision, and comprehension; and coma. These are commonly lumped under the general heading of stroke. Disorders of awareness or consciousness can include coma, delirium, and confusion, but transitory episodes of delirium and confusion are often dismissed as being caused by anesthesia or medications. More subtle losses are determined by comparison of preoperative and postoperative performances using a standard battery of neuropsychologic tests prepared by a group of neuropsychologists. A neuropsychologic examination is basically an extension of the neurologic examination with a much greater emphasis on higher cortical function. Dysfunction is objectively defined as a deviation from the expected, relative to a large population. For example, although performing at a 95 IQ level is in the normal range, it is low for a physician, and a search for a neurologic impairment would be triggered by such a poor performance. A 20% decline in two or more of these tests, compared to the patient's own baseline, suggests a neuropsychologic deficit that should be followed until resolved or not resolved. In studies involving long-term follow-up, the inclusion of a control group of unoperated patients with the same disease and of similar demographics helps define the causes of neuropsychologic decline that occurs later than 3 to 6 months after surgery.

Computed axial tomograms or magnetic resonance imaging (MRI) scans are essential for the definitive diagnosis of stroke, delirium, or coma. Preoperative imaging is usually not necessary when new techniques such as diffusion-weighted MRI imaging, MRI spectroscopy, or MRI angiography are used to assess possible new lesions after surgery. However, recent studies demonstrate patients with dementia have a loss in cell volume as a result of micro-infarctions that are not detectable with current radiologic techniques. Histologic studies performed on patients who did not survive cardiac surgery have demonstrated millions of small lipid microemboli, which may result in massive cell loss and increased volume of ventricles ( Fig. 62-1 ).

FIGURE 62-1, Preoperative brain MRI from patient undergoing extensive cardiac surgery superimposed on identical images taken at 3 months and 1 year after surgery. The appearance of the ventricles at 1 year indicates brain shrinkage, presumably from apoptosis of neurons.

Biochemical markers of neurologic injury after cardiac surgery are relatively nonspecific and inconclusive. Neuron-specific enolase (NSE) is an intracellular enzyme found in neurons, normal neuroendocrine cells, platelets, and erythrocytes. S-100 is an acidic calcium-binding protein found in the brain. The beta dimer resides in glial and Schwann cells. Both S-100 and NSE increase in spinal fluid with neuronal death and may correlate with stroke or spinal cord injury after CPB. However, plasma levels are contaminated by aspiration of wound blood into the pump and hemolysis and are often elevated following prolonged CPB in patients without otherwise detectable neurologic injury. Newer bloodborne biochemical markers are being identified but, as of yet, have not been shown to be diagnostic for subtle neurologic injury.

Populations at Risk

Advancing age increases the risk of stroke or cognitive impairment in the general population, and surgery, regardless of type, increases the risk still higher. In 1999 Hogue and colleagues reported the risk of stroke during coronary artery bypass graft (CABG) surgery to be directly related to age and other factors. A European study compared 321 older adult patients without surgery to 1218 patients who had noncardiac surgery and found a 26% incidence of cognitive dysfunction 1 week after operation and a 10% incidence at 3 months. Between 1974 and 1990 the number of patients undergoing cardiac surgery who were older than 60 years and older than 70 years increased twofold and sevenfold, respectively. Today patients 75 years of age and older commonly receive cardiac surgery. Genetic factors also influence the incidence of cognitive dysfunction following cardiac surgery. The incidence of cognitive dysfunction at 1 week following cardiac surgery is approximately double that of noncardiac surgery.

As the age of patients undergoing cardiac surgery increases, the number of patients with multiple risk factors for neurologic injury also increases. Risk factors for adverse cerebral outcomes are listed in Table 62-1 . These factors are divided into stroke with a permanent fixed neurologic deficit (type 1) and coma or delirium (type 2). Hypertension and diabetes occur in approximately 55% and 25% of cardiac surgical patients, respectively. Fifteen percent have carotid stenosis of 50% or greater, and up to 13% have had a transient ischemic attack or prior stroke. The total number of MRI atherosclerotic lesions in the brachiocephalic vessels adds to the risk of stroke or cognitive dysfunction, as does the severity of atherosclerosis in the ascending aorta as detected by epiaortic ultrasound scanning. Palpable ascending aortic atherosclerotic plaques markedly increase the risk of right carotid arterial emboli as detected by Doppler ultrasound. The incidence of severe aortic atherosclerosis is 1% in cardiac surgical patients younger than 50 years and is 10% in those aged 75 to 80 years.

TABLE 62-1
Adjusted Odds Ratios for Type I and Type II Cerebral Outcomes Associated with Selected Risk Factors
Modified from Roach GW, Kanchuger M, Mangano CM, et al: Adverse cerebral outcomes after coronary bypass surgery. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators. N Engl J Med 335:1857–1863, 1996.
Factor Model for Type I Cerebral Outcome Model for Type II Cerebral Outcome
Significant Factors, P < 0.05
Proximal aortic atherosclerosis 4.52
History of neurologic disease 3.19
Use of intra-aortic balloon pump 2.60
Diabetes mellitus 2.59
History of hypertension 2.31
History of pulmonary disease 2.09 2.37
History of unstable angina 1.83
Age (per additional decade) 1.75 2.20
Systolic blood pressure > 180 mm Hg at admission 3.47
History of excessive alcohol consumption 2.64
History of CABG 2.18
Dysrhythmia on day of surgery 1.97
Antihypertensive therapy 1.78
Other Factors ( P not significant)
Perioperative hypotension 1.92 1.88
Ventricular venting 1.83
Congestive heart failure on day of surgery 2.46
History of peripheral vascular disease 1.64
CABG, Coronary artery bypass graft.

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