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Ann Thorac Surg 1995;59:1340-1344
© 1995 The Society of Thoracic Surgeons
Departments of Anesthesia and Neurology, The Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina
Abstract
There have been major advancements in cardiac surgery over the past two decades and a concomitant decrease in mortality and major morbidity. The improved safety in cardiac procedures permitted 330,000 operations involving cardiopulmonary bypass in 1992. However, several recent studies have demonstrated that cardiac surgery poses substantial risk of negative neurologic and neuropsychologic outcomes. Although very few patients die as a result of a cardiac operation, more than two thirds of patients demonstrate evidence of neuropsychologic dysfunction postoperatively. The mechanisms contributing to neuropsychologic deficits after cardiopulmonary bypass are uncertain. To characterize the incidence and severity of such deficits after cardiac operations, a concise battery of neuropsychologic tests that provides reliable evidence of subtle brain trauma is essential. With an objective, valid measure of brain injury, the etiology of neuropsychologic deficits can be identified and either eliminated or the effects ameliorated. The proper selection and use of neurobehavioral tools provides a basis to evaluate the efficacy of surgical and pharmacologic interventions to further improve neurologic outcome after cardiopulmonary bypass.
At the inception of every research plan to evaluate the effect of cardiopulmonary bypass (CPB) on the brain, one of the major areas of contention is how best to describe evidence of brain trauma. The purpose of this discussion is to explore the differences in the development of a traditional neuropsychologic battery of tests as opposed to a research battery whose variables are defined not only by the clinical question but by environmental and patient demographics.
There are a variety of reasons why a patient may be referred for a clinical neuropsychologic evaluation: (1) to determine if the patient has experienced a brain trauma, (2) to determine if the patient has developed a psychiatric dysfunction, or (3) to determine whether the patient has both an organic and a psychiatric complaint.
The historical purpose of the clinical neuropsychologic evaluation was localization of the lesion site, but given the advances in imaging, localization of lesions has taken a secondary role. Assessment, with an emphasis on determining the level of social and cognitive impairment, has taken precedence.
The traditional approach for a clinical referral is to give the patient an extensive battery of tests that will survey his or her abilities and elicit errors that can be evaluated for clinical significance and diagnostic importance. The rationale for the use of an exhaustive neuropsychologic battery is to ensure that all modalities are explored for any potential deficits. Any errors are carefully examined to determine if they are evidence for labeling the patient with a specific syndrome or higher cortical dysfunction. Although it might take only a few moments to recognize a patient has a language disorder, it might take several hours of testing to tease out the specifics of a subcortical aphasia, for example.
When asked to provide a battery of tests to answer a research question, experienced neuropsychologists tend to fall back on the familiar basic clinical examination, which covers a broad spectrum of behaviors and takes 2 or more hours to administer. However, when asked to study cardiac surgical patients, these neuropsychologists are rudely awakened when it becomes apparent that they have only 45 minutes to evaluate the most complicated system in the body, the organ of behavior, the brain. The task to refine the question in line with the limited access one has to the patient becomes a series of compromises.
The first level on the decision tree to provide an abbreviated 45-minute evaluation is to answer this question: What is the research question? In other words, what are we ultimately trying to accomplish with the study of patients undergoing CPB? Essentially, it is already known that patients experience varying levels of brain insult secondary to CPB. What is needed is to either eliminate the source of the trauma or ameliorate its effect.
The question then becomes what level of refinement is necessary to describe and define the deficit. Is it sufficient to just determine that a brain trauma has occurred, or is a more complete description of the deficits necessary? To answer the principal question of whether or not an intervention has affected outcome, it is not necessary to exquisitely define specific neurobehavioral deficits. Reliability and sensitivity are more key to a research evaluation than the names of specific deficits. In other words, it is more important to be able to reliably determine the patient has a visual deficit than it is to label the impairment a prosopagnosia.
Another highly controversial question attendant on the issue of CPB and neuropsychologic outcome is the clinical significance of the deficits exhibited by these patients. This is the quality of life issue, that is, if the patients are not ``significantly'' impaired, such as after a major stroke, do we need to intervene? There are two possible answers to this concern: (1) yes, the neuropsychologic deficits are important and should be avoided, and (2) it does not matter if the deficits are behaviorally important as long as they are reliable markers of brain injury and can be used to improve CPB.
If the research were limited to eliminating the factors associated with CPB that cause death, an impossibly large number of patients would be needed to obtain significance. By using as an end point an objective, reliable, and valid measure of brain trauma, such as the relative change between preoperative and postoperative neuropsychologic performance of the patient, then fewer patients, hundreds instead of thousands, are adequate to assess the efficacy of a treatment.
Remarkably few patients die or are completely disabled as a by-product of CPB. However, most individuals would agree that a decrement in memory or coordination would be a major inconvenience. Further, it seems reasonable to presume that if it were possible to eliminate the cause of the small problems, the number of ``major'' events would probably be reduced as well.
The criteria for defining a deficit is critical. If the definition is too stringent, then few patients meet the criteria. If the definition is too broad, then most patients have some level of trauma and the ability to evaluate an intervention is lost. However, there is not a consensus in the literature on what constitutes an impairment. There is little agreement on how ``severe'' a deficit must be before it is considered clinically important.
A Question of Severity, or Not All Lesions Are Created Equal
For the purposes of reducing cognitive impairment after CPB, severity can be described in two ways, behaviorally and structurally. The first describes the human condition, meaning that a small left-hemispheric central cortical stroke resulting in an expressive dysphasia, dominant hand weakness, and eye movement incoordination is a socioeconomic disaster for the patient. Conversely, a larger anterior right frontal lobe stroke may go unnoticed, although causing a greater level of tissue destruction. The second description of severity is the quantity of tissue damaged, which, we can see from the example given, does not necessarily correlate with the socioeconomic consequences of a focal stroke.
Which is the best approach to ranking severity? An analogy might be along the line of attempting to stop drivers from running a red light. It is important to the victim and society whether the vehicle is struck on the driver or passenger side but largely irrelevant to the engineer assigned to stopping the violators. If the side on which the victim is struck is relatively random, then half the time the consequences to the driver of someone running the light are severe and the other half, merely inconvenient. It would be inappropriate to attempt to control only the driver-side accidents. It would be best to try to prevent all accidents, and presume if you decreased the number of fender-benders, you would also proportionally reduce the number of socioeconomically important left-sided crashes where the driver is hospitalized. The goal of the ``engineer'' is to keep the ``embolic driver'' from entering the intersection, thereby preventing the severe accidents by preventing all accidents.
This example helps explain why the number of tests on which a patient performs abnormally might possibly reflect only the socioeconomic consequences of the lesion and not its severity. A left-hemispheric stroke would cause a patient to do poorly in the following categories of function (tests) relative to preoperative performance: (1) vocabulary test; (2) verbal learning test; (3) visual-motor coordination task; (4) visual-motor, frontal lobe function; (5) motor coordination task; (6) motor coordination, visual scanning, and planning; (7) visual learning and reaction time; and (8) visual scanning, attention, and concentration. The same size stroke in the same location in the right hemisphere would cause deficits in these tests: (1) motor coordination (nondominant hand), and (2) motor coordination (nondominant hand), visual scanning, and planning.
One interpretation of these results is that the first (left hemisphere) lesion is four times as severe as the second (right hemisphere), even though they are the same size. From the patient's point of view, the first lesion is far more devastating than the right-hemispheric stroke, certainly worse than a 4 on a severity scale, even though anatomically equal.
This problem could potentially be addressed using standardized scores (Z-scores) and categories of dysfunction where a category such as motor function would be the composite score of four motor and visual-motor tests using the dominant and nondominant hands. Memory would be the composite of two tests (verbal and nonverbal) and perceptual motor functioning, five tests. The composite scores would be independent of the side of the lesion but would still be subject to location versus size of lesion inequalities. This is not a satisfactory solution because it is not possible to equate the amount of tissue disruption with the behavioral consequences of a lesion. At best, a relative rating of the level of impairment for a given behavioral domain, memory, for example, could be used, but it would be a description of impairment rather than an indication of severity.
Alternatively, a cutoff score could be used such that a given level or change in performance is abnormal. Again, this approach does not actually address a ``severity scale.'' Further, the social consequences of a deficit are dependent on individual factors such as employment, education, hobbies, and age. A language impairment would be more devastating to a lawyer than a mechanic, whereas a major left-sided weakness would be a 100% disability for the mechanic but not a career-ending deficit for a lawyer or politician.
Perhaps the most objective method of scaling the relative structural severity of a frank stroke is with neuroimaging techniques. This approach avoids the subjective social bias that ranks behavioral attributes as opposed to lesion size and tissue destruction. The problem with this approach is that it is accurate only for relatively large lesions. If the cause of the behavioral deficit is the absolute volume of small ischemic lesions, the behavioral manifestation may far exceed any radiologic evidence of structural abnormality. A similar example is the early stages of Alzheimer's disease where the patient is obviously impaired but the radiologic examination is equivocal.
The preceding discussion highlights several of the dilemmas associated with the question of how to assign a level of severity to a neurobehavioral symptom. It is important to stay focused on the central goal of improving outcome after CPB and not be driven by the accountants in the study of the consequences of cardiac surgery. All brain insults should be prevented, not just those that have quantifiable monetary cost to the individual or society. However, most studies are directed toward reducing the ``major'' deficits. The reason is most behavioral and neurologic tests are designed to assess either the social consequences of a brain injury or its location. These tests do not determine the size or the destructiveness of a lesion, which, if the brain is to be protected, is the important issue.
Currently, there is no way to selectively influence where the lesions occur. There is some possibility that the factors related to lesion site are not random. Microemboli may preferentially go to the right hemisphere. The deficits may be an expression of bilateral watershed infarctions if the lesions are ischemic in nature, secondary to hypoperfusion. Anatomic location will determine the ``social relevance'' of the lesions independent of their size and destructiveness. It is probably more important to determine the relative size and distribution of lesions than their exact anatomic site. Small strokes 2 cm apart can cause radically different symptoms.
Development of Neuropsychologic Assessment Battery
Precise characterization of the neuropsychologic deficits occurring after cardiac operations poses a unique challenge. Although the test battery must quantify the incidence of brain dysfunction occurring after CPB, a short battery cannot be sufficiently detailed to exhaustively characterize subtle higher cortical dysfunctions. The test battery must be concise because of the number of time-consuming perioperative activities and because of patient fatigue, which may reduce patient cooperation and data validity. In addition, the battery must offer good interobserver and intraobserver reproducibility, good discriminative capacity, and appropriate controls for practice effects.
Because of patient time constraints, the selection and the evaluation of the battery of tests described in Appendix 1 emphasized specificity and test-retest reliability. Tests were deleted if previous studies or personal experience proved they were insensitive and unlikely to identify any abnormalities. Such tests, including the complete Wechsler adult intelligence scale and other measures of general intelligence, show only minor changes in scores [1, 2]. Other tests were chosen to facilitate comparison between the event rates reported by other investigators [3, 4], and several tests were chosen because they had proved to be sensitive in other series. The psychometric examination requires approximately 50 to 60 minutes preoperatively and somewhat longer postoperatively because of longer rest periods between tests.
Tests that typically reveal deficits, such as the trail-making test [5–8], the digit-symbol test [2, 8], and the grooved-pegboard [8, 9] and maze tests [2, 10], are timed tests that require a triad of skills: (1) sustained motor performance, (2) focused attention, and (3) visuopractic (including eye-hand coordination and manual dexterity).
All of these abilities can be adversely, but reversibly, diminished by anesthesia, fatigue, and pain, all of which inevitably accompany thoracic surgical procedures [11]. Therefore, the postoperative testing interval is delayed until postoperative day 4 to 8 to minimize those effects. Postoperative visual acuity should be assessed, as several studies [3, 12–16] suggest that a substantial number of patients undergoing CPB sustain retinal infarctions. Finally, the time and place of testing should be standardized to eliminate the variability in performance that occurs in individual patients as a function of the time of day. The testing should take place in the patient's room or a laboratory at the same time of day, preferably in the morning. A more comprehensive assessment of the psychosocial consequences of CPB can be obtained preoperatively and at the 1- to 3-month follow-up.
It is essential to define a clinically important level of deterioration in performance. Individuals who do not have operation (controls) demonstrate highly consistent performance between tests, that is, the standard deviation of intrasubject mean performance is small. Unlike the controls, nearly all patients show deterioration in performance from preoperative to postoperative testing. However, many deficits detected by excessively sensitive criteria are clinically trivial.
In our laboratory, no normal, older control has ever demonstrated a decline in performance from the initial test interval that exceeded 20% on any test. Consequently, in our laboratory, a clinically important deterioration in performance is considered a deficit when a patient demonstrates a decrease of at least 20% on two or more neuropsychologic tests from preoperative to postoperative performance. This is a rigorous criterion. Most individuals are approximately 10% more coordinated with their dominant hand than their nondominant hand on tests of fine motor coordination. For a person to have a deficit by this criterion, the postoperative coordination with the dominant hand would have to fall considerably below that of the nondominant hand on tests of manual dexterity.
The 4- to 8-day postoperative test interval followed by an evaluation at least 1 month and preferably 3 months later should be performed to document any improvement and what type of improvements can be expected in neurologic function.
The following is a list of the tests used at Bowman Gray, but it is the categories of function that should be emphasized and not the specific tests. The tests named have been selected to describe the following brain functions:
After a surgical procedure, pain may interfere with the finger-tapping and trail-making tests, thereby suggesting the presence of cortical dysfunction. If the patient shows bilateral slowing on the finger-tapping test but performs well on the visual reaction time test, the likely cause is pain rather than cortical injury. Impaired function on both tests more strongly suggests neurologic injury. If both tests demonstrate consistent unilateral deficits, a focal injury is likely. Performance on several of the tests may decline as a result of visual deficits after CPB [12, 13, 15, 24, 25]. Blauth and associates [24] reported that transient retinal vessel occlusion commonly occurs during CPB. These findings suggest that visual dysfunction rather than neurologic injury could account for the high incidence of abnormalities in neuropsychologic batteries that rely on tests requiring intact visuopractic function. However, the positive correlation between retinal occlusion and neuropsychologic determination noted by Blauth and his group [24] suggests that frequent retinal arterial occlusion could also reflect diffuse embolic cerebral vascular occlusion.
When selecting tests for inclusion in a neuropsychologic battery, the initial choices can be focused by the probability that certain anatomic regions are at greater risk. If microemboli are the most probable cause of the neuropsychologic deficits, then tests that evaluate the distal regions supplied by the middle cerebral arteries should be selected with an emphasis on comparing focal right-sided and left-sided functions. A heterogeneous pattern of deficits would be consistent with microemboli as the cause. If the damage is secondary to hypoperfusion, then tests evaluating the watershed areas would be most appropriate, with a more homogeneous and predictable pattern of deficits expected.
Conclusion
The premise is that mortality and morbidity after CPB can be reduced by changes in surgical techniques, anesthesia management, perfusion methodology, and use of new neuroprotective drugs. To evaluate the efficacy of these manipulations on reducing cerebral dysfunction, a reliable outcome measure is required.
Neurobehavioral testing provides a sensitive, objective, reliable, and valid means to evaluate the function of the brain to determine the presence of trauma. The severity of behavioral dysfunction does not necessarily correlate with the amount of structural trauma. The location and etiology of the lesion are generally more important than the volume of tissue disrupted for predicting the social consequences of central nervous system insult.
Neuropsychologic testing can be useful in assessing the efficacy of clinical interventions in both comparing groups and monitoring individual progress. The most powerful use of these behavioral tools is in combination with other measures of central nervous system functional integrity such as magnetic resonance imaging or positron emission tomography or when correlated with physiologic monitoring such as for cerebral blood flow or embolic load.
Finally, it is a testimony to the dedication of the cardiovascular research and clinical community that death and stroke are so uncommon, tests of subtle higher cortical function are necessary to evaluate new interventions.
Acknowledgments
Supported by grants NS 28955 and NS 27500 from the National Institutes of Health.
I thank Professor Stanton P. Newman for assisting in the development of the neuropsychologic battery; Rosie Hibawi, MS, for statistical assistance; Susan Hart, MS, Barbara Ruby, MS, and Kristen Morris, BA, for performing the neuropsychologic evaluations; and Julia Phipps, RN and Jo Beth Holliday, RN, for intraoperative monitoring.
Footnotes
Presented at the Conference on CNS Dysfunction After Cardiac Surgery: Defining the Problem, Fort Lauderdale, FL, Dec 10–11, 1994.
Address reprint requests to Dr Stump, Department of Anesthesia, Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1009.
References
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