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Ann Thorac Surg 1999;67:1887-1890
© 1999 The Society of Thoracic Surgeons

Temporary neurological dysfunction after deep hypothermic circulatory arrest: a clinical marker of long-term functional deficit

^a Department of Cardiothoracic Surgery, Mount Sinai Medical Center, New York, New York, USA

Address reprint requests to Dr Ergin, Department of Cardiothoracic Surgery, Mount Sinai Medical Center, Box 1028, One Gustave L. Levy Place, New York, NY 10029

Presented at the Aortic Surgery Symposium VI, April 30–May 1, 1998, New York, NY.

	Abstract

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Background. With increasing clinical experience, it has become clear that two distinct forms of neurological injury occur after operations on the thoracic aorta that require temporary exclusion of the cerebral circulation. Traditionally, evaluation of neurological outcome was limited to reporting the incidence of postoperative stroke related to ischemic infarcts due to particulate embolization. More recently, the symptom complex defined as "temporary neurological dysfunction" (TND) was recognized as a functional manifestation of subtle and presumably transient brain injury, but whether this early postoperative syndrome is associated with long-term deficits of cognitive and intellectual functions has not been established.

Methods. With Institution Review Board approval, 105 patients undergoing elective thoracic aortic surgery were entered into a protocol involving neuropsychological evaluation with a battery of tests preoperatively, and 1 and 6 weeks postoperatively. Patients who could not be tested adequately or had documented strokes were eliminated from final analysis. Seventy-one patients completed the neuropsychological evaluation, which consisted of eight tests consolidated into five domains: attention, cognitive speed, memory, executive function, and fine motor function. Independent observers also determined whether temporary dysfunction was present, and graded its severity based on a fixed but subjective clinical scale, ranging from simple disorientation and lethargy or confusion (grade 1–2) to prolonged extreme agitation or psychotic behavior requiring treatment with psychotropic drugs (grade 3–5). Data were normalized to baseline values, and were analyzed using analysis of variance, analysis of covariance (ANCOVA), and ² as necessary.

Results. A previous analysis had shown that patients who could not be tested or had poor scores 1 week postoperatively were more likely to perform poorly at 6 weeks (odds ratio 5.27, p < 0.01). In the current study, in order to determine the clinical relevance of TND, patients were analyzed retrospectively according to their performance in neuropsychological testing: patients with no change or a decline of less than 50% in tests of memory, motor function, and attention 1 week postoperatively (group 1, n = 49) were compared with those with a negative change exceeding 50% in the same functions at 1 week (group 2, n = 22). The overall incidence of TND was 28.1% (20/71). The incidence of TND in group 2 (14/22, 63%) was significantly higher than in group 1 (6/49, 12%; p = 0.0006). Similarly, the severity of TND (as assessed by clinical score > 2) was also significantly higher in group 2 (11/14) compared with group 1 (0/6; p = 0.006.)

Conclusions. The incidence and severity of clinically apparent temporary neurological dysfunction correlates significantly with poor performance on neuropsychological tests 1 week postoperatively. Such poor performance predicts continued deficits in memory and motor function at 6 weeks. Thus, TND may not be a benign self-limited condition as previously supposed, but rather a clinical marker for insidious but significant neurological injury associated with measurable long-term deficits in cerebral function. A concerted effort to reduce the incidence of this complication is therefore necessary.

	Introduction

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The last decade of cumulative clinical experience has taught us that two distinct types of neurological injury, due to two different mechanisms, occur during operations on the thoracic aorta that require temporary exclusion of the cerebral circulation [1]. Localized and sometimes devastating strokes are caused by embolic events, and are independent of the method of brain protection utilized. In contrast, subtle but diffuse injury undetectable by conventional imaging techniques is more commonly observed, and is directly related to inadequate brain protection [1].

The postoperative symptom complex that we have defined as "temporary neurological dysfunction" (TND) occurs in about a quarter of patients after periods of deep hypothermic circulatory arrest (DHCA). It is not associated with any structural abnormality in the brain detectable by the usual imaging methods. Its incidence is significantly related to the duration of the circulatory arrest interval as as well as to advanced age [2]. We believe that "temporary neurological dysfunction" represents a functional manifestation of subtle—and presumably transient—brain injury, but whether this early postoperative syndrome is associated with long-term deficits of cognitive and intellectual function has not previously been investigated. The current study was undertaken to determine the relationship between clinical TND and the occurrence of long-term deficits in motor function and memory detected by perioperative neuropsychological testing.

	Material and methods

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Under an Institutional Review Board-approved protocol with informed patient consent, 105 patients undergoing elective thoracic aortic surgery with varying periods of DHCA were evaluated with a battery of neuropsychological tests at three times: preoperatively for a baseline measurement, then as early in the postoperative period (during the same hospitalization) as was compatible with their medical condition (1 week), and finally at an outpatient follow-up visit (6 weeks after discharge). Patients who were not adequately tested or had documented strokes were eliminated from the final analysis. Surgical techniques and use of DHCA were constant throughout the duration of the study, and have been described in detail previously [2].

The neuropsychological evaluation consisted of a battery of eight tests divided into five domains: attention, cognitive speed, executive function, memory, and fine motor function. The details of the methods of neuropsychological evaluation have been described previously by Reich and associates [3]: this study showed that poor test results 1 week postoperatively were predictive of deficits in performance at 6 weeks (odds ratio 5.27; p < 0.01) [3]. Consequently, patients in the current study were divided into two groups according to their neuropsychological evaluation one week postoperatively. Patients with no change or less than a 50% decline in memory or fine motor function and attention 1 week postoperatively (group 1, n = 49) were compared with those with more than a 50% early negative change in the same functions (group 2, n = 22).

Independent observers also determined the presence of TND in individual patients in both groups, and graded its severity based on a fixed but subjective clinical scale. TND ranged from simple disorientation and lethargy or confusion (grade 1–2) to prolonged extreme agitation or psychotic behavior requiring treatment with psychotropic drugs (grade 3–5; Table 1). The incidence and severity of TND between groups were compared.

	Results

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Seventy-one patients completed the protocol and constitute the cohort subject to final analysis; some of their clinical characteristics are outlined in Table 2. There were 52 men and 19 women, with an average age of 62.2 years. Average age in group 1 was 61, vs 68.5 years in group 2 (NS). Overall hospital mortality was 4.2% (3/71). In group 2, 45% (10/22) of patients had atherosclerotic aneurysms vs only 11% (5/49) in group 1 (p < 0.002, ²). Significantly more patients in group 1 (89%, 44/49) had operations confined to the ascending aorta or the proximal portion of the aortic arch than in group 2 (54%, 12/22; p < 0.002, ²). Probably reflecting the extent of operation, more patients in group 2 (72%, 16/22) had DHCA for an interval exceeding 25 min than in group 1 (40%, 20/49, p < 0.02 ²). There was no significant difference in average cardiopulmonary bypass times between the groups (group 1, 218.7 min vs 211.3 minutes in group 2). The average duration of circulatory arrest was significantly longer in group 2 (33.5 vs 23 minutes; p > 0.001 Mann-Whitney Rank Sum). In group 2, 77% (17/22) of the patients had some form of supplemental cerebral perfusion in addition to DHCA—either retrograde or antegrade selective cerebral perfusion alone or in combination, compared with only 22% (11/49) with supplemental cerebral perfusion in group 1 (p < 0.0001 ²). The use of supplemental cerebral perfusion reflects our deliberate policy to limit duration of circulatory arrest, especially in older patients.

	Discussion

Top Abstract Introduction Material and methods Results Discussion References

 
The evaluation of neurological outcome in adult patients undergoing DHCA has generally been limited to reports of the incidence of postoperative stroke and of gross neurological dysfunction [4]. Our earlier experience indicated that there are two distinct types of cerebral injury after DHCA in surgery of the thoracic aorta. Permanent neurological sequelae, observed in 7% of the patients, were related to embolic strokes, with defects verified by computerized tomography of the brain [2]. The multivariable predictors of stroke were age, severe atheromatous disease of the aorta, and surgery involving the descending aorta. The stroke incidence was not related to the duration of circulatory arrest, and was therefore independent of the method of cerebral protection.

In contrast, TND, defined by us as postoperative confusion, agitation, delirium, prolonged obtundation, or parkinsonism without localizing neurological signs, occurred in 19% of patients, and was clearly correlated with the duration of DHCA as well as with patient age [2]. The significant relationship between TND and circulatory arrest duration was of concern to us, although the progress of most patients appeared to be quite benign after recovery from what was thought to be a self-limited syndrome of altered neurological function. But even at that early time, we recommended that every effort be made to limit arrest duration, especially in older patients, because we suspected that this clinical syndrome was a manifestation of subtle brain injury due to inadequate cerebral protection.

To investigate further whether DHCA in the adult is associated with long-term neuropsychological deficits, we embarked upon a detailed study comparing patients undergoing routine cardiac surgery with cardiopulmonary bypass with patients who have surgery of the thoracic aorta with periods of DHCA. This recently completed study showed unequivocally that poor performance or inability to be tested early (at 1 week) were significant predictors of poor late performance (at 6 weeks) in all domains (odds ratio 5.27; p < 0.01). The decline in memory function at 6 weeks (-0.48 ± 0.27) roughly approximates a 20-point decrease in IQ. Prolonged DHCA (> 25 minutes) and advanced age were significant predictors of poor performance at 6 weeks for both memory and fine motor domains. Prolonged DHCA (> 25 minutes, odds ratio 4.0; p = 0.02) was also a determinant of prolonged hospital stay (> 21 days) [3].

The current study was undertaken as an extension of this previous one in order to answer three questions: 1) What is the incidence of TND in patients who perform poorly in early neuropsychological testing? 2) Is there a correlation between poor performance in early postoperative testing and the severity of TND? 3) Does supplementary brain perfusion prevent TND?

The results clearly show a significantly higher incidence of TND among patients who performed poorly in early postoperative testing (63% vs 12%); 50% of these patients suffered from severe TND. Since the earlier study had shown that poor performance in the early postoperative test was a multivariable predictor of poor performance on the late test and hence a harbinger of long-lasting deficit in the domains of memory and fine motor function, it is reasonable to conclude that TND may be a clinical marker for long-lasting neuropsychological deficit after DHCA.

Our earlier findings showed a clear, almost linear relationship between circulatory arrest time and the development of TND, with exactly one-third of the patients exhibiting severe TND after 50 min of DHCA [2]. The recent study based on neuropsychological evaluations showed that a duration of circulatory arrest exceeding 25 minutes is a predictor of long-term deficits in function [3]. These findings suggest that past projections of the theoretical safe duration of circulatory arrest calculated from information on rates of oxygen consumption at various brain temperatures (Q10 and cerebral metabolic rate for oxygen (CMRO₂)) [5] may have been too optimistic. McCullough and colleagues have recalculated Q10 for the adult human brain based on direct measurement of CMRO₂ during DHCA [6]. Based on their findings, the safe period of arrest at 15°C is only about 30 min, and at 10°C it is still only 40 min. Beyond these time limits, anoxic cellular injury is inevitable. The earliest manifestations of such injury are likely to occur in the regions of the brain with higher metabolic rates, where metabolic activity may persist even during profound hypothermia. In experimental models, the hippocampus emerges as the region most vulnerable to such injury [7]: this region of the brain is the locus for acquisition of new information, and is particularly sensitive to anoxic or ischemic injury because of its high metabolic rate [8]. It is quite possible that the impairment in memory function in prolonged DHCA patients is related to neuronal injury in the hippocampus. The prevalence of this injury in older patients, manifest as motor and memory dysfunction, may be related to slower recovery from injury due to an age-related reduction in brain reserve capacity [9].

Since our early report, we have made a concerted effort to limit arrest duration, especially in older patients [1]. In pursuing this strategy, we have primarily used antegrade selective cerebral perfusion. Although some investigators have claimed that retrograde cerebral perfusion (RCP) extends the safe duration of DHCA [10], the experience reported here shows no protective effect of RCP in reducing the development of TND, and RCP therefore probably has no influence in preventing its associated long-term neuropsychological deficits. In fact, in our experience the incidence of TND increases in patients who receive supplemental RCP, although it must be acknowledged that RCP is used more frequently when prolonged HCA is anticipated, and in patients judged to have an increased risk of embolization. Only one other series in the literature contains analysis of the incidence of TND after RCP: Okita and associates report a substantially increased (25%) incidence of severe TND following RCP [10], suggesting that use of prolonged RCP does not prevent but may in fact compound neuronal injury. This clinical finding confirms our laboratory experience with RCP, in which prolonged and effective RCP was associated with significant brain edema and increased cellular injury [11].

It is quite clear that the clinical syndrome of TND after DHCA is not a totally benign condition. It is an easily recognizable clinical marker of subtle but significant neuropsychological deficits due to neuronal injury in specific regions of the brain. The most effective means of preventing injury is to limit arrest duration, especially in the elderly. Logic dictates that antegrade selective cerebral perfusion should be the method of choice to achieve this goal. Unfortunately, there are no data in the literature that allow a meaningful comparison of the influence of various protective methods on the incidence of TND, since this complication goes unmentioned by many investigators. In the evolution of thoracic aortic surgery, we have reached a stage in which mere survival and absence of gross neurological deficit cannot any longer be viewed as an acceptable result. All of us who work in this field should make a concerted effort to standardize our reporting to allow meaningful comparisons. Only then will we be able to further refine our protective methods to prevent the subtle brain injury manifested by TND and its later associated functional deficits.

	References

Top Abstract Introduction Material and methods Results Discussion References

 

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