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CARDIOVASCULAR ANESTHESIA

Serum Creatinine Patterns in Coronary Bypass Surgery Patients With and Without Postoperative Cognitive Dysfunction

Madhav Swaminathan, MD^*, Brian J. McCreath, FRCA^*, Barbara G. Phillips-Bute, PhD^*, Mark F. Newman, MD^*, Joseph P. Mathew, MD^*, Peter K. Smith, MD, James A. Blumenthal, PhD, and Mark Stafford-Smith, MD, FRCPC^* the Perioperative Outcomes Research Group

Departments of *Anesthesiology, Surgery (Cardiothoracic Division), and Medicine and Psychiatry, Duke University Medical Center, Durham, North Carolina

Address correspondence and reprint requests to Mark Stafford-Smith, FRCPC, Department of Anesthesiology, Box 3094, Duke University Medical Center, Durham, NC 27710. Address e-mail to staff002{at}mc.duke.edu

	Abstract

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Renal dysfunction is common after coronary artery bypass graft (CABG) surgery. We have previously shown that CABG procedures complicated by stroke have a threefold greater peak serum creatinine level relative to uncomplicated surgery. However, postoperative creatinine patterns for procedures complicated by cognitive dysfunction are unknown. Therefore, we tested the hypothesis that postoperative cognitive dysfunction is associated with acute perioperative renal injury after CABG surgery. Data were prospectively gathered for 282 elective CABG surgery patients. Psychometric tests were performed at baseline and 6 wk after surgery. Cognitive dysfunction was defined both as a dichotomous variable (cognitive deficit [CD]) and as a continuous variable (cognitive index). Forty percent of patients had CD at 6 wk. However, the association between peak percentage change in postoperative creatinine and CD (parameter estimate = -0.41; P = 0.91) or cognitive index (parameter estimate = -1.29; P = 0.46) was not significant. These data indicate that postcardiac surgery cognitive dysfunction, unlike stroke, is not associated with major increases in postoperative renal dysfunction.

IMPLICATIONS: We previously noted that patients with postcardiac surgery stroke also have greater acute renal injury than unaffected patients. However, in the same setting, we found no difference in renal injury between patients with and without cognitive dysfunction. Factors responsible for subtle postoperative cognitive dysfunction do not appear to be associated with clinically important renal effects.

	Introduction

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Postoperative renal dysfunction is still a major complication of coronary artery bypass graft (CABG) surgery. There is a lack of consensus on the definition of postoperative acute renal dysfunction (1). However, serum creatinine (Cr) or Cr-derived variables have consistently proved to be robust markers of renal dysfunction with predictive value in clinical studies involving large populations (2). Patients with greater Cr increase, a marker of renal injury after cardiac surgery, require disproportionately more resources and are associated with poorer short- and long-term outcome and greater expense (3). Proposed mechanisms contributing to postcardiac surgery renal dysfunction include athero- and thromboemboli, systemic inflammation, and hypoperfusion and reperfusion injury (4,5). All these factors have potential for systemic distribution and have also been incriminated as contributors to postoperative cognitive dysfunction (6,7). Despite general advances in the perioperative care of cardiac surgical patients, postoperative renal and neurologic dysfunction are still concerns that lack effective measures for treatment or prevention.

Post-CABG surgery Cr values typically increase and peak on the second postoperative day, returning to preoperative levels by the fourth or fifth day (8). We recently reported postoperative Cr patterns in patients whose CABG surgery was complicated by stroke compared with patients without this complication (9). Patients with postoperative stroke showed a similar Cr pattern but on average had a threefold greater increase in Cr compared with unaffected patients. Detachment of aortic atheroma has been proposed as a mechanism for post-CABG stroke, a mechanism that may also be responsible for embolic kidney injury. Although both cognitive and renal dysfunction after CABG surgery have been associated with transcranial Doppler-detected embolic phenomena (10,11), the potential for linkage between acute renal injury and cognitive dysfunction in this setting has not been evaluated. Therefore, we tested the hypothesis that postoperative cognitive dysfunction is associated with acute perioperative renal injury after CABG surgery.

	Methods

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After IRB approval and written, informed consent were obtained, data were collected for all elective, primary CABG surgery patients who were prospectively enrolled in the control arms of neurocognitive outcome studies at our institution from April 1995 to August 1999. Patients with chronic illnesses, including a history of cerebrovascular disease with residual deficits, uncontrolled hypertension, alcoholism, psychiatric illness, renal disease (Cr >177 µmol/L), or active liver disease were excluded. Pregnant women and patients with less than a seventh grade education were also excluded. Patients who died sooner than 2 days after surgery were also excluded from the analysis because their Cr values did not accurately reflect a perioperative renal injury; i.e., there was inadequate time for Cr to increase.

Demographic variables were gathered for all patients with reference to previously reported renal risk factors (4,12), including age; sex; weight; African American race; history of hypertension, diabetes, and obstructive lung disease (each noted as being present when they required treatment for adequate control); history of stroke without residual deficits or transient ischemic attacks; carotid bruit on physical examination; history of congestive heart failure (defined as history of paroxysmal or nocturnal dyspnea responsive to afterload reduction drug therapy); previous myocardial infarction; ASA class; preoperative ejection fraction; and unstable angina. Additionally, perioperative variables were gathered, including cardiopulmonary bypass (CPB) duration, number of aortocoronary grafts, intraaortic balloon pump use, mean arterial blood pressure (MAP), inotrope use, and transfusion requirements.

Anesthesia was managed according to the attending anesthesiologist’s preference. Use of drugs with potential renal effects (e.g., IV dopamine, furosemide, and mannitol) was not regulated. The induction and maintenance of anesthesia was achieved with a continuous infusion of fentanyl and midazolam. Supplemental isoflurane (0.5%–1.0%) was used as required to maintain heart rate and MAP within 25% of preinduction values. Extracorporeal perfusion was performed with a Cobe CML Duo blood oxygenator with sealed hard-shell filtered venous reservoir (Cobe Laboratories, Lakewood, CO), a Cobe Century Perfusion System, and a 43-µm arterial line filter (Cobe Sentry^TM arterial line filter with Primegard; Cobe Cardiovascular, Inc., Arvada, CO). Blood obtained by cardiotomy suction was routed by the roller pump into the integrated oxygenator-venous reservoir. Nonpulsatile perfusion was maintained at 2–2.4 L · min^-1 · m^-2. The CPB circuit was primed with mannitol (50 g of 20% solution), crystalloid solution (0.9% normal saline), and packed red blood cells, if required, to achieve a hematocrit of 18% or more during CPB. All patients were perfused during CPB through an ascending aortic cannula. The arterial carbon dioxide tension was maintained throughout CPB at 35–40 mm Hg (uncorrected for temperature), with the arterial oxygen tension maintained at 150–250 mm Hg. MAP was maintained between 50 and 90 mm Hg during CPB by using IV phenylephrine or sodium nitroprusside, as required. Patients were cooled to a nasopharyngeal temperature of 34°C to 28°C during aortic cross-clamp and rewarmed to a nasopharyngeal temperature of 37°C or a bladder temperature of at least 36°C before separation from CPB.

Cr was measured as part of routine biochemical laboratory investigations for all elective CABG patients by using a dry-slide enzymatic reflectance technique (VITROS 950; Johnson & Johnson, New Brunswick, NJ) with a normal range of 62 to 124 µmol/L. The preoperative Cr (CrPre) was the value on the day before surgery for all inpatients and was assessed within 1 wk before surgery for all outpatients scheduled to undergo elective CABG surgery. Peak postoperative Cr (Cr_maxPost) was defined as the highest of the daily in-hospital postoperative values. Peak percentage change in postoperative Cr (%Cr) was defined as the difference between the CrPre and Cr_maxPost, represented as a percentage of the preoperative value. By using the Cockroft-Gault equation (13), CrPre clearance was estimated from CrPre, and lowest postoperative Cr clearance (CrClPost) was estimated from Cr_maxPost.

The primary outcome variable selected was %Cr, because this marker demonstrates the best association with mortality and major morbidity when compared with other Cr-derived markers of renal function (14). Patients underwent neurocognitive testing on two occasions: the day before the operation (baseline) and at 6 wk after surgery. A trained psychometrician administered the neuropsychological test battery. The battery of tests used to assess cognitive function is described in Table 1. The testing procedure adhered to previously described institutional protocols (15,16).

A dichotomous measure of cognitive dysfunction (cognitive deficit [CD]) was defined as a decline in performance (relative to baseline) of 1 SD or more for any of the four independent cognitive factor scores. Cognitive function was also described as the sum of the four independent cognitive factor scores (cognitive index [CI]). Cognitive dysfunction was then measured as a continuous variable, which was defined as a change in CI (CI) by subtracting the baseline from the 6-wk CI scores.

The methodology used for missing neurocognitive test data has been previously described (16). Briefly, missing data were imputed by using "place-holder" values that do not affect group mean change scores but allow the rest of the patient’s data to be included in the analysis. Patients missing both baseline and 6-wk scores on a test were given the group mean for baseline, to which the mean change for that test was added for the 6-wk score. Patients missing only the 6-wk score were assigned their own baseline plus the mean change for that test for a 6-wk score. Similarly, if only the baseline score was missing, it was imputed from the patient’s 6-wk score minus the mean change for that test. Imputation was not performed for patients who were missing more than two scores from a testing period. Patients whose 6-wk scores were missing because of death or stroke were given worst possible scores on 6-wk tests.

Baseline and demographic characteristics for patients with and without CD were compared by using the ² test for categorical variables and Student’s t-test or Wilcoxon’s ranked sum test for numeric variables. The primary multivariate linear regression analysis for our hypothesis was performed to determine the independent association of CD with %Cr. To assess the generalizability and robustness of the results, we performed similar linear regression analyses to test the association of CI with %Cr and both CD and CI with Cr_maxPost. Demographic variables previously reported to be renal risk factors (4) were included as covariates in both analyses. All demographic variables were considered as covariates in the multivariate model, and only significant covariates were retained in the final model. A P value of 0.05 was considered significant. All statistical analyses were performed with SAS statistical software Version 8.0 (SAS Institute, Inc., Cary, NC).

	Results

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Complete data were obtained for 282 patients. The 282 patients represent 45.1% of the total number of patients (625) who were enrolled in various neurocognitive outcome studies performed at our institute. Only one patient, who was dialysis dependent before surgery, was excluded from analysis. There were no postoperative dialyses or deaths within 48 h of surgery in this patient population. In general, our patient population had similar renal risk factors as comparable populations (4) (Tables 2 and 3).

Univariate analysis of demographic data between the two groups of patients (i.e., with [n = 112] and without [n = 170] CD) is shown in Table 2. In general, demographic variables were similar to those of previously reported comparable populations (4).

Both groups were compared in a univariate analysis with regard to several Cr-derived variables (Table 3). There was no significant difference between the two groups in any of the variables, except that estimated CrClPost was lower in patients without CD (74.2 vs 80.6 mL/min; P = 0.04).

We did not find an independent association between CD and %Cr (parameter estimate [PE] = -0.41; P = 0.91) (Table 4). There was also no significant independent association of CI with %Cr (PE = -1.29; P = 0.46) (Table 5). However, risk factors previously reported to be independently associated with postoperative Cr increase (12) were confirmed, including CrPre, weight, diabetes, and a low cardiac output state (as defined by postoperative inotrope use) (Tables 4 and 5).

View this table: [in this window] [in a new window]   Table 4. Multivariate Linear Regression Analysis of Association Between Percentage Change in Creatinine (%Cr) and Cognitive Deficit (CD)

View this table: [in this window] [in a new window]   Table 5. Multivariate Linear Regression Analysis of the Association Between Percentage Change in Creatinine (%Cr) and Change in Cognitive Index (CI)

View this table: [in this window] [in a new window]   Table 7. Multivariate Linear Regression Analysis of the Association Between Change in Cognitive Index (CI) and CrmaxPost

	Discussion

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We did not confirm the hypothesis that postoperative cognitive dysfunction is associated with acute perioperative renal injury after CABG surgery. However, we did confirm significant associations of several previously reported renal risk factors (4,12) with %Cr. The population-averaged daily percentage peak postoperative fractional change in Cr between patients with and without six-week postoperative CD is shown in Figure 1. These findings contrast with those from our recent study demonstrating that CABG surgery complicated by another major neurologic complication, stroke, was associated with a threefold greater %Cr compared with unaffected patients (9). The findings in our study were consistent in both multivariate models that analyzed the data looking at both indexes of cognitive dysfunction—a dichotomous outcome (CD at six weeks) and a continuous measure (CI). Factors strengthening the validity of the results of this study include the use of a reliable test of renal filtration, power to identify a small change in %Cr, and confirmation of renal risk factors similar to those reported in other populations. Our study indicates that different neurologic complications of cardiac surgery have different patterns of association with perioperative acute renal injury, a finding that with further investigation may shed light on the pathophysiology underlying insults to both major organ systems.

View larger version (22K): [in this window] [in a new window]   Figure 1. Ten-day trend of the peak percentage change in postoperative creatinine in both groups of patients: those with (n = 112) and without (n = 170) cognitive deficit at 6 wk.

Our study has limitations with regard to measurement of renal function. We used Cr as a marker of renal injury. Although the information provided by %Cr and Cr_maxPost is limited to filtration function of the kidneys, these measures have strong established associations, not only with postoperative renal injury, but also with major morbidities and mortality after cardiac surgery (3,12,22). There may be more sensitive markers of renal injury than Cr, e.g., ß₂-micro-globulinuria and urinary N-acetyl ß-D-glucosamin-idase. Moreover, the association of these subtle measures of tubular function and cell injury with outcome from cardiac surgery is not established (23), particularly in large patient groups. In addition, we have previously reported the limitations of tubular proteinuria markers, such as ß₂-microglobulinuria, to indicate renal injury after cardiac surgery (24). The measurement of cognitive dysfunction as a dichotomous outcome (CD) has some limitations because it is based on impaired performance in only one of four factor scores. However, we also assessed cognitive dysfunction as a continuous variable (CI) in which all four factor scores were included in the analysis. We were confident that assessment of CI improved the chance of detecting any aspect of cognitive dysfunction that may have been missed by analyzing CD alone.

The analysis of an association between an in-hospital variable (Cr) with a postdischarge variable (six-week cognitive function test) may be viewed as a limitation. We chose the six-week postoperative assessment of neurocognitive function in accord with data previously reported by our institution (16). There is a substantial reduction in measured neurocognitive deficits between discharge and four- and 6-week testing (25,26). There is little difference between the incidence of cognitive dysfunction measured at the six-week time point and the six-month or three-year follow-up (27). The stability of measured neurocognitive decline at this time point and the consideration of retaining patient compliance for follow-up were the deciding factors in our selection of the six-week neurocognitive follow-up as our primary outcome. Neville et al. (25) have suggested that for purposes of neurobehavioral assessment, clinical neuroprotection trials can be limited to a one-month follow-up. Our study accounted for 12% of the variability in %Cr in the total study population. In previous studies in which it has been assessed, multivariate regression models were unable to account for a large part of the variability in postoperative Cr increase in cardiac surgical patients. In a study of 2009 patients, Andersson et al. (28) found that significant covariates accounted for only 28% (r² = 0.28) of the variation in Cr_maxPost after cardiac surgery. We have previously demonstrated in a multivariate regression analysis of 1502 postcardiac surgery patients that significant covariates also accounted for 28% of the variation in CrClPost (29). However, in our study, the significant covariates accounted for 46% of the variability in Cr_maxPost (Tables 6 and 7). As can be appreciated from these studies, CrPre accounts for a large part of this variability. In any analysis of fractional change in Cr (i.e., %Cr), the contributory effect of CrPre is absorbed, and therefore covariates will account for much less of the variability in %Cr. In our previous article, we showed that, in a sample size of 564 CABG patients, the total predictive value for all covariates in the model was 37.8% (r² = 0.378) (30). However, in this model, CrPre alone accounted for 34.4% of this variability, and other covariates accounted for only 3.4%. In this study, for the multivariate models predicting %Cr (Tables 4 and 5), the r² was 0.12 and was adjusted for CrPre (because it tested %Cr). As the study sample size decreases, only factors with larger effect sizes will appear as significant covariates in any multivariate analysis of factors associated with Cr increase. In our sample size of 282 patients, only factors with significant renal effects were apparent in the multivariate analysis. These independent variables accounted for only 12% of the variation in %Cr. Our inability to confirm an association between cognitive dysfunction and renal injury after cardiac surgery contrasts with the strong relationship between postoperative stroke and renal injury (9).

Preoperative risk factors for acute renal injury and CD in cardiac surgical patients are different (31). Systemic influences, including microemboli, temperature management during CPB, and genetic polymorphisms, appear to play a role in the occurrence of postcardiac surgery CD (6,32,33). However, our findings suggest that the systemic effects that contribute to the pathophysiology of CD in this group of patients did not also contribute significantly to acute renal injury. Possible interpretations of this evidence are that local factors may be predominantly responsible for the occurrence of cognitive dysfunction (e.g., inflammatory mediators) or that systemic factors with opposing effects may have important influences on postoperative cognitive and renal function (e.g., genetic polymorphisms). We demonstrated that the apolipoprotein E ₄ allele confers a protective effect on the kidneys during cardiac surgery (30); this contrasts with the reportedly increased susceptibility to post-CABG surgery cognitive dysfunction in the presence of this allele (33). However, this interpretation of postcardiac surgery renal and neurologic complications may be simplistic, because a complex interplay of several factors, including atheromatous emboli and genetic and inflammatory mechanisms, appears to be important (19,20,30,33,34). Further prospective investigation using a variety of tests of renal function in a large cardiac surgical population may elucidate the mechanisms underlying the pathophysiology of acute perioperative renal injury.

In summary, we found no significant difference in postoperative Cr increase for CABG surgery patients with and without six-week postoperative cognitive impairment. These data are intriguing when compared with our previous demonstration of threefold increases in postoperative Cr with postoperative stroke relative to unaffected patients—a finding that prompts speculation as to a common systemic pathophysiology responsible for both adverse renal and neurologic outcomes (e.g., atheromatous emboli). In contrast, our findings in this study suggest that the factors responsible for subtle cognitive dysfunction after cardiac surgery may occur at a local level or have clinically insignificant effects on the kidneys. However, this conclusion is based on a single test of renal function and requires validation in a large prospective trial using a variety of renal function tests.

	Appendix 1: Members of the Perioperative Outcomes Research Group of the Duke Heart Center

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Neurologic Outcome Research Group: Director, Joseph P. Mathew, MD; and Co-Director, James A. Blumenthal, PhD. Renal Outcome Research Group: Director, Mark Stafford-Smith, FRCPC. Anesthesiology: Mark F. Newman, MD; Hilary P. Grocott, MD; Steven E. Hill, MD; J. G. Reves, MD; Debra A. Schwinn, MD; Mark Stafford-Smith, FRCPC; David Warner, MD; Malissa Harris, RN, BSN; Jerry L. Kirchner, BS; Brenda Mickley, BS; Mandy Barnes, RN, BSN; Elizabeth Carver, RN, BSN; Bonita L. Funk, RN; E. D. Derilus, BS; Jason Hawkins, RN, BSN; Terri Moore, BA; Chonna Campbell, BS; Amanda Cheek, AS; Tanya Kagarise, BS; Tori Latiker, BS; Erich Lauff, BA; Melanie Tirronen, BS; Regina DeLacy, BA; William Hansley, BS; Yvonne M. Connelly, MA, MPH; Barbara Phillips-Bute, PhD; and William D. White, MPH. Behavioral Medicine: Michael A. Babyak, PhD; and James A. Blumenthal, PhD. Cardiology: Daniel B. Mark, MD, MPH; and Michael H. Sketch, MD. Neurology: Carmelo Graffagnino, MD; Daniel T. Laskowitz, MD; John R. Lynch, MD; Ann M. Saunders, PhD; Warren J. Strittmatter, MD; and Kathleen A. Welsh-Bohmer, PhD. Pathology: Ellen Bennett, PhD. Perfusion Services: Greg Smigla, BS, CCP; and Ian Shearer, BS, CCP. Surgery: Robert W. Anderson, MD; Thomas A. D’Amico, MD; Peter K. Smith, MD; R. Duane Davis, MD; Donald D. Glower, MD; R. David Harpole, MD; James Jaggers, MD; Robert H. Jones, MD; Kevin Landolfo, MD; James E. Lowe, MD; Robert H. Messier, MD; Carmelo Milano, MD; Eric M. Toloza, MD, PhD; and Walter G. Wolfe, MD.

	Acknowledgments

 
Supported in part by National Institutes of Health (NIH) Grants 5RO1-HL-54316, AG-09663, and MO1-RR-30 (National Center for Research Resources, Clinical Research Centers Program, NIH) and by the Cardiothoracic Division of the Department of Anesthesiology, Duke University Medical Center, Durham, NC.

The authors would like to gratefully acknowledge the assistance and secretarial efficiency of LaTanya Rhames, Department of Anesthesiology, Duke University Medical Center, in the preparation of this manuscript.

	Footnotes

 
Presented in part at the 23rd annual meeting of the Society of Cardiovascular Anesthesiologists, Vancouver, BC, Canada, May, 2001.

See Appendix 1 for members of the Perioperative Outcomes Research Group of the Duke Heart Center.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999