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Anesth Analg 1999;89:1091
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Attempting to Maintain Normoglycemia During Cardiopulmonary Bypass with Insulin May Initiate Postoperative Hypoglycemia

Mark A. Chaney, MD*, Mihail P. Nikolov, MD*, Bradford P. Blakeman, MD{dagger}, and Mamdouh Bakhos, MD{dagger}

Departments of *Anesthesiology and {dagger}Thoracic and Cardiovascular Surgery, Loyola University Medical Center, Maywood, Illinois

Address correspondence and reprint requests to Mark A. Chaney, MD, Department of Anesthesiology, Loyola University Medical Center, Foster G. McGaw Hospital, 2160 S. First Ave., Maywood, IL 60153. Address e-mail to MCHANEY{at}LUC.EDU


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Appendix 1. "Tight Control"...
 References
 
We attempted to develop an insulin administration protocol that maintains normoglycemia in patients undergoing cardiac surgery and to study the effects of intraoperative blood glucose management on serum levels of creatine phosphokinase isoenzyme BB (CK-BB) and S-100 protein. Twenty nondiabetic patients were randomly allocated to receive either "tight control" of blood glucose with a standardized IV insulin infusion intraoperatively (Group TC) or "no control" of blood glucose intraoperatively (Group NC). Perioperative serum levels of glucose, CK-BB, and S-100 protein were determined in all patients. Group TC patients received 90.0 ± 49.2 units of insulin, whereas Group NC patients received none. Despite insulin, both Group TC (P = 0.00026) and Group NC (P = 0.00003) experienced similar significant increases in blood glucose levels during hypothermic cardiopulmonary bypass. However, mean blood glucose level upon intensive care unit arrival was significantly decreased in Group TC, compared with Group NC (84.7 ± 41.0 mg/dL, range 32–137 mg/dL vs 201.4 ± 67.5 mg/dL, range 82–277 mg/dL, respectively; P = 0.0002). Forty percent of Group TC patients required treatment for postoperative hypoglycemia (blood glucose level <60 mg/dL). Substantial interindividual variability existed in regard to insulin resistance. The investigation was terminated after we realized that normoglycemia was unattainable with the study protocol and that postoperative hypoglycemia was unpredictable. All patients in both groups experienced similar significant increases in postoperative serum levels of CK-BB and S-100 protein. These results indicate that "tight control" of intraoperative blood glucose in nondiabetic patients undergoing cardiac surgery was unattainable with the study protocol and may initiate postoperative hypoglycemia.

Implications: The appropriate intraoperative management of hyperglycemia and whether it adversely affects neurologic outcome in patients after cardiac surgery remains controversial. This investigation reveals that attempting to maintain normoglycemia in this setting with insulin may initiate postoperative hypoglycemia.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Appendix 1. "Tight Control"...
 References
 
Because of cardiopulmonary bypass (CPB)-induced alterations in insulin secretion and resistance, profound hyperglycemia occurs in patients undergoing cardiac surgery (levels may approach 1000 mg/dL). Hyperglycemia has been shown to worsen neurologic injury after focal and global cerebral ischemia, probably because of anaerobic glycolysis-induced conversion of glucose to lactate, which causes intracellular acidosis and impairment of cellular metabolism (1,2). The appropriate intraoperative management of hyperglycemia, and whether it adversely affects neurologic outcome in patients after cardiac surgery, remains controversial1 2 3 (3–7).Previous investigations have assessed neurologic injury as either perioperative gross neurologic change or perioperative changes in a battery of neuropsychologic examinations. However, interpretation and clinical significance of perioperative changes in neuropsychologic examinations is controversial for a number of reasons (8). Biochemical markers (measured in cerebrospinal fluid and/or serum) have been used to assess subtle neurologic injury in patients after cardiac surgery in a manner less subject to measurement vagaries (9). The most promising biochemical markers for assessing subtle neurologic injury in patients after cardiac surgery are the creatine phosphokinase isoenzyme BB (CK-BB) and S-100 protein. In this prospective, randomized, clinical study, we attempted to develop an insulin administration protocol that maintains normoglycemia in patients undergoing cardiac surgery and study the effects of intraoperative blood glucose management on serum levels of CK-BB and S-100 protein.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Appendix 1. "Tight Control"...
 References
 
After institutional review board approval and informed consent, 20 nondiabetic patients scheduled for elective coronary artery bypass grafting (CABG) participated in the study. Patients receiving preoperative insulin and/or oral hypoglycemics were not studied. Patients requiring preoperative IV inotropic drugs, intraaortic balloon support, or mechanical ventilation were excluded from participation in the study. Any patient exhibiting significant pulmonary, endocrine, metabolic, or neurologic pathology was also excluded.

All patients had their cardiac medications continued through the morning of surgery. Prior to arrival to the operating room, each patient was randomized to receive either "tight control" of blood glucose intraoperatively (Group TC) or "no control" of blood glucose intraoperatively (Group NC). Group TC patients had an IV insulin (Humulin® R regular insulin, Eli Lilly and Company, Indianapolis, IN) infusion initiated during induction of anesthesia that was continued until sternal closure at the end of surgery (see the Appendix for insulin administration protocol). In all patients, arterial blood samples were obtained prior to induction of anesthesia (baseline) and every 20 min after induction of anesthesia for determination of blood glucose levels. The last intraoperative blood glucose level was obtained during sternal closure at the end of surgery when the insulin infusion was stopped. Group NC patients were not administered insulin to control intraoperative blood glucose levels. All patients in both groups received only normal saline for perioperative IV infusion.

The intraoperative anesthetic technique was the same for all patients and consisted of IV fentanyl (20 µg/kg), midazolam (14 mg, total), and vecuronium. All of the fentanyl was administered prior to sternotomy. Regarding midazolam, 10 mg was administered prior to sternotomy and 4 mg administered during rewarming. If required, inhaled isoflurane and/or IV nitroglycerin were used for blood pressure control before initiation of CPB. Hypothermic CPB (to a lowest temperature of 28°C) with a membrane oxygenator and crystalloid prime (2.0 L of lactated Ringer’s solution, 50 mEq of sodium bicarbonate, and 12.5 g of mannitol) was used in all patients. Nonpulsatile flows were maintained between 2.4–2.8 L · min-1 · m-2 and, if needed, isoflurane was used by the perfusionist to maintain perfusion pressure in the range of 50–70 mm Hg. Alpha-stat blood gas management was used in all patients. Separation from CPB was facilitated with IV inotropic and/or vasoactive drugs at the discretion of the anesthesiologist managing the case. Intraoperative surgical care was not altered in any way in either group.

To assess the effects of intraoperative blood glucose management on changes in serum CK-BB and S-100 protein, six arterial blood samples were obtained from each patient: immediately prior to induction of anesthesia (baseline); immediately after separation from CPB; and 2, 4, 6, and 24 h after separation from CPB. Blood samples were centrifuged within 15 min, and the serum was stored at -20°C until analysis. CK-BB concentrations were measured with the use of a commercially available two-site monoclonal antibody technique as described by Rossi et al. (10). S-100 protein concentrations were measured with the use of a commercially available two-site monoclonal immunoradioactive assay as described by Westaby et al. (11).

After completion of CABG, patients were transferred to the intensive care unit. Postoperative care was standardized for all patients, and extubation was accomplished at the earliest clinically appropriate time. Postoperative complications and treatments were recorded daily for all patients until hospital discharge.

Fisher’s exact test was applied to categorical data. Student’s t-test (two-tailed) was used to test the difference between means in the two groups. A P value of <0.05 was considered statistically significant, and P values are reported only when significance was found. Results are expressed as the mean ± 1 SD unless otherwise indicated.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Appendix 1. "Tight Control"...
 References
 
Of the 20 nondiabetic patients enrolled and participating in the study, 10 were randomly allocated to Group TC and 10 to Group NC. Demographic and clinical characteristics of patients and intraoperative data are presented in Tables 1 and 2, respectively.


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  		Table 1. Demographic and Clinical Characteristics of Patients
 

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  		Table 2. Intraoperative Data
 
In Group TC patients, despite administration of IV insulin (increased infusion rate, supplementary injections), we were unable to attain normoglycemia with the study protocol. Group TC patients received 90.0 ± 49.2 units of insulin (range 40–161 units), whereas Group NC patients received none. Table 3 presents perioperative blood glucose levels for both groups. Although both Group TC (P = 0.00026) and Group NC (P = 0.00003) experienced significant increases in blood glucose levels during CPB (when compared with baseline), there was no difference between groups. However, mean blood glucose level at sternal closure and upon intensive care unit arrival was significantly decreased in Group TC (Table 3).


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  		Table 3. Perioperative Blood Glucose Levels
 
Table 4 presents individual data for the 10 Group TC patients. Four patients (40%) required treatment for postoperative hypoglycemia (blood glucose level <60 mg/dL).


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  		Table 4. "Tight Control" Patients
 
Perioperative CK-BB and S-100 protein levels are presented in Table 5. Both Group TC (P = 0.005) and Group NC (P = 0.006) experienced significant increases in serum levels of CK-BB (comparing baseline with peak). Likewise, both Group TC (P = 0.009) and Group NC (P = 0.001) experienced significant increases in serum levels of S-100 protein (comparing baseline with peak). However, there were no differences between groups.


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  		Table 5. Perioperative CK-BB and S-100 Protein Levels
 
All patients in both groups had an uneventful intraoperative course. Postoperatively, two patients in Group TC and four patients in Group NC developed new-onset atrial fibrillation. No patient in either group experienced perioperative myocardial infarction. The only clinical neurologic morbidity encountered postoperatively occurred in one Group NC patient who developed transient left arm and left leg weakness with aphasia on the second postoperative day that was completely resolved by the fourth postoperative day. This patient had a history of seizures and was taking phenytoin preoperatively. All patients in both groups were eventually discharged from the hospital. Mean postoperative discharge day in Group TC patients (5.5 ± 2.3 days, range 4–10 days) was similar to Group NC patients (6.5 ± 2.0 days, range 3–9 days).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Appendix 1. "Tight Control"...
 References
 
This investigation revealed that "tight control" of intraoperative blood glucose was not attainable in these nondiabetic patients undergoing elective CABG and hypothermic CPB with our protocol. Furthermore, 40% of patients receiving insulin required treatment for postoperative hypoglycemia (blood glucose level <60 mg/dL) and insulin administration did not affect postoperative serum levels of CK-BB and S-100 protein. These results indicate that attempting to maintain normoglycemia in this setting with insulin may initiate postoperative hypoglycemia.

The appropriate intraoperative management of hyperglycemia and whether or not it adversely affects neurologic outcome in patients after cardiac surgery remains controversial (3–7). Part of the reason for this controversy is that postoperative neurologic dysfunction is difficult to define and assess (8). Biochemical markers (measured in cerebrospinal fluid and/or serum) can be used to assess subtle neurologic injury in patients after cardiac surgery in a manner less subject to measurement vagaries (9). Although less brain-specific than first expected, CK-BB remains the most extensively studied marker in cardiac surgery, and its presence in serum strongly suggests cerebral damage (9). Although the presence of S-100 protein in serum after CPB may represent either cerebral injury or increased blood-brain barrier permeability, studies indicate that it may be a highly sensitive and specific biochemical marker of neurologic injury in patients after cardiac surgery (9). Both of our groups experienced significant postoperative increases in serum levels of CK-BB and S-100 protein. However, there was no difference between groups, perhaps because of similar intraoperative blood glucose levels and/or small sample size.

Although a large body of convincing evidence indicates that glucose worsens outcome from focal and global cerebral ischemia (1), investigations using a battery of neuropsychologic examinations have failed to show a correlation between intraoperative blood glucose levels and neurologic outcome (1,2). One investigation demonstrated that perioperative hyperglycemia actually benefited patients undergoing cardiac surgery by decreasing perioperative fluid requirements and decreasing postoperative fluid retention (6). However, other investigations indicate that hyperglycemia during profound hypothermic circulatory arrest (10,12)3 or during normothermic CPB (13) may contribute to neurologic dysfunction. Although not extensively studied, likely causes of hyperglycemia during and after CPB include decreased insulin secretion and peripheral glucose use (hypothermia, pancreatic hypoperfusion) and/or increased activity of insulin antagonists (glucagon, epinephrine, norepinephrine, growth hormone, and cortisol)4 (14).

We were unable to attain normoglycemia in Group TC patients despite administration of IV insulin (increased infusion rate, supplementary injections) with a standardized protocol. Both groups experienced similar significant increases in blood glucose levels during CPB. This lack of difference between groups may have been a result of the small number of patients studied and/or the large interindividual variability among patients. However, patients receiving insulin had significantly decreased blood glucose levels postoperatively, and 40% required treatment for hypoglycemia. Although the cause(s) of hyperglycemia during and after CPB remains to be elucidated (14),4 this investigation suggests that insulin resistance and temperature (not decreased insulin secretion) likely play major roles.

Despite aggressive administration of insulin with our protocol (up to 161 units), normoglycemia was unattainable during hypothermic CPB, and hypoglycemia occurred after CPB (normothermia). Furthermore, after review of individual patient data in Table 4, it is apparent that there is substantial interindividual variability in insulin resistance and in predicting which patients will develop postoperative hypoglycemia. For example, Patient 7 experienced a peak CPB blood glucose level of 496 mg/dL, despite receiving 160 units of insulin, and did not become hypoglycemic postoperatively. On the other hand, Patient 10 required only 40 units of insulin to maintain a peak CPB blood glucose level of 178 mg/dL, yet did become hypoglycemic postoperatively. After review of the initial 20 patients enrolled in this investigation and realizing that normoglycemia was unattainable with our protocol and that postoperative hypoglycemia was unpredictable, the investigation was terminated.

In conclusion, this investigation revealed that "tight control" of intraoperative blood glucose was not attainable in nondiabetic patients undergoing elective CABG and hypothermic CPB with our protocol. Furthermore, 40% of patients receiving insulin required treatment for postoperative hypoglycemia (blood glucose level <60 mg/dL) and insulin administration did not affect postoperative serum levels of CK-BB and S-100 protein. These results indicate that attempting to maintain normoglycemia in this setting with insulin may initiate postoperative hypoglycemia.


   Appendix 1. "Tight Control" Group Insulin Administration Protocol
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix 1. "Tight Control"...
References
 
Appendix 1


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  		Table 1A.
 


   Acknowledgments
 
This study was supported by Loyola University Medical Center, Department of Anesthesiology, Research Fund.


   Footnotes
 
1 Shevde K, Kharode S, Harigopal P. Neuropsychological dysfunction following cardiac surgery. The role of intraoperative plasma glucose [abstract]. Anesthesiology 1994;81:A222. Back

2 Frasco P, Croughwell N, Blumenthal J, et al. Association between blood glucose level during cardiopulmonary bypass and neuropsychiatric outcome [abstract]. Anesthesiology 1991;75:A55. Back

3 Steward DJ, Da Silva CA, Flegel T. Elevated blood glucose levels may increase the danger of neurological deficit following profoundly hypothermic cardiac arrest [correspondence]. Anesthesiology 1988;68:653. Back

4 Rogers AT, Zaloga GP, Prough DS, et al. Hyperglycemia during cardiac surgery: central vs peripheral mechanisms [abstract]. Anesth Analg 1990;70:S328. Back


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix 1. "Tight Control"...
 References
 

  1. Lanier WL. Glucose management during cardiopulmonary bypass: cardiovascular and neurologic implications. Anesth Analg 1991;72:423–7.[Free Full Text]
  2. Sieber FE, Traystman RJ. Special issues: glucose and the brain. Crit Care Med 1991;20:104–14.
  3. Metz S. Pro. Glucose priming solutions should be used for cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1995;9:603–4.[Medline]
  4. Hindman B. Con. Glucose priming solutions should not be used for cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1995;9:605–7.[Medline]
  5. Freerick AE, Johnston WE, Jenkins LW, et al. Hyperglycemia during hypothermic canine cardiopulmonary bypass increases cerebral lactate. Anesthesiology 1995;82:512–20.[Medline]
  6. Metz S, Keats AS. Benefits of a glucose-containing priming solution for cardiopulmonary bypass. Anesth Analg 1991;72:428–34.[Abstract/Free Full Text]
  7. Nussmeier NA, Fish KJ. Neuropsychological dysfunction after cardiopulmonary bypass: a comparison of two institutions. Cardiothorac Vasc Anesth 1991;5:584–8.
  8. Borowicz LM, Goldsborough MA, Selnes OA, McKhann GM. Neuropsychologic change after cardiac surgery: a critical review. J Cardiothorac Vasc Anesth 1996;10:105–12.[Web of Science][Medline]
  9. Johnsson P. Markers of cerebral ischemia after cardiac surgery. Vasc Anesth 1996;10:120–6.
  10. Rossi R, van der Linden J, Ekroth R, et al. No flow or low flow? A study of the ischemic marker creatine kinase BB after deep hypothermic procedures. J Thorac Cardiovasc Surg 1989;98:193–9.[Abstract]
  11. Westaby S, Johnsson P, Parry AJ, et al. Serum S100 protein: a potential marker for cerebral events during cardiopulmonary bypass. Ann Thorac Surg 1996;61:88–92.[Abstract/Free Full Text]
  12. Ekroth R, Thompson RJ, Lincoln C, et al. Elective deep hypothermia with total circulatory arrest: changes in plasma creatine kinase BB, blood glucose, and clinical variables. J Thorac Cardiovasc Surg 1989;97:30–5.[Abstract]
  13. Mora CT, Henson MB, Weintraub WS, et al. The effect of temperature management during cardiopulmonary bypass on neurologic and neuropsychologic outcomes in patients undergoing coronary revascularization. J Thorac Cardiovasc Surg 1996;112:514–22.[Abstract/Free Full Text]
  14. Rogers A, Stump D, Coker L, et al. Does insulin treatment improve neurobehavioral outcome following coronary artery bypass grafting [abstract]? Anesthesiology 1997;87:A126.
Accepted for publication June 22, 1999.




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Lippincott, Williams & Wilkins 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 HighWire Press