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Anesth Analg 2002;95:1489-1495
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Hyperthermia in the Forty-Eight Hours After Cardiopulmonary Bypass

Weng Y. Thong, MD*, Andrew G. Strickler, MS*, Shu Li, MD*, Elester E. Stewart, RN*, Connie L. Collier, RN*, William K. Vaughn, PhD{dagger}, and Nancy A. Nussmeier, MD*

Departments of *Cardiovascular Anesthesiology and {dagger}Biostatistics and Epidemiology, Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston

Address correspondence and reprint requests to Nancy A. Nussmeier, MD, Department of Cardiovascular Anesthesiology, Texas Heart Institute, PO Box 20345, MC 1–226, Houston, TX 77225. Address e-mail to nnussmeier{at}heart.thi.tmc.edu


   Abstract
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 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
The adverse consequences of perioperative hypothermia have been emphasized. However, postoperative hyperthermia may be equally hazardous after cardiac surgery, owing to increased oxygen demand and potential exacerbation of neurologic injury. To determine the incidence of hyperthermia (bladder temperature [BT] >= 38.5°C) after cardiopulmonary bypass, we recorded hourly postoperative BT (n = 305), nasopharyngeal (n = 40), and jugular venous bulb (n = 20) temperatures for up to 48 h after admission to the intensive care unit (ICU). At least 38% of the patients developed postoperative hyperthermia, although all patients did not remain in the ICU for 48 h. The incidence of hyperthermia peaked with a bimodal distribution at 9.1 ± 4.0 h (26%) and at 27.7 ± 6.3 h (26%). Of these, 14% of the patients were hyperthermic at both times. For the first 5 postoperative h, jugular venous bulb temperature was 0.4°C higher than the BT (P < 0.05). There was no difference between BT and nasopharyngeal temperature. Higher temperature on ICU entry and age <60 yr were independently associated with hyperthermia (P < 0.05). In summary, postoperative hyperthermia is common, with both early and late occurrences during the first 48 h after cardiac surgery with cardiopulmonary bypass.

IMPLICATIONS:Postoperative hyperthermia is common in cardiac surgery patients, with a bimodal distribution during the first 48 h. Jugular venous bulb temperature is slightly higher than bladder temperature for several hours. Postoperative cerebral hyperthermia may contribute to the severity of cerebral injury after cardiopulmonary bypass.


   Introduction
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 Introduction
Materials and Methods
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 Discussion
 References
 
Neurologic injury remains a devastating complication of cardiac surgery, leading to excess mortality and resource use and decreased quality of life (1,2). Among patients undergoing operations with cardiopulmonary bypass (CPB), 25%–65% of all in-hospital strokes occur after initial uneventful recovery from surgery (3,4). Induced hypothermia is the only reliable method of neuroprotection from injuries related to cerebral ischemia from any cause (5–8). Nevertheless, even mild degrees of postoperative hypothermia are treated vigorously to prevent shivering, impaired blood coagulation, arrhythmia, and possibly wound infection (9).

In the course of observing patients after studies of intraoperative temperature gradients (at several measurement sites) (10,11), we noted that postoperative hyperthermia (>38.5°C) early after operation was not unusual and was frequently untreated. In intraoperative studies, we and others (10–14) observed that jugular venous bulb temperature (JVBT), a reasonable approximation of global brain temperature, was significantly higher than nasopharyngeal (NPT) or esophageal temperatures and 3°C–4°C higher than bladder (BT) or rectal temperature during rewarming from hypothermia. Bissonnette et al. (14) reported that JVBT was 1°C–2°C higher than simultaneous tympanic, rectal, or esophageal temperatures in 15 infants and children after cardiac operations. Because postoperative core temperature is most often measured in the bladder or rectum, it is possible that there is cerebral hyperthermia in many patients during the period in which they are vulnerable to cerebral injury and could increase the severity of such injury.

We therefore performed this study to prospectively determine in consecutive patients the incidence of postoperative hyperthermia and potential patient and procedure factors that contribute to the incidence. In addition, in small subsets of patients, we planned to confirm the temperature gradients observed during surgery.


   Materials and Methods
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 Materials and Methods
Results
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 References
 
With the approval of our IRB, we prospectively studied 305 consecutive patients for elective cardiac procedures requiring CPB. Two-hundred-fifty-one patients underwent coronary artery bypass grafting, 43 had valve repair or replacement, and 11 had coronary artery bypass grafting plus a valve procedure. Anesthesia and CPB with a membrane oxygenator were managed according to a uniform institutional protocol. NPT and BT were monitored in all patients. NPT was monitored with a 12F temperature probe (Mon-a-thermTM, Mallinkrodt Inc, St Louis, MO). BT was monitored with a 16F catheter with temperature-sensing capability (Bardex LubricathTM Temperature-Sensing Foley Catheter, C.R. Bard Inc, Covington, GA).

CPB was performed with a standard bypass circuit, crystalloid prime (except in markedly anemic patients), roller pumps, and membrane oxygenators. Blood cardioplegia was administered in an antegrade fashion in most cases. Retrograde cardioplegia was used occasionally. During CPB, the degree of induced hypothermia was selected by each surgeon and monitored by the NPT probe. Patients were rewarmed to a target temperature of 36.5°C before the end of CPB, and the temperature of the CPB perfusate was never more than 38.0°C. Heating blankets were not used during surgery, but crystalloid, colloid, and blood products were warmed with an IV fluid warmer (HotlineTM, Sims Level 1, Inc, Rockland, MA). The room temperature was maintained at 13°C–18°C. Postoperatively, all patients were transferred to the intensive care unit (ICU) where intermittent positive-pressure ventilation was maintained for a minimum of 3 h. Rewarming by means of forced air blanket was performed when temperature on admission was <35.0°C. Acetaminophen 325 mg or 650 mg orally or rectal suppository every 4 h as required was routinely ordered for a BT exceeding 38.5°C.

Postoperatively, the BT was monitored continuously and recorded hourly from ICU admission to ICU discharge or the 48th postoperative h by nursing staff using digital data storage, which was then transcribed hourly into the ICU record. In 40 unselected patients, the intraoperative NPT probe remained in place and was monitored until extubation. In 20 un-selected patients, in whom JVBT was monitored during surgery as part of the study of intraoperative temperature gradients, the probe remained in place and was monitored for 24 h. This 5F catheter with thermistor capability (7.5-cm Swan-GanzTM Catheter, Baxter, Irvine, CA) was inserted after the anesthetic induction without special methods (e.g., fluoroscopy) to ensure exact localization in the jugular bulb. The catheter was inserted retrograde until resistance was encountered and then pulled back approximately one-half centimeter until blood could be freely aspirated.

Clinically significant hyperthermia was defined as a BT of >=38.5°C (101.3 °F) (14–17) at any hour during the first 48 h after ICU admission. When hyperthermia was present, its duration was recorded in hourly units. All data were transcribed daily from the ICU record onto a separate data sheet.

In addition, the following demographic and intraoperative factors were recorded: age, weight, sex, surgical procedure, duration of CPB, nadir NPT during CPB, antifibrinolytic drugs, intraoperative blood components, and NPT at the end of CPB and on leaving the operating room. We also recorded postoperative usage of blood components, antipyretic drugs, and a forced air warmer (Bair HuggerTM, Augustine Medical Inc, Eden Prairie, MN). Univariate associations between potential risk factors for hyperthermia were assessed with Student’s t-test, {chi}2 analysis, or analysis of variance, followed by stepwise logistic modeling, which included all significant (P < 0.10) variables. Differences in temperatures at simultaneously monitored sites were assessed with paired t-tests for each patient.


   Results
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 Materials and Methods
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Discussion
 References
 
The 305 patients underwent 32.8 ± 24 min of hypothermic CPB with a total CPB time of 75.9 ± 37 min and a mean rewarming time of 39.8 ± 21 min. Mean nadir NPT during CPB was 30.5°C ± 2.2°C. Mean NPT was 36.4°C ± 0.4°C at the end of CPB and 35.2°C ± 0.7°C on leaving the operating room.

Because temperature monitoring was terminated on discharge from the ICU, all 305 patients were continuously monitored for 12 h, 243 patients for 24 h, 178 patients for 36 h, and 74 patients for 48 h. In this group, at least 38% (117 of 305) had clinically significant hyperthermia (BT >=38.5°C) during the first 48 postoperative h. Of the 117, only 19 patients had hyperthermia (>=38.5°C) recorded for one hourly observation; nine patients had it recorded for two observations, and 17 had it recorded for three observations. In the other 72 patients, hyperthermia lasted more than 3 h.

The development of hyperthermia peaked at two intervals after the operation (Fig. 1). Twenty-six percent of the patients became hyperthermic 9.1 ± 4.0 h after ICU admission. Twenty-six percent developed hyperthermia 27.7 ± 6.3 h after ICU admission. Of these, 14% of the patients were hyperthermic at both intervals, only seven of them being continuously hyperthermic. The mean duration of hyperthermic episodes was 3.8 ± 2.6 h early and 4.9 ± 4.3 h late. Mean peak temperature at both intervals was 38.7°C ± 0.2°C.



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  		Figure 1. Postoperative development of bladder temperature (BT) >38.5°C in 117 of 305 patients after admission to the intensive care unit (n = 305 at 12 h, 243 at 24 h, 178 at 36 h, and 74 at 48 h). Patients included in the solid black areas represent those whose initial hyperthermia recurred later in the ICU period.

 
Preoperative, intraoperative, and postoperative patient characteristics were compared by means of univariate analyses in the hyperthermic and nonhyperthermic groups (Table 1). Patients who developed hyperthermia were younger (P = 0.008), with a median age of 60 yr compared with 65 yr in the nonhyperthermic group. Hyperthermic patients also weighed more (P = 0.05). Notably, all but two patients were hypothermic (mean BT, 34.9°C ± 0.8°C) when admitted to the ICU. BT on ICU admission was significantly lower in the nonhyperthermic group (34.8°C ± 0.8°C) than in the hyperthermic group (35.1°C ± 0.8°C) (P = 0.0005; Table 1). A forced air warmer was used more frequently in the nonhyperthermic group (55.3% versus 41.9%; P = 0.07). Administration of fresh frozen plasma in the intraoperative or postoperative period and administration of packed red blood cells in the postoperative period were significantly associated with development of hyperthermia (Table 1). We separately examined the use of intraoperative and postoperative blood products with respect to the development of early or late hyperthermia. No relationship with any individual type of blood product or with combinations of blood products was noted for the early versus late occurrences. As expected, significantly more hyperthermic patients were treated with antipyretic drugs (47.0% versus 10.6%; P = 0.0001).


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  		Table 1. Demographic and Perioperative Patient Characteristics
 
The following characteristics, having P < 0.10 in univariate analysis, were included in the multivariate analysis: age <60 yr, body weight, temperature on admission to ICU, use of a forced air warmer, and total units of any blood product. Higher mean temperature on admission to the ICU (35.1°C ± 0.8°C versus 34.8°C ± 0.8°C; odds ratio, 1.8 [95% confidence interval, 1.3–2.4]; P = 0.001) and age <60 yr (odds ratio, 0.51 [95% confidence interval, 0.31–0.83]; P = 0.01) remained significantly associated with postoperative hyperthermia.

During gradual rewarming in the first 5 postoperative h, mean JVBT remained significantly higher than mean BT (P < 0.05; Fig. 2). The maximum difference between the JVBT and BT was 0.39°C, occurring at both 3 and 4 h after ICU admission. There were no significant differences between the NPT and BT.



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  		Figure 2. Mean postoperative jugular venous bulb temperature (JVBT) versus bladder temperature (BT) (n = 20).

 
Although this study was not designed to evaluate the neurologic consequences of postoperative hyperthermia, we performed a retrospective chart review of progress notes after the study was completed, revealing 3 strokes (2.6%) in the 117 hyperthermic patients and 4 strokes (2.1%) in the 188 nonhyperthermic patients. In addition, 5 hyperthermic patients (4.2%) and 5 nonhyperthermic patients (2.7%) developed postoperative confusion, lethargy, or poor responsiveness.


   Discussion
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 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In this study of adult patients after hypothermic CPB, at least 38% developed postoperative hyperthermia of >=38.5°C, with a mean peak temperature of nearly 39°C. We chose 38.5°C as the criterion for hyperthermia because this temperature triggers clinical treatment at our center and other institutions (14,15) and is associated with a poorer prognosis in stroke patients (16,17) as well as lower neuropsychological scores in cardiac surgery patients (18). Because many of the overt strokes associated with cardiac surgery occur after operation (3,4), cerebral hyperthermia of this magnitude can only exacerbate the ensuing tissue injury.

Abundant animal data confirm the deleterious effects of hyperthermia on a variety of experimental brain injuries. Hyperthermia during or after ischemia delays neuronal metabolic recovery (19), and increases excitotoxic neurotransmitter release (20), oxygen free radical production (21), intracellular acidosis (19), and blood-brain barrier permeability (22), as well as modulating protein kinase (23) and destabilizing the cytoskeleton (24). Even small (2°C) increases in cerebral temperature significantly enhance ischemic neuronal injury and accelerate neuronal death (5,25). In rats, Dietrich et al. (25) demonstrated that mildly increasing the intraischemic brain temperature by 2°C converted cell injury to frank infarction in susceptible regions, increasing the mortality.

Clinical data are equally convincing. In stroke patients, lower body temperatures were associated with decreased mortality and a better neurologic outcome in survivors (16,17,26). Even small (1°C–2°C) differences in temperature predicted substantial differences in outcomes. Two recent randomized studies of induced mild-to-moderate hypothermia (32°C–34°C) in resuscitated survivors of cardiac arrest demonstrated improved neurologic outcome (7,8). Furthermore, two studies (16,17) in patients with acute strokes showed that hyperthermia after stroke worsened the prognosis with respect to stroke severity, infarct size, mortality, and outcome in survivors. Recently, Grocott et al. (18) reported that higher maximum postoperative temperature correlated with a greater degree of cognitive dysfunction six weeks after cardiac surgery. In that study, patients were monitored for 24 hours, with peak temperature occurring after six to 10 hours. The finding of an association between postoperative hyperthermia and cognitive dysfunction stresses the importance of temperature management beyond the operative period.

Although large temperature gradients during intraoperative rewarming are well documented (10–14), these gradients nearly disappeared in our patients by the time of ICU admission. During the first five hours in the ICU, NPT was not different from BT, and mean JVBT exceeded the BT by only 0.4°C, a smaller gradient than that observed in pediatric patients during this same postoperative period (14). In our data, younger age was a significant predictor of postoperative hyperthermia, suggesting perhaps a greater hazard of postoperative cerebral hyperthermia in younger patients.

The exact etiology of hyperthermia after cardiac surgery is unknown. Certainly, procedures performed with CPB involve greater thermal perturbations than other types of surgery in that the use of a heat exchanger minimizes the role of other sources of heat loss and gain, with resultant large alterations in tissue heat content and regional distribution of heat (27). However, after the operation, a likely cause of postoperative hyperthermia may be the well-known inflammatory response to CPB, which persists despite improvements in CPB equipment and technology (28–31). A similar response occurs however, even during cardiac operations without CPB, although to a lesser degree (28) and probably during all operations associated with significant tissue injury (30). In addition, our univariate analyses showed a significant association between transfusion of either packed red blood cells or fresh frozen plasma and postoperative hyperthermia, suggesting the febrile response to blood products as another cause (32,33). Our multivariate analyses revealed only younger age and higher temperature on ICU admission as potential predictors of postoperative hyperthermia. Perhaps younger patients mount a more aggressive inflammatory response to the same stimulus (14). Although atelectasis is often cited as a potential cause of fever, Engoren et al. (15) found no such association in patients after CPB. Possibly, overly aggressive rewarming to prevent postoperative hypothermia contributed to the increased frequency of hyperthermia we observed. Our observation of a second peak incidence of hyperthermia at 28 hours suggests that the etiology is probably multiple.

The major limitation of this study is that temperature monitoring was terminated on discharge from the ICU, with attrition of 62 patients by 24 hours, additional loss of 65 patients by 36 hours, and only 74 patients remaining by 48 hours. Therefore, we undoubtedly underestimated the overall incidence of hyperthermia. Other potential limitations include inaccuracy in positioning of the jugular bulb catheter and the reliability of this site to monitor global brain temperature. Although JVBT does not precisely measure cerebral cortical temperature, it cannot be greater than brain temperature, as shown by direct measurements of cerebral temperature in patients with head injuries (34). Another limitation is that the BT was recorded only hourly. Given these limitations, we did not expect to find such a frequent incidence of hyperthermia (at least 38%).

The risks of postoperative hypothermia have been widely emphasized (35–37). In cardiac surgery patients, efforts to minimize postoperative hypothermia have focused on vigorous rewarming after CPB, using forced air warmers, fluid-filled warming blankets, IV fluid warmers, and heated humidifiers (9). These efforts require increased resource use and costs for warming devices and additional nursing care. In this effort, the neuroprotective effect of perioperative hypothermia may have been overlooked (7,8,38) as well as potential hazards of excessive rewarming, which include increased oxygen consumption, increased myocardial demand, arrhythmias, and tachycardia, all of which may increase cardiac morbidity. Gradual establishment of normothermia without overshooting in the postoperative period and with continued vigilance to avoid delayed hyperthermia is probably the optimal clinical regimen (39,40).

In summary, our data indicate that postoperative hyperthermia is common, occurring in at least 38% of 305 cardiac surgical patients. When hyperthermia did occur, it was undertreated in our patients. Excessive concern regarding hazards of hypothermia may encourage tolerance of hyperthermia. Overly aggressive intraoperative rewarming and the use of blood products probably contribute to its frequency. Considering that a significant portion of cerebral injuries after CPB occur during the postoperative period and that the brain temperature may be higher than the monitored temperature for part of this period, postoperative hyperthermia should receive the same attention and aggressive treatment as hypothermia. A much larger study will be required to determine whether such treatment improves cerebral or other outcomes after CPB.


   Acknowledgments
 
The authors appreciate the professional reviews of J.R. Cooper, Jr, MD, and Arthur S. Keats, MD, in the preparation of this manuscript.


   References
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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