Cerebral Hyperthermia Research Articles

A computational model of a thermoelectric device for the correction of cerebral hyperthermia

A computational model of a thermoelectric device for the correction of cerebral hyperthermia

Hypoxic irreversible brain cells damage, associated risk factors and antihypoxants

It is reported that in the final stage of many diseases the immediate cause of biological death in humans and warm-blooded animals is hypoxic irreversible damage to brain cells. This explains the fact that to prevent biological death in all critical conditions without exception, inhalation with breathing gases containing oxygen has long been successfully used. This is also why oxygenation of the blood is considered one of the main conditions for preserving human life in all critical situations and forms the basis of emergency medical care in the intensive care unit. However, inhalation of oxygen gas and increasing blood oxygen saturation should be carried out as early as possible, and more precisely - before the onset of the stage of hypoxic irreversible damage in brain cells. The fact is that after the onset of irreversible damage brain cells die even in the presence of oxygen. In this connection, the mechanisms of adaptation of the organism to oxygen deficiency play a great role for longer preservation of brain cells viability and human life in conditions of hypoxemia. In order to increase resistance to hypoxemia, antihypoxants are traditionally used. But they can preserve the viability of brain cells not always, but only if they are introduced into the body before the onset of hypoxic irreversible damage to brain cells and in the case of unused reserves of adaptation to hypoxemia in the body. Risk factors of hypoxic irreversible damage of brain cells are indicated, among which excessively long duration of hypoxemia and hyperthermia are emphasized. It is shown that the most important circumstance for the development of hypoxic irreversible damage of brain cells is not so much the degree of hypoxemia as the degree of hypoxia of brain tissue and its duration, which exceeds the period of human resistance to hypoxia. It has been shown that human resistance to hypoxia can be assessed using the Stange test. It has been reported that fever and local cerebral hyperthermia decrease, and hibernation and local cerebral hypothermia increase, the resistance of brain cells to hypoxia. In this regard, recommendations not only to eliminate fever and local inflammatory processes in the head, but also recommendations to reduce brain temperature are highly appropriate to improve resistance to hypoxia. It is pointed out that among the methods of local therapeutic hypothermia, targeted temperature management is the most advanced. In addition, it is reported that in recent years a new group of promising antihypoxants - alkaline solutions of hydrogen peroxide - has been created. It is shown that hydrogen peroxide is able to decompose very quickly into water and oxygen gas under the action of catalase, which is found in all tissues. The peculiarities of using alkaline solutions of hydrogen peroxide as antihypoxants we all have to study in the future.

Abstract WP311: Novel Computational Framework for Modelling the Effects of Temperature on Survival Time in Ischemic Stroke

Introduction: The detrimental influence of cerebral hyperthermia is well known, with notably deleterious effects in the ischemic brain, where even mild increases (<1°C) may rapidly potentiate ischemic injury. Experimental models of ischemic hyperthermia are undermined by the lack of pragmatic means for temporally- and spatially-resolved, direct cerebral thermometry. Computational models of cerebrovascular ischemia are well-suited to such exploration, and the use of digital phantoms for sophisticated biophysical modeling has been facilitated by emergent hardware, software, and computational solutions. We present a realistic computational environment for the simulation of thermal disturbance in cerebrovascular ischemia, permitting multiscale demonstration of hemodynamic, metabolic, and thermal aberrations in ischemic brain Methods: A multi-tissue biophysical numerical model of the human head and brain was extended to incorporate the dynamics of nutritive flow, metabolic need, tissue heating, and cytotoxicity. By restricting perfusion in a region of brain using a rudimentary representation of vascularization, we could quantify tissue heating arising from impaired radiative cooling, and time-dependent cell death. The procedure was iterated with an expected proportionality between temperature and metabolic rate Results: Fig 1 demonstrates simulated hypoperfusion affecting one hemisphere with resultant cerebral hyperthermia arising from impaired countercurrent heat exchange. Incorporating the effects of hyperthermia upon metabolic demand, the downward influence of heating on survivability is apparent, with ~30-minute acceleration to cytotoxicity. Conclusion: We present a combined model for tissue physiology and survival time following ischemic stroke using a multi-tissue model of whole-head bio-thermodynamics to examine effects of critical temperature disturbance on predicted tissue survival time.

Microwave Radiothermometry in Evaluating Brain Temperature Changes (Review)

Aim. This review aims to inform physicians of different specialties (anesthesiologists, intensivists, neurologists, neurosurgeons, oncologists) about the diagnostic capabilities of microwave radiothermometry, which enables to identify and analyze features of alterations of cerebral temperature in brain damage.The review displays a critical analysis of 80 recent Russian and foreign open access publications found by keywords.The review presents major clinical features and pathophysiological mechanisms of cerebral thermal balance disruptions in brain lesions. Slow responsiveness and vulnerability of cerebral thermal homeostasis regulation mechanisms that underlie development of different temperature heterogeneity levels in the cerebral cortex in healthy brain and brain lesions are highlighted. The authors postulate their concept about the critical role of hyperthermia in the pathogenesis of brain damage and disruption of interconnections in the global central regulation system. A body of evidence explaining direct association between the depth of consciousness impairment and degree of cerebral cortex temperature heterogeneity manifestation is presented. It is emphasized that a significant increase in temperature heterogeneity with areas of focal hyperthermia accompanies an acute period of ischemic stroke, while in post-comatose state usually associated with prolonged impairment of consciousness, the temperature heterogeneity significantly subsides. It has been suggested that lowering of an increased and rising of the reduced temperature heterogeneity, for example by using temperature exposure, can improve altered level of consciousness in patients with brain damage. The diagnostic capabilities of various technologies used for cerebral temperature measurement, including microwave radiothermometry (MWR), are evaluated. Data on high accuracy of MWR in measurement of the cerebral cortex temperature in comparison with invasive methods are presented.Conclusion. In healthy individuals MWR revealed a distinct daily rhythmic changes of the cerebral cortex temperature, and badly violated circadian rhythms in patients with brain lesions. Since MWR is an easy-toperform, non-invasive and objective diagnostic tool, it is feasible to use this technology to detect latent cerebral hyperthermia and assess the level of temperature heterogeneity disruption, as well as to study the circadian rhythm of temperature changes.

Craniocerebral hypothermia in the acute period of ischemic stroke

To determine the effect of craniocerebral hypothermia (CCH) on neurological deficit regression, hemodynamics, fever and functional outcome of therapy in patients with moderate ischemic stroke (IS). This study included 60 patients with IS (the first day). The main group consisted of 30 patients who underwent CCH, and the comparison (control) group consisted of 30 patients without CCH. The National Institutes of Health Stroke Scale (NIHSS), the Glasgow Coma Scale (GCS), the modified Rankin Scale (mRs) were used. Recorded parameters were mortality, heart rate (HR), blood pressure (BP), axial temperature, cerebral temperature of the frontal cortex. Cerebral temperature was obtained noninvasively by using a RTM-01-RES radiothermometer (Russia). CCH (for 24 hours) in the main group was implemented by ATG-01 device (Russia). Results were recorded on the day of admission, after 24 hours and at discharge. In both groups, basic neuroprotective, hypotensive, antiplatelet and antiedemic therapy was administered. No fatal outcomes were reported in both groups. Side-effects and complications of CCH were not recorded. In the main group, neurological deficit assessed by NIHSS decreased by 75% after the CCH procedure and by 93.75% at the time of discharge from the hospital. In patients of the comparison group, regression of neurological deficit was 35% on the second day and 55% at the day of discharge. The use of CCH suppressed systemic and cerebral hyperthermia. Functional outcome of therapy in the main group was higher compared to the comparison one. The dynamics in blood pressure and heart rate didn't differ in both groups. A pronounced positive effect of CCH on the course of the acute period and therapy results in patients with IS was demonstrated.

Mechanisms of low-temperature rehabilitation technologies. Sports traumatic brain injury

According to various data, sports traumatic brain injury (TBI) accounts for up to 20% of all injuries in athletes, and the number of cases of traumatization is progressively increasing year by year due to an increase in the number of people involved in sports, the growing popularity of extreme and contact sports, as well as a high level of motivation to achieve record results. The structure of sports TBI is dominated by mild TBI, which can provoke the development of a very wide range of complications and negative consequences that affect not only the result, but, most importantly, the quality of life of athletes. The pathogenesis of mild TBI has been studied, therapy and rehabilitation programs have been developed. At the same time, the features of sports TBI that significantly distinguish it from domestic, road or criminal injuries are not sufficiently taken into account: repeated frequent TBI, increased body and brain temperature, peripheral redistribution of blood flow and hypocapnia associated with physical exertion and significantly affecting cerebral blood flow. An athlete receives a TBI during the most vulnerable period for the brain. To a large extent, these features are associated with the high incidence of various kinds of neurological complications of sports TBI (cognitive disorders, memory impairment, sleep disorders, migraines, etc.). Special techniques that can prevent complications of sports TBI have not been developed. Brain injury is an independent cause of the development of cerebral hyperthermia, which significantly worsens the course and consequences of TBI. The well-known technology of craniocerebral hypothermia (CCG) allows to reduce physical general and cerebral hyperthermia, to increase the resistance of neurons of the cerebral cortex to hypoxia and trauma. However, this technology is used sporadically, which, apparently, is due to the lack of awareness of coaches and doctors of sports teams specializing in sports medicine and rehabilitation. The purpose of the review is to analyze the features of the action of selective hypothermia of the cerebral cortex, used to prevent complications of mild sports TBI.

Influence of cerebral hyperthermia on intracranial pressure and autoregulation of cerebral circulation in patients with acute brain injury

To study the effect of hyperthermia on intracranial pressure (ICP) and cerebral autoregulation (Prx). There were 8 patients with acute brain injury, signs of brain edema and intracranial hypertension. Cerebral autoregulation was assessed by using of PRx. ICP, CPP, BP, PRx were measured before and during hyperthermia. We have analyzed 33 episodes of cerebral hyperthermia over 38.30 C. Statistica 10.0 (StatSoft) was used for statistical analysis. Only ICP was significantly increased by 6 [3; 11] mm Hg (p<0.01). In patients with initially normal ICP, hyperthermia resulted increase of ICP in 48% of cases (median 24 [22; 28] mm Hg). In patients with baseline intracranial hypertension, progression of hypertension was noted in 100% cases (median 31 [27; 32] mm Hg) (p<0.01). Hyperthermia resulted intracranial hypertension regardless brain autoregulation status. Cerebral hyperthermia in patients with initially normal ICP results intracranial hypertension in 48% of cases. In case of elevated ICP, further progression of intracranial hypertension occurs in 100% of cases. Cerebral hyperthermia is followed by ICP elevation in both intact and impaired cerebral autoregulation.

The pathogenetic role of cerebral hyperthermia in brain lesion

Cerebral hyperthermia is a factor of pathogenesis of secondary brain injury. Microwave recording of temperature allows to identify thermal anomalies in the brain while craniocerebral hypothermia arrests their development. Craniocerebral hypothermia has marked neuroprotective effects in patients with brain lesions.

Cerebral Temperature Dysregulation: MR Thermographic Monitoring in a Nonhuman Primate Study of Acute Ischemic Stroke.

Cerebral thermoregulation remains poorly understood. Temperature dysregulation is deeply implicated in the potentiation of cerebrovascular ischemia. We present a multiphasic, MR thermographic study in a nonhuman primate model of MCA infarction, hypothesizing detectable brain temperature disturbances and brain-systemic temperature decoupling. Three Rhesus Macaque nonhuman primates were sourced for 3-phase MR imaging: 1) baseline MR imaging, 2) 7-hour continuous MR imaging following minimally invasive, endovascular MCA stroke induction, and 3) poststroke day 1 MR imaging follow-up. MR thermometry was achieved by multivoxel spectroscopy (semi-localization by adiabatic selective refocusing) by using the proton resonance frequency chemical shift. The relationship of brain and systemic temperatures with time and infarction volumes was characterized by using a mixed-effects model. Following MCA infarction, progressive cerebral hyperthermia was observed in all 3 subjects, significantly outpacing systemic temperature fluctuations. Highly significant associations were observed for systemic, hemispheric, and global brain temperatures (F-statistic, P = .0005 for all regressions) relative to the time from stroke induction. Significant differences in the relationship between temperature and time following stroke onset were detected when comparing systemic temperatures with ipsilateral (P = .007), contralateral (P = .004), and infarction core (P = .003) temperatures following multiple-comparisons correction. Significant associations were observed between infarction volumes and both systemic (P ≤ .01) and ipsilateral (P = .04) brain temperatures, but not contralateral brain temperature (P = .08). Successful physiologic and continuous postischemic cerebral MR thermography was conducted and prescribed in a nonhuman primate infarction model to facilitate translatability. The results confirm hypothesized temperature disturbance and decoupling of physiologic brain-systemic temperature gradients. These findings inform a developing paradigm of brain thermoregulation and the applicability of brain temperature as a neuroimaging biomarker in CNS injury.

The Society of Thoracic Surgeons, The Society of Cardiovascular Anesthesiologists, and The American Society of ExtraCorporeal Technology: Clinical Practice Guidelines for Cardiopulmonary Bypass--Temperature Management During Cardiopulmonary Bypass.

In order to improve our understanding of the evidence-based literature supporting temperature management during adult cardiopulmonary bypass, The Society of Thoracic Surgeons, the Society of Cardiovascular Anesthesiology and the American Society of ExtraCorporeal Technology tasked the authors to conduct a review of the peer-reviewed literature, including: 1) optimal site for temperature monitoring, 2) avoidance of hyperthermia, 3) peak cooling temperature gradient and cooling rate, and 4) peak warming temperature gradient and rewarming rate. Authors adopted the American College of Cardiology/American Heart Association method for development clinical practice guidelines, and arrived at the following recommendations: CLASS I RECOMMENDATIONS: a)The oxygenator arterial outlet blood temperature is recommended to be utilized as a surrogate for cerebral temperature measurement during CPB. (Class I, Level C) b)To monitor cerebral perfusate temperature during warming, it should be assumed that the oxygenator arterial outlet blood temperature under-estimates cerebral perfusate temperature. (Class I, Level C) c)Surgical teams should limit arterial outlet blood temperature to<37°C to avoid cerebral hyperthermia. (Class 1, Level C) d)Temperature gradients between the arterial outlet and venous inflow on the oxygenator during CPB cooling should not exceed 10°C to avoid generation of gaseous emboli. (Class 1, Level C) e)Temperature gradients between the arterial outlet and venous inflow on the oxygenator during CPB rewarming should not exceed 10°C to avoid out-gassing when blood is returned to the patient. (Class 1, Level C) CLASS IIa a)Pulmonary artery or nasopharyngeal temperature recording is reasonable for weaning and immediate post-bypass temperature measurement. (Class IIa, Level C)b)Rewarming when arterial blood outlet temperature ≥30° C: i.To achieve the desired temperature for separation from bypass, it is reasonable to maintain a temperature gradient between arterial outlet temperature and the venous inflow of≤4°C. (Class IIa, Level B) ii.To achieve the desired temperature for separation from bypass, it is reasonable to maintain a rewarming rate≤0.5°C/min. (Class IIa, Level B) NO RECOMMENDATION: No recommendation for a guideline is provided concerning optimal temperature for weaning from CPB due to insufficient published evidence.

Plasma protein denaturation with graded heat exposure

During cardiopulmonary bypass (CPB), perfusion at tepid temperatures (33-35 °C) is recommended to avoid high temperature cerebral hyperthermia during and after the operation. However, the ideal temperature for uncomplicated adult cardiac surgery is an unsettled question. Typically, the heat exchanger maximum temperature is monitored between 40-42 °C to prevent denaturation of plasma proteins, but studies have not been performed to make these conclusions. Therefore, our hypothesis was to determine the temperature in which blood plasma protein degradation occurs after 2 hours of heat exposure. As a result, blood plasma proteins were exposed to heat in the 37-50 °C range for 2 hours. Plasma protein samples were loaded onto an 8-12% gradient gel for SDS-PAGE and low molecular weight plasma protein degradation was detected with graded heat exposure. Protein degradation was first detected between 43-45 °C of heat exposure. This study supports the practice of monitoring the heat exchanger between 40-42 °C to prevent denaturation of plasma proteins.

Brachial Arterial Temperature as an Indicator of Core Temperature: Proof of Concept and Potential Applications

There is potential for heat loss and hypothermia during anesthesia and also for hyperthermia if heat conservation and active warming measures are not accurately titrated. Accurate temperature monitoring is particularly important in procedures in which the patient is actively cooled and then rewarmed such as during cardiopulmonary bypass surgery (CPB). We simultaneously measured core, nasopharyngeal, and brachial artery temperatures to investigate the last named as a potential peripheral temperature monitoring site. Ten patients undergoing hypothermic CPB were instrumented for simultaneous monitoring of temperatures in the pulmonary artery (PA), aortic arterial inflow (AI), nasopharynx (NP), and brachial artery (BA). Core temperature was defined as PA temperature before and after CPB and the AI temperature during CPB. Mean deviations of BA and NP temperatures from core temperature were calculated for three steady-state periods (before, during, and after CPB). Mean deviation of BA and NP temperatures from AI temperature was also calculated during active rewarming. A total of 1862 measurements were obtained and logged from eight patients. Mean BA and NP deviations from core temperature across the steady-state periods (before, during, and after CBP) were, respectively: .23 ± .25, −.26 ± .3, and −.09 ± .05°C (BA), and .11 ± .19, −.1 ± .47, and −.04 ± .3°C (NP). During steadystate periods, there was no evidence of a difference between the mean BA and NP deviation. During active rewarming, the mean difference between the BA and AI temperatures was .14 ± .36°C. During this period, NP temperature lagged behind AI and BA temperatures by up to 41 minutes and was up to 5.3°C lower than BA (mean difference between BA and NP temperatures was 1.22 ± .58°C). The BA temperature is an adequate surrogate for core temperature. It also accurately tracks the changing AI temperature during rewarming and is therefore potentially useful in detecting a hyperthermic perfusate, which might cause cerebral hyperthermia.

Neurocognitive Function in Patients Undergoing Coronary Artery Bypass Graft Surgery With Cardiopulmonary Bypass: The Effect of Two Different Rewarming Strategies

Hypothermia followed by rewarming during cardiopulmonary bypass can lead to cerebral hyperthermia, which has been implicated as 1 of the causes for postoperative deterioration in neurocognitive function in patients undergoing coronary revascularization. Hence, the authors studied the effects of 2 different rewarming strategies on postoperative neurocognitive function in adult patients undergoing coronary artery bypass graft surgery with the aid of cardiopulmonary bypass. This was a randomized clinical trial. A cardiothoracic center of a tertiary level referral, teaching hospital. A total of 80 adult patients aged 45 to 70 years undergoing elective primary isolated coronary artery bypass graft surgery with cardiopulmonary bypass under moderate hypothermia at 30 degrees C were included in this study. The patients were randomly allocated into 2 groups of 40 each. In group A, patients were rewarmed to a nasopharyngeal temperature of 37 degrees C; whereas, in group B, patients were rewarmed to a nasopharyngeal temperature of 33 degrees C before weaning off bypass. The anesthetic and bypass management were standardized for both groups. All patients were assessed for neurocognitive function preoperatively and on the fifth postoperative day using the Post Graduate Institute Memory Scale. The amount of blood loss and need for blood and blood product transfusion postoperatively, the need for pacing, increased inotrope or vasodilator use, and time to extubation were also noted. Serum S100beta levels were measured after anesthetic induction and at 24 hours postoperatively. The jugular venous oxygen saturation and oxygen tension were noted at 30 degrees C and at the end of full rewarming (ie, at 37 degrees C or 33 degrees C, respectively, in the 2 groups). There was a significant deterioration in neurocognitive function postoperatively as compared with preoperative function in patients of group A (37 degrees C). This was associated with higher S100beta levels 24 hours postoperatively in group A (37 degrees C) compared with group B (33 degrees C) patients. Also, there was a significant decrease in jugular venous oxygen saturation in group A (37 degrees C) as compared with group B (33 degrees C) at the end of rewarming. The time to extubation was longer in group B (33 degrees C). No significant differences were noted in the amount of postoperative blood loss, blood and blood product use, inotrope or vasodilator use, and the need for pacing. Weaning from CPB at 33 degrees C may be a simple and useful strategy to lower the postoperative impairment of neurocognitive function and may be used as a tool to decrease morbidity after coronary revascularization.

The Effect of Limited Rewarming and Postoperative Hypothermia on Cognitive Function in a Rat Cardiopulmonary Bypass Model

Clinical studies have failed to demonstrate significant benefits of hypothermia for the prevention of postoperative cognitive dysfunction (POCD) after cardiopulmonary bypass (CPB). One explanation for this might be that potentially injurious cerebral hyperthermia occurs during rewarming at the end of CPB, off-setting the protective benefits of hypothermia. In this study, we investigated the relative influence of CPB temperature, rewarming strategies, and postoperative temperature in a rat CPB model. Four groups of male Sprague-Dawley rats were surgically prepared and subjected to 90 min of CPB. Group A was normothermic (37.5 degrees C) during and after CPB. Group B underwent hypothermic (32 degrees C) CPB, followed by rewarming to 37.5 degrees C at the end of bypass. Group C had hypothermic (32 degrees C) CPB, followed by limited rewarming to 35 degrees C. Group D had normothermic CPB with hypothermia (35 degrees C) induced only postoperatively. Groups were compared for POCD determined by the performance in the Morris water maze on postoperative days 3-9. Histologic analysis of the brains (CA1 and CA3 hippocampal regions) was also performed. Hypothermia induced only during (group B versus group A) or after CPB (group D versus group A) conferred no significant POCD benefit. Hypothermia when induced during CPB and continued into the postoperative period resulted in a significant improvement in water maze performance versus all other temperature regimens (group C versus group A, P = 0.044; group C versus group B, P = 0.011; group C versus group D, P = 0.012). No histological differences among groups were demonstrated. The combination of hypothermic (32 degrees C) CPB coupled with limited rewarming and prolonged postoperative hypothermia (35 degrees C) decreased POCD after CPB in rats.

Effects of sustained mild hypothermia on neurocognitive function after coronary artery bypass surgery: A randomized, double-blind study

Neurocognitive deficits occur frequently in patients undergoing cardiac surgery and may be caused, in part, by ischemic cerebral injury. Cerebral hypothermia has been proposed as a neuroprotective strategy to reduce ischemic injury in animal studies, in postcardiac arrest, and during cardiac surgery. We sought to evaluate the effects of sustained mild intraoperative hypothermia, without rewarming, on neurocognitive function after coronary artery bypass surgery. Patients (aged >/= 60 years) undergoing non-urgent coronary surgery were randomized to an intraoperative nasopharyngeal temperature of 34 degrees C (hypothermic; n = 133) or 37 degrees C (normothermic; n = 134), maintained using water-circulating thermal control pads. No active rewarming was used. Transcranial Doppler was used intraoperatively to monitor middle cerebral artery emboli. Neuropsychometric testing, consisting of a battery of 16 tests, was performed by blinded observers preoperatively, before discharge, and at 3 months, and tests were divided into 4 cognitive domains. A deficit was prospectively defined as a 1 standard deviation decrease in individual scores from baseline in 1 or more domains. The number of intraoperative cerebral emboli was similar between the control and the treated groups (188 [115-331] vs 182 [100-305], P = .71). At discharge, neurocognitive deficits were present in 45% of control patients and in 49% of treated patients (P = .49) and at 3 months decreased to 8% in control patients and 4% in treated patients (P = .28). There was no correlation between the total number of cerebral emboli and the occurrence of neurocognitive deficits (r = -0.01; P = .88). Hypothermic patients demonstrated trends toward reduced intensive care unit stay (1.4 +/- 1.0 days vs 1.2 +/- 0.7 days, P = .06) and increased chest tube output (655 +/- 327 mL/24 h vs 584 +/- 325 mL/24 h, P = .09). Mild intraoperative hypothermia has no major adverse effects but does not decrease the incidence of neurocognitive deficits in patients undergoing coronary artery bypass surgery. In the absence of rewarming and cerebral hyperthermia, sustained mild hypothermia does not improve cognitive outcome.

Intracardiac temperature monitoring in infants after cardiac surgery

Hyperthermia after cerebral ischemia is associated with worse neurologic outcome. Our goals were 3-fold: (1) to describe the postoperative temperature course in infants after cardiac surgery, (2) to compare intracardiac temperature monitoring with traditional monitoring in infants, and (3) to determine variables that influence the patients' temperatures. Longitudinal temperature data were collected for 100 infants undergoing cardiac surgery. Intra-atrial, nasopharyngeal, esophageal, rectal, and axillary temperatures were recorded in all patients. The mean age at the time of operation was 128 +/- 166 days, and the mean weight was 5.1 +/- 2.4 kg. Circulatory arrest was used for 54 patients. In the operating room, the maximum intra-atrial temperature (37.5 degrees C +/- 0.6 degrees C) was significantly greater than both the simultaneous esophageal temperature (36.9 degrees C +/- 1.9 degrees C, P = .03) and nasopharyngeal temperature (36.3 degrees C +/- 2.5 degrees C, P < .001). In the cardiac intensive care unit, intra-atrial temperature was significantly greater than both axillary and rectal temperatures. During the first 24 postoperative hours, intra-atrial temperature was greater than 38 degrees C in 48 (48%) patients, rectal temperature was greater than 38 degrees C in 36 (36%) patients, and axillary temperature was greater than 38 degrees C in 7 (7%) patients. In patients less than 2 years of age undergoing cardiac surgery requiring cardiopulmonary bypass, intra-atrial temperature peaked 4 to 6 hours after leaving the operating room. Traditional methods of temperature monitoring significantly underestimate core temperature after cardiac surgery in infants. Use of intracardiac temperature monitoring might result in avoidance of cerebral hyperthermia.

The effect of head hypothermia on the large-acreage cerebral insarction(LCI) and hyperthermia patient's serum CORT,SOD and LPO level

目的 探讨大面积脑梗死(LCI)高热患者血清皮质醇(CORT)、脂质过氧化物(LPO)、超氧化物歧化酶(SOD)的含量变化,观察头部低温降温对三者的影响.方法采用放射免疫法、羟胺氧化法、丙二醛法测定49例(A组)LCI应用头部低温降温与43例(B组)应用温水擦浴、冰盐水灌肠降温者入院第2天及高热后第2天、第3天、第4天血清中CORT、LPO、SOD含量,并与30例健康人(C组)作对照.同时对两组生存者生活质量进行比较.结果 A、B两组入院第2天较C组CORT、LPO明显升高和SOD降低(P＜0.01).A、B两组高热第2天较入院第2天CORT、LPO均明显升高和SOD显著降低(P＜0.05,P＜0.01).A组高热第4天较入院第2天和高热第2天CORT、LPO显著降低(P＜0.05,P＜0.01),SOD升高(P＜0.01).B组高热第4天CORT、LPO仍高于和SOD低于入院第2天(P＜0.05).结论头部低温可有效使LCI高热患者CORT、LPO降低和SOD升高,提高预后生活质量。

Rapport sommaire: l’incidence décroissante de l’hyperthermie cérébrale pendant la cardiochirurgie, sept ans d’expérience auprès de 6 334 patients

PurposeCerebral hyperthermia during rewarming from hypothermic cardiopulmonary bypass (CPB) commonly occurs and has been associated with postoperative neurocognitive dysfunction. Increased awareness of this has likely led to changes in rewarming strategies, including the reduction of rewarming rates and lowering of target rewarming temperatures. As a result, we hypothesized that the maximum temperature reached during cardiac surgery has decreased at our institution over time.MethodsWe retrospectively reviewed the maximum intraoperative nasopharyngeal (NP) temperature in 6,334 patients having undergone cardiac surgery utilizing hypothermic CPB from January 1993 to June 2000. The incidence of cerebral hyperthermia (defined by a NP temperature > 38°C) was examined over time using Chisquare testing and the relationship between maximum temperature and date of surgery was studied using linear regression.ResultsMaximum temperature decreased over time (P < 0.0001; r2 = 0.40) having the greatest reduction from January 1993 to December 1996 (0.34ºC temperature drop per year), while from January 1997 to June 2000, it continued to decrease, but at a slower rate (0.10ºC per yr;P < 0.0001). The incidence of cerebral hyperthermia decreased over time with 83% of the first 10% of patients and 3% of the latter 10% of patients during the study period having a maximum temperature > 38°C (P < 0.0001).ConclusionThe incidence of cerebral hyperthermia has decreased at our institution suggesting that a change in temperature management has occurred at our institution from January 1993 to June 2000 thereby outlining a temporal evolution in temperature management during CPB.

Temperature Inaccuracies During Cardiopulmonary Bypass

Cerebral hyperthermia caused by perfusate temperature greater than 37°C during the rewarming phase of CPB has been linked to postoperative neurologic deficits. The purpose of this study was to determine the accuracy of the coupled temperature measurement system and the CDI 500 arterial temperature sensor. Seventeen patients undergoing CPB were divided into four groups, each with a different temperature probe coupled to the oxygenator. The coupled temperature measurement system and CDI temperature sensors were compared with an indwelling probe placed in direct contact with the arterial perfusate. Blood, bladder, room and water temperatures, arterial line pressure, blood flow, and hemoglobin were recorded while the patients were supported with CPB. The actual blood temperature was significantly higher than the coupled temperature measurement system for two of the four groups (mean = 1.61°C and 0.91°C,p&lt; 0.0001). A significant positive correlation between the actual temperature and the coupled temperature measurement system error was observed for the same two groups (r = 0.44,p&lt; 0.0001). The actual temperature was significantly higher than the CDI temperature in all patients (mean = 1.2°C,p&lt; 0.0001). The coupling mechanism on the oxygenator generates inconsistent temperature readings. The perfusionist should consider these inconsistencies when using coupled temperature measurements and may consider the use of a direct temperature measurement system. The CDI temperature error is probably the result of inadequate flow through the sensor. On the test circuit, the flow of 170 mL/min was inadequate for circuit temperature accuracy. The accuracy of the CDI temperature drastically improved when the flow-through the sensor was increased to approximately 400 mL/min. Thus, the perfusionist must ensure adequate flow through the sensor in order for the temperature mechanism to function properly. Finally, the perfusionist can prevent cerebral hyperthermia by not allowing water temperature to exceed 37°C, when using a coupled temperature measurement system.

Safety of deliberate intraoperative and postoperative hypothermia for patients undergoing coronary artery surgery: A randomized trial

Background Hypothermia in the perioperative period is associated with adverse effects, particularly bleeding. Before termination of cardiopulmonary bypass, rewarming times and perfusion temperatures are often increased to avoid post–cardiopulmonary bypass hypothermia and the presumed complications. This practice may, however, also have adverse effects, particularly cerebral hyperthermia. We present safety outcomes from a trial in which patients undergoing coronary artery surgery were randomly assigned to normothermia or hypothermia for the entire surgical procedure. Methods Consenting patients over the age of 60 years presenting for a first, elective coronary artery surgery with cardiopulmonary bypass were randomly assigned to having their nasopharyngeal temperature maintained at either 37°C (group N; 73 patients) or 34°C (group H; 71 patients) throughout the intraoperative period, with no rewarming before arrival in the intensive care unit. All received tranexamic acid. Results There was no clinically important difference in intraoperative blood product or inotrope use. Temperatures on arrival in the intensive care unit were 36.7°C ± 0.38°C and 34.3°C ± 0.38°C in groups N and H, respectively. Blood loss during the first 12 postoperative hours was 596 ± 356 mL in group N and 666 ± 405 mL in group H (mean difference ± 95% confidence interval, 70 ± 126 mL; P = .28). There was no significant difference in blood product utilization, intubation time, time in the hospital, myocardial infarction, or mortality. The mean time in the intensive care unit was 8.4 hours less in the hypothermic group ( P = .02). Conclusions Our data support the safety of perioperative mild hypothermia in patients undergoing elective nonreoperative coronary artery surgery with cardiopulmonary bypass. These findings suggest that complete rewarming after hypothermic cardiopulmonary bypass is not necessary in all cases.