Trans-vaccenic acid reprograms CD8+ T cells and anti-tumour immunity.

Diet-derived nutrients are inextricably linked to human physiology by providing energy and biosynthetic building blocks and by functioning as regulatory molecules. However, the mechanisms by which circulating nutrients in the human body influence specific physiological processes remain largely unknown. Here we use a blood nutrient compound library-based screening approach to demonstrate that dietary trans-vaccenic acid (TVA) directly promotes effector CD8+ T cell function and anti-tumour immunity in vivo. TVA is the predominant form of trans-fatty acids enriched in human milk, but the human body cannot produce TVA endogenously1. Circulating TVA in humans is mainly from ruminant-derived foods including beef, lamb and dairy products such as milk and butter2,3, but only around 19% or 12% of dietary TVA is converted to rumenic acid by humans or mice, respectively4,5. Mechanistically, TVA inactivates the cell-surface receptor GPR43, an immunomodulatory G protein-coupled receptor activated by its short-chain fatty acid ligands6-8. TVA thus antagonizes the short-chain fatty acid agonists of GPR43, leading to activation of the cAMP-PKA-CREB axis for enhanced CD8+ T cell function. These findings reveal that diet-derived TVA represents a mechanism for host-extrinsic reprogramming of CD8+ T cells as opposed to the intrahost gut microbiota-derived short-chain fatty acids. TVA thus has translational potential for the treatment of tumours.

Continuous bupivacaine infusion post-iliac crest bone graft harvesting in pediatric cleft surgery: role and comparison with ketorolac.

OBJECTIVE: To investigate the use of intravenous ketorolac and iliac crest bupivacaine infusion in the management of iliac crest donor-site pain in the pediatric cleft population. The null hypothesis was there is no difference with respect to pain scores between ketorolac and iliac crest bupivacaine infusion as analgesic adjuncts to intravenous opioids. METHODS: A total of 54 children and adolescents (27 boys, 27 girls) undergoing alveolar cleft repair or Le Fort I osteotomy were assigned randomly in a prospective, single-blinded fashion to one of three groups: intravenous ketorolac plus iliac crest normal saline infusion, intravenous ketorolac plus iliac crest bupivacaine infusion, or iliac crest bupivacaine infusion alone. Iliac crest infusions and ketorolac were administered for 48 hours or until discharge, whichever occurred first. All patients received morphine via a patient-controlled analgesia device. MAIN OUTCOME MEASURE(S): Primary outcome was pain score, and secondary outcomes were morphine consumption and satisfaction scores. RESULTS: Pain scores, morphine consumption, and satisfaction scores were not significantly different among groups. Estimated costs were significantly higher for bupivacaine infusion than intravenous ketorolac. CONCLUSIONS: Iliac crest donor-site pain is well managed in this patient population. Intravenous ketorolac and iliac crest bupivacaine infusion provide comparable analgesia for iliac crest bone graft donor-site pain in children and adolescents.

Cerebral blood flow velocity increases when propofol is changed to desflurane, but not when isoflurane is changed to desflurane in children.

BACKGROUND: Children may exhibit delayed emergence following maintenance of anesthesia with propofol or isoflurane. Desflurane is often used towards the end of procedures to facilitate emergence. This study evaluated the effect on middle cerebral artery blood flow velocity (Vmca) in anesthetized children when propofol or isoflurane was substituted with desflurane. METHODS: Forty-two healthy children aged 1-6 years were enrolled. A standardized anesthetic induction was used. Anesthesia was maintained with remifentanil (0.5 microg.kg(-1) bolus followed by an infusion of 0.2 microg.kg(-1).min(-1)) and a randomly selected sequence of propofol/desflurane/propofol, desflurane/propofol/desflurane, isoflurane/desflurane/isoflurane or desflurane/isoflurane/desflurane. Propofol was administered to maintain a steady-state serum concentration of 3 microg.ml(-1). Desflurane and isoflurane were administered at age-corrected 1 MAC. Hemodynamic stability was maintained. Transcranial Doppler sonography was used to measure Vmca. Hemodynamic variables as well as Vmca were measured 30 min after skin incision and repeated 30 min after each change in anesthetic maintenance agent. RESULTS: The mean age and weight was 2.3 +/- 1.3 years and 13.0 +/- 3.7 kg, respectively. The Vmca (mean) increased by 35% from 37.7 +/- 10.5 cm s(-1) to 57.8 +/- 14.6 cm s(-1) (P < 0.0001) when propofol was changed to desflurane but was unaffected when desflurane replaced isoflurane. CONCLUSION: When propofol is changed to desflurane, cerebral blood flow velocity increases significantly in normal children. This cerebral vasodilatory effect may have important implications in the neurosurgical setting.

The effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with sevoflurane.

To determine the effects of nitrous oxide on middle cerebral artery blood flow velocity (CBFV) during sevoflurane anaesthesia in children, CBFV was measured using transcranial Doppler sonography in 16 ASA I or II children. Anaesthesia consisted of 1.0 MAC sevoflurane in 30% oxygen with intermittent positive pressure ventilation maintaining FEco2 at 38 mmHg (5.0 kPa) and a caudal epidural block using 0.25% bupivacaine 1.0 ml.kg-1. The remainder of the inspired gas was varied in one of two sequences either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide. The results showed that CBFV decreased when nitrous oxide was replaced by air (p = 0.03) and returned to its initial value when nitrous oxide was reintroduced. CBFV increased when air was replaced by nitrous oxide (p = 0.04) and returned to its initial value when air was reintroduced. Mean heart rate and blood pressure remained constant. We conclude that nitrous oxide increases cerebral blood flow velocity in healthy children anaesthetised with 1.0 MAC sevoflurane.

The effect of sevoflurane on cerebral blood flow velocity in children.

BACKGROUND: Sevoflurane is a suitable agent for neuroanesthesia in adult patients. In children, cerebrovascular carbon dioxide reactivity is maintained during hypo- and normocapnia under sevoflurane anesthesia. To determine the effects of sevoflurane on middle cerebral artery blood flow velocity (Vmca) in neurologically normal children, Vmca was measured both at different MAC values and at one MAC over a specified time period, using transcranial Doppler sonography. METHODS: Twenty-six healthy children undergoing elective urological surgery were enrolled (16 patients in part I and 10 in part II). In part I of the study anesthesia comprised sevoflurane 0.5, 1.0 and 1.5 MAC in 30% oxygen and a caudal epidural block. Once steady state had been reached at each sevoflurane MAC level, three measurements of Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded. In part II of the study patients received sevoflurane 1.0 MAC over a 90-min period, with the same variables being recorded at 15-min intervals. RESULTS: Vmca did not vary significantly at 0.5, 1.0 and 1.5 MAC sevoflurane. There was a significant decrease in MAP between 0.5 MAC and 1.0 MAC sevoflurane (P < 0.005) and also between 1.0 MAC and 1.5 MAC (P < 0.01). There was no significant change in Vmca over 90 min at 1.0 MAC sevoflurane. CONCLUSION: Sevoflurane does not significantly affect cerebral blood flow velocity in healthy children at working concentrations.

The effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during propofol anesthesia.

Nitrous oxide (N(2)O) increases cerebral blood flow when used alone and in combination with propofol. We investigated the effects of N(2)O on cerebrovascular CO(2) reactivity (CCO(2)R) during propofol anesthesia in 10 healthy children undergoing elective urological surgery. Anesthesia consisted of a steady-state propofol infusion and a continuous caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Randomization determined the sequence order of N(2)O (N(2)O/air or air/N(2)O) and end-tidal (ET)CO(2) concentration (25, 35, 45, and 55 mm Hg) using an exogenous source of CO(2). At steady state, three sets of measurements of middle cerebral artery blood flow velocity, mean arterial blood pressure, and heart rate were recorded. A linear preservation of CCO(2)R was observed above 35 mm Hg of ETCO(2), irrespective of N(2)O. A decrease in CCO(2)R to 1.4%-1.9% per millimeters of mercury was seen in the hypocapnic range (ETCO(2) 25-35 mm Hg) with both air and N(2)O. We conclude that N(2)O does not affect CCO(2)R during propofol anesthesia in children. When preservation of CCO(2)R is required, the combination of N(2)O with propofol anesthesia in children would seem suitable. The cerebral vasoconstriction caused by propofol would imply that hyperventilation to ETCO(2) values less than 35 mm Hg may not be required because no further reduction in cerebral blood flow velocity would be achieved.

Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia.

BACKGROUND: Sevoflurane and nitrous oxide have intrinsic cerebral vasodilatory activity. To determine the effects of nitrous oxide on cerebrovascular reactivity to carbon dioxide (CCO(2)R) during sevoflurane anaesthesia in children, middle cerebral artery blood flow velocity (V(mca)) was measured over a range of end-tidal carbon dioxide concentrations (E'(CO(2))), using transcranial Doppler (TCD) ultrasonography. METHODS: Ten children aged 1.5-6 yr were anaesthetized with sevoflurane and received a caudal block. Patients were allocated randomly to receive either air-nitrous oxide or nitrous oxide-air. Further randomization determined the sequence of E'(CO(2)) (25, 35, 45, and 55 mm Hg) and sevoflurane (1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Once steady state had been reached, three measurements of V(mca), mean arterial pressure (MAP), and heart rate (HR) were recorded. RESULTS: Cerebrovascular carbon dioxide reactivity was reduced in the 25-35 mm Hg E'(CO(2)) range on the addition of nitrous oxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau in CCO(2)R of 0.4-0.6% per mm Hg was seen in all groups between E'(CO(2)) values of 45 and 55 mm Hg. Mean HR and MAP remained constant throughout the study period. CONCLUSIONS: Cerebrovascular carbon dioxide reactivity is reduced at and above an E'(CO(2)) of 45 mm Hg during 1.0 and 1.5 MAC sevoflurane anaesthesia. The addition of nitrous oxide to 1.5 MAC sevoflurane diminishes CCO(2)R in the hypocapnic range. This should be taken into consideration when hyperventilation techniques for reduction of brain bulk are being contemplated in children with raised intracranial pressure.

[Cerebral oedema in children compared to cerebral oedema in adults]. / Oedème cérébral chez l'enfant par rapport à l'adulte: quelles sont les différences?

About 50% of deaths, in the pediatric population between 1-15 years of age, are due to trauma. This high mortality rate, associated with the frequent sequelae, leading sometimes to severe handicaps, constitutes a major problem for public health in the developed countries. Pediatric trauma has some particularities, due to anatomic and physiologic differences, and to specific injury mechanisms. In a busy traumatology center, a child will be admitted daily in the emergency department with head trauma injury. The anaesthesiologist must have a complete understanding of the pathophysiology involved in this clinical presentation if one wishes to develop a practical knowledge of initial management of such patients. Traumatic brain injury may have intracranial and systemic effects that combine to give global cerebral ischaemia.

The effect of nitrous oxide on cerebral blood flow velocity in children anesthetized with propofol.

BACKGROUND: Propofol for maintenance of anesthesia by continuous infusion is gaining popularity for use in pediatric patients. Nitrous oxide (N2O) has been shown to increase cerebral blood flow velocity (CBFV) in both children and adults. To determine the effects of N2O on middle cerebral artery blood flow velocity (Vmca) during propofol anesthesia in children, Vmca was measured with and without N2O using transcranial Doppler (TCD) sonography. METHODS: Thirty ASA I or II children aged 18 months to 6 years undergoing elective urological surgery were enrolled. Anesthesia comprised propofol aimed at producing an estimated steady-state serum concentration of 3 micro g.ml-1 and a caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomized to receive a sequence of either Air/N2O/Air or N2O/Air/N2O in 35% oxygen. Fifteen min after each change in the N2O concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Ventilatory parameters and EtCO2 were kept constant throughout the study period. RESULTS: CBFV increased by 12.4% when air was replaced by N2O, and returned to baseline when N2O was subsequently removed. There was a 14% decrease in CBFV when N2O was replaced with air, which increased to baseline when air was subsequently replaced with N2O. Mean heart rate and blood pressure remained constant throughout the study period. CONCLUSION: The effects of nitrous oxide on CBFV are preserved in children during propofol anesthesia.

The effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane.

The aim of this study was to determine the effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane. Eighteen healthy children scheduled for elective surgery were enrolled into the study. Anaesthesia was induced using sevoflurane, and a caudal block was performed following tracheal intubation. Anaesthesia was maintained with 1 age-adjusted MAC desflurane. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomised to receive a sequence of either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide in 30% oxygen. Fifteen minutes after each change in the nitrous oxide concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Neither the addition nor removal of nitrous oxide caused any significant changes in middle cerebral artery blood flow velocity, heart rate or blood pressure. This may be due to a more potent cerebral vasodilatory effect of desflurane in children.

Cerebrovascular carbon dioxide reactivity in children anaesthetized with sevoflurane.

BACKGROUND: To determine the effects of sevoflurane on cerebrovascular carbon dioxide reactivity (CCO2R), middle cerebral artery blood flow velocity (CBFV) was measured at different levels of PE'CO2 by transcranial Doppler sonography in 16 ASA I or II children, aged 18 months to 7 yr undergoing elective urological surgery. METHODS: Anaesthesia comprised 1.0 MAC sevoflurane and air in 30% oxygen delivered through an Ayre's T piece by intermittent positive-pressure ventilation, and a caudal epidural block with 0.25% bupivacaine 1.0 ml kg(-1) without epinephrine. PE'CO2 was randomly adjusted to 25, 35, 45 and 55 mm Hg (3.3, 4.6, 5.9 and 7.2 kPa) with an exogenous source of CO2, while maintaining ventilation variables constant. RESULTS: CBFV increased as PE'CO2 increased from 25 to 35, and to 45 mm Hg (P<0.001), but did not increase significantly with an increase in PE'CO2 from 45 to 55 mm Hg. Mean heart rate and arterial pressure remained constant. CONCLUSION: CCO2R is preserved in healthy children anaesthetized with 1.0 MAC sevoflurane.

Effects of temperature and haematocrit on the relationships between blood flow velocity and blood flow in a vessel of fixed diameter.

BACKGROUND: To determine whether temperature and haematocrit (Hct) alter the relationship between blood flow (BF) and blood flow velocity (BFV). METHODS: Using a transcranial Doppler apparatus, we measured the peak velocity of whole blood cells pumped by a cardiopulmonary bypass (CPB) circuit, through a 0.15-cm internal diameter segment of rigid tubing. BF and BFV relationships were obtained at temperatures of 19, 28, and 37 degrees C and at Hct of 0.05, 0.22, 0.39, and 0.54, by altering CPB flow over a range from 10 to 100 cc/min. Linear regression analysis was performed. RESULTS: The relationship between velocity and flow for the pooled Hct data was y=(0.43)x+0.86, r2=0.998 and 95% CI (0.999-1) whereas the association for the temperature data was y=(0.42)x+0.02, r2=0.9998 and 95% CI (0.999-0.9997). Changes of blood viscosity had no effect on velocity at a given flow rate. The combined effect of Hct and temperature on velocity for the relationship with flow is expressed by: y=1.3+2.4x. CONCLUSION: In fixed diameter vessels with laminar flow, the linear relationship between flow and velocity is not affected by changes in temperature and Hct in clinical ranges. These results are explained by the Fahraeus-Lindquist effect. They support the use of transcranial Doppler sonography to estimate cerebral blood flow in infants who may have large variations of Hct and/or temperature during bypass.

[Traumatic head injury in children: physiopathology and clinical management]. / Les différentes lésions cérébrales traumatiques du nourrisson et du petit enfant: mécanismes et clinique.

Traumatic brain injury (TBI) constitutes a major health and economic problem for developed countries, being one of the main causes of mortality and morbidity in children. In a busy traumatology center, a child will be admitted daily in the emergency department with head trauma injury. The anaesthesiologist must have a complete understanding of the pathophysiology and develop a practical knowledge of initial management of such patients. Traumatic brain injury may have intracranial and systemic effects that combine to give global cerebral ischaemia. Injury to the nervous system, irrespective of the primary injury, initiates a multitude of inflammatory cascades resulting in secondary brain injury. The consequence of these secondary brain injuries is most often as important, if not, more important than the primary injury. This period of brain inflammation can last up to three weeks and renders the brain more susceptible to the effects of systemic insults such as hypotension, hypoxia and or pyrexia. It has been shown in post-mortem examination of patients dying from severe traumatic brain injury that more than 91% had evidence of secondary ischaemic damage. These secondary injuries may be responsible for the clinical presentation of the "child who talk and die". The concept of "cerebral protection" has been extended to encompass the active treatment of secondary injury and the prevention of cerebral ischaemia. Initial care focuses on achieving oxygenation, airway control and treatment of arterial hypotension.

[The specificity of neurosurgical anesthesia for the child]. / Spécificité de l'anesthésie de l'enfant en neurochirurgie.

Anaesthesia for paediatric neurosurgical procedures presents an interesting challenge to the anaesthesiologist. The child is not simply a small adult. At birth the central nervous system (CNS) development is incomplete and will not be mature until the end of the first year of life. Because of this delay in the maturation of the CNS, several specific pathophysiological and psychological differences ensue. Although one has little control on the child primary lesion, the selection of an anaesthetic technique designed to protect the perilesional area and the recognition of perioperative events and changes may well have a profound effect in the reduction or prevention of significant morbidity. Current neuroanaesthestic practice is based on the understanding of cerebral anatomy and physiology. Paediatric neuroanaesthesiologists must face the added challenge of the physiological differences between developing children and their adult counterparts.

Midazolam premedication reduces propofol dose requirements for multiple anesthetic endpoints.

PURPOSE: This study investigates the interactions between midazolam premedication and propofol infusion induction of anesthesia for multiple anesthetic endpoints including: loss of verbal contact (LVC; hypnotic), dropping an infusion flex (DF; motor), loss of reaction to painful stimulation (LRP; antinociceptive) and attainment of electroencephalographic burst suppression (BUR; EEG). METHODS: In a double blind, controlled, randomized and prospective study, 24 ASA I-II patients received either midazolam 0.05 mg x kg(-1) (PM; n = 13) or saline placebo (PO; n = 11) i.v. as premedication. Twenty minutes later, anesthesia was induced by propofol infusion at 30 mg x kg(-1) x hr(-1). ED50, ED95 and group medians for times and doses were determined and compared at multiple anesthetic endpoints. RESULTS: At the hypnotic, motor and EEG endpoints, midazolam premedication significantly and similarly reduced propofol ED50 (reduction: 18%, 13% and 20% respectively; P <0.05 vs unpremedicated patients) and ED95 (reduction: 20%, 11% and 20% respectively; P <0.05 vs unpremedicated patients). For antinociception (LRP), dose reduction by premedication was greater for propofol ED95 (reduction: 41%; P <0.05 vs unpremedicated patients) than ED50 (reduction: 18%; P <0.05 vs unpremedicated patients). Hemodynamic values were similar in both groups at the various endpoints. CONCLUSIONS: Midazolam premedication 20 min prior to induction of anesthesia reduces the propofol doses necessary to attain the multiple anesthetic endpoints studied without affecting hemodynamics in this otherwise healthy population. The interaction differs for different anesthetic endpoints (e.g., antinociception vs hypnosis) and propofol doses (e.g., ED50 vs ED95).

Effect of halothane on the cerebral circulation in young children: a hysteresis phenomenon.

To determine the effect of halothane on the cerebral blood flow velocity (CBFV) with increasing then decreasing concentrations, 11 children scheduled for minor surgery were studied. Anaesthesia consisted of halothane, vecuronium, nitrous oxide in oxygen and a caudal block. End-tidal carbon dioxide, temperature, heart rate and systolic arterial pressure were maintained constant. CBFV increased significantly between 0.5 and 1.0 MAC (p <0.001), and 0.5 and 1.5 MAC of halothane (p <0.001), but was not different after increasing concentration from 1.0 to 1.5 MAC. During the decreasing phase, CBFV decreased significantly from 1.5 to 1.0 MAC of halothane (p <0.001), whereas there was no difference in CBFV when decreasing halothane MAC from 1.0 to 0.5 MAC. In children, the decrease in CBFV during decreasing halothane concentration is not superimposable to the increase in CBFV seen when increasing halothane concentration, suggesting the presence of cerebrovascular hysteresis to halothane.

Human errors in a multidisciplinary intensive care unit: a 1-year prospective study.

OBJECTIVES: To determine the incidence and identify risk factors of critical incidents in an ICU. DESIGN: Prospective observational study of consecutive patients admitted over 1 year to an ICU. Critical incidents were recorded using predefined criteria. Their causes and consequences were analysed. The causes were classified as technical failure, patient's underlying disease, or human errors (subclassified as planning, execution, or surveillance). The consequences were classified as lethal, leading to sequelae, prolonging the ICU stay, minor, or without consequences. The correlation between critical incidents and specific factors including patient's diagnosis and severity score, use of monitoring and therapeutic modalities was analysed by uni- and multivariate analysis. SETTING: An 11-bed multidisciplinary ICU in a non-university teaching hospital. PATIENTS: 1,024 consecutive patients admitted to the ICU. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: The median length of ICU stay by the 1,024 patients was 1.9 days. Of the 777 critical incidents reported 2% were due to technical failure and 67 % to secondary to underlying disease. There were 241 human errors (31%) in 161 patients, evenly distributed among planning (n = 75), execution (n = 88), and surveillance (n = 78). One error was lethal, two led to sequelae, 26 % prolonged ICU stay, and 57 % were minor and 16 % without consequence. Errors with significant consequences were related mainly to planning. Human errors prolonged ICU stay by 425 patient-days, amounting to 15 % of ICU time. Readmitted patients had more frequent and more severe critical incidents than primarily admitted patients. CONCLUSIONS: Critical incidents add morbidity, workload, and financial burden. A substantial proportion of them are related to human factors with dire consequences. Efforts must focus on timely, appropriate care to avoid planning and execution mishaps at the beginning of the ICU stay; surveillance intensity must be maintained, specially after the fourth day.

Cerebral hyperthermia in children after cardiopulmonary bypass.

BACKGROUND: Cerebral hyperthermia after hypothermic cardiopulmonary bypass has been poorly documented for adults and never in children. This study was designed to monitor brain temperature during and up to 6 h after cardiopulmonary bypass in infants and children. METHODS: Fifteen infants and children, between 3 months and 6 yr of age, were studied. A right retrograde jugular bulb catheter was used to measure the jugular venous bulb temperature (JVBT) during the procedure and the first 6 h in the critical care unit. The temperature of the blood from the bypass machine was measured at the aorta through the cannula using an indwelling temperature probe. All data were acquired every minute. RESULTS: The age of the patients ranged from 3 to 71 months (median, 15 months). The mean weight was 11.5 +/- 8.4 kg. The mean JVBT recorded at the end of cardiopulmonary bypass was 36.9 +/- 1.4 degrees C but reached 39.6 +/- 0.8 degrees C after six h (P < 0.01). The kinetics of brain rewarming was determined by the slope of the mean JVBT and corresponded to y +/- 0.006x + 37.21 (r2 = 0.97). The JVBT differed from the tympanic temperature after 200 min (P < 0.01) and the lower esophageal (P < 0.05) and rectal (P < 0.001) temperatures after 300 min. After 6 h, the tympanic, rectal, and lower esophageal temperatures were 37.8 +/- 0.9, 37.7 +/- 0.6, and 38.4 +/- 0.7 degrees C, respectively, whereas the JVBT was 39.6 +/- 0.8 degrees C (P < 0.001). However, the correlation coefficients between the JVBT and the tympanic, rectal, and esophageal temperatures were 0.98, 0. 85, and 0.97, respectively. No complications were recorded with placement of the jugular bulb catheter. CONCLUSIONS: Mean JVBT was significantly increased over the mean core temperature at all times from rewarming by cardiopulmonary bypass onward. Although the lower esophageal, rectal, and tympanic temperatures correlated well with JVBT, all three failed to reflect JVBT during recovery. This observation might help to elucidate factors involved in the functional and structural neurologic injury known to occur in pediatric patients.