Local brain surface temperature compared to temperatures measured at standard extracranial monitoring sites during posterior fossa surgery

Mild hypothermia is assumed to protect against secondary brain injury. However, the accuracy of brain temperature estimation remains debatable if direct measurement in the target area is to be avoided or is impossible. Furthermore, intracerebral temperature gradients exist, especially under intraoperative conditions. We aimed to establish how brain surface temperatures (TBrain) relate to temperatures taken at standard sites in posterior fossa surgery. Ten patients undergoing cerebellopontine angle tumor removal were monitored for TBrain, esophageal temperature (TEso), bladder temperature (TBlad), ipsi- and contralateral tympanic membrane (TTymp-I, TTymp-C), and scalp temperatures (TScalp). During monitoring, TEso increased from 35.3+/-0.2 degrees C to 36.0+/-0.3 degrees C. After dura opening, TBrain was -0.14+/-0.1 degrees C below TEso. At the end of tumor removal, this difference increased to -0.43+/-0.31 degrees C (P < 0.05). TTymp-C was -0.29+/-0.18 degrees C below TBrain at dura opening. TTymp-C reflected the behavior of TEso adequately (r = 0.938), however, with a mean difference of -0.39+/-0.04 degrees C. In contrast, TTymp-I readings closely followed temperature changes in the area of surgery. TBlad reflected TEso except in periods of rapid temperature changes. In posterior fossa (PF) surgery, local TBrain is most accurately reflected by TEso. For clinical use TBlad and TTymp-C are also sufficient to assess brain surface temperature in the PF. Intraoperative surface cooling of the brainstem is less than the previously described cooling rate of exposed cerebral cortex.     

Local saline infusion into ischemic territory induces regional brain cooling and neuroprotection in rats with transient middle cerebral artery occlusion

OBJECTIVE: The neuroprotective effect of hypothermia has long been recognized. Use of hypothermia for stroke therapy, which is currently being induced by whole-body surface cooling, has been limited primarily because of management problems and severe side effects (e.g., pneumonia). The goal of this study was to determine whether local infusion of saline into ischemic territory could induce regional brain cooling and neuroprotection. METHODS: A novel procedure was used to block the middle cerebral artery of rats for 3 hours with a hollow filament and locally infuse the middle cerebral artery-supplied territory with 6 ml cold saline (20 degrees C) for 10 minutes before reperfusion. RESULTS: The cold saline infusion rapidly and significantly reduced temperature in cerebral cortex from 37.2 +/- 0.1 to 33.4 +/- 0.4 degrees C and in striatum from 37.5 +/- 0.2 to 33.9 +/- 0.4 degrees C. The significant hypothermia remained for up to 60 minutes after reperfusion. Significant (P < 0.01) reductions in infarct volume (approximately 90%) were evident after 48 hours of reperfusion. In ischemic rats that received the same amount of cold saline systemically through a femoral artery, a mild hypothermia was induced only in the cerebral cortex (35.3 +/- 0.2 degrees C) and returned to normal within 5 minutes. No significant reductions in infarct volume were observed in this group or in the ischemic group with local warm saline infusion or without infusion. Furthermore, brain-cooling infusion significantly (P < 0.01) improved motor behavior in ischemic rats after 14 days of reperfusion. This improvement continued for up to 28 days after reperfusion. CONCLUSION: Local prereperfusion infusion effectively induced hypothermia and ameliorated brain injury from stroke. Clinically, this procedure could be used in acute stroke treatment, possibly in combination with intra-arterial thrombolysis or mechanical disruption of clot by means of a microcatheter.     

The importance of brain temperature in patients after severe head injury: relationship to intracranial pressure,cerebral perfusion pressure,cerebral blood flow,and outcome

Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The temperature difference between brain and rectal temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 +/- 0.4 degrees C in the normothermic group to 38.2 +/- 0.5 degrees C in the hyperthermic group, 35.3 +/- 0.5 degrees C in the mild therapeutic hypothermia group, and 34.3 +/- 1.5 degrees C in the hypothermia group without active cooling. The mean DeltaT(br-rect) was positive for patients with a T(br) above 36.0 degrees C (0.0 +/- 0.5 degrees C) and negative for patients during mild therapeutic hypothermia (-0.2 +/- 0.6 degrees C) and also in those with a brain temperature below 36 degrees C without active cooling (0.8 +/- -1.4 degrees C) - the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0 degrees C and 37.5 degrees C was 37.8 +/- 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0 degrees C and a negative brain-rectal temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.     

Brain magnetic resonance imaging increases core body temperature in sedated children

An increasing number of children now undergo magnetic resonance imaging (MRI) under sedation. MRI requires a cool environment. Because children have a larger surface area to body weight ratio than adults and because active warming devices are not MRI compatible, hypothermia as a result of passive heat loss is a risk. Absorption of radiofrequency radiation generated by the scanning process, however, may partially offset this heat loss. To determine the effect of absorbed radiofrequency radiation on body temperature during MRI, we measured pre-MRI and post-MRI tympanic temperatures in 30 children who underwent brain MRI while sedated with chloral hydrate and covered with a hospital gown and blanket. The mean (+/- sd) age was 14.9 +/- 8.6 mo, and weight was 9.8 +/- 2.8 kg. During an average scan duration of 42 +/- 13 min, mean tympanic temperatures increased 0.5 degrees C from 36.9 degrees C +/- 0.4 degrees C to 37.4 degrees C +/- 0.3 degrees C; (95% CI difference, 0.3 degrees C to 0.7 degrees C; P < 0.001). Our findings suggest that children sedated with chloral hydrate for brain MRI did not become hypothermic but rather had increased body temperature despite minimal barriers to heat loss and no active warming. These results imply that aggressive measures to prevent passive heat loss during MRI studies may not be needed in all patients.     

Atropine prevents midazolam-induced core hypothermia in elderly patients.

STUDY OBJECTIVE: To test the hypothesis that core temperature is well preserved when atropine and midazolam are combined. DESIGN: Randomized, blinded study. SETTING: Department of Anesthesia, Yamanashi Medical University. PATIENTS: 40 elderly, ASA physical status I and II patients (aged more than 60 years). INTERVENTIONS: Patients were randomly assigned (n = 10 per group) to premedication with: 1) saline control; 2) midazolam 0.05 mg/kg; 3) atropine 0.01 mg/kg; and 4) midazolam 0.05 mg/kg combined with atropine 0.01 mg/kg. All premedication was given on the ward at approximately 8:30 am, approximately 30 minutes before induction of anesthesia. MEASUREMENTS AND MAIN RESULTS: Core temperatures were measured at the right tympanic membrane. Mean skin temperature was calculated as 0.3 x (T(chest) + T(arm)) + 0.2 x (T(thigh) + T(calf)). Fingertip perfusion was evaluated using forearm minus fingertip and calf minus toe, skin-surface temperature gradients. Temperatures were evaluated at the time of premedication and 30 minutes later, just before induction of anesthesia. Core temperature remained nearly constant in the control patients (0.1 +/- 0.2 degrees C; mean +/- SD), whereas it decreased significantly in the patients given midazolam alone (-0.3 +/- 0.1 degrees C). Atropine alone increased core temperature (0.3 +/- 0.2 degrees C), although the increase was not statistically significant. The combination of midazolam and atropine attenuated the hypothermia induced by midazolam alone (0.0 +/- 0.2 degrees C). Initial skin-temperature gradients exceeded 0 degrees C in all groups, indicating that the patients were vasoconstricted. The gradients were unchanged by premedication with saline or atropine. Midazolam significantly decreased the gradient (-1.8 +/- 1.1 degrees C), as did the combination of midazolam and atropine (-1.4 +/- 0.9 degrees C). CONCLUSIONS: The thermoregulatory effects of benzodiazepine receptor agonist and cholinergic inhibitors oppose each other, and the combination leaves core temperature unchanged.     

The effect of selective brain cooling on intracerebral temperature during craniotomy

In this study we investigated the effect of topical application of cool irrigation fluid on brain tissue temperature during craniotomy. Eight patients were given a standard general anaesthetic for craniotomy. Distal oesophageal and nasopharyngeal temperatures were measured continuously and systemic normothermia was maintained. A sterile needle temperature probe was inserted 18 mm into the cerebrum to measure brain temperature. Brain temperatures were recorded for five minutes while the brain was irrigated with 1000 ml of normal saline at a temperature of 30 degrees C. Measurement continued until the brain temperature returned to baseline. The mean maximum decrease in cerebralparenchymal temperaturefollowing irrigation was 1.6 +/- 0.5 degrees C (P<0.01). The average time to return to baseline temperature after cessation of irrigation was 5.3 +/- 1.5 minutes. Cooling the brain has a marked protective effect after brain injury, but systemic hypothermia can produce significant harmful effects. This study demonstrates that the use of cool irrigation fluid during neurosurgery is a simple and effective method of cooling the brain whilst minimizing the use of systemic hypothermia.     

Covering the head and face maintains intraoperative core temperature

PURPOSE: To determine the effect of covering the patient's head and face on the prevention of intraoperative hypothermia (<35.5 degrees C). METHODS: This randomized, prospective trial included 44 adults undergoing elective abdominal surgery. After the induction of anesthesia with thiopental, in 44 patients their extremities and trunk were covered with towels and sheets. In addition, 22 patients (covered group) had their face and head fully covered. Anesthesia was maintained with N2O 50-66% (2-3 L x min(-1)) and isoflurane (相似文献   

Hypothermia and rewarming by peritoneal dialysis and temperature-controlled inhalate.

In 12 rabbits hypothermia and rewarming were induced with temperature-controlled circulating peritoneal dialysis in combination with temperature-controlled hypoxic and hypercapnic gas mixtures. The average cooling time necessary for the esophageal temperature to decrease from 37.7 degrees +/- 0.7 to 20.6 degrees +/- 1.0 degrees C was 81 +/- 34 minutes with a range of 41 to 150 minutes. The average warming time for esophageal temperature to increase from 20.6 degrees +/- 1.0 degrees C to 35.2 degrees +/- 1.8 degrees C was 90 +/- 35 minutes. Time of cooling was related to the proportions of inspired carbon dioxide and oxygen. In contrast to surface and bypass methods, esophageal and muscular temperatures agreed very closely, suggesting an absence of regional temperature gradients.     

Mild hypothermia improves survival after prolonged, traumatic hemorrhagic shock in pigs

INTRODUCTION: Clinical studies have demonstrated improved survival after cardiac arrest with induction of mild hypothermia (34 degrees C). Infusion of ice-cold saline seems beneficial. The American Heart Association recommends therapeutic hypothermia for comatose survivors of cardiac arrest. For hemorrhagic shock (HS), laboratory studies suggest that mild hypothermia prolongs the golden hour for resuscitation. Yet, the effects of hypothermia during HS are unclear since retrospective clinical studies suggest that hypothermia is associated with increased mortality. Using a clinically relevant, large animal model with trauma and intensive care, we tested the hypothesis that mild hypothermia, induced with intravenous cold saline (ice cold or room temperature) and surface cooling, would improve survival after HS in pigs. METHODS: Pigs were prepared under isoflurane anesthesia. After laparotomy, venous blood (75 mL/kg) was continuously withdrawn over 3 hours (no systemic heparin). At HS 35 minutes, the spleen was transected. At HS 40 minutes, pigs were divided into three groups (n = 8, each): 1) Normothermia (Norm)(38 degrees C), induced with warmed saline; 2) Mild hypothermia (34 degrees C) induced with i.v. infusion of 2 degrees C saline (Hypo-Ice) and surface cooling; and 3) Mild hypothermia (34 degrees C), induced with room temperature (24 degrees C) i.v. saline (Hypo-Rm) and surface cooling. Fluids were given when mean arterial pressure (MAP) was <30 mmHg. At HS 3 hours, shed blood was returned and splenectomy was performed. Intensive care was continued to 24 hours. RESULTS: At 24 hours, there were two survivors in the Norm group, four in the Hypo-Ice group and seven in the Hypo-Rm group (p < 0.05 versus the Norm group, Log Rank). Time required to achieve 34 degrees C was 17 +/- 9 minutes in the Hypo-Ice group and 15 +/- 4 minutes in the Hypo-Rm group (NS). Compared with the Hypo-Rm group, the Hypo-Ice group required less saline during early HS (321 +/- 122 versus 571 +/- 184 mL, p < 0.05). The Hypo-Ice group also had higher lactate levels than the Hypo-Rm group (p < 0.05). Hypothermia did not cause any increase in bleeding compared with normothermia. CONCLUSION: Mild hypothermia during HS, induced by infusion of room temperature saline and surface cooling, improves survival in a clinically relevant model of HS and trauma. However, the use of iced saline in this model had detrimental effects and did not cool the animal more quickly than room temperature fluids. These findings suggest that optimal methods for induction of hypothermia need to be addressed for each potential indication, e.g. cardiac arrest versus HS.     

Profound hypothermia (less than 10 degrees C) compared with deep hypothermia (15 degrees C) improves neurologic outcome in dogs after two hours' circulatory arrest induced to enable resuscitative surgery

Deaths from uncontrollable hemorrhage might be prevented by arresting the circulation under protective hypothermia to allow resuscitative surgery to repair these injuries in a bloodless field. We have shown previously that in hemorrhagic shock, circulatory arrest of 60 minutes under deep hypothermia (tympanic membrane temperature, Ttm = 15 degrees C) was the maximum duration of arrest that allowed normal brain recovery. We hypothesize that profound cerebral hypothermia (Ttm less than 10 degrees C) could extend the duration of safe circulatory arrest. In pilot experiments, we found that the cardiopulmonary system did not tolerate arrest at a core (esophageal) temperature (Tes) of less than 10 degrees C. Twenty-two dogs underwent 30-minute hemorrhagic shock (mean arterial pressure 40 mm Hg), rapid cooling by cardiopulmonary bypass (CPB), blood washout to a hematocrit of less than 10%, and circulatory arrest of 2 hours. In deep hypothermia group 1 (n = 10), Ttm was maintained at 15 degrees C during arrest. In profound hypothermia group 2 (n = 12), during cooling with CPB, the head was immersed in ice water, which decreased Ttm to 4 degrees-7 degrees C. The Tes was 10 degrees C in all dogs during arrest. Reperfusion and rewarming were by CPB for 2 hours. Controlled ventilation was to 24 hours, intensive care to 72 hours. In the 20 dogs that followed protocol, best neurologic deficit scores (0% = normal, 100% = brain death) at 24-72 hours were 23% +/- 19% in group 1 and 12% +/- 8% in group 2 (p = 0.15). Overall performance categories and histologic damage scores were significantly better in group 2 (p = 0.04 and p less than 0.001, respectively). We conclude that profound cerebral hypothermia with CPB plus ice water immersion of the head can extend the brain's tolerance of therapeutic circulatory arrest beyond that achieved with deep hypothermia.     

Renal hypothermia: experience in pigs and clinical trial

PURPOSE: This study was designed to compare the effectiveness of two methods of inducing renal hypothermia through laparoscopy in pigs and humans. MATERIALS AND METHODS: Twelve pigs were divided into four groups of three animals each. Both kidneys of the animals in Groups A, B, and C were submitted to pelvic irrigation with cold saline (4 degrees C) for 20 minutes, with flow rates of 5 mL/min, 10 mL/min, and 15 mL/min, respectively. In Group D renal hypothermia was induced by intracorporeal ice slush applied to the surface for 20 minutes. All maneuvers were performed laparoscopically and renal cortex temperature was measured by a thermocouple needle. Five human patients also underwent laparoscopic partial nephrectomy due to renal cell carcinoma. In one case renoprotection was induced by retrograde endoscopic cold saline perfusion at a flow rate of 10 mL/min. In the remaining four patients we induced renal hypothermia via laparoscopic application of ice slush. The renal temperature of the human patients was also monitored using a thermocouple needle. RESULTS: In the pigs, at 20 minutes of renal pelvis perfusion the mean renal temperature, the temperature drop, and saline flow per gram of kidney were: Group A, -29.5 degrees C +/- 1.1 (-6.3 degrees C; 0.10 mL); Group B, -22.8 degrees C +/- 1.1 (-13.1 degrees C; 0.22 mL); and Group C, -21.1 degrees C +/- 0.9 (-14.9 degrees C; 0.31 mL). In Group D the mean renal cortex temperature at 20 minutes was 13.6 degrees C +/- 1.2, a drop of -22.5 degrees C. There were striking differences among the groups (P < 0.0001). The laparoscopic partial nephrectomy was uneventful in all five human patients. The lowest renal cortex temperature was 32.5 degrees C, seen in the patient who submitted to pelvic irrigation with cold saline, and the mean temperature drop was 19.1 degrees C +/- 2.5 degrees C in the patients who submitted to ice slush-induced renal hypothermia. CONCLUSIONS: Induction of renal hypothermia using intracorporeal ice slush confers lower kidney temperatures than endoscopically-induced cold saline perfusion.     

The effect of maternal hypothermic cardiopulmonary bypass on fetal lamb temperature, hemodynamics, oxygenation, and acid-base balance

OBJECTIVE: To evaluate fetal-maternal temperature relationship and fetal cardiovascular and metabolic response during maternal hypothermic cardiopulmonary bypass in pregnant ewes. METHODS: Cardiopulmonary bypass was instituted in 9 pregnant ewes, reaching 2 different levels of maternal hypothermia: 24 degrees C to 20 degrees C (deep hypothermia) in group A (5 cases) and less than 20 degrees C (very deep hypothermia) in group B (4 cases). Hypothermic levels were maintained for 20 minutes, then the rewarming phase was started. Fetal and maternal temperature, blood pressure, heart rate, electrocardiogram, blood gases, and acid-base balance were evaluated at different levels of hypothermia and during recovery. RESULTS: Fetal survival was related to maternal hypothermia: all group A fetuses survived, while 2 of 4 fetuses of group B in which maternal temperature was lowered below 18 degrees C died in a very deep acidotic and hypoxic status. Maternal temperature was always lower than fetal temperature during cooling; during rewarming the gradient was inverted. The start of cardiopulmonary bypass and cooling was associated with transient fetal tachycardia and hypertension; then, both fetal heart rate and blood pressure progressively decreased. The reduction of fetal heart rate was of 7 beats per minute for each degree of fetal cooling. Deep maternal hypothermia was associated with fetal alkalosis and reduction of Po(2). Very deep hypothermia, in particular below 18 degrees C, caused irreversible fetal acidosis and hypoxia. CONCLUSIONS: Deep maternal hypothermic cardiopulmonary bypass was associated with reversible modifications in fetal cardiovascular parameters, blood gases, and acid-base balance and therefore with fetal survival. On the contrary, fetuses did not survive to a very deep hypothermia below 18 degrees C.     

Effect of mild hypothermia on brain dialysate lactate after fluid percussion brain injury in rodents

OBJECTIVE: To investigate the effects of mild hypothermia on brain microdialysate lactate after fluid percussion traumatic brain injury (TBI) in rats. METHODS: Brain dialysate lactate before and after fluid percussion brain injury (2.1 +/- 0.2 atm) was measured in rats with preinjury mild hypothermia (32 degrees C), postinjury mild hypothermia (32 degrees C), injury normothermia (37 degrees C), and the sham control group. Mild hypothermia (32 degrees C) was induced by partial immersion in a water bath (0 degrees C) under general anesthesia and maintained for 2 hours. RESULTS: In the normothermia TBI group, brain extracellular fluid lactate increased from 0.311 +/- 0.03 to 1.275 +/- 0.08 mmol/L within 30 minutes after TBI (P < 0.01) and remained at a high level (0.546 +/- 0.05 mmol/L) (P < 0.01) at 2 hours after injury. In the postinjury mild hypothermic group, brain extracellular fluid lactate increased from 0.303 +/- 0.03 to 0.875 +/- 0.05 mmol/L at 15 minutes after TBI (P < 0.01) and then gradually decreased to 0.316 +/- 0.04 mmol/L at 2 hours after TBI (P > 0.05). In the preinjury mild hypothermic group, brain extracellular fluid lactate remained at normal levels after injury (P > 0.05). CONCLUSION: The cerebral extracellular fluid lactate level increases significantly after fluid percussion brain injury. Preinjury mild hypothermia completely inhibits the cerebral lactate accumulation, and early postinjury mild hypothermia significantly blunts the increase of cerebral lactate level after fluid percussion injury.     

Safety and performance of a novel intravascular catheter for induction and reversal of hypothermia in a porcine model

OBJECTIVE: This study was undertaken to assess the acute safety and feasibility of rapidly inducing, maintaining, then reversing hypothermia using a novel heat transfer catheter and a closed-loop automatic feedback temperature control system to overcome limitations imposed by current clinical practices used for perioperative cooling and warming. METHODS: Six swine (mean mass, 53.8 +/- 3.6 kg) were studied. The heat transfer catheter was placed in the inferior vena cava via the femoral vein. Hypothermia to 32 degrees C was induced, maintained for 6 hours, then reversed to 36 degrees C. The time needed to induce and reverse hypothermia was recorded via continuous temperature monitoring of the lower esophagus, cerebrum, and rectum. Electrocardiography provided continuous monitoring, and blood draws were made at baseline and at 2-hour intervals. Examination of the catheter in situ was performed after the animals were killed. RESULTS: Cooling from 36.2 to 32.0 degrees C was rapid and uniform (mean, 7.3 +/- 0.7 degrees C/h), with animals reaching the target temperature within 60 minutes. Rewarming was also easily controlled, with animals' temperatures reaching 36 degrees C within 130 minutes. No arrhythmia was observed, and all hematological variables were within the normal range for swine. There was no evidence of hemolysis or platelet changes. Little to no thrombosis was observed. CONCLUSION: The data presented here suggest that rapid induction and reversal of hypothermia are technically possible using a core intravenous cooling catheter; this method would provide a safe, rapid, and exquisitely reproducible way to induce hypothermia with subsequent restoration of normothermia.     

Focal epidural cooling reduces the infarction volume of permanent middle cerebral artery occlusion in swine

BACKGROUND: The protective effect against ischemic stroke by systemic hypothermia is limited by the cooling rate and it has severe complications. This study was designed to evaluate the effect of SBH induced by epidural cooling on infarction volume in a swine model of PMCAO. METHODS: Permanent middle cerebral artery occlusion was performed in 12 domestic swine assigned to groups A and B. In group A, the cranial and rectal temperatures were maintained at normal range (37 degrees C-39 degrees C) for 6 hours after PMCAO. In group B, cranial temperature was reduced to moderate (deep brain, <30 degrees C) and deep (brain surface, <20 degrees C) temperature and maintained at that level for 5 hours after 1 hour after PMCAO, by the epidural cooling method. All animals were euthanized 6 hours after MCAO; their brains were sectioned and stained with 2,3,5-triphenyltetrazolium chloride and their infarct volumes were calculated. RESULTS: The moderate and deep brain temperature (at deep brain and brain surface) can be induced by rapid epidural cooling, whereas the rectal temperature was maintained within normal range. The infarction volume after PMCAO was significantly reduced by epidural cooling compared with controls (13.73% +/- 1.82% vs 5.62% +/- 2.57%, P < .05). CONCLUSIONS: The present study has demonstrated, with histologic confirmation, that epidural cooling may be a useful strategy for reducing infarct volume after the onset of ischemia.     

After spontaneous hypothermia during hemorrhagic shock,continuing mild hypothermia (34 degrees C) improves early but not late survival in rats

BACKGROUND: Spontaneous hypothermia is common in victims of severe trauma. Laboratory studies have shown benefit of induced (therapeutic) mild hypothermia (34 degrees C) during hemorrhagic shock (HS). Clinical data, however, suggest that hypothermia, which often occurs spontaneously in trauma patients, is detrimental. Because critically ill trauma patients are usually cool, the clinical question, which has not been explored in the laboratory with long-term outcome, is whether maintaining hypothermia or actively rewarming the patient improves outcome. We hypothesized that after spontaneous cooling during HS, continuing mild therapeutic hypothermia during resuscitation is beneficial compared with active rewarming. METHODS: In study A, under light isoflurane anesthesia, 24 Sprague-Dawley rats were bled over 10 minutes to, and maintained at, mean arterial pressure (MAP) of 40 mm Hg until reuptake of 30% of maximal shed blood volume was needed. Rectal temperature (Tr) decreased spontaneously to, and was then maintained at, 35 degrees C during HS. Fluid resuscitation included the remaining shed blood and up to 400 mL/kg of lactated Ringer's solution with 5% dextrose over 4 hours. During resuscitation, three groups (n = 8 each) were studied: normothermia (rapid rewarming to Tr 37.5 degrees C at the beginning of resuscitation); hypothermia-2 h (cooling to Tr 34 degrees C to resuscitation time 2 hours); and hypothermia-12 h (cooling to Tr 34 degrees C to 12 hours). Rats were observed to 72 hours. In study B, more severe HS than in study A was studied. HS was induced with 3 mL/100 g blood withdrawal over 15 minutes followed by maintenance of MAP of 40 mm Hg until 50% of maximal shed blood volume was needed. Two groups (n = 8 each) were studied: normothermia and hypothermia-12 h. Data are presented as mean +/- SD or median (range). RESULTS: In study A, both hypothermia groups had higher MAP and lower heart rates during resuscitation than the normothermia group (p < 0.01). Survival to 72 hours was achieved in three of eight rats in the normothermia group and two of eight in each hypothermia group. Thirteen of 17 deaths occurred after 24 hours. In study B, for resuscitation, the hypothermia group needed less fluid (53 +/- 6 mL vs. 79 +/- 32 mL, p < 0.05), but had higher MAP (p < 0.01), lower heart rate (p < 0.01), and lower lactate level (p = 0.06). All rats died before 72 hours. The hypothermia group had longer survival time (24.5 [13-48.5] hours) than the normothermia group (7.5 [1.5-19] hours) (p = 0.003 by life table analysis). CONCLUSION: After spontaneous cooling during moderately severe HS, mild, controlled hypothermia during resuscitation does not seem to affect long-term survival. After more severe HS, hypothermia increases survival time. Hypothermia supports arterial pressure during resuscitation from severe HS.     

Is Maintenance of Cerebral Hypothermia the Principal Mechanism by which Retrograde Cerebral Perfusion Provides Better Brain Protection than Hypothermic Circulatory Arrest?

OBJECTIVE: Retrograde cerebral perfusion (RCP) provides better brain protection than hypothermic circulatory arrest (HCA) alone. The mechanism by which RCP improves brain protection during circulatory arrest remains unknown. The purpose of the study in pigs was to determine if RCP improves brain protection mainly as a result of its ability to maintain cerebral hypothermia. METHODS: Fifteen pigs were subjected to 120 minutes of HCA alone (HCA group, n = 5), HCA + RCP at perfusion pressures of 23 to 29 mmHg (RCP-low group, n = 5), or at perfusion pressures of 34-40 mmHg (RCP-high group, n = 5) at 15 degrees C, followed by 60 minutes of normothermic cardiopulmonary bypass (CPB). After brain temperature reached 15 degrees C, HCA was initiated with or without RCP. Temperatures in the brain, esophagus, and perfusate/blood were monitored continuously. Brain tissue blood flow was measured continuously using a laser flowmeter. Brain oxygen extraction was calculated from the oxygen contents in arterial and venous blood samples. RESULTS: During cooling and rewarming, the change in temperature was slower in the brain than in the esophagus. A similar degree of spontaneous rewarming (from 15 degrees C to 17/18 degrees C) occurred in the brain during HCA and RCP. This indicates that RCP does not provide better maintenance of cerebral hypothermia during circulatory arrest than HCA alone. The esophageal temperature rose more slowly during RCP than during HCA alone, indicating that RCP maintains better hypothermia in the body. During RCP, the brain extracted oxygen continuously from the blood, indicating that RCP may provide nutrient flow to the brain. CONCLUSION: In an acute pig model, maintenance of cerebral hypothermia does not appear to be the principal mechanism by which RCP provides better brain protection than HCA alone. Retrograde cerebral perfusion provides nutrient flow/oxygen to brain tissue, leading to better brain protection than HCA alone.     

Effect of induction rate for mild hypothermia on survival time during uncontrolled hemorrhagic shock in rats

BACKGROUND: Rapid induction of hypothermia has been shown to improve survival in uncontrolled hemorrhagic shock (UHS) rat studies. We hypothesized that prolonged induction of hypothermia would be equally beneficial for survival during UHS. METHODS: Light anesthesia was induced with halothane in 30 rats, and spontaneous breathing was maintained. Rectal temperature (Tr) was monitored and maintained at 38 degrees C. UHS was induced by blood withdrawal of 2.5 mL/100 g during a 15-minute period, followed by 75% tail amputation. Immediately after cutting the tail, rats were randomized into three groups of 10 rats each: Group 1, maintained at Tr 38 degrees C; group 2, passively cooled to 34 degrees C by exposure to room temperature (23 degrees C); and group 3, actively cooled to 34 degrees C by applying alcohol to the skin and under an electric fan. Next, rats were controlled at each target Tr and observed without fluid resuscitation until either death or a maximum of 240 minutes. RESULTS: Cooling rate was -0.09 +/- 0.01 degrees C/min in group 2 and -0.36 +/- 0.9 degrees C/min in group 3 (p < 0.01). Mean survival time was 72 +/- 21 minutes in group 1 (38 degrees C), and was nearly doubled by hypothermia to 132 +/- 62 minutes for group 2 (p < 0.01 vs. group 1) and 150 +/- 69 minutes for group 3 (p < 0.01 vs. group 1). No significant difference in survival was noted between groups 2 and 3. Additional blood loss from the tail stump did not differ significantly between groups. CONCLUSION: Therapeutic mild hypothermia, induced either slowly (approximately -0.1 degrees C/min) or rapidly (approximately -0.4 degrees C/min) prolongs survival during lethal UHS in rats.     

Physiologic characteristics of cold perfluorocarbon-induced hypothermia during partial liquid ventilation in normal rabbits.

Because perfluorocarbon (PFC) liquid contacts closely with the alveolar capillaries during partial liquid ventilation (PLV), PLV with cold PFC may be used for the induction of hypothermia. Twenty rabbits were randomized to PFC-induced hypothermia (PH) (n = 7; core temperature 35 degrees +/- 1 degrees C), surface hypothermia (SH) (n = 7; 35 degrees +/- 1 degrees C), or normothermia (n = 6; 39 degrees +/- 1 degrees C). We induced PH by repeated in situ exchanges of 0 degrees C perfluorodecalin during PLV. At the establishment (0 min) of hypothermia in the PH group, oxygen consumption (P = 0.04) and oxygen extraction ratio (P = 0.01) decreased from normothermic condition. Metabolic (oxygen consumption, oxygen extraction ratio, serum lactate level) and hemodynamic variables (heart rate, blood pressure, cardiac output, pulmonary artery pressure) of the PH group were not different from those of the SH group at 0, 30, 60, 90, and 120 min of hypothermia. The difference in temperature between the pulmonary artery and rectum during the hypothermic period was smaller in the PH group compared with the SH group (P = 0.033). In conclusion, hypothermia may be induced during PLV by using cold PFC. This "pulmonary method" of cooling was comparable to a systemic method of cooling with regard to a few important physiologic variables, while maintaining a narrower interorgan temperature difference. IMPLICATIONS: The induction of moderate hypothermia was feasible in rabbits by administrating cold perfluorocarbon liquid into the lung. Physiologic changes induced by this pulmonary cooling were comparable to those induced by systemic cooling. Our method may be regarded as a methodological advance in the field of therapeutic hypothermia.     

Rapid and selective cerebral hypothermia achieved using a cooling helmet

OBJECT: Hypothermia is by far the most potent neuroprotectant. Nevertheless, timely and safe delivery of hypothermia remains a clinical challenge. To maximize neuroprotection yet minimize systemic complications, ultra-early delivery of selective cerebral hypothermia by Emergency Medical Service (EMS) personnel in the field would be advantageous. The authors (W.E. and H.W.) have developed a cooling helmet by using National Aeronautics and Space Administration spinoff technology. In this study its effectiveness in lowering brain temperature in patients with severe stroke or head injury is examined. METHODS: Patients were randomly assigned to groups receiving either the cooling helmet or no cooling, and brain temperatures (0.8 cm below the cortical surface) were continuously monitored for a mean of 48 to 72 hours with a Neurotrend sensor and then compared with the patients' core temperatures. There were eight patients in the study group and six in the control group. The mean change in temperature (brain-body temperature) calculated from 277 data hours in the study group was -1.6 degrees C compared with a mean change in temperature of +0.22 degrees C calculated from 309 data hours in the control group. This was statistically significant (p < 0.0001). On average, 1.84 degrees C of brain temperature reduction (range 0.9-2.4 degrees C) was observed within 1 hour of helmet application. It took a mean of 3.4 hours (range 2-6 hours) to achieve a brain temperature lower than 34 degrees C and 6.67 hours (range 1-12 hours) before systemic hypothermia (< 36 degrees C) occurred. Use of the helmet resulted in no significant complications. There was, however, one episode of asymptomatic bradycardia (heart rate < 40) that responded to a 0.5 degrees C body temperature increase. CONCLUSIONS: This helmet delivers initial rapid and selective brain cooling and maintains a significant temperature gradient between the core and brain temperatures throughout the hypothermic period to provide sufficient regional hypothermia yet minimize systemic complications. It results in delayed systemic hypothermia, creating a safe window for possible ultra-early delivery of regional hypothermia by EMS personnel in the field.