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PubMed2004

Prevention of cerebral hyperthermia during cardiac surgery by limiting on-bypass rewarming in combination with post-bypass body surface warming: a feasibility study.

Cerebral hyperthermia is common during the rewarming phase of cardiopulmonary bypass (CPB) and is implicated in CPB-associated neurocognitive dysfunction. Limiting rewarming may prevent cerebral hyperthermia but risks postoperative hypothermia. In a prospective, controlled study, we tested whether using a surface-warming device could allow limited rewarming from hypothermic CPB while avoiding prolonged postoperative hypothermia (core body temperature <36 degrees C). Thirteen patients undergoing primary elective coronary artery bypass grafting surgery were randomized to either a surface-rewarming group (using the Arctic Sun thermoregulatory system; n = 7) or a control standard rewarming group (n = 6). During rewarming from CPB, the control group was warmed to a nasopharyngeal temperature of 37 degrees C, whereas the surface-warming group was warmed to 35 degrees C, and then slowly rewarmed to 36.8 degrees C over the ensuing 4 h. Cerebral temperature was measured using a jugular bulb thermistor. Nasopharyngeal temperatures were lower in the surface-rewarming group at the end of CPB but not 4 h after surgery. Peak jugular bulb temperatures during the rewarming phase were significantly lower in the surface-rewarming group (36.4 degrees C +/- 1 degrees C) compared with controls (37.7 degrees C +/- 0.5 degrees C; P = 0.024). We conclude that limiting rewarming during CPB, when used in combination with surface warming, can prevent cerebral hyperthermia while minimizing the risk of postoperative hypothermia[corrected].

Adult↗
PubMed2002

Severe accidental hypothermia with or without hemodynamic instability: rewarming without the use of extracorporeal circulation.

BACKGROUND: The optimal rewarming technique for patients in deep accidental hypothermia with core temperatures below 28 degrees C is not established. Several authors believe that extracorporeal rewarming is essential, especially for patients with hemodynamic instability. Others believe that invasive rewarming ought to be reserved for patients in cardiac arrest. We describe our experience with a strictly conservative technique without the use of invasive rewarming devices in patients with severe accidental hypothermia and a sustained perfusion rhythm. METHODS: A cohort study extending from 1991 to 2000, including all patients received at the emergency department of the University Hospital of Vienna with severe hypothermia, a core temperature of maximum 28 degrees C and no preclinical cardiac arrest. RESULTS: 36 patients with deep hypothermia were included in the study. Their core temperatures ranged from 20.2 degrees C to 28 degrees C; the median temperature was 25.75 degrees C (25th and 75th percentile, 24.2/27.3). Fourteen patients were intoxicated and their multimorbidity was high. All of 19 patients with stable hemodynamics and 14 of 17 patients with unstable hemodynamics were successfully rewarmed to normothermia with warmed infusions, inhalation rewarming and forced air rewarming. The rewarming process took 9.5 hours (8/10.5) and required a volume load of 4820 ml (2735/5770). The rewarming rate was 1.09 degrees C per hour (0.94/1.25). Although 92% of the patients were successfully rewarmed to normothermia, in-hospital mortality was 42%, but was largely related to comorbidity. DISCUSSION: A conservative approach is highly successful in achieving normothermia in patients with deep hypothermia with or without stable hemodynamics. In-hospital mortality of severe accidental hypothermia in urban conditions is high; comorbidity might play a major role. The influence of the rewarming strategy on late in-hospital mortality remains unclear.

Austria↗
PubMed2004

Uncomplicated rapid posthypothermic rewarming alters cerebrovascular responsiveness.

BACKGROUND AND PURPOSE: Recently, we focused on the cerebrovascular protective effects of moderate hypothermia after traumatic brain injury, noting that the efficacy of posttraumatic hypothermia is related to the rate of posthypothermic rewarming. In the current communication, we revisit the use of hypothermia with varying degrees of rewarming to ascertain whether, in the normal cerebral vasculature, varying rates of rewarming can differentially affect cerebrovascular responsiveness. METHODS: Pentobarbital-anesthetized rats equipped with a cranial window were randomized to 3 groups. In 1 group, a 1-hour period of hypothermia (32 degrees C) followed by slow rewarming (over 90 minutes) was used. In the remaining 2 groups, either a 1- or 2-hour period of hypothermia was followed by rapid rewarming (within 30 minutes). Vasoreactivity to hypercapnia and acetylcholine was assessed before, during, and after hypothermia. Additionally, the vascular responses to sodium nitroprusside (SNP) and pinacidil, a K(ATP) channel opener, were also examined. RESULTS: Hypothermia itself generated modest vasodilation and reduced vasoreactivity to all utilized agents. The slow rewarming group showed restoration of normal vascular responsivity. In contrast, hypothermia followed by rapid rewarming was associated with continued impaired responsiveness to acetylcholine and arterial hypercapnia. These abnormalities persisted even with the use of more prolonged (2-hour) hypothermia. Furthermore, posthypothermic rapid rewarming impaired the dilator responses of SNP and pinacidil. CONCLUSIONS: Posthypothermic rapid rewarming caused cerebral vascular abnormalities, including a diminished response to acetylcholine, hypercapnia, pinacidil, and SNP. Our data with acetylcholine and SNP suggest that rapid rewarming most likely causes abnormality at both the vascular smooth muscle and endothelial levels.

Acetylcholine↗
PubMed1995

Inhalation rewarming from hypothermia: an evaluation in -20 degrees C simulated field conditions.

The present study evaluates the efficacy of inhaling warm moist air as a method of rewarming from hypothermia in -20 degrees C field conditions. The method of inhalation rewarming is compared to two other methods of rewarming: a) passive rewarming; and b) passive rewarming, with a respiratory heat exchanger designed to minimize respiratory heat loss. Eight male subjects were rendered hypothermic by immersion in 15 degrees C water for 1 h. They were withdrawn from the tank earlier, in the event that their rectal temperature (Tre) decreased to 35 degrees C, or by 1.5 degrees C from the pre-immersion value. Upon completion of the immersion, they were placed in a well-insulated sleeping bag assembly and transferred to a cold room maintained at -20 degrees C for a 2 h rewarming period. They participated in 3 trials: Control-passive rewarming; Heat Treat-inhalation rewarming with the Heat Treat; HME-passive rewarming in conjunction with a respiratory heat and moisture exchanger (HME). During the rewarming period, inspired air temperature was -19.4 +/- 1.1 degrees C in the control trial. In the HME and Heat Treat trials subjects breathed via an oro-nasal mask. The inspired air temperature was +20.5 +/- 1.2 degrees C in the HME and +36.2 +/- 2.9 degrees C in the Heat Treat trial. The post-immersion drop in Tre was significant in all conditions. The reduction in the post-exposure drop in Tre observed with the Heat Treat may be attributed to the minimization of respiratory heat loss, since the magnitude of the reduction was similar to that observed with the HME.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of a standardized rewarming protocol and acetaminophen on core temperature after coronary artery bypass.

BACKGROUND: Cardiac surgical patients who require hypothermic cardiopulmonary bypass experience hypothermia, normothermia, and hyperthermia during the early postoperative period. Research-based rewarming protocols are needed to manage temperature variations. OBJECTIVE: To describe the effect of a standardized rewarming protocol and acetaminophen on the following outcome variables: core temperature, peak core temperature, rewarming time, and hyperthermia. METHODS: Patients (N = 60) were rewarmed using a standardized rewarming protocol. Electric heating blankets were used for subjects with core temperatures less than 36 degrees C on admission to the intensive care unit; other subjects were covered with cotton bath blankets. Subjects were also assigned to one of three acetaminophen groups (650 mg at 38.1 degrees C, 650 mg at 37 degrees C, 1300 mg at 37 degrees C). RESULTS: Using the protocol, subjects warmed to normothermia in 3.6 to 6 hours. The 16-hour core temperature thermal curves of heating blanket versus cotton bath blanket subjects differed significantly; thermal curves of the acetaminophen groups were similar. Peak core temperature was significantly lower in heating blanket subjects and unaffected by acetaminophen group. The onset of hyperthermia was not significantly affected by the method of rewarming (electric heating blanket versus cotton blankets) or acetaminophen group. Rewarming time was significantly longer for electric heating blanket subjects. CONCLUSIONS: Our results indicate that mildly hypothermic subjects rewarmed with electric heating blankets during the early postoperative period have lower peak core temperatures and longer rewarming times than those rewarmed with cotton bath blankets. Acetaminophen administration at normothermia does not significantly affect peak core temperature or the onset of hyperthermia.

Acetaminophen↗
PubMed1979

Accidental hypothermia and rewarming in dogs.

1. Twenty lightly anaesthetized dogs were cooled to 29 degrees C by cold-water immersion. Ventilation was spontaneous and the animals were allowed to shiver freely. Metabolic heat production and respiratory heat exchange were measured during rewarming. 2. The animals were divided into four groups each of five dogs and each group was rewarmed by a different technique. The control group was allowed to rewarm spontaneously; a second group was given warm (45-50 degrees C) fully humidified air to breathe in addition; a third group was rewarmed in a hot-water bath (42-44 degrees C) and the remaining group was given in muscle relaxant to abolish shivering and rewarmed by warm inspired air only. 3. The group rewarmed in hot water achieved normal core temperature most rapidly but there was no difference in the rewarming rates of the group rewarmed spontaneously and of the group given warm air to breathe in addition. 4. The group given a muscle relaxant and rewarmed with warm inspired air required 12 h to achieve the same core temperature as the shivering groups achieved in 2 h. Compared with the heat produced by shivering the amount of heat which it was possible to transfer across the respiratory tract was so small that it did not materially influence the rate of rewarming.

Animals↗
PubMed1966

Survival of Plant Tissue at Super-Low Temperatures. IV. Cell Survival with Rapid Cooling and Rewarming.

Thin unmounted cortical tissue sections from winter twigs of the mulberry tree were held with a thin forceps and rapidly immersed in liquid nitrogen from room temperatures without prefreezing. They were rewarmed; rapidly in water at 10 degrees to 40 degrees , or slowly, in air at room temperatures. In those sections rapidly rewarmed, all survived. None survived in those sections rewarmed slowly in air.Tissue sections mounted between coverglasses with water were extracellulary prefrozen at the temperatures low enough to dehydrate almost all of the freezable water in cells. These sufficiently prefrozen cells could survive immersion in liquid nitrogen, and the survival value was very little affected by the rates of cooling to and rewarming from super-low temperatures. With insufficient prefreezing at higher temperatures, however, the rewarming process seriously influenced the survival value of cells frozen at super-low temperatures. Slow rewarming in air destroyed all of the cells, while rapid rewarming in water at 30 degrees did not affect them. An abrupt decrease in the survival value in insufficiently prefrozen cells during rewarming was also observed at temperatures above approximately -50 degrees following immersion in liquid nitrogen. Very little decrease in the survival value was observed in any of the cells that had been sufficiently prefrozen.These results indicate that cells which are insufficiently prefrozen may contain freezable water which nucleates during rapid cooling in liquid nitrogen and then grows during the subsequent slow rewarming into ice masses which destroy the viability of the cells. Such fatal intracellular freezing rarely occurs in sufficiently prefrozen cells, irrespective of the rate of cooling to or rewarming from super-low temperatures.

Journal Article↗
PubMed1992

Comparison of four noninvasive rewarming methods for mild hypothermia.

Four noninvasive rewarming techniques for mildly hypothermic subjects were compared. Seven subjects were cooled in a water bath of 15 degrees C for 2 h to an average esophageal temperature (Tes) of 36 degrees C. Thereafter, the subjects were rewarmed by immersion of the body in a water bath of 42 degrees C (Method 1), the body but not the extremities in water of 42 degrees C (Method 2), only the extremities in water of 42 degrees C (Method 3), or spontaneous rewarming in blankets (Method 4). Method 1 showed the highest rewarming rate in Tes (10.1 degrees C/h) and an afterdrop in Tes of 0.18 degrees C. Method 2 showed the same afterdrop, but a lower rewarming rate (7.5 degrees C/h). In Method 3, the heat uptake of the extremities was too low to rewarm the subjects effectively. The afterdrop and rewarming rate were 0.38 degrees C and 0.8 degrees C/h, respectively. Method 4 had the lowest rewarming rate (0.2 degrees C/h), and an afterdrop (0.14 degrees C) which was not significantly lower than that of Method 1 or 2. Therefore, Method 1 is recommended for rewarming mild hypothermic subjects because of its high rewarming rate and small afterdrop.

Adult↗
PubMed1986

Partial cardiopulmonary bypass for core rewarming in profound accidental hypothermia.

Six cases of treatment of severe accidental hypothermia using cardiopulmonary bypass for core rewarming are reported and eleven cases from the literature are analyzed. Thirteen patients survived. Overall survival was more likely in patients who had vital signs initially. Initial mean core temperatures in the new cases was 22.8 C. Surface and conventional core rewarming methods resulted in an average temperature increase of 2.4 C per hr. Electrical defibrillation was generally without success until the core temperature had been raised to above 30 C. Between one and six hours after admission, partial femoral-femoral cardiopulmonary bypass (CPB) for core rewarming was started, causing a mean temperature increase of 9.5 C per hr. Four patients required a thoracotomy. Two patients had a massively dilated heart with contusions, and could not be weaned off bypass. None of the four long-term survivors had a demonstrable central nervous system (CNS) deficit. All patients developed temporary pulmonary problems; two developed wound infections. The average hospital stay was 21 days. CPB for core rewarming allows circulatory support while avoiding myocardial damage from prolonged external cardiac massage; rapidly increases the myocardial temperature and counteracts myocardial temperature gradients so that DC electroversion is successful; avoids "rewarming shock"; and improves microcirculatory flow. A prospective randomized trial to compare rapid surface rewarming and CPB rewarming is suggested. Immediate CPB for rewarming is recommended for patients in ventricular fibrillation with core temperatures below 30 C. Prolonged external cardiac massage (ECM) should not be used. The value of surface rewarming and non-CPB core rewarming methods remains undefined.

Accidents↗
PubMed1995

Pretreatment with 3,5,3'triiodo-L-thyronine (T3). Effects on myocyte contractile function after hypothermic cardioplegic arrest and rewarming.

Circulating levels of 3,5,3'triiodo-L-thyronine are depressed after cardiopulmonary bypass and have been implicated to play a contributory role in the alterations in left ventricular function after hypothermic cardioplegic arrest and rewarming. The central hypothesis of the present study was that pretreatment of isolated myocytes with triiodothyronine will have a direct and beneficial effect on contractile performance after hypothermic cardioplegic arrest and rewarming. Contractile function in isolated pig left ventricular myocytes was examined by video microscopy after the following treatment protocols: (1) 37 degrees C incubation in medium (normothermia) for 2 hours with triiodothyronine followed by a 2-hour normothermic incubation with no triiodothyronine, (2) 4 hours of normothermic incubation with no triiodothyronine, (3) normothermic incubation for 2 hours with triiodothyronine followed by 2 hours of hyperkalemic, hypothermic cardioplegic arrest ([K+]:24 mmol/L; 4 degrees C) and subsequent rewarming, and (4) normothermic incubation for 2 hours with no triiodothyronine followed by 2 hours of hyperkalemic, hypothermic cardioplegic arrest and rewarming. Two hours of normothermia with triiodothyronine increased myocyte contractile function by 30% compared with values in untreated control myocytes, and this increase persisted after a subsequent 2-hour incubation under normothermic conditions with no triiodothyronine. For example, myocyte velocity of shortening in triiodothyronine-pretreated myocytes was 84 +/- 4.9 microns/sec compared with 62 +/- 2.8 microns/sec in control myocytes (p < 0.05). Cardioplegic arrest and subsequent rewarming caused a significant reduction in myocyte velocity of shortening from normothermic values (37 +/- 3.4 microns/sec, p < 0.05). However, in myocytes pretreated with triiodothyronine, myocyte contractile function was significantly higher after hypothermic cardioplegic arrest and rewarming (54 +/- 2.5 microns/sec, p < 0.05). In a second series of experiments, beta-adrenergic responsiveness was examined after pretreatment with triiodothyronine. In the presence of the beta-adrenergic agonist isoproterenol (25 nmol/L), myocyte contractile function was increased by 26% in the triiodothyronine-treated myocytes compared with that in untreated control myocytes. This enhanced beta-adrenergic responsiveness with triiodothyronine pretreatment persisted with subsequent exposure to hypothermic cardioplegic arrest and rewarming. In summary, triiodothyronine pretreatment caused an increase in myocyte contractile function and beta-adrenergic responsiveness under normothermic conditions and after hypothermic cardioplegic arrest and rewarming. Thus the present study provides direct evidence to suggest that preemptive treatment with triiodothyronine may improve left ventricular contractile performance after hypothermic cardioplegic arrest and rewarming.

Animals↗
PubMed1998

The role of inhalation rewarming in the early management of hypothermia.

OBJECTIVE: To evaluate the effectiveness of inhalation rewarming in early resuscitative efforts for hypothermic victims. DATA SOURCES: Search of MEDLINE and manual retrieval using the terms hypothermia, resuscitation, inhalation and treatment. All articles and papers published within the last 5 years were searched. Earlier literature was also included if considered vital to documenting the scientific basis and rationale for using airway rewarming. STUDY SELECTION: Letters to the editor, review articles, case reports and original research were included in this review. Material was considered for inclusion if it contributed generally to the understanding of the role of inhalation rewarming in the stabilization or treatment of accidental hypothermia. RESULTS: The literature reported many instances in which inhalation rewarming appeared to contribute to a successful outcome during hypothermic resuscitative efforts. The maximum contribution that inhalation rewarming provides to overall core rewarming does not appear to endorse it as a sole method of core rewarming. CONCLUSIONS: The safety and efficacy of inhalation rewarming suggest that it is a viable adjunct of treatment during hypothermic resuscitation. Its routine use may be more appropriate for a field rescue situation where more advanced rewarming modalities may not be available or practicable. Also, its primary value may be to minimize further core temperature loss during early management of accidental hypothermia.

Cardiopulmonary Resuscitation↗
PubMed2002

Effects of hypothermia and rewarming on evoked potentials during transient focal cerebral ischemia in cats.

We examined the effects of mild to moderate hypothermia and the influence of rewarming on electrophysiological function using somatosensory evoked potentials (SEPs) in transient focal ischemia in the brain. Nineteen cats underwent 60 min of left middle cerebral artery occlusion under normothermic (36 degrees-37 degrees C, n = 6) or hypothermic (30 degrees -31 degrees C, n = 13) conditions followed by 300 min of reperfusion with slow (120 min, n = 6) or rapid (30 min, n = 7) rewarming. Whole-body hypothermia was induced during ischemia and the first 180 min of reperfusion. SEPs and regional cerebral blood flow were measured before and during ischemia and during reperfusion. The specific gravity of gray and white matter was examined as the indicator of edema. During rewarming, SEP amplitudes recovered gradually. After rewarming, SEPs in the normothermic and rapid rewarming groups remained depressed (20%-40% of pre-occlusion values); however, recovery of SEPs was significantly enhanced in the slow rewarming group (p < 0.05). Hypothermia followed by slow rewarming reduced edema in gray and white matter. Rapid rewarming did not reduce edema in the white matter. The recovery of SEPs correlated with the extent of brain edema in transient focal ischemia. Rapid rewarming reduced the protective effect of hypothermia.

Animals↗
PubMed2006

Rewarming rates in urban patients with hypothermia: prediction of underlying infection.

BACKGROUND: In the urban setting, hypothermia is commonly associated with illness or intoxication, with death often secondary to infection. OBJECTIVES: To evaluate factors that affect the rewarming rate (RWR) and the ability of the RWR and other clinical markers to predict the presence or absence of underlying infection in an adult urban population. METHODS: This was a prospective observational study of hypothermic patient visits to a large emergency department. Serial temperatures were obtained during rewarming to construct rewarming curves. Rewarming modalities selected by emergency physicians were correlated with admission temperatures. Univariate associates of RWR and infection were assessed. RESULTS: The authors identified 96 patient visits. The median temperature was 89.5 degrees F (31.9 degrees C; range, 73.0 degrees F to 95.0 degrees F [22.8 degrees C to 35.0 degrees C]). Thirteen patients had temperatures of < 80.0 degrees F (26.0 degrees C). Seven died within 14 hours of presentation; six, of infection. No patient experienced ventricular fibrillation. Potential candidate predictors of infection from a multivariate analysis were a RWR of < 1.80 degrees F (1.0 degrees C) per hour and a serum albumin of < 2.7 g/dL. Rapid rewarming was associated with the absence of infection and a temperature below 86.0 degrees F (30.0 degrees C). In patients without significant underlying illness, rewarming rates appeared to be independent of the modality of rewarming. CONCLUSIONS: Rewarming rates reflect intrinsic capacity for thermogenesis. Increased RWRs were associated with the absence of infection. The achievement of normothermia did not prevent death in infected patients. Initiation of invasive rewarming in urban patients with hypothermia who have not had hypothermic cardiac arrest may be unwarranted. Management of this population should emphasize support, detection, and treatment of underlying illness.

Age Distribution↗
PubMed1999

Influence of rewarming conditions after hypothermia in gerbils with transient forebrain ischemia.

OBJECT: Recently, several studies have demonstrated that hypothermia has a beneficial effect on clinical outcome; however, it is difficult to determine the appropriate rewarming conditions in clinical use. The purpose of the present study was to examine the influence of rewarming conditions in gerbils with transient forebrain ischemia. METHODS: Ischemia was induced in the gerbils by a 5-minute bilateral common carotid artery occlusion, after which the animals were immediately subjected to moderate or deep hypothermia. After moderate hypothermia (30.5 degrees C for 4 hours) the animals were rewarmed over standard, fast, or slow time periods. After deep hypothermia (24 degrees C for 2 hours) the animals were rewarmed in a standard, fast, slow, or stepwise manner. Cerebral blood flow (CBF), extracellular glutamate, and lactate were monitored. Hippocampal CA I cell damage was assessed 7 days after induction of ischemia. In animals treated with moderate hypothermia, the rewarming rate had no influence on the number of surviving neurons. However, fast rewarming from deep hypothermia (to 37 degrees C for 30 minutes) failed to provide the neuroprotective effect of hypothermia. Furthermore, this group showed a poor recovery of CBF (p < 0.01) and, consequently, an increase in extracellular glutamate (p < 0.01) and lactate (p < 0.01) in the hippocampus. CONCLUSIONS: The results of this study indicate a transient uncoupling of CBF and cerebral metabolism during fast rewarming from deep hypothermia, whereas slow and stepwise rewarming periods were found to be useful for protection against uncoupling of CBF and cerebral metabolism during rewarming.

Animals↗
PubMed2003

Radiant heat affects thermoregulation and energy expenditure during rewarming from torpor.

The high expenditure of energy required for endogenous rewarming is one of the widely perceived disadvantages of torpor. However, recent evidence demonstrates that passive rewarming either by the increase of ambient temperature or by basking in the sun appears to be common in heterothermic birds and mammals. As it is presently unknown how radiant heat affects energy expenditure during rewarming from torpor and little is known about how it affects normothermic thermoregulation, we quantified the effects of radiant heat on body temperature and metabolic rate of the small (body mass 25 g) marsupial Sminthopsis macroura in the laboratory. Normothermic resting individuals exposed to radiant heat were able to maintain metabolic rates near basal levels (at 0.91 ml O(2) g(-1) h(-1)) and a constant body temperature down to an ambient temperature of 12 degrees C. In contrast, metabolic rates of individuals without access to radiant heat were 4.5-times higher at an ambient temperature of 12 degrees C and body temperature fell with ambient temperature. During radiant heat-assisted passive rewarming from torpor, animals did not employ shivering but appeared to maximise uptake of radiant heat. Their metabolic rate increased only 3.2-times with a 15- degrees C rise of body temperature (Q(10)=2.2), as predicted by Q(10) effects. In contrast, during active rewarming shivering was intensive and metabolic rates showed an 11.6-times increase. Although body temperature showed a similar absolute change between the beginning and the end of the rewarming process, the overall energetic cost during active rewarming was 6.3-times greater than that during passive, radiant heat-assisted rewarming. Our study demonstrates that energetic models assuming active rewarming from torpor at low ambient temperatures can substantially over-estimate energetic costs. The low energy expenditure during passive arousal provides an alternative explanation as to why daily torpor is common in sunny regions and suggests that the prevalence of torpor in low latitudes may have been under-estimated in the past.

Acclimatization↗
PubMed1986

Bath rewarming from immersion hypothermia.

Trunk-only bath rewarming has often been recommended over whole-body bath rewarming as a method for the treatment of immersion hypothermia. At present, no report of a direct comparison of the relative merits of these techniques has been made. Authorities in favor of trunk-only bath rewarming base their proposal on the assumption that core temperature afterdrop would be minimized by preventing peripheral vasodilation when the subject's limbs are not immersed in the rewarming bath. In the present study, trunk-only and whole-body bath rewarming are compared by rewarming eight mildly hypothermic male subjects twice, once via each technique. It was concluded that trunk-only rewarming is not superior to whole-body bath rewarming as a therapy for mild immersion hypothermia, based on the findings that no significant differences existed between the two techniques, either in size or duration of core temperature afterdrop, or in rate of rewarming.

Adult↗
PubMed2001

The immunophilin ligand FK506 attenuates the axonal damage associated with rapid rewarming following posttraumatic hypothermia.

Our laboratory has shown that traumatically induced axonal injury (TAI) is significantly reduced by posttraumatic hypothermia followed by slow rewarming. Further, TAI can be exacerbated by rapid rewarming, and the damaging consequences of rapid rewarming can be reversed by cyclosporin A, which is believed to protect via blunting mitochondrial permeability transition (MPT). In this communication, we continue investigating the damaging consequences of rapid posthypothermic rewarming and the protective role of immunophilin ligands using another member of the immunophilin family, FK506, which does not affect MPT but rather inhibits calcineurin. Rats were subjected to impact-acceleration brain injury followed by the induction of hypothermia with subsequent rapid or slow posthypothermic rewarming. During rewarming, animals received either FK506 or its vehicle. Three hours postinjury, animals were prepared for the visualization of TAI via antibodies targeting impaired axoplasmic transport (APP) and/or overt neurofilament alteration (RMO-14). Rapid rewarming exacerbated TAI, which was attenuated by FK506. This protection was statistically significant for the APP-immunoreactive fibers but not for the RMO-14-positive fibers. Combined labeling, using one chromagen to visualize both axonal changes, suggested that these two immunoreactive profiles revealed two distinct pathologies not occurring along the same axon. Collectively, these studies confirmed previous observations identifying the adverse consequences of rapid rewarming while also showing the complexity of the pathobiology of TAI. Additionally, the demonstration that FK506 is protective suggests that calcineurin may be a major target for neuroprotection.

Animals↗
PubMed1997

[Determination of core body temperature. A comparison of esophageal, bladder, and rectal temperature during postoperative rewarming].

OBJECTIVE: The data of 60 postoperatively sedated and ventilated patients were studied for analysis of oesophageal, bladder, and rectal temperatures. The purpose of the investigation was to clarify whether changes of oesophageal temperature are adequately reflected by bladder and rectal temperatures and whether the rate of rewarming has an influence on the accuracy of the latter two sites. METHODS: For temperature recording, a Hi-Lo Temp esophageal stethoscope (Mallinckrodt Medical), a Foley FC400-18 catheter temperature sensor (Respiratory Support Products, Mallinckrodt Medical), and a rectal temperature probe N401 (YSI) were used. Each probe and matching recording unit was calibrated over a range of 30-40 degrees C against a reference quartz thermometer (Hewlett packard Model 2801 A) in a thermostated water bath before the investigation. Five measuring points distributed over the whole period of rewarming were evaluated. Patients were assigned to groups with slow and fast rewarming, respectively. Agreement between the methods of measurement was assessed as described by Bland and Altman. Furthermore, differences between the oesophageal and bladder or rectal temperature were checked at each measuring point for statistical significance using the t-test. RESULTS: In regard to oesophageal temperature, the bladder and rectal temperatures had biases of -0.01 degree C and -0.03 degree C, respectively. Limits of agreement (+/- s) were +/-0.68 degree C and +/-0.82 degree C, respectively. The bias of the bladder temperature was independent of the rate of rewarming (Fig. 3). The bias of the rectal temperature, however, differed in regard to the rewarming rate, being +0.06 degree C in the group with slow rewarming and -0.13 degree C in the group with fast rewarming (Tables 1 and 2, Fig. 1 and 2). These differences were significant for the measuring points 4 and 5 (Fig. 4). CONCLUSIONS: Bladder and rectal temperatures can accurately indicate the oesophageal temperature with a very small bias in postoperatively sedated and ventilated patients. Since the rate of rewarming influences the accuracy of rectal temperature readings, monitoring of bladder temperature seems to be more favourable in the postoperative period.

Body Temperature↗