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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An attempt was made to demonstrate the importance of increased perfusion of cold tissue in core temperature afterdrop. Five male subjects were cooled twice in water (8 degrees C) for 53-80 min. They were then rewarmed by one of two methods (shivering thermogenesis or treadmill exercise) for another 40-65 min, after which they entered a warm bath (40 degrees C). Esophageal temperature (Tes) as well as thigh and calf muscle temperatures at three depths (1.5, 3.0, and 4.5 cm) were measured. Cold water immersion was terminated at Tes varying between 33.0 and 34.5 degrees C. For each subject this temperature was similar in both trials. The initial core temperature afterdrop was 58% greater during exercise (mean +/- SE, 0.65 +/- 0.10 degrees C) than shivering (0.41 +/- 0.06 degrees C) (P < 0.005). Within the first 5 min after subjects entered the warm bath the initial rate of rewarming (previously established during shivering or exercise, approximately 0.07 degrees C/min) decreased. The attenuation was 0.088 +/- 0.03 degrees C/min (P < 0.025) after shivering and 0.062 +/- 0.022 degrees C/min (P < 0.025) after exercise. In 4 of 10 trials (2 after shivering and 2 after exercise) a second afterdrop occurred during this period. We suggest that increased perfusion of cold tissue is one probable mechanism responsible for attenuation or reversal of the initial rewarming rate. These results have important implications for treatment of hypothermia victims, even when treatment commences long after removal from cold water.
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PMID:A second postcooling afterdrop: more evidence for a convective mechanism. 144 67

This study determined the efficiency of a reflective blanket in preventing hypothermia during intra-abdominal gynecological procedures. Forty female patients were studied. A table of random numbers was used to assign patients to the reflective blanket group (experimental) or the warmed cotton blanket group (control). Esophageal and room temperatures were measured. Data were recorded regarding age, height, weight, body surface area, first-hour intravenous fluid volume, time from induction to skin incision and time from skin incision to peritoneal incision. The study showed no significant differences between groups in regard to esophageal or room temperatures (ANOVA, p greater than .05). No significant differences between groups in regard to patient characteristics were found (ANCOVA). No correlation was found between esophageal temperature and room temperature in either group. A significant decrease in esophageal temperatures was found in both groups during the first 45 minutes of the study (p less than .01), after which temperatures stabilized. In conclusion, the reflective blanket was no more efficient than warmed cotton blankets in preventing intraoperative hypothermia. Previous studies showing the greatest decrease in temperature occurred within the first hour of anesthesia and surgery were supported. The reflective blanket may be useful for operating rooms where the storage and heating of cotton blankets is not feasible due to limited space or cost.
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PMID:The efficiency of a reflective heating blanket in preventing hypothermia in patients undergoing intra-abdominal procedures. 237 37

Oesophageal temperature was recorded after induction of anesthesia, and further, at one, two and three hours. Temperature in the operation hall was continuously monitored. In relation to the temperature in the operating hall the effects on the patient were of three kinds: 1. operating halls with low temperatures (under 21 degrees C) where all the patients become hypothermic; 2. operating halls with an intermediate temperature (21-24 degrees C), where 67% of the patients remain normothermic; 3. operating halls with high temperatures (above 24 degrees C) where all the patients remain normothermic, although these temperatures are uncomfortable for the medical personnel, and increase the septic risk of the patient. When the oesophageal temperature of the patients falls by 0.5 degrees C chills will occur in 40% of the patients. Thermal falls of less than 0.5 degrees C will also determine chills but in only 10.5% of the cases. Immediate postanesthesia chills are also recorded in normothermic patients, but there is a direct relationship between the temperature in the operating hall, the degree of hypothermia and the frequency of chills, while the site of the surgery or the duration of the operation have but an unsignificant influence on intra-anesthetic temperature.
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PMID:[Intra-anesthetic hypothermia]. 253 99

Hypothermia is a well recognized consequence of severe injury, even in temperate climates, and the physiologic consequences of hypothermia are known to be detrimental. To analyze the frequency and risk factors for hypothermia and its effect on patient outcome, we prospectively studied 94 intubated injured patients at a regional trauma center during a 16-month period. Esophageal temperature probes were placed in the field or ER and core temperatures (T) were followed for 24 hours or until rewarming. Patients were designated as normothermic (greater than 36 degrees C), mildly hypothermic (34 degrees C-36 degrees C) or severely hypothermic (less than 34 degrees C) based on initial T. The risk factors for hypothermia evaluated included age, severity and location of injuries, blood alcohol level, blood transfusion requirements, and time spent in the field, ER, or OR. The average initial T was 35 degrees C, with no seasonal variation. Injury severity and survival correlated with severe hypothermia. Normothermic patients had an average ISS of 28 with a 78% survival. Severely hypothermic patients had an average ISS of 36 with a 41% survival (p less than 0.05). Patient age strongly correlated with outcome although there was no relationship between age and initial temperature. Sixty-two per cent of patients tested were positive for blood alcohol, and one half were legally intoxicated (BAC greater than 100 mg%). However, no consistent correlation was found between alcohol intoxication and initial temperature or patient survival. Blood transfusion requirements paralleled injury severity and patients receiving greater than 10 unit transfusions had significantly lower core temperature (p less than 0.05). The average temperature change was positive in the ER, OR, and ICU with time to rewarming correlating with the aggressiveness of warming measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence and effect of hypothermia in seriously injured patients. 365 63

Intraoperative hypothermia has become a common occurrence. Postoperative rewarming often is accompanied by shivering and results in increased metabolic and circulatory demands. We examined the metabolic, hemodynamic, and biochemical variables in 2 groups of hypothermic (greater than 35.8 degrees C) patients requiring mechanical ventilation after a major operation. One was observed during routine medical management whereas the other group received 40 mg of metocurine iodide and then observed during routine medical management. All patients were allowed to rewarm passively. O2 consumption (VO2, ml/min, STPD), CO2 production (VCO2, ml/min, STPD) and respiratory quotient (RQ) measurements were made every 15 min using a Beckman Metabolic Measurement Cart. Esophageal temperature, arterial blood pressure, heart rate (HR), rate pressure product, CVP, arterial blood gases, serum lactate concentration, and duration of shivering also were recorded. Suppression of the shivering by metocurine increased rewarming time significantly and decreased VCO2, VO2, HR, rate pressure product, mean arterial pressure (MAP), and the O2 cost of rewarming. Thus, the elimination of shivering during postoperative rewarming is associated with a decrease in caloric, metabolic demands and myocardial work (as assessed by the rate pressure product) while rewarming time is prolonged. In the postoperative, hypothermic, critically ill patient, suppression of the shivering response in selected patients may be indicated.
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PMID:Physiologic requirements during rewarming: suppression of the shivering response. 640 3

Forced-air warming is used for prevention or reversal of hypothermia in surgical patients. In the present study, the efficacy of this system for treatment of immersion hypothermia was evaluated. Six men and two women were twice immersed in 8 degrees C water until hypothermic. They were then rewarmed by either: 1) shivering-only inside a sleeping bag; or 2) forced-air warming. Esophageal and skin temperature, cutaneous heat flux and metabolism were measured. Afterdrop (+/- SD) during forced-air warming (0.43 +/- 0.26 degrees C) was approximately 30% less than during shivering (0.61 +/- 0.26 degrees C) (p < 0.001). Rewarming rate during forced-air warming (3.26 +/- 1.8 degrees C.h-1) was not significantly different from shivering (3.02 +/- 1.2 degrees C.h-1). Skin temperature was higher during forced-air warming by 3.7 degrees C early and 4.5 degrees C after 35 min of warming. Heat production increased by 77 W over the initial 20 min of shivering, and subsequently declined, compared to an immediate decrease with forced-air warming. During shivering heat flux ranged from 30 W early in rewarming, to 50 W after 35 min, compared to -237 W and -163 W respectively, for forced-air warming. Forced-air warming attenuated afterdrop and the metabolic stress of shivering while maintaining an average rate of rewarming comparable to shivering. Forced-air warming is a safe, simple, noninvasive treatment and could be used effectively in an emergency medical facility, and possibly in some rescue/emergency vehicles or marine vessels.
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PMID:Treatment of mild immersion hypothermia by forced-air warming. 781 48

A 68-year-old woman with an aneurysm of the distal arch involving an aberrant right subclavin artery was surgically treated successfully. Computed tomography suggested distal arch aneurysm with the abnormal branching of the arch vessels, which was confirmed as an aberrant right subclavian artery (ARSA) by angiogram. ARSA originated from Kommerell's aortic diverticulum and its orifice developed an aneurysmal change, which severely compressed esophagus and was thought to be the cause of preoperative dysphagia. Distal arch reconstruction was performed with woven Dacron graft using retrograde cerebral perfusion technique under deep hypothermia. Esophageal compression was satisfactorily released by resection of the aneurysm of ARSA which was reconstructed with the same material. Dysphagia disappeared postoperatively. Esophagogram showed no stenosis, and angiogram indicated successful distal arch and ARSA reconstructions.
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PMID:[Successful surgical treatment for distal arch aneurysm involving an aberrant right subclavian artery]. 892 31

Maintenance of pneumoperitoneum to perform laparoscopic surgery with carbon dioxide (CO2) could induce hypothermia. The authors assessed the mean body temperature (MBT) and changes in total body heat content (TBHC) under laparoscopic cholecystectomy. Thirty-six ASA I-II female patients underwent open cholecystectomy (Group-O, n = 18) or laparoscopic cholecystectomy (Group-L, n = 18). Esophageal temperature and four skin-surface temperatures were measured before induction and then every 10 minutes, and at arrival to the postanesthesia care unit. Operating room temperature was 22.9 +/- 1.2 degrees C. Operating time was as follows: G-O, 74 +/- 21 minutes; G-L, 94 +/- 16 minutes. After 60 minutes of surgery, decrease in TBHC was as follows: G-L = 54.9 kJ and G-O = 40.9 kJ. Decrease in MBT after 60 minutes intervention and at arrival to the postanesthesia care unit was as follows: G-L = 0.13 and 0.66 degree C and G-O = 0.17 and 0.49 degree C, respectively. There were no statistically significant differences between groups. Minor differences were attributed to longer surgery duration in the laparoscopic group.
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PMID:Can hypothermia be evidenced during laparoscopic cholecystectomy? 934 16

The purpose of this study was to determine the effects of adenosine agonists and an antagonist on ischemia-induced extracellular glutamate concentrations in an animal model of transient cerebral ischemia using in vivo cerebral microdialysis. Fifty New Zealand white rabbits were randomly assigned to one of five groups (normothermia, hypothermia, cyclopentyladenosine (CPA), theophylline, or propentofylline). Microdialysis probes were stereotactically placed in the dorsal hippocampus. Twenty minutes before the onset of ischemia, either 1 mg/kg CPA, 5 mg/kg propentofylline, or 20 mg/kg theophylline were administered intravenously. Esophageal temperature was maintained at 38 degrees C, except in the hypothermic animals, which were cooled to 30 degrees C throughout the entire experiment. Two 12-min periods of cerebral ischemia, separated by a 105-min interval of reperfusion, were produced by inflating a neck tourniquet. High-performance liquid chromatography was used to determine the glutamate concentration in the microdialysate. There were no significant increases in glutamate concentrations during the first ischemic period in any of the five groups. During the second ischemic episode, glutamate concentrations in the normothermic group peaked at levels approximately three times higher than the initial values. A similar pattern of changes in glutamate concentrations was observed in the CPA, propentofylline, and theophylline groups. In the hypothermic group, the concentrations of glutamate remained at baseline levels during the entire experiment. Contrary to expectations, neither the adenosine agonists (CPA, propentofylline) nor the antagonist (theophylline) had any effect on extracellular glutamate concentrations in the peri-ischemic period. Although adenosine and its analogs may be cerebroprotective agents, their mechanism of action is not fully understood. The data derived from this study indicates that the acute administration of such agents had no effect on ischemia-induced glutamate release within the hippocampus under these experimental conditions. Based on these results, further work is needed to compare in vivo versus in vitro experimental results in acute and long-term treatment studies with adenosine receptor agonists and antagonists.
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PMID:Effects of adenosine agonists and an antagonist on excitatory transmitter release from the ischemic rabbit hippocampus. 1092 82

The excessive release of glutamate during cerebral ischemia may play an important role in subsequent neuronal injury. Both lamotrigine and hypothermia have independently been shown to attenuate the release of glutamate. In this study, the authors sought to determine whether these effects were additive. Thirty-five New Zealand White rabbits were randomized to one of six groups: a normothermic control group; a lamotrigine-treated group; two hypothermic groups at 33 degreesC or 34.5 degreesC; or two groups treated with both hypothermia at 33 degreesC or 34.5 degreesC plus lamotrigine. Animals were anesthetized before implanting microdialysis probes in the hippocampus. Esophageal temperature was maintained at 38 degreesC in the control and lamotrigine groups, while the temperatures of animals in the hypothermia and hypothermia-plus-lamotrigine groups were cooled to 33 degreesC or 34.5 degreesC. Two 10 minute periods of global cerebral ischemia were produced by inflating a neck tourniquet. Levels of glutamate in the microdialysate were then determined using high-performance liquid chromatography. Extracellular glutamate concentrations increased only slightly from baseline during the first ischemic period. Glutamate levels during the second ischemic episode in the hypothermia-plus-lamotrigine group (34.5 degreesC) were significantly lower than those in the hypothermia group alone (34.5 degreesC), lamotrigine, or control groups (P < .01). The fact that mild hypothermia (34.5 degreesC) plus lamotrigine (20 mg/kg) together were more effective in inhibiting extracellular glutamate accumulation than hypothermia (34.5 degreesC) or lamotrigine (20 mg/kg) alone, suggests the potential for increased neuroprotection by the addition of lamotrigine to mild hypothermia.
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PMID:The combination of lamotrigine and mild hypothermia prevents ischemia-induced increase in hippocampal glutamate. 1129 51


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