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Activated cytokine production in patients with accidental hypothermia.

We have demonstrated recently that therapeutic moderate hypothermia of 32-33 degrees C, induced by surface cooling under the administration of narcotics, sedatives and muscle relaxant, suppresses cytokine production after traumatic brain injury. We present here the first documented case report of augmented cytokine production in two accidental hypothermia patients, unconscious 84- (acute immersion) and 87- (non-immersion) year-old women, whose rectal temperatures were below 28 degrees C. The victims were artificially ventilated after sedation with midazolam and buprenorphine in accordance with our protocol. Rewarming at the rate of approximately 1 degrees C/h was done by blowing forced-air with appropriate fluid resuscitation. Plasma interleukin(IL)-6 and/or IL-8 levels were measured using ELISA in the patients. In both patients, plasma IL-6 levels on admission were already elevated and the cytokine levels further increased during and after the rewarming period. In the patient with the poorer prognosis, the plasma IL-8 level on admission was not elevated remarkably but after rewarming the level rose significantly. Augmented IL-6 production in accidental hypothermia was sustained for 6 days in the patient with the poorer prognosis but not in the subject with good recovery, who was treated with anti-thrombin III in the early phase. Since the mechanisms for developing accidental hypothermia were different, simple comparisons between the two cases should be limited. But, these findings may suggest a need for testing a hypothesis whether cytokine modulation could be a therapeutic approach worthy of consideration. The results presented here also suggest that in hypothermia, changes in cytokine release may vary depending on procedures such as the anesthetic drugs used, the duration of the therapy, or the rate of rewarming from hypothermia.

Aged↗

Cold-induced apoptosis in isolated rat hepatocytes: protective role of glutathione.

Liver conservation for transplantation is usually made at 2-4 degrees C. We studied the effect of rewarming to 37 degrees C for up to 3 h of rat hepatocytes kept at 4 degrees C for 20 h, modulating intracellular glutathione (GSH) concentration either with a GSH precursor (N-acetyl-L-cysteine, NAC), or with GSH depleting agents (diethylmaleate and buthionine sulfoximine, DEM/BSO). Untreated hepatocytes showed time-dependent production of reactive oxygen species (ROS), lipid peroxidation, chromatin condensation and membrane blebbing, decrease in GSH concentration, and protein sulfhydryl groups. Fluorochromatization with Propidium Iodide (PI) and Annexin V (AnxV) of cells rewarmed for 1 h caused an increase of AnxV-positive cells without PI staining and any observed lactate dehydrogenase leakage. TUNEL and DNA-laddering tests were negative for all times and treatments, indicating that apoptosis may occur without DNA fragmentation. Cold preservation and rewarming in the presence of NAC induced a significant improvement in the morphology, less oxidative stress and apoptosis. Conversely, DEM/BSO caused a marked deterioration of morphology, increase of oxidative stress and apoptosis. These results suggested that marked changes in GSH status might play a critical role in triggering apoptosis during cold preservation of isolated rat hepatocytes. NAC, added before rewarming, might represent a therapeutic approach for preventing the early events of apoptosis during cold storage.

Acetylcysteine↗

Effect of mild hypothermia during cardiopulmonary bypass on erythrocytic hemoglobin oxygen delivery.

OBJECTIVES: To observe and define the degree of change in hemoglobin oxygen affinity induced by hypothermic extracorporeal circulation (ECC). DESIGN: A prospective, nonrandomized, observational study. SETTING: A single university medical center. PARTICIPANTS: Seventeen patients presenting for elective cardiac surgery. INTERVENTIONS: Systemic hypothermia during ECC. MEASUREMENTS AND MAIN RESULTS: During and after ECC, simultaneous arterial and mixed-venous whole-blood samples were obtained and immediately analyzed for gas tensions and hemoglobin saturation. Samples were obtained during the following times on ECC: initially after cardiopulmonary bypass onset during normothermia (37 degrees C), after cooling to 32 degrees C, and after rewarming to 37 degrees C. A fourth sample was obtained 10 to 20 minutes after discontinuation of cardiopulmonary bypass. Extracorporeal pump flow and thermodilution-determined cardiac output were also recorded for calculation of oxygen delivery and consumption. Mixed-venous results were used to calculate in vivo the blood gas tension at which hemoglobin was 50% saturated with oxygen (P50). There were no differences in P50 for the 17 patients by analysis of variance (ANOVA) for repeated measures with paired t-test with Bonferroni correction. Furthermore, no change in P50 was observed during the course of cooling and rewarming in any individual patient's samples. Oxygen delivery decreased after hypothermia and rewarming from mild hypothermia; oxygen consumption was decreased after rewarming and markedly increased after discontinuation from ECC. CONCLUSION: Mild hypothermia to 32 degrees C during ECC does not result in in vivo alterations in oxyhemoglobin dissociation and thus does not induce changes in oxygen delivery to peripheral tissues. However, oxygen usage appears to be markedly increased after cardiopulmonary bypass.

Adult↗

Analysis of factors related to jugular venous oxygen saturation during cardiopulmonary bypass.

OBJECTIVE: To investigate preoperative clinical conditions and/or intraoperative physiologic variables related to jugular venous oxygen saturation (SjO2) during cardiopulmonary bypass (CPB). DESIGN: Prospective study. SETTING: General hospital, single institution. PARTICIPANTS: One hundred forty patients (52 women, 88 men) who underwent coronary artery bypass grafting. MEASUREMENTS AND MAIN RESULTS: The authors measured SjO2 at five times during surgery. Multiple stepwise regression analysis showed a significant correlation of SjO2 with (1) arterial carbon dioxide partial pressure (PaCO2) before CPB (standard regression coefficient [(SC)] = 0.435), (2) cerebral perfusion pressure (CPP) during initiation of CPB (SC = 0.259), (3) PaCO2, tympanic temperature (TT), bubble oxygenator, and cerebral small infarctions (CSIs) during hypothermic CPB (SC = 0.507, -0.237, -0.192, and -0.189, respectively), (4) CPP, PaCO2, CSIs, and bubble oxygenator during rewarming (SC = 0.476, 0.294, -0.220, and -0.189, respectively), and (5) PaCO2 after CPB (SC = 0.480; p < 0.01). Correlation coefficients between SjO2 and CPP during rewarming were 0.40 (0.46 without CSI and 0.37 with CSI; p < 0.01). These results indicate that the relationship between CPP and SjO2 was significant in patients with CPP less than 40 mmHg during rewarming. CONCLUSION: During rewarming, when cerebral perfusion and oxygen demand change abruptly, but not during stable hypothermic CPB, CPP was a significant factor related to sjO2.

Aged↗

Hemodynamic and echocardiographic effects of hemofiltration performed during cardiopulmonary bypass.

OBJECTIVE: To evaluate the effects of hemofiltration performed during rewarming before emergence from cardiopulmonary bypass on hemodynamic and echocardiographic parameters. DESIGN: Prospective randomized study; blind analysis of echocardiographic parameters and hemodynamic parameters. SETTING: Single-center study performed in a university hospital. PARTICIPANTS: Two groups of 13 adult patients undergoing coronary artery bypass graft surgery. INTERVENTION: Patients were randomized to conventional procedure or hemofiltration performed with a polysulfone hemofilter. Hemofiltration, started at the time of rewarming on cardiopulmonary bypass, was performed with a flow rate adjusted to achieve an ultrafiltrate volume of 15 mL/kg on completion of rewarming. MEASUREMENTS AND MAIN RESULTS: Hemodynamic (systemic mean arterial pressure, right atrial pressure, heart rate) and echocardiographic parameters (shortening fraction, segmental kinetic score, cardiac output, systemic vascular resistance) were measured before and after hemofiltration and on arrival in the intensive care unit. Heart rate and cardiac index were increased significantly in both groups during the postoperative period. In the control group, systemic vascular resistance was decreased significantly, and cardiac index was increased during the postoperative period, together with significant alterations of segmental kinetic score and shortening fraction. In the hemofiltration group, systemic vascular resistance remained unchanged, associated with a significantly improved segmental kinetic score compared with the control group. CONCLUSIONS: Hemofiltration performed during rewarming before emergence from cardiopulmonary bypass is associated with stability of hemodynamic parameters and improved segmental myocardial kinetics.

Adult↗

Oxygen consumption after hypothermic cardiopulmonary bypass: the effect of continuing a propofol infusion postoperatively.

OBJECTIVE: To evaluate the effect of a fixed rate of infusion of propofol on total body oxygen consumption during the postoperative rewarming phase after cardiopulmonary bypass. DESIGN: Prospective, randomized, controlled study. SETTING: Cardiac intensive care unit, university hospital. PARTICIPANTS: Twenty-four male and female patients undergoing elective first-time coronary artery bypass graft surgery. INTERVENTIONS: Total body oxygen consumption was measured using a pulmonary artery catheter and thermodilution during postoperative rewarming. Twelve patients had propofol infused at 2 mg/kg/h for 4 hours or until rewarmed. MEASUREMENTS AND MAIN RESULTS: Total body oxygen consumption was reduced in the propofol group compared with the control group. Oxygen consumption was a median of 30.0 mL/min/m(2) less in the patients receiving propofol (p = 0.01). One patient receiving propofol shivered compared with 4 in the control group (p = 0.14). CONCLUSION: Administration of propofol during postoperative rewarming reduces total body oxygen consumption and may reduce shivering.

Anesthetics, Intravenous↗

Regional oxygenation and systemic inflammatory response during cardiopulmonary bypass: influence of temperature and blood flow variations.

OBJECTIVE: To evaluate the role of target temperature (28 degrees or 34 degrees C) in cardiac surgery on regional oxygenation during hypothermia and rewarming and systemic inflammatory response. DESIGN: Prospective, controlled, and randomized clinical study. SETTING: University hospital. PARTICIPANTS: Elderly patients (mean age 70 +/- 2 years) with acquired heart disease with an anticipated bypass time exceeding 120 minutes (n = 30). INTERVENTIONS: The patients were cooled to either 28 degrees C (n = 15) or 34 degrees C (n = 15). At hypothermia, bypass blood flow was reduced twice from full flow (2.4 L/min/m(2) body surface area [BSA]) to 2.0 L/min/m(2). MEASUREMENTS AND MAIN RESULTS: Hepatic and jugular venous oxygen tension and saturation were higher at 28 degrees C than at 34 degrees C. In comparison with the preoperative values, at 28 degrees C hepatic venous values were higher; whereas at 34 degrees C, they were lower. The reduction of pump blood flow during hypothermia, from 2.4 to 2.0 L/min/m(2)was accompanied by reductions of central, jugular, and hepatic oxygenation at both target temperatures. During rewarming, central and regional venous oxygenation decreased irrespective of the preceding temperature. The decrease was most pronounced in hepatic venous blood, with the lowest individual values <10%. Serum concentrations of C3a and IL-6 increased during hypothermia and increased further during rewarming irrespective of the preceding temperature. CONCLUSION: During cardiopulmonary bypass, hypothermia at 28 degrees C increases regional and central venous oxygenation better than at 34 degrees C. In contrast, venous oxygenation decreases during rewarming irrespective of the preceding temperature. No significant difference in the systemic inflammatory response associated with target temperature was detected.

Aged↗

Posttraumatic hypothermia is neuroprotective in a model of traumatic brain injury complicated by a secondary hypoxic insult.

OBJECTIVE: Human traumatic brain injury frequently results in secondary complications, including hypoxia. In previous studies, we have reported that posttraumatic hypothermia is neuroprotective and that secondary hypoxia exacerbates histopathologic outcome after fluid-percussion brain injury. The purpose of this study was to assess the therapeutic effects of mild (33 degrees C) hypothermia after fluid-percussion injury combined with secondary hypoxia. In addition, the importance of the rewarming period on histopathologic outcome was investigated. DESIGN: Prospective experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTION: Intubated, anesthetized rats underwent normothermic parasagittal fluid-percussion brain injury (1.8-2.1 atmospheres) followed by either 30 mins of normoxia (n = 6) or hypoxic (n = 6) gas levels and by 4 hrs of normothermia (37 degrees C). In hypothermic rats, brain temperature was reduced immediately after the 30-min hypoxic insult and maintained for 4 hrs. After hypothermia, brain temperature was either rapidly (n = 6) or slowly (n = 5) increased to normothermic levels. Rats were killed 3 days after traumatic brain injury, and contusion volumes were quantitatively assessed. MEASUREMENTS AND MAIN RESULTS: As previously shown, posttraumatic hypoxia significantly increased contusion volume compared with traumatic brain injury-normoxic animals (p <.02). Importantly, although posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (p <.03) reduced contusion volumes, compared with hypoxic normothermic rats. CONCLUSIONS: These data emphasize the beneficial effects of posttraumatic hypothermia in a traumatic brain injury model complicated by secondary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.

Analysis of Variance↗

Very hot intravenous fluid in the treatment of hypothermia.

The efficacy and safety of very hot (65 degrees C/149 degrees F) intravenous fluid (IVF) were compared with those of conventional warm (38 degrees C/100.4 degrees F) IVF in the treatment of hypothermia. Eight anesthetized beagles (11-20 kg) were studied. Blood pressure (BP), pulse (P), and core temperature (cT degrees) were recorded at baseline, during hypothermia, and during rewarming. The plasma free hemoglobin (PFHg) was measured to assess hemolysis. Each subject was cooled to 32 degrees C/89.6 degrees F and assigned to receive either 65 degrees C or 38 degrees C IVF via a specially designed multiport balloon-tipped catheter in the superior vena cava (SVC). The IV fluid rate was 80% of the blood volume per hour. Conventional rewarming methods were used in all subjects. After 2 hours the subjects were killed and the SVC was examined for injury. The rate of rewarming was 2.9 degrees C/hour in the 65 degrees C IVF group and 1.25 degrees C/hour in the 38 degrees C IVF group. The cT degrees was significantly different in all subjects after 1 (35.2 degrees +/- 1.03 degrees C vs. 33.2 degrees +/- 0.5 degrees C; p < 0.006) and 2 (37.6 degrees +/- 1.17 degrees C vs. 34.3 degrees +/- 0.9 degrees C; p < 0.004) hours of rewarming. The BP, P, and PFHg were not different. Visual examination of the SVC revealed two lesions in the 65 degrees C IVF group and one in the 38 degrees C group. Mechanical or thermal injury could not be differentiated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Coagulation defects resulting from ambient temperature-induced hypothermia.

Ambient temperature-induced hypothermia noted in trauma patients is frequently accompanied by a bleeding diathesis despite "laboratory normal" coagulation values. To document this impression, the following experiment was conducted. Coagulation studies and platelet function studies were performed in ten minipigs during induced whole body hypothermia (40 degrees C to 34 degrees C) and rewarming. Cooling was achieved in 2 to 3 hours and rewarming took 4 to 5 hours. In addition, similar coagulation and platelet function studies were conducted on plasma samples from the same animals that were cooled and then rewarmed in a water bath. Platelet counts and function as measured by Sonoclot analysis and aggregation did not decrease significantly with hypothermia in either model. Plasma cooled in a water bath demonstrated abnormal PT and aPTT (p < 0.001). Whole body hypothermia demonstrated abnormal bleeding time and PT (p < 0.001). Ambient temperature-induced hypothermia produced significant coagulation defects in a porcine model. Some of the coagulation defects were most pronounced during rewarming.

Animals↗

Important aspects in the treatment of severe accidental hypothermia: the Innsbruck experience.

The purpose of this paper is to review important aspects in the treatment of accidental hypothermia, based on our own experience in rewarming 55 patients with severe accidental hypothermia and a core temperature < 30 degrees C. We used three different methods of rewarming, adjusted to the patients' hemodynamics: airway rewarming, warmed fluids and insulation in patients with stable hemodynamics (group 1, n = 24), peritoneal dialysis in patients with unstable hemodynamics (group 2, n = 7) and extracorporeal circulation in patients with cardiocirculatory arrest (group 3, n = 24). Survival rates were 100% (group 1), 72% (group 2) and 13% (group 3) retrospectively. Published data supporting our strategy and alternative approaches are reviewed. The method used to rewarm a patient with severe accidental hypothermia should be adjusted to the hemodynamic status. The prognosis is excellent in patients in whom no hypoxic event precedes hypothermia and no serious underlying disease exists.

Adult↗

Moderate hypothermia may be detrimental after traumatic brain injury in fentanyl-anesthetized rats.

OBJECTIVES: To determine whether transient, moderate hypothermia is beneficial after traumatic brain injury in fentanyl-anesthetized rats. DESIGN: Prospective, randomized study. SETTING: University-based animal research facility. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: All rats were intubated, mechanically ventilated, and anesthetized with fentanyl (10 microg/kg intravenous bolus and then 50 microg.kg(-1).hr(-1) infusion). Controlled cortical impact was performed to the left parietal cortex, followed immediately by 1 hr of either normothermia (brain temperature 37 +/- 0.5 degrees C) or hypothermia (brain temperature 32 +/- 0.5 degrees C). Hypothermic rats were rewarmed gradually over 1 hr. Fentanyl anesthesia and mechanical ventilation were continued in both groups until the end of rewarming (2 hrs after traumatic brain injury). MEASUREMENTS AND MAIN RESULTS: Histologic assessment performed 72 hrs after traumatic brain injury was the primary outcome variable. Secondary outcome variables were physiologic variables monitored during the first 2 hrs after traumatic brain injury and plasma catecholamine and serum fentanyl concentrations measured at the end of both hypothermia and rewarming (1 and 2 hrs after traumatic brain injury). Contusion volume was larger in hypothermic vs. normothermic rats (44.3 +/- 4.2 vs. 28.6 +/- 4.0 mm, p <.05), but hippocampal neuronal survival did not differ between groups. Physiologic variables did not differ between groups. Plasma dopamine and norepinephrine concentrations were increased at the end of hypothermia in hypothermic (vs. normothermic) rats (p <.05), indicating that hypothermia augmented the systemic stress response. Similarly, serum fentanyl concentrations were higher in hypothermic (vs. normothermic) rats at the end of both hypothermia and rewarming (p <.05), demonstrating that hypothermia reduced the clearance and/or metabolism of fentanyl. CONCLUSIONS: Moderate hypothermia was detrimental after experimental traumatic brain injury in fentanyl-anesthetized rats. Since treatment with hypothermia has provided reliable benefit in experimental traumatic brain injury with inhalational anesthetics, these results indicate that the choice of anesthesia/analgesia after traumatic brain injury may dramatically influence response to other therapeutic interventions, such as hypothermia. Given that narcotics commonly are administered to patients after severe traumatic brain injury, this study may have clinical implications.

Anesthesia, Intravenous↗

Effects of sympathetic stimulation during cooling on hypothermic as well as posthypothermic hemodynamic function.

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n=7) were cooled to 15 degrees C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 microg/min Epi, i.v., for 1 h during cooling to 28 degrees C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 degrees C. Group 2 served a saline solution control. At 37 degrees C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 degrees C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 degrees C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 degrees C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.

Anesthesia↗

Phosphorylation of c-Jun N-terminal kinase in human hepatoblastoma cells is transiently increased by cold exposure and further enhanced by subsequent warm incubation of the cells.

During a cold preservation and reperfusion process of organs, cells are exposed to two major stresses, i.e. changes in oxygen concentration and temperature. c-Jun N-terminal kinase (JNK) /stress-activated protein kinase is activated by various stresses through its phosphorylation. Although hypoxia and subsequent reoxygenation is known to activate JNK, little is known about effects of hypothermia and subsequent rewarming on JNK activation. Thus, we investigated the activation of JNK in human hepatoblastoma (HepG2) cells exposed to a temperature of 5 degrees C and in those rewarmed at 37 degrees C. Western blot analysis using an anti-phospho-JNK antibody revealed that p54 JNK was transiently phosphorylated in cold-stressed cells. In addition, the phosphorylation of p54 JNK was further increased by rewarming of the cells. Since translational and transcriptional abilities were markedly reduced in the cold-stressed cells, effects of translation and transcription inhibitors on the phosphorylation of p54 JNK were determined. Cycloheximide, but not actinomycin D, increased the phosphorylation of p54 JNK in HepG2 cells. These results suggest that hypothermia alone transiently increases the p54 JNK phosphorylation possibly through reduction of protein synthesis and that rewarming after hypothermia stimulates the phosphorylation of p54 JNK.

Apoptosis↗

Raynaud's phenomenon in vibration syndrome: the impact of cold feet on skin temperature and vasomotion of the hand after immersion in cold water.

Patients with vibration syndrome, suffering from Raynaud's phenomenon, are sensitive to cold. Rewarming time, after local cooling, is delayed. The present study evaluated whether rewarming of the hand after cooling is influenced by the temperature of the feet. In five Japanese patients (former forest workers) with vibration syndrome, suffering from Raynaud's phenomenon, and in five healthy controls, temperature changes of the hand after cooling were registered under the two test situations (on different days) with the feet immersed in water of 35 degrees C or 20 degrees C, respectively. In both patients and controls (in both groups, in four of five cases) rewarming of the hand after cooling was faster when the feet were immersed in cold water, compared with when the feet were immersed in warm water. In this test situation, the systemic thermoregulative counterreaction appears to be more important for rewarming of the hand after cooling than a possible synchronous passive reaction accompanying warming of the feet. A deliberate training of the systemic counterreaction may prove beneficial for patients with Raynaud's phenomenon.

Adult↗

Increase in leukotrienes in the coronary circulation by cooling: a study in the anesthetized dog.

Pentobarbital-anesthetized dogs were instrumented for hemodynamic measurements and cooled by heat exchange tubes. Through a catheter in the coronary sinus, blood samples were obtained and plasma leukotrienes measured using a high-pressure liquid chromatography technique. Hemodynamic function was significantly reduced during cooling, and during subsequent rewarming hemodynamic function was only partly restored. Leukotriene C4 and B4 were significantly increased at a body core temperature of 31 degrees C and 25 degrees C during cooling but not during rewarming (28 degrees C) and after rewarming (37 degrees C). This indicates that during decreasing body temperature elevated leukotriene levels may increase vascular permeability, inflammation, and vasoactivity and counteract temperature-dependent decrease in these functions. Disturbed microcirculation may thus diminish cardiac recovery during rewarming.

Animals↗

[Treatment of accidental hypothermia].

New knowledge about accidental hypothermia acquired in recent years may simplify treatment and aid the evaluation of prognosis. Evidence of death or severe collapse due to the feared afterdrop has not been published. Afterdrop is a phenomenon of conductive heat loss. Evaluation of rewarming techniques shows that results from forced air rewarming techniques are equivalent to or better than results from invasive rewarming methods, except for rewarming with cardiopulmonary bypass. In hypothermia the most important differential diagnosis is death. Patients who are cold and could be resuscitated must be differentiated from patients, who are cold because they are dead. Experience from abroad has shown that extreme hyperkalaemia may be a useful diagnostic tool.

Accidents↗

[Treatment of severe, accidental hypothermia with a warm air bed].

Patients suffering from severe accidental hypothermia are by many authors recommended to be rewarmed by extra-corporal circulation. Some authors argue in favour of other approaches in treatment of severe hypothermia, as long as the patient has a sufficient circulation. One of these is rewarming using forced air warming. We rewarmed a patient with severe hypothermia using forced air warming. The patient arrived with a core temperature of 25.9 degrees C and had sufficient circulation despite of atrial fibrillation. The patient was rewarmed to a core temperature of 36.1 degrees C over seven hours. No other arrhythmias or complications were observed.

Accidents↗