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The identification of hypothermia as the cause of death remains challenging in forensic pathology because of unspecific radiological, morphological, and biochemical results. Hyperemia, edema, and petechial hemorrhages within the cerebral parenchyma were described in cases of death by hypothermia. On the other hand, the effect of low temperatures in the brain has been speculated to cause local injuries on a cellular level with potential occurrences of necrosis and inflammation. In the study herein described, endocan, alkaline phosphatase, neuron-specific enolase, S100 protein subunit B, glial fibrillary acidic protein, and C-reactive protein were measured in postmortem serum from femoral blood and cerebrospinal fluid in a series of hypothermia fatalities and control cases. The combination of data collected failed to identify a specific biochemical profile for death by hypothermia in postmortem serum and/or the cerebrospinal fluid, thus suggesting that an alternative panel of brain damage biomarkers indicative of diffuse hypoxic brain injury needs to be defined in hypothermia fatalities.

Objective: To determine whether hypothermia within 24 hours of sepsis diagnosis is associated with development of persistent lymphopenia, a feature of sepsis-induced immunosuppression., Design: Retrospective cohort study., Setting: A 1,200-bed university-affiliated tertiary care hospital., Patients: Adult patients diagnosed with bacteremia and sepsis within 5 days of hospital admission between January 1, 2010, and July 31, 2012., Interventions: None., Measurements and Main Results: Leukocyte counts were recorded during the first 4 days following sepsis diagnosis. Persistent lymphopenia was defined as an absolute lymphocyte count less than 1.2 cells/μL×10(3) present on the fourth day after diagnosis. Of the 445 patients with sepsis included, hypothermia developed in 64 patients (14.4%) (defined as a body temperature<36.0°C) within 24 hours of sepsis diagnosis. Hypothermia was a significant independent predictor of persistent lymphopenia (adjusted odds ratio, 2.70 [95% CI, 1.10, 6.60]; p=0.03) after accounting for age, disease severity, comorbidities, source of bacteremia, and type of organism. Compared with the nonhypothermic patients, hypothermic patients had higher 28-day (50.0% vs 24.9%, p<0.001) and 1-year mortality (60.9% vs 47.0%, p=0.001)., Conclusions: Hypothermia is associated with higher mortality and an increased risk of persistent lymphopenia in patients with sepsis, and it may be an early clinical predictor of sepsis-induced immunosuppression.

Background: Hypothermia, which can result from tissue hypoperfusion, body exposure, and transfusion of cold resuscitation fluids, is a major factor contributing to coagulopathy of trauma and surgery. Despite considerable efforts, the mechanisms of hypothermia-induced blood coagulation impairment have not been fully understood. We introduce a kinetic modeling approach to investigate the effects of hypothermia on thrombin generation., Methods: We extended a validated computational model to predict and analyze the impact of low temperatures (with or without concomitant blood dilution) on thrombin generation and its quantitative parameters. The computational model reflects the existing knowledge about the mechanistic details of thrombin generation biochemistry. We performed the analysis for an "average" subject, as well as for 472 subjects in the control group of the Leiden Thrombophilia Study., Results: We computed and analyzed thousands of kinetic curves characterizing the generation of thrombin and the formation of the thrombin-antithrombin complex (TAT). In all simulations, hypothermia in the temperature interval 31°C to 36°C progressively slowed down thrombin generation, as reflected by clotting time, thrombin peak time, and prothrombin time, which increased in all subjects (P < 10(-5)). Maximum slope of the thrombin curve was progressively decreased, and the area under the thrombin curve was increased in hypothermia (P < 10(-5)); thrombin peak height remained practically unaffected. TAT formation was noticeably delayed (P < 10(-5)), but the final TAT levels were not significantly affected. Hypothermia-induced fold changes in the affected thrombin generation parameters were larger for lower temperatures, but were practically independent of the parameter itself and of the subjects' clotting factor composition, despite substantial variability in the subject group. Hypothermia and blood dilution acted additively on the thrombin generation parameters., Conclusions: We developed a general computational strategy that can be used to simulate the effects of changing temperature on the kinetics of biochemical systems and applied this strategy to analyze the effects of hypothermia on thrombin generation. We found that thrombin generation can be noticeably impaired in subjects with different blood plasma composition even in moderate hypothermia. Our work provides mechanistic support to the notion that thrombin generation impairment may be a key factor in coagulopathy induced by hypothermia and complicated by blood plasma dilution.

Background: Hypothermia may be accidental or therapeutic. Therapeutic hypothermia is increasingly used as treatment for various conditions, e.g., neuroprotection after cardiac arrest. Hypothermia leads to an impairment of the coagulation system, but the degree of impairment has been difficult to determine. Most studies have been performed on plasma instead of whole blood. We therefore evaluated whole blood investigating the effects of hypothermia on the coagulation system over a wide range of temperatures (25-40 degrees C)., Methods: Blood was drawn from six healthy volunteers into citrated test tubes. Samples were then placed in water baths with temperatures ranging from 25 to 40 degrees C for 30 min before the coagulation system was studied using rotational thromboelastometry. A contact activator (Ellagic acid) was used for initiation of coagulation. Clotting time, clot formation time, alpha angle, and maximum clot strength were measured. All tests were run for 60 min and they were performed at the same temperature as the temperature in the water bath., Results: Coagulation was increasingly impaired with decreasing temperatures in the temperature range studied. All variables measured were significantly impaired in a stepwise pattern (P < 0.0001)., Conclusions: Evaluation using a whole blood analysis shows that hypothermia progressively impairs the coagulation system.

Background: Hypothermia and hemorrhagic shock contribute to coagulopathy after trauma. In this study, we investigated the independent and combined effects of hypothermia and hemorrhage with resuscitation on coagulation in swine and evaluated clinically relevant tests of coagulation., Methods: Pigs (n = 24) were randomized into four groups of six animals each: sham control, hypothermia, hemorrhage with resuscitation, and hypothermia, hemorrhage with resuscitation combined. Hypothermia to 32 degrees C was induced with a cold blanket. Hemorrhage was induced by bleeding 35% of total blood volume followed by resuscitation with lactated Ringer's solution. Coagulation was assessed by thrombin generation, prothrombin time (PT), activated partial thromboplastin time (aPTT), activated clotting time (ACT), and thrombelastography (TEG) from blood samples taken at baseline and 4 hour after hypothermia and/or hemorrhage with resuscitation. Data were compared with analysis of variance., Results: Baseline values were similar among groups. There were no changes in any measurements in the control group. Compared with baseline values, hemorrhage with resuscitation increased lactate to 140% +/- 15% (p < 0.05). Hypothermia decreased platelets to 73% +/- 3% (p < 0.05) with no effect on fibrinogen. Hemorrhage with resuscitation reduced platelets to 72% +/- 4% and fibrinogen to 71% +/- 3% (both p < 0.05), with similar decreases in platelets and fibrinogen observed in the combined group. Thrombin generation was decreased to 75% +/- 4% in hypothermia, 67% +/- 6% in hemorrhage with resuscitation, and 75% +/- 10% in the combined group (all p < 0.05). There were no significant changes in PT or aPTT by hemorrhage or hypothermia. ACT was prolonged to 122% +/- 1% in hypothermia, 111% +/- 4% in hemorrhage with resuscitation, and 127% +/- 3% in the combined group (all p < 0.05). Hypothermia prolonged the initial clotting time (R) and clot formation time (K), and decreased clotting rapidity (alpha) (all p < 0.05). Hemorrhage with resuscitation only decreased clot strength (maximum amplitude [MA], p < 0.05). TEG parameters in the combined group reflected the abnormal R, K, MA, and alpha observed in the other groups., Conclusion: Hypothermia inhibited clotting times and clotting rate, whereas hemorrhage impaired clot strength. Combining hypothermia with hemorrhage impaired all these clotting parameters. PT, aPTT were not sensitive whereas ACT was not specific in detecting these coagulation defects. Only TEG differentiated mechanism related to clotting abnormalities, and thus may allow focused treatment of clotting alterations associated with hypothermia and hemorrhagic shock.

Background: Hypothermia and acidosis were reported to influence coagulopathy in different clinical settings. We evaluated whole blood coagulation to determine the effects of hypothermia and/or acidosis on hemostasis., Methods: Whole blood samples (3.000 microL) from 10 healthy volunteers (2 female, 8 male) were acidified by adding 40 microL of hydrochloric acid of increasing molarity to achieve a blood pH (alpha-stat) between 7.0 and 7.37, and coagulation was analyzed by rotational thromboelastometry after an incubation period of 30 min using both intrinsically (InTEM) and extrinsically (ExTEM) activated assays. To assess temperature-dependent effects, all tests were performed at blood/thromboelastometer temperatures of 30, 33, 36, and 39 degrees C, respectively. An additional extrinsically activated test with addition of cytochalasin D was performed to examine clot formation without platelet contribution., Results: Hypothermia at a normal pH produced an increased coagulation time [ExTEM: 65 s +/- 3.6 (36 degrees C) vs 85 +/- 4 (30 degrees C), P < 0.001; coagulation time, InTEM: 181 s +/- 10 (36 degrees C) vs 226 +/- 9, P < 0.001] and clot formation time [ExTEM: 105 s +/- 5 (36 degrees C) vs 187 +/- 6 (30 degrees C), P < 0.001]; clot formation time [InTEM: 101 s +/- 5 (36 degrees C) vs 175 +/- 7, P < 0.001], as well as decreased alpha angle [ExTEM: 65.6 +/- 1.8 (36 degrees C) vs 58 +/- 1.1, P < 0.01, P < 0.01; InTEM: 70.5 +/- 1.8 (36 degrees C) vs 60.2 +/- 1.5, P < 0.001]. Maximum clot firmness was significantly impaired only in InTEM assays [56.9 mm +/- 0.9 (36 degrees C) vs 52.7 +/- 0.9, P < 0.05]. In contrast, acidosis per se had no significant effects during normothermia. Acidosis amplified the effects of hypothermia, and synergistically impaired clotting times, alpha angle, and decreased maximum clot firmness, again in both extrinsically and intrinsically activated assays. Formation of a fibrin clot tested after abolition of platelet function by cytochalasin D was not impaired. Clot lysis decreased under hypothermic and/or acidotic conditions, but increased with hyperthermia., Conclusions: In this in vitro study, hypothermia produced coagulation changes that were worsened by acidosis whereas acidosis without hypothermia has no significant effect on coagulation, as studied by thromboelastometry. This effect was mediated by the inhibition of coagulation factors and platelet function. Thus, thromboelastometry performed at 37 degrees C overestimated integrity of coagulation during hypothermia in particular in combination with acidosis.

In trauma patients, continuous arteriovenous (AV) rewarming can effectively reverse hypothermia even if associated with hypovolemia. In battlefield conditions, however, portable fluid warmers driven by battery power show limited capacities. We studied the efficacy and safety of a portable fluid warmer that utilizes controlled hydrocarbon combustion (nonflame) for heat generation during continuous AV rewarming in a large animal model of hypothermia and hemorrhagic shock. Six dogs (26.1 +/- 0.8 kg) were cooled to a core temperature of 30 degrees C (hypo 1). After rewarming to 37 degrees C, dogs were bled by 20% of their estimated blood volume and cooled again to 30 degrees C (hypo 2) followed by rewarming. We recorded temperature (blood, esophageal, rectal, and bladder), left ventricular performance, hemodynamic parameters including superior mesenteric artery (SMA) flow and blood flow through the fluid warmer. Especially, we measured the effect of the AV-shunt on cardiac output and regional blood flow (superior mesenteric artery). Rewarming after hypothermia took 45 +/- 6 minutes (hypothermia 1) and 55 +/- 6 minutes (hypothermia 2), respectively. The AV-shunt flow was correlated to the cardiac output and affected neither cardiac output nor regional blood flow at any time point during the experiment. Arteriovenous rewarming, using the tested portable fluid warmer, effectively reversed hypothermia without compromising hemodynamics or regional blood flow.

Background: Recombinant activated factor VII (rFVIIa) is currently administered off-label to control diffuse coagulopathic bleeding of patients with traumatic injuries. These patients are often cold, acidotic, and coagulopathic upon arrival and each responds differently to rFVIIa therapy. This study investigated the effects of hypothermia on clotting and the potential benefit of rFVIIa administration on blood coagulation at different hypothermic temperatures., Method: Citrated blood samples were collected from eight healthy volunteers (20-45 years old) and incubated at 37 degrees C, 34 degrees C, 31 degrees C, and 28 degrees C for 30 minutes. rFVIIa (1.26 microg/mL equivalent to 90 microg/kg in vivo dose) or vehicle solution (saline) was added to each blood sample, incubated (10 minutes), and analyzed at the respective temperatures by standard coagulation tests and thrombelastography., Results: The clot reaction time of blood samples, measured as prothrombin time, activated partial thromboplastin time, and R time (thrombelastography analysis), was significantly prolonged at 31 degrees C or below compared with at 37 degrees C. The clot formation rate ([alpha] angle, maximum clotting velocity [Vmax]) was decreased at all cold temperatures. Maximum clot strength (maximum amplitude) was only affected (reduced) at 28 degrees C. Addition of rFVIIa shortened the prothrombin time, activated partial thromboplastin time, and R times at every temperature, surpassing the normal (37 degrees C) temperature values in 31 degrees C and 34 degrees C cold samples. Similarly, clot formation rate parameters (clotting time, [alpha] angle, Vmax) were also improved by rFVIIa addition and normothermic values were restored in 31 degrees C and 34 degrees C cold blood samples. rFVIIa did not affect maximum amplitude at any temperature., Conclusions: Mild to moderate hypothermia delayed the initial clot reaction and reduced clot formation rate without affecting ultimate clot strength. FVIIa effectively compensated for the adverse effects of hypothermia except in severe cases. These results suggest that administration of FVIIa should be beneficial in enhancing hemostasis in hypothermic trauma patients without the need for prior correction of the patient's body temperature.

Background: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control., Methods: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39 degrees C), acidotic (pH, 7.1; 39 degrees C), hypothermic (pH, 7.4; 32 degrees C), and acidotic and hypothermic (pH, 7.1; 32 degrees C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4 degrees C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved., Results: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47%, 57%, and 72% increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18% and 17% in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0%, 12.5%, and 5.7%, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-alpha and interleukin-6 in any group during the study., Conclusion: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.

Background: Hemorrhage is a major complication of trauma and often becomes more severe in hypothermic patients. Although it has been known that platelets are activated in the cold, studies have been focused on platelet behavior at 4 degrees C, which is far below temperatures encountered in hypothermic trauma patients. In contrast, how platelets function at temperatures that are commonly found in hypothermic trauma patients (32-37 degrees C) remains largely unknown, especially when they are exposed to significant changes in fluid shear stress that could occur in trauma patients due to hemorrhage, vascular dilation/constriction, and fluid resuscitation., Methods: Using a cone-plate viscometer, we have examined platelet activation and aggregation in response to a wide range of fluid shear stresses at 24, 32, 35, and 37 degrees C., Results: We found that shear-induced platelet aggregation was significantly increased at 24, 32, and 35 degrees C as compared with 37 degrees C and the enhancement was observed in whole blood and platelet-rich plasma. In contrast to observation made at 4 degrees C, the increased shear-induced platelet aggregation at these temperatures was associated with minimal platelet activation as determined by the P-selectin expression on platelet surface. Blood viscosity was also increased at low temperature and the changes in viscosity correlated with levels of plasma total protein and fibrinogen., Conclusion: We found that platelets are hyper-reactive to fluid shear stress at temperatures of 24, 32, and 35 degrees C as compared with at 37 degrees C. The hyperreactivity results in heightened aggregation through a platelet-activation independent mechanism. The enhanced platelet aggregation parallels with increased whole blood viscosity at these temperatures, suggesting that enhanced mechanical cross-linking may be responsible for the enhanced platelet aggregation.

Objective: Especially in pediatric patients with severe hypothermia, intraosseous access may be more readily available than intravascular access during an early phase of treatment and therefore, may be helpful to optimize management. The purpose of this study was to determine whether intraosseous blood gases are comparable with arterial, mixed venous, and sagittal sinus blood gases during different degrees of hypothermia., Design: Prospective, descriptive laboratory investigation using a porcine model., Setting: University hospital laboratory., Subjects: Twelve anesthetized, 12- to 16-wk-old domestic pigs weighing 30-35 kg., Interventions: Volume-controlled ventilated animals were instrumented with arterial, pulmonary artery, sagittal sinus, and 16-gauge intraosseous catheters. Blood samples were obtained from each site every 15 mins during surface cooling with crushed ice until mean +/- SEM core temperature decreased from 38.5+/-0.1 degrees C [101.3+/-0.2 degrees F] to 27+/-0.5 degrees C [80.5+/-0.9 degrees F] over 2 hrs., Measurements and Main Results: Intraindividual correlation of Pco2 and pH values were determined as the difference (delta) between intraosseous and reference blood samples. With hypothermia, absolute values of Pco2 decreased and pH increased in samples from all sites. At 27 degrees C, intraosseous--arterial delta P(CO2) and delta pH (mean +/- 95% confidence intervals) were 2.6+/-10.6 torr [0.35+/-1.4 kPa] and -0.11+/-0.07 units; intraosseous - mixed venous were 0.4+/-12.2 torr [0.05+/-1.6 kPa] and -0.06+/-0.08 units; and intraosseous - sagittal sinus were -7.3+/-16 torr [-0.97+/-2.1 kPa] and 0.001+/-0.14 units, respectively. Intraosseous Pco2 was not comparable to end-tidal values (deltaP(CO2) 17.4+/-14.6 torr [2.3+/-1.9 kPa]), and intraosseous lactate did not correlate with arterial, mixed venous, or sagittal sinus values., Conclusions: During hypothermia, intraosseous P(CO2) values were predictable for mixed venous Pco2 and arterial P(CO2). Intraosseous pH values also correlated with mixed venous and sagittal sinus blood samples. Accordingly, interpretation of blood gas values obtained from bone marrow aspirates may be helpful to adjust ventilation and optimize fluid and drug therapy during the early treatment of patients with severe hypothermia.

Objective: To determine if samples obtained from arterial and capillary sources are comparable in children with diverse pathologic conditions during their stay in a pediatric intensive care unit., Study Design: Prospective, descriptive study in patients admitted to a multidisciplinary pediatric intensive care unit., Interventions: Seventy-five simultaneous paired samples (arterial and capillary) were obtained from patients with different degrees of capillary reperfusion, hemodynamic stability, blood pressure, and temperature. Both samples were analyzed < or =5 mins after collection., Measurements and Main Results: The average correlations between arterial and capillary samples were 0.87 for pH, 0.86 for CO2, and 0.65 for oxygen. Neither poor perfusion nor low temperature altered the correlation for pH or CO2. The only condition that significantly affected the correlation was hypotension., Conclusion: Capillary blood sampling is a useful alternative to gasometric evaluation of critically ill children, even in the presence of hypothermia or hypoperfusion, provided that hypotension is not present.

Unlabelled: Moderate hypothermia (32-33 degrees C) occurs in anesthetic practice. However, intrapulmonary gas exchange and the effect of temperature correction of blood gases on oxygen and carbon dioxide exchange have not been investigated in these patients. We investigated alveolar-arterial difference in oxygen tension (AaDO2) and arterial to end-tidal difference in carbon dioxide (Pa-ETCO2) during rewarming of eight ASA physical status I patients from hypothermia of 32 degrees C. Anesthesia was maintained with fentanyl/propofol. AaDO2 and Pa-ETCO2 were assessed by analyzing arterial blood gases and saturated water vapor pressure, uncorrected or corrected to actual body temperature. The respiratory quotient (RQ) was measured by calorimetry. After temperature correction of blood gases and water vapor pressure, the AaDO2 was significantly higher at 33 and 32 degrees C compared with 36 degrees C (56 +/- 13 and 64 +/- 14 vs 39 +/- 10 mm Hg; P < 0.05 and P < 0.01). The deterioration of pulmonary oxygen exchange was not detected if arterial blood gases and water vapor pressure were not corrected. The RQ did not change during moderate hypothermia compared with 36 +/-C. The temperature-corrected Pa-ETCO2 was not affected by hypothermia. We conclude that AaDO2 is increased during moderate hypothermia. This is only detected when water vapor pressure and arterial blood gases are corrected to actual body temperature., Implications: We investigated intrapulmonary oxygen and carbon dioxide exchange during moderate hypothermia (32 degrees C) in eight patients. If oxygen, carbon dioxide, and water vapor pressure were corrected to actual body temperature, the alveolar-arterial oxygen tension difference was increased during hypothermia. The carbon dioxide tension difference and the respiratory quotient were unaffected by hypothermia.

Background: Mild hypothermia is accompanied by metabolic changes. Epidural local anesthetic agents attenuate the surgical stress response, but it is not known whether they modulate thermal stress., Methods: Thirty patients undergoing colorectal surgery, performed by one surgical team, received epidural 0.5% bupivacaine to achieve T3-S5 sensory block. They were then assigned randomly to two groups of 15 patients each. The control or unwarmed group was left to cool during surgery, whereas active warming was used in the warmed group. General anesthesia was induced by thiopentone, vecuronium, fentanyl, nitrous oxide in oxygen, and enflurane. At the end of surgery, both groups received epidural 0.25% bupivacaine to maintain a T5-L3 sensory block. Aural canal (core) and skin surface (15 sites) temperatures; oxygen consumption; pain visual analogue score; and concentrations of epinephrine, norepinephrine, glucose, cortisol, lactate, and free fatty acids in plasma were measured before epidural blockade, 30 min after epidural blockade, at the end of surgery, and for 4 h after surgery. Patients and those measuring the outcomes were unaware of group allocation., Results: Core and mean skin temperatures decreased significantly in the control group (P < 0.001) but not in the warmed group. Catecholamine concentrations in plasma decreased significantly after epidural block, and although concentration of epinephrine in plasma increased from baseline sharply in the control group at the end of surgery (P = 0.004), it decreased in the warmed group (P = 0.007). During recovery, there was no difference between the two groups for norepinephrine concentrations in plasma, body weight-adjusted oxygen consumption, pain visual analogue score, and metabolites., Conclusions: The postoperative metabolic changes obtained with epidural block were similar except for an attenuated concentration of epinephrine in normothermic patients compared with those who were mildly hypothermic.

Background: The coagulopathy noted in hypothermic trauma patients has been variously theorized to be caused by either enzyme inhibition, platelet alteration, or fibrinolytic processes, but no study has examined the possibility that all three processes may simultaneously contribute to coagulopathy, but are perhaps triggered at different levels of hypothermia. The purpose of this study was to determine whether, at clinically common levels of hypothermia (33.0-36.9 degrees C), there are specific temperature levels at which coagulopathic alterations are seen in each of these processes., Methods: Of 232 consecutive adult trauma patients presenting to a Level I trauma center, 112 patients met the inclusion criteria of an Injury Severity Score of 9 or greater and time since injury of less than 2 hours. Of the included patients, 40 were normothermic and 72 were hypothermic (> or =37 degrees C, n = 40; 36.9-36 degrees C, n = 29; 35.9-35 degrees C, n = 20; 34.9-34 degrees C, n = 16; 33.9-33 degrees C, n = 7). Included patients were prospectively studied with thrombelastography adjusted to core body temperature. Additionally, PT, aPTT, platelets, CO2, hemoglobin, hematocrit, and Injury Severity Score were measured., Results: Analysis by multivariate analysis of variance of the relationship between coagulation and temperature demonstrated that in hypothermic trauma patients, 34 degrees C was the critical point at which enzyme activity slowed significantly (p < 0.0001), and at which significant alteration in platelet activity was seen (p < 0.001). Fibrinolysis was not significantly affected at any of the measured temperatures (p > 0.25)., Conclusions: Patients whose temperature was > or =34.0 degrees C actually demonstrated a significant hypercoagulability. Enzyme activity slowing and decreased platelet function individually contributed to hypothermic coagulopathy in patients with core temperatures below 34.0 degrees C. All the coagulation measures affected are part of the polymerization process of platelets and fibrin, and this process may be the mechanism by which the alteration in coagulation occurs.

Background: Unintended hypothermia occurs frequently during surgery and may have adverse effects on the cardiovascular system. Although the mechanisms responsible for the cardiovascular manifestations of hypothermia are unclear, it is possible that they are sympathetically mediated. In this prospective study, relationships between body temperature, the neuroendocrine response, and hemodynamic changes in the perioperative period were examined., Methods: Seventy-four elderly patients, undergoing abdominal, thoracic, or lower extremity vascular surgical procedures, were randomly assigned to either "routine care" (n = 37) or "forced-air warming" (n = 37) groups. Throughout the intraoperative and early postoperative periods, the routine care group received standard thermal care, and the forced-air warming group received forced-air skin-surface warming. Core temperature, forearm minus fingertip skin-surface temperature gradient, and plasma concentrations of epinephrine, norepinephrine, and cortisol were measured throughout the perioperative period, and the two groups were compared. In addition, heart rate and arterial blood pressure were compared between groups., Results: The routine care and forced-air warming groups did not differ with regard to age, sex, type of surgical procedures, anesthetic techniques, or postoperative analgesia. Mean core temperature was lower in the routine care group on admission to the postanesthetic care unit (routine care, 35.3 +/- 0.1 degree C; forced-air warming, 36.7 +/- 0.1 degree C; P = 0.0001) and remained lower during the early postoperative period. Forearm minus fingertip skin-surface temperature gradient (an index of peripheral vasoconstriction) was greater in the routine care group in the early postoperative period. The mean norepinephrine concentration (pcg/ml) was greater in the routine care group immediately after surgery (480 +/- 70 vs. 330 +/- 30, P = 0.02) and at 60 min (530 +/- 50 vs. 340 +/- 30, P = 0.002) and 180 min (500 +/- 80 vs. 320 +/- 30, P = 0.004) postoperatively. Mean epinephrine concentrations were not significantly different between groups. Mean cortisol concentrations were increased in both groups during the early postoperative period (P < 0.01), but the differences between groups were not significant. Systolic, mean, and diastolic arterial blood pressures were significantly higher in the routine care group., Conclusions: Compared with patients in the forced-air warming group, patients receiving routine thermal care had lower core temperatures, a greater degree of peripheral vasoconstriction, higher norepinephrine concentrations, and higher arterial blood pressures in the early postoperative period. These findings suggest a possible mechanism for hypothermia-related cardiovascular morbidity in the perioperative period.

This in vivo study confirmed impaired hemostasis during hypothermia in a swine model. Group I (normothermic, n = 8) and group II (hypothermic, n = 8) animals were anesthetized and instrumented for continuous peritoneal irrigation and monitoring of heart rate and blood pressure. The effects of hypothermia, hypotension, and inotrope on bleeding time and bleeding from two types of arterial injuries were evaluated. Our findings were that (1) bleeding time was significantly prolonged in hypothermic animals; (2) the differences in blood loss from partially torn artery (PTA) and completely cut artery (CCA) at both normothermic and hypothermic temperatures did not reach statistical significance; and (3) blood loss from PTA was greater than CCA when norepinephrine (Levophed) was infused to elevate blood pressure in hypotensive animals at normal core temperature.

Background: Hypothermia occurs commonly during surgery and can be associated with increased metabolic demands during rewarming in the postoperative period. Although cardiac complications remain the leading cause of morbidity after anesthesia and surgery, the relationship between unintentional hypothermia and myocardial ischemia during the perioperative period has not been studied., Methods: One hundred patients undergoing lower extremity vascular reconstruction received continuous Holter monitoring throughout the first 24 h postoperatively. Myocardial ischemia was determined by a cardiologist masked to clinical variables. The patient's sublingual temperature on arrival at the intensive care unit immediately after the surgical procedure was used to divide the patients into two groups: hypothermic (temperature, < 35 degrees C; n = 33) and normothermic (temperature, > or = 35 degrees C; n = 67). The relationship between intentional hypothermia and myocardial ischemia occurring during the first postoperative day was evaluated by univariate and multivariate analyses., Results: A greater percentage of patients had electrocardiographic changes consistent with myocardial ischemia in the hypothermic group (36%, 12 of 33) compared with those in the normothermic group (13%, 9 of 67, P = 0.008). Preoperative risk factors for perioperative cardiac morbidity were similar between the two groups, except for patient age. The mean age was 70 +/- 2 yr and 62 +/- 1 yr in the hypothermic and normothermic groups, respectively (P = 0.001). When subgroup and multivariate analyses were used to adjust for differences in age, temperature remained an independent predictor of ischemia (odds ratio, 1.82 per degree Celsius; 95% confidence interval, 1.09-3.02). The incidence of postoperative angina was greater in the hypothermic group (18%, 6 of 33) than in the normothermic group (1.5%, 1 of 67, P = 0.002). The incidence of PaO2 < 80 mmHg in the arterial blood was greater in the hypothermic group (52%, 17 of 33) than in the normothermic group (30%, 20 of 67, P = 0.03)., Conclusions: Unintentional hypothermia is associated with myocardial ischemia, angina, and PaO2 < 80 mmHg during the early postoperative period in patients undergoing lower extremity vascular surgery.

The increased metabolic and respiratory demand during naloxone recovery from opioid-based anesthesia could be related to the return of thermoregulation in hypothermic patients and thus be avoided by preventing intraoperative hypothermia. In this study, we measured O2 uptake (VO2) during naloxone-induced recovery in two groups of patients to determine the effect of intraoperative heat loss on postoperative VO2 changes. In seven patients, intraoperative hypothermia was prevented (normothermic group), whereas hypothermia was allowed to develop in seven other patients (hypothermic group). Core and skin temperatures were measured throughout the study to calculate changes in body heat content. Before naloxone antagonism of fentanyl-supplemented anesthesia, core temperature (mean +/- SEM) was 36.8 +/- 0.1 degrees C in the normothermic group and 34.2 +/- 0.2 degrees C in the hypothermic group (P less than 0.001). After titrated administration of naloxone during recovery, VO2 and minute ventilation (VE) increased in the hypothermic group, by 114 +/- 37% and 97 +/- 52% respectively (P less than 0.05), with a three-fold increase in four patients. In the normothermic group, VO2 increased significantly less (25 +/- 5%), without any significant change in VE. The change in VO2 and VE was significantly greater in patients who were hypothermic. VO2 was integrated throughout the recovery period to calculate recovery energy expenditure. Recovery energy expenditure and intraoperative heat loss were highly correlated (r = 0.88; P less than 0.01). This study demonstrates that the metabolic and respiratory stresses associated with naloxone-induced recovery from opioid-based anesthesia depend on the intraoperative heat loss and can therefore be reduced by preventing intraoperative hypothermia.

Objective: To determine if there was a difference between reflection and transmission pulse oximeters in their ability to regain data display after hypothermia in patients recovering from open-heart surgery., Design: Prospective, randomized, controlled study., Patients: Nineteen adult patients scheduled for open-heart surgery were studied immediately after surgery in the ICU., Interventions: Transmission and reflection sensors were used in random order in two simultaneously monitoring identical oximeters and probes. The time difference at the start of display between the oximeters was measured and the skin temperatures in the region of the probes, cardiac index, systolic BP, pulse pressure, and systemic vascular resistance index were recorded., Results: The mean skin temperatures at the probe sites differed significantly (p = .001) at the moment of data acquisition. The mean forehead, ear lobe, and fingertip temperatures (simultaneously measured) were 33.9 degrees C, 31.8 degrees C, and 28.8 degrees C, respectively. The hemodynamic variables were comparable at the moment when the oximeters resumed display. The reflection probe was the first to resume function in 12 patients and the transmission probe was the first to resume function in four patients (p less than .02). The bias of the reflection probe was 1.4% (SD 2.2) and that of the transmission probe was -0.4% (SD 2.7). All the patients were normoxic throughout the study., Conclusion: The forehead reflection probe regained signal detection earlier than the transmission probe on the ear lobe in patients with compromised peripheral blood flow and cool periphery. This finding may be due to higher skin temperature at the reflection probe site, since the systemic hemodynamic conditions were equal at the time of the data acquisition of both sensors.

Oxygen tension, oxyhemoglobin saturation, and pH were measured in arterial and in venous blood from heart, brain, kidney, liver, gut and pulmonary artery in anesthetized hypoxemic dogs during a reduction of blood oxygen affinity due to increasing acidosis caused by the administration of CO2 and NH4Cl (pH range 7.40-6.80). In dogs with hypoxemia due to right to left shunt (anastomosis between inferior vena cava and left atrium), a reduction in blood oxygen affinity was followed by increasing Pao2 and Pvo2 at unchanged Sao2. In dogs with hypoxemia caused by alveolar hypoxia, or a combination of alveolar hypoxia and right to left shunt, a reduction of blood oxygen affinity was followed by arterial and venous desaturation at unchanged Pao2 values. Infusions of sodium bicarbonate or blood transfusions with reduced 2,3-diphosphoglycerate (2,3-DPG)-concentrations, if given to patients suffering from hypoxemia due to right to left shunt, may reduce the Pao2. Such therapy should be prescribed with caution.