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

Sublethal doses of vincristine (VNC) and bacterial lipopolysaccharide (LPS) administered simultaneously to adult male mice resulted in markedly enhanced mortality. All of 10 strains of Pseudomonas aeruginosa tested, 4 of 7 strains of Bacteroides, and 6 of 10 strains of Listeria monocytogenes were able to substitute for purified LPS in enhancing mortality in VNC-treated mice. Inoculation of mice with each of 10 strains of Pseudomonas, each of 7 strains of Bacteroides, and about half of the 10 strains of Listeria tested elicited increased resistance to the lethal action of purified LPS. The patterns of responses of mice receiving a lethal combination of 2 mg of LPS/kg and 1 mg of VNC/kg resembled those of mice receiving a lethal dose of 10 mg of VNC/kg alone or 15 mg of LPS/kg alone with respect to (i) serum glutamic pyruvate transaminase activity, (ii) hematocrit values, and (iii) thrombocytopenia. The patterns of responses of mice receiving a lethal combination of LPS and VNC resembled those of mice receiving a lethal dose of LPS alone with respect to (i) hypothermia, (ii) retention of sulfobromophthalein, (iii) fibrinogen level, (iv) prothrombin activity, (v) blood urea nitrogen levels, and (vi) time of death. These data are consistent with the proposition that the combination of VNC and LPS produces a fatal renal failure. Histological studies confirmed that there was extensive renal damage in mice treated with lethal doses of LPS alone or a lethal combination of LPS and VNC.
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PMID:Enhanced toxicity for mice of combinations of bacterial lipopolysaccharide and vincristine. 94 80

Hypothermic patients commonly develop coagulopathy, but the effects of hypothermia on coagulation remain unclear because clinical laboratories routinely perform clotting tests only at 37 degrees C. Measurements of activated partial thromboplastin times (APTT), prothrombin times (PT), and thrombin times (TT) were performed on plasma from normothermic and hypothermic rats at a range of temperatures (25 degrees-37 degrees C) to assess the effects of hypothermia on apparent clotting factor levels and clotting factor activities. In general, clotting times were more severely prolonged when test temperatures were hypothermic than when body temperatures were hypothermic. Indeed, little to no prolongation resulted from body hypothermia alone. These findings reveal the observed disparity between clinically evident hypothermic coagulopathy and near-normal clotting studies. Clotting studies performed at 37 degrees C will not confirm hypothermic coagulopathy. These results indicate that the appropriate treatment for hypothermia-induced coagulopathy is rewarming rather than administration of clotting factors.
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PMID:The disparity between hypothermic coagulopathy and clotting studies. 140 19

Planned intra-abdominal packing for surgically uncontrollable hemorrhage from liver and retroperitoneal injuries exacerbated by hypothermia, acidosis, and coagulopathy regained popularity over the past decade. The authors reviewed 39 patients injured between August 1985 and September 1990; 31 packed for liver injuries, eight for nonliver injuries. The overall mortality rate was 44% (17/39); 9 (23%) exsanguinated, 3 (8%) died of head injuries, 3 (8%) of multisystem organ failure, 2 (5%) of late complications. The mean age was 33.9 +/- 16.2 (range, 16 to 79); there were 26 men and 13 women. Relaparotomy for pack removal was performed 2.0 +/- 1.1 days (range, 1 to 7) after initial operation. The authors identified intraoperative risk factors of pH less than or equal to 7.18, temperature less than or equal to 33 C, prothrombin time greater than or equal to 16, partial thromboplastin time greater than or equal to 50, and transfusion of 10 units or more of blood as highly predictive of outcome. Patients with four to five risk factors (n = 3) had a 100% mortality rate (p less than 0.04); two to three risk factors (n = 12), 83% mortality rate (p less than 0.003), compared with zero to one risk factors (n = 24), 18% mortality rate. Complications developed in six of 22 survivors (27%): 5 abdominal abscesses (23%), 2 wound dehiscences (9%), and 2 enterocutaneous fistulae (9%). Intra-abdominal packing will not stop all bleeding; 23% of the patients exsanguinated. In 77%, packing helped achieve hemostasis we believed was not otherwise possible. Packing may be done to prevent the development of acidosis, hypothermia, and coagulopathy or may be done early in the treatment of cold, acidotic patients rather than massive transfusion in the face of surgically uncorrectable bleeding.
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PMID:Abdominal packing for surgically uncontrollable hemorrhage. 161 83

Previous studies of hypothermia and blood coagulation have focused on alterations in the levels of blood clotting elements using coagulation tests performed under normothermic conditions. However, because of the enzymatic nature of activated clotting factors, hypothermia should also be expected to affect clotting factor activities. Multiple determinations of activated partial thromboplastin times (APTT), prothrombin times (PT), and thrombin times (TT) were performed on commercially available normal human plasma at assay temperatures similar to those encountered clinically (25-37 degrees C). Both the APTT and the PT were significantly prolonged at temperatures below 35 degrees C (P less than 0.05). Clotting time correlated significantly with assay temperature in a negative exponential fashion for all three tests (r = -0.97 for APTT, -0.93 for PT, -0.71 for TT, P less than 0.001 for all regressions). Clotting time prolongation appears proportional to the number of enzymatic steps involved. These data indicate that the coagulopathy observed during hypothermia is, in part, independent of clotting factor levels.
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PMID:Hypothermia and blood coagulation: dissociation between enzyme activity and clotting factor levels. 225 17

In an attempt to assess the changes occurring to the coagulation profile during internal active core rewarming with partial cardiopulmonary bypass (CPB) without heparin anticoagulation, five pigs were anesthetized, and a model for severe to moderate hypothermia was created. Femoral-femoral bypass with Bio-Pump, heat exchanger, and a membrane oxygenator were used during the rewarming for 64.8 +/- 8.5 minutes. There were no statistically significant changes in platelet count, platelet index, activated clotting time (ACT), partial thromboplastin time (PTT), prothrombin time (PT), fibrinogen, fibrinogen index and fibrin split products (p greater than 0.05). There were no thromboembolic sequelae seen at autopsy. The components of the CPB circuit showed no signs of formation of aggregates or thrombi. The results of this study are attributed to the nonthrombogenic, atraumatic design of the Bio-Pump and the enhanced physiological fibrinolysis seen in the first hour of CPB. We concluded that heparinless CPB may serve as a safe alternative for active core rewarming for severe to moderate hypothermia.
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PMID:Heparinless extracorporeal bypass for treatment of hypothermia. 229 71

In the present study, an effort was made to establish the procedure for 60 minutes selective profound hypothermia below 20 degrees C of the abdominal viscera. In 6 mongrel dogs, hemodynamic changes were investigated during 60 minutes normothermic vascular exclusion of the abdominal viscera by occluding the aorta and inferior caval vein just above the diaphragm. Hemodynamic state just after the combined occlusion of these vessels was stable, but 60 minutes occlusion was followed by hypoperfusion of the cranial half of the body. In 15 mongrel dogs, the 60 minutes selective profound hypothermia below 20 degrees C of the abdominal viscera was performed after occluding these vessels with an aid of extracorporeal circuit. Pooled blood in the splanchnic region during hypothermia was warmed and drained to jugular vein to maintain the hemodynamic state in the cranial half of the body. Twelve of 15 dogs survived 2 weeks after the procedure with minimal hepatic damage. In 7 mongrel dogs, blood coagulation system was investigated. Decrease of platelet, fibrinogen, plasminogen, anti-thrombin III, prothrombin and cold insoluble globulin concentration, elongation of prothrombin time and partial thromboplastin time, and elevation of FDP occurred during and after the selective profound hypothermia. But these changes were self limiting and recovered soon after heparin neutralization. In 9 mongrel dogs, extended pancreatectomy with splenectomy and combined resection of portal vein using selective profound hypothermia was performed. Bleeding and splanchnic congestion during extended pancreatectomy was minimum. Five of 9 dogs survived 2 weeks with slight hepatic and renal damage.
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PMID:[Experimental studies on the selective profound hypothermia of the abdominal viscera by descending aorta and inferior caval vein occlusion]. 667 63

The haemostatic status of twenty children with cyanotic and acyanotic cardiopathies was studied before, during and after cardiopulmonary bypass (CPB) under deep hypothermia and haemodilution. Eleven patients had various haemostatic troubles before surgery. Haemodilution with a crystalloid solution to an haematocrit of 21,8 vol. +/- 1,3% resulted in a severe lowering of all coagulation factors. Forced diuresis after CPB induced partial normalization. The observed alterations included moderate thrombocytopenia, prolongation of the prothrombin time, transient decrease of factors V and plasminogen, elevation of fibrin degradation products (FDP), significant lowering of factor VII-X, marked elevation of factor VIII and mild increase of fibrinogen. No correlation was found between coagulation abnormalities and postoperative bleeding, duration of CPB or type of cardiopathies. It is concluded that CPB with haemodilution proves as safe as more conventional approaches in respect to coagulant activities.
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PMID:Haemostatic changes during open heart surgery with extracorporeal circulation and deep hypothermia in children. 708 21

Hypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series of 36 patients with severe head injuries (Glasgow Coma Scale 3-7) enrolled in a prospective, randomized, clinical trial of therapeutic moderate hypothermia. Patients were randomized to a normothermic group (n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of injury (n = 20). Prothrombin times, partial thromboplastin times, and platelet counts were obtained in the emergency room and then again within 24 hours of randomization. Delayed traumatic intracerebral hemorrhage occurred in 6 of 20 (30%) hypothermic patients and 5 of 16 (31%) normothermic patients. In the hypothermic group, 9 of 17 patients had an increased prothrombin time during hypothermic therapy, as opposed to 11 of 16 in the normothermic group during the corresponding time period. The partial thromboplastin time was prolonged in 2 of 17 hypothermic patients and 2 of 16 normothermic patients. Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.
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PMID:The effect of hypothermia on the incidence of delayed traumatic intracerebral hemorrhage. 817 85

Definitive laparotomy (DL) for penetrating abdominal wounding with combined vascular and visceral injury is a difficult surgical challenge. Physiologic derangements such as dilutional coagulopathy, hypothermia, and acidosis often preclude completion of the procedure. "Damage control" (DC), defined as initial control of hemorrhage and contamination followed by intraperitoneal packing and rapid closure, allows for resuscitation to normal physiology in the intensive care unit and subsequent definitive re-exploration. The purpose of the study was to compare the damage control technique with definitive laparotomy. Over a 3 1/2-year period, 46 patients with penetrating abdominal injuries required laparotomy and urgent transfusion of greater than 10 units packed red blood cells for exsanguination. Medical records were retrospectively reviewed for degree and pattern of injury, probability of survival, actual survival, transfusion requirements for the preoperative and postoperative phases, resuscitation and operative times, lowest perioperative temperature, pH, and HCO3. No significant differences were identified between 22 DL and 24 DC patients and actual survival rates were similar (55% DC vs. 58% DL). However, in a subset of 22 patients with major vascular injury and two or more visceral injuries (maximum injury subset), otherwise similar to the overall group, survival was markedly improved in patients treated with damage control (10 of 13, 77%*) vs. DLM (1 of 9, 11%) (Fisher's exact test, * p < 0.02). In preparation for return to the operating room, DC survivors averaged 8.4 units of packed red blood cells transfused and 10.3 units fresh frozen plasma over a mean ICU stay of 31.7 hours. Resolution of coagulopathy (mean prothrombin time/partial thromboplastin time 19.5/70.4 to 13.3/34.9), normalization of acid-base balance (mean pH/HCO3 7.37/20.6 to 7.42/24.2), and core rewarming (mean 33.2 degrees C to 37.7 degrees C) were achieved. All patients had gastrointestinal procedures at reoperation (mean operative time, 4.3 hours). We conclude that damage control is a promising approach for increased survival in exsanguinating patients with major vascular and multiple visceral penetrating abdominal injuries.
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PMID:'Damage control': an approach for improved survival in exsanguinating penetrating abdominal injury. 837 Dec 95

The occurrence of bleeding in trauma patients is a life-threatening problem which can be explained by different mechanisms. The infusion of cristalloids, colloids, packed red blood cells, or even fresh frozen plasma is very rarely responsible for bleeding but it can contribute to dilute the patient's platelet pool, and especially dilutional thrombocytopenia is the first cause of bleeding after massive transfusion. Blood coagulation factor activity is decreased after a massive fluid infusion is performed but it has to reach a dramatically low plasma level in order to induce troubles. It has to be emphasized that colloids and especially dextrans can impair the patient's haemostasis by interfering the same way with the factor VIII-von Willebrand complex and fibrin formation. Gelatins do not interfere with platelets or with the coagulation system. A third mechanism that can explain the strong link between haemostasis and haemodilution is the haemostatic role of red cells. It has been shown in experimental models that red cells play a definite function in promoting platelet accretion on the damaged vessel surface. Higher values of haematocrit (Ht) are responsible for a better platelet adhesion On the opposite, platelet adhesion decreases when low values of Ht (< 20%) are reached. Hypothermia can also impair platelet function and worsen the bleeding. A simplified monitoring of haemostasis can be proposed with platelet count, whole blood coagulation clotting time, immediately available activated partial thromboplastin time and prothrombin time with bedside portable monitors and thromboelastography. Haematocrit and body temperature have to be monitored as well.
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PMID:[Traumatic emergencies and hemostasis]. 856 76


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