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

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

Patients at risk for clinically significant bleeding and who require urgent or emergent surgical procedures are encountered. Usually local causes are responsible, but a generalized hematologic defect may be uncovered. Quickly and effectively distinguishing the cause may be critical to rapid treatment and survival. A careful history, appropriate use of laboratory tests (e.g., partial thromboplastin time, prothrombin time, and platelet count), and knowledge of possible causes are key to prompt diagnosis and treatment. Bleeding from multiple sites, spontaneous bleeding, or unexpectedly severe bleeding suggests a systemic process. Immunocompromised or suppressed patients or systemically ill patients with chronic hepatic renal, lymphatic, and hematologic disorders are seen with urgent surgical problems. The key is rapid diagnosis and effective systemic and local therapy to counter the problem. The syndrome of diffuse "medical bleeding" frequently confronts the surgeon treating a patient who has received transfusions of more than 1.5 times blood volume. The coagulation defect is almost always associated with hypothermia and acidosis. Treatment consists in control of large-vessel bleeding by appropriate surgical techniques, blunt packing, and tamponade of diffuse bleeding, rapid rewarming of the patient, and adequate resuscitation for shock. Transfusion of platelets and fresh frozen plasma is empiric initially and subsequently guided by the clinical and laboratory coagulation profiles of the patient.
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PMID:Emergency surgery in hematologic patients. 886 72

A porcine model of hemorrhagic shock was used to study the effect of hypothermia on hemodynamic, metabolic, and coagulation parameters. The model was designed to simulate the events of severe blunt injury with hemorrhage occurring initially, to a systolic blood pressure of 30 mm Hg, followed by simultaneous hemorrhage and crystalloid volume replacement, followed by cessation of hemorrhage and blood replacement. Half of the animals were rendered hypothermic by external application of ice, and half remained normothermic. There was seven pigs in each group. Two deaths occurred in each during the hemorrhage phase. The hypothermic pigs demonstrated larger reduction in cardiac output than normothermic pigs. Volume replacement in the normothermic group restored cardiac output to baseline values. In the hypothermic group, cardiac output remained depressed despite volume replacement. Prothrombin times and partial thromboplastin times showed significantly more prolongation in the hypothermic group. Furthermore, this was not corrected by replacement of shed blood in the hypothermic group, as was seen in the normothermic group. We conclude that when shock and hypothermia occur together, their deleterious effect on hemodynamic and coagulation parameters are additive. The effects of hypothermia persist despite the arrest of hemorrhage and volume replacement. Thus, it is necessary to aggressively address both shock and hypothermia when they occur simultaneously.
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PMID:Hypothermia-induced coagulopathy during hemorrhagic shock. 1077 71

It often takes longer to achieve hemostasis when performing an operation on a patient in cerebral hypothermia therapy than in a normal patient, despite the lack of abnormal clinical blood coagulation findings, and this study was conducted to investigate the cause of delays in coagulation in patients with hypothermia. In this study, 93 samples of plasma were collected at our center from 10 patients(7 men and 3 women; mean age, 33.7) who were in cerebral hypothermia therapy with a urinary bladder temperature maintained at 32-34 degrees C. Each sample was divided into two, and PT(prothrombin time) and APTT(activated partial thromboplastin time) were measured at the normal analysis temperature of 37 degrees C in one sample, and at the hypothermia temperature of 32-34 degrees C in the other sample. The results showed that PT and APTT tended to shorter at 37 degrees C, than those measured at 32-34 degrees C. Thus, we suggest that it is necessary to regulate the temperature of patients with accidental hypothermia or in whom hypothermia therapy is performed.
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PMID:[Clinical data obtained through coagulation testing suggests that hypothermia exerts influence on a patient's blood coagulation reaction]. 1121 18

In management of severe trauma patients, trauma surgeons need to decide which patients are eligible for damage control. Such decision may be supported by utilizing models that predict the patient's outcome. The study described in this paper investigates the possibility to construct patient outcome prediction models from retrospective patient's data at the end of initial damage control surgery by using feature mining and machine learning techniques. As the data used comprises rather excessive number of features, special attention was paid to the problem of selecting only the most relevant features. We show that a small subset of features may carry enough information to construct reasonably accurate prognostic models. Furthermore, the techniques used in our study identified two factors, namely the pH value when admitted to ICU and the worst partial active thromboplastin time, to be of highest importance for prediction. This finding is pathophysiologically reasonable and represents two of three major problems with severe trauma patients, metabolic acidosis, hypothermia, and coagulopathy.
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PMID:Feature mining and predictive model construction from severe trauma patient's data. 1151 64

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.
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PMID:Successful treatment of uterine torsion in a cat with severe metabolic and haemostatic complications. 1171 4

Massive haemorrhage in elective surgery can be either anticipated (e.g. organ transplantation) or unexpected. Management requires early recognition, securing haemostasis and maintenance of normovolaemia. Transfusion management involves the transfusion of packed red cells, platelet concentrates and plasma (fresh frozen plasma and cryoprecipitate). Blood product support should be based on clinical judgment and be guided by repeated laboratory tests of coagulation. Although coagulation tests may not provide a true representation of in vivo haemostasis, they do assist in management of haemostatic factors. Below critical levels (prothrombin time or activated partial thromboplastin time >1.8; fibrinogen <1.0 g/l; platelet count < 80 x 10(9) 1(-1)) it is difficult to achieve haemostasis. Despite seemingly adequate blood component therapy there remain situations where haemorrhage is uncontrollable. In this setting, alternative approaches must be considered. These include the use of other blood products (e.g. prothrombin complex concentrates; fresh whole blood; fibrin glue) and pharmacological agents (e.g. aprotinin). Complications of massive transfusion result in significant morbidity and mortality. These may be secondary to the storage lesion of the transfused blood products, disseminated intravascular coagulation, hypothermia or hypovolaemic shock. The use of fresh blood products and leucocyte-reduced packed red cells and platelets, may minimise some of the adverse clinical sequelae.
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PMID:Massive blood transfusion in the elective surgical setting. 1220 74

The initial aim in massive transfusion (MT) is to supply crystalloids, colloids, and plasma-poor red cell concentrates (RCCs) to maintain normovolemia and oxygen supply. This frequently leads to dilution coagulopathy, which is frequently aggravated and accelerated by hypothermia, acidosis, shock-induced impairment of liver function and disseminated intravascular coagulation (DIC), and increased consumption of clotting factors and platelets at extensive wound sites. Disorders of hemostasis deteriorate the prognosis of massively transfused patients dramatically. Therefore, the second therapeutic objective is the timely administration of plasma and platelet concentrates as required to halt the microvascular bleeding (MVB) induced by impaired hemostasis. Close laboratory monitoring, to include as a minimum platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen, is essential to identify hemostatic disorders requiring therapeutic intervention. Coagulopathy promoting microvascular bleeding can be assumed when PT or APTT values exceed 1.5 times mean controls and/or when fibrinogen levels fall below 1.0 g/l. Repeated rapid infusion of 10-15 ml plasma per kg of body weight will be required to raise clotting factor levels significantly and to achieve adequate hemostasis. The turnaround time for obtaining laboratory results and for readying plasma for transfusion must be taken into particular consideration in cases of rapid blood loss.
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PMID:Indications for plasma in massive transfusion. 1237 88


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