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

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 reproducible experimental animal model of fulminant hepatic failure (FHF) resembling the clinical condition is needed. We have developed such a model in the rat by combining resection of the two anterior liver lobes (68% liver mass) with ligation of the right lobes pedicle (24% liver mass), resulting in liver necrosis; the remaining two omental lobes (8% liver mass) are left intact. Adult Sprague-Dawley rats (250-300 g) were used. Survival time was determined in 60 rats. Because maintenance of body temperature at 37 degrees C shortened survival time by half, FHF rats were not warmed during the postinduction period and were allowed to gradually enter a state of mild to moderate hypothermia (29-32 degrees C). Additionally, 42 FHF rats were killed in batches of six rats each 2, 6, 12, 18, 24, 30, and 36 hours postoperatively to evaluate changes in blood chemistry (glucose, lactate, liver function tests, prothrombin time) and to assess liver regenerative response in the residual omental liver lobes (weight, protein content, incorporation of bromodeoxyuridine [BrdU], expression of proliferation cell nuclear antigen [PCNA], mitotic activity), plasma levels of hepatocyte growth factor (HGF) and transforming growth factor beta (TGF-beta1), and tissue expression of the HGF and it's receptor c-met. Rats undergoing partial hepatectomy of 68% (PH; n = 42) and a sham operation (SO; n = 42) served as controls. All SO and PH controls survived. PH rats showed only transient decreases in body temperature, signs of modest early hepatic dysfunction (hyperlactemia, hyperammonemia, prolonged PT time), and normal restitution of liver mass. All FHF rats became comatose by 24 hours postoperatively. Most animals (90%) died within 24-48 hours postoperatively (mean, 39 +/- 11 hours). Changes in blood chemistry reflected rapid development of liver failure. Plasma HGF levels were markedly elevated and at all time points were higher than in PH controls (P < .05). At the same time, expression of HGF and c-met messenger RNA in the remnant liver was delayed. Plasma TGF-beta1 levels increased early (18 hours) and remained twofold to threefold higher than that of PH and SO controls (P < .05). There was only a 20% increase in the weight of the remnant liver lobes due to swelling. No hepatocytes stained positively for BrdU and PCNA, and none showed mitotic figures. In contrast, all PH controls showed vigorous liver regeneration. In conclusion, we have developed and characterized a novel model of FHF in rats that has a number of physiological and biochemical features seen clinically in FHF, including severely impaired ability of the residual liver tissue to regenerate.
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PMID:Fulminant hepatic failure in rats: survival and effect on blood chemistry and liver regeneration. 893 80

Whether febrile illnesses in the intensive care unit (ICU) have unique spectrum, etiologies, and outcome has not been determined in liver transplant recipients. We studied 78 consecutive febrile patients over a 4-yr period; 49% (38/78) were in the ICU and 51% (40/78) were in the non-ICU setting. Of febrile patients in the ICU, 87% (33/38) had infection and 13% had non-infectious etiology for fever. Seventy-nine percent (26/33) of the infections associated with fever in the ICU were bacterial, 9% (3/33) were viral, and 9% (3/33) were fungal in etiology. Pneumonia (30%), catheter-related bacteremia (15%), and biliary tree (9%) were the predominant sources of infections associated with fever in the ICU. Bacteremia was documented in 45% of the patients with fever in the ICU. Fifty-three percent (20/38) of the febrile episodes in the ICU occurred during the initial post-transplant stay, and 47% (18/ 38) during a subsequent readmission. Pneumonia accounted for 41% of all febrile infections during the first 7 d of ICU stay, but only 14% of those after 7 d. Febrile patients in the ICU had higher APACHE II scores (p = 0.001), higher APS scores (p = 0.0001), higher bilirubin (p = 0.001), lower cholesterol (p = 0.019), higher prothrombin time (p = 0.001), were more tachycardiac (p = 0.002), and were more likely to have abnormal blood pressure (p = 0.001) than those in the non-ICU setting. Twenty-three percent of all infections in the ICU were unaccompanied by fever and 9% were accompanied by hypothermia. Mortality at 14 d (24 versus 0%, p = 0.001) and at 30 d (34 versus 5%, p = 0.001) was significantly higher in febrile patients in the ICU, as compared to the patients in the non-ICU setting. These data have implications for diagnostic evaluation and management of critically ill febrile liver transplant recipients.
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PMID:Fever in liver transplant recipients in the intensive care unit. 1061 41

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

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

The purpose of the study is to comparatively evaluate the impact of normo- and hypothermic perfusion on acid-base balance (ABB), gas blood composition, metabolic parameters, and hemostasis. Fifty patients undergone multiple aortocoronary bypass under extracorporeal circulation (EC) were examined. Twenty four patients and 26 (Groups 1 and 2, respectively) had been operated on under normo- and hypothermia. The groups did not differ in age, body weight, the duration of an operation, the number of shunts, the time of EC, and myocardial ischemia. ABB, gas blood composition, the concentrations of hemoglobin, lactate, fibrinogen, prothrombin time, thrombin time, activated partial thromboplastin time, activated coagulation time, blood coagulation time as described by Leigh-White, the count of platelets, and ADP-induced platelet aggregation in the early postperfusion and postoperative periods, following 24 and 48 hours after surgery. There were no significant differences in the values of ABB, gas blood composition, blood lactate levels in patients from both groups. However, metabolic acidosis, elevated blood lactate concentrations were more frequently encountered in Group 2 patients, which suggests that hypothermia prduces a more aggressive effect on systemic homeostasis. Impact of normo- and hypothermia on the coagulative link of homeostasis was not revealed. Nevertheless, hypothermic EC halved the functional activity of platelets, which has a substantial effect on the size of postoperative blood loss.
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PMID:[Temperature regimen of extracorporeal circulation during aortocoronary bypass surgery]. 1261 Dec 98

Many pesticides are formulated in organic solvents. An example is amitraz, one of the formamidine groups of pesticidal chemicals. It is commonly used for the treatment of generalized demodicosis in dogs and for the control of ticks and mites in cattle and sheep. In this article, the clinical and laboratory findings of eight children with amitraz intoxication are reviewed. The purpose was to enlighten the findings of amitraz intoxication in children. Of the eight patients, five (62.5%) were boys, three (37.5%) were girls, and the ages ranged from 1 to 4 years. All children accidentally ingested amitraz orally, with no dermal exposure. The most common observed signs were decreased consciousness and bradycardia. Leukocytosis, hyperglycemia, hypernatremia, increased serum aspartate transaminase level, and prolonged partial prothrombin time were diagnosed in children. None of the children had hypothermia, hypotension, or convulsion and none of the patients died. The findings show that the initial signs and symptoms of acute amitraz intoxication appeared severe but they disappeared, with only supportive care needed in most cases within a few days.
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PMID:Report of eight children with amitraz intoxication. 1269 34

Vipera palaestinae (Vp), formerly a subspecies of the near east viper Vipera xanthina, is the most common poisonous snake in Israel and neighbouring countries (Jordan, Lebanon and Syria), and is responsible for most envenomations in humans and domestic animals. Hospital records were retrospectively reviewed for confirmed cases of Vp envenomations in dogs over a 13-year period and 327 cases were included in the study. Most envenomations occurred between May and October, and between 02:00 and 10:00 PM. The most frequent clinical signs included: local swelling and oedema (99.6%), viper teeth penetration marks (51%), tachypnoea (50%), panting (44%), increased body temperature (19.2%), tachycardia (>160/min, 19%), salivation (18%) and lameness (15.6%). Common haematological findings included: increased haematocrit (47%), increased haemoglobin concentration (45%), leucocytosis (39%), and thrombocytopenia (30%). The prothrombin time and activated partial thromboplastin time were prolonged in 68 and 21% of the dogs, respectively. Blood biochemistry abnormalities included increased activities of muscle enzymes, hyperglycaemia, hyperbilirubinaemia, hyperglobulinaemia and hypocholesterolaemia. The mortality rate was 4% (13 dogs). The following variables were significantly (p < 0.05) associated with mortality: body weight below 15 kg (p = 0.01), limb envenomation (0.008), envenomation at night (p = 0.025), severe lethargy (P < 0.001), hypothermia (p = 0.04), systemic bleeding (p = 0.001), shock (p = 0.007), dyspnoea (p = 0.002), tachycardia (p = 0.002), thrombocytopenia (p = 0.02), and glucocorticosteroid therapy (p = 0.002). Dogs younger than 4 years had a lower death risk (p = 0.01). The association of steroid therapy with increased mortality suggests that the use of steroids in Vp envenomations may be harmful. Specific antivenom therapy (10 ml/dog) was not associated with a higher survival rate, thus its use, dose and timing of administration should be further investigated.
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PMID:Vipera palaestinae envenomation in 327 dogs: a retrospective cohort study and analysis of risk factors for mortality. 1510 90

Hypoxic-ischemic injury may cause multisystem organ damage with significant aberrations in clotting, renal, and cardiac functions. Systemic hypothermia may aggravate these medical conditions, such as bradycardia and increased clotting times, and very little safety data in neonatal hypoxic-ischemic injury is available. This study reports a multicenter, randomized, controlled pilot trial of moderate systemic hypothermia (33 degrees C) vs normothermia (37 degrees C) for 48 hours in infants with neonatal encephalopathy instituted within 6 hours of birth or hypoxic-ischemic event. The best outcome measures of safety were determined, comparing rates of adverse events between normothermia and hypothermia groups. A total of 32 hypothermia and 33 normothermia neonates were enrolled in seven centers. Adverse events and serious adverse effects were collected by the study team during the hospital admission, monitored by an independent study monitor, and reported to Institutional Review Boards and the Data and Safety Monitoring Committee. The following adverse events were observed significantly more commonly in the hypothermia group: more frequent bradycardia and lower heart rates during the period of hypothermia, longer dependence on pressors, higher prothrombin times, and lower platelet counts with more patients requiring plasma and platelet transfusions. Seizures as an adverse event were more common in the hypothermia group. These observed side effects of 48 hours of moderate systemic hypothermia were of mild to moderate severity and manageable with minor interventions.
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PMID:Moderate hypothermia in neonatal encephalopathy: safety outcomes. 1645 38


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