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

Plasma heparin activity in 11 patients undergoing open-heart surgery was measured by comparing thrombin time of patient plasma to thrombin time of plasma containing known heparin concentrations. Although all patients received 300 units/kg of heparin, their initial plasma heparin levels varied significantly, from 1.8 units/ml in lighter petients to 3 units/ml in heavier patients. During hypothermia (25 degrees C), heparin decay was insignificant. At 37 degrees C, heparin decayed at a rate between 0.37 and 2.01 units/ml/hr. This decay was significantly faster in those patients with higher initial posthypothermia plasma heparin levels. When heparin was reversed with a protamine dose based on circulating plasma heparin levels, the mean difference between the predicted and the actual residual heparin activity was 0.025 units/ml. Heparin levels vary widely becuase of the influence of temperature on decay rates and because the space into which heparin is distributed is not simply proportional to weight. Evaluation and reversal of plasma heparin activity require ongoing analysis rather than any 1 dosage protocol.
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PMID:Plasma heparin activity and antagonism during cardiopulmonary bypass with hypothermia. 56 Jan 45

A method of heparinless, oxygenatorless, left heart bypass perfusion rewarming following surface hypothermia, with the use of a closed circuit with 130 ml. prime volume including heat exchanger, has been devised. The use of polyurethane-polyvinyl-graphite (PPG)-coated tubing has previously been reported. In this text, the use of an athrombogenic coating with cetyl-pyridinium chloride (CPC) as a regional heparin carrier was studied in dogs, comparing groups with PPG tubing and total systemic heparinization or plain polyvinyl tubing without systemic heparinization. Heparin compounded in the CPC coating eluted into the blood and caused mild transient whole-body heparinization during rewarming from 20 degrees to 25 degrees C., as evidenced by prolongation of the thrombin time. Alterations of hematologic parameters in all three groups were similar to those during surface rewarming except for those affected by heparinization. The left heart bypass method was found useful for hypothermic open-heart surgery when utilized with an athrombogenic surface coating or total body heparinization. It was concluded that the CPC coating is superior to the PPG coating since no cracking surface develops, it is translucent, and it provides a more effective athrombogenic surface.
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PMID:Use of athrombogenic tubing for perfusion rewarming following surface-induced deep hypothermia. 76 68

An investigation of 78 cases of adrenal haemorrhage and necrosis disclosed that 32 were examples of adrenal venous infarction. In all these cases there was thrombosis of the main adrenal vein and in most there was also thrombosis of the capsular veins, a finding which has not been well established. In a number of cases with venous infarction there was clinical and pathological evidence that disseminated intravascular coagulation (DIC) had occurred, but it appears that it was not the direct cause of venous thrombosis. The majority of cases of venous infarction occur in patients with severe infection, frequently of the respiratory tract. Venous infarction was found in five cases with hypothermia an association which had rarely been described, and in three of these there was evidence of DIC. This is apparently the first occasion on which DIC has been demonstrated in cases of hypothermia in man. The cause of venous thrombosis in the adrenal glands is obscure in most cases of venous infarction, although in three it was due to involvement by metastatic carcinoma. It is suggested that the factors responsible for the initiation of thrombosis in the adrenal veins are catecholamines, thrombin, fibrin and endotoxin. Localisation of the thrombi to the adrenal vein is due to the unique anatomical structure of the vein which, under certain circumstances, results in the local stasis of blood.
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PMID:Venous infarction of the adrenal glands. 93 79

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

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 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

A hypothermia-induced hemorrhagic diathesis is associated with cardiopulmonary bypass, major surgery, and multiple trauma, but its pathophysiological basis is not well understood. We examined the hypothesis that hypothermia reversibly inhibits human platelet activation in vitro and in vivo. Platelet activation was studied in normal volunteers by whole blood flow cytometric analysis of modulation of platelet surface GMP-140 and the glycoprotein (GP) Ib-IX complex in: a) shed blood emerging from a standardized in vivo bleeding time wound; b) peripheral blood activated in vitro with either thrombin (in the presence of gly-pro-arg-pro, an inhibitor of fibrin polymerization) or the stable thromboxane (TX) A2 analogue U46619. Platelets in peripheral whole blood were activated at temperatures between 22 degrees C and 37 degrees C. the forearm skin temperature was maintained at temperatures between 22 degrees C and 37 degrees C prior to and during the bleeding time incision. Platelet aggregation was studied in shed blood by flow cytometry and in peripheral blood by aggregometry. Generation of TXB2 (the stable metabolite of TXA2) was determined by radioimmunoassay. In vitro, hypothermia inhibited both thrombin- and U46619-induced upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregation, and TXB2 generation. These inhibitory effects of hypothermia were all completely reversed by rewarming the blood to 37 degrees C. In vivo, platelet activation was inhibited by hypothermia as shown by 5 independent assays of shed blood: upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregate formation, TXB2 generation, and the bleeding time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversible inhibition of human platelet activation by hypothermia in vivo and in vitro. 752 54

The activated clotting time (ACT) is routinely used for monitoring of heparin effects during cardiopulmonary bypass (CPB). However, ACT is not a specific assay for heparin and may be influenced by several other factors, which may be misleading with regard to the proper administration of heparin and protamine. In this pilot study, we compared a new test, the high-dose thrombin time (HiTT), with the conventional ACT test for both in vitro and in vivo heparin-induced anticoagulation. Our in vitro results showed that there were heparin dose-dependent increases in ACT and HiTT. Data on 30 adult cardiac patients indicated that HiTT correlated well with heparin concentration both after initial heparin administration and during CPB (r = 0.645 and 0.515). Hypothermia and hemodilution occurring during CPB did not alter HiTT results. ACT also correlated well with both heparin concentration and HiTT before CPB, but the linear relationship was lost during CPB. Our results suggest that HiTT is a useful assay for monitoring heparin effects during cardiac surgery, even during hypothermia and hemodilution.
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PMID:Comparison of high-dose thrombin time with activated clotting time for monitoring of anticoagulant effects of heparin in cardiac surgical patients. 801 Apr 61

The paper gives indications for surgical management and describes a surgical technique on the basis of the author's experience with 36 reconstructive interventions on pulmonary arteries in persistent post-embolic occlusion. The absolute indication for elimination of occlusion is central pulmonary arterial lesion which exists no more than 3 years and which is accompanied by elevated systolic pulmonary pressure (ranging from 51 to 100 mm Hg) and relatively preserved right ventricular myocardial function. The optimal surgical method is thrombin-thymectomy performed in deep hypothermia using intermittent extracorporeal perfusion.
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PMID:[Indications and techniques of surgical intervention in chronic postembolic pulmonary hypertension]. 814 63

The haemostatic system and the use of heparin during cardiopulmonary bypass (CPB) have been studied extensively in adults but not in children. Results from adult trials cannot be extrapolated to children because of age-dependent physiologic differences in haemostasis. We studied 22 consecutive paediatric patients who underwent CPB at The Hospital for Sick Children, Toronto. Fibrinogen, factors II, V, VII, VIII, IX, XII, prekallikrein, protein C, protein S, antithrombin (AT), heparin cofactor II, alpha 2-macroglobulin, plasminogen, alpha 2-antiplasmin, tissue plasminogen activator (tPA), plasminogen activator inhibitor, thrombin-AT complexes (TAT), D-dimer, heparin (by both anti-factor Xa assay and protamine titration) and activated clotting time (ACT) were assayed perioperatively. The timing of the sampling was: pre heparin, post heparin, after initiation of CPB, during hypothermia, post hypothermia, post protamine reversal and 24 h post CPB. Plasma concentrations of all haemostatic proteins decreased by an average of 56% immediately following the initiation of CPB due to haemodilution. During CPB, the majority of procoagulants, inhibitors and some components of the fibrinolytic system (plasminogen, alpha 2 AP) remained stable. However, plasma concentrations of TAT and D-dimers increased during CPB showing that significant activation of the coagulation and fibrinolytic systems occurred. Mechanisms responsible for the activation of haemostasis are likely complex. However, low plasma concentrations of heparin (< 2.0 units/ml in 45% of patients) during CPB were likely a major contributing etiology. ACT values showed a poor correlation (r = 0.38) with heparin concentrations likely due to concurrent haemodilution of haemostatic factors, activation of haemostatic system, hypothermia and activation of platelets. In conclusion, CPB in paediatric patients causes global decreases of components of the coagulation and fibrinolytic systems, primarily by haemodilution and secondarily by consumption.
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PMID:Coagulation and fibrinolytic profile of paediatric patients undergoing cardiopulmonary bypass. 915 80


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