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

In this study we assessed the effects of changes in pH, temperature, and their combination in whole blood on thromboelastographic variables. Blood was collected from six healthy volunteers. Thromboelastograph (TEG series 5000; Haemoscope Corporation, Illinois, USA) channels were set at temperatures of 32, 37, and 39 degrees C and each was filled with artificially acidified, alkalified, and neutral blood, respectively. Acidification (pH 6.95) significantly impairs thromboelastographic variables reaction time r (from 23.3 to 33.7 min; P = 0.0280), kinetic time k (from 8.7 to 16.1 min; P = 0.028), angle alpha (from 24.3 degrees to 13.8 degrees ; P = 0.028), prothrombin time (from 11.4 to 12.1 s; P = 0.044), and activated partial thromboplastin time (from 29.3 to 45.0 s; P = 0.028). A temperature drop from 37 to 32 degrees C in blood of neutral pH significantly impaired k (from 8.7 to 10.2 min; P = 0.028) and alpha (from 24.3 degrees to 21.0 degrees ; P = 0.027), whereas maximum amplitude ma significantly increased (from 46.5 to 52.5 mm; P = 0.027). A temperature rise from 37 to 39 degrees C at pH 7.37 did not affect any of the TEG variables. Artificial alkalization (pH 7.68) at a temperature of 37 degrees C had no effect on any of the measured variables. Acidosis causes a significant impairment of clot formation and clot strength. Hypothermia had the same effects, but to a lesser extent. These findings emphasize the need for correction of acidosis and hypothermia to normalize haemostasis.
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PMID:Effects of acidosis, alkalosis, hyperthermia and hypothermia on haemostasis: results of point-of-care testing with the thromboelastography analyser. 1949 62

Acute traumatic coagulopathy (ATC) is an early endogenous process, driven by the combination of tissue injury and shock that is associated with increased mortality and worse outcomes in the polytrauma patient. This review summarizes our current understanding of the pathophysiology of ATC and the role of rapid diagnostics in the management of severe trauma hemorrhage. In particular we consider diagnostic and therapeutic strategies for bleeding trauma patients with short versus long prehospital times and the concept of remote damage control resuscitation. Endothelial activation of Protein C is a central mechanism of ATC, which produces rapid anticoagulation and fibrinolysis following severe trauma. Continued blood loss, hypothermia, acidosis, and hemodilution potentiate ATC and lead to a global derangement in all components of hemostasis. The contribution and interplay between platelet activity, fibrinogen utilization, endothelial dysfunction, and neurohormonal pathways remain to be defined in ATC pathogenesis but may offer novel therapeutic targets. Conventional laboratory-based tests of coagulation have a limited role in the early management of major trauma hemorrhage. TEG and ROTEM provide a rapid evaluation of clot dynamics in whole blood and are of greater value than coagulation screens in diagnosing and managing trauma hemorrhage.
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PMID:Pathogenesis of acute traumatic coagulopathy. 2330 69