The effects of hypothermia and acidosis on Haemostasis




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De Montfort University


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Peer reviewed


Hypothermia and acidosis are often seen in trauma patients and the critically ill. Both significantly contribute towards the pathology of these conditions. These patients are often investigated for coagulopathy, often as a result of bleeding. Traditionally routine coagulation screening is performed in buffered systems at 37°C. Therefore the information returned by the laboratory tells the clinician what the clotting will be like if the hypothermia and acidosis are corrected. This is useful clinical information but does not accurately reflect the clinical situation at the time. Blood was taken from 40 consenting healthy adults and 17 critically ill patients to examine the effects of hypothermia and acidosis upon “normal” clotting. The STart®4 coagulometer was used to assess the prothrombin time (PT) and the activated partial thromboplastin time (APTT), the ROTEM® analyzer to assess thromboelastometry and the Fluoroscan Ascent to assess thrombin generation using calibrated automated thrombography (CAT). The results show a difference in interpretation between assays using fibrin polymerisation as an end-point as opposed to the generation of thrombin. The results of the CAT assay under hypothermic and/or acidotic conditions suggest that in spite of having initially a delayed lag time (lag time at 37°C = 7.91 min; lag time at 31°C = 8.37 min (Table 4.3.)), once the thrombin burst occurs it will generate more thrombin which will increase the overall ETP (ETP at 37°C = 1777nmol of thrombin; ETP at 31°C = 2681nmol of thrombin (Table 4.3.)). Therefore a thrombotic profile may be seen instead of a bleeding tendency. In general, it seems that both parameters (lag time and ETP) are affected by both hypothermic and acidotic conditions on their own but when combining both of them together (hypothermia + acidosis) there was a cumulative effect which exaggerates the changes even more (lag time at 37°C/ pH 7.35 =.7.91min; lag time at 31°C/ pH 6.9 =.10.46min. and ETP at 37°C/ pH 7.35 =.1777nmol of thrombin; ETP at 31°C/ pH 6.9 =.2852 nmol of thrombin (Table 4.3.)). These particular observations have not been observed previously in any published literature to date, where a hypocoagulable coagulopathy is described under abnormal conditions, such as hypothermia and acidosis. Although these standard clotting tests are performed at 37°C and physiological pH, in vitro testing of any given sample should ideally be performed at the patient’s own body temperature and pH as well as under the corrected conditions. This will give a picture of what is happening now compared to what will happen when the hypothermia/acidosis is corrected. It is possible that global assays of haemostasis may offer some insight into the pathology of hypothermia and acidosis. However, as always in science many more questions are raised than are answered.



Haemostasis, hypothermia, acidosis



Research Institute