CONTEXT: Hypothermia is known to influence thromboelastography (TEG). TEG reproducibility is generally low. OBJECTIVE: The aim of this study was to evaluate the rationale of TEG temperature adjustment in patients during hypothermia. We hypothesised that temperature adjustment would not be important because of low TEG reproducibility. DESIGN: Prospective observational study. SETTING: Single-centre, secondary care study performed 01/2009 to 07/2010. PATIENTS: Survivors of cardiopulmonary resuscitation in whom therapeutic hypothermia (32 to 34°C) was indicated for 24 h were recruited to the study which lasted 36 h. Four hundred samples from 30 patients (22 men and eight women) were obtained. No specific exclusion criteria were defined. MAIN OUTCOME MEASURES: Temperature adjusted and non-adjusted Kaolin-Heparinase and Rapid-TEG were done at 12-h intervals during the first 36 h. RESULTS: Bland-Altman plots were used for analysis. During hypothermia, the bias of adjusted measurements was greater in clot formation variables for both Kaolin-Heparinase-TEG (from -15 to -19%) and Rapid-TEG (-9 to -25%) compared to normothermia (from -3 to 3% for Kaolin-Heparinase-TEG and -10 to 2% for Rapid-TEG). Bias of clot strength variables was not influenced by temperature adjustment (median -1%). The 95% limits of agreement were wide for clot formation variables and independent of temperature. In Kaolin-Heparinase-TEG (R -42 to 40% normothermia, -47 to 18% hypothermia) and in Rapid-TEG (R -117 to 97% normothermia, -114 to 95% hypothermia). Limits of agreement of clot strength variables were narrower and independent of temperature in Kaolin-Heparinase-TEG (MA -16 to 13% normothermia, -9 to 10% hypothermia) and also in Rapid-TEG (MA -27 to 24% normothermia, -18 to 20% hypothermia). CONCLUSION: Although TEG analysis with temperature adjusted to the in-vivo value during hypothermia yields results with small systematic bias, the importance of temperature adjustment in clinical routine is low because of the precision limits of TEG measurement itself. Therefore, we see no need to perform TEG analysis at the in-vivo temperature.
CONTEXT: Hypothermia is known to influence thromboelastography (TEG). TEG reproducibility is generally low. OBJECTIVE: The aim of this study was to evaluate the rationale of TEG temperature adjustment in patients during hypothermia. We hypothesised that temperature adjustment would not be important because of low TEG reproducibility. DESIGN: Prospective observational study. SETTING: Single-centre, secondary care study performed 01/2009 to 07/2010. PATIENTS: Survivors of cardiopulmonary resuscitation in whom therapeutic hypothermia (32 to 34°C) was indicated for 24 h were recruited to the study which lasted 36 h. Four hundred samples from 30 patients (22 men and eight women) were obtained. No specific exclusion criteria were defined. MAIN OUTCOME MEASURES: Temperature adjusted and non-adjusted Kaolin-Heparinase and Rapid-TEG were done at 12-h intervals during the first 36 h. RESULTS: Bland-Altman plots were used for analysis. During hypothermia, the bias of adjusted measurements was greater in clot formation variables for both Kaolin-Heparinase-TEG (from -15 to -19%) and Rapid-TEG (-9 to -25%) compared to normothermia (from -3 to 3% for Kaolin-Heparinase-TEG and -10 to 2% for Rapid-TEG). Bias of clot strength variables was not influenced by temperature adjustment (median -1%). The 95% limits of agreement were wide for clot formation variables and independent of temperature. In Kaolin-Heparinase-TEG (R -42 to 40% normothermia, -47 to 18% hypothermia) and in Rapid-TEG (R -117 to 97% normothermia, -114 to 95% hypothermia). Limits of agreement of clot strength variables were narrower and independent of temperature in Kaolin-Heparinase-TEG (MA -16 to 13% normothermia, -9 to 10% hypothermia) and also in Rapid-TEG (MA -27 to 24% normothermia, -18 to 20% hypothermia). CONCLUSION: Although TEG analysis with temperature adjusted to the in-vivo value during hypothermia yields results with small systematic bias, the importance of temperature adjustment in clinical routine is low because of the precision limits of TEG measurement itself. Therefore, we see no need to perform TEG analysis at the in-vivo temperature.
Authors: Aleksander Trąbka-Zawicki; Marek Tomala; Aleksander Zeliaś; Elżbieta Paszek; Wojciech Zajdel; Ewa Stępień; Krzysztof Żmudka Journal: Cardiol J Date: 2017-07-11 Impact factor: 2.737
Authors: Torstein Schanche; Ole Magnus Filseth; Bjarne Østerud; Timofei V Kondratiev; Gary C Sieck; Torkjel Tveita Journal: Front Physiol Date: 2022-04-29 Impact factor: 4.755
Authors: James H Lantry; Phillip Mason; Matthew G Logsdon; Connor M Bunch; Ethan E Peck; Ernest E Moore; Hunter B Moore; Matthew D Neal; Scott G Thomas; Rashid Z Khan; Laura Gillespie; Charles Florance; Josh Korzan; Fletcher R Preuss; Dan Mason; Tarek Saleh; Mathew K Marsee; Stefani Vande Lune; Qamarnisa Ayoub; Dietmar Fries; Mark M Walsh Journal: J Clin Med Date: 2022-01-12 Impact factor: 4.241