Independent contributions of hypothermia and acidosis to coagulopathy in swine

Wenjun Z. Martini, Anthony E. Pusateri, John M. Uscilowicz, Angel V. Delgado, John B. Holcomb, James G. Tyburski, Peter M Rhee, Martin A. Schreiber

Research output: Contribution to journalArticle

186 Citations (Scopus)

Abstract

Background: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control. Methods: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39°C), acidotic (pH, 7.1; 39°C), hypothermic (pH, 7.4; 32°C), and acidotic and hypothermic (pH, 7.1; 32°C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4°C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved. Results: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47%, 57%, and 72% increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18% and 17% in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0%, 12.5%, and 5.7%, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-α and interleukin-6 in any group during the study. Conclusion: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.

Original languageEnglish (US)
Pages (from-to)1002-1010
Number of pages9
JournalJournal of Trauma
Volume58
Issue number5
DOIs
StatePublished - May 2005
Externally publishedYes

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Acidosis
Hypothermia
Swine
Thrombin
Bleeding Time
Prothrombin Time
Thrombelastography
Thrombin Time
Induced Hypothermia
Hydrochloric Acid
Fibrinogen
Interleukin-6
Tumor Necrosis Factor-alpha
Hemorrhage
Control Groups
Water
Wounds and Injuries
Serum
Population

ASJC Scopus subject areas

  • Surgery

Cite this

Martini, W. Z., Pusateri, A. E., Uscilowicz, J. M., Delgado, A. V., Holcomb, J. B., Tyburski, J. G., ... Schreiber, M. A. (2005). Independent contributions of hypothermia and acidosis to coagulopathy in swine. Journal of Trauma, 58(5), 1002-1010. https://doi.org/10.1097/01.TA.0000156246.53383.9F

Independent contributions of hypothermia and acidosis to coagulopathy in swine. / Martini, Wenjun Z.; Pusateri, Anthony E.; Uscilowicz, John M.; Delgado, Angel V.; Holcomb, John B.; Tyburski, James G.; Rhee, Peter M; Schreiber, Martin A.

In: Journal of Trauma, Vol. 58, No. 5, 05.2005, p. 1002-1010.

Research output: Contribution to journalArticle

Martini, WZ, Pusateri, AE, Uscilowicz, JM, Delgado, AV, Holcomb, JB, Tyburski, JG, Rhee, PM & Schreiber, MA 2005, 'Independent contributions of hypothermia and acidosis to coagulopathy in swine', Journal of Trauma, vol. 58, no. 5, pp. 1002-1010. https://doi.org/10.1097/01.TA.0000156246.53383.9F
Martini WZ, Pusateri AE, Uscilowicz JM, Delgado AV, Holcomb JB, Tyburski JG et al. Independent contributions of hypothermia and acidosis to coagulopathy in swine. Journal of Trauma. 2005 May;58(5):1002-1010. https://doi.org/10.1097/01.TA.0000156246.53383.9F
Martini, Wenjun Z. ; Pusateri, Anthony E. ; Uscilowicz, John M. ; Delgado, Angel V. ; Holcomb, John B. ; Tyburski, James G. ; Rhee, Peter M ; Schreiber, Martin A. / Independent contributions of hypothermia and acidosis to coagulopathy in swine. In: Journal of Trauma. 2005 ; Vol. 58, No. 5. pp. 1002-1010.
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abstract = "Background: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control. Methods: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39°C), acidotic (pH, 7.1; 39°C), hypothermic (pH, 7.4; 32°C), and acidotic and hypothermic (pH, 7.1; 32°C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4°C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved. Results: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47{\%}, 57{\%}, and 72{\%} increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18{\%} and 17{\%} in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0{\%}, 12.5{\%}, and 5.7{\%}, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-α and interleukin-6 in any group during the study. Conclusion: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.",
author = "Martini, {Wenjun Z.} and Pusateri, {Anthony E.} and Uscilowicz, {John M.} and Delgado, {Angel V.} and Holcomb, {John B.} and Tyburski, {James G.} and Rhee, {Peter M} and Schreiber, {Martin A.}",
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T1 - Independent contributions of hypothermia and acidosis to coagulopathy in swine

AU - Martini, Wenjun Z.

AU - Pusateri, Anthony E.

AU - Uscilowicz, John M.

AU - Delgado, Angel V.

AU - Holcomb, John B.

AU - Tyburski, James G.

AU - Rhee, Peter M

AU - Schreiber, Martin A.

PY - 2005/5

Y1 - 2005/5

N2 - Background: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control. Methods: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39°C), acidotic (pH, 7.1; 39°C), hypothermic (pH, 7.4; 32°C), and acidotic and hypothermic (pH, 7.1; 32°C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4°C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved. Results: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47%, 57%, and 72% increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18% and 17% in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0%, 12.5%, and 5.7%, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-α and interleukin-6 in any group during the study. Conclusion: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.

AB - Background: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control. Methods: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39°C), acidotic (pH, 7.1; 39°C), hypothermic (pH, 7.4; 32°C), and acidotic and hypothermic (pH, 7.1; 32°C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4°C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved. Results: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47%, 57%, and 72% increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18% and 17% in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0%, 12.5%, and 5.7%, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-α and interleukin-6 in any group during the study. Conclusion: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.

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