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Journal Article
Research Support, Non-U.S. Gov't
Evaluation for effects of severe acidosis on hemostasis in trauma patients using thrombelastography analyzer.
American Journal of Emergency Medicine 2018 August
OBJECTIVE: To investigate effects of metabolic acidosis on hemostasis function in trauma patients using thromboelastography analyzer.
METHODS: 65 critically injured patients and 19 healthy volunteers were enrolled in the study. Three samples of whole blood were collected from each patient or healthy volunteer. These three samples were acidified with 50mmol/l phosphate-buffered saline (PBS) (pH5.8) or a neutral buffer (50mmol/l phosphate, pH7.4) and acidified blood sample with target pH of 6.95, 7.15 or 7.35 was obtained respectively. These three samples with target pH value were added into thrombelastography analyzer (TEG® 5000 Thrombelastograph Hemostasis Analyzers; Haemoscope Corporation, Niles, Illinois, USA) respectively and variables of Clot time (r), Rate of clot formation (α Angle), Clot formation time (K), Coagulation Index (CI) and Maximum strength (MA) were monitored at 37°C. Besides, association between TEG® parameters and clinicopathological features was analyzed by the Pearson χ2 test.
RESULTS: In trauma patients, all 5 thrombelastographic variables, Clot time (r), Clot formation time (K), Maximum Amplitude (MA), Rate of clot formation (α Angle) and Coagulation Index (CI), were significantly affected by blood acidification, F(1.321,83.213)=88.960, P<0.001, F(2,128)=112.738, P<0.001, F(1.199,76.748)=37.964, P<0.001, F(1.195,76.452)=16.789, P<0.001 and F(2,128)=178.674, P<0.001. Post hoc tests showed that moderate acidosis (pH7.15) significantly elongated K time (from 2.6 to 3.4min, P=0.0013) and increased α Angle (from 51.9°to 52.2°, P=0.0040). r, MA and CI were not markedly influenced under moderate acidification. Comparing to mild acidosis (pH7.15), severe acidosis (pH6.95) induced more serious impairment to hemostasis and all 5 variables was substantially affected, r (from 5.9 to 6.8min, P<0.001), K (from 3.4 to 3.9min, P<0.001), α Angle (from 52.2°to 50.8°, P=0.002), MA (from 52.9 to 51.6mm, P<0.001) and CI (from -2.3 to -4.2, P<0.001). Additionally, higher r elongation under severe acidosis was significantly associated with an increased mortality rate and transfusion requirement (P=0.019 and 0.031). In healthy volunteers, similar effects on hemostasis were detected. Inhibition ratios of thrombelastographic parameters were significantly higher in trauma patients than in healthy volunteers indicating severer impairment of metabolic acidosis to hemostasis in critically injured patients.
CONCLUSIONS: The degree of metabolic acidosis in trauma patients is positively correlated to the severity of hemostasis dysfunction. Additionally, acidosis induces more serious impairment to hemostasis in trauma patients than in healthy volunteers. Moreover, acidosis-induced r time elongation is positively related to a higher death rate and increased transfusion requirement and this indicates a predictive role of TEG® variables for prognosis of traumatized patients.
METHODS: 65 critically injured patients and 19 healthy volunteers were enrolled in the study. Three samples of whole blood were collected from each patient or healthy volunteer. These three samples were acidified with 50mmol/l phosphate-buffered saline (PBS) (pH5.8) or a neutral buffer (50mmol/l phosphate, pH7.4) and acidified blood sample with target pH of 6.95, 7.15 or 7.35 was obtained respectively. These three samples with target pH value were added into thrombelastography analyzer (TEG® 5000 Thrombelastograph Hemostasis Analyzers; Haemoscope Corporation, Niles, Illinois, USA) respectively and variables of Clot time (r), Rate of clot formation (α Angle), Clot formation time (K), Coagulation Index (CI) and Maximum strength (MA) were monitored at 37°C. Besides, association between TEG® parameters and clinicopathological features was analyzed by the Pearson χ2 test.
RESULTS: In trauma patients, all 5 thrombelastographic variables, Clot time (r), Clot formation time (K), Maximum Amplitude (MA), Rate of clot formation (α Angle) and Coagulation Index (CI), were significantly affected by blood acidification, F(1.321,83.213)=88.960, P<0.001, F(2,128)=112.738, P<0.001, F(1.199,76.748)=37.964, P<0.001, F(1.195,76.452)=16.789, P<0.001 and F(2,128)=178.674, P<0.001. Post hoc tests showed that moderate acidosis (pH7.15) significantly elongated K time (from 2.6 to 3.4min, P=0.0013) and increased α Angle (from 51.9°to 52.2°, P=0.0040). r, MA and CI were not markedly influenced under moderate acidification. Comparing to mild acidosis (pH7.15), severe acidosis (pH6.95) induced more serious impairment to hemostasis and all 5 variables was substantially affected, r (from 5.9 to 6.8min, P<0.001), K (from 3.4 to 3.9min, P<0.001), α Angle (from 52.2°to 50.8°, P=0.002), MA (from 52.9 to 51.6mm, P<0.001) and CI (from -2.3 to -4.2, P<0.001). Additionally, higher r elongation under severe acidosis was significantly associated with an increased mortality rate and transfusion requirement (P=0.019 and 0.031). In healthy volunteers, similar effects on hemostasis were detected. Inhibition ratios of thrombelastographic parameters were significantly higher in trauma patients than in healthy volunteers indicating severer impairment of metabolic acidosis to hemostasis in critically injured patients.
CONCLUSIONS: The degree of metabolic acidosis in trauma patients is positively correlated to the severity of hemostasis dysfunction. Additionally, acidosis induces more serious impairment to hemostasis in trauma patients than in healthy volunteers. Moreover, acidosis-induced r time elongation is positively related to a higher death rate and increased transfusion requirement and this indicates a predictive role of TEG® variables for prognosis of traumatized patients.
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