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      비외상성 중증 출혈 질환에서 급성 혈액응고장애의 발생 = Acute Coagulopathy in Non-Traumatic Bleeding

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      https://www.riss.kr/link?id=A104608502

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      Purpose: To find the incidence of acute coagulopathy following non-traumatic bleeding and to evaluate the factors related to the development of coagulopathy.
      Methods: Non-traumatic bleeding patients that visited the emergency department of a university teaching hospital from March 2007 to March 2010 were enrolled retrospectively.
      Patients >18-years-of-age with altered mental status and unstable vital signs, who required resuscitations, transfusion and emergency surgery were included. Patients with liver cirrhosis, chronic renal failure and warfarin medication were excluded. The presence of coagulopathy was defined as prothrombin time (PT) > 18 sec or PT (%) < 50% or activated partial thromboplastin time (APTT) > 60 sec. We analyzed the relationship between coagulopathy and age, presence of circulatory shock (systolic blood pressure < 90mmHg), hypothermia (body temperature (BT) < 36􀆆C),acidity of arterial blood (arterial pH < 7.35), tissue hypoperfusion (base deficit ≤ -6 mmol/L), thrombocytopenia (<100000/uL) and sequential organ failure assessment (SOFA) score. Multiple logistic regression analysis was used to find factors that predicted the development of acute coagulopathy.
      Results: Non-traumatic bleeding patients (n=149) were analyzed. Sixteen patients (10.7%) showed acute coagulopathy.
      Ten patients (6.7%) expired during hospitalization.
      There were no significant differences in mortality, age, sex and full term for glasgow coma scale (GCS) according to presence of early coagulopathy. The presence of shock,metabolic acidosis, thrombocytopenia and high SOFA score were risk factors for the development of acute coagulopathy following non-traumatic bleeding. The group that had early coagulopathy received more much fluid and transfusions compared to the group that did not have coagulopathy (p<0.05).
      Conclusion: Acute coagulopathy causes organ dysfunction due to tissue hypoperfusion. Presently, patients who had acute coagulopathy following non-traumatic bleeding required large amounts of fluid and transfusion during acute resuscitation comparison with non-coagulopathy patients.
      Further study is needed to find whether the correction of coagulopathy improves the outcome of non-traumatic bleeding patients.
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      Purpose: To find the incidence of acute coagulopathy following non-traumatic bleeding and to evaluate the factors related to the development of coagulopathy. Methods: Non-traumatic bleeding patients that visited the emergency department of a universit...

      Purpose: To find the incidence of acute coagulopathy following non-traumatic bleeding and to evaluate the factors related to the development of coagulopathy.
      Methods: Non-traumatic bleeding patients that visited the emergency department of a university teaching hospital from March 2007 to March 2010 were enrolled retrospectively.
      Patients >18-years-of-age with altered mental status and unstable vital signs, who required resuscitations, transfusion and emergency surgery were included. Patients with liver cirrhosis, chronic renal failure and warfarin medication were excluded. The presence of coagulopathy was defined as prothrombin time (PT) > 18 sec or PT (%) < 50% or activated partial thromboplastin time (APTT) > 60 sec. We analyzed the relationship between coagulopathy and age, presence of circulatory shock (systolic blood pressure < 90mmHg), hypothermia (body temperature (BT) < 36􀆆C),acidity of arterial blood (arterial pH < 7.35), tissue hypoperfusion (base deficit ≤ -6 mmol/L), thrombocytopenia (<100000/uL) and sequential organ failure assessment (SOFA) score. Multiple logistic regression analysis was used to find factors that predicted the development of acute coagulopathy.
      Results: Non-traumatic bleeding patients (n=149) were analyzed. Sixteen patients (10.7%) showed acute coagulopathy.
      Ten patients (6.7%) expired during hospitalization.
      There were no significant differences in mortality, age, sex and full term for glasgow coma scale (GCS) according to presence of early coagulopathy. The presence of shock,metabolic acidosis, thrombocytopenia and high SOFA score were risk factors for the development of acute coagulopathy following non-traumatic bleeding. The group that had early coagulopathy received more much fluid and transfusions compared to the group that did not have coagulopathy (p<0.05).
      Conclusion: Acute coagulopathy causes organ dysfunction due to tissue hypoperfusion. Presently, patients who had acute coagulopathy following non-traumatic bleeding required large amounts of fluid and transfusion during acute resuscitation comparison with non-coagulopathy patients.
      Further study is needed to find whether the correction of coagulopathy improves the outcome of non-traumatic bleeding patients.

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      참고문헌 (Reference)

      1 Hess JR, "The coagulopathy oftrauma: A review of mechanism" 65 : 748-754, 2008

      2 Rady MY, "Resuscitation of thecritically ill in the ED; Responses of blood pressure, heartrate, shock index, central venous oxygen saturation andlactate" 14 : 218-, 1996

      3 College of American pathologists, "Practice parameters forthe use of fresh frozen plasma, cryoprecipitate andplatelets" 271 : 777-781, 1994

      4 Hirshberg A, "Minimizing dilutionalcoagulopathy in exanauinating hemorrhage: a computersimulation" 54 : 454-463, 2003

      5 Hewitt PE, "Massive blood transfusion" BMJPublishing Group 38-40, 1992

      6 Sauaia A, "Epidemiology oftrauma deaths: a reassessment" 38 : 185-193, 1995

      7 Rohrer MJ, "Effect of hypothermia on thecoagulation cascade" 20 : 1402-1405, 1992

      8 Cohen MJ, "Early coagulopathy after traumatic braininjury: the role of hypoperfusion and the protein C pathway" 63 : 1254-1262, 2007

      9 Martini WZ, "Does bicarbonate correct coagulationfuction impaired by acidosis in swine" 61 : 99-106, 2006

      10 Kristen C, "Complication of massive transfusion" 137 : 209-220, 2010

      1 Hess JR, "The coagulopathy oftrauma: A review of mechanism" 65 : 748-754, 2008

      2 Rady MY, "Resuscitation of thecritically ill in the ED; Responses of blood pressure, heartrate, shock index, central venous oxygen saturation andlactate" 14 : 218-, 1996

      3 College of American pathologists, "Practice parameters forthe use of fresh frozen plasma, cryoprecipitate andplatelets" 271 : 777-781, 1994

      4 Hirshberg A, "Minimizing dilutionalcoagulopathy in exanauinating hemorrhage: a computersimulation" 54 : 454-463, 2003

      5 Hewitt PE, "Massive blood transfusion" BMJPublishing Group 38-40, 1992

      6 Sauaia A, "Epidemiology oftrauma deaths: a reassessment" 38 : 185-193, 1995

      7 Rohrer MJ, "Effect of hypothermia on thecoagulation cascade" 20 : 1402-1405, 1992

      8 Cohen MJ, "Early coagulopathy after traumatic braininjury: the role of hypoperfusion and the protein C pathway" 63 : 1254-1262, 2007

      9 Martini WZ, "Does bicarbonate correct coagulationfuction impaired by acidosis in swine" 61 : 99-106, 2006

      10 Kristen C, "Complication of massive transfusion" 137 : 209-220, 2010

      11 Hewson JR, "Coagulopathy related todilution and hypotension during massive transfusion" 13 : 387-391, 1985

      12 Moore FA, "Blood transfusion. Anindependent risk factor for postinjury multiple organ failure" 132 : 620-624, 1997

      13 Malone DL, "Blood transfusion, independentof shock severity, is associated with worse outcomein trauma" 54 : 898-905, 2003

      14 Malone D, "Age of blood transfusion intrauma: does it alter outcome" 30 (30): 72-21, 2003

      15 Brohi K, "Acute traumaticcoagulopathy" 54 : 1127-1130, 2003

      16 Brohi K, "Acute traumatic coagulopathy: initiated byhypoperfusion modulated through the protein C pathway" 245 : 812-818, 2007

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      2027 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2020-05-08 학회명변경 영문명 : The Korean Society Of Emergency Medicine -> The Korean Society of Emergency Medicine KCI등재
      2018-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2005-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2003-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.23 0.23 0.22
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.22 0.22 0.339 0.06
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