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Journal of The Korean Society of Emergency Medicine 2011;22(1): 100-105. |
| Acute Coagulopathy in Non-Traumatic Bleeding |
| Sun Bum Lee, Sung Woo Lee, Yun Sik Hong, Sung Hyuck Choi, Sung Woo Moon, Su Jin Kim, Young Hoon Yoon |
| Department of Emergency Medicine, Korea University College of Medicine, Korea. kuedlee@korea.ac.kr |
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| ABSTRACT |
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 < 90 mmHg), hypothermia (body temperature (BT) < 36degrees C), acidity of arterial blood (arterial pH < 7.35), tissue hypoperfusion (base deficit < or = -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. |
| Key words:
Hemorrhage, Coagulopathy, Hypoperfusion, Shock |
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