Acute Coagulopathy in Non-Traumatic Bleeding

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 (%) 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.

Acute Coagulopathy in Non-Traumatic Bleeding

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 (%) 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.

The Clinical Utility of End-tidal Carbon Dioxide as a Non-invasive Monitoring of Hyperventilation in Severe Brain Injury

PURPOSE: Hyperventilation is no longer recommended as a prophylactic intervention during the first 24 hours after severe head injury. The vasoconstriction caused by reducing carbon dioxide (CO2) levels leads to cerebral ischemia, and multiple arterial punctures may be required in order to monitor hyperventilation in severe brain injury. However, end-tidal CO2 (Petco2) reflects arterial CO2 (Paco2) noninvasively. The aim of this study was to determine whether Petco2 can be successfully used instead of Paco2 to monitor hyperventilation in brain injury patients. METHODS: From July 1, 2006 to June 30, 2007, 71 patients who visited the emergency department of a hospital after severe brain injury (trauma or acute cerebral disorder) were enrolled. Ten patients with chest trauma, 6 patients who received CPR in the emergency department (ED), and 1 patient who had COPD were excluded. Hemodynamic variables (Glasgow coma scale, mean arterial pressure, heart rate, respiration rate, body temperature, emergency operation, serum lactate concentration) under mechanical ventilation support were measured. The concordance between Petco2 and Paco2 was analyzed by employing a Bland-Altman plot. We defined the normal range for Paco2 and Petco2 [P(a-et)co2] is -5~5 mmHg. We compared the normal and high P(a-et)co2 groups to identify factors affecting the P(a-et)co2. RESULTS: Excepting 17 patients under exclusion criteria, we analyzed 54 of the total of 71 patients. Thirteen patients (24.1%) were seen to be below 30 mmHg for Paco2. The Pearson correlation coefficient between Paco2 and Petco2 is 0.834 (p < 0.001), and the concordance between Paco2 and Petco2 was similarly high. The patients with high P(aet) co2 showed significantly lower mean arterial pressure and lower arterial pH than patients with normal P(a-et)co2. CONCLUSION: Petco2 shows high concordance with Paco2 in severe brain injury. However, patients with high P(a-et)co2 showed evidence of poor tissue perfusion. Therefore, the hemodynamic and tissue perfusion state should be considered when attempting to monitor hyperventilation in severe brain injury patients using Petco2.

Experiences of Using Extracorporeal Life Support in Cardiac Arrest Unresponsive to Standard Cardiopulmonary Resuscitation

PURPOSE: Extracorporeal life support has been used as an extension of conventional cardiopulmonary resuscitation (CPR). However, the appropriate indications for extracorporeal CPR (ECPR) including the duration of CPR are unknown. We analyzed the cases of patients who received ECPR in our institute to find indicators for ECPR. METHODS: Patients who received ECPR in the emergency department of Korea University Ansan hospital from April 2006 to March 2007 were candidates for enrolment. Inclusion criteria were 1) a witnessed sudden cardiac arrest with correctable cause, 2) age <75 years, 3) cardiac arrest unresponsive to standard CPR, 4) absence of serious underlying disease such as advanced cancer, 5) impending arrest state due to respiratory failure or cardiogenic shock. Cardiac arrest related to trauma was excluded from the study. Tracked outcomes were hospital survival, improvement of Glasgow Coma Scale-motor respones, and return of spontaneous circulation. We analyzed the cause of arrest, arrest rhythm, time of administration of extracorporeal life support, and laboratory values. RESULTS: A total of seven patients received ECPR during one year. All patients achieved spontaneous circulation after ECPR and four patients showed improvement of GCS-motor response. Two patients were discharged alive. Their GCS and CPC were 15 points and 1 point, respectively. Intervention to correct underlying cause of arrest during ECPR, rapid start of ECPR during chest compression, and recovery of mean arterial pressure, heart rate, and urine output during ECPR all correlated with good outcomes. CONCLUSION: ECPR as a method of extended CPR improved the survival of cardiac arrest patients unresponsive to standard CPR.