BACKGROUND: In trauma patients, the admission value of arterial base deficit stratifies injury severity, predicts complications, and is correlated with arterial lactate concentration. In theory, elevated base deficit and lactate concentrations after shock are related to oxygen transport imbalance at the cellular level. The purpose of this study was to test the hypothesis that an elevated base deficit in trauma patients is indicative of impaired systemic oxygen utilization and portends poor outcomes. METHODS: This study was a retrospective analysis of a prospectively collected database. The study population included all patients admitted to the trauma intensive care unit at a Level 1 trauma center during a 12-month period who were monitored with a pulmonary artery catheter and serial measurements of lactate and base deficit, and who achieved a normal arterial lactate concentration (< 2.2 mmol/L) with resuscitation. The patients were divided into those who maintained a persistently high base deficit (> or = 4 mmol/L) and those who achieved a low base deficit (< 4 mmol/L) during resuscitation. RESULTS: One-hundred patients (mortality 20%) were monitored with a pulmonary artery catheter and achieved a normal arterial lactate concentration. The mean age+/-SD (SEM) of the group was 37+/-17 years and the Injury Severity Score was 25+/-11. Subgroup analysis revealed that patients with a persistently high base deficit (n=26) had higher rates of multiple organ failure (35% versus 5%, p < 0.001) and death (50% versus 9%, p < 0.00001) compared with patients who achieved a low base deficit. Patients with a persistently high base deficit also had lower oxygen consumption (126+/-40 mL/m2 versus 156+/-30 mL/m2, p=0.01 at 48 hours) and a lower oxygen utilization coefficient (0.20+/-0.05 versus 0.24+/-0.03, p=0.01 at 48 hours) compared with patients with a low base deficit. At 48 hours, both oxygen consumption (r=-0.44, [r, correlation coefficient] p=0.002) and oxygen utilization (r=-0.46, p=0.001) had a significant negative correlation with base deficit. CONCLUSIONS: In trauma patients, a persistently high arterial base deficit is associated with altered oxygen utilization and an increased risk of multiple organ failure and mortality. Serial monitoring of base deficit may be useful in assessing the adequacy of oxygen transport and resuscitation.
BACKGROUND: In traumapatients, the admission value of arterial base deficit stratifies injury severity, predicts complications, and is correlated with arterial lactate concentration. In theory, elevated base deficit and lactate concentrations after shock are related to oxygen transport imbalance at the cellular level. The purpose of this study was to test the hypothesis that an elevated base deficit in traumapatients is indicative of impaired systemic oxygen utilization and portends poor outcomes. METHODS: This study was a retrospective analysis of a prospectively collected database. The study population included all patients admitted to the trauma intensive care unit at a Level 1 trauma center during a 12-month period who were monitored with a pulmonary artery catheter and serial measurements of lactate and base deficit, and who achieved a normal arterial lactate concentration (< 2.2 mmol/L) with resuscitation. The patients were divided into those who maintained a persistently high base deficit (> or = 4 mmol/L) and those who achieved a low base deficit (< 4 mmol/L) during resuscitation. RESULTS: One-hundred patients (mortality 20%) were monitored with a pulmonary artery catheter and achieved a normal arterial lactate concentration. The mean age+/-SD (SEM) of the group was 37+/-17 years and the Injury Severity Score was 25+/-11. Subgroup analysis revealed that patients with a persistently high base deficit (n=26) had higher rates of multiple organ failure (35% versus 5%, p < 0.001) and death (50% versus 9%, p < 0.00001) compared with patients who achieved a low base deficit. Patients with a persistently high base deficit also had lower oxygen consumption (126+/-40 mL/m2 versus 156+/-30 mL/m2, p=0.01 at 48 hours) and a lower oxygen utilization coefficient (0.20+/-0.05 versus 0.24+/-0.03, p=0.01 at 48 hours) compared with patients with a low base deficit. At 48 hours, both oxygen consumption (r=-0.44, [r, correlation coefficient] p=0.002) and oxygen utilization (r=-0.46, p=0.001) had a significant negative correlation with base deficit. CONCLUSIONS: In traumapatients, a persistently high arterial base deficit is associated with altered oxygen utilization and an increased risk of multiple organ failure and mortality. Serial monitoring of base deficit may be useful in assessing the adequacy of oxygen transport and resuscitation.
Authors: Elliott J Kim; Samuel N Crosby; Gregory A Mencio; Neil E Green; Steven A Lovejoy; Jonathan G Schoenecker; Jeffrey E Martus Journal: JBJS Essent Surg Tech Date: 2014-10-08