Trauma is among the most common causes of disability and mortality worldwide [1-5]. ey are a major cause of mortality, disability and huge costs to the society. The target of their acute management is to prevent or to reverse the primary and the secondary injuries.
Severity of trauma and development of systemic inammatory response syndrome have been studied as eective factors by causing inammation [6, 7]. Recent studies have shown that decreased tissue perfusion, without clear clinical symptoms, led to an increase in the levels of lactate and carbonic acid in trauma patients and was introduced as a predictor of mortality in these patients, and its criterion is measuring serum lactic acid [6, 8, 9]. However, it is not possible to measure this parameter in all trauma centers. Base excess (BE) is the levels of base that is required for titration of one liter of full blood to reach pH 7.4 in the case of full saturation of blood with oxygen, at 37°C and PaCO2 =40 mmHg [10, 11]. Studies have shown that in cases of severe base decit, most of the trauma patients suer from shock due to bleeding. However, in the absence of shock, it seems that this criterion can be a sign of lactic acidosis [10 - 13]. Some studies have suggested that the mortality of trauma patients can be predicted by the levels of base decit within the rst 24 hours after the trauma [14, 15]. Hamed et al. focused in their research on the benets of measuring the BE level to early predict the risk of death. These authors aimed to test the prognostic value of the baseline base excess level of injured patients admitted in the emergency department. is was a prospective monocenter study with a 479-patient sample. e primary endpoint was to compare the base excess in the groups of survivors and deaths during the rst day of trauma. The secondary endpoint was to compare the base excess levels among survivors and dead at day 7 post-trauma. e immediate death rate was at 2.2%. The mortality rate was at 17.5% at the seventh day post-trauma and at 21% at the 21th day post-trauma. The major nding of this study was that the BE level was statistically dierent between deceased and survivors both for the immediate and early mortalities. The analysis of the cuto by the ROC curve showed that a base excess lower that 6.5 mmol/l on admission was correlated with a higher risk of mortality during the rst 24 hours of trauma (AUC 0.8; p
In multivariate analysis, the baseline base excess level was the only predictor with low systolic blood pressure. Patients with a base excess level lower than 6.5 mmol/l had a 3.1 higher risk of death the rst 24 hours of management (p=0.005; CI [1.4- 7.1]) and 1.5 higher risk of death during the rst seven days after trauma (p=0.003; CI [1.1-1.9]). e eorts of the authors should be highlighted, the early accurate management of severe injured patients is a challenging task for the emergency physician. Nevertheless, these results should be conrmed by a larger sample, focusing on correlation between base excess levels and the diagnosed organ failures and the dierent types of injuries. In this study, the authors did not explain the dierent ndings of the imaging, nor the dierent lesions secondary to trauma. The BE levels were not clearly correlated to the number of organ failures. It was highly associated with elevated ISS (p=0.004), but it was not explained which lesion was statistically associated with low BE level. Moreover, the follow-up rhythm was not determined, nor the cause of death.
Future studies should distinguish sub-groups of patients by initial severity, type of lesion and cause of death.
Base Excess in severe trauma patients: useful or excess?
