Guidelines for initial triage, trauma team activation, and early resuscitation following trauma are largely based on studies performed in younger trauma patients . The geriatric population appears to be a relevant subset of patients in whom traditional physical signs of cHI such as SBP and HR may not identify severe injury and blood loss [6, 7], and in whom additional indicators of cHI such as VL are important in predicting mortality. The results of this study demonstrate that a VL ≥ 2.5 mM was independently associated with a 2.6-fold increased odds of mortality in geriatric trauma patients. The TVS of SBP, HR, and SI were not independently associated with mortality in geriatric trauma patients, and activation based on abnormal TVS does not appear to independently identify a population of patients at risk of mortality. These results were demonstrated in a high volume level I trauma center with a large percentage of elderly trauma patients.
Perhaps more importantly, OH was exceedingly common in elderly trauma patients, occurring in 20.03%, and was associated with a two-fold increased odds of mortality. There continues to be a high frequency of OH ranging from 16% to 70% in hemodynamically stable severely injured patients [27–29]. At our institution we identified elderly trauma patients who appeared to be hemodynamically stable in the ED, and would later deteriorate in the operating room or in a non-intensive care unit setting because they were not adequately resuscitated or triaged. A protocol was implemented that utilizes VL on admission, and sets in motion a resuscitative protocol for patients with a VL ≥ 2.5 mM. It is important for inadequate perfusion to be recognized during initial resuscitation efforts, because prolonged OH in elderly trauma increases mortality from 12% to 35% . A cut-off for VL of ≥ 2.5 mM was used for the geriatric resuscitation protocol based on existing literature [23–25]. A receiver operator characteristic curve analysis was performed in our population, and the results of this analysis support our definition of elevated VL: the optimal cut-off was found to be > 2.4 mM, with a sensitivity of 52.6% and a specificity of 79.5% for mortality.
Our results demonstrate that standard physiologic variables of SBP and HR may not identify increased risk of mortality in older trauma patients, while an elevated lactate can be used to identify patients with an increased risk for in-hospital mortality, signifying that an increased risk of mortality may not be recognized in current triage and resuscitation protocols that do not incorporate VL. The geriatric population may be especially susceptible to under-evaluation of risk because of comorbidities, polypharmacy and decreased physiologic reserve. We believe an initial VL drawn in the ED or in a pre-hospital setting may improve the identification of significantly injured geriatric patients. Further, we advocate the implementation of a geriatric-specific resuscitation protocol that includes an initial VL to aid in resuscitation and care protocols.
Several recent studies in non-geriatric trauma patients corroborate our findings that lactate is more strongly associated with mortality following trauma than standard physiologic variables [14, 30, 31]. Meregalli et al. examined 44 high-risk, hemodynamically stable trauma patients, and showed that nonsurvivors had higher lactate than survivors at 12 hours, 24 hours, and 48 hours, whereas there were no differences in mean arterial pressure, HR, and arterial blood oxygenation at any time between survivors and nonsurvivors . On receiver operator characteristic curve analysis, the area under the curve was greater for lactate than for mean arterial pressure, HR, arterial bicarbonate, PaO2/FiO2, and urine output for predicting mortality. Vandromme et al. studied trauma patients in whom hemodynamic measures were indeterminate (SBP between 90–110 mm Hg), and demonstrated that lactate was a significantly better predictor of mortality than pre-hospital SBP and ED SBP . Lavery and colleagues compared VL ≥ 2 mM against standard triage criteria in their ability to identify major injury, and showed that VL was significantly better in predicting ISS, intensive care unit resource utilization, and hospital length of stay .
Additionally, two studies in elderly trauma patients have shown that standard physiologic variables may not identify severe injury [3, 6]: Lehmann et al. studied nearly 14000 geriatric trauma patients, and showed that HR and SBP were not predictive of severe injury , while Zarzuar and colleagues demonstrated that only in geriatric patients was age x SI a better predictor of mortality than HR, SBP, and SI alone .
A recent systematic review reported that initial lactate is useful for risk assessment, and an elevated lactate requires close monitoring for signs of deterioration ; yet few guidelines incorporate an initial lactate measurement [17–19]. Based on the results of this study, VL measurements should be used in the ED for patients for whom no activation occurs based on TVS. Further, we recommend that future studies examine the value of adding a point-of-care measurement of VL for either pre-hospital activation or delayed activation in the ED. While both venous and arterial lactate measurements have been shown to be markers of serious injury following trauma, VL eliminates the need for arterial sampling and correlates strongly with arterial lactate [15, 30].
There are several potential limitations to our study: First, the study evaluated mortality in our geriatric trauma population, who sustained predominantly minor blunt injuries from fall and motor vehicle mechanisms of injury, which limits the ability to generalize our findings for trauma populations unlike our own. However, we believe the majority of elderly trauma patients seen at other institutions present with similar injury characteristics . Second, compliance with VL measurements was 75.39%. Patients without a VL closely resembled patients with a VL < 2.5 mM for mortality and probability of survival; therefore, we believe the association between elevated VL and mortality would remain had all patients received a VL measurement. Third, due to the retrospective design we do not have all potentially relevant data to compare our studies to the existing literature, including emergent interventions in the ED, pre-injury location (e.g. home, nursing facility) and withdrawal of support. Fourth, there are additional activation and resuscitation parameters that we did not compare VL with, such as revised trauma score, GCS, and respiratory rate. Our study was intended to compare predictive ability of physical signs of cHI (SBP and HR) and metabolic indicators of cHI (VL) for mortality. Other institutions use base deficit as a metabolic marker of cHI; we did not examine base deficit because our geriatric resuscitation protocol specifies routine collection of VL.