Prehospital end-tidal carbon dioxide predicts massive transfusion and death following trauma

Abstract

BACKGROUND The lack of an accurate marker of prehospital hemorrhagic shock limits our ability to triage patients to the correct level of care, delays treatment in the emergency department, and inhibits our ability to perform prehospital interventional research in trauma. End-tidal carbon dioxide (ETCO2) is the measurement of alveolar carbon dioxide concentration at end expiration and is measured noninvasively in the ventilator circuit for intubated patients in continuous manner. Several hospital-based studies have been able to demonstrate that either low or decreasing levels of ETCO2 as well as disparities between ETCO2 and plasma carbon dioxide correlate with increasing mortality in trauma. We hypothesized that prehospital ETCO2 values will be predictive of mortality and need for massive transfusion following injury. METHODS This is a single-center retrospective study from an urban level 1 trauma center. We reviewed all intubated adult patients transported for injury who had prehospital ETCO2 values available. Unadjusted comparisons of continuous variables were done with the Wilcoxon two-sample test. The predictive performance of prehospital ETCO2, the prehospital shock index, and prehospital systolic blood pressure were assessed and compared using areas under the receiver operating characteristic curves. Optimal cutoffs were estimated by maximizing the Youden index. Massive transfusion was defined as >10 U of blood or death in 24 hours. RESULTS A total of 173 patients were identified with prehospital ETCO2 values during the 2-year study period. Population was 78.5% male with a median age of 37.5 years (interquartile range, 23.5–53.5 years). Injury mechanism was penetrating in 22.8%. This cohort had a median Injury Severity Score of 26 (interquartile range, 17–36), massive transfusion rate of 34.7%, and mortality of 42.1%. In the evaluation of prediction of postinjury mortality and massive transfusion, ETCO2 outperformed systolic blood pressure and shock index, but these differences did not reach statistical significance. CONCLUSION End-tidal carbon dioxide is a novel prehospital predictor of mortality and massive transfusion after injury. LEVEL OF EVIDENCE Prognostic/Epidemiologic, level III.

Prehospital end-tidal carbon dioxide is predictive of death and massive transfusion in injured patients: An Eastern Association for Surgery of Trauma multicenter trial

“…In addition, two other recent studies demonstrated that prehospital ETCO 2 was predictive of the need for blood transfusion in trauma patients. 9,11 These prior works were limited by relatively small numbers and were performed at single institutions. Our study confirms similar results but has the advantage of significantly larger numbers and a diverse 2.9 ± 1.9 2.9 ± 1.9 3.5 ± 1.9 Min-max 0.0-9.0 0.0-9.0 0.0-6.0 Median (IQR group of trauma centers contributing data leading to increased generalizability.…”

“…[5][6][7][8] However, studies of ETCO 2 in the prehospital setting have been limited to small single center series. [9][10][11] Consequently, we conducted a multicenter study with the hypothesis that prehospital ETCO 2 values will be predictive of mortality and need for massive transfusion (MT) following injury in intubated patients.…”

Prehospital Hemorrhage Assessment Criteria: A Concise Review

“…It is measured noninvasively either in the ventilator circuit of intubated patients or with specialized nasal cannulas in nonintubated patients. End-tidal carbon dioxide is widely available across emergency medical services agencies and holds promise as prehospital levels have been shown to correlate with mortality and the need for massive transfusion or early death (Campion et al, 2020).…”

Low intraoperative end-tidal carbon dioxide: a promising target to improve outcomes or a marker of physiologic instability?

“…Nevertheless, low ETCO 2 in trauma is unlikely to be the direct cause of mortality, rather it reflects more severe hemorrhagic shock and inadequate cardiac output to transfer CO 2 from the blood to alveoli, despite systemically elevated PaCO 2 . 12 It is therefore possible that some of the association between low ETCO 2 and 90-day mortality could be related to a higher burden of hemorrhage (and inaccurate estimations of blood loss) in the low ETCO 2 group, rather than being causally connected.…”

“…Néanmoins, un ETCO 2 bas en cas de traumatisme est peu probablement la cause directe de la mortalité; il est plutôt le reflet d'un choc hémorragique plus sévère et d'un débit cardiaque insuffisant pour transférer le CO 2 du sang aux alvéoles, en dépit d'une PaCO 2 systémique élevée. 12 Il est donc possible qu'une part de l'association entre l'ETCO 2 bas et la mortalité à 90 jours soit liée aux conséquences de l'hémorragie (et à une estimation incorrecte de la perte sanguine) dans le groupe ETCO 2 bas, plutôt qu'à un lien causal.…”