Benjamin J Ramser (Denver, CO / US), Christopher Erickson (Denver, CO / US), Benjamin W Stocker (Denver, CO / US), Lauren T Gallagher (Denver, CO / US), Otto Thielen (Denver, CO / US), William Hallas (Denver, CO / US), Sanchayita Mitra (Denver, CO / US), Kirk Hansen (Denver, CO / US), Angelo D'Alessandro (Denver, CO / US), Christopher Silliman (Denver, CO / US), Ernest E. Moore (Denver, CO / US), Mitchell J Cohen (Denver, CO / US)
Introduction: Respiratory failure (RF) plays a major role in the morbidity and mortality of trauma; however, the pathophysiology remains unknown. We sought to determine the biological pathways that differ between patients who progress to RF versus those who do not via Multiomic analysis.
Patients & Methods: Patients were enrolled in a randomized prospective trial. Patients less than 18 years old or with a new injury severity score (nISS) less than 25 were excluded. The Denver Organ Failure Score was used to determine RF status. Plasma was collected upon arrival and at multiple time points after arrival. Mass spectrometry was used to obtain Multiomic signatures. Statistical analyses were performed using the Kruskal-Wallis T-test with a raw P-value of <0.05.
Results: Of the 63 patients who met inclusion criteria, 25 had RF (39.7%) and 38 did not have RF (60.3%). There was no difference between age, sex, BMI, injury type, nISS, GCS, lactate, base deficit, and resuscitation with crystalloid and blood products. The RF group had a significantly longer hospital course (6 vs. 32 days, P<0.0001), ICU days (3 vs. 18 days, P< 0.0001), and ventilator-free days (26 vs. 14 days, P< 0.0001). The non-RF group had a higher mortality rate (31.6% v 4%, P 0.01); however, 10/13 patients died within 6 hours of presentation from non-respiratory causes. Patients with RF had elevated levels of transferrin receptors, beta-oxidation enzymes, and decreased levels of acylcarnitines, which are beta-oxidation substrates (see Figure 2).
Conclusion: Severely injured trauma patients who progress to RF have higher levels of beta-oxidation and transferrin receptors, which are associated with elevated oxidative stress. Mitochondrial energy crisis may represent a potential mechanism for RF after trauma.
Figure 1: Clinical outcomes of the non-RF group vs RF group
Figure 2: Levels of TFRC (panel A), beta-oxidation enzymes (panel B), and acylcarnitines (panel C) between RF and non-RF groups.
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