Evidence for early supply independent mitochondrial dysfunction in patients developing multiple organ failure after trauma

Abstract

Objective: To determine whether early supply independent mitochondrial oxidative dysfunction occurs in trauma patients who develop multiple organ failure (MOF).

Design: Prospective focused observational trial.

Methods: High-risk patients were aggressively resuscitated while being continuously monitored by near infrared spectroscopy. Near infrared spectroscopy monitoring strips allow for a direct comparison of changes in tissue oxyhemoglobin levels (HbO2), which reflect local oxygen supply, and cytochrome a,a3 redox, which reflects mitochondrial oxygen consumption. Under normal conditions, HbO2 and a,a3 redox are tightly coupled. On the other hand, decoupled HbO2 and a,a3 redox is a sign of mitochondrial oxidative dysfunction. Outcomes included MOF, oxygen delivery, oxygen consumption, lactate, and the presence of decoupled HbO2 and a,a3 redox.

Results: Twenty-four high-risk patients were studied; nine (38%) developed MOF. At 12 hours of resuscitation, MOF and non-MOF patients did not have statistically different oxygen delivery and oxygen consumption, but lactate levels were significantly higher in MOF patients. Additionally, HBO2 and a,a3 redox were decoupled in eight (89%) MOF patients compared with two (13%) non-MOF patients (p < 0.05).

Conclusion: Severely injured trauma patients who develop MOF preferentially display evidence of mitochondrial oxidative dysfunction early in the course of their resuscitation despite early goal-oriented maximization of oxygen delivery.