Pre-emptive hypothermia during resuscitated porcine hemorrhagic shock

Introduction

The role of hypothermia in hemorrhagic shock is still a matter of debate [1]. Therefore, we studied the effects of deliberate, pre-emptive hypothermia on hemodynamics and organ function during long-term porcine hemorrhage and resuscitation.

Methods

Anesthetized and instrumented pigs were randomly assigned to 32°C (n = 7), 35°C (n = 7), and 38°C (n = 6) of core temperature and subjected to 4 hours of hemorrhage (removal of 40% of the calculated blood volume, additional removal/retransfusion of blood to maintain mean arterial pressure (MAP) = 30 mmHg). After 12 hours of reperfusion comprising retransfusion of shed blood, colloid fluid resuscitation and noradrenaline to keep MAP at pre-shock levels, animals were rewarmed to 38°C. Data (median, quartiles) were obtained before and at the end of the shock phase as well as at 12 and 22 hours of resuscitation, intergroup differences were analyzed using a Kruskal-Wallis ANOVA on ranks.

Results

Fluid balance and noradrenaline requirements did differ between groups. At 12 hours of reperfusion - that is, immediately before rewarming - the 32°C group showed the lowest blood levels of creatinine (P = 0.026), troponin I (P = 0.053), the thrombin-antithrombin complexes (P = 0.012), and von Willebrand factor (P = 0.012). At the end of the experiment - that is, after rewarming - all these intergroup differences had disappeared, but the 32°C group presented with arterial hypotension (P = 0.039), the most severe visceral organ acidosis (portal and hepatic venous base excess: P = 0.044, P = 0.022, respectively), and the highest TNFα blood levels (P = 0.030).

Conclusion

Deliberate, pre-emptive moderate hypothermia slowed but did not protect against hemorrhagic shock and resuscitation-induced organ dysfunction, possibly due to a delayed but not attenuated inflammatory response.