Pathways to Reduce Late Mortality of Hemorrhagic Shock

Abstract

Patients with progressing hemorrhagic shock (HS) die rapidly of cardiac arrest by insufficient venous return or within days by second-hit multiple organ dysfunction/failure (MOD/MOF). Once earliest source control has been effectuated and macro-hemodynamics is normalized, only three variables affect mortality, namely microcirculation, temperature, and oxygen. Late, non-immediate, mortality is usually preceded by a period of cryptic shock, essentially a disease of microcirculation in the midst of a seemingly functional macrocirculation. The persistence of the effects of ischemia-reperfusion toxemia (IRT) underlying a subclinical cryptic shock is the fundamental pathogenetic factors for clinical observed second hit deterioration. Rewarming a hypothermic hemorrhagic patient and administration of supplementary high dosages of oxygen are standard practices for the management of hemorrhagic shock in acute phase. A complete shift of paradigm prospects an answer to the above tactics’ limitations, drawbacks, and contra-indications. Mild-to-moderate hypothermia, titrated supplementary oxygen, and timely-given vasodilators should instead be given during damage control surgery (DCS) for advanced shock with the aim of reducing ischemia repercussion injury (IRI) e microcirculation dysfunction. A new strategy is suggested: preoperative hypothermia and titrated oxygen before hemorrhage source control, and intra-operative vasodilation and anti-inflammatory tactics after source control.