Management of Hemorrhagic Shock: Physiology Approach, Timing and Strategies

Abstract

Hemorrhagic shock (HS) management is based on a timely, rapid, definitive source control of bleeding/s and on blood loss replacement. Stopping the hemorrhage from progressing from any named and visible vessel is the main stem fundamental praxis of efficacy and effectiveness and an essential, obligatory, life-saving step. Blood loss replacement serves the purpose of preventing ischemia/reperfusion toxemia and optimizing tissue oxygenation and microcirculation dynamics. The "physiological classification of HS" dictates the timely management and suits the 'titrated hypotensive resuscitation' tactics and the 'damage control surgery' strategy. In any hypotensive but not yet critical shock, the body's response to a fluid load test determines the cut-off point between compensation and progression between the time for adopting conservative treatment and preparing for surgery or rushing to the theater for rapid bleeding source control. Up to 20% of the total blood volume is given to refill the unstressed venous return volume. In any critical level of shock where, ab initio, the patient manifests signs indicating critical physiology and impending cardiac arrest or cardiovascular accident, the balance between the life-saving reflexes stretched to the maximum and the insufficient distal perfusion (blood, oxygen, and substrates) remains in a liable and delicate equilibrium, susceptible to any minimal change or interfering variable. In a cardiac arrest by exsanguination, the core of the physiological issue remains the rapid restoration of a sufficient venous return, allowing the heart to pump it back into systemic circulation either by open massage via sternotomy or anterolateral thoracotomy or spontaneously after aorta clamping in the chest or in the abdomen at the epigastrium under extracorporeal resuscitation and induced hypothermia. This is the only way to prevent ischemic damage to the brain and the heart. This is accomplishable rapidly and efficiently only by a direct approach, which is a crush laparotomy if the bleeding is coming from an abdominal +/- lower limb site or rapid sternotomy/anterolateral thoracotomy if the bleeding is coming from a chest +/- upper limbs site. Without first stopping the bleeding and refilling the heart, any further exercise is doomed to failure. Direct source control via laparotomy/thoracotomy, with the concomitant or soon following venous refilling, are the two essential, initial life-saving steps.

Keywords: damage control surgery; exsanguination; fluid load test; hemorrhagic shock; hypotensive resuscitation; titrated-to-response anesthesia.

Figure 1

Diagnostic classification of hemorrhagic shock.

Figure 2

Therapeutical classification of hemorrhagic shock. NOM = non-operative management; PRC = packed red cells; OT = operating theatre; CA = cardiac; ARREST St-Y = sternotomy; TACC = thoracic aorta cross-clamping; HR = hypotensive resuscitation; ERT = emergency resuscitative thoracotomy; ALT = anterolateral thoracotomy; THR = titrated hypotensive resuscitation.

Figure 3

Management of stage III HS. TBV = total blood volume; CVL = central venous line; PRC = packed red cells; PLTS = platelets; PCC = prothrombin complex concentrates; TA = tranexamic acid; HR = hypotensive resuscitation; ADH = anti-diuretic hormone; NA = noradrenaline; LL = lower limbs; UL = upper limbs.

Figure 4

Management of stage IV HS. DCR = damage control resuscitation; DCA = damage control anesthesia; DCS = damage control; SURGERY LL = lower limbs; UL = upper limbs; PRC = packed red cells, PLTS = platelets; PCC = prothrombin complex concentrates; TA = tranexamic acid, IHD = ischemic heart disease; CVD = cerebrovascular disease.

Figure 5

Criteria for damage control surgery. DCS = damage control surgery; SBP= systolic blood pressure; NBE = negative base excess; ScvO2 =central venous oxygen saturation.