Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock

Shock as a result of blood loss results in inadequate organ perfusion and tissue oxygenation, with subsequent tissue acidosis and lactic acidemia. Central hemodynamic endpoints for resuscitation from compensated hemorrhagic shock, when taken alone, fail to measure adequate organ perfusion and oxygen delivery. Two separate clinical studies by Scalea et al. 1 and Abou-Khalil et al. 2 document that despite normalization of blood pressure, heart rate, and urine output, tissue hypoperfusion persists in 80% to 85% of patients, as evidenced by lactic acidemia and decreased mixed venous oxygen saturation. Other clinical studies have shown that the level and the rate of normalization of serum lactate (indirect measures of tissue oxygen utilization) correlated with mortality both in degree of elevation and in the time-dependent rate of normalization. 3,4 Systemic base deficit (an indicator of tissue perfusion) also shows a similar predictive pattern of mortality. 5 However, interventions that focus on correction of this oxygen debt by driving oxygen transport variables, such as cardiac index or oxygen delivery index following resuscitation, to supernormal levels fail to reduce mortality in severely injured patients. 6,7 Taken as a whole, those studies indicate that systemic markers of tissue perfusion fail to account for the distribution of blood flow to different tissue beds. Certain tissues appear to benefit from a redistribution of flow (e.g., heart, brain, and striated muscle), while the splanchnic vascular bed shows a persistent hypoperfusion following conventional intravenous resuscitation (CR) from shock. Intestinal ischemia after hemorrhagic shock (HS) has been documented in both experimental 8,9 and clinical 10 studies. It appears that this splanchnic hypoperfusion results from local microvascular endothelial cell dysfunction, 11,12 and the resultant intestinal injury leads the gut-associated lymphatic tissue (GALT) to become a cytokine-generating organ. 13 Recent experimental data suggest that those proinflammatory cytokines cause remote organ injury through lymphatic drainage from the gut. 14 Standard therapies for hemorrhagic shock focus on intravascular volume replacement and preservation of cell membrane function. Additional systemic therapies that are designed to preserve endothelial cell function and splanchnic perfusion appear to have other adverse consequences. 15–19 Despite a better understanding of the physiologic events of fluid resuscitation regimens 20–22 that emphasize rapid hemodynamic stabilization, reversal of the pathophysiologic course in the splanchnic circulation after CR continues to constitute a major but elusive treatment goal. Investigators have adopted several approaches to alleviate the hemorrhage-induced host-stress response and gut hypoperfusion. Blockage of proinflammatory mediators, integrins, and other cell adhesion molecules or addition of radical scavengers to CR regimens gives marginal alterations in the inflammatory response and microvascular injury. 23,24 Pentoxifylline-supplemented resuscitation 8,17 or pretreatment with selective inhibitors of the complement system 9 or with heparin 16 can prevent the microvascular impairment to restore tissue perfusion after CR from HS. Commercial peritoneal dialysis solutions possess a vasodilation effect on visceral and parietal arterioles. 25 Our laboratory has recently demonstrated a generalized and sustained dilation effect of these solutions on the intestinal microcirculation. 26 Thus, we hypothesized that initiation of peritoneal resuscitation (PR) with commercially available hyperosmolar dextrose-based solution (Delflex 2.5%) during CR from HS prevents the progressive intestinal vasoconstriction and hypoperfusion and the sequelae of impaired microvascular dilation.