Effects of primary and secondary intra-abdominal hypertension on mesenteric lymph flow: implications for the abdominal compartment syndrome

Abstract

Intra-abdominal hypertension leading to abdominal compartment syndrome complicates trauma resuscitation. The purpose of this study was to determine the effect of primary (1 degrees) and secondary (2 degrees) intra-abdominal hypertension (IAH) on hemodynamics, intestinal fluid balance, and mesenteric lymph flow. Anesthetized dogs were instrumented with vascular catheters, intra-abdominal manometer, and mesenteric lymphatic fistulae. 1 degrees IAH was created by infusing 0.9% saline into the peritoneal cavity to increase abdominal pressure. 2 degrees IAH was created by elevating the inferior vena cava (IVC) pressure between 20 and 25 mmHg and crystalloid resuscitation to create intestinal edema to induce IAH. At baseline and at 30-min intervals, hemodynamics, lymph flow (QL), IVC, and intra-abdominal pressures were measured. Tissue water was determined using microgravimetry to assess gut edema. Results are reported as mean +/- SEM, with n = 7-8 dogs per group. 1 degrees IAH significantly increased CVP and decreased QL. 1 degrees IAH stopped mesenteric QL, thus transvascular fluid flux necessarily exceeded QL, contributing to gut edema formation. 2 degrees IAH significantly increased CVP and QL. 2 degrees IAH increased QL despite elevated IAP. Interstitial protein washdown maintained the plasma-to-interstitial oncotic gradient, thus increased transvascular fluid flux was due principally to increased capillary pressure. Transvascular fluid flux exceeded QL as manifested by increasing gut tissue water as QL plateaued. Modest elevations in IAP significantly affect mesenteric QL and the development of gut edema. The principle of early abdominal decompression to reduce mesenteric/IVC venous hypertension and capillary pressure is supported by these data.