title: Fluid resuscitation preserves cardiac output but cannot prevent organ damage in a porcine model during 24 h of intraabdominal hypertension.
abstract: According to a previous study, a pathologically increased intraabdominal pressure (IAP) reduces cardiac output (CO) and results in medium- to high-grade organ damage in a porcine model of the abdominal compartment syndrome (ACS). The purpose of this study was to evaluate whether fluid resuscitation can preserve organ integrity together with CO. We examined 12 domestic pigs with a mean body weight of 48 kg. We used a CO2 pneumoperitoneum to increase the IAP to 30 mmHg in 6 animals, and the others served as control group. The investigation period was 24 h. In addition to a standard infusion regimen, Ringer's solution was infused to maintain CO at the level of control animals. Hemodynamic parameters (ITBV, EVLW, MAP, CVP), urine output, inspiratory pressure, as well as serum parameters (e.g., ALT, lipase, AP, lactate, creatinine) were recorded. In the end histological examination of liver, bowel, kidney, and lung was performed. CO, ITBV, EVLW, and urine output did not change when compared with control. Fluid intake was increased (P < 0.01) when compared with control (10,570 +/- 1,928 vs. 3,918 +/- 1,042 mL). CVP, MAP, and inspiratory pressure were increased. Serum parameters did not change. Acidosis occurred in the study group. Liver, bowel, kidney, and lung displayed mean- to high-grade damage (P < 0.01). Although extensive fluid resuscitation preserved CO, diuresis, and serum parameters in this previously described model of the ACS, organ damage occurred. In the clinical regard, these results support decompressive treatment in the presence of pathologically high IAP despite "normalized" parameters.
authors.affiliation: Department of Surgery, Technical University of Aachen, Aachen, Germany. alexander.schachtrupp@post.rwth-aachen.de
authors.forename: Alexander
authors.initials: A
authors.lastname: Schachtrupp
authors.forename: Gilbert
authors.initials: G
authors.lastname: Lawong
authors.forename: Mamdouh
authors.initials: M
authors.lastname: Afify
authors.forename: Juergen
authors.initials: J
authors.lastname: Graf
authors.forename: Christian
authors.initials: C
authors.lastname: Toens
authors.forename: Volker
authors.initials: V
authors.lastname: Schumpelick
mesh_terms: D000138:Acidosis; D000704:Analysis of Variance; D000818:Animals; D001158:Arteries / Q000473:pathology; D001794:Blood Pressure; D001835:Body Weight; D002245:Carbon Dioxide / Q000494:pharmacology; D002248:Carbon Monoxide / Q000737:chemistry; D002302:Cardiac Output; D005440:Fluid Therapy / Q000379:methods*; D006439:Hemodynamics; D006973:Hypertension / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000473:pathology; D008168:Lung / Q000473:pathology; D008297:Male; D011312:Pressure; D012151:Resuscitation / Q000379:methods*; D013552:Swine; D013997:Time Factors
chemical_list: D018799:Intercellular Adhesion Molecule-1; D002245:Carbon Dioxide; D002248:Carbon Monoxide