title: Development of a fatal noncompressible truncal hemorrhage model with combined hepatic and portal venous injury in normothermic normovolemic swine.
abstract: Noncompressible truncal hemorrhage and brain injury currently account for most early mortality of warfighters on the battlefield. There is no effective treatment for noncompressible truncal hemorrhage, other than rapid evacuation to a surgical facility. The availability of an effective field treatment for noncompressible truncal hemorrhage could increase the number of warfighters salvaged from this frequently-lethal scenario. Our intent was to develop a porcine model of noncompressible truncal hemorrhage with a ∼ 50% one-hour mortality so that we could develop new treatments for this difficult problem. Normovolemic normothermic domestic swine (barrows, 3 months old, 34-36 kg) underwent one of three injury types through a midline incision: 1) central stellate injury (N = 6); 2) excision of a portal vein branch distal to the main PV trunk (N = 6); or 3) hemi-transection of the left lateral lobe of the liver at its base (N = 10). The one-hour mortality of these injuries was 0, 82, and 40%, respectively; the final mean arterial pressure was 65, 24, and 30 mm Hg, respectively; and the final hemoglobin was 8.3, 2.3, and 3.6 g/dL, respectively. Hemi-transection of the left lateral lobe of the liver appeared to target our desired mortality rate better than the other injury mechanisms.
authors.affiliation: Department of Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America; Department of Surgery, VA Nebraska-Western Iowa Health Care System, Omaha, Nebraska, United States of America.
authors.forename: Ujwal R
authors.initials: UR
authors.lastname: Yanala
authors.affiliation: Department of Vascular Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America; Department of Surgery, VA Nebraska-Western Iowa Health Care System, Omaha, Nebraska, United States of America.
authors.forename: Jason M
authors.initials: JM
authors.lastname: Johanning
authors.affiliation: Department of Vascular Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America; Department of Surgery, VA Nebraska-Western Iowa Health Care System, Omaha, Nebraska, United States of America.
authors.forename: Iraklis I
authors.initials: II
authors.lastname: Pipinos
authors.affiliation: Department of Chemical and Biomolecular Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Larsen
authors.affiliation: Department of Chemical and Biomolecular Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
authors.forename: William H
authors.initials: WH
authors.lastname: Velander
authors.affiliation: Department of Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America; Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska, United States of America; Department of Surgery, VA Nebraska-Western Iowa Health Care System, Omaha, Nebraska, United States of America.
authors.forename: Mark A
authors.initials: MA
authors.lastname: Carlson
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006470:Hemorrhage / Q000209:etiology / Q000401:mortality* / Q000503:physiopathology; D006503:Hepatic Veins / Q000293:injuries*; D006801:Humans; D008297:Male; D011169:Portal Vein / Q000293:injuries*; D034421:Sus scrofa