78.04 A Combat-Relevant Model of Noncompressible Torso Hemorrhage with Hilum Clamping

A. Batchinsky1,2, V. Karaliou1, J. Choi1,2, B. Beely1,2, T. Roberts1,2, G. Harea1, J. Cannon3, L. Cancio6, S. Nessen6, V. Sams4, P. Mason4, J. Lantry5, A. Batchinsky1,2  1The Geneva Foundation,Tacoma, WA, USA 2University Of The Incarnate Word, School Of Osteopathic Medicine,Department Of Translational Medicine,San Antonio, TX, USA 3University Of Pennsylvania,Penn Presbyterian,Philadelphia, PA, USA 4Brooke Army Medical Center,Ft Sam Houston, TX, USA 5University Of Maryland,Medical Center,Baltimore, MD, USA 6United States Army Institute Of Surgical Research,JBSA Ft. Sam Houston, TX, USA

Introduction:  Noncompressible torso hemorrhage (NCTH) is highly lethal. We developed a model of NCTH with single lung ventilation due to pulmonary contusion, hemorrhage, and unilateral hilum clamping, hypothesizing that it leads to severe shock, acidosis, and ARDS.

Methods: After anesthesia, instrumentation, volume controlled mechanical ventilation (10ml/kg tidal volume (TV) and 5 cm H2O PEEP), and baseline data recording (BL), 8 swine (54±7kg) received right-sided contusion (PC) with a captive bolt device; chest tube; hemorrhage (Post Hem) to 40 mm Hg of mean arterial pressure (MAP); 30 minutes of shock (Post Shock); then thoracotomy with hilum clamping (Hilum Clamp); crystalloid resuscitation (36 ml/kg) followed by transfusion of the shed blood (Post Transf) and 12 and 24 hour follow up. Body temperature was not controlled. Data presented as means±SEM, statistics by Kruskal-Wallis test with a Dunnett adjustment, p-value < 0.05 (*).

Results: See Table 1. Injury led to progressive sustained tachycardia; sustained hypotension; desaturation with increased O2 needs; transient increase in Peak and Plateau pressure, ARDS, and lactic acidosis. Mortality was 38% at 24 hr with mean survival time of 16.5± 3.6 hr. In 7 animals, continuous epinephrine was administered at 0.1-5 mcg/kg/min; 2 animals required direct heart massage, and repeat defibrillations with CPR occurred in 4 animals. Histology confirmed diffuse alveolar damage consistent with ARDS in all animals.

Conclusion: We developed a model of NCTH which led to sustained tachycardia, profound hypotension; transient ARDS and lactic acidosis. This model will be used to investigate rescue interventions such as extracorporeal life support and normothermic vs. hypothermic resuscitation.