TY - JOUR
T1 - Partial Resuscitative Endovascular Balloon Occlusion of the Aorta in Swine Model of Hemorrhagic Shock
AU - Russo, Rachel M.
AU - Neff, Lucas P.
AU - Lamb, Christopher M.
AU - Cannon, Jeremy W.
AU - Galante, Joseph M.
AU - Clement, Nathan F.
AU - Grayson, J. Kevin
AU - Williams, Timothy K.
N1 - Publisher Copyright:
© 2016
PY - 2016/8/1
Y1 - 2016/8/1
N2 - Background Complete resuscitative endovascular balloon occlusion of the aorta (C-REBOA) increases proximal mean arterial pressure (MAP) at the cost of distal organ ischemia, limiting the duration of intervention. We hypothesized that partial aortic occlusion (P-REBOA) would maintain a more physiologic proximal MAP and reduce distal tissue ischemia. We investigated the hemodynamic and physiologic effects of P-REBOA vs C-REBOA. Study Design Fifteen swine were anesthetized, instrumented, splenectomized, and subjected to rapid 25% blood volume loss. They were randomized to C-REBOA, P-REBOA, or no intervention (controls). Partial REBOA was created by partially inflating an aortic balloon catheter to generate a 50% blood pressure gradient across the balloon. Hemodynamics were recorded and serum makers of ischemia and inflammation were measured. After 90 minutes of treatment, balloons were deflated to evaluate the immediate effects of reperfusion. End organs were histologically examined. Results Complete REBOA produced supraphysiologic increases in proximal MAP after hemorrhage compared with more modest augmentation in the P-REBOA group (p < 0.01), with both groups significantly greater than controls (p < 0.01). Less rebound hypotension after balloon deflation was seen in the P-REBOA compared with C-REBOA groups. Complete REBOA resulted in higher serum lactate than both P-REBOA and controls (p < 0.01). Histology revealed early necrosis and disruption of duodenal mucosa in all C-REBOA animals, but none in P-REBOA animals. Conclusions In a porcine hemorrhagic shock model, P-REBOA resulted in more physiologically tolerable hemodynamic and ischemic changes compared with C-REBOA. Additional work is needed to determine whether the benefits associated with P-REBOA can both extend the duration of intervention and increase survival.
AB - Background Complete resuscitative endovascular balloon occlusion of the aorta (C-REBOA) increases proximal mean arterial pressure (MAP) at the cost of distal organ ischemia, limiting the duration of intervention. We hypothesized that partial aortic occlusion (P-REBOA) would maintain a more physiologic proximal MAP and reduce distal tissue ischemia. We investigated the hemodynamic and physiologic effects of P-REBOA vs C-REBOA. Study Design Fifteen swine were anesthetized, instrumented, splenectomized, and subjected to rapid 25% blood volume loss. They were randomized to C-REBOA, P-REBOA, or no intervention (controls). Partial REBOA was created by partially inflating an aortic balloon catheter to generate a 50% blood pressure gradient across the balloon. Hemodynamics were recorded and serum makers of ischemia and inflammation were measured. After 90 minutes of treatment, balloons were deflated to evaluate the immediate effects of reperfusion. End organs were histologically examined. Results Complete REBOA produced supraphysiologic increases in proximal MAP after hemorrhage compared with more modest augmentation in the P-REBOA group (p < 0.01), with both groups significantly greater than controls (p < 0.01). Less rebound hypotension after balloon deflation was seen in the P-REBOA compared with C-REBOA groups. Complete REBOA resulted in higher serum lactate than both P-REBOA and controls (p < 0.01). Histology revealed early necrosis and disruption of duodenal mucosa in all C-REBOA animals, but none in P-REBOA animals. Conclusions In a porcine hemorrhagic shock model, P-REBOA resulted in more physiologically tolerable hemodynamic and ischemic changes compared with C-REBOA. Additional work is needed to determine whether the benefits associated with P-REBOA can both extend the duration of intervention and increase survival.
UR - http://www.scopus.com/inward/record.url?scp=84991230575&partnerID=8YFLogxK
U2 - 10.1016/j.jamcollsurg.2016.04.037
DO - 10.1016/j.jamcollsurg.2016.04.037
M3 - Article
C2 - 27138649
AN - SCOPUS:84991230575
SN - 1072-7515
VL - 223
SP - 359
EP - 368
JO - Journal of the American College of Surgeons
JF - Journal of the American College of Surgeons
IS - 2
ER -