Factors associated with abdominal compartment syndrome complicating endovascular repair of ruptured abdominal aortic aneurysms.

BACKGROUND: Endovascular treatment of ruptured abdominal aortic aneurysms (r-AAAs) has the potential to offer improved outcomes. As our experience with endovascular repair of r-AAA evolved, we recognized that the development of abdominal compartment syndrome (ACS) led to an increase in morbidity and mortality. We therefore reviewed our experience to identify risk factors associated with the development of ACS. METHODS: From January 2002 to December 2004, 30 patients underwent emergent endovascular repair of r-AAA by using commercially available stent grafts. All patients who developed ACS underwent emergent laparotomy. Physiological and clinical parameters were analyzed between patients with and without ACS after endovascular r-AAA repair. RESULTS: Over the past 3 years, 30 patients underwent endovascular r-AAA repair, and 6 (20%) patients developed ACS. Patients with ACS had a higher incidence of the need for aortic occlusion balloon (67% vs 12%; P = .01), a markedly longer activated partial thromboplastin time (128 +/- 84 seconds vs 49 +/- 31 seconds; P = .01), a greater need for blood transfusion (8 +/- 2.5 units vs 1.8 +/- 1.7 units; P = .08), and a higher incidence of conversion to aortouni-iliac devices because of ongoing hemodynamic instability and an inability to expeditiously cannulate the contralateral gate (67% vs 8%) when compared with patients without ACS. The mortality was significantly higher in the patients with ACS (67%; 4 of 6) compared with patients without ACS (13%; 3 of 24; P = .01). CONCLUSIONS: ACS is a potential complication of endovascular repair of r-AAA and negatively affects survival. Factors associated with the development of ACS include (1) use of an aortic occlusion balloon, (2) coagulopathy, (3) massive transfusion requirements, and (4) conversion of bifurcated stent grafts into aortouni-iliac devices. We recommend that, after endovascular repair of r-AAA, these patients undergo vigilant monitoring for the development of ACS.

Cutting edge: transplantation tolerance through enhanced CTLA-4 expression.

Knockout and blocking studies have shown a critical role for CTLA-4 in peripheral tolerance, however, it is unknown whether augmenting CTLA-4 expression actually promotes tolerance. Here we demonstrate a specific and requisite role for CTLA-4 and its up-regulation in tolerance through anti-CD45RB. First, long-term murine islet allograft survival induced by anti-CD45RB is prevented by CTLA4-Ig, which interferes with B7:CTLA-4 interactions. Second, anti-CD45RB is ineffective in recipients lacking CTLA-4, B7-1, and B7-2. In contrast, CTLA4-Ig, which targets B7 on allogeneic cells, promotes long-term engraftment in these mice. Moreover, anti-CD45RB was effective in B7-deficient controls expressing CTLA-4. Finally, in wild-type mice, CTLA-4 expression returned to baseline 17 days after receiving anti-CD45RB, and was refractory to further increase. Transplantation and anti-CD45RB therapy at this time could neither augment CTLA-4 nor prolong engraftment. These data demonstrate a specific role for CTLA-4 in anti-CD45RB-mediated tolerance and indicate that CTLA-4 up-regulation can directly promote allograft survival.