PURPOSE: To describe our experience with a novel technique to decompress abdominal compartment syndrome after endovascular aneurysm repair (EVAR) of ruptured abdominal aortic aneurysm (rAAA). METHODS: From January 2003 to April 2010, 13 patients (12 men; mean age 75 years) treated for rAAA with EVAR underwent tissue plasminogen activator (tPA)-assisted decompression for intra-abdominal hypertension. All of the patients but one had intra-abdominal pressure >20 mmHg, with signs of multiple organ failure or abdominal perfusion pressure <60 mmHg. With computed tomography guidance, a drain was inserted into the retroperitoneal hematoma, and tPA solution was injected to facilitate evacuation of the coagulated hematoma and decrease the abdominal pressure. RESULTS: In the 13 patients, the mean intra-abdominal pressure decreased from 23.5 mmHg (range 12-35) to 16 mmHg (range 10-28.5). A mean 1520 mL (range 170-2900) of blood was evacuated. Urine production (mean 130 mL/h, range 50-270) increased in 7 patients at 24 hours after tPA-assisted decompression; among the 5 patients in which urine output did not increase, 3 underwent hemodialysis by the 30-day follow-up. One patient did not respond with clinical improvement and required laparotomy. The 30-day, 90-day, and 1-year mortality was 38% (5/13 patients); none of the deaths was related to the decompression technique. CONCLUSION: tPA-assisted decompression of abdominal compartment syndrome after EVAR can decrease the intra-abdominal pressure and could be useful in preventing multiple organ failure. It is a minimally invasive technique that can be used in selected cases but does not replace laparotomy or retroperitoneal surgical procedures as the gold standard treatments.
PURPOSE: To describe our experience with a novel technique to decompress abdominal compartment syndrome after endovascular aneurysm repair (EVAR) of ruptured abdominal aortic aneurysm (rAAA). METHODS: From January 2003 to April 2010, 13 patients (12 men; mean age 75 years) treated for rAAA with EVAR underwent tissue plasminogen activator (tPA)-assisted decompression for intra-abdominal hypertension. All of the patients but one had intra-abdominal pressure >20 mmHg, with signs of multiple organ failure or abdominal perfusion pressure <60 mmHg. With computed tomography guidance, a drain was inserted into the retroperitoneal hematoma, and tPA solution was injected to facilitate evacuation of the coagulated hematoma and decrease the abdominal pressure. RESULTS: In the 13 patients, the mean intra-abdominal pressure decreased from 23.5 mmHg (range 12-35) to 16 mmHg (range 10-28.5). A mean 1520 mL (range 170-2900) of blood was evacuated. Urine production (mean 130 mL/h, range 50-270) increased in 7 patients at 24 hours after tPA-assisted decompression; among the 5 patients in which urine output did not increase, 3 underwent hemodialysis by the 30-day follow-up. One patient did not respond with clinical improvement and required laparotomy. The 30-day, 90-day, and 1-year mortality was 38% (5/13 patients); none of the deaths was related to the decompression technique. CONCLUSION: tPA-assisted decompression of abdominal compartment syndrome after EVAR can decrease the intra-abdominal pressure and could be useful in preventing multiple organ failure. It is a minimally invasive technique that can be used in selected cases but does not replace laparotomy or retroperitoneal surgical procedures as the gold standard treatments.