Mechanism of acute ascites formation after trauma resuscitation

Severely injured patients have been observed to acutely develop ascites; however, the pathogenesis of this rare phenomenon is poorly understood.

To report the factors common among severely injured patients developing ascites and to formulate a hypothesis regarding its origin.

Retrospective review of case series.

We identified 9 injured patients between January 1, 1993, and December 31, 1998, who acutely developed significant amounts of ascites. The mean +/- SD estimated ascites volume was 2.0 +/- 0.8 L. All 9 patients had severe shock and were mechanically ventilated before abdominal decompression for the abdominal compartment syndrome. The mean +/- SD peak inspiratory pressure was 39.0 +/- 5.8 cm H2O. The mean +/- SD volumes of crystalloid and blood product infusion before decompression were 16.1 +/- 10.2 L and 5.2 +/- 4.8 L, respectively, in a mean +/- SD of 17 +/- 15 hours. In comparison, the mean +/- SD volumes of crystalloid and blood product transfusion among 100 contemporary, randomly selected patients undergoing trauma laparotomy were 5.1 +/- 5.5 L and 1.1 +/- 2.5 L, respectively (P<.001). Eight patients had only extra-abdominal injuries, while 1 patient had a combination of extra- and intra-abdominal injuries. Two patients were found to be cirrhotic by liver biopsy, but the other 7 patients had no known preexisting hepatic disease. Eight patients had absorbable mesh temporary abdominal closure, and 1 patient had primary fascial closure. There was persistent ascitic drainage in 5 patients; however, in all but 1 patient with cirrhosis, the drainage did not persist beyond 3 days. Two patients died, 1 of sepsis and the other of a closed head injury.

Common denominators of posttraumatic ascites include shock, massive fluid resuscitation, and elevated intrathoracic pressure. The rapid onset of ascites in the setting of elevated intrathoracic pressure suggests that the patient's ability to clear ascitic fluid is overwhelmed.