You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 138 No. 7, July 2003 TABLE OF CONTENTS
  Archives
  •  Online Features
  Original Article
 This Article
 •Full text
 •PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citing articles on ISI (23)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Topic Collections
 •Surgery, Other
 •Alert me on articles by topic

Mechanism of Acute Ascites Formation After Trauma Resuscitation

John C. Mayberry, MD; Kenneth J. Welker, MD; Robert K. Goldman, MD; Richard J. Mullins, MD

Arch Surg. 2003;138:773-776.

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

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

Methods  Retrospective review of case series.

Results  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.

Conclusions  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.


From the Department of Surgery, Oregon Health & Science University, Portland.







HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2003 American Medical Association. All Rights Reserved.