Acute abdominal compartment syndrome

Abstract

Acute abdominal compartment syndrome can be an elusive clinical diagnosis for which critical care physicians must exercise a high index of suspicion in the differential diagnosis of hemodynamic compromise and hemorrhagic shock. The purpose of these Rounds is to describe a case of abdominal compartment syndrome and to summarize the pathophysiology, differential diagnosis, etiology, and treatment of this entity. The Research Ethics Committee of the Montreal Heart Institute granted approval for use of the related images for publication purposes. A middle-aged male was admitted to the intensive care unit (ICU) for management of lower gastro-intestinal bleeding and hemorrhagic shock. His medical history was remarkable for cirrhosis (Child-Pugh Stage C) secondary to hepatitis C, with previous ligature of esophageal varices. He also had undergone a colonoscopy with a cecal polyp resection five days earlier. The initial blood work-up showed a 6.0 g decrease in hemoglobin. The patient was mechanically ventilated and transfused with six units of packed red blood cells. Despite blood transfusion and aggressive resuscitation with crystalloids, noradrenaline was required at an infusion rate of 15 lg min to maintain a mean arterial pressure (MAP) [65 mmHg. Esophagogastric endoscopy showed no active bleeding. A colonoscopy was planned, and 4 L of an oral preparation (Golytely) were to be administered via a nasogastric tube (NGT). After 30 min and 1 L of the oral preparation had been administered, the patient’s blood pressure decreased to 50 mmHg and the noradrenaline infusion was increased to 53 lg min (Fig. 1a). The patient’s abdomen became increasingly tense and he developed anuria. His intravesical pressure at this time was 28 mmHg (Fig. 1b). A diagnosis of acute compartment syndrome (ACS) was made, and ultrasound-guided paracentesis (Figs. 2 and 3a, b) and nasogastric aspiration were performed. Two and one-half litres of ascitic fluid and 1 L of the enteral solution were removed through aspiration. Shortly after this intervention, the noradrenaline requirements decreased to 10 lg min to maintain the MAP [65 mmHg. On angiography, an intracecal bleeding site was identified and the cecal artery was embolized. The bleeding stopped and the patient later stabilized. A review of computed tomography scans of the abdomen performed one week prior to this acute event revealed signs of liver cirrhosis with portal hypertension and ascitis (Fig. 4 [videos #1 and #2 online at www.springerlink.com]). Note was made of the fact that the inferior vena cava was significantly narrowed in its intrahepatic portion. Abdominal compartment syndrome is defined as a sustained abdominal pressure [20 mmHg with evidence of organ dysfunction relieved by abdominal decompression. Electronic supplementary material The online version of this article (doi:10.1007/s12630-009-9140-8) contains supplementary material, which is available to authorized users.