Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure

The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury.

IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity.

IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema.

IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.