Intraabdominal Hypertension, Abdominal Compartment Syndrome, and the Open Abdomen

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Abstract

Abdominal compartment syndrome (ACS) is the end point of a process whereby massive interstitial swelling in the abdomen or rapid development of a space-filling lesion in the abdomen (such as ascites or a hematoma) leads to pathologically increased pressure. This results in so-called intraabdominal hypertension (IAH), causing decreased perfusion of the kidneys and abdominal viscera and possible difficulties with ventilation and maintenance of cardiac output. These effects contribute to a cascade of ischemia and multiple organ dysfunction with high mortality. A few primary disease processes traditionally requiring large-volume crystalloid resuscitation account for most cases of IAH and ACS. Once IAH is recognized, nonsurgical steps to decrease intraabdominal pressure (IAP) can be undertaken (diuresis/dialysis, evacuation of intraluminal bowel contents, and sedation), although the clinical benefit of such therapies remains largely conjectural. Surgical decompression with midline laparotomy is the standard ultimate treatment once ACS with organ dysfunction is established. There is minimal primary literature on the pathophysiological underpinnings of IAH and ACS and few prospective randomized trials evaluating their treatment or prevention; this concise review therefore provides only brief summaries of these topics. Many modern studies nominally dealing with IAH or ACS are simply epidemiologic surveys on their incidence, so this paper summarizes the incidence of IAH and ACS in a variety of disease states. Especially emphasized is the fact that modern critical care paradigms emphasize rational limitations to fluid resuscitation, which may have contributed to an apparent decrease in ACS among critically ill patients.

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