Compartment syndrome is known to occur in the extremities, but some believe it can also occur in the abdomen and in the cranial cavity. Compartment syndrome occurs when narrow compartments defined by fascial elements or bone are exposed to increased pressure, resulting in ischemia and organ dysfunction. The exact clinical condition that defines abdominal compartment syndrome (ACS) remains controversial. However, organ dysfunction caused by intra-abdominal hypertension (IAH) is considered as abdominal compartment syndrome. Intraperitoneal hypertension is defined as sustained IAP above 12 mm Hg, and ACS results from repeated pressure elevations above 20 mm Hg with associated organ dysfunction. Organ dysfunction may be respiratory failure due to impaired tidal volume, decreased urine output due to decreased renal blood flow, or organ dysfunction due to increased intra-abdominal pressure. Surgical decompression remains the main treatment for ACS. Although first recognized over 150 years ago, the pathophysiological effects of increased intra-abdominal pressure (IAP) have essentially been rediscovered only in the last 20 years. Explosive scientific research and accumulation of clinical experience have confirmed the significant adverse effects of both 'intra-abdominal hypertension' (IAH), the presence of elevated intra-abdominal pressure, and 'abdominal compartment syndrome' (ACS). His study of IAH-induced organ dysfunction and dysfunction in critically ill patients. IAH has been identified as a continuum of pathophysiologic changes that begins with focal perfusion failure leading to overt end-organ damage and development of ACS. ACS has been found to cause significant morbidity and mortality in critical surgical, medical, and pediatric patients. Once present and underestimated, IAH and ACS are now recognized as common occurrences in the intensive care unit (ICU). Elevated IAP has been identified as an independent predictor of mortality during critical illness and is critical for the development of multiple organ failure, a syndrome that has plagued critically ill patients and physicians for decades. Evidence-based consensus definitions and recommendations for resuscitation and rehabilitation of patients with IAH and ACS have recently been published. Central to this evolving strategy is the use of early serial IAP measurements to detect the presence of IAH and the use of comprehensive medical management strategies to reduce elevated IAP and restore end-organ perfusion, timely surgical abdominal decompression, and early attempts for refractory organ dysfunction. Fascial closure at physiologically relevant time points. Such strategies have been shown to significantly improve patient survival, reduce complications (such as intestinal fistula), and reduce resource utilization. The following overview discusses both the pathophysiological impact of increased IAP on various organ systems and the currently accepted definitions surrounding IAH and ACS. Diagnosis, prevention, and treatment of IAH/ACS have been addressed in many recent publications. In most patients, the critical IAP appears to be 10-15 mmHg. At this pressure, microcirculatory blood flow is reduced and the first signs of organ dysfunction and failure appear. ACS is a natural consequence of end-organ changes due to these pressures and develops when IAH is not recognized and treated in time. Although ACS is generally fatal if not recognized and treated appropriately, prevention and/or timely intervention is associated with significant improvements in organ function and patient survival.