Practice Essentials Although compartment syndrome is well recognized to occur in the extremities, it also occurs in the abdomen and, some believe, in the intracranial cavity. Compartment syndrome occurs when a fixed compartment, defined by myofascial elements or bone, becomes subject to increased pressure, leading to ischemia and organ dysfunction. The exact clinical conditions that define abdominal compartment syndrome (ACS) are controversial; however, organ dysfunction caused by intra-abdominal hypertension (IAH) is considered to be abdominal compartment syndrome. The dysfunction may be respiratory insufficiency secondary to compromised tidal volumes, decreased urine output caused by falling renal perfusion, or any organ dysfunction caused by increased abdominal compartment pressure. Surgical decompression remains the mainstay treatment of ACS. However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS. [1, 2, 3, 4, 5, 6, 7, 8]
Abdominal compartment syndrome was recognized clinically in the 19th century when Marey and Burt observed its association with declines in respiratory function. In the early 20th century, Emerson's animal experiments demonstrated mortality associated with abdominal compartment syndrome. Initially, cardiorespiratory compromise was thought to be the cause; however, renal failure was hypothesized by Wendt and was later studied by Thorington and Schmidt.
More recently, Kron and Iberti developed a simple method of accurately measuring intra-abdominal pressure. This has led to a better understanding of the relationship between IAH and abdominal compartment syndrome.
The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations  :
Intra-abdominal pressure (IAP) is approximately 5-7 mm Hg in critically ill adults. Intra-abdominal hypertension is defined by a sustained or repeated pathological elevation in IAP of ≥12 mm Hg. ACS is defined as a sustained IAP >20 mm Hg associated with organ dysfunction/failure. IAH is graded as follows: Grade I: IAP 12-15 mm Hg; Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg. Recommend measuring intra-abdominal pressure when any known risk factor for IAH/ACS is present in critically ill or injured patients. Recommend that studies of IAH or ACS adopt the trans-bladder technique as a standard IAP measurement technique. Recommend decompressive laparotomy to decrease IAP in cases of overt ACS. Suggest brief trials of neuromuscular blockade as temporizing measure in treatment of IAH. Three categories As the diagnosis of abdominal compartment syndrome became easier to establish, it was observed to occur as a consequence of a variety of primary clinical events. Abdominal compartment syndrome can be divided into the following 3 categories:
Primary or acute abdominal compartment syndrome occurs when intra-abdominal pathology is directly and proximally responsible for the compartment syndrome
Secondary abdominal compartment syndrome occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation
Chronic abdominal compartment syndrome occurs in the presence of cirrhosis and ascites or related disease states, often in the later stages of the disease
In the ED and ICU In the emergency department and intensive care unit, abdominal compartment syndrome is recognized with growing frequency as the cause of morbidity such as metabolic acidosis, decreased urine output, and decreased cardiac output. The cause of these events might easily be mistaken for other pathologic events such as hypovolemia if the clinician is not alert to the morbidity associated with abdominal compartment syndrome.
Therapy should include fluid resuscitation and transfusion if needed. Pharmacologic therapy is less effective than mechanical drainage. Paracentesis may be a superior alternative to decompressive laparotomy in this patient population. (See Treatment and Medication.)
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