Abdominal Pain, Anemia, and Oliguria in a Distressed Woman

Eva Nourbakhsh, MD; Kenneth M. Nugent, MD; Rishi Raj, MD


April 30, 2021


This patient presented with refractory hypotension, oliguria, metabolic acidosis, and anemia. A CT scan revealed a large abdominal wall hematoma, with collapse of the inferior vena cava. Her bladder pressure was initially high and further increased during a relatively short period of observation. The diagnosis of abdominal compartment syndrome (ACS) was made based on the multiorgan failure, evidence of abdominal wall hematoma secondary to anticoagulants, and increasing IAPs.

Compartment syndrome (CS) refers to a fixed compartment that becomes subject to increased pressure, whether from injury or other means, leading to reduced capillary circulation or outright venous collapse followed by ischemia and organ dysfunction. CS occurs most frequently in the extremities, but it may also occur in the abdomen and the organs. ACS often presents with pain and complaint of distended or bloated abdomen; however, it often occurs in unconscious patients and goes unnoticed. In the comatose patient, signs include a distended or overly "round" abdomen and vital sign deterioration with tachycardia and hypotension; if untreated, this leads to multiorgan failure and shock later.

ACS is defined as the adverse physiologic consequences that occur with an acute increase in IAP. The consensus statement from the World Society of the Abdominal Compartment Syndrome defines intra-abdominal hypertension (IAH) as an IAP of 12 mm Hg or higher and ACS as a sustained IAP of 20 mm Hg or higher associated with new organ dysfunction or failure.[1] The organ dysfunction occurs as a result of direct compression of hollow systems.[2] These structures collapse under high pressure, and thrombosis or bowel wall edema occurs, leading to translocation of bacterial products and additional fluid accumulation that further increases IAP.

At the cellular level, oxygen delivery is impaired, which causes ischemia and anaerobic metabolism. Vasoactive substances, such as histamine and serotonin, increase endothelial permeability, and this capillary leakage impairs red cell transport and oxygen delivery.

ACS can be divided into primary, secondary, and chronic forms. Primary or acute presentations occur when an intra-abdominal pathology is directly responsible for the CS. Examples of this include penetrating trauma, intraperitoneal hemorrhage, pancreatitis, pelvic fracture, rupture of an abdominal aortic aneurysm, and a perforated peptic ulcer. Secondary presentations occur when no visible intra-abdominal injury is present but injuries outside of the abdomen cause fluid accumulation; examples of this include large-volume resuscitation (>3 L), large areas of full-thickness burns, postoperative packing and primary fascial closure, and sepsis. Chronic ACS can develop in cases of cirrhosis with excessive ascites.[3]


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