The Compartment Syndrome of the Abdominal Cavity: A State of the Art Review

Abstract

Abdominal compartment syndrome gains increasing recognition. It impairs physiology and requires treatment. It occurs more commonly with acute rather than chronic abdominal hypertension. Functional impairments involve the cardiovascular system, respiratory system, hepatic, renal, and gastrointestinal function, and intracranial pressure. Abdominal hypertension decreases venous return, increases systemic vascular resistance and intrathoracic pressure, and therefore reduces cardiac output. It also adversely affects cardiovascular monitoring. In the presence of increased abdominal pressure, atelectasis and pneumonia are likely to develop and impaired ventilation may lead to respiratory failure. Also, blood flow to the liver and kidney may be reduced, resulting in functional impairment of both organs. The adverse effects on gastrointestinal function result from impairing lymphatic, venous, and arterial flow. Anastomotic healing may become a problem under these circumstances. Decreased venous return through the inferior vena cava in obese patients may lead to venous stasis ulcers and hemorrhage. The correlation of increased intracranial pressure and intra-abdominal pressure may be a problem for trauma patients with simultaneous injuries to the head and the abdomen. There are three severity grades of increased intra-abdominal pressure: Acute sustained elevation of intra-abdominal pressure above 10–20 mmHg is called mild abdominal hypertension. Physiologic effects are generally well compensated and usually clinically nonsignificant. Nonoperative therapy may be required. Moderate hypertension is defined as sustained elevation of 21–35 mmHg. Therapy is generally necessary. Surgical abdominal-decompression may be critical. Severe hypertension or abdominal compartment syndrome is defined as sustained elevation above 35 mmHg. Operative decompression is always indicated. The gap between the abdominal wound edges must be temporarily covered to prevent fascia retraction and formation of a huge hernia. All detrimental effects of elevated intra-abdominal pressure and the methods and benefits of its decompression have been well studied, both in the laboratory and in clinical practice. Diagnostic suspicion may be confirmed with objective measurements of intra-abdominal pressure to select patients who may benefit from decompression. Operative decompression is achieved by abdominal fasciotomy and covering the fascial gap with mesh made of Marlex®, Gore-Tex®, silastic, or by a Velcro-like closure mesh (artificial bur). All meshes help to effectively decompress the abdomen. The artificial bur offers further advantages by permitting successive reapproximation of the fascia until final fascial closure, and avoiding the fistula and hernia formation seen with the other meshes.

V.A.C.® Abdominal Dressing System

“…The management of abdominal compartment syndrome (ACS), with its effect on pulmonary, cardiac and renal functions, or the concept of damage-control laparotomy are techniques that proved to be an important advance of life-saving in trauma care [1][2][3]. A massive early resuscitation of trauma patients is often accompanied by marked visceral edema, retroperitoneal hematoma or a packing of the peritoneal cavity and results in an open abdomen situation.…”

Perspectives in Using Resonant Git Stimulation in Acute Pancreatitis

“…Последний аспект следует считать достаточно важным показателем висцеральной перфузии [20], в том числе в связи с тем, что он является критерием инфузионной терапии [11], так как уровень абдоминального перфузион-ного давления ниже 60 мм рт. ст.…”

Abdominal Compartment Syndrome

“…20 Gastric pressure is determined by infusing 50-100 ml water through a nasogastric tube into the lumen of the stomach. The proximal end of the open tube is held perpendicular to the fl oor.…”

“…All these reduce the stroke volume by compensatory tachycardia. 20,21,26,[30][31][32] Despite the very high left and right atrial pressure, radionucleotide-gated pool scans and echocardiography showed an adequate ejection fraction averaging 55% and ventricular volumes that were small or normal. If ACS is not treated, patients die due to left ventricular failure.…”

“…The pathogenesis of this malfunction is multifactoral, 34 and restoration of the CO to normal or supranormal values by blood volume expansion does not appear to prevent it reliably. 20 Changes in CO, direct compression of the abdominal aorta and the renal arteries, compression of the renal vein causing outfl ow obstruction, and compression of renal parenchyma with diminished renal blood fl ow, an increase in the renal vascular resistance and a redistribution of blood from the renal cortex to the medulla are the basic causes for the decrease in glomerular fi ltration rate (GFR). Furthermore, the direct compression of the kidneys increases cortical pressure, thus leading to a "renal compartment syndrome."…”