ACUTE ABDOMINAL COMPARTMENT SYNDROME
 R.A.S HEMAT, MB;BCh, FRCSI, Dip.Urol.UCL.
A healthy awake man generates 60-80 mmHg of intraabdominal pressure with Valsalva manoeuvre. Intraabdominal pressure is 8 cmH2O at rest, 35 cmH2O with defecation, 60 cmH2O with vomiting, and 80 cmH2O and above with coughing. Intraabdominal pressure of 200 mmHg is associated with abdominal burst.
Compartment syndrome as a reperfusion injury is a cyclic event. Compartment syndrome is a condition in which increased pressure in a confined anatomical space adversely affect the circulation and threatens the function and viability of the tissues therein. The abdomen is also a space in which elevated pressure can cause a compartment syndrome.
AACS induces severe multiple organ systems effects. EIAP, due to whatever mechanism, creates a compartment syndrome, and all intraabdominal viscera including the abdominal wall, are placed under ischaemic conditions. The compression of the renal parenchyma itself by perirenal processes, described by Page 1939, produces renal ischaemia without renal artery stenosis.
The physiological changes that occur with raised intra-abdominal pressure leads to the reduction in thoracic compliance. ACS causes organ failure secondary to increased intra-abdominal pressure. The physiologic basis for visceral oedema lies in the body’s normal response to trauma (acute inflammatory response). Ischaemia to abdominal wall muscle leads to myoglobinuria. 30 minutes after intraabdominal pressure abolition significant quantities of reactive oxygen metabolic production of free radical are produced, the malondialdehyde (MDA), an intermediate of lipid peroxidation are released from intestine, liver, and spleen. Increased MDA levels are also found in the lung, it has a potential role in the development of lung oedema. During 60 minutes of EIAP signs of severe ischaemia will be shown. The infusion of dopamine during raised pressure would not alter the decrease in RVF or the fall in urine output. There is profound reduction in renal cortical perfusion (60%) after a 15 mmHg pressure rise, results in a 50% reduction in urine output. Increased intrathoracic pressure, by elevation of the diaphragm, lead to increase in ventricular filling pressure and decrease in cardiac compliance. Both hemidiaphragms are pushed upward by the increased intra-abdominal pressure, which decreases thoracic volume and compliance. So, mechanical ventilation is required to compensate, but positive end-expiratory pressure (PEEP) ventilation causes further physiological abnormalities when combined with an increased intra-abdominal pressure.
AACS raises the intracranial pressure, which may increase the risk of neuronal damage by decreasing cerebral perfusion pressure. Elevated IAP significantly increase intracranial pressure (ICP) at pressures routinely used during diagnostic laparoscopy. There are 2 possible mechanisms by which the increased in intracranial pressure possibly occur: A- decrease in thoraco-abdominal compliance caused by EIAP results in increased mean intrathoracic pressure, and B- decrease in or restriction of lumber venous plexus outflow potentially causes increased spinal canal pressure, increases cerebral spinal fluid pressure and secondary increases in intracranial pressure. Diminishing venous return increases ICP. Insignificant decrease in CPP that occurs at lower IAPs may be clinically significant. This is because CPP is the most important determinant of cerebral haemodynamic responses. EIAP increases ICP by impeding venous return, via the jugular venous system, from the cranial vault. Because the spinal canal and the intracranial vault are continuous, a sudden rise in intraspinal pressures causes a concomitant increase in the intracranial pressure. The aetiology of the sudden increase of capillary permeability remains unclear. Gingko biloba extract is a powerful and specific platelet activating factor receptor antagonist had been used with success. The colloid solutions may further elevate the compartment pressures in the tissue and may contribute or precipitate the compartment syndrome. Ischaemia-reperfusion syndrome of the kidney may result from resuscitation following systemic hypotension.
The urinary bladder is the most reliable viscus to use to measure abdominal pressure. High intra-abdominal pressure (IAP) can exist even though the urinary bladder pressure monitoring is not elevated.
Decompressive laparotomy leads to a rapid improvement in pulmonary parameters and oxygen delivery. The ACS is an example of ischaemia/reperfusion injury. After decompression of AACS, cardiac, respiratory, renal function, and cerebral haemodynamics, immediately improve.
Skin closure alone may produce intra-abdominal pressure of 50 mmHg or more. The 3L plastic cystoscopy fluid irrigation bag is large, soft, pliable, strong, and cost-effective. It helps retain body heat, minimises fluid loss, and loss does not irritate the underlying tissue. The underlying tissue will not adhere to silo bag.
Decompression of raised intra-abdominal pressure can be a life-saving, complications are manageable by vigilant nursing team.
October, 2004
Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology (urotext-Basics volume 1), Principles of modern urology, by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.
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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.
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