ACS OVERVIEW
» Overview
» Impact on Outcome
» Does monitoring and
   intervention improve
   outcome in IAH?
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» IAH and Renal
» IAH and Gut
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» IAH and Hemodynamic
   Monitoring Errors
» IAH and Pancreatitis
» IAH and Sepsis
» IAH and Burns
» IAH and Pediatrics
» IAH Interventions
» ACS and IAH Prevalence
» ACS and Multiple Organ
   Failure
» Volume of Infusion
» Abdominal Perfusion Pressure
» No such thing as an open abdomen
» Catheter Associated UTI
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Intra-abdominal pressure and the gut

The effect of elevated intra-abdominal pressure has direct impact on gut and liver physiology. Numerous events are occurring simultaneously:

  1. Direct compression of mesenteric and hepatic capillaries leading to reduced tissue flow.[1, 2]
  2. Direct compression of mesenteric, vena caval and portal veins leading to venous congestion, edema and worsened IAP.[1-3]
  3. Reduced cardiac output (see cardiovascular physiology) and increased afterload further exacerbating arterial flow.
  4. Reduced oxygenation (see pulmonary physiology) further exacerbating tissue ischemia.
Elevated IAP results in tissue ischemia throughout the abdominal cavity, affecting all organs (except perhaps the adrenal gland). These events begin with pressures as low as 8 to 12 mm Hg.[1, 4] The process is a vicious cycle – as the pressure increases, venous congestion increases and arterial blood flow drops leading to tissue ischemia. Ischemia leads to further capillary leak and cellular damage, which causes more edema. Increasing edema results in further increases in intra-abdominal pressure and a self-perpetuating condition of ischemia, capillary leak and increased pressure.

As the gut becomes increasingly more hypoxic, inflammatory mediators are released and bacterial translocation occurs. These events may lead to sepsis and multiple organ dysfunction syndromes.[5] Hypoxia and congestion of the liver also result in reduced clotting factor production and coagulopathies may develop.[3] Finally, as the abdominal wall tension increases, blood flow decreases and significant problems may occur with wound healing.[6]

In summary, elevated intra-abdominal pressure leads a vicious cycle of ischemia, inflammation, bacterial translocation and additional edema with resultant worsening abdominal hypertension. The end result is multiple organ failure and possibly death.


References
  1. Diebel, L.N., S.A. Dulchavsky, and R.F. Wilson, Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma, 1992. 33(1): p. 45-8.
  2. Hunter, J.D. and Z. Damani, Intra-abdominal hypertension and the abdominal compartment syndrome. Anaesthesia, 2004. 59(9): p. 899-907.
  3. Diebel, L.N., et al., Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma, 1992. 33(2): p. 279-82.
  4. Schwarte, L.A., et al., Moderate increase in intraabdominal pressure attenuates gastric mucosal oxygen saturation in patients undergoing laparoscopy. Anesthesiology, 2004. 100(5): p. 1081-7.
  5. Diebel, L.N., S.A. Dulchavsky, and W.J. Brown, Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma, 1997. 43(5): p. 852-5.
  6. Diebel, L., J. Saxe, and S. Dulchavsky, Effect of intra-abdominal pressure on abdominal wall blood flow. Am Surg, 1992. 58(9): p. 573-5.