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Intra-abdominal hypertension and the gut

It is not surprising that intraabdominal hypertension leads to serious pathophysiologic changes in the gut and the retroperitoneal space.  A brief review of the pathophysiology of this syndrome shows that critical illness and the ensuing inflammatory changes lead to profound capillary permeability that manifests primarily with edema in the bowel wall and mesentery (see detailed discussion of this physiology by clicking here). This edema leads to compression of the venous structures of the bowel causing venous and lymphatic obstruction and congestion with increasing tissue edema and ischemia.[1-5] As the pressure continues to rise to the level of capillary perfusion pressure (15-25 mm Hg) the capillary structures begin to become compressed – a point at which severe ischemic injury will ensue.

Another symptom of IAH related to the bowel is feeding intolerance. Because the intestinal villa are underperfused during IAH, patients tend to not absorb nutrients well and can suffer problems with feeding intolerance. Dr. Reintam and her team have come up with a score for this - the GIF score or gastrointestinal failure score which they have found to be another predictor of mortality.[16] They also found a close relationship between IAH and gastrointestinal symptoms with higher pressures correlating with worse GIF scores/ worse feeding intolerance.[17] However, patients with IAH but no feeding intolerance did well. (click here for open access article.) The current belief is that we should still try to begin enteral feedings at 36-48 hours if possible, even if only at trophic levels to enhance gut function, but be aware of gut dysfunction and rising IAP levels to adjust this or potentially discontinue feedings if the patients IAP continues to rise.

Another concept that is being actively investigated is the concept of abdominal perfusion pressure - what flow is actually occurring to the gut in the face of elevated intraabdominal pressure - Click here to read about abdominal perfusion pressure.

 IAH pathophysiology

Figure – Pathophysiology of IAH

(click here for high resolution 8MB  file of this diagram including a section on its impact on gut capillary perfusion)

This bowel edema and progressive ischemia lead to the production of pro-inflammatory cytokines that accumulate in the bowel and ascitic fluid. As the levels increase they are transported into the lymphatic system and blood stream, leading to increasingly elevated serum cytokine levels.[6-11] Several investigators have shown a direct link between intraabdominal pressure increases, inflammatory mediator levels and organ injury in critical illness.[7, 8, 12, 13]  Kowal-Vern found markedly elevated peritoneal and plasma cytokine levels in patients suffering from IAH, suggesting this as a reservoir for systemic inflammation.[6] Al-Bahrani noted patients with abdominal sepsis to have a 75% and 25% rate of IAH and ACS respectively.[12] Those patients with IAH/ACS had much higher plasma endotoxin levels that resolved as the IAP was reduced.  Kubiak et al provide data from a trauma/sepsis model showing that increasing intraabdominal pressure is associated with massive increases in inflammatory mediators within the gut milieu.[7] These mediators and the resulting IAH can be attenuated by negative pressure removal of bowel fluid. The treatment leads to reduced IAP, reduced inflammatory mediators in the bowel and the systemic circulation, and dramatic improvements in the histopathology of the lung, liver and kidney (see photos below). In other words, by treating the inflammatory and pressure problems occurring in the gut, they were able to attenuate multiple organs dysfunction syndrome (MODS). The authors conclude that sepsis can result in inflammatory ascites and intraabdominal hypertension, which may perpetuate organ injury. By removing this ascites and reducing the abdominal pressure the cycle can be broken and MODS can be stopped. Shah and colleagues found that the peritoneal fluid of animals subjected to IAH was proinflammatory and would prime naïve immune cells – suggesting a therapeutic advantage of removing that fluid in patients suffering from IAH.[14]

 histology slide of the gut mucosa following IAHIL-6 cytokine levels are reduced with negative pressure therapy for IAH

Click slide to enlarge

Figure: This histology slide shows the damage to the intestinal mucosa from the adverse affects of IAH cytokine production.  The left slide is in an animal that had no therapy beyond decompression, the right slide is from and animal that had the IAP actively decreased and the cytokines suctioned out of the bowel and peritoneal space with negative pressure therapy. Cleary the active treatment group did better. Similar histologic improvements were seen in the kidney, liver and lung (go to those sections to see the slides).The second slide shows how active treatment not only reduced inflammatory mediators in the peritoneal fluid, but also in the circulating plasma.

 

Summary:

As the gut becomes increasingly more hypoxic due to the cardiovascular effects of IAH, inflammatory mediators are produced and bacterial translocation from the gut lumen to the lymphatic and circulatory systems occur. If untreated, these events may lead to multiple organ dysfunction syndromes.[2]  Hypoxia and congestion of the liver also result in reduced clotting factor production and coagulopathies may develop.[4] Finally, as the abdominal wall tension increases, blood flow decreases and significant problems may occur with wound healing.[15] In summary, elevated intra-abdominal pressure leads a viscous cycle of ischemia, inflammation, bacterial translocation and additional edema with resultant worsening abdominal hypertension.  The end result is multiple organ dysfunction / failure and possibly death.

Free articles:

Reintham-Blaser, A., et al., Intra-abdominal hypertension and gastrointestinal symptoms in mechanically ventilated patients. Critical Care Res and Pract, 2011. 1: p. 1-5. (Click here for open access free article)

Hill L, et al., The effect of intra-abdominal hypertension on gastrointestinal function. South African J Crit Care 2011. 27 (1). (Click here for the abstract)

References:

1.            Malbrain, M.L., et al., Lymphatic drainage between thorax and abdomen: please take good care of this well-performing machinery. Acta Clin Belg Suppl, 2007(1): p. 152-61.

2.         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.

3.         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.

4.         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.

5.            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.

6.            Kowal-Vern, A., et al., Elevated cytokine levels in peritoneal fluid from burned patients with intra-abdominal hypertension and abdominal compartment syndrome. Burns, 2006.

7.            Kubiak, B.D., et al., Peritoneal Negative Pressure Therapy Prevents Multiple Organ Injury in a Chronic Porcine Sepsis and Ischemia/Reperfusion Model. Shock, 2010.

8.            Marinis, A., et al., Ischemia as a possible effect of increased intra-abdominal pressure on central nervous system cytokines, lactate and perfusion pressures. Crit Care, 2010. 14(2): p. R31.

9.         Oda, S., et al., Management of Intra-abdominal Hypertension in Patients With Severe Acute Pancreatitis With Continuous Hemodiafiltration Using a Polymethyl Methacrylate Membrane Hemofilter. Ther Apher Dial, 2005. 9(4): p. 355-61.

10.            Rezende-Neto, J.B., et al., The abdominal compartment syndrome as a second insult during systemic neutrophil priming provokes multiple organ injury. Shock, 2003. 20(4): p. 303-8.

11.            Rezende-Neto, J.B., et al., Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure. J Trauma, 2002. 53(6): p. 1121-8.

12.       Al-Bahrani, A.Z., et al., Gut barrier dysfunction in critically ill surgical patients with abdominal compartment syndrome. Pancreas, 2010. 39(7): p. 1064-9.

13.       Raraty, M.G., et al., Acute pancreatitis and organ failure: pathophysiology, natural history, and management strategies. Curr Gastroenterol Rep, 2004. 6(2): p. 99-103.

14.       Shah, S.K., et al., A novel mechanism for neutrophil priming in trauma: potential role of peritoneal fluid. Surgery, 2010. 148(2): p. 263-70.

15.       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.

16.     Reintam, A., et al., Gastrointestinal failure score in critically ill patients: a prospective observational study. Crit Care, 2008. 12(4): p. R90.

17.     Reintham-Blaser, A., et al., Intra-abdominal hypertension and gastrointestinal symptoms in mechanically ventilated patients. Critical Care Res and Pract, 2011. 1: p. 1-5. (Click here for open access free article)