ACS OVERVIEW
» Overview
» Impact on Outcome
» Does monitoring and
   intervention improve
   outcome in IAH?
» IAH and Cardiac
» ACS and Pulmonary
» IAH and Renal
» IAH and Gut
» IAH and Brain
» 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
ACS Overview >>
Multiple organ failure and intra-abdominal hypertension

Intra-abdominal hypertension leads to organ dysfunction via two distinct and separate pathways. First, early on in the disease process there is a purely mechanical effects that cause significant and measurable organ dysfunction largely related to the effect of the elevated pressure on organ function and organ perfusion (please see individual organ system discussions for further detail). However, untreated IAH also causes immune and inflammatory effects that can result in progressive organ failure. In fact, an emerging body of experimental and clinical evidence suggests that untreated intra-abdominal hypertension (IAH) acts as the second insult in the two-event model of multiple organ failure (MOF).[1-8] The two-event model of multiple organ failure postulates that an initial insult causing cellular ischemia primes the patients immune system for an exaggerated response to any secondary insult.[9] This "priming" occurs for a limited time - about 3-16 hours following the initial insult - at which point the hyperresponsiveness of the immune system begins to taper.[10, 11] Interestingly, the most common time for IAH to develop is within an 8-16 hour time range following an initial tissue insult - the exact period of maximal immune responsiveness.[1, 10, 11] Rezende-Neto el al found that IAH causes elevated levels of pro-inflammatory cytokines (tumor necrosis factor, and interleukins IL-6 and IL-1) as well a lung myeloperoxidase (MPO) in an animal model.[2] They also found that the presence of IAH during the 8-16 hour "critical" time period resulted in a 3-fold increase in inflammatory neutrophil expression.[3] However, animals subjected to IAH insults < 2 hours or > 18 hours after initial insult fared much better. These authors conclude that a vulnerable period exists following ischemic injury and a second insult such as IAH causes a hyper-inflammatory immune response leading to a high incidence of MOF and death.[3] Other investigators have also found increases in inflammatory mediators as well as bacterial translocation across the bowel wall during the ischemic insult that occurs during from intra-abdominal pressure.[4-6, 12-15] These data suggest that abdominal compartment syndrome is not the terminal event caused by refractory shock/multiple organ failure. Instead, elevated intra-abdominal pressure acts as a "secondary insult" in the two-event model of multiple organ failure, leading to an overly aggressive immune response with inflammatory cytokine release.[1-8] The end result of this undetected and untreated "secondary insult" is multiple organ failure.

Solutions proposed to reduce the incidence of MOF related to elevated intra-abdominal pressures are several:

  1. Optimizing crystalloid infusion to avoid over-resuscitation and reduce the amount of capillary leak that occurs.[1, 16](See IAH algorithm in this web site for a multi-pronged approach to managing these patients. Also see cardiovascular physiology to understand some of the downfalls associated with standard CVP and wedge pressure measurements in the face of IAH).
  2. Further investigation into the role of colloids, blood substitutes and hypertonic saline in this patient group since there is evidence that these fluids reduce the hyper-inflammatory response.[1, 16-22]
  3. Early recognition of intra-abdominal hypertension through serial measurements of IAP (and perhaps pHi) with prompt medical and/or surgical interventions to prevent the development of significant mesenteric ischemia and the inflammatory cascade that accompanies this ischemia

References:
  1. Balogh, Z., et al., Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma, 2003. 54(5): p. 848-59.
  2. 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.
  3. 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.
  4. Kacmaz, A., et al., Octreotide: a new approach to the management of acute abdominal hypertension. Peptides, 2003. 24(9): p. 1381-6.
  5. Kacmaz, A., et al., Octreotide improves reperfusion-induced oxidative injury in acute abdominal hypertension in rats. J Gastrointest Surg, 2004. 8(1): p. 113-9.
  6. Sener, G., et al., Melatonin ameliorates oxidative organ damage induced by acute intra-abdominal compartment syndrome in rats. J Pineal Res, 2003. 35(3): p. 163-8.
  7. Bathe OF, Chow AW, and P. PT., Splanchnic origin of cytokines in a porcine model of mesenteric ischemia-reperfusion. Surgery, 1998. 123: p. 79-88.
  8. Bathe, O.F., A.W. Chow, and P.T. Phang, Splanchnic origin of cytokines in a porcine model of mesenteric ischemia-reperfusion. Surgery, 1998. 123(1): p. 79-88.
  9. Moore, F.A., E.E. Moore, and R.A. Read, Postinjury multiple organ failure: role of extrathoracic injury and sepsis in adult respiratory distress syndrome. New Horiz, 1993. 1(4): p. 538-49.
  10. Botha, A.J., et al., Postinjury neutrophil priming and activation: an early vulnerable window. Surgery, 1995. 118(2): p. 358-64.
  11. Zallen, G., et al., Circulating postinjury neutrophils are primed for the release of proinflammatory cytokines. J Trauma, 1999. 46(1): p. 42-8.
  12. 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.
  13. Eleftheriadis, E., et al., Gut ischemia, oxidative stress, and bacterial translocation in elevated abdominal pressure in rats. World J Surg, 1996. 20(1): p. 11-6.
  14. Gargiulo, N.J., 3rd, et al., Hemorrhage exacerbates bacterial translocation at low levels of intra-abdominal pressure. Arch Surg, 1998. 133(12): p. 1351-5.
  15. Moore, E.E., Mesenteric lymph: the critical bridge between dysfunctional gut and multiple organ failure. Shock, 1998. 10(6): p. 415-6.
  16. Balogh, Z., et al., Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg, 2003. 138(6): p. 637-43.
  17. Gonzalez, R.J., et al., Hyperosmolarity abrogates neutrophil cytotoxicity provoked by post-shock mesenteric lymph. Shock, 2002. 18(1): p. 29-32.
  18. Angle, N., et al., Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock. Shock, 1998. 9(3): p. 164-70.
  19. Rizoli, S.B., et al., Immunomodulatory effects of hypertonic resuscitation on the development of lung inflammation following hemorrhagic shock. J Immunol, 1998. 161(11): p. 6288-96.
  20. Zallen, G., et al., Hypertonic saline resuscitation abrogates neutrophil priming by mesenteric lymph. J Trauma, 2000. 48(1): p. 45-8.
  21. Johnson, J.L., et al., Resuscitation with a blood substitute abrogates pathologic postinjury neutrophil cytotoxic function. J Trauma, 2001. 50(3): p. 449-55; discussion 456.
  22. Johnson, J.L., et al., Alteration of the postinjury hyperinflammatory response by means of resuscitation with a red cell substitute. J Trauma, 2003. 54(1): p. 133-9.