The "critical IAP"that causes organ dysfunction and impacts ultimate patient outcome varies from patient to patient due to differences in physiologic reserve and comorbidities.[1] For this reason, there is no “black and white” IAP threshold that clinicians can use to definitively decide if a patient is suffering end-organ damage from elevated IAP. In an effort to improve predictability of the impact of IAP on patients’ outcomes, the concept of abdominal perfusion pressure was developed. Abdominal perfusion pressure combines not only the absolute IAP but also the physiologic parameter of mean arterial pressure to better understand abdominal end organ perfusion. Research studies now demonstrate that abdominal perfusion pressure is superior to IAP, pH, base deficit, and arterial lactate in predicting patient outcomes.[1] Abdominal perfusion pressure may become the most useful parameter to guide clinicians in their resuscitation and management of patients suffering from ACS.[1]

The perfusion pressure of any anatomic compartment (extremity, skull, thorax, abdomen) is dependent on three factors[1].

1. The arterial inflow pressure
2. The venous outflow pressure
3. The compliance of the compartment to expand with increased volumes

The concept of perfusion pressure is best understood in the neuro-critical care ICU where patients with brain injuries have their intracranial pressure (ICP) and mean arterial pressure (MAP) carefully measured to insure that the perfusion of their brain (cerebral perfusion pressure – CPP) exceeds a critical threshold of 60 mm Hg. This perfusion is represented by the formula: CPP = MAP-ICP. An increase in MAP will improve cerebral perfusion, while an increase in ICP will reduce blood delivery to the brain tissue and reduce perfusion. If CPP falls below this threshold of 60 mm Hg, aggressive efforts are instituted to either increase the MAP or reduce the ICP. ICP can only be decreased by reducing the volume within the cranial vault (or expanding the vault with a craniectomy). Because the brain is contained within the non-compliant confines of the skull, as the volume within the brain begins to increase, so does the intracranial pressure (ICP). At a critical volume there is no additional space and the pressure dramatically increases, leading to significant tissue ischemia due to reduction in blood flow (see the diagram of the Monro-Kellie Doctrine).

Monroe-Kellie doctrine diagram

Abdominal perfusion pressure may be considered analogous to cerebral perfusion pressure. Abdominal perfusion pressure (APP) is determined by the arterial inflow pressure (MAP) and the intra-abdominal pressure (IAP) that resists blood delivery to the abdominal organs. This perfusion pressure is represented by the formula: APP = MAP-IAP. While the abdominal cavity is more complaint that the skull, it is not freely compliant and becomes increasingly rigid as it distends. At some point the compliance of the abdominal wall drops dramatically and the pressure begins to increase in a similar fashion (though not as steep of a slope) as that shown in the Monroe Kellie diagram. As this compliance threshold is crossed, IAP rises, APP decreases and organ ischemia worsens leading to intra-abdominal hypertension and if untreated – the abdominal compartment syndrome.

Early investigations into abdominal perfusion pressure have noted patients’ outcomes more closely related to the APP than to the IAP, MAP, or arterial lactate.[2] Cheatham et al retrospectively reviewed 144 patients with IAH and found that maintenance of an APP of at least 50 mm HG maximized the value of APP for predicting patient survival. Malbrain et al prospectively confirmed the utility of APP as an outcome predictor and concluded that maintaining an APP over 60 mm Hg with an IAP less than 12 mm Hg was best to optimize patient outcomes.[3] A management strategy that includes frequent IAP monitoring, optimization of abdominal perfusion pressure (greater than 50 to 60 mm Hg) through careful fluid and vasopressor support, medical interventions to reduce IAP and immediate abdominal decompression should IAP continue to rise or APP remain inadequate is necessary to ensure optimal patient survival. (See Management algorithm for a graphic display of such a management method). Utilizing and approach like this, Cheatham et al were able to improve patient outcomes – reducing the incidence of ACS from 64% to 43% and reducing patient mortality from 44% to 28% in a high-risk surgical population.[2]

In summary, early goal directed therapy to improve tissue perfusion and oxygen delivery is essential to ensure optimal survival and reduced morbidity in critically ill patients. Intra-abdominal pressure has a dramatic impact on the perfusion pressure and oxygen delivery to the organs within the abdominal cavity and retroperitoneal space. Focusing more attention on enhancing abdominal perfusion pressure and reducing intra-abdominal pressure to maintain adequate organ oxygen delivery can improve critically ill patient outcomes.

1. Cheatham, M.L. and M.L.N.G. Malbrain, Abdominal perfusion pressure, in Abdominal compartment syndrome, R.R. Ivatury, Editor. 2006, Landes Bioscience: Georgetown. p. 69-81.
2. Cheatham, M.L., et al., Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma, 2000. 49(4): p. 621-6.
3. Malbrain, M.L.N.G., Abdominal perfusion pressure as a prognostic marker in intra-abdominal hypertension, in Yearbook of Intensive Care and Emergency Medicine, J.L. Vincent, Editor. 2002, Springer: New York, Berlin, Heidelberg. p. 792-814.