Interestingly, intra-abdominal hypertension impacts intra-cranial pressure. In fact, IAH is an independent risk factor for secondary brain injury after traumatic brain injury.[1] The physiology is fairly straight forward: As intra-abdominal pressure goes up, it pushes up the diaphragms, reducing intra-thoracic volume and causing elevated intrathoracic pressure. Elevated intra-thoracic pressure results in elevated central venous pressure and subsequent elevated internal jugular venous pressure. The result is a functional obstruction of cerebral venous outflow, resulting in increases in intra-cranial pressure and reduction in cerebral perfusion pressure.[2, 3] Citerio et al graphically demonstrated the direct correlation between IAH and ICP in a clinical setting.[2] They found that artificially induced IAP elevation led to immediate (in seconds) and significant increases in ICP, internal jugular pressure and central venous pressure (See figure). The impact of IAH on ICP has implications in trauma surgery since any use of laparoscopic techniques leads to substantial elevations in IAH and may cause further CNS ischemia.[4, 5]

Figure: Effect of IAP elevation on ICP and CVP

This figure from Citerio el al demonstrates the direct correlation between IAP and multiple other pressure measurements.[2] As demonstrated in the graph, IAP elevation leads to immediate (in seconds) and significant increases in ICP, IJP and CVP due to direct transmission of the IAP into the thorax, the central veins and the jugular veins. The result is venous outflow obstruction from the brain and concomitant elevations of ICP.

Another interesting insight from this data is the direct and immediate impact IAP has on CVP. For those clinicians who base fluid resuscitation and preload assessment on CVP (or on wedge pressures) this diagram graphically demonstrates that IAP causes a direct, non-fluid related increase in CVP - in effect a "false elevation" of the central venous pressure that has nothing to do with preload. Interpretation and use of CVP measurements without concomitant IAP data to correct for this false elevation may cause clinicians to misinterpret cardiac pressure data. It is not uncommon to see a very high CVP and PAOP (wedge) with poor cardiac index and suspect heart failure, when in fact these cardiac measurements are all a result of IAP elevation that has caused severe reduction in venous return to the heart with simultaneous elevations in intrathoracic pressure. In this setting, an echocardiogram of the heart will demonstrate an actively contracting left ventricle (i.e. not a failing heart) that simply cannot fill due to venous obstruction from the elevated IAP. Failure to recognize these IAP induced pathophysiologic changes may lead to treating the patient for heart failure rather than treating the cause of the problem - elevated intra-abdominal pressure.

1. Hunter, J.D. and Z. Damani, Intra-abdominal hypertension and the abdominal compartment syndrome. Anaesthesia, 2004. 59(9): p. 899-907.
2. Citerio, G., et al., Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med, 2001. 29(7): p. 1466-71.
3. Bloomfield, G.L., et al., A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med, 1997. 25(3): p. 496-503.
4. Josephs, L.G., et al., Diagnostic laparoscopy increases intracranial pressure. J Trauma, 1994. 36(6): p. 815-818.
5. Joseph, D.K., et al., Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma, 2004. 57(4): p. 687-95.