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Ischemia as a possible effect of increased intra-abdominal pressure on central nervous system cytokines, lactate and perfusion pressures

Athanasios Marinis1*, Eriphili Argyra2, Pavlos Lykoudis1, Paraskevas Brestas1, Kassiani Theodoraki2, Georgios Polymeneas1, Efstathios Boviatsis3 and Dionysios Voros1

Author Affiliations

1 Second Department of Surgery, Aretaieion University Hospital, 76 Vassilisis Sofia's Av, GR-11528, Athens, Greece

2 First Department of Anesthesiology, Aretaieion University Hospital, 76 Vassilisis Sofia's Av., GR-11528, Athens, Greece

3 Department of Neurosurgery, "Evangelismos" Athens General Hospital, 45-47 Ipsilantou STR, GR-10676, Athens, Greece

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Critical Care 2010, 14:R31 doi:10.1186/cc8908

Published: 15 March 2010

Abstract

Introduction

The aims of our study were to evaluate the impact of increased intra-abdominal pressure (IAP) on central nervous system (CNS) cytokines (Interleukin 6 and tumor necrosis factor), lactate and perfusion pressures, testing the hypothesis that intra-abdominal hypertension (IAH) may possibly lead to CNS ischemia.

Methods

Fifteen pigs were studied. Helium pneumoperitoneum was established and IAP was increased initially at 20 mmHg and subsequently at 45 mmHg, which was finally followed by abdominal desufflation. Interleukin 6 (IL-6), tumor necrosis factor alpha (TNFa) and lactate were measured in the cerebrospinal fluid (CSF) and intracranial (ICP), intraspinal (ISP), cerebral perfusion (CPP) and spinal perfusion (SPP) pressures recorded.

Results

Increased IAP (20 mmHg) was followed by a statistically significant increase in IL-6 (p = 0.028), lactate (p = 0.017), ICP (p < 0.001) and ISP (p = 0.001) and a significant decrease in CPP (p = 0.013) and SPP (p = 0.002). However, further increase of IAP (45 mmHg) was accompanied by an increase in mean arterial pressure due to compensatory tachycardia, followed by an increase in CPP and SPP and a decrease of cytokines and lactate.

Conclusions

IAH resulted in a decrease of CPP and SPP lower than 60 mmHg and an increase of all ischemic mediators, indicating CNS ischemia; on the other hand, restoration of perfusion pressures above this threshold decreased all ischemic indicators, irrespective of the level of IAH.