Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: A prospective study

Citation
G. Citerio et al., Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: A prospective study, CRIT CARE M, 29(7), 2001, pp. 1466-1471
Citations number
26
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
29
Issue
7
Year of publication
2001
Pages
1466 - 1471
Database
ISI
SICI code
0090-3493(200107)29:7<1466:IACSII>2.0.ZU;2-P
Abstract
pObjective: To evaluate the effect of a stepwise increase in intra-abdomina l pressure (IAP) on intracranial pressure (ICP) and to further define the p ressure transmission characteristics of different body compartments. Design: A prospective, nonrandomized study. Setting: A multidisciplinary intensive care unit at a university medical ce nter. Patients: Fifteen patients with moderate-to-severe head injury. Interventions: All patients were studied after the initial stabilization an d resolution of intracranial hypertension. Measurements were carried out be fore and 20 mins after IAP was increased by positioning a soft, 15-L water bag on the patient's abdomen. Measurements and Main Results: Placing weights upon the abdomen generated a significant increase in IAP, which rose from 4.7 +/- 2.9 to 15.5 +/- 4.1 m m Hg (p < .001). The rise in IAP caused concomitant and rapid increases in central venous pressure (from 6.2 +/- 2.4 to 10.4 +/- 2.9 mm Hg; p < .001), internal jugular pressure (from 11.9 +/- 3.2 to 14.3 +/- 2.4 mm Hg; p < .0 01), and ICP (from 12.0 +/- 4.2 to 15.5 +/- 4.4 mm Hg; p < .001). Thoracic transmural pressure, calculated as the difference between central venous pr essure and esophageal pressure, remained constant during the protocol. Resp iratory system compliance decreased from 58.9 +/- 9.8 to 44.9 +/- 9.4 mL/cm H2O (p < .001) in all patients because of decreased chest wall compliance. The mean arterial pressure increased from 94 +/- 11 to 100 +/- 13 mm Hg (p < .01), which allowed the maintenance of a stable cerebral perfusion press ure (82.4 +/- 10.3 vs. 84.7 +/- 11.5 mm Hg; p = NS) despite the ICP increas e. Conclusions: Increased IAP causes a significant rise in ICP in head trauma patients. This effect seems to be the result of an increase in intrathoraci c pressure, which causes a functional obstruction to cerebral venous outflo w. Routine assessment of IAP may help clinicians to identify remediable cau ses of increased ICP. Caution should be used when applying laparoscopic tec hniques in neurotrauma patients.