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Open Access Highly Accessed Research

Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test

Szilárd Szatmári1, Tamás Végh1, Ákos Csomós2, Judit Hallay1, István Takács3, Csilla Molnár1 and Béla Fülesdi1*

Author Affiliations

1 Department of Anesthesiology and Intensive Care, University of Debrecen, Health and Medical Science Center, H-4032. Debrecen, Nagyerdei krt. 98, Hungary

2 1st Department of Surgery, Semmelweis University, H-1082 Budapest, Üllõi út 78, Hungary

3 Department of Surgery, University of Debrecen, Health and Medical Science Center, H-4032 Debrecen, Nagyerdei krt. 98

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Critical Care 2010, 14:R50  doi:10.1186/cc8939

Published: 31 March 2010

Abstract

Introduction

The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.

Methods

Patients fulfilling the criteria of clinical sepsis and showing disturbance of consciousness of any severity were included (n = 14). Non-septic persons whithout previous diseases affecting cerebral vasoreactivity served as controls (n = 20). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity, CVR) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity, CRC) were compared among the groups.

Results

Absolute blood flow velocities after adminsitration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that patients with SAE reacted to a lesser extent to the drug than did control subjects (CRC controls:46.2 ± 15.9%, CRC SAE: 31,5 ± 15.8%, P < 0.01).

Conclusions

We conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.