Acetazolamide-induced cerebrovascular reactivity is impaired in sepsis-associated encephalopathy

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. Nonseptic persons without previous diseases affecting cerebral vasoreactivity served as controls. Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kg BW 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

Fourteen patients with SAE and 20 controls were included. Absolute blood flow velocities after administration 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 SAE: 46.2 ± 15.9%, CRC controls: 29.4 ± 15.8%, P < 0.01).

Conclusions

We conclude that cerebrovascular reactivity is impaired in patients with SAE.