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

Szilárd Szatmári, Tamás Végh, Akos Csomós, Judit Hallay, István Takács, Csilla Molnár, Béla Fülesdi, Szilárd Szatmári, Tamás Végh, Akos Csomós, Judit Hallay, István Takács, Csilla Molnár, Béla Fülesdi

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 without 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 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 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.

Figures

Figure 1
Figure 1
Percentage increase of the middle cerebral artery mean blood flow velocity in patients with sepsis-associated encephalopathy and in controls at 5, 10, 15 and 20 minutes after injection of acetazolamide. Means and standard errors are shown.
Figure 2
Figure 2
Maximal percentage increase of the middle cerebral artery mean blood flow velocity in patients with sepsis-associated encephalopathy and in controls after injection of acetazolamide. Means and standard errors are shown.
Figure 3
Figure 3
Illustration of the rationale and the background of transcranial Doppler-assessed cerebral vasomotor reactivity testing. MCA: middle cerebral artery.

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Source: PubMed

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