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

Szilárd Szatmári, Tamás Végh, Ákos Csomós, Judit Hallay, István Takács, Csilla Molnár, B. Fülesdi

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Article numberR50
JournalCritical Care
Volume14
Issue number2
DOIs
Publication statusPublished - Mar 31 2010

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Acetazolamide
Blood Flow Velocity
Cerebrovascular Circulation
Aptitude
Drug and Narcotic Control
Arterioles
Sepsis-Associated Encephalopathy
Consciousness
Vasodilator Agents
Intravenous Administration
Sepsis
Inflammation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Medicine(all)

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Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test. / Szatmári, Szilárd; Végh, Tamás; Csomós, Ákos; Hallay, Judit; Takács, István; Molnár, Csilla; Fülesdi, B.

In: Critical Care, Vol. 14, No. 2, R50, 31.03.2010.

Research output: Contribution to journalArticle

Szatmári S, Végh T, Csomós Á, Hallay J, Takács I, Molnár C et al. Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test. Critical Care. 2010 Mar 31;14(2). R50. https://doi.org/10.1186/cc8939
Szatmári, Szilárd ; Végh, Tamás ; Csomós, Ákos ; Hallay, Judit ; Takács, István ; Molnár, Csilla ; Fülesdi, B. / Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test. In: Critical Care. 2010 ; Vol. 14, No. 2.
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AB - 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.

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