Abstract
IntroductionThe 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.MethodsPatients 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.ResultsAbsolute 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).ConclusionsWe conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.
Highlights
The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear
When assessing cerebral microvascular contributing factors, in previous human investigations Matta and Stow [6] found cerebral autoregulation and carbon dioxide reactivity to be normal in patients with sepsis, whereas Terborg and colleagues reported on severely disturbed vasomotor reactivity (VMR) [7]
When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during 20 minutes of vasomotor testing, we found that patients with sepsis-associated encephalopathy reacted to the drug to a lesser extent than control subjects
Summary
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. Sepsis-associated encephalopathy is defined as a diffuse cerebral dysfunction induced by the systemic response to the infection without clinical or laboratory evidence of direct infectious involvement of the central nervous system [1]. According to the studies of Wilson and colleagues and Young and colleagues, electroencephalogram (EEG) may be abnormal in 87% of patients with bacteriemia They diagnosed 70% with disturbance of consciousness of differing severity ranging from somnolence. When assessing cerebral microvascular contributing factors, in previous human investigations Matta and Stow [6] found cerebral autoregulation and carbon dioxide reactivity to be normal in patients with sepsis, whereas Terborg and colleagues reported on severely disturbed vasomotor reactivity (VMR) [7]. With respect to the debated involvement of the above cerebral microvascular alterations, in the present study we intended to test whether acetazolamideinduced cerebral VMR is altered in patients with sepsisassociated encephalopathy. To the best of our knowledge this is the first study that uses the transcranial Doppleracetazolamide test to assess cerebral VMR in sepsisrelated encephalopathy
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