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Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated delirium

Patrick Schramm1*, Klaus Ulrich Klein14, Lena Falkenberg1, Manfred Berres2, Dorothea Closhen1, Konrad J Werhahn3, Matthias David1, Christian Werner1 and Kristin Engelhard1

Author Affiliations

1 Department of Anaesthesiology, University Medical Centre of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany

2 Institute of Medical Biometry, Epidemiology and Informatics (IMBEI), University Medical Centre of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany and RheinAhrCampus Remagen, Germany

3 Department of Neurology, University Medical Centre of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany

4 Department of Anaesthesiology, Intensive Care Medicine and Pain Therapy, Vienna General Hospital, University Vienna, Währinger Gürtel 18-20, 1090 Wien, Austria

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Critical Care 2012, 16:R181  doi:10.1186/cc11665

Published: 4 October 2012

Abstract

Introduction

Sepsis-associated delirium (SAD) increases morbidity in septic patients and, therefore, factors contributing to SAD should be further characterized. One possible mechanism might be the impairment of cerebrovascular autoregulation (AR) by sepsis, leading to cerebral hypo- or hyperperfusion in these haemodynamically unstable patients. Therefore, the present study investigates the relationship between the incidence of SAD and the status of AR during sepsis.

Methods

Cerebral blood flow velocity was measured using transcranial Doppler sonography and was correlated with the invasive arterial blood pressure curve to calculate the index of AR Mx (Mx>0.3 indicates impaired AR). Mx was measured daily during the first 4 days of sepsis. Diagnosis of a SAD was performed using the confusion assessment method for ICU (CAM-ICU) and, furthermore the predominant brain electrical activity in electroencephalogram (EEG) both at day 4 after reduction of sedation to RASS >-2.

Results

30 critically ill adult patients with severe sepsis or septic shock (APACHE II 32 ± 6) were included. AR was impaired at day 1 in 60%, day 2 in 59%, day 3 in 41% and day 4 in 46% of patients; SAD detected by CAM-ICU was present in 76 % of patients. Impaired AR at day 1 was associated with the incidence of SAD at day 4 (p = 0.035).

Conclusions

AR is impaired in the great majority of patients with severe sepsis during the first two days. Impaired AR is associated with SAD, suggesting that dysfunction of AR is one of the trigger mechanisms contributing to the development of SAD.

Trial registration

clinicalTrials.gov ID NCT01029080