Cerebral perfusion in sepsis-associated delirium

David Pfister¹ , Martin Siegemund¹ , Salome Dell-Kuster¹ , Peter Smielewski² , Stephan Rüegg³ , Stephan P Strebel¹ , Stephan CU Marsch⁴ , Hans Pargger¹ and Luzius A Steiner¹

¹Department of Anaesthesia, Operative Intensive Care Unit, University Hospital Basel, Spitalstrasse 21, CH-4031 Basel, Switzerland

²Academic Neurosurgery, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge CB2 0QQ, UK

³Department of Neurology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland

⁴Medical Intensive Care Unit, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland

author email corresponding author email

Critical Care 2008, 12:R63doi:10.1186/cc6891


Published:	5 May 2008

Abstract

Introduction

The pathophysiology of sepsis-associated delirium is not completely understood and the data on cerebral perfusion in sepsis are conflicting. We tested the hypothesis that cerebral perfusion and selected serum markers of inflammation and delirium differ in septic patients with and without sepsis-associated delirium.

Methods

We investigated 23 adult patients with sepsis, severe sepsis, or septic shock with an extracranial focus of infection and no history of intracranial pathology. Patients were investigated after stabilisation within 48 hours after admission to the intensive care unit. Sepsis-associated delirium was diagnosed using the confusion assessment method for the intensive care unit. Mean arterial pressure (MAP), blood flow velocity (FV) in the middle cerebral artery using transcranial Doppler, and cerebral tissue oxygenation using near-infrared spectroscopy were monitored for 1 hour. An index of cerebrovascular autoregulation was calculated from MAP and FV data. C-reactive protein (CRP), interleukin-6 (IL-6), S-100β, and cortisol were measured during each data acquisition.

Results

Data from 16 patients, of whom 12 had sepsis-associated delirium, were analysed. There were no significant correlations or associations between MAP, cerebral blood FV, or tissue oxygenation and sepsis-associated delirium. However, we found a significant association between sepsis-associated delirium and disturbed autoregulation (P = 0.015). IL-6 did not differ between patients with and without sepsis-associated delirium, but we found a significant association between elevated CRP (P = 0.008), S-100β (P = 0.029), and cortisol (P = 0.011) and sepsis-associated delirium. Elevated CRP was significantly correlated with disturbed autoregulation (Spearman rho = 0.62, P = 0.010).

Conclusion

In this small group of patients, cerebral perfusion assessed with transcranial Doppler and near-infrared spectroscopy did not differ between patients with and without sepsis-associated delirium. However, the state of autoregulation differed between the two groups. This may be due to inflammation impeding cerebrovascular endothelial function. Further investigations defining the role of S-100β and cortisol in the diagnosis of sepsis-associated delirium are warranted.

Trial registration

ClinicalTrials.gov NCT00410111.