Cerebral perfusion in sepsis-associated delirium

David Pfister , Martin Siegemund , Salome Dell-Kuster , Peter Smielewski , Stephan Rueegg , Stephan P Strebel , Stephan CU Marsch , Hans Pargger and Luzius A Steiner

Critical Care 2008, 12:R63doi:10.1186/cc6891


Published:	5 May 2008

Abstract (provisional)

Introduction

The pathophysiology of sepsis-associated delirium is not completely understood and the data on cerebral perfusion in sepsis are conflicting. We tested the hypotheses 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 an intracranial pathology. Patients were investigated after stabilisation within 48 h after admission to the intensive care unit. Sepsis-associated delirium was diagnosed using the confusion assessment method for the intensive care unit (CAM-ICU). Mean arterial pressure (MAP), blood flow velocity in the middle cerebral artery using transcranial Doppler, and cerebral tissue oxygenation using near-infrared spectroscopy were monitored for one hour. An index of cerebrovascular autoregulation was calculated from MAP and FV data. CRP, IL-6, S-100b and cortisol were measured during each data acquisition.

Results

Data from 16 patients, of which 12 had sepsis-associated delirium, were analysed. There were no significant correlations or associations between MAP, cerebral blood flow velocity 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-100b (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).

Conclusions

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-100b and cortisol in the diagnosis of sepsis-associated delirium are warranted. Trial registration: ClinicalTrials.gov NCT00410111