Early evidence of sepsis-associated hyperperfusion - A study of cerebral blood flow measured with magnetic resonance imaging arterial spin labeling in critically-ill septic patients and healthy volunteers
CCCF ePoster library. Palanchuck S. Oct 4, 2017; 198138; 114
Steven Palanchuck
Steven Palanchuck
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Early evidence of sepsis-associated hyperperfusion - A study of cerebral blood flow measured with magnetic resonance imaging arterial spin labeling in critically-ill septic patients and healthy volunteers

Masse MH1,11, Richard MA9, Palanchuck S6, Mayette M1, St-Arnaud C1, D’Aragon F1, 2, 11, Adhikari N3, Fraser W4,11, Carpentier A5,11,  Gauthier D2, Lanthier L6, Touchette M6, Lamontagne A7, Chenard J8, Mehta S10, Sansoucy Y2, Croteau É9,11, Lepage M9,11, Lamontagne F1,6,11.





1Dept. of Medicine/Division of Critical Care Medicine, University of Sherbrooke, Sherbrooke, QC, Canada 

2Dept. of Anesthesiology, University of Sherbrooke, Sherbrooke, QC, Canada 

3Depart of Critical Care Medicine, Sunnybrook Health Sciences Centre, Toronto, Canada 

4Dept. of Gynecology/Obstetrics, University of Sherbrooke, Sherbrooke, QC, Canada 

5Dept. of Medicine/Division of Endocrinology, University of Sherbrooke, Sherbrooke, QC, Canada 

6Dept. of Medicine/Division of Internal Medicine, University of Sherbrooke, Sherbrooke, QC, Canada 

7Dept. of Medicine/Division of Neurology, University of Sherbrooke, Sherbrooke, QC, Canada 

8Dept. of Diagnostic Radiology, University of Sherbrooke, Sherbrooke, QC, Canada 

9Department of Nuclear Medicine and Radiobiology, University of Sherbrooke, Sherbrooke, QC, Canada 

10 Mount Sinai Hospital and Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Ontario, Canada 

11Centre de recherche du CHUS, Sherbrooke, QC, Canada

Introduction:
The precise mechanisms underlying sepsis-associated encephalopathy remain unclear, but reduced cerebral blood flow (CBF), alone or in conjunction with altered autoregulation, is reported as a potential contributor. The objectives of this study were to compare CBF in 1) healthy volunteers with and without sedation; 2) septic patients receiving vasopressors to achieve higher vs. lower mean arterial pressure (MAP) targets; and 3) between septic patients and healthy volunteers.
 
Methods:
We measured CBF using magnetic resonance imaging (MRI) with arterial spin labeling (ASL) conducted in a 3.0 T MRI scanner (Ingenia, Philips Healthcare, Best, Netherlands).
 
CBF was measured in healthy volunteers (with/without chronic hypertension) while awake and under moderate sedation with a continuous propofol infusion. In septic patients (with/without chronic hypertension) sedated with propofol and receiving norepinephrine, we measured CBF at a MAP of 65 and 75 mmHg. The sequence of sedation/no sedation (in healthy subjects) and MAP targets (in septic patients) was randomized. Calculation of CBF was blind to allocation.
 
Results:
Twelve healthy volunteers (6 with controlled chronic hypertension) and 10 sedated septic patients on mechanical ventilation (4 with controlled chronic hypertension) were enrolled; mean ages were 44±12.8 and 61±10.2 years respectively (p=0.003). Mean APACHE II score of septic patients at ICU admission was 28±6.6 and the study was conducted, on average, 1.5 days following ICU admission.
 
In healthy volunteers, we observed no difference in global CBF measured with and without sedation (24.9 vs. 24.8 mL/100 g/min; p=0.93). In septic patients, CBF measured at a MAP target of 65 mmHg (40.4 mL/100 g/min) was not different from CBF measured at a MAP target of 75 mmHg (41.3 mL/100 g/min; p=0.65). We found no interaction between chronic hypertension and the effect of sedation or MAP targets. CBF measured in sedated septic patients was 62% higher than in sedated healthy volunteers (p=0.001).
 
Conclusion:
In septic patients, CBF was higher than in sedated healthy volunteers and did not vary with MAP targets. Further research is required to understand the clinical significance of sepsis or vasopressor-induced cerebral hyperperfusion and to reassess the neurological effects of current protocols of vasopressor therapy in sepsis.

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