Severe traumatic brain injury with increased intracranial pressure can lead to decreased cerebral blood flow. Low cerebral blood flow is responsible for secondary lesions, leading to bad prognosis. It is not yet established whether increasing cardiac output in these patients can lead to an increase in cerebral blood flow, although there are some arguments in favor of this hypothesis. The aim of this study is to demonstrate that increasing cardiac output will improve cerebral blood flow in patients with severe traumatic injury and high cerebral pressure.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
SINGLE
Enrollment
20
Grenoble University Hospital
Grenoble, France
RECRUITINGMean blood flow velocity
Mean blood flow velocity averaged on the two middle cerebral arteries (right and left) measured one after after the initiation of treatment. Each velocity is calculated as an average on the 10 last minutes form continuous transcranial doppler monitoring
Time frame: After one hour of treatment
Evolution of brain oxygenation under treatment
Comparison of the brain tissue oxygenation curves (PbrO2) under treatment with and without dobutamine
Time frame: During one hour of treatment
Dobutamine doses
Dobutamine doses required to reach the same cerebral perfusion pressure than noradrenaline alone
Time frame: After one hour of treatment
Resistivity index on renal doppler
Measure of resistivity index on renal doppler after one hour of treatment with and without dobutamine
Time frame: After one hour of treatment
Pulsatility index on renal doppler
Measure of pulsatility index (PI) on renal doppler before and after one hour of treatment with and without dobutamine prediction of cerebral blood flow increase (patients with high initial renal PI)
Time frame: After one hour of treatment
Cardiac output modifications
Comparison of cardiac blood flow modifications under treatment for one hour with and without dobutamine
Time frame: During one hour of treatment
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