Brain tissue oxygenation guided therapy and outcome in non-traumatic subarachnoid hemorrhage

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作者
Elisa Gouvea Bogossian
Daniela Diaferia
Narcisse Ndieugnou Djangang
Marco Menozzi
Jean-Louis Vincent
Marta Talamonti
Olivier Dewitte
Lorenzo Peluso
Sami Barrit
Mejdeddine Al Barajraji
Joachim Andre
Sophie Schuind
Jacques Creteur
Fabio Silvio Taccone
机构
[1] Université Libre de Bruxelles,Department of Intensive Care, Erasme Hospital
[2] Université Libre de Bruxelles,Department of Neurosurgery, Erasme Hospital
[3] Université Libre de Bruxelles,Department of Radiology, Erasme Hospital
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Scientific Reports | / 11卷
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摘要
Brain hypoxia can occur after non-traumatic subarachnoid hemorrhage (SAH), even when levels of intracranial pressure (ICP) remain normal. Brain tissue oxygenation (PbtO2) can be measured as a part of a neurological multimodal neuromonitoring. Low PbtO2 has been associated with poor neurologic recovery. There is scarce data on the impact of PbtO2 guided-therapy on patients’ outcome. This single-center cohort study (June 2014–March 2020) included all patients admitted to the ICU after SAH who required multimodal monitoring. Patients with imminent brain death were excluded. Our primary goal was to assess the impact of PbtO2-guided therapy on neurological outcome. Secondary outcome included the association of brain hypoxia with outcome. Of the 163 patients that underwent ICP monitoring, 62 were monitored with PbtO2 and 54 (87%) had at least one episode of brain hypoxia. In patients that required treatment based on neuromonitoring strategies, PbtO2-guided therapy (OR 0.33 [CI 95% 0.12–0.89]) compared to ICP-guided therapy had a protective effect on neurological outcome at 6 months. In this cohort of SAH patients, PbtO2-guided therapy might be associated with improved long-term neurological outcome, only when compared to ICP-guided therapy.
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[1]  
Mozaffarian D(2015)Heart disease and stroke statistics–2015 update: A report from the American Heart Association Circulation 131 e29-322
[2]  
Krishnamurthi RV(2013)Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990–2010: Findings from the Global Burden of Disease Study 2010 Lancet Glob. Health 1 e259-281
[3]  
Connolly ES(2012)Guidelines for the management of aneurysmal subarachnoid hemorrhage: A guideline for healthcare professionals from the American Heart Association/american Stroke Association Stroke 43 1711-1737
[4]  
Grote E(1988)The critical first minutes after subarachnoid hemorrhage Neurosurgery 22 654-661
[5]  
Hassler W(2017)Mechanisms of global cerebral edema formation in aneurysmal subarachnoid hemorrhage Neurocrit. Care 26 301-310
[6]  
Hayman EG(2004)Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage J. Neurosurg. 101 408-416
[7]  
Wessell A(2006)Mechanisms of early brain injury after subarachnoid hemorrhage J. Cereb. Blood Flow Metab. 26 1341-1353
[8]  
Gerzanich V(2007)Cerebral vasospasm after subarachnoid hemorrhage: The emerging revolution Nat. Clin. Pract. Neurol. 3 256-263
[9]  
Sheth KN(2015)Intracranial pressure after subarachnoid hemorrhage Crit. Care Med. 43 168-176
[10]  
Simard JM(2005)Reduced mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen monitoring J. Neurosurg. 103 805-811