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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
"Triple h" therapy for aneurysmal subarachnoid haemorrhage: real therapy or chasing numbers?
1Department of Intensive Care Medicine, The St George Hospital, Sydney, NSW 2217, Australia j.myburgh@unsw.edu.au.
Despite technological and medical advances for the treatment of SAH that have had a positive impact on outcomes over the last 20 years, but the all-cause mortality for this often-catastrophic condition remains high at 12 - 15%. Survival will ultimately depend on the severity of the haemorrhage, the subsequent loss of functional neurones and the extracranial reserve of the patient. In this regard, advances in neuroradiology and operative techniques together with expert neurocritical care and rehabilitation provide the best chances of short- and long- term survival respectively. In this context, the contribution of cerebral vasospasm to attributable morbidity and mortality remains conjectural albeit real, and whilst medical anti-vasospastic therapies should be considered in vulnerable patients, they should be used with circumspection and caution. There is little or no evidence to justify the aggressive use of anti-vasospastic therapies as a preventative manner with exception of oral nimodipine in patients with low-grade aneurysmal subarachnoid haemorrhage. Concomitant use of induced hypertension/hypervolaemia/haemodilution cannot be recommended on current evidence, but if employed should be done on an individualised basis, considering the patients underlying neurological condition, cardiopulmonary reserve, adequacy of systemic and neurological monitoring and access to expert neuroradiological, neurosurgical and neurocritical care services.
Despite technological and medical advances for the treatment of SAH that have had a positive impact on outcomes over the last 20 years, but the all-cause mortality for this often-catastrophic condition remains high at 12 - 15%. Survival will ultimately depend on the severity of the haemorrhage, the subsequent loss of functional neurones and the extracranial reserve of the patient. In this regard, advances in neuroradiology and operative techniques together with expert neurocritical care and rehabilitation provide the best chances of short- and long- term survival respectively. In this context, the contribution of cerebral vasospasm to attributable morbidity and mortality remains conjectural albeit real, and whilst medical anti-vasospastic therapies should be considered in vulnerable patients, they should be used with circumspection and caution. There is little or no evidence to justify the aggressive use of anti-vasospastic therapies as a preventative manner with exception of oral nimodipine in patients with low-grade aneurysmal subarachnoid haemorrhage. Concomitant use of induced hypertension/hypervolaemia/haemodilution cannot be recommended on current evidence, but if employed should be done on an individualised basis, considering the patients underlying neurological condition, cardiopulmonary reserve, adequacy of systemic and neurological monitoring and access to expert neuroradiological, neurosurgical and neurocritical care services.
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