Updates on aneurysmal subarachnoid hemorrhage: is there anything really new?

Aneurysmal subarachnoid hemorrhage (aSAH) is a severe disease, with systemic involvement and complex diagnosis and treatment. Since the current guidelines were published by the AHA/ASA, Neurocritical Care Society and the European Stroke Organization in 2012-2013,there has been an evolution in the comprehension of SAH-associated brain injury and its multiple underlying mechanisms. As a result, several clinical and translational trials were developed or are underway. Objective: The aim of this article is to review some updates in the diagnosis and treatment of neurological complications of SAH. Methods: A review of PubMed (May, 2010 to February, 2022) was performed. Data was summarized. Results: Content of five meta-analyses, nine review articles and 23 new clinical trials, including pilots, were summarized. Conclusions:Advances in the comprehension of pathophysiology and improvements in critical care have been reflected in the reduction of mortality in SAH. However, despite the number of publications, the only treatments shown to be effective in adequate, well-controlled clinical trials are nimodipine and repair of the ruptured aneurysm. Thus, doubts about the optimal management of SAH still persist.

Keywords:
Subarachnoid Hemorrhage; Aneurysm; Vasospasm, Intracranial

Study	Study type	Agent	Biological Background	Result
STASH (Simvastatin in Aneurysmal Subarachnoid Hemorrhage)³¹	RCT	Simvastatin 40 mg/d orally for 21 days	Complex and multiple mechanism. Success phase II trials with others statins	No differences for long-term or short-term outcome
NEWTON2 (Study of EG-1962 Compared to Standard of Care Oral Nimodipine in Adults With Aneurysmal Subarachnoid Hemorrhage)³²	RCT	Microparticle formulation of 600mg nimodipine. Application intratecal	Oral nimodipine improves clinical outcome, no reduction radiologic VSP	Trial stopped early due to high rate of vasospasm and DCI
Intraventricular Tissue Plasminogen Activator in Subarachnoid Hemorrhage Patients: A Prospective, Randomized, Placebo Controlled Pilot Trial³⁵	Pilot trial Phase II	Dose 2 mg 12/12h intraventricular tissue plasminogen activator (TPA)	Amount of intracranial hemorrhage directly associated with worse clinical outcome.	TPA as a potent clot clearance accelerator. No clinical outcome assessment
Prospective, randomized, open-label phase II trial on concomitant intraventricular fibrinolysis and low-frequency rotation after severe subarachnoid hemorrhage³⁶	Prospective randomized Phase II	5 mg of rt-PA was diluted in 2 mL of NaCl and given as an intraventricular bolus every 12 hours	Amount of intracranial hemorrhage directly associated with worse clinical outcome.	No reduction of delayed cerebral ischemia or poor functional outcome
Low-dose intravenous heparin infusion in patients with aneurysmal subarachnoid hemorrhage: a preliminary assessment³⁹	Controlled retrospectively	Low-dose intravenous heparin infusion:8 U/kg/hr progressing over 36 hours to 10 U/kg/hr	Microthrombotic mechanisms in intracranial vasculature shown to be associated with DCI in bench study	Reduction in the occurrence of DCI and vasospasm in the intervention group. No increase in bleeding.

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[1] Conflict of interest:

There is no conflict of interest to declare