Aneurysmal subarachnoid hemorrhage (aSAH) is a fatal neurosurgical emergency that may reach to a mortality of up to nearly 60% within one month of symptoms onset in untreated cases. Accounting for almost 5% of all stroke cases, aSAH predominantly affects the working age population with significant socioeconomic effect due to its impact on their quality of healthy life. Despite refined contemporary neurosurgical techniques and advancements in neurocritical care, secondary/delayed ischemia neurological deficits due to cerebral vasospasm, have been implicated as the main contributing factor, related to poor clinical outcome in nearly 30% of the patients. Although, over the years, many different treatment modalities have been used to counter the detrimental effects of vasospasm including calcium channel blockers and triple-H therapy (hypervolemic, hemodilution, hypertension) with no substantiative improvement in clinical outcome and a search for an effective management strategy continues.

In aSAH, hyponatremia due to increased release of natriuretic factors and reduction in intravascular volume have been attributed to cause clinical vasospasm and delayed ischemic neurological deficits as a part of natural course of the disease. Reduced cerebral blood flow during aSAH has been explained based on two etiological factors. Firstly, immediately with the clinical onset of aSAH, there is a generalized decrease in brain oxidative metabolism that contributes to drop in global cerebral blood flow (CBF). This disruption in brain metabolic harmony is primarily caused by presence of toxic blood products in subarachnoid spaces although other contributing factors including acute hydrocephalus, brain edema and rise in intracranial pressure may also play their roles to already compromised CBF. Secondly, during the course of subsequent days to weeks when cerebral vasospasm sets in, it can further cause drop in CBF and cerebral metabolism. This drop in CBF is topographically heterogenous in brain parenchyma and this manifests as the delayed cerebral ischemia causing neurological deficits. Based on these pathophysiological mechanisms, the standard use of hypervolemic therapy was rationalized in neurosurgical practice in the past to mitigate the detrimental effects of hypoperfusion and it used to be achieved by routine use of crystalloids/isotonic solutions and complementary colloidal agents including dextran, hypertonic saline and human albumin in neurocritical care.

In animal studies with rat models for acute focal ischemia, albumin treatment has effectively reduced size of penumbra. In contemporary clinical practice, the beneficial effects of human albumin has been investigated in cerebral strokes, acute brain injury, intracranial hemorrhages, including aSAH with promising results. In a pilot study conducted by Suarez et al (ALISAH) for a clinically safe dosage regimen for aSAH, it has also been observed that the use of albumin may be effective to prevent the deleterious effects of cerebral vasospasm by enhanced CBF leading to improvements in neurological outcome in aSAH patients. Ali A. et al recently published a systematic review that underscores obvious gaps in literature for the use of human albumin with no randomized control trial published to-date and highlighting the lack of any robust clinical evidence for the role of albumin to treat cerebral vasospasm in aSAH This single center RCT will aim to explore potential beneficial role of human albumin to improve clinical outcome in patients with aSAH.