Critical Care volume 29,
Article number: 414 (2025) Published: 30 September
2025
Abstract
Aneurysmal subarachnoid hemorrhage is a critical condition
with high case-fatality and lasting impacts on survivors. Acute events that are
the direct result of aneurysm rupture, such as acute ischemia, elevated
intracranial pressure, cerebral edema, seizures, and hydrocephalus, lead to
early brain injury. A delayed cascade of processes, including a prominent
systemic inflammatory response, may lead to secondary brain injury and delayed
cerebral ischemia, which often further impairs recovery. Systemic complications,
including cardiac and pulmonary dysfunction, fever, and electrolyte imbalances,
arise in the interplay between early and secondary brain injury and challenge
the clinical course. Early management focuses on the prevention of rebleeding
mainly through aneurysm securement, amelioration of early brain injury through
cerebrospinal fluid drainage, control of intracranial pressure, and organ
support to avoid or attenuate secondary brain injury. Nimodipine remains the
only pharmacological agent shown to reduce delayed cerebral ischemia, and
lumbar drainage of cerebrospinal fluid to reduce subarachnoid blood may improve
outcome. Management strategies for hemodynamic interventions, seizures,
intracranial pressure control, large artery vasospasm, and electrolytes remain
consensus-based and with large variation in practice. Several advances in
understanding inflammation and delayed cerebral ischemia, as well as in
monitoring and interventions hold promise, but robust trials are needed to
refine protocols and improve patient recovery. Understanding and mitigating the
cascade of damage from rupture to recovery is essential to reduce the burden of
this devastating condition. In this review, we appraise the current
understanding of the pathophysiology of post-rupture complications as well as
scientific and management data, with a focus on recent advances.
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