From the Guidelines
Pathophysiology of Aneurysmal Subarachnoid Hemorrhage (SAH)
The pathophysiology of aneurysmal subarachnoid hemorrhage (SAH) is complex and involves multiple mechanisms, including early brain injury, cerebral vasospasm, and delayed cerebral ischemia (DCI).
- The initial rupture of the aneurysm leads to increased intracranial pressure, global cerebral ischemia, and blood-brain barrier breakdown, contributing to early brain injury within 72 hours of SAH 1.
- Cerebral vasospasm, which occurs most frequently 7 to 10 days after aneurysm rupture, is initiated when oxyhemoglobin comes in contact with the abluminal side of the vessel, leading to arterial narrowing and potentially ischemic neurological symptoms 1.
- DCI, which remains a major cause of death and disability in patients with SAH, is hypothesized to be caused by the combined effects of large-vessel cerebral vasospasm and multiple brain injury processes triggered by aneurysm rupture and early brain injury, including arteriolar constriction, cerebral microthrombosis, cortical spreading depolarization/ischemia, and cerebral autoregulation impairment 1.
- Neuroinflammation has also been identified as a potential target for intervention in the pathophysiology of SAH 1.
- The clinical correlate of early brain injury is the neurological grade of the patient, with high-grade global cerebral edema after SAH being an independent predictor of DCI and unfavorable outcome 1.
- The management of SAH-induced vasospasm is complex, and many significant advances in the understanding of aSAH-induced vasospasm and DCI have been made, but few effective treatments exist, and further research is needed 1.
From the Research
Pathophysiology of Aneurysmal Subarachnoid Hemorrhage (SAH)
The pathophysiology of aneurysmal subarachnoid hemorrhage (SAH) is complex and involves multiple mechanisms. Some of the key processes include:
- Angiographic vasospasm, which is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome 2
- Early brain injury (EBI), which may be causally connected to DCI 2
- Neuroinflammation, which plays a critical role in injury expansion and brain damage 3
- Release of inflammatory cytokines triggered by red blood cell breakdown products, leading to vasospasm and tissue injury 3
- Inflammation-induced cellular changes, including changes in parenchymal brain and peripheral immune cells 4
Key Determinants of Functional Outcome
The key determinants of functional outcome in aneurysmal subarachnoid hemorrhage include:
- Early brain injury
- Rebleeding of the ruptured aneurysm
- Delayed cerebral ischemia 5 Securing the ruptured aneurysm quickly is the only effective way to reduce the risk of rebleeding 5.
Current Understanding and Management
Despite advances in the comprehension of pathophysiology and improvements in critical care, the only treatments shown to be effective in adequate, well-controlled clinical trials are nimodipine and repair of the ruptured aneurysm 6. Prompt diagnosis, transfer to specialized centers, and meticulous management in the intensive care unit (ICU) significantly improve the prognosis of aSAH 5. Multimodality monitoring with specific interventions to correct pathophysiological imbalances has been proposed, and vigilance extends beyond intracranial concerns to encompass systemic respiratory and haemodynamic monitoring 5.