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Cerebral vasospasm in subarachnoid hemorrhage: Fisher scale classification, treatment challenges, and prognosis

Dimitar Monov

Abstract

Cerebral vasospasm is one of the most serious complications after subarachnoid hemorrhage (SAH), leading to significant morbidity and mortality. Vasospasm is characterized by prolonged and unpredictable narrowing of blood vessels in the brain, which can lead to ischemia and secondary stroke. Understanding the pathophysiological mechanisms and developing effective diagnostic and therapeutic strategies is critical to improving clinical outcomes in patients with SAH(1).

Subarachnoid hemorrhage usually occurs as a result of aneurysm rupture or trauma, leading to hemorrhage into the subarachnoid space. The blood in this space causes an inflammatory reaction, which is a major factor in the subsequent vasospasm(2).

The pathophysiology of vasospasm is multifactorial and complex. The main mechanisms include:

1. Inflammatory reactions: Blood in the subarachnoid space triggers the release of inflammatory mediators such as cytokines and free radicals, which can cause direct vasoconstriction and endothelial cell damage.

2. Mechanical factors: The presence of blood and products of its degradation (for example, hemoglobin) can lead to mechanical irritation and narrowing of the vessels.

3. Endothelial dysfunction: Endothelial cell damage reduces the production of vasodilator agents such as nitric oxide, thereby predominating the vasoconstrictor effects.

4. Neurogenic mechanisms: Activation of the sympathetic nervous system may contribute to vasoconstriction by releasing catecholamines.

Vasospasm usually occurs between the 3rd and 14th day after the onset of SAH. Clinical symptoms include:

• Headache

• Changes in consciousness

• Neurological deficits such as hemiparesis or aphasia

• New ischemic strokes

Diagnosis

Instrumental methods

1. Transcranial Doppler sonography (TCD): TCD is a non-invasive method for monitoring blood flow in the basal arteries of the brain. An increase in blood flow rate may indicate vasospasm.

2. Cerebral angiography: The gold standard for the diagnosis of vasospasm, allowing visualization of vessel narrowing.

3. CT angiography: A non-invasive method that can provide additional information about the vascular status of patients.

Treatment

Prevention and early treatment

1. Hemodynamic management: Maintenance of adequate blood flow through hypervolemia and hypertension (triple H therapy) is a standard approach to the prevention and treatment of vasospasm.

2. Pharmacological therapy:

• Nimodipine: A calcium antagonist that reduces the risk of ischemic complications through vasodilation.

• Vasodilators: Intra-arterial administration of papaverine or nicardipine can be used for severe vasospasm.

3. Endovascular interventions: Balloon angioplasty or intra-arterial infusion of vasodilators can be used in patients with resistant vasospasm.


Keywords

subarachnoid hemorrhage, Fischer scale, cerebral vasospasm

Full Text


References

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DOI: http://dx.doi.org/10.14748/vmf.v13i2.9817

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