What are the characteristics of the vasospasm phase in subarachnoid hemorrhage (SAH)?

From the Guidelines

Vasospasm in subarachnoid hemorrhage (SAH) is characterized by delayed narrowing of large-capacitance arteries, typically occurring 3 to 5 days after the hemorrhage, with maximal narrowing at 5 to 14 days, and gradual resolution over 2 to 4 weeks. The characteristics of the vasospasm phase in SAH include:

• Angiographic vasospasm is seen in 30% to 70% of patients [ 1 ]
• Typical onset is 3 to 5 days after the hemorrhage, with maximal narrowing at 5 to 14 days [ 1 ]
• Gradual resolution over 2 to 4 weeks [ 1 ]
• Often manifested by the occurrence of a delayed neurological ischemic deficit, which may resolve or progress to cerebral infarction [ 1 ]
• Accounts for nearly 50% of the deaths in patients surviving to treatment after SAH [ 1 ]
• May be asymptomatic in comatose patients, requiring a high index of suspicion [ 1 ]
• Monitoring with transcranial Doppler (TCD) technology and clinical observation in the intensive care unit is crucial, although TCD monitoring is operator-dependent and requires establishment of critical thresholds and quality control [ 1 ] Key signs of symptomatic vasospasm include new focal deficits, unexplained by hydrocephalus or rebleeding, and unexplained increases in mean arterial pressure [ 1 ].

From the FDA Drug Label

Although the clinical studies described below demonstrate a favorable effect of nimodipine on the severity of neurological deficits caused by cerebral vasospasm following SAH, there is no arteriographic evidence that the drug either prevents or relieves the spasm of these arteries

The characteristics of the vasospasm phase in subarachnoid hemorrhage (SAH) are not directly described in the provided drug labels. However, it is mentioned that nimodipine has a favorable effect on the severity of neurological deficits caused by cerebral vasospasm following SAH.

• Key points:
  • No arteriographic evidence that nimodipine prevents or relieves vasospasm
  • Nimodipine reduces the severity of neurological deficits resulting from vasospasm in patients with SAH 2
  • The precise mechanism of action of nimodipine in humans is unknown 3

From the Research

Characteristics of Vasospasm Phase in Subarachnoid Hemorrhage (SAH)

• The vasospasm phase in SAH typically develops between 5 and 15 days after the initial hemorrhage 4
• Radiographic vasospasm is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients 4
• The pathophysiology of vasospasm involves structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells, triggered by blood in the subarachnoid space 4
• Cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function, leading to reduction in cerebral blood flow and potentially causing ischemia and infarction 4

Clinical Presentation and Diagnosis

• The initial and main symptom of cerebral vasospasm is diffuse headache, which may be accompanied by a slight increase in discomfort from neck stiffness and fever 5
• Clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness or a new focal neurologic deficit 5
• Diagnosis can be made by a combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors 4

Treatment and Management

• Nimodipine, a calcium channel antagonist, is the only available therapy with proven benefit for reducing the impact of DID 4, 6
• Triple-H therapy, which combines hemodynamic augmentation, hypervolemia, and hypertension, is used to improve cerebral perfusion and neurological outcome 5, 7
• Endovascular administration of intra-arterial anti-spasmodic agents and balloon angioplasty are becoming more commonly utilized 8, 7
• Other medications, such as magnesium sulfate, HMG-CoA reductase inhibitors, and enoxaparin, are being investigated with promising results 6, 5, 7