What are the methods and scores used to determine the risk of vasospasm in patients with subarachnoid hemorrhage (SAH)?

From the Guidelines

To determine the risk of vasospasm in subarachnoid hemorrhage (SAH), the most recent and highest quality study recommends using a combination of validated methods and scoring systems, including the modified Fisher scale, Hunt and Hess scale, and World Federation of Neurological Surgeons (WFNS) scale, as well as Transcranial Doppler (TCD) ultrasonography and CT angiography 1.

Methods for Determining Vasospasm Risk

The following methods can be used to determine the risk of vasospasm in SAH:

• Modified Fisher scale: grades SAH severity from 1-4 based on the amount of blood on CT scans and the presence of intraventricular hemorrhage, with grades 3-4 indicating high vasospasm risk
• Hunt and Hess scale: grades clinical presentation from 1-5, with higher grades correlating with increased risk
• World Federation of Neurological Surgeons (WFNS) scale: also helps predict vasospasm risk based on clinical presentation
• Transcranial Doppler (TCD) ultrasonography: essential for monitoring, with mean flow velocities >120 cm/s in the middle cerebral artery suggesting vasospasm
• CT angiography: can detect vessel narrowing and perfusion deficits

Scoring Systems and Monitoring

The Lindegaard ratio (comparing middle cerebral artery to extracranial internal carotid artery flow) >3 helps distinguish vasospasm from hyperemia 1. Clinical monitoring for new neurological deficits between days 3-14 post-SAH is crucial, as vasospasm typically develops during this period. Continuous electroencephalography may detect early changes before clinical deterioration.

Treatment and Intervention

These methods should be used in combination for optimal risk assessment and early intervention with calcium channel blockers (nimodipine 60mg every 4 hours for 21 days), hemodynamic augmentation, or endovascular treatments when necessary, as recommended by the American Heart Association/American Stroke Association guidelines 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 trials used doses ranging from 20 to 30 mg to 90 mg every 4 hours, with drug given for 21 days in 3 studies, and for at least 18 days in the other Three of the four trials followed patients for 3 to 6 months. Three of the trials studied relatively well patients, with all or most patients in Hunt and Hess Grades I - III The fourth studied much sicker patients, Hunt and Hess Grades III - V. Two studies, one U.S., one French, were similar in design, with relatively unimpaired SAH patients randomized to nimodipine or placebo. In each, a judgment was made as to whether any late-developing deficit was due to spasm or other causes, and the deficits were graded Both studies showed significantly fewer severe deficits due to spasm in the nimodipine group; the second (French) study showed fewer spasm-related deficits of all severities.

The Hunt and Hess grading system is used to determine the risk of vasospasm in subarachnoid acute hemorrhage.

• Grades I-III are considered to be relatively well patients, with all or most patients being essentially free of focal deficits after the initial bleed.
• Grades III-V are considered to be much sicker patients, with a high rate of death and disability. The Glasgow Outcome Scale is also used to assess the outcome of patients with subarachnoid hemorrhage, with good recovery being the most favorable outcome. Key points to determine the risk of vasospasm include:
• Delayed ischemic deficits, which can result from spasm
• Spasm-related deficits, which can be assessed using the Hunt and Hess grading system
• Permanent deficits, which can be a result of vasospasm
• Glasgow Outcome Scale, which can be used to assess the outcome of patients with subarachnoid hemorrhage 2 2 2

From the Research

Methods to Determine Risk of Vasospasm in Subarachnoid Acute Hemorrhage

• The risk of vasospasm in subarachnoid acute hemorrhage can be determined using various clinical grading scales, such as the Hunt and Hess scale 3 and the World Federation of Neurological Surgeons Scale (WFNSS) 3.
• Another grading system based on the Glasgow Coma Scale (GCS) has been proposed, which compresses the 15-point GCS into five grades that are comparable with those of the Hunt and Hess and WFNSS 4.
• The GCS grading system has been shown to have equal or greater predictive value regarding outcome after SAH than the currently used grading systems, and it has greater reproducibility across observers 4.

Scores to Determine Risk of Vasospasm

• The Hunt and Hess scale divides patients into 5 groups or levels, whose severity is progressively increasing 3.
• The WFNSS is based on the Glasgow Coma Scale score and the finding of a motor focal deficit 3.
• The GCS grading system uses a simplified grading system based entirely on the Glasgow Coma Scale, which compresses the 15-point GCS into five grades 4.
• The predictive value of each scale has been tested using ordinal logistic regression models, logistic regression models, and linear regression models, and the results show that the GCS grade has the best predictive value regarding discharge Glasgow Outcome score 4.

Management of Vasospasm

• Delayed cerebral ischemia secondary to cerebral vasospasm should be treated with induced hypertension and endovascular therapies once confirmed 5.
• However, emerging clinical evidence suggests potential harmful impact of historic empiric treatments for SAH-associated vasospasm, such as prophylactic induction of hypertension, hypervolemia, and hemodilution (triple H therapy) 6.
• The management of patients with SAH should adhere to currently available treatment guidelines, which include admission of patients to high-volume centers, early identification and management of the bleeding source, and management of patients in the neurocritical care unit with oral nimodipine, blood pressure control, euvolemia, and frequent monitoring for neurologic and systemic complications 5.