Computed Tomography Grading Schemes Used to Predict Cerebral Vasospasm
Computed Tomography Grading Schemes Used to Predict Cerebral Vasospasm
The elucidation of predictive factors of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major area of both clinical and basic science research. It is becoming clear that many factors contribute to this phenomenon. The most consistent predictor of vasospasm has been the amount of SAH seen on the postictal computed tomography scan. Over the last 30 years, it has become clear that the greater the amount of blood within the basal cisterns, the greater the risk of vasospasm. To evaluate this risk, various grading schemes have been proposed, from simple to elaborate, the most widely known being the Fisher scale. Most recently, volumetric quantification and clearance models have provided the most detailed analysis. Intraventricular hemorrhage, although not supported as strongly as cisternal SAH, has also been shown to be a risk factor for vasospasm.
Blood released under high pressure into the basal subarachnoid cisterns as a result of a ruptured an eurysm can trigger a cascade of molecular events that leads to a narrowing of the major intracranial arteries, which is called cerebral vasospasm. Radio graphically apparent vasospasm will develop in approximately 60 to 70% of all patients with aneurysmal SAH. Of these, two thirds will suffer ischemia severe enough to cause transient or permanent neurological deficits, so-called symptomatic or clinical vasospasm, or DINDs. Extreme vasospasm can ultimately lead to infarction. Vasospasm follows a typical time course in that its onset usually occurs within 1 week after the hemorrhage, it reaches its maximum severity between Days 7 and 10 post-SAH, and it usually dissipates after 14 to 21 days.
Although the impact of vasospasm on the outcome of SAH has steadily declined because of medical and surgical advances, both the disease and its treatment continue to be major sources of morbidity and mortality. Based on data from the International Cooperative Study on the Tim ing of Aneurysm Surgery, which was conducted in the early 1980s, researchers showed that clinical vasospasm permanently affected 13.5% of all patients and accounted for 33% of deaths and disabilities. More recent studies indicate that 5 to 11% of patients continue to suffer permanent disability as a result of vasospasm.
Abstract and Introduction
Abstract
The elucidation of predictive factors of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major area of both clinical and basic science research. It is becoming clear that many factors contribute to this phenomenon. The most consistent predictor of vasospasm has been the amount of SAH seen on the postictal computed tomography scan. Over the last 30 years, it has become clear that the greater the amount of blood within the basal cisterns, the greater the risk of vasospasm. To evaluate this risk, various grading schemes have been proposed, from simple to elaborate, the most widely known being the Fisher scale. Most recently, volumetric quantification and clearance models have provided the most detailed analysis. Intraventricular hemorrhage, although not supported as strongly as cisternal SAH, has also been shown to be a risk factor for vasospasm.
Introduction
Blood released under high pressure into the basal subarachnoid cisterns as a result of a ruptured an eurysm can trigger a cascade of molecular events that leads to a narrowing of the major intracranial arteries, which is called cerebral vasospasm. Radio graphically apparent vasospasm will develop in approximately 60 to 70% of all patients with aneurysmal SAH. Of these, two thirds will suffer ischemia severe enough to cause transient or permanent neurological deficits, so-called symptomatic or clinical vasospasm, or DINDs. Extreme vasospasm can ultimately lead to infarction. Vasospasm follows a typical time course in that its onset usually occurs within 1 week after the hemorrhage, it reaches its maximum severity between Days 7 and 10 post-SAH, and it usually dissipates after 14 to 21 days.
Although the impact of vasospasm on the outcome of SAH has steadily declined because of medical and surgical advances, both the disease and its treatment continue to be major sources of morbidity and mortality. Based on data from the International Cooperative Study on the Tim ing of Aneurysm Surgery, which was conducted in the early 1980s, researchers showed that clinical vasospasm permanently affected 13.5% of all patients and accounted for 33% of deaths and disabilities. More recent studies indicate that 5 to 11% of patients continue to suffer permanent disability as a result of vasospasm.
