Clinical Pearls & Morning Reports
Published July 19, 2017
Subarachnoid hemorrhage without a preceding trauma is caused by the rupture of an intracranial aneurysm in 80% of cases; other causes include vascular malformations and vasculitis. Intracranial aneurysms occur in 1 to 2% of the population. The risk of intracranial aneurysms is increased among persons with a family history (defined as at least one first-degree relative who has had an intracranial aneurysm, with a greater risk if two or more first-degree relatives have had such an event), among persons with certain connective-tissue disorders (e.g., the Ehlers–Danlos syndrome), and among persons with polycystic kidney disease. Read a new review on this topic.
Q. Is there ever a warning sign before the overt rupture of an intracranial aneurysm?
A. The hallmark presenting symptom of aneurysmal subarachnoid hemorrhage is “the worst headache of my life.” The onset of the headache is sudden, and the headache is severe and reaches maximal intensity in seconds (known as a thunderclap headache). In 10 to 40% of patients, this headache is preceded by a warning leak or “sentinel” headache, which typically occurs within 2 to 8 weeks before overt subarachnoid hemorrhage.
Q. What is the risk of rerupture after the initial rupture of an intracranial aneurysm?
A. Aneurysm rerupture is associated with a very high risk of death and worse neurologic recovery among survivors. The risk of rerupture is 4 to 14% in the first 24 hours after aneurysmal subarachnoid hemorrhage, but the risk remains elevated for 30 days after the initial rupture if the aneurysm is not treated.
Figure 2. CT Scan of the Head Showing Evidence of Subarachnoid Hemorrhage.
Q: What are some of the mainstays of treatment of a ruptured intracranial aneurysm?
A: Data from randomized trials have shown better functional outcomes overall with endovascular treatment than with open-surgical treatment. However, open-surgical treatment (surgical clipping) may be preferred on the basis of certain features of the aneurysm (e.g., morphologic characteristics of the aneurysm and an associated large hematoma) or in younger patients, given the greater durability of the open-surgical treatment in the randomized trials. The calcium-channel blocker nimodipine is the only drug known to reduce the risk of delayed cerebral ischemia and improve neurologic outcome after subarachnoid hemorrhage. Currently, it is recommended that nimodipine be administered orally to all patients from the time of presentation to 21 days after the occurrence of subarachnoid hemorrhage. A Cochrane review of randomized trials indicated that nimodipine reduced the risk of poor outcomes in patients with subarachnoid hemorrhage by one third. The goals for blood pressure and volume status after intervention and the appropriate management of delayed cerebral ischemia remain uncertain.
Q: What are some of the sequelae of subarachnoid hemorrhage?
A: Delayed cerebral ischemia is a clinical syndrome of focal neurologic deficits that develops in one third of patients, typically 4 to 14 days after aneurysm rupture, and is a major cause of death and disability after subarachnoid hemorrhage has occurred. Despite a general belief that vasospasm causes delayed cerebral ischemia, recent evidence suggests that a variety of vascular and neural changes that take place after subarachnoid hemorrhage may contribute to its pathogenesis. Hydrocephalus develops soon after subarachnoid hemorrhage in 15 to 85% of patients, owing to the presence of extravasated blood blocking normal cerebrospinal fluid circulation through the subarachnoid cisterns that surround major arteries at the base of the brain; most cases are not clinically significant. Seizures occur in up to 20% of patients, especially in patients with intraparenchymal bleeding, and can cause hemodynamic instability that precipitates aneurysm rerupture; however, data are lacking from randomized trials to support routine administration of antiseizure medication, and routine prophylaxis is not recommended.