- Of the 18,000 persons who survive the initial rupture of an aneurysm annually, 3,000 either die or are disabled from rebleeding.
- Some believe the incidence of rebleeding is as high as 30%.
- The highest incidence occurs in the first 2 weeks after initial hemorrhage.
- Peaks in the incidence of rebleeding occur in the first 24 to 28 hours and at 7 to 10 days.
- Rebleeding within the first 24 to 48 hours is the leading cause of death in persons surviving the initial bleed.
- Approximately 70% of patients who rebleed will die.
The onset of rebleeding is usually accompanied by sudden severe headache, often associated with severe nausea and vomiting; a decrease in or loss of consciousness; and new neurological deficits. Death may occur. Rebleeding can be confirmed by a CT scan or a sudden spike in ICP with new blood seen in the bag if a ventricular drain is in place. Early treatment, with either surgical or endovascular methods, of the aneurysm is the most effective means of preventing rebleeding.
- Of the 18,000 persons annually who survive initial aneurysmal rupture, 3,000 either die or are disabled from cerebral vasospasm.
- Vasospasm occurs in approximately 30% of patients.
- By definition, cerebral vasospasm is narrowing of a cerebral blood vessel and causes reduced blood flow distally, which may lead to delayed ischemic deficit and cerebral infarction if left untreated.
- Besides the damage done by the initial SAH, brain damage produced by vasospasm is an important cause of morbidity and mortality after hemorrhage, with 14% to 36% of patients suffering disability and death.
- Since improved treatment of aneurysmal subarachnoid hemorrhage has occurred with early and improved microsurgery, new endovascular techniques and better post operative care and monitoring, vasospasm has significantly decreased as the cause of death over the last ten years (from 35% in the seventies to less than 10% at this time).
- The present rescue therapies, which include ‘triple H therapy’ HHH, (hypertension/hypervolemia/ hemodilution), interventional procedures such as balloon angioplasty, intra-arterial nicardipine and other vasodilators, are associated with significant morbidity, and are labor intensive and expensive.120 A drug that would prevent delayed ischemic effects and minimize the amount of rescue therapy and optimize late outcome is desirable. When the patient’s condition deteriorates 3 to 14 days after SAH, vasospasm should be considered as the possible cause. A CT scan should be performed immediately to rule out hydrocephalus, infarction, or rebleeding.
- Vasospasm can decrease cerebral perfusion to an area, causing ischemia and perhaps infarction, and can lead to further deterioration of neurological function.
- Vasospasm may be differentiated as either angiographic or symptomatic.
- Angiographic vasospasm refers to narrowing of a cerebral arterial territory, as noted on angiography, without clinical symptoms.
- Symptomatic vasospasm is the clinical syndrome of delayed cerebral ischemia associated with angiographically documented narrowing of a major cerebral arterial territory and TCD elevation of a specific arterial territory.
- Vasospasm develops 3 to 14 days after SAH (peaking at 7 to 10 days), although the onset may be delayed up to 21 days.
Hydrocephalus is a condition in which there is either an obstruction to the flow of CSF within the ventricular system or subarachnoid space (noncommunicating hydrocephalus) either due to intraventricular mass lesions or to external compression or a problem with reabsorption of CSF (communicating hydrocephalus). The type of hydrocephalus that occurs with SAH is communicating hydrocephalus. Hydrocephalus can be classified as acute, subacute, or delayed. The profiles for each are different and are briefly discussed here. With SAH, hydrocephalus develops as a result of blood in the CSF, which plugs the arachnoid villi, thus interfering with the reabsorption of CSF. Diagnosis is established on the basis of CT findings, which will reveal dilated ventricles with blood within the ventricles.
Signs and Symptoms/Treatment
The following summarizes the signs and symptoms of the three types of hydrocephalus, as well as the appropriate treatment for each.
- Occurs within the first 24 hours after hemorrhage
- Occurs in up to 20% to 67% of affected patients within 3 days following SAH
- Associated with intraventricular hemorrhage or excessive blood in the basal cisterns of posterior fossa
- Characterized by the abrupt onset of stupor or persistence of coma
- Management: immediate ventriculostomy to drain the CSF periodically, especially when ICP is elevated above a predetermined level such as 20 mm Hg
- Occurs within the first few days to 7 days after hemorrhage
- Associated with blood in the CSF secondary to SAH
- Characterized by drowsiness, the onset of which is gradual, although an abrupt onset is possible
- Management: ventriculostomy, or serial lumbar puncture or lumbar drainage of CSF
- Occurs 10 or more days after hemorrhage
- Associated with blood in the CSF secondary to SAH
- Characterized by a gradual onset of symptoms when the patient is recovering from surgery; symptoms include gait difficulty, behavioral changes (dull, quiet, and blunted animation)
- Management: surgical placement of a ventriculoperitoneal shunt
Because signs and symptoms of hydrocephalus are nonspecific, changes in responsiveness may be attributed to other problems, thus delaying appropriate treatment.
The frequency of seizures following SAH is not known with certainty. In the early period, seizures occur between 16% and 90%. Risk factors for seizures in the early period after SAH include previous history of hypertension, CT-documented presence of focal intraparenchymal blood, occurrence of a cerebral infarction, middle cerebral aneurysm location, and duration of coma after SAH. Seizures generally occur within 18 months (if they do occur) and may be generalized, focal, or complex. On the basis of available data, many treat all aneurysmal SAH patients with anticonvulsants. If the hemorrhage is mild, anticonvulsants are tapered after 1 month. If the hemorrhage is more severe and if intraparenchymal brain injury has occurred, extended therapy and EEG monitoring are employed.