Risks and Complications

A patient’s condition, the type, location, and size of the aneurysm, as well as other factors determine the potential risks and complications associated with these surgical procedures. The current combined morbidity and mortality rate related to the neurosurgical clipping of an incidental cerebral aneurysm is between 5% and 10%. The risk may be somewhat higher with large aneurysms, particularly the deepest ones. Surgery poses the lowest risk when it is performed before an aneurysm ruptures. However, there are certain risks and complications associated with these treatment options. They include:

  • Blood Clots
  • Swelling in the Brain
  • Bleeding in the Brain
  • Weakness
  • Paralysis
  • Loss of Sensation
  • Loss of Vision
  • Confusion
  • Loss of Speech & Other Cognitive Functions
  • Short-term Memory Problems
  • Infections
  • Vasospasm
  • Seizures
  • Hydrocephalus
  • Stroke
  • Death


  • 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.

Cerebral Vasospasm

  • 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.