– A localized dilation of the wall of a cerebral artery. Most ruptured aneurysms (95%) are classified as saccular (berry) aneurysms. Other categories include fusiform and mycotic aneurysms.
Causes and Incidence
Cerebral aneurysms come from congenital defects in the vessel wall coupled with secondary factors such as atherosclerosis, head trauma, arterial hypertension, infection, and polycystic disease. It is the fourth leading cerebrovascular disorder in the United States, with 24,000 new cases diagnosed annually. The peak incidence is between 35 and 60 years of age, and women are affected slightly more often than men.
Saccular aneurysms are small, berrylike sacs that protrude outward in a pouch formation on cerebral arteries, primarily at bifurcations or branches of major arteries in the circle of Willis. A weakness in the vessel wall allows the intima to bulge outward, creating a sac that fills with blood to the point of rupture. Rupture occurs when pulse pressure creates a hole in the sac, leading to subarachnoid hemorrhage and irritation of the cranial nerves and underlying cortex. The damage depends on the severity of bleeding.
A fusiform aneurysm involves the entire circumference of the artery. It develops over time as the elastic fibers undergo degenerative changes, smooth muscle is replaced by fibrous tissue, and cholesterol deposits build up on the intima. These aneurysms usually form at the trunk of the basilar artery, and they rarely rupture. Mycotic aneurysms, which are rare, occur as a result of a systemic infectious process that causes arterial necrosis and leads to the formation of multiple aneurysms along the distal branches of the anterior or middle cerebral arteries.
Most aneurysms cause no symptoms until they rupture. At that point, typical symptoms include severe, abrupt-onset headache; stiff neck; nausea; vomiting; steadily increasing neurologic deficits; seizures; and loss of consciousness. The extent of the symptoms depends on the location of the aneurysm and the severity of the bleeding. Ruptures are divided into five grades. Grade I ruptures involve minimal bleeding, no neurologic deficit, and no loss of consciousness. The person is alert, and the only symptoms may be a slight headache and a stiff neck. Grade II ruptures involve mild bleeding, and the person displays mild neurologic deficits (e.g., weakness) in addition to headache and nuchal rigidity. With grade III (moderate) bleeding, the person is confused or drowsy (or both) and has a severe headache, nuchal rigidity, and mild focal neurologic deficits. Grade IV (severe) bleeding produces stupor, mild hemiparesis, and possibly decerebrate posturing. Grade V bleeding produces coma and decerebrate posturing.
Rupture often leads to residual neurologic deficits, a permanent vegetative state, or death.
Computed tomography/ magnetic resonance imaging
To detect blood in subarachnoid space and displaced cerebral structures.
To determine whether aneurysm is intact.
Contraindicated with any sign of increased intracranial pressure (ICP).
Calcification of aneurysm wall.
Shifts in cerebral structures.
Resection, clipping, ligating, or wrapping of intact or remaining aneurysm after bleeding; ventriculostomy to treat increased ICP; ventriculoatrial shunt to treat hydrocephalus; evacuation of blood clots.
Anticonvulsants to control seizures; antihypertensives to control elevated blood pressure; corticosteroids to reduce cerebral edema; drugs to control vasospasms; stool softeners to prevent constipation and straining; analgesics for pain; chlorpromazine for shivering; antifibrinolytic agents to prevent bleeding in individuals who are not candidates for surgery.
Ventilatory support; seizure precautions; antiembolic stockings; monitoring of neurologic, cardiovascular, and hemodynamic systems; safety precautions; prevention of disuse syndrome; rehabilitation for residual neurologic deficits or coma stimulation; instruction in how to avoid straining at stool.