Aneurysm, cerebral
Aneurysm, cerebral: Excerpt from Handbook of Diseases
With cerebral aneurysm, localized dilation of a cerebral artery results from a weakness in the arterial wall. Its most common form is the berry aneurysm, a saclike outpouching in a cerebral artery. Cerebral aneurysms usually arise at an arterial junction in the circle of Willis, the circular anastomosis forming the major cerebral arteries at the base of the brain. Cerebral aneurysms usually rupture, causing subarachnoid hemorrhage.
The prognosis is guarded. About half of all patients who suffer a subarachnoid hemorrhage die immediately; of those who survive untreated, 40% die from the effects of hemorrhage and another 20% die later from recurring hemorrhage. With new and better treatment, the prognosis is improving.
Causes
Cerebral aneurysms may result from a congenital defect, a degenerative process, or a combination of both. For example, hypertension and atherosclerosis may disrupt blood flow and exert pressure against a congenitally weak arterial wall, stretching it like an overblown balloon and making it likely to rupture. Such a rupture is followed by subarachnoid hemorrhage, in which blood spills into the space normally occupied by cerebrospinal fluid (CSF). Sometimes, blood also spills into brain tissue and subsequently forms a clot. This may result in potentially fatal increased intracranial pressure (ICP) and brain tissue damage.
These aneurysms are slightly more common in women than in men, especially those in their late 40s or early to middle 50s, but a cerebral aneurysm may occur at any age, in women and men.
Signs and symptoms
Occasionally, rupture of a cerebral aneurysm causes premonitory symptoms that last several days, such as headache, nuchal rigidity, stiff back and legs, and intermittent nausea. Usually, however, the rupture occurs abruptly and without warning, causing a sudden severe headache, nausea, vomiting and, depending on the severity and location of bleeding, altered level of consciousness (LOC), including a deep coma.
Bleeding causes meningeal irritation, resulting in nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision. Bleeding into the brain tissues causes hemiparesis, hemisensory defects, dysphagia, and visual defects. If the aneurysm is near the internal carotid artery, it compresses the oculomotor nerve and causes diplopia, ptosis, dilated pupil, and inability to rotate the eye.
Degrees of severity
The severity of symptoms varies from patient to patient, depending on the site and amount of bleeding. Patients with ruptured cerebral aneurysms are grouped as follows:
Grade I: minimal bleeding. The patient is alert with no neurologic deficit; he may have a slight headache and nuchal rigidity.
Grade II: mild bleeding. The patient is alert, with a mild to severe headache, nuchal rigidity and, possibly, third-nerve palsy.
Grade III: moderate bleeding. The patient is confused or drowsy, with nuchal rigidity and, possibly, a mild focal deficit.
Grade IV: severe bleeding. The patient is stuporous, with nuchal rigidity and, possibly, mild to severe hemiparesis.
Grade V: moribund (commonly fatal). If the rupture is nonfatal, the patient is decerebrate or in a deep coma.
Life-threatening factors
Generally, a cerebral aneurysm poses three major threats:
Death from increased ICP. Increased ICP may push the brain downward, impair brain stem function, and cut off blood supply to the part of the brain that supports vital functions.
Bleeding episode. Generally, after the initial bleeding episode, a clot forms and seals the rupture, which reinforces the wall of the aneurysm for 7 to 10 days. However, after the 7th day, fibrinolysis begins to dissolve the clot and increases the risk of rebleeding. This rebleeding produces signs and symptoms similar to those accompanying the initial hemorrhage. Rebleeding episodes during the first 24 hours after the initial hemorrhage aren’t uncommon, and they contribute to the high mortality associated with this disorder.
Vasospasm. The reason for this complication isn’t clearly understood. Usually, vasospasm occurs in blood vessels adjacent to the cerebral aneurysm, but it may extend to major vessels of the brain, causing ischemia and altered brain function.
Other complications of a cerebral aneurysm include acute hydrocephalus (due to abnormal accumulation of CSF within the cranial cavity because of CSF blockage by blood or adhesions) and pulmonary embolism (an adverse effect of deep vein thrombosis [DVT] or aneurysm treatment). (See Danger signals in cerebral aneurysm.)
Diagnosis
With cerebral aneurysm, diagnosis is based on patient history; neurologic examination; a computed tomography (CT) scan, which reveals subarachnoid or ventricular blood; and magnetic resonance imaging or magnetic resonant angiography, which can identify a cerebral aneurysm as a “flow void” or by computer reconstruction of cerebral vessels.
Cerebral angiography remains the procedure of choice for helping to diagnose a cerebral aneurysm. Lumbar puncture may be used to identify blood in CSF when the CT scan is normal. However, its use is contraindicated in patients with signs of increased ICP.
Other baseline laboratory studies include a complete blood count, urinalysis, arterial blood gas (ABG) analysis, coagulation studies, serum osmolality, and electrolyte and glucose levels.
Treatment
The risk of vasospasm and cerebral infarction is reduced by repairing the aneurysm. Usually, surgical repair (by clipping, ligating, or wrapping the aneurysm neck with muscle) takes place 7 to 10 days after the initial hemorrhage; however, surgery performed within 1 to 2 days after the hemorrhage has also shown promise in grades I and II aneurysms.
When surgical correction is risky, when the aneurysm is in a dangerous location, or when surgery is delayed because of vasospasm, treatment includes:
bed rest in a relaxing environment that allows the patient to participate in activities that reduce stress and allow for stabilization of blood pressure (If immediate surgery isn’t possible, bed rest may continue for 4 to 6 weeks.)
avoidance of coffee, other stimulants, and aspirin
codeine or another analgesic as needed
CLINICAL TIP: To avoid the constipating effect of codeine, a stool softener is crucial to prevent straining and resultant rebleeding.
hydralazine or another antihypertensive if the patient is hypertensive
a calcium channel blocker to decrease spasm
a corticosteroid to reduce edema
phenytoin or another anticonvulsant
phenobarbital or another sedative
aminocaproic acid, a fibrinolytic inhibitor, to minimize the risk of rebleeding by delaying blood clot lysis. However, this drug’s effectiveness has been disputed.
After surgical repair, the patient’s condition depends on the extent of damage from the initial hemorrhage and the degree of success of the treatment of resulting complications. Surgery can’t improve the patient’s neurologic condition unless it removes a hematoma or reduces the compression effect.
Special considerations
During initial treatment after a hemorrhage, establish and maintain a patent airway because the patient may need supplemental oxygen. Position the patient to promote pulmonary drainage and prevent upper airway obstruction. If he’s intubated, preoxygenation with 100% oxygen before suctioning to remove secretions will prevent hypoxia and vasodilation from carbon dioxide accumulation.
Provide frequent nose and mouth care.
Institute aneurysm precautions to minimize the risk of rebleeding and to avoid increased ICP. Such precautions include bed rest in a quiet, darkened room (keeping the head of the bed flat or under 30 degrees); limited visits; avoidance of caffeine, other stimulants, and strenuous physical activity; and restricted fluid intake. Be sure to explain to the patient why these restrictive measures are necessary.
Turn the patient often. Encourage deep breathing and leg movement. Warn the patient to avoid all unnecessary physical activity. Assist him with active range-of-motion (ROM) exercises (unless the physician has forbidden them); if the patient is paralyzed, perform regular passive ROM exercises.
Monitor ABG levels, LOC, and vital signs often, and accurately measure intake and output. Avoid taking the patient’s temperature rectally because vagus nerve stimulation may cause cardiac arrest.
Watch for ominous signs of life-threatening complications.
Give fluids and monitor I.V. infusions to avoid increased ICP.
Assess the patient for dysphagia: gurgling voice, coughing, pulmonary secretions, delayed swallowing, food pocketing, and cranial nerve dysfunction (V, VII, IX, X, or XII).
Initiate a speech evaluation for assessment and recommendations for maximum safety during feeding, such as positioning, food consistency, and strategies for swallowing. If the patient is at risk for aspiration, insert a nasogastric or gastric tube.
If the patient can eat, provide a high-bulk diet (bran, salads, and fruit) to prevent straining during defecation, which can increase ICP.
Administer a stool softener, such as dioctyl sodium sulfosuccinate, or a mild laxative as needed. Don’t force fluids. Implement a bowel elimination program based on previous habits. If the patient is receiving a steroid, check the stool for blood.
If the patient is experiencing weakness of cranial nerve III (impaired lid closure), V (impaired sensation), or VII (impaired tearing), administer artificial tears or ophthalmic ointment to minimize corneal damage. An occlusive metal eye patch may also be needed.
Give the patient a sedative to help minimize stress. Be alert for signs of oversedation. Raise the side rails to help protect him from injury. If possible, avoid using restraints because they can cause agitation and raise ICP.
Administer hydralazine or another antihypertensive, if necessary. Carefully monitor blood pressure, and be alert for any significant change, especially a rise in systolic pressure. Be careful to avoid activities that may suddenly increase blood pressure.
Administer aminocaproic acid I.V. in dextrose 5% in water or orally at least every 2 hours to maintain therapeutic blood levels. (Renal insufficiency may necessitate a dosage adjustment.) Monitor the patient for adverse reactions, such as nausea and diarrhea (most common with oral administration) and phlebitis (most common with I.V. administration).
Reduce DVT by applying antiembolism stockings or sequential compression sleeves.
If the patient can’t speak, establish a simple means of communication, or use cards or a slate. Try to limit conversation to topics that won’t further frustrate him. Encourage his family to speak to him in a normal tone, even if he doesn’t seem to respond.
Provide the patient with emotional support, and include his family in his care as much as possible. Encourage family members to adopt a realistic attitude, but don’t discourage hope.
Before discharge, refer the patient to a visiting nurse or a rehabilitation center, if necessary, and teach the patient and family how to recognize signs of rebleeding. Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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