eMedicine Specialties > Neurology > Neuro-vascular Diseases

Cerebral Aneurysms: Treatment & Medication

Author: David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
Contributor Information and Disclosures

Updated: Mar 10, 2009

Treatment

Medical Care

  • Prehospital care should include assessment of vital signs and neurological status. Airway, breathing, and circulation should be addressed with endotracheal intubation, if necessary, and establishment of intravenous access.
  • Medical therapy of cerebral aneurysms involves general supportive measures and prevention of complications for individuals who are in the periprocedural period or are poor surgical candidates. Treatment decisions should be based on the clinical status of the patient, vascular anatomy of the aneurysm, and surgical or endovascular considerations.
    • Medical management of aneurysmal SAH is orchestrated in the ICU, with cardiac monitoring and placement of an arterial line.
    • Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures.
    • Following surgical or endovascular aneurysm treatment, blood pressure is maintained at higher levels to diminish complications associated with vasospasm. Vasospasm usually occurs between days 3 and 21, presenting with headache, decreased level of consciousness, and variable neurological deficits. Serial TCD may be employed to detect trends in cerebral blood flow during this period.
    • Induced hypertension, hypervolemia, and hemodilution (ie, "triple-H therapy") aims to maintain adequate cerebral perfusion pressure in the setting of impaired cerebrovascular autoregulation.
    • Intraarterial papaverine or endovascular balloon angioplasty may be used to treat vasospasm in select patients.
  • Infectious aneurysms are friable, with an increased propensity for hemorrhage. Anticoagulation is avoided in this setting. As these lesions resolve with antibiotic therapy, surgical approaches usually are deferred. Regression or evolution of these aneurysms is monitored with serial angiography.
  • The management of unruptured intracranial aneurysms is highly controversial. The International Study of Unruptured Intracranial Aneurysms (ISUIA) indicated a relatively low risk of rupture in small aneurysms without history of SAH. Aneurysms less than 10 mm in size had an annual rupture rate of approximately 0.05%. For posterior communicating, vertebrobasilar/posterior cerebral, or basilar tip aneurysms less than 10 mm, the risk of rupture over 7.5 years approximated 2%, with all other locations harboring a risk of almost 0%. Recent guidelines and an evidence-based systematic review of the literature have formulated recommendations for the care of patients with unruptured intracranial aneurysms, principally based on age, history, and aneurysm size.
    • The anatomical characterization and morphology of unruptured aneurysms are not readily standardized, however. Some investigators have advocated endovascular or surgical treatment of all aneurysms less than 10 mm if age is less than 50 years, in the absence of contraindications. The presence of cigarette smoking, family history of aneurysms, polycystic kidney disease, or systemic lupus erythematosus may elevate the risk of rupture and should be considered. Asymptomatic aneurysms greater than 10 mm should also be considered for treatment, accounting for age, coexisting medical conditions, and relative risks for treatment.
    • Considerable surgical mortality and morbidity rates at 1 year (as high as 3.8% and 15.7%, respectively) have been demonstrated in preventive treatment of unruptured aneurysms. The surgeon's experience may be a significant and highly variable factor in operative morbidity rate and functional outcome. More recently, application of diffusion-weighted MRI has demonstrated silent thromboembolic events associated with endovascular treatment of unruptured cerebral aneurysms. Quality-of-life issues, including the psychological morbidity of living with an unruptured intracranial aneurysm, also must be addressed.
    • Therapeutic decision making must balance endovascular or surgical morbidity and mortality rates with the risk of hemorrhage and other considerations on an individual basis. Future studies in the management of unruptured intracranial aneurysms may systematically account for the evolving technology of advanced endovascular approaches, detailed aneurysm morphology, novel neuroimaging correlates, ethnic and geographical variation, neurocognitive impairment following endovascular or surgical treatment, and quality-of-life issues.

Surgical Care

  • Microsurgical techniques focus on exclusion of the aneurysm from the cerebral circulation and reduction of mass effects on adjacent structures. Various approaches have been developed and tailored to the anatomy and location of the aneurysm. A surgical clip usually is placed across the aneurysm neck with preservation of the parent vessel, eliminating any aneurysmal rests that may redevelop subsequently. Alternative surgical techniques involve proximal or Hunterian ligation, wrapping of the aneurysm, or trapping (ie, a combination of proximal and distal vessel occlusion).
  • Adjunctive measures have been developed to reduce operative morbidity and to provide cerebral protection. Aneurysmal rupture, the principal surgical complication, may be avoided with induced hypotension, CSF drainage, diuretics, hyperventilation, and use of minimal brain retraction. Hypothermia, with or without circulatory arrest, and systemic hypotension are used commonly. A large recent study of mild intraoperative hypothermia, however, failed to demonstrate benefit of this adjunctive technique. Lumbar spinal drainage allows for relaxation of brain parenchyma and provides a clean surgical field. Postoperative angiography is performed routinely to check for major vessel occlusion or persistence of an aneurysmal rest. Operative morbidity rate increases with aneurysm size (2.3% for <5 mm; 6.8% for 6-15 mm, 14% for 16-25 mm) and varies by location.
  • Optimal timing of aneurysm surgery depends on the clinical status of the patient and associated factors. Early surgery (ie, <48-96 h after SAH) is favored for candidates in good condition or those with unstable blood pressure, seizures, mass effect from thrombus, large amounts of blood, or evidence of aneurysm growth or rebleeding. Early surgery carries an increased operative morbidity, although the risks of vasospasm and rebleeding are reduced considerably. Delayed surgery (ie, 10-14 d after SAH) may be considered for large aneurysms in difficult locations or for candidates in poor clinical condition. Surgery is indicated for ruptured or symptomatic aneurysms in patients without extenuating contraindications or considerably advanced age. Surgery generally is precluded if the clinical status is poor, corresponding to Hunt and Hess grade 4 or 5.
  • Advances in endovascular techniques have provided novel therapeutic alternatives that may be employed even in the setting of acute aneurysmal SAH. These techniques allow for parent vessel preservation and may be combined with surgical approaches. Electrolytically detachable platinum coils (eg, Guglielmi detachable coils [GDC]) may be deployed strategically within the aneurysm, promoting thrombosis and eventual obliteration. Wide-neck aneurysms may be more difficult to occlude with these devices. Other materials, such as balloons or glue, also may be used. Complications include vessel perforation, hemorrhage, or distal thromboembolism.
  • Endovascular therapy or coiling of cerebral aneurysms has proliferated during the last several years. The respective roles of coiling versus surgical clipping of particular cerebral aneurysms are likely influenced by numerous factors. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated the superiority of coiling with improved clinical outcomes. Seizures were also less common in patients with endovascular treatment, yet late rebleeding was also more common. Selection bias may also have influenced ISAT and, therefore, treatment for a given individual must still be tailored to each case.
  • Progressive refinement in endovascular techniques and devices tailored for the cerebrovasculature have expanded therapeutic options available for definitive treatment of cerebral aneurysms. More pliable, low profile stents may be used for stent-assisted coiling for obliteration of wide-necked aneurysms.
    • Self-expanding or balloon-expandable covered stents may be used for treatment of selected carotid or vertebral artery pseudoaneurysms.4
    • Large or giant intracranial aneurysms may be treated with a combination of devices, such as stent-assisted coil placement.5 However, the requirement of dual antiplatelet therapy in stent-assisted coiling may increase the risk of intracranial hemorrhage.6
    • Refinement of endovascular techniques for very small intracranial aneurysms has expanded treatment options, yet complications may also increase in this particular subset.7

Consultations

A multidisciplinary approach to the treatment of cerebral aneurysms is recommended. The following specialists should be a part of the multidisciplinary team:

  • Neurosurgeon
  • Interventional neuroradiologist
  • Neurologist
  • Rehabilitation specialist

Diet

  • Restrict possible surgical candidates to taking nothing by mouth (NPO).
  • Employ nasogastric feedings for individuals with a decreased level of consciousness.
  • Recommend a soft, high-fiber diet to alert patients; patients should avoid caffeine.

Activity

  • Advise bed rest in a quiet dark environment during the initial week following aneurysmal SAH.
  • Perform passive range of motion exercises and frequent turning.
  • Assist patients with self-care activities, followed by slow advancement in activity as tolerated.

Medication

Nimodipine has been demonstrated to improve outcome and decrease the incidence of delayed neurological deficits when administered for the first 21 days after aneurysmal SAH. Although the prophylactic role of antiepileptic medications in aneurysmal SAH is controversial, seizures may be treated with these medications. Antihypertensive medications may be needed to control blood pressure. After aneurysmal occlusion, these medications are held typically for 2 weeks. Sedatives and pain control may be needed for aneurysmal SAH. Antiemetics, antacids, and stool softeners also are used routinely.

Calcium channel blockers

These agents are administered to minimize sequelae of cerebral vasospasm.


Nimodipine (Nimotop)

For improvement of neurological impairments resulting from spasms following SAH caused by ruptured congenital intracranial aneurysm in patients in good postictal neurological condition.
While studies show benefit in severity of neurological deficits caused by cerebral vasospasm following SAH, no evidence shows that the drug either prevents or relieves spasm of cerebral arteries. Actual mechanism of action unknown but may involve protection of brain against ischemia.
Therapy should start within 96 h of SAH. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a hole can be made at both ends of capsule with 18-gauge needle, and contents extracted into a syringe. Contents then can be emptied into patient's nasogastric tube in situ and washed down tube with 30 mL isotonic saline.

Adult

60 mg PO q4h for 21 d

Pediatric

Not established

Although advantageous in some patients, beta-blockers may result in increased adverse effects due to depressant effects on myocardial contractility or AV conduction; fentanyl may cause severe hypotension; may increase fluid volume requirements; cimetidine may increase blood levels

Documented hypersensitivity; systolic blood pressure <90 mm Hg; sick sinus syndrome; second- or third-degree AV block except when using pacemaker

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Rare cases of elevated levels of LDH, alkaline phosphatase, and ALT may occur

Antiepileptics

These agents are administered for treatment and prevention of seizures.


Fosphenytoin (Cerebyx)

Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.
To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV is route of choice and should be used in emergency situations.
Concomitant administration of IV benzodiazepine usually necessary to control status epilepticus. Full antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate.

Adult

Loading dose: 15-20 mg PE/kg IV/IM, 100-150 mg PE/min
Maintenance dose: 4-6 mg PE/kg/d IV/IM, 150 mg PE/min to minimize risk of hypotension

Pediatric

Loading dose: 15-20 mg PE/kg IV/IM
Initial dose: 5 mg PE/kg/d IV/IM
Maintenance dose: 4-8 mg PE/kg IV/IM
>6 years: May require minimum adult dose (300 mg PE/d); not to exceed 300 mg PE/d

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, disulfiram, ethanol (acute ingestion), omeprazole, phenacemide, phenylbutazone, succinimides, fluconazole, isoniazid, metronidazole, miconazole, sulfonamides, trimethoprim, and valproic acid may increase toxicity
Barbiturates, carbamazepine, theophylline, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, or sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, methadone, metyrapone, mexiletine, oral contraceptives, quinidine, theophylline, valproic acid

Documented hypersensitivity; sino-atrial block; second- and third-degree AV block; Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Death from cardiac arrest has occurred after too-rapid IV administration, preceded sometimes by marked QRS widening
Blood dyscrasias have occurred; therefore, perform blood counts and urinalyses when therapy initiated and at monthly intervals for several mo thereafter; discontinue use if skin rash appears—if rash is exfoliative, bullous, or purpuric do not resume use; use caution in acute intermittent porphyria and diabetes (may raise blood glucose levels); discontinue drug if hepatic dysfunction occurs

Antihypertensives

These agents help in controlling systemic blood pressure.


Labetalol (Normodyne, Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, thereby decreasing blood pressure.

Adult

20-30 mg IV over 2 min, followed by 40-80 mg at 10-min intervals; not to exceed 300 mg/dose

Pediatric

Not established; suggested dose is 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use caution in impaired hepatic function (discontinue therapy if signs of liver dysfunction) and in elderly patients (lower response rate and higher incidence of toxicity may be observed)


Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Adult

10-20 mg/dose PO q4-6h prn initially; increase to 40 mg/dose if necessary; change to PO as soon as possible

Pediatric

Not established

MAOIs and beta-blockers may increase toxicity; indomethacin may decrease pharmacologic effects

Documented hypersensitivity; mitral valve rheumatic heart disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Has been implicated in myocardial infarction; caution in suspected coronary artery disease

Analgesics

These agents help in pain relief.


Morphine sulfate (MSIR, Duramorph, Astramorph, MS Contin)

Drug of choice for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Various IV doses used; commonly titrated until desired effect obtained.

Adult

Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; reassess hemodynamic effects of dose

Pediatric

Infants and children: 0.1-0.2 mg/kg dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; can initiate at 0.05 mg/kg/dose

Phenothiazines may antagonize analgesic effects; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; use caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Antiemetics

These agents help in minimizing nausea and vomiting.


Prochlorperazine (Compazine)

May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory response, acting as respiratory stimulant at high altitude.

Adult

5-10 mg PO/IM tid/qid; not to exceed 40 mg/d
2.5-10 mg IV q3-4h prn; not to exceed 10 mg/dose or 40 mg/d
Alternatively, 25 mg PR bid

Pediatric

2.5 mg PO/PR q8h or 5 mg q12h prn; not to exceed 15 mg/d; IV dosing not recommended for children
0.1-0.15 mg/kg/dose IM and change to PO as soon as possible

CNS depressants or anticonvulsants may cause additive effects; may cause hypotension with epinephrine

Documented hypersensitivity; bone marrow suppression; narrow-angle glaucoma; severe liver or cardiac disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Drug-induced Parkinson syndrome or pseudoparkinsonism occurs quite frequently; akathisia is most common extrapyramidal reaction in elderly patients; lowers seizure threshold; use caution in patients with history of seizures

Antacids

These agents help in relieving gastrointestinal acid reflux.


Ranitidine (Zantac)

Inhibits stimulation of H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen-ion concentration.

Adult

150 mg PO bid; not to exceed 600 mg/d
Alternatively, 50 mg/dose IV/IM q6-8h

Pediatric

<12 years: Not established
>12 years: 1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use caution in renal or liver impairment—if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

Stool softeners

These agents help in softening stools and minimizing straining.


Docusate sodium (Colace, Dialox, Surfak, Regulax, Sulfalax)

For patients who should avoid straining during defecation; allows incorporation of water and fat into stool, causing stool to soften.

Adult

50-500 mg/d PO qd or divided qid

Pediatric

3-6 years: 20-60 mg/d PO qd or divided qid
6-12 years: 40-150 mg/d qd or divided qid

Decreases effects of warfarin and increases effects of phenolphthalein

Documented hypersensitivity; nausea, vomiting, or acute abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use may result in electrolyte imbalance

More on Cerebral Aneurysms

Overview: Cerebral Aneurysms
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Treatment & Medication: Cerebral Aneurysms
Follow-up: Cerebral Aneurysms
Multimedia: Cerebral Aneurysms
References
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Further Reading

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Keywords

intracranial aneurysm, intracerebral aneurysm, saccular aneurysm, berry aneurysm, giant aneurysm, fusiform aneurysm, dolichoectasia, infectious aneurysm, mycotic aneurysm

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Contributor Information and Disclosures

Author

David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Draga Jichici, MD, FRCP, Associate Clinical Professor, Department of Medicine, Division of Neurology and Critical Care Medicine, McMaster University, Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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