eMedicine Specialties > Neurosurgery > Vascular

Subarachnoid Hemorrhage: Treatment

Author: Jennifer Oman, MD, Associate Clinical Professor, Department of Emergency Medicine, University of California at Irvine
Coauthor(s): Sean David Lavine, MD, Assistant Professor of Neurosurgery and Radiology, Columbia College of Physicians and Surgeons; Adjunct Assistant Professor of Radiology and Neurological Surgery, Weill Medical College of Cornell University; Clinical Director, Neuroendovascular Services, New York Presbyterian Hospital, Columbia Presbyterian Medical Center
Contributor Information and Disclosures

Updated: Aug 3, 2009

Treatment

Medical Therapy

The initial management of patients with SAH is directed at patient stabilization. Assess the level of consciousness and airway, as well as breathing and circulation (ABCs).

Endotracheal intubation should be performed for patients presenting with coma, depressed level of consciousness, inability to protect their airway, or increased ICP. Rapid sequence intubation should be employed, if possible, including the use of sedation, defasciculation, short-acting neuromuscular blockade, and agents to blunt an increase in ICP.

Intravenous (IV) access should be obtained, including central and arterial lines. A short-acting benzodiazepine, such as midazolam, should be administered prior to all procedures. Monitoring should include the following:

  • Cardiac monitoring
  • Pulse oximetry
  • Automated and/or arterial blood pressure monitoring (arterial BP monitoring is indicated in high-grade SAH or when blood pressure is labile)
  • End-tidal carbon dioxide, if applicable
  • Urine output via placement of a Foley catheter

The traditional treatment of ruptured cerebral aneurysms included strict blood pressure control, with fluid restriction and antihypertensive therapy. This approach was associated with a high rate of morbidity and mortality from the ischemic complications of hypovolemia and hypotension.

The current recommendations advocate the use of antihypertensive agents when the mean arterial pressure (MAP) exceeds 130 mm Hg. Intravenous beta-blockers, which have a relatively short half-life, can be titrated easily and do not increase ICP. Beta-blockers are the agents of choice in patients without contraindications. Most clinicians avoid the use of nitrates, such as nitroprusside or nitroglycerin, which elevate ICP. Hydralazine and calcium channel blockers have a fast onset and lead to relatively less increase in ICP than do nitrates. Angiotensin-converting enzyme inhibitors have a relatively slow onset and are not first-line agents in the setting of acute SAH.

Patients with signs of increased ICP or herniation should be intubated and hyperventilated. Minute ventilation should be titrated to achieve a PCO2 of 30-35 mm Hg. Avoid excessive hyperventilation, which may potentiate vasospasm and ischemia.

Other interventions for increased ICP include the following:

  • Osmotic agents (eg, mannitol), which can decrease ICP dramatically (50% after 30 min postadministration)
  • Loop diuretics (eg, furosemide) also can decrease ICP
  • The use of IV steroids (eg, Decadron) is controversial but is recommended by some authors.

All patients should receive frequent neurological evaluation.

Use sedatives and analgesics cautiously to avoid masking the neurological examination. Emergent neurosurgical consultation should be obtained in all cases of suspected SAH.

Prophylaxis and treatment of complications

Additional medical management is directed to prevent and treat the following common complications of SAH:

  • Rebleeding
  • Vasospasm
  • Hydrocephalus
  • Hyponatremia
  • Seizures
  • Pulmonary complications
  • Cardiac complications

Ideally, management of the complications of SAH should take place in a neurologic intensive care unit or in an intensive care unit similarly equipped.

Rebleeding is the most dreaded early complication of SAH. The greatest risk of rebleeding occurs within the first 24 hours of rupture (4.1%). The cumulative risk of rebleeding is 19% at 14 days. The overall mortality rate from rebleeding is reported to be as high as 78%. Measures to prevent rebleeding include the following:
  • Bedrest in a quiet room
  • Analgesia, preferably with a short-acting and reversible agent such as fentanyl: Pain is associated with a transient elevation in blood pressure and increased risk of rebleeding.
  • Sedation (used with caution to avoid distorting subsequent neurologic evaluation) with a short-acting benzodiazepine such as midazolam
  • Stool softeners
  • Antifibrinolytics have been shown to reduce the occurrence of rebleeding. However, outcome likely does not improve because of a concurrent increase in the incidence of cerebral ischemia.
Cerebral vasospasm, the delayed narrowing of the large capacitance vessels at the base of the brain, is a leading cause of morbidity and mortality in survivors of nontraumatic SAH. Vasospasm is reported to occur in as many as 70% of patients with SAH and is clinically symptomatic in as many as 30% of patients. Most commonly, this occurs 4-14 days after the hemorrhage. Vasospasm can lead to impaired cerebral autoregulation and may progress to cerebral ischemia and infarction. Most often, the terminal internal carotid artery or the proximal portions of the anterior and middle cerebral arteries are involved. The arterial territory involved is not related to the location of the ruptured aneurysm. Risk factors for vasospasm include the following:
  • Larger volumes of blood in the subarachnoid space
  • Clinically severe SAH
  • Female sex
  • Young age
  • Smoking

Symptoms vary with the arterial territory involved, but patients typically present with a new-onset general decrease in consciousness or focal neurological deficit. Vasospasm may be clinically indistinguishable from rebleeding; imaging studies are required to exclude the latter. Conventional angiography is the definitive imaging study for vasospasm. The diagnosis of vasospasm can be made reliably at the bedside in a noninvasive fashion with transcranial Doppler.

Other tests, such as single photon emission computed tomography (SPECT), positron emission tomography (PET), xenon CT scan, and radioactive xenon clearance, can be useful for evaluation of regional cerebral blood flow in patients with vasospasm but often are difficult to perform on critically ill patients. Approximately 15-20% of patients with symptomatic vasospasm will have a poor outcome despite maximal medical therapy, including mortality in 7-10% of patients and severe morbidity in 7-10% of patients. Measures used for prevention of vasospasm include the following:

  • Maintenance of normovolemia, normothermia, and normal oxygenation are paramount to vasospasm prophylaxis. Volume status should be monitored closely, with avoidance of volume contraction, which can predispose to vasospasm.
  • Prophylaxis with oral nimodipine: Calcium channel blockers have been shown to reduce the incidence of ischemic neurological deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. Although the mechanism is unproved, it appears that nimodipine may prevent the ischemic complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged neurons. Calcium channel blockers and other antihypertensives should be used cautiously to avoid the deleterious effects of hypotension.2,3
  • Some evidence indicates that subarachnoid clot removal achieved via intracisternal injections of recombinant tissue plasminogen activator (rTPA) may dramatically reduce the risk of vasospasm. This is performed after the clipping of the aneurysm. Thrombolytic therapy is associated with the theoretical risk of intracranial bleeding, and, although the results of preliminary studies are favorable, rigorous clinical trials are needed to establish the safety and efficacy of this approach. Intracisternal antioxidants and anti-inflammatory agents are of uncertain value.
  • Aspiration and irrigation of the subarachnoid clot at the time of aneurysmal clipping usually results in suboptimal removal of the clot and is associated with a significant risk of iatrogenic trauma to pial surfaces and small vessels.
  • Intraoperative sodium chloride lavage to clear blood products from the subarachnoid space may be of some benefit, but its effectiveness remains unproved.
  • Some authors suggest that early CSF drainage via a ventricular drain may decrease the incidence of vasospasm. This intervention is performed after the aneurysm has been secured. Use caution to prevent rapid or overly aggressive drainage of CSF, which may precipitate aneurysmal rebleeding. One author suggests draining the CSF if the ICP exceeds 20 mm Hg. The drain should be set at a height to drain at 20 mm Hg to avoid an excessive reduction in ICP.

If vasospasm becomes symptomatic, most authors advocate the use of hypertensive, hypervolemic, and hemodilutional (HHH) therapy. While the efficacy of HHH therapy still is subject to debate, a number of studies have demonstrated improved cerebral blood flow and resolution of the ischemic effects of vasospasm.

Initiation of HHH therapy requires placement of a pulmonary artery catheter in order to guide volume expansion and inotropic or vasopressor therapy. This therapy should be reserved for patients with aneurysms secured by surgical clipping or endovascular techniques in order to reduce the risk of rebleeding.

Hypervolemia may be achieved by using packed erythrocytes, isotonic crystalloid, and colloid and albumin infusions in conjunction with vasopressin injection. Corticosteroids may be of some benefit; however, such treatment remains controversial. The hematocrit should be maintained at 30-35% via hemodilution or transfusion in order to optimize blood viscosity and oxygen delivery. Central venous pressure (CVP) should be maintained at 10-12 mm Hg. Pulmonary artery wedge pressure (PAWP) should be maintained at 19-20 mm Hg. Aggressive hypertensive therapy with inotropes and vasopressors (eg, dobutamine) can be initiated, if warranted.

Transluminal balloon angioplasty is recommended for treatment of vasospasm after failure of conventional therapy. One study reported improved neurologic outcome in 70% of patients with symptomatic vasospasm after transluminal angioplasty. Case series reports have indicated that angioplasty appears to be effective in treating vasospasm of large proximal vessels.4 It is not effective in direct treatment of vasospasm of more distal vessels; however, distal blood flow may be increased as a result of increased proximal vessel diameter. The potential complications of angioplasty include vessel rupture, dissection, or occlusion, as well as intracerebral hemorrhage.

Intra-arterial injection of papaverine has been reported to improve outcome, but more data are needed before routine use can be recommended. The beneficial effects of papaverine infusion appear to be short-lived compared to those of angioplasty.

Acute obstructive hydrocephalus complicates 20% of SAH cases and usually occurs within the first 24 hours after hemorrhage. This condition can precipitate life-threatening brainstem compression and occlusion of blood vessels. Hydrocephalus presents as a relatively abrupt mental status change, including lethargy, stupor, or coma. CT scan differentiates hydrocephalus from rebleeding.

Treatment for acute hydrocephalus includes external ventricular drainage, depending on the severity of clinical neurologic dysfunction or CT scan findings. Rapid lowering of ICP during intraventricular catheter placement is associated with a higher risk of rebleeding and should be avoided. Resolution of hydrocephalus may be assessed periodically by blocking CSF drainage while monitoring ICP.

Late or chronic hydrocephalus, caused by scarring of the arachnoid granulations and alterations in CSF absorption, occurs in 10-15% of patients with SAH. Typically, late hydrocephalus is of the communicating type and develops 10 or more days after SAH. Patients may present with incontinence, gait instability, and cognitive deterioration. It may be impossible to distinguish late hydrocephalus from vasospasm clinically.

Symptomatic cases of hydrocephalus may be managed by temporary lumbar CSF drainage, serial LPs, or placement of a permanent ventricular shunt. Shunt placement may not be necessary in mild cases.

Hyponatremia following SAH occurs in 10-34% of cases. Elevated levels of atrial natriuretic factor (ANF) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been implicated in recent studies of post-SAH hyponatremia. Administration of isotonic fluid can prevent volume contraction but not hyponatremia. Use of slightly hypertonic sodium chloride (1.5% sodium chloride) at rates above maintenance requirements usually is efficacious for SAH-induced hyponatremia. Avoid fluid restriction in patients with SAH.Seizures occur in as many as 25% of patients following SAH and are most common after rupture of middle cerebral artery aneurysms. Seizures can lead to increased cerebral blood flow, hypertension, and elevated ICP, thereby escalating the risk of rebleeding and neurologic deterioration. Generalized, partial, and complex-partial seizures are observed after SAH. Agents used for seizure prophylaxis include the following:
  • Phenytoin, the agent of choice, can achieve rapid therapeutic concentrations when loaded intravenously, and it does not cause alterations in consciousness.
  • Phenobarbital produces a sedative effect, which may mask the neurological evaluation; phenobarbital is used less frequently than phenytoin.
  • Chronic anticonvulsants are not recommended in patients without prior seizure activity or risk factors such as hematoma, infarct, or middle cerebral artery aneurysm.
Acute pulmonary edema and hypoxia are almost universal in severe SAH. The pulmonary edema in SAH is believed to be neurogenic in origin and unrelated to HHH therapy; however, the latter is associated with an increased risk of fluid overload. SAH-induced hypoxemia likewise is believed to be partially neurogenic in origin because it is out of proportion to what would be expected from cardiac insufficiency or fluid overload. Treatment of acute pulmonary edema may include the use of gentle diuresis, dobutamine, and positive end-expiratory pressure (PEEP).Cardiac dysfunction occurs in a significant number of people with SAH. Neurogenic sympathetic hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in SAH-associated cardiac dysfunction. Arrhythmias occur in as many as 90% of patients and most commonly include the following:
  • Premature ventricular complexes (PVCs)
  • Bradyarrhythmias
  • Supraventricular tachycardia

Arrhythmias are most prevalent in the first 48 hours following SAH. Only a small percentage of arrhythmias (usually those associated with hypokalemia) are life threatening.

Because most ECG abnormalities that occur with SAH are benign and reversible, differentiating true myocardial ischemia from these benign changes is important. The perioperative therapy to prevent secondary cerebral ischemia (hypervolemia, hypertension) may exacerbate myocardial ischemia. Conversely, therapy for myocardial ischemia, such as nitrates, may increase ICP, lower cerebral perfusion pressure, and exacerbate cerebral ischemia. Two-dimensional echocardiography often is more sensitive in detecting myocardial ischemia than is ECG, and 2-dimensional echocardiography is useful in the setting of SAH.

Surgical Therapy

Surgical methods for treatment of SAH have improved dramatically with the advent of modern microsurgical techniques and, more recently, with the success of endovascular therapy. See Indications for discussion of the specific indications for treating an aneurysm surgically, endovascularly, or both. Current surgical options include the following:

Direct aneurysmal clipping is still considered first-line treatment in the United States. The aneurysmal neck is obliterated via application of a clip that occludes blood flow to the aneurysmal dome without compromising flow to the parent artery. Clips are available in various sizes and shapes. Giant aneurysms or aneurysms with a calcified neck require specialized clips with added strength (tandem or booster clips).

Of the various endovascular options currently available, most authors believe that GDCs will have the largest influence with respect to treatment of SAH. GDCs are first-line therapy in Europe. They are soft, flexible, and can be contoured to the configuration of the aneurysm. Sizes range from 2-20 mm in diameter and 2-30 cm in length. In limited clinical trials, GDCs have been reported to achieve excellent rates of aneurysmal occlusion combined with a low complication rate in appropriate patients. Two experimental coils, the bidimensional GDC and the 3-dimensional GDC may have even better potential for aneurysm occlusion than the current generation of GDCs, but further study is needed.

Balloon embolization is efficacious in selected patients, but it has a higher incidence of complications than coil embolization.

Other surgical options include the following:

Proximal ligation of the parent artery or trapping of aneurysms with or without bypass: Proximal ligation is effective for giant aneurysms. Trial balloon occlusion can be used to assess which cases necessitate a bypass graft during the trapping procedure.

Wrapping or coating of aneurysms may be the only option in rare cases of dissecting or fusiform aneurysms

Preoperative Details

The presurgical examination should consist of a general assessment, a neurologic assessment, and a radiologic assessment.

General assessment

Cardiac and pulmonary function can decline with SAH; therefore, all patients should undergo ECG and ABG monitoring. Hemodynamic status should be monitored with a pulmonary artery catheter in patients that show evidence of compromise. A funduscopic examination should be performed. As many as 10% of patients with SAH have subretinal hemorrhage, which can lead to loss of vision.

Neurologic assessment

Serial neurologic examinations should be performed until the time of surgery for early detection of complications. Minor changes in mood, mentation, or focal neurologic function can be an early indicator of an impending complication, such as arterial vasospasm.

Radiologic assessment

Transfemoral cerebral angiography can provide important information about the size, shape, and configuration of the aneurysmal dome and neck, as well as the relationship of the parent vessel and perforators. Multiple views should be obtained to best delineate the anatomy of the aneurysmal neck. During diagnostic angiography, a trial balloon occlusion of the parent artery can be performed. This can be important in giant and fusiform aneurysms that may need to be "trapped" because they lack a defined neck for surgical clipping. A trial balloon occlusion also may provide important information about collateral blood flow.

Transcranial Doppler studies are useful in detecting and following the course of arterial vasospasm.

CT scan may detect calcification of the aneurysmal dome and neck, as well as the presence of thrombus. This information can have important surgical implications. CT angiography may be helpful in demonstrating the anatomy and relationships to other vessels.

An MRI can help delineate the degree of intramural thrombus in giant aneurysms.

Timing of surgical intervention

The timing of surgery for SAH has been a controversial topic for over 3 decades. Early surgery (0-3 d) has the following advantages:

  • Prevention of rebleeding, which is associated with a high mortality rate
  • Possible prophylaxis against vasospasm by removal of subarachnoid clot
  • Prevention and treatment of ischemic complications
  • Prevention of medical complications
  • Decreased duration of hospitalization

Disadvantages of early surgery for SAH include the following:

  • Technical problems associated with edematous brain tissue
  • High risk of intraoperative rupture of fragile aneurysm
  • Higher surgical morbidity and mortality rates

Delayed surgery for SAH (>10 d posthemorrhage) has the following advantages:

  • Brain tissue is less edematous.
  • Lower risk of intraoperative aneurysm rupture
  • Lower surgical morbidity and mortality rates
  • Flexibility of scheduling

The disadvantages of delayed surgery are as follows:

  • Increased rate of morbidity and mortality due to rebleeding
  • Technical difficulties due to adhesions around the aneurysm

The International Cooperative Study on Timing of Aneurysm Surgery findings are as follows:

  • Surgical outcomes usually are superior with delayed surgery; however, the increased morbidity and mortality rate associated with delay (as high as 30% in some studies for patients with low-grade SAH) negated these results.
  • Overall results were comparable for early and delayed surgery with the exception that patients with low-grade SAH (Hunt and Hess/WFNS grades 1-2) had a better outcome with early surgery.
  • Subsequently, many centers have published favorable results with early surgery for low-grade SAH, and it now is a common treatment decision.

For patients with an intermediate grade of SAH (Hunt and Hess/WFNS grade 3), the published results are less conclusive.

  • Several studies show no difference in morbidity and mortality rates between early and delayed surgery.
  • A 1995 study in Japan suggests that early surgery is beneficial in this group of patients.
  • Greater microsurgical experience and advances in neuroanesthesia and neurointensive management are likely to improve the outcomes for early surgery in this group of patients.

The timing of surgical management for patients with high-grade SAH (Hunt and Hess/WFNS grades 4-5) must be individualized depending on the following criteria:

  • Admission clinical examination findings and GCS
  • CT scan evidence of brain destruction
  • ICP
  • Concurrent medical problems
  • Presence of absence of cerebral vasospasm

Data suggest that some patients with an initial GCS less than 5 can have good outcomes if the following occur:

  • A ventricular drain is placed emergently.
  • ICP does not exceed 30 mm Hg.
  • Angiography shows normal intracranial filling.

Patients with significant evidence of brain destruction, increased ICP, and angiogram revealing poor intracranial filling have a universally poor outcome regardless of treatment.

The overall outcome in patients with high-grade SAH is poor with or without surgical intervention; however; because surgical treatment seems to benefit some patients, many authors suggest an aggressive approach to management.

Intraoperative Details

Surgical clipping

Most anterior circulation aneurysms can be approached from the pterion. Exceptions include (1) aneurysms arising from the division of the anterior cerebral artery into the pericallosal and callosal marginal branches and (2) small mycotic aneurysms on distal branches of the middle cerebral artery.

Posterior circulation aneurysms are less accessible, and a number of modified approaches have been developed.

  • The modified pterional approach can be employed for aneurysms arising from the head of the basilar artery where the head is above the dorsum sellae.
  • The subtemporal approach is used for aneurysms that initiate at the head of the basilar artery in which the bifurcation of the basilar artery is below the dorsum sellae.
  • A posterior subtemporal approach can be used for most aneurysms arising from the trunk of the basilar artery.
  • A far lateral inferior approach can be used for certain lower basilar trunk and midline vertebral artery aneurysms. A midline suboccipital approach can be utilized for aneurysms extending from the vertebral artery where it pierces the dura. The midline suboccipital approach also may be used for a group of aneurysms that arise from the distal posterior inferior communicating artery.

Skillful brain retraction is paramount in aneurysm surgery, with care taken to minimize tissue and vessel damage. Use of one blade only of a self-retaining retractor (eg, Yasargil, Greenburg, Sugita) usually is sufficient for adequate exposure of most saccular aneurysms and allows for the compensatory expansion and displacement of nonretracted areas of the brain, thus minimizing tissue trauma.

The general approach to surgical clipping of saccular aneurysms is as follows:

  • Dissection is undertaken to identify the parent artery for possible temporary clipping in the event of aneurysmal rupture.
  • Incision of the arachnoid overlying the aneurysm is accomplished with the tip of a #11 blade scalpel.
  • The walls of the aneurysm are dissected away from the perforating vessels with a small aneurysm dissector or spatula. Aneurysmal sac volume can be decreased, under hypotension, by compression with a suction device placed over a cotton pad.
  • Mobilization of the aneurysm in all directions is necessary for visualization of any perforating vessels that might inadvertently be incorporated by clip misplacement.
  • Occlusion of the aneurysm is accomplished with an appropriately sized clip placed across the base. Use of a clip that is as small as possible helps facilitate the visualization of perforating vessels after aneurysm repair.
    • Avoid placing the clip too close to the parent artery, which may cause a tear in the aneurysmal sac.
    • If a tear does occur, a clip graft is used for repair. Use of a clip graft is associated with the risk of damage to perforating vessels, so it should be employed only when necessary.
    • Suturing in close proximity to an aneurysm can result in damage to the parent artery and should be avoided.
  • An attempt should be made to gently open the basal cisterns and to carefully remove as much of the subarachnoid blood as possible with suction, lavage, and, possibly, intracisternal infusion of antifibrinolytics, when appropriate.

Endovascular treatment with the Guglielmi detachable coil system

Adequate airway protection, oxygenation, sedation, blood pressure management, and ICP management are paramount during the procedure. Ideally, endovascular treatment for patients with SAH should be performed under general anesthesia. Complete immobilization of the patient during catheterization and embolization is mandatory.

  • After the femoral artery puncture and initial angiogram, anticoagulation is initiated with heparin. The risk of thromboembolic events during the procedure in patients with acute SAH eclipses the risk of hemorrhage.
  • A guide catheter (6F) is placed in the internal carotid or vertebral artery. This allows for the passage of the microcatheter and facilitates contrast injection for angiograms and road mapping. Road mapping is a computer-generated technique that allows for real-time visualization of endovascular equipment superimposed over a map of the intracranial arteries.
  • The size of the aneurysm must be approximated before embolization by estimation based on the size of the adjacent intracranial arteries, by using objects such as coins for reference, or by use of a guiding catheter with a known size.
  • The clinician should find the projection that allows for optimal visualization of the parent artery in relation to the aneurysm; this usually requires views in multiple planes.
  • The plastic microcatheter tip and the Micro-Guide wire are shaped according to the configuration of the aneurysm.
  • The aneurysm is catheterized with the microcatheter and guide wire using road mapping. The microcatheter should not touch the walls of the aneurysm.
  • When the microcatheter is in the desired position within the aneurysm, the first GDC can be delivered. The first coil should be slightly smaller than the diameter of the aneurysm, and it should cross the neck of the aneurysm several times to form a receptacle. Delivery of the GDC typically takes 1-4 minutes; however, newer GDC systems can detach in 20-30 seconds.
  • After placement of the first coil has been achieved, the aneurysm is filled with coils of decreasing size until densely packed. Complete packing of the aneurysmal sac and neck usually is possible with small aneurysms. In some larger aneurysms, the neck cannot be occluded completely. These aneurysms have a higher risk of recurrence. Often, aneurysms with larger necks can be treated successfully with a balloon-assisted GDC technique.
  • The microcatheter is withdrawn cautiously from the aneurysm, and a final angiogram is obtained.
  • Heparinization is reversed with protamine, the femoral sheath is removed, and the patient is transferred to the neurologic intensive care unit.

Postoperative Details

The postoperative management of SAH is directed at prophylaxis and treatment of the complications of SAH (see Prophylaxis and treatment of complications).

Follow-up

Patients with neurologic deficits may require outpatient rehabilitation. Cognitive and psychological rehabilitation often is needed.

SAH often causes nonspecific symptoms similar to postconcussion syndrome and include the following:

  • Headache
  • Dizziness
  • Blurred vision
  • Poor concentration
  • Poor short-term memory
  • Emotional lability
  • Insomnia
  • Fatigue

Specific postsurgical problems include the following:

  • Jaw pain and stiffness due to temporalis muscle scarring
  • Paralysis of the frontalis muscle
  • Deranged or absent sense of smell due to intraoperative traction on the olfactory tract
  • Local neuralgias
  • Wound infection

Some patients may require steroid and/or anticonvulsant therapy as outpatients. Oral nimodipine therapy often is continued for 3-4 weeks after SAH.

Complications

Complications of surgical clipping include the following:

  • Hemorrhagic complications
  • Ischemic complications
  • Damage to parent artery or perforating arteries
  • Acute or delayed neurological deficits from iatrogenic trauma
  • Meningitis
  • Cellulitis and wound infection
  • Nonspecific postsurgical syndrome similar to postconcussive syndrome

Common complications of endovascular therapy include the following:

  • Aneurysm rupture (GDCs, balloons)
  • Thromboembolism (GDCs) with acute or delayed neurologic deficit
  • Balloon rupture or deflation

More on Subarachnoid Hemorrhage

Overview: Subarachnoid Hemorrhage
Workup: Subarachnoid Hemorrhage
Treatment: Subarachnoid Hemorrhage
Follow-up: Subarachnoid Hemorrhage
Multimedia: Subarachnoid Hemorrhage
References
Further Reading
[ CLOSE WINDOW ]

References

  1. [Best Evidence] Molyneux AJ, Kerr RS, Yu LM. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascualr coiling in 2143 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding, subgroups and. Lancet. 2005;366(9488):809-817. [Medline].

  2. Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med. Mar 17 1983;308(11):619-24. [Medline].

  3. Pickard JD, Murray GD, Illingworth R. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. Mar 11 1989;298(6674):636-42. [Medline].

  4. Elliott JP, Newell DW, Lam DJ, et al. Comparison of balloon angioplasty and papaverine infusion for the treatment of vasospasm following aneurysmal subarachnoid hemorrhage. J Neurosurg. Feb 1998;88(2):277-84. [Medline].

  5. [Guideline] Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. Oct 2008;52(4):407-36. [Medline].

  6. Bejjani GK, Bank WO, Olan WJ, Sekhar LN. The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery. May 1998;42(5):979-86; discussion 986-7. [Medline].

  7. Bonita R, Thomson S. Subarachnoid hemorrhage: epidemiology, diagnosis, management, and outcome. Stroke. Jul-Aug 1985;16(4):591-4. [Medline].

  8. Brilstra EH, Rinkel GJ, van der Graaf Y, et al. Treatment of intracranial aneurysms by embolization with coils: a systematic review. Stroke. Feb 1999;30(2):470-6. [Medline].

  9. Brisman JL, Song JK, Newall DW. Cerebral Aneurysms. N Engl J Med. 2006;355 (9):928-939.

  10. Brouwers PJ, Wijdicks EF, Van Gijn J. Infarction after aneurysm rupture does not depend on distribution or clearance rate of blood. Stroke. Mar 1992;23(3):374-9. [Medline].

  11. Bryan RN, Rigamonti D, Mathis JM. The treatment of acutely ruptured cerebral aneurysms: endovascular therapy versus surgery. AJNR Am J Neuroradiol. Nov-Dec 1997;18(10):1826-30. [Medline].

  12. Dandapani BK, Suzuki S, Kelley RE, et al. Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke. Jan 1995;26(1):21-4. [Medline].

  13. Dandy WE. Intracranial aneurysm of the internal carotid artery: cured by operation. Ann Surg. 1938;107:654-659.

  14. Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium. Neurosurgery. Dec 1990;27(6):855-65; discussion 865-6. [Medline].

  15. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. Jan 6 2000;342(1):29-36. [Medline].

  16. Edlow JA, Wyer PC. Evidence-based emergency medicine/clinical question. How good is a negative cranial computed tomographic scan result in excluding subarachnoid hemorrhage?. Ann Emerg Med. Nov 2000;36(5):507-16. [Medline].

  17. Eskridge JM, Song JK. Endovascular embolization of 150 basilar tip aneurysms with Guglielmi detachable coils: results of the Food and Drug Administration multicenter clinical trial. J Neurosurg. Jul 1998;89(1):81-6. [Medline].

  18. Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology. Apr 1998;50(4):876-83. [Medline].

  19. Firlik KS, Kaufmann AM, Firlik AD, et al. Intra-arterial papaverine for the treatment of cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Surg Neurol. Jan 1999;51(1):66-74. [Medline].

  20. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. Jan 1980;6(1):1-9. [Medline].

  21. Guglielmi G, Vinuela F, Dion J, Duckwiler G. Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: Preliminary clinical experience. J Neurosurg. Jul 1991;75(1):8-14. [Medline].

  22. Guglielmi G, Vinuela F, Sepetka I, Macellari V. Electrothrombosis of saccular aneurysms via endovascular approach. Part 1: Electrochemical basis, technique, and experimental results. J Neurosurg. Jul 1991;75(1):1-7. [Medline].

  23. Hacein-Bey L, Connolly ES, Mayer SA, et al. Complex intracranial aneurysms: combined operative and endovascular approaches. Neurosurgery. Dec 1998;43(6):1304-12; discussion 1312-3. [Medline].

  24. Hackett ML, Anderson CS. Health outcomes 1 year after subarachnoid hemorrhage: An international population-based study. The Australian Cooperative Research on Subarachnoid Hemorrhage Study Group. Neurology. Sep 12 2000;55(5):658-62. [Medline].

  25. Haley EC, Kassell NF, Apperson-Hansen C, et al. A randomized, double-blind, vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in North America. J Neurosurg. Mar 1997;86(3):467-74. [Medline].

  26. Hop JW, Rinkel GJ, Algra A, et al. Randomized pilot trial of postoperative aspirin in subarachnoid hemorrhage. Neurology. Feb 22 2000;54(4):872-8. [Medline].

  27. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. Jan 1968;28(1):14-20. [Medline].

  28. Johnston SC, Dudley RA, Gress DR, Ono L. Surgical and endovascular treatment of unruptured cerebral aneurysms at university hospitals. Neurology. Jun 10 1999;52(9):1799-805. [Medline].

  29. Johnston SC, Selvin S, Gress DR. The burden, trends, and demographics of mortality from subarachnoid hemorrhage. Neurology. May 1998;50(5):1413-8. [Medline].

  30. Juvela S, Heiskanen O, Poranen A, et al. The treatment of spontaneous intracerebral hemorrhage. A prospective randomized trial of surgical and conservative treatment. J Neurosurg. May 1989;70(5):755-8. [Medline].

  31. Kasner SE. Stroke treatment-specific considerations. Neurol Clin. May 2000;18(2):399-417. [Medline].

  32. Kassell NF, Boarini DJ, Adams HP, et al. Overall management of ruptured aneurysm: comparison of early and late operation. Neurosurgery. Aug 1981;9(2):120-8. [Medline].

  33. Kassell NF, Peerless SJ, Durward QJ, et al. Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery. Sep 1982;11(3):337-43. [Medline].

  34. Kassell NF, Torner JC. Aneurysmal rebleeding: a preliminary report from the Cooperative Aneurysm Study. Neurosurgery. Nov 1983;13(5):479-81. [Medline].

  35. Kassell NF, Torner JC, Haley EC, et al. The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg. Jul 1990;73(1):18-36. [Medline].

  36. Kassell NF, Torner JC, Jane JA, et al. The International Cooperative Study on the Timing of Aneurysm Surgery. Part 2: Surgical results. J Neurosurg. Jul 1990;73(1):37-47. [Medline].

  37. Kazzi AA, Ellis K. Subarachnoid Hemorrhage. eMedicine Journal [serial online]. 2001. Available at: http://www.emedicine.com/emerg/topic559.htm. [Full Text].

  38. Kowalski RG, Claassen J, Kreiter KT, et al. Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA. Feb 18 2004;291(7):866-9. [Medline].

  39. Lang DT, Berberian LB, Lee S, Ault M. Rapid differentiation of subarachnoid hemorrhage from traumatic lumbar puncture using the D-dimer assay. Am J Clin Pathol. Mar 1990;93(3):403-5. [Medline].

  40. Le Roux PD, Newell DW, Eskridge J, et al. Severe symptomatic vasospasm: the role of immediate postoperative angioplasty. J Neurosurg. Feb 1994;80(2):224-9. [Medline].

  41. Le Roux PD, Winn HR. Intracranial aneurysms and subarachnoid hemorrhage management of the poor grade patient. Acta Neurochir Suppl (Wien). 1999;72:7-26. [Medline].

  42. Leblanc R. The minor leak preceding subarachnoid hemorrhage. J Neurosurg. Jan 1987;66(1):35-9. [Medline].

  43. Linn FH, Rinkel GJ, Algra A, van Gijn J. Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis. Stroke. Apr 1996;27(4):625-9. [Medline].

  44. Mancuso PA, Weinstein PR. Pathophysiology and management of hydrocephalus after subarachnoid hemorrhage. In: Ratchenson RA, Wirth FP, eds. Ruptured cerebral aneurysms: Perioperative management. Concepts in Neurosurgery. Vol 6. Baltimore, Md:. Williams and Wilkins;1994:124-133.

  45. Martin NA. The combination of endovascular and surgical techniques for the treatment of intracranial aneurysms. Neurosurg Clin N Am. Oct 1998;9(4):897. [Medline].

  46. Mayberg MR, Batjer HH, Dacey R, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. Nov 1994;25(11):2315-28. [Medline].

  47. Miller J, Diringer M. Management of aneurysmal subarachnoid hemorrhage. Neurol Clin. Aug 1995;13(3):451-78. [Medline].

  48. Mizoi K, Yoshimoto T, Takahashi A, et al. Prospective study on the prevention of cerebral vasospasm by intrathecal fibrinolytic therapy with tissue-type plasminogen activator. J Neurosurg. Mar 1993;78(3):430-7. [Medline].

  49. Morgenstern LB, Luna-Gonzales H, Huber JC Jr, et al. Worst headache and subarachnoid hemorrhage: prospective, modern computed tomography and spinal fluid analysis. Ann Emerg Med. Sep 1998;32(3 Pt 1):297-304. [Medline].

  50. Muizelaar JP, Becker DP. Induced hypertension for the treatment of cerebral ischemia after subarachnoid hemorrhage. Direct effect on cerebral blood flow. Surg Neurol. Apr 1986;25(4):317-25. [Medline].

  51. Newell DW, Elliott JP, Eskridge JM, Winn HR. Endovascular therapy for aneurysmal vasospasm. Crit Care Clin. Oct 1999;15(4):685-99, v. [Medline].

  52. Newell DW, Winn HR. Transcranial Doppler in cerebral vasospasm. Neurosurg Clin N Am. Apr 1990;1(2):319-28. [Medline].

  53. Nichols DA, Meyer FB, Piepgras DG. Endovascular treatment of intracranial aneurysms. Mayo Clin Proc. Mar 1994;69(3):272-85. [Medline].

  54. Ohman J, Servo A, Heiskanen O. Effect of intrathecal fibrinolytic therapy on clot lysis and vasospasm in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg. Aug 1991;75(2):197-201. [Medline].

  55. Olafsson E, Hauser WA, Gudmundsson G. A population-based study of prognosis of ruptured cerebral aneurysm: mortality and recurrence of subarachnoid hemorrhage. Neurology. May 1997;48(5):1191-5. [Medline].

  56. Oropello JM, Weiner L, Benjamin E. Hypertensive, hypervolemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? No. Crit Care Clin. Jul 1996;12(3):709-30. [Medline].

  57. Pinto AN, Canhao P, Ferro JM. Seizures at the onset of subarachnoid haemorrhage. J Neurol. Feb 1996;243(2):161-4. [Medline].

  58. Rhoney DH, Tipps LB, Murry KR, et al. Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology. Jul 25 2000;55(2):258-65. [Medline].

  59. Rinkel GJ, van Gijn J, Wijdicks EF. Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke. Sep 1993;24(9):1403-9. [Medline].

  60. Roginski RS, Abramowicz AS. Intracranial hypertension and neurosurgery. Anesthesiol Clin North America. 1999;17(3):633-643.

  61. Roos EJ, Rinkel GJ, Velthuis BK, Algra A. The relation between aneurysm size and outcome in patients with subarachnoid hemorrhage. Neurology. Jun 27 2000;54(12):2334-6. [Medline].

  62. Roos Y. Antifibrinolytic treatment in subarachnoid hemorrhage: a randomized placebo-controlled trial. STAR Study Group. Neurology. Jan 11 2000;54(1):77-82. [Medline].

  63. Roos YB, Vermeulen M, Rinkel GJ, et al. Systematic review of antifibrinolytic treatment in aneurysmal subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. Dec 1998;65(6):942-3. [Medline].

  64. Schievink WI. Intracranial aneurysms. N Engl J Med. Jan 2 1997;336(1):28-40. [Medline].

  65. Schwartz RB, Tice HM, Hooten SM, et al. Evaluation of cerebral aneurysms with helical CT: correlation with conventional angiography and MR angiography. Radiology. Sep 1994;192(3):717-22. [Medline].

  66. Shah MV, Heros RC. Intracerebral hemorrhage due to cerebral arteriovenous malformations. Neurosurg Clin N Am. Jul 1992;3(3):567-76. [Medline].

  67. Solenski NJ, Haley EC Jr, Kassell NF, et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med. Jun 1995;23(6):1007-17. [Medline].

  68. Solomon RA, Fink ME, Pile-Spellman J. Surgical management of unruptured intracranial aneurysms. J Neurosurg. Mar 1994;80(3):440-6. [Medline].

  69. Stieg PE, Kase CS. Intracranial hemorrhage: diagnosis and emergency management. Neurol Clin. May 1998;16(2):373-90. [Medline].

  70. Sztajnkrycer M, Jauch EC. Unusual headaches. Emerg Med Clin North Am. Nov 1998;16(4):741-60, vi. [Medline].

  71. Thrift AG, McNeil JJ, Forbes A, Donnan GA. Risk factors for cerebral hemorrhage in the era of well-controlled hypertension. Melbourne Risk Factor Study (MERFS) Group. Stroke. Nov 1996;27(11):2020-5. [Medline].

  72. Ullman JS, Bederson JB. Hypertensive, hypervolemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? Yes. Crit Care Clin. Jul 1996;12(3):697-707. [Medline].

  73. van der Wee N, Rinkel GJ, Hasan D, van Gijn J. Detection of subarachnoid haemorrhage on early CT: is lumbar puncture still needed after a negative scan?. J Neurol Neurosurg Psychiatry. Mar 1995;58(3):357-9. [Medline].

  74. van Gijn J, Bromberg JE, Lindsay KW, et al. Definition of initial grading, specific events, and overall outcome in patients with aneurysmal subarachnoid hemorrhage. A survey. Stroke. Aug 1994;25(8):1623-7. [Medline].

  75. Vermeulen M. Subarachnoid haemorrhage: diagnosis and treatment. J Neurol. Jul 1996;243(7):496-501. [Medline].

  76. Vespa PM, Gobin YP. Endovascular treatment and neurointensive care of ruptured aneurysms. Crit Care Clin. Oct 1999;15(4):667-84. [Medline].

  77. Weaver JP, Fisher M. Subarachnoid hemorrhage: an update of pathogenesis, diagnosis and management. J Neurol Sci. Sep 1994;125(2):119-31. [Medline].

  78. Wermer MJ, Buskens E, van der Schaaf IC, et al. Yield of screening for new aneurysms after treatment for subarachnoid hemorrhage. Neurology. Feb 10 2004;62(3):369-75. [Medline].

[ CLOSE WINDOW ]

Further Reading

Clinical guidelines

Acute stroke management. Management of subarachnoid and intracerebral hemorrhage. In: Canadian best practice recommendations for stroke care: 2006. Ottawa (ON): Canadian Stroke Network, Heart & Stroke Foundation of Canada; 2006. p. 61-3.

Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW, American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med 2008 Oct;52(4):407-36. 5

[ CLOSE WINDOW ]

Keywords

SAH, nontraumatic subarachnoid hemorrhage, nontraumatic SAH, extravasation of blood into the subarachnoid space between the pial and arachnoid membranes, spontaneous atraumatic intracranial hemorrhage, ruptured cerebral aneurysm, ruptured arteriovenous malformation

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Jennifer Oman, MD, Associate Clinical Professor, Department of Emergency Medicine, University of California at Irvine
Disclosure: Nothing to disclose.

Coauthor(s)

Sean David Lavine, MD, Assistant Professor of Neurosurgery and Radiology, Columbia College of Physicians and Surgeons; Adjunct Assistant Professor of Radiology and Neurological Surgery, Weill Medical College of Cornell University; Clinical Director, Neuroendovascular Services, New York Presbyterian Hospital, Columbia Presbyterian Medical Center
Sean David Lavine, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and Neurosurgical Society of America
Disclosure: Nothing to disclose.

Medical Editor

Paul L Penar, MD, Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine
Paul L Penar, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.