AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Intracranial saccular aneurysms represent the most common etiology of nontraumatic subarachnoid hemorrhage (SAH), with about 80% of SAH resulting from ruptured aneurysms. SAH is responsible for the death and/or disability of 18,000 persons each year in North America alone. Unfortunately, the difficulties in detecting unruptured aneurysms in asymptomatic patients practically preclude the possibility of preventing most SAH.

About 6-8% of all strokes are caused by SAH from ruptured berry aneurysms. Over the past several decades, the incidence of other types of strokes has decreased; however, the incidence of SAH has not decreased.

Pathophysiology

Aneurysms are acquired lesions related to hemodynamic stress on the arterial walls at bifurcation points and bends. Saccular or berry aneurysms are specific to the intracranial arteries because their walls lack an external elastic lamina and contain a very thin adventitia—factors that may predispose to the formation of aneurysms. An additional feature is that they lie unsupported in the subarachnoid space.

Aneurysms mostly arise from the terminal portion of the internal carotid artery (ICA) and from the major branches of the anterior portion of the circle of Willis. In a 25-year autopsy study of 125 patients with ruptured or unruptured aneurysms conducted at Johns Hopkins, hypertension, cerebral atherosclerosis, vascular asymmetry in the circle of Willis, persistent headache, pregnancy-induced hypertension, long-term analgesic use, and family history of stroke all were correlated positively with the formation of saccular aneurysms.

The occurrence of aneurysms in children indicates the role of intrinsic vascular factors. A number of disease states resulting in weakness of the arterial wall are associated with an increased incidence of berry aneurysms.

Hypertension (previously documented acute severe hypertension with diastolic value over 110 mm Hg), smoking, alcohol, multiple aneurysms, increasing aneurysm size, fatty metamorphosis of the liver, long-term analgesic use, and oral contraceptives have been linked to aneurysmal SAH.

Disease states associated with higher incidence of berry aneurysms include the following:

• Increased blood pressure - Fibromuscular dysplasia, polycystic kidney disease, and aortic coarctation
• Increased blood flow - Cerebral arteriovenous malformation (AVM); persistent carotid-basilar anastomosis; ligated, aplastic, or hypoplastic contralateral vessel
• Blood vessel disorders – Systemic lupus erythematosus (SLE), Moyamoya disease, and granulomatous angiitis
• Genetic - Marfan syndrome, Ehlers-Danlos syndrome, Osler-Weber-Rendu syndrome, pseudoxanthoma elasticum, and Klippel-Trenaunay-Weber syndrome
• Congenital - Persistent fetal circulation and hypoplastic/absent arterial circulation
• Metastatic tumors to cerebral arteries - Atrial myxoma, choriocarcinoma, and undifferentiated carcinoma
• Infectious - Bacterial, fungal

Frequency

United States

The frequency of ruptured and unruptured aneurysms has been estimated at 1-9% in different autopsy series, with a prevalence (of unruptured aneurysms) of 0.3-5%. Generally, the older age group is more likely to be hospitalized; therefore, these studies may not be representative of the general population.

Retrospective arteriographic studies show a prevalence of less than 1% with the limitation that some cases did not receive adequate evaluation and thus some aneurysms may have been missed. Overall estimated prevalence of unruptured aneurysms in the general population is around 1%.

The incidence of SAH from ruptured saccular aneurysms in North America is approximately 12 cases per 100,000 population. Approximately 28,000 people experience aneurysmal SAH each year.

International

The reported incidence of SAH is high in the United States, Finland, and Japan, while it is low in New Zealand and the Middle East. In Finland, the estimated incidence based on different studies is 14.4-19.6 cases per 100,000 population, although numbers as high as 29.7 have been reported. In Japan, the reported rates vary between 11 and 18.3 cases per 100,000 population, with one study showing an incidence of 96.1 cases per 100,000 population (this study included only patients aged 40 and older in the data collection, and results were not adjusted for sex and age to the same reference population). In New Zealand, age-adjusted incidence was reported as 14.3 cases per 100,000 population.

An Australian study reported an incidence of 26.4 cases per 100,000 population but only for patients older than 35 years, as age was not adjusted in the reference population. In the Netherlands, the age-specific incidence was reported as 7.8 cases per 100,000 population (this is believed to be an underestimate). Iceland reported 8 cases per 100,000 population, but a significant portion of the affected rural population was believed to be missed. Greenland Eskimos had 9.3 cases per 100,000 population, while ethnic Danes in the same country were found to have an incidence of 3.1 cases per 100,000 population. This latter figure is consistent with the figures in Denmark—marked differences are postulated to be related to genetic factors. On the Faeroe Islands (part of Denmark with an isolated population of the same genetic ancestry), the reported incidence is 7.4 cases per 100,000 population.

In China, the reported incidence is low but no good studies have been published to support this statement. Indians and Rhodesian Africans also have significantly lower incidence than those from European nations; this can be explained partly by the low incidence of atherosclerosis in these populations. In the Middle East, the numbers are very low as well; the best available estimate is 5.1 cases per 100,000 population in Qatar.

Mortality/Morbidity

• As many as 60% of patients die in the first 30 days as the result of SAH. About 10% die immediately without any warning; an additional 25% die or become disabled as a result of the initial hemorrhage.
• Hospitalized patients have an average mortality rate of 40% in the first month. Rebleeding, a major complication, carries a mortality rate of 51-80%.
• Delayed cerebral ischemia due to vasospasm, the most deadly of all complications, affects 20% of angiographically visualized cases of vasospasm.

Race

North American blacks have been found to have a 2.1 times greater risk of SAH than whites.

Sex

The incidence of SAH is slightly higher in women than in men.

Age

The mean age for SAH is 50 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Aneurysmal SAH presents with severe headache of sudden onset ("thunderclap headache") that can be accompanied by loss of consciousness at onset. The headache is frequently described as "worst headache of my life."
• Neck stiffness, photophobia, and low back pain are symptoms of meningeal irritation. Nausea and vomiting are due to increased intracranial pressure (ICP) and meningeal irritation.
• Focal neurological deficits may also occur.
• Approximately 10-25% of patients with SAH have a seizure, usually in the first few minutes after onset. This is due to the sudden rise in ICP or direct cortical irritation by blood.
• An estimated 10-15% of patients with ruptured aneurysms have symptoms related to their aneurysm prior to the rupture. The most common symptoms are headache (48%), dizziness (10%), orbital pain (7%), diplopia (4%), and visual loss (4%).
• Signs present before SAH include sensory or motor disturbance (6%), seizures (4%), ptosis (3%), bruits (3%), and dysphasia (2%). Some studies estimate an even higher incidence of premonitory symptoms—as many as 40-50%, with signs appearing 10-20 days prior to rupture.
• The premonitory symptoms may represent small leaks ("sentinel bleed") or expansion of the aneurysm.
• Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional strain, defecation, coitus, and head trauma contribute to varying degrees in the remaining 60-70% of cases.

Physical

• The physical examination findings may be normal.
• Global depression of neurological function may be noted, including altered level of consciousness and confusional state.
• Focal neurological findings may include the following:
• • Cranial nerve deficits: Oculomotor palsy (posterior communicating artery aneurysm) is most frequent. Abducens palsy is usually due to increased ICP rather than a true localizing sign. Monocular loss of vision can occur with ophthalmic artery aneurysms.
  • Hemiparesis: With or without aphasia, hemiparesis is due to middle cerebral artery (MCA) aneurysm, ischemia or hypoperfusion in the vascular territory, or intracerebral clot.
  • Leg monoparesis or paraparesis with or without akinetic mutism/abulia points to anterior communicating aneurysm rupture.
• Funduscopic findings include papilledema and subhyaloid retinal hemorrhages.

Causes

• Eighty percent of nontraumatic SAHs are due to a ruptured berry aneurysm.
• Other vascular malformations such as AVMs and mycotic aneurysms cause most of the remaining 20%.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Arterial supply, orbit
Back pain
Diplopia
Computed tomography (CT) in neurovascular diseases

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Serum chemistry panel
• CBC count
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests
• Blood typing/screening tests

Imaging Studies

• CT without contrast
• • CT is the most sensitive imaging study in SAH (see Images 1-3).
  • Findings may be negative in 10-15% of patients with SAH.
  • Maximum sensitivity is within 24 hours after the event; sensitivity is 80% at 3 days, 50% at 1 week.
  • Look for evidence of hydrocephalus (trapped temporal horns and "Mickey Mouse" appearance of ventricular system).
  • Look for intraparenchymal clot, intraventricular hematoma, and interhemispheric hematoma.
  • Degree and location of SAH are significant prognostic factors. The Fisher grading system is used to classify SAH, as follows:
  • • Grade I - No subarachnoid blood seen on CT scan
    • Grade II - Diffuse or vertical layers of SAH less than 1 mm thick
    • Grade III - Diffuse clot and/or vertical layer greater than 1 mm thick
    • Grade IV - Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
• Cerebral angiography - To assess the following:
• • Vascular anatomy (see Images 4-7)
  • Site of bleed (location of aneurysm that bled this time)
  • Presence of other aneurysms (about 20% have multiple aneurysms)
  • Operative planning
  • Negative angiographic findings do not rule out aneurysm. Approximately 10-20% of patients with clinically diagnosed SAH (CT and/or lumbar puncture [LP]) have negative angiographic findings. A repeat angiogram is usually required in 10-21 days.
• MRI is inferior to CT in an acute setting to detect SAH.
• MR angiography (MRA) is less sensitive than cerebral angiography to detect small aneurysms.
• CT angiography is beneficial in very unstable patients who cannot undergo angiography or in emergent settings prior to operative intervention for clot evacuation.

Other Tests

• ECG
• • Nonspecific ST and T changes, prolongation of QRS segments or QT intervals, deeply inverted T waves, and U waves sometimes are seen in SAH.
  • Patients with SAH can have myocardial ischemia due to the increased level of circulating catecholamines or to autonomic stimulation from the brain.

Procedures

• Lumbar puncture
• • If the CT scan shows no SAH, an LP needs to be performed to evaluate the cerebrospinal fluid (CSF) for the presence of RBCs and xanthochromia.
  • LP is most sensitive 12 hours after onset of symptoms.
  • LP findings can be negative in approximately 10-15% of patients with SAH.
  • Patients with negative CT and LP findings have a favorable prognosis.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

The patient with acute SAH needs to be managed in an intensive care (ICU) setting, placed in a quiet room, and given mild sedation if agitated. The head end of the bed should be kept elevated at 30° to ensure optimal venous drainage. Blood pressure must be maintained with consideration of the patient's neurological status. Optimally, systolic blood pressure (SBP) of no more than 130-140 mm Hg should be the goal, unless clinical evidence of vasospasm is noted. Indwelling catheters include arterial line, central venous access, and Foley catheter. Seizure prophylaxis and calcium channel blockade are standard medical measures. Stool softeners are given to prevent Valsalva maneuvers with resultant peaks in SBP and ICP.

• Hydrocephalus
• • Since acute hydrocephalus (HCP) is associated with lower preoperative grade and poorer prognosis, the clinician must carefully monitor the patient for early signs of acute HCP. The most reliable clinical measure is the patient's level of consciousness. Any change in the level of consciousness requires an emergent CT scan to evaluate ventricular size. An obtunded patient with dilated ventricles deserves an immediate ventriculostomy.
  • Increased risk for rebleeding may be associated with ventriculostomy placement, along with known infectious risk; therefore, patients with dilated ventricles (but no compromise of level of consciousness) should be treated conservatively with close monitoring of mental status and prompt intervention in case their clinical status declines. Some have used serial LPs to monitor such patients.
  • Ventriculostomy, when done correctly, is a relatively low-risk procedure that can result in dramatic and immediate clinical improvement in about two thirds of patients. If the patient's grade improves enough as a result of ventriculostomy, the patient may become a candidate for early surgery.
  • When grading patients clinically, great care must be taken to note possibly reversible deficits related to HCP, which may be contributing to the patients' poor condition. According to a study of 47 patients with poor-grade aneurysm without CT evidence of irreversible brain destruction who underwent ventriculostomy, early control of the ICP and aggressive management appeared to be the appropriate treatment in this subset of patients.
• Vasospasm lethargy
• • Lethargy with or without focal neurological deficit is vasospasm, until proven otherwise.
  • Emergency CT must be performed to rule out other pathology.
  • Swan-Ganz catheterization is indicated; hypertensive hypervolemic hemodilution (ie, triple H) management is used to target a pulmonary capillary wedge pressure (PCWP) of 14.
  • The goal is to maximize cerebral blood flow (CBF) to areas of vasospasm to prevent or reverse neurological symptoms.
  • Cardiac output and cardiac index should be monitored.

Surgical Care

• Surgical treatment involves clipping of the ruptured berry aneurysm. Endovascular treatment (ie, coiling) is an increasingly practiced alternative to surgical clipping. At many institutions, higher-grade patients and those with significant medical comorbidities tend to be treated by coiling as opposed to clipping. Posterior circulation aneurysms are preferentially treated by coiling because of the significant morbidity and mortality associated with surgical clipping.
• The large randomized prospective study ISAT found coiling to be significantly safer when comparing ruptured aneurysms that were deemed equally suitable candidates for either surgical or endovascular treatment. The incidence of rebleeding was slightly higher in the coiled group, but the endovascularly treated group did so much better overall that the study was stopped after reviewing the one-year outcome data. Partially because of the ISAT study, endovascular treatment is becoming the first-line treatment for many aneurysms.
• The data to establish long-term results of endovascular treatment are insufficient, however. In general, the incidence of recanalization is higher with coiling. Significant advances have been made in recent years with the introduction of new coated coils that either swell within the aneurysm or promote fibrous tissue formation and organization of the intraarterial clot.
• Other advances include the use of intracranial stents to promote coiling (especially in aneurysms with wide necks) and decrease inflow into the aneurysm in certain instances. The stents have also provided a novel approach to treating certain types of aneurysms that have historically been untreatable. At the moment, no long-term follow-up data exist to assess the efficacy of these new treatment modalities.
• The timing of surgery has been the subject of controversy for more than 40 years. Early surgery/coiling is generally recommended in patients with straightforward aneurysms of a favorable clinical grade. Poor-grade patients who fail to improve after stabilizing measures (including ventriculostomy placement), may not get treated in the acute period or may be preferentially treated by coiling.
  The goals of early surgical/endovascular treatment are to prevent rebleeding and to enable the treating physicians to institute triple H therapy (for vasospasm prevention).
• Delayed surgery/coiling is recommended in patients with poor-grade aneurysms, those with medical complications, and those with giant or complicated aneurysms.

Consultations

• The neurosurgeon/neurointerventionalist must be involved early in the care of the patient with an aneurysmal SAH.
• A physician with critical care experience, pulmonologist, cardiologist, or anesthesiologist should manage the patient in the ICU.

Activity

Patients must be admitted to the ICU with strict bed rest until the etiology of hemorrhage is determined. Patients should not be allowed out of bed for any reason.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Therapeutic goals are blood pressure control, prevention of seizures, treatment of nausea, management of ICP, prevention of vasospasm, control of pain, and maintenance of cerebral perfusion.

Drug Category: Calcium channel blocker

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Drug Category: Antiepileptic agents

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.

Drug Category: Stool softeners

These agents prevent elevation of intracranial pressure associated with Valsalva maneuver.

Drug Category: Antihypertensive agents

After SAH due to ruptured aneurysm, blood pressure must be maintained in a range that allows for sufficient cerebral perfusion yet limits the risk of rebleeding.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Inpatient or subacute rehabilitation (ie, physical, occupational, and speech therapy) is often appropriate.

Further Outpatient Care

• Neurosurgery clinic follow-up in 4-6 weeks
• Outpatient physical therapy/occupational/speech therapy as needed

Transfer

• Rehabilitation

Complications

• Hydrocephalus
• • SAH can cause HCP by 2 mechanisms—obstruction of CSF pathways (ie, acute, obstructive, noncommunicating type) and blockage of arachnoid granulations by blood breakdown products (ie, delayed, nonobstructive, communicating type).
    • Acute HCP may present immediately or within the first 7 days after SAH.
    • Delayed HCP has a more insidious and indolent presentation.
  • Acute (ie, obstructive) HCP is caused by compromise of CSF circulation pathways by interfering with CSF outflow through the sylvian aqueduct, fourth ventricular outlet, basal cisterns, and subarachnoid space. CSF production and absorption rates are unaltered. The presence of intraventricular blood is the strongest determinant for the development of acute HCP due to either blockage of CSF pathways by blood clot or diminished CSF outflow as a result of significantly elevated CSF viscosity.
  • Other factors increasing the risk of developing acute (obstructive) HCP include bilateral ambient cisternal blood, increased age, vasospasm, and use of antifibrinolytic drugs. HCP results in increased ICP and ventricular dilatation, decreased basal blood flow, and decreased level of consciousness. It is associated with lower preoperative grade and poorer prognosis.
• Rebleeding
• • The incidence of this dreadful complication is greatest in the first 2 weeks. The peak is within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5% per day for the next 12-13 days. The cumulative 2-week incidence is 20-30% in unoperated patients. The rebleeds in the first days ("blow out" hemorrhages) are thought to be related to the unstable nature of the aneurysmal thrombus as opposed to lysis of the clot sitting over the rupture site. Clinical factors that increase the likelihood of rebleeding include hypertension, anxiety, agitation, and seizures. Rebleeding is the cause of 7% of deaths in aneurysmal SAH.
  • After the first 30 days, rebleed rate decreases to 1.5% per year for the first 10 years. In another study, rebleeding was reported at a rate of 3% per year after 6 months, with a 67% mortality rate at 20 years. Initially, the high complication rate related to early clipping of the aneurysms was thought to outweigh the risk of rebleeding, and a philosophy of delayed surgery was generally accepted. With the improvement of surgical technique, especially since the routine use of microneurosurgical techniques, a major change in this thinking has occurred in favor of early surgery for patients with aneurysms of favorable grade.
• Delayed ischemia
• • Presently, delayed ischemia is the most common cause of death and disability following aneurysmal SAH. It has to some degree "compensated for" the improved rebleed rate related to early surgical clipping. An estimated 10-20% of patients with aneurysmal SAH suffer delayed cerebral ischemia, resulting in permanent disability or death. This complication alone accounts for 14-32% of deaths and permanent disability in large studies, while the direct effect of aneurysm rupture accounts for 25% and rebleeding for 17.6%.
  • Incidence of angiographic vasospasm is 30-70%; of these patients, 20% become symptomatic. Vasospasm is believed to be induced in areas of thick subarachnoid clot. The putative agent responsible for vasospasm is oxyhemoglobin, but its true etiology and pathogenesis remain to be elucidated. Vasospasm has its onset on day 3 after SAH, is maximal about days 6-8, and usually resolves around day 12. The actual distribution of risk of clinical vasospasm differs according to whether the patient has had a prior SAH. In patients with no prior SAH, most frequent time of onset is between days 10 and 17, with only a 4.2% incidence on day 3. In patients with previous SAH, incidence of vasospasm is 38.7% in the first 3 days and only 20% between days 10 and 17.
  • Overall, close to 50% of patients develop vasospasm in the peak period. Correlation between the initial CT scan and the incidence of vasospasm is well established. When the CT scan fails to demonstrate blood or shows only a thin layer, vasospasm is unlikely. If the CT shows significant blood clot of 5 x 3 mm or larger size, severe angiographic spasm and clinical deficits follow in nearly all cases.
• Intracerebral hemorrhage (ICH): Radiologically, ICH from aneurysmal rupture can look identical to hypertensive hemorrhage. The mechanism of ICH is direct rupture of aneurysm into the brain; it accounts for about 40% of cases of ICH. It commonly results from internal cerebral artery (ICA), pericallosal, and anterior cerebral artery (ACA) aneurysms. Secondary rupture of subarachnoid hematoma into the brain parenchyma most commonly arises from MCA aneurysms. Overall incidence of ICH from ACA is 44%; MCA 26%; ICA 21%; and pericallosal 10%.
• Intraventricular hemorrhage (IVH): Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy cases, IVH is a significant predictor of poor neurological grade and outcome. Patients with IVH are at higher risk of developing HCP. In one study of 91 patients, it was associated with an overall mortality rate of 64%. Key prognostic indicator is the degree of ventricular dilatation. Sources of IVH are ACA (40%), ICA (25%), MCA (21%), and vertebrobasilar artery (VBA, 14%).
• Subdural hematoma (SDH): SDH is rare following aneurysmal SAH, with reported incidence of 1.3-2.8% in clinical series and as high as 20% in autopsy series. The mechanisms of SDH involve tearing of arachnoid adherent to the dome of the aneurysm at the time of rupture, direct tearing of arachnoid by a jet of blood, and disruption of arachnoid by ICH, with secondary decompression of ICH into the subdural space.
• Seizures: Seizures occur in 13-24% of patients with SAH, commonly in the first 24 hours after the bleed. Some studies argue that anticonvulsant therapy can be limited safely to the immediate perioperative period in patients with no parenchymal clot, ischemic infarct, or postoperative hematoma.
• Increased ICP: Elevations in ICP are due to mass effect of blood (subarachnoid, ICH, IVH, or SDH) or acute HCP. Once ICP reaches mean arterial pressure (MAP), cerebral perfusion pressure becomes 0 and cerebral blood flow stops, resulting in loss of consciousness and death.

Prognosis

• The prognosis of patients who have suffered a SAH depends upon several factors, which include age, Hunt and Hess grade, smoking history, and location of the aneurysm.
• • Age: Younger patients do better.
  • Hunt and Hess grade
    • Grade 0 - Unruptured aneurysm
    • Grade 1 - Asymptomatic or mild headache and slight nuchal rigidity
    • Grade 1a - Fixed neurological deficit without acute meningeal/brain reaction
    • Grade 2 - Cranial nerve palsy, moderate to severe headache, nuchal rigidity
    • Grade 3 - Mild focal deficit, lethargy, or confusion
    • Grade 4 - Stupor, moderate to severe hemiparesis, early decerebrate rigidity
    • Grade 5 - Deep coma, decerebrate rigidity, moribund appearance
    • The lower the grade, the better the prognosis. Grades 1-3 generally are associated with favorable outcome; these patients are candidates for early surgery. Grades 4 and 5 carry poor prognosis; these patients need stabilization and improvement to grade 3 before surgery is undertaken. Some recommend more aggressive management for patients with poor clinical grade.
  • Smoking: Patients with a history of cigarette smoking have a poorer prognosis.
  • Location of aneurysm: Anterior circulation aneurysms carry a more favorable prognosis.

Patient Education

• For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article, Aneurysm, Brain.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• The usual medicolegal risks of delayed diagnosis, misdiagnosis, surgical risk and complications, and medication complications are pertinent in SAH.
• Missing SAH obviously carries major medical-legal consequences. In the emergency department, clinicians should err on the side of "overtapping" patients. A good history of the current headache is essential, even in known migraineurs, and if anything unusual presents (eg, worst ever headache, episode of loss of consciousness, first ever episode of diplopia), obtain a CT scan of the head and LP even if the CT scan is negative for blood. Do not forget to measure opening pressure and adequately check for xanthochromia.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.
	View Full Size Image
Media type:  CT

Media file 2:  CT scan reveals subarachnoid hemorrhage in the sylvian fissure, right more than left.
	View Full Size Image
Media type:  CT

Media file 3:  A 47-year-old woman presented with headache and vomiting; her CT scan in the emergency department revealed subarachnoid hemorrhage.
	View Full Size Image
Media type:  CT

Media file 4:  Cerebral angiogram reveals a middle cerebral artery aneurysm.
	View Full Size Image
Media type:  X-RAY

Media file 5:  Cerebral angiogram reveals a middle cerebral artery aneurysm.
	View Full Size Image
Media type:  X-RAY

Media file 6:  Cerebral angiogram (lateral view) reveals a large aneurysm arising from the left anterior choroidal artery.
	View Full Size Image
Media type:  X-RAY

Media file 7:  Cerebral angiogram (anteroposterior view) reveals a large aneurysm arising from the left anterior choroidal artery.
	View Full Size Image
Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Caplan LR. Subarachnoid hemorrhage. In: Stroke: A Clinical Approach. Boston, Butterworth-Heinemann; 1993:. 389-423.
• Greenberg MS. SAH and aneurysms. In: Handbook of Neurosurgery. New York: Thieme Medical Publishers; 1999:. 711-52.
• Jayaraman MV, Mayo-Smith WW, Tung GA, et al. Detection of intracranial aneurysms: multi-detector row CT angiography compared with DSA. Radiology. Feb 2004;230(2):510-8. [Medline].
• Langer DJ, Zager EL, Flamm ES. Parasurgical management of aneurysmal subarachnoid hemorrhage. Neurologic and Neurosurgical Emergencies.
• Le Roux PD, Winn HR. Management of the ruptured aneurysm. Neurosurg Clin N Am. Jul 1998;9(3):525-40. [Medline].
• Liebenberg WA, Worth R, Firth GB, et al. Aneurysmal subarachnoid haemorrhage: guidance in making the correct diagnosis. Postgrad Med J. Jul 2005;81(957):470-3. [Medline].
• Lin CL, Dumont AS, Lieu AS, et al. Characterization of perioperative seizures and epilepsy following aneurysmal subarachnoid hemorrhage. J Neurosurg. Dec 2003;99(6):978-85. [Medline].
• Marden FA, Roy SS. Endovascular management of intracerebral and subarachnoid hemorrhage. Curr Treat Options Cardiovasc Med. Jul 2005;7(3):197-209. [Medline].
• Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet. Oct 26 2002;360(9342):1267-74. [Medline].
• Morris PG, Wilson JT, Dunn L. Anxiety and depression after spontaneous subarachnoid hemorrhage. Neurosurgery. Jan 2004;54(1):47-52; discussion 52-4. [Medline].
• Ratcheson RA, Wirth FP. Ruptured cerebral aneurysms: perioperative management. In: Concepts in Neurosurgery. Baltimore: Williams & Wilkins; 1994.
• Schievink WI. Intracranial aneurysms. N Engl J Med. Jan 2 1997;336(1):28-40. [Medline].

Article Last Updated: Jan 11, 2007