Introduction
The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20% of all strokes.
SAH is a devastating condition with high morbidity and mortality, and, in the United States, it is associated with an annual cost of $1.75 billion. SAH occurs in various clinical contexts, the most common being head trauma. However, the familiar medical use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM). The scope of this chapter is confined to nontraumatic SAH.
CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.
History of the Procedure
Ancient Greek, Egyptian, and Arabic literature all have references to intracranial aneurysms. The first successful treatment of an intracranial aneurysm was reported in the early 19th century; however, such outcomes did not become routine until the Dandy era and the advent of modern neurosurgical techniques.
Dandy performed the first successful clipping of an aneurysm in 1937, using a vascular clip designed by Harvey Cushing. In the following years, advancements in microneurosurgical techniques, including the operating microscope, microsurgical instruments, better anesthesia, and improved management of subarachnoid hemorrhage (SAH) complications, have led to significant improvements in surgical outcomes.
Endovascular therapy for the treatment of intracranial aneurysms was pioneered in the mid 1970s by Serbinenko at the Moscow Institute of Neurosurgery. This initial approach, which attempted to achieve parent vessel occlusion using latex balloons, was moderately successful in a limited subset of cases. However, it never gained widespread applicability.
Other balloon devices, including detachable silicon and latex balloons, subsequently were developed in the United States, Europe, and Japan. The success of balloon embolization has been tempered by the associated complications of deflation and aneurysmal rupture.
Arguably, the most significant recent development in endovascular therapy occurred in 1990, when Guglielmi and colleagues at the University of California Los Angeles (UCLA) Medical Center developed the Guglielmi detachable coil system (GDC).
The GDC is a radiopaque platinum coil that is delivered through a microcatheter into an aneurysm, which then is detached by electrolysis. GDCs gained approval by the Food and Drug Administration (FDA) in 1995 for treatment of aneurysms that have the potential for high surgical morbidity and mortality. In Europe, GDCs have been used as a first-line intervention in lieu of surgical treatment for patients without contraindications to endovascular therapy. In the last 5 years, endovascular coiling has become first-line treatment for aneurysms at several centers in the United States and is continuing to gain popularity in those patients appropriate for the procedure.
Other endovascular techniques under investigation include liquid embolic agents, intravascular laser treatments, and intravascular stents. As endovascular occlusive techniques evolve, it seems likely that they will play a larger role in the management of SAH.
Problem
Nontraumatic subarachnoid hemorrhage (SAH) usually is the result of a ruptured cerebral aneurysm or AVM. Blood extravasation into the subarachnoid space has a detrimental effect on both local and global brain function and leads to high morbidity and mortality rates.
Although mortality rates of SAH have decreased since 1979, it remains a devastating neurological problem. An estimated 15% of patients die before reaching the hospital. Approximately 25% of patients die within 24 hours, with or without medical attention. The mortality rate at the end of 1 week approaches 40%. Half of all patients die in the first 6 months.
Age-adjusted mortality rates are 62% greater in females than in males and 57% greater in blacks than in whites. While advances in the management of SAH have led to an overall decrease in mortality rates, approximately 40% of all survivors have major neurologic deficits. Morbidity and mortality increase with age and are related to the overall health status of the patient.
Frequency
Subarachnoid hemorrhage (SAH) is a major clinical problem worldwide.
The annual incidence of aneurysmal SAH in the United States is 6-16 cases per 100,000 population, with approximately 30,000 episodes occurring each year. Unlike other subcategories of stroke, the incidence of SAH has not decreased over time. However, since 1970, population-based survival rates have improved. The incidence of SAH worldwide varies widely (2-49 cases per 100,000 population), with the highest rates occurring in Japan and Finland.
Age: Incidence increases with age and peaks at age 50 years. Approximately 80% of cases of SAH occur in people aged 40-65 years, with 15% occurring in people aged 20-40 years. Only 5% of cases of SAH occur in people younger than 20 years. The prevalence of SAH is rare in children younger than 10 years; SAH in children younger than 10 years accounts for only 0.5% of all cases.
Sex: Incidence of SAH in women is higher than in men (3:2). The risk of SAH is significantly higher in the third trimester of pregnancy, and SAH from aneurysmal rupture is a leading cause of maternal mortality, accounting for 6-25% of maternal deaths during pregnancy. A higher incidence of AVM rupture also has been reported during pregnancy.
Race: The risk is higher in blacks than in whites; however, people of all ethnic groups develop intracranial aneurysms. The disparity in frequency of rupture has been attributed to population variance with respect to prevalence of risk factors and age distribution.
Etiology
Nontraumatic cases of subarachnoid hemorrhage (SAH) usually are caused by extravasation of blood from abnormal blood vessels onto the surface of the brain. Usually, this is the result of aneurysmal or AVM leakage or rupture. Rupture of "berry," or saccular, aneurysms of the basal vessels of the brain comprises 77% of nontraumatic SAH cases.
The etiology of cerebral aneurysms is unknown, but both congenital and acquired factors are thought to play a role. Evidence supporting the role of congenital causes in aneurysm formation includes the following:
- Clusters of familial occurrence, such as in Finland where the incidence of familial cerebral aneurysm is 10%
- Significant incidence of multiple aneurysms in patients with SAH (15%)
- Aneurysms have been associated with specific congenital diseases (eg, coarctation of the aorta, Marfan syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, polycystic kidney disease).
Congenital defects in the muscle and elastic tissue of the arterial media in the vessels of the circle of Willis are found in approximately 80% of normal vessels at autopsy. These defects lead to microaneurysmal dilatation in 20% of the population (<2 mm) and larger dilation (>5 mm) and aneurysms in 5% of the population.
Acquired factors thought to be associated with aneurysmal formation include the following:
- Atherosclerosis
- Hypertension
- Hemodynamic stress
AVMs are the second most identifiable cause of SAH, accounting for 10% of cases of SAH. Familial cases of AVM are rare, and the problem may result from sporadic abnormalities in embryologic development. AVMs are thought to occur in approximately 4-5% of the general population, of which 10-15% are symptomatic.
Less common causes of SAH include the following:
- Fusiform and mycotic aneurysms
- Fibromuscular dysplasia
- Blood dyscrasias
- Moyamoya disease
- Infection
- Neoplasm
- Trauma (fracture at the base of the skull leading to internal carotid aneurysm)
- Amyloid angiopathy (especially in elderly people)
- Vasculitis
- Idiopathic SAH
Risk factors
Although risk factors for SAH have been evaluated extensively, little conclusive evidence has been derived. Smoking appears to be a significant risk factor, as does heavy alcohol consumption. Data regarding the relationship between hypertension and SAH are conflicting. The following do not appear to be significant risk factors for SAH:
- Use of oral contraceptives
- Hormone replacement therapy
- Hypercholesterolemia
- Vigorous physical activity
The risk of AVM rupture is greater during pregnancy.
Pathophysiology
Aneurysms usually occur at the branching sites on the large cerebral arteries of the circle of Willis. The early precursors of aneurysms are small outpouchings through defects in the media of the arteries. These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations. A mature aneurysm has a paucity of media, replaced by connective tissue, and has diminished or absent elastic lamina.
The probability of rupture is related to the tension on the aneurysm wall. The law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm. Thus, the rate of rupture is directly related to the size of the aneurysm. Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosis.
Although hypertension has been identified as a risk factor for aneurysm formation, the data with respect to rupture are conflicting. However, certain hypertensive states, such as those induced by use of cocaine and other stimulants, clearly promote aneurysm growth and rupture earlier than would be predicted by the available data.
Brain injury from cerebral aneurysm formation can occur in the absence of rupture via compressive forces that cause injury to local tissues and/or compromise of distal blood supply (mass effect).
When an aneurysm ruptures, blood extravasates under arterial pressure into the subarachnoid space and quickly spreads through the cerebrospinal fluid (CSF) around the brain and spinal cord. Blood released under high pressure may directly cause damage to local tissues. Blood extravasation causes a global increase in intracranial pressure (ICP). Meningeal irritation occurs.
Rupture of AVMs can result in both intracerebral hemorrhage and SAH. Currently, no explanation can be provided for the observation that small AVMs (<2.5 cm) rupture more frequently than large AVMs (>5 cm).
Presentation
The signs and symptoms of subarachnoid hemorrhage (SAH) range from subtle prodromal events, which often are misdiagnosed, to the classic presentation of catastrophic headache. The history and physical examination, especially the neurologic examination, are essential components in the diagnosis and clinical staging of SAH.
Prodromal signs and symptoms usually are the result of one or more of the following: sentinel leaks, mass effect of aneurysm expansion, or emboli.
- Sentinel, or "warning," leaks that produce minor blood leakage are reported to occur in 30-50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or generalized head pain that may be severe. Sentinel headaches precede aneurysm rupture by a few hours to a few months, with a reported mean of 2 weeks prior to discovery of the SAH. In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. These symptoms may be ignored by the physician. Therefore, a high index of suspicion is necessary for accurate diagnosis. Sentinel leaks usually do not generate symptomatology suggestive of elevated ICP. Sentinel leaks usually do not occur in the setting of AVM.
- Mass effect: Prodromal presentations occasionally are caused by the mass effect of an expanding aneurysm and have characteristic features based upon aneurysm location.
- Posterior communicating artery/internal carotid artery - Focal, progressive retro-orbital headaches and oculomotor nerve palsy
- Middle cerebral artery - Contralateral face or hand paresis, aphasia (left side), contralateral visual neglect (right side)
- Anterior communicating artery - Bilateral leg paresis and bilateral Babinski sign
- Basilar artery apex - Vertical gaze, paresis, and coma
- Intracranial vertebral artery/posterior inferior cerebellar artery - Vertigo, components of lateral medullary syndrome
- Emboli: Transient ischemic attacks can occur from emboli originating from intra-aneurysmal thrombus formation. The classic symptoms and signs of aneurysmal rupture into the subarachnoid space comprise one of the most pathognomonic presentations in all of clinical medicine. Symptomatology is as follows:
- A sudden onset of severe headache, often described as the "worst headache of my life" (Absence of headache in the setting of a ruptured intracranial aneurysm is rare, and probably represents amnesia for the event.)
- Nausea and/or vomiting
- Symptoms of meningeal irritation, including nuchal rigidity and pain, back pain, and bilateral leg pain, occur in as many as 80% of patients with SAH (but may take several hours to manifest).
- Photophobia and visual changes are common.
- A sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as ICP exceeds cerebral perfusion pressure.
- LOC often is transient; however, approximately 10% of patients are comatose for several days, depending on the location of the aneurysm and the amount of bleeding.
- Seizures during the acute phase of SAH occur in 10-25% of patients.
- No correlation exists between seizure focus and the anatomical site of aneurysm rupture.
- Less severe hemorrhages may present with headache of moderate intensity, neck pain, and nonspecific symptoms.
- Findings on physical examination of the patient with SAH may be normal or consistent with one or more of the following:
- Focal neurologic abnormalities, including hemiparesis, aphasia, hemineglect, cranial nerve palsies, and memory loss, are present in 25% of patients.
- Motor neurologic deficits occur in 10-15% of patients, usually from middle cerebral artery aneurysms.
- Ophthalmologic examination may reveal subhyaloid retinal hemorrhages (20-30%) and papilledema.
- Blood pressure elevation is observed in about 50% of patients. Blood pressure often becomes labile as ICP increases.
- Temperature elevation, secondary to chemical meningitis from subarachnoid blood products, is common after the fourth day following bleeding.
- Tachycardia often is present for several days after SAH.
Clinical grading scales
Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical scales most often employed are the Hunt and Hess and the World Federation of Neurological Surgeons (WFNS) grading systems. A third, the Fischer scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood.
- Hunt and Hess grading system
- Grade 1 - Asymptomatic or mild headache
- Grade 2 - Moderate-to-severe headache, nuchal rigidity, and no neurological deficit other than possible cranial nerve palsy
- Grade 3 - Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit
- Grade 4 - Stupor and/or hemiparesis
- Grade 5 - Comatose and/or decerebrate rigidity
- WFNS scale
- Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent
- Grade 2 - GCS of 13-14, motor deficit absent
- Grade 3 - GCS of 13-14, motor deficit present
- Grade 4 - GCS of 7-12, motor deficit absent or present
- Grade 5 - GCS of 3-6, motor deficit absent or present
- Fischer scale (CT scan appearance)
- Group 1 - No blood detected
- Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm
- Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness
- Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present
The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The Fischer classification has been used successfully to predict the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH. All 3 grading systems are useful in determining the indications for and timing of surgical management. For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm.
Indications
The indications for surgery in patients with SAH can be stratified based on clinical grade. Other factors, such as overall medical condition of the patient, aneurysm size and location, accessibility of the aneurysm for surgical repair, and presence or absence of thrombus, also are important.
For patients with a mild- or intermediate-grade SAH (Hunt and Hess/WFNS grades 1-3), surgical treatment is strongly recommended because the risks of SAH complications greatly exceed the risk of surgical complications.
For patients with a poor grade of SAH (Hunt and Hess/WFNS grades 4-5), the decision whether to operate is controversial and largely institution-dependent. The overall outcome is poor, with or without surgical intervention.
Patients with a higher grade of SAH or poor medical status that do not qualify for early surgery may be candidates for delayed surgery or endovascular obliteration of the aneurysm.
Other indications for surgical management have been described recently and include the following:
- Large and giant aneurysm
- Wide-necked aneurysms
- Vessels emanating from the aneurysm dome
- Mass effect or hematoma associated with the aneurysm
- Recurrent aneurysm after coil embolization
Indications for endovascular treatment
Endovascular therapy (eg, coil embolization) has been used increasingly in recent years in lieu of surgical clipping, with promising results. More definitive data are required comparing the traditional treatment modality (aneurysmal clipping) with newer endovascular techniques before conclusive recommendations can be made.
An attempt to answer this question was recently published in Lancet by Molyneux et al.1 In a randomized multicenter trial mainly in Europe and the United Kingdom, 2143 patients were randomized to either neurosurgical clipping or endovascular coiling. It was found that independent survival was improved in the endovascular coiling group. The risk of late rebleeding, although low in both groups was higher in the endovascular coiling group. Even with the results of this study, controversy still exists over which treatment is superior. In general, endovascular treatment of aneurysms is favored over surgery in the following situations:
- Patients with poor clinical grade
- Patients who are medically unstable
- In situations where aneurysm location imparts an increased surgical risk, such as cavernous sinus and many basilar tip aneurysms
- Small-neck aneurysms in the posterior fossa
- Patients with early vasospasm
- Cases where the aneurysm lacks a defined surgical neck (although these are also difficult to "coil")
- Patients with multiple aneurysms in different arterial territories if surgical risk is high
Surgery remains the standard reference for therapy and is favored over endovascular treatment when surgical risk is low or equal to that of endovascular therapy. However, many patients may be treated adequately with either method, and the ultimate choice of intervention often is guided by physician and institution preference.
A combined approach may benefit a particular subset of patients, eg, those with a poor clinical grade and an aneurysm that cannot be occluded completely by endovascular therapy.
Surgical indications for unruptured symptomatic aneurysms
Surgery usually is indicated in patients with unruptured symptomatic aneurysms because the rate of subsequent rupture is high. Most symptomatic aneurysms are giant (large) aneurysms rather than saccular aneurysms. Patients with giant aneurysms face an increased surgical risk; however, this risk usually is much less than the morbidity and mortality associated with aneurysm rupture.
Surgical indications for asymptomatic aneurysms
The risk of aneurysmal rupture increases relative to the size of the aneurysm; however, the critical size with respect to increased risk of rupture is unknown.
Unruptured aneurysms are reported to rupture at a rate of 1-1.4% per year. Most authors propose that surgical risks are eclipsed by the risks of mass effect and aneurysm rupture in patients younger than 65 years who have aneurysms larger than 1 cm in size. The impact of the size of the aneurysm is controversial.
Relevant Anatomy
Circle of Willis
Most saccular aneurysms occur at bifurcations of the vessels that comprise the circle of Willis. The circle of Willis is in close proximity to the ventral surface of the diencephalon and is adjacent to the optic nerves and tracts. It extends from the superior border of the pons to the longitudinal fissure between the cerebral hemispheres. The circle of Willis is an important anastomosis for the 4 arteries that supply the brain—the 2 vertebral and the 2 internal carotid arteries. It can be divided into anterior and posterior sections.
Anterior portion of the circle of Willis
The anterior section of the circle of Willis consists of the internal carotid arteries, the anterior cerebral artery, and the anterior communicating artery.
- The right internal carotid artery, along with the right external carotid artery, branches from the common carotid artery most often at C3 or C4, with a range of C1-T2.
- The right common carotid artery originates from the brachiocephalic trunk, the first branch of the aorta.
- The left common carotid artery, the second branch of the aorta, branches into the right internal and right external carotid arteries at about the same level as the right common carotid bifurcation.
- The cerebral portions of the internal carotid arteries branch into the anterior and middle cerebral arteries at the medial end of the lateral sulcus.
- The anterior communicating artery is a short segment that connects the 2 anterior cerebral arteries and forms the anterior border of the circle.
Posterior portion of the circle of Willis
The posterior segment of the circle of Willis consists of the proximal portions of the posterior cerebral arteries and the paired posterior communicating arteries.
- The 2 posterior cerebral arteries arise from the terminal bifurcation of the basilar artery.
- The basilar artery is formed by the union of the 2 vertebral arteries, each of which begins as a branch of the first part of the subclavian artery.
- The posterior communicating arteries connect the internal carotid and the posterior cerebral arteries and form the posterior-lateral borders of the circle of Willis.
Location of aneurysm rupture
Approximately 85% of saccular aneurysms occur in the anterior circulation. The most common sites of rupture are as follows:
- The internal carotid artery, including the posterior communicating junction (41%)
- The anterior communicating artery/anterior cerebral artery (34%)
- The middle cerebral artery (20%)
- The vertebral-basilar arteries (4%)
- Other arteries (1%)
Contraindications
No strict contraindications to surgery for aneurysmal SAH exist other than unstable medical status or a lesion not amenable to surgical therapy. Patient stratification with respect to endovascular therapy versus surgery is discussed in Treatment.
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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
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
