• Internationally: The real incidence of intracranial aneurysms is unknown, since most aneurysms remain unknown until they rupture or produce neurological deficits. Autopsy studies estimate that approximately 5% of the adult population harbors cerebral aneurysms. However, over 50% of aneurysms identified at postmortem examinations were asymptomatic and unrecognized until then. More is known about the incidence of ruptured aneurysms. In Western countries, the average incidence of SAH is approximately 10/10,000/y.

Mortality/Morbidity: Ruptured intracranial aneurysms are associated with high morbidity and mortality. Approximately 10-20% of the patients die before reaching the hospital; approximately 8% die from progressive deterioration from the initial hemorrhage. In untreated patients with SAH, the risk of rebleed is 4.1% on the first day, and then 1.5% per day for 2 weeks. By 6 months, 50% of patients with SAH rebleed at least once. After 6 months, the risk of rebleeding stabilizes at approximately 3% per year. Without treatment, approximately 18% of patients who suffer SAH are functional survivors at 10 years, 8% are disabled, and 74% die. Following surgical or endovascular treatment, one third of patients with SAH achieve good, functional neurologic outcomes.

Complications that follow SAH can be divided into medical and neurological subsets. Although the largest proportion of major morbidity and mortality of SAH is attributed to neurological complications (aneurysmal rebleeding, vasospasm), medical complications contribute significantly to the morbidity in these patients and are responsible for 23% of deaths.

• Electrolyte abnormalities: Fluid and electrolyte abnormalities are relatively common in patients with SAH. The most common abnormality probably is hyponatremia, which is present in 35% of patients with SAH. In most patients, natriuresis results from abnormal secretion of the atrial natriuretic factor that produces urinary loss of sodium (cerebral salt wasting). Clinically, hyponatremia may exacerbate alterations in level of consciousness and cause seizures and cerebral edema. It is important to distinguish the syndrome of inappropriate atrial natriuretic factor from the syndrome of inappropriate antidiuretic hormone secretion. In the former, patients are sodium depleted and hypovolemic, while patients with inappropriate antidiuretic hormone secretion are normovolemic or hypervolemic. Fluid restriction in a patient with incipient hyponatremia and hypovolemia secondary to natriuresis may be detrimental, particularly in those with cerebral vasospasm.

• Cardiac complications: Arrhythmias and waveform abnormalities on electrocardiography (ECG) are common immediately after the hemorrhage and are likely to contribute both to the initial loss of consciousness and to the sudden death that can occur after SAH. Arrhythmias have been recorded in 91% of patients after onset of SAH. Although these arrhythmias usually are benign, ventricular tachycardia and ventricular fibrillation can be life threatening. Serious arrhythmias are more likely to occur in patients with advanced age, hypokalemia, and prolonged QT interval. Therefore, continuous ECG monitoring is recommended in all patients with SAH.

• Pulmonary complications: The immediate period following SAH may be complicated by severe hypoxia resulting from aspiration pneumonia or, less frequently, from neurogenic pulmonary edema.

• Neurologic complications: The most common neurological complications in SAH patients are rebleeding, vasospasm, and hydrocephalus.
  • Rebleeding: Aneurysmal rebleeding is the most serious and disabling event following SAH. Maximum frequency (4%) of rebleeding occurs in the first day following the event, then decreases to 1.5% per day for the following 13 days. Therefore, approximately 15-20% will rebleed by 2 weeks and 50% by 6 months post-SAH. Mortality rates from rebleeding range from 70-90%. Early surgical or endovascular treatment of the aneurysm eliminates rebleeding potential.

  • Vasospasm: In the first 14 days after aneurysmal SAH, angiographic vasospasm may occur in approximately 70-90% of patients. The incidence of vasospasm correlates with the amount of blood in the subarachnoid space. Half of these patients develop an ischemic stroke.

  • Hydrocephalus: The frequency of acute hydrocephalus during the first 3 days after aneurysmal SAH has been estimated at approximately 20%. However, the reported incidence of acute hydrocephalus following subarachnoid hemorrhage is widely variable. Reports from the literature range from as low as 12% to 63%. In a series of 3,521 patients admitted within 3 days of the hemorrhage, an admission CT showed hydrocephalus in 15% while another series showed an incidence of acute hydrocephalus of 20%. Chronic hydrocephalus develops in 10 to 37% of patients surviving aneurysmal subarachnoid hemorrhage. Some radiologic findings that correlate with the development of hydrocephalus include the presence of intraventricular blood and focal areas of thick layers of subarachnoid blood. A significant number of patients without intraventricular hemorrhage can develop chronic, symptomatic, communicating hydrocephalus.

Race: Differences in the incidence of cerebrovascular disease and intracranial aneurism exist in racial and ethnic groups.

• A low incidence of intracranial arterial aneurysms has been reported from some countries, including India, Iran, and many parts of Africa.

• An analysis of 244 patients performed in Detroit showed a white-to-black ratio of 2.3:1 in intracranial aneurysms; however, when only those patients with SAH bleeding aneurysms were considered, the ratio was 1.6:1.

• In a study by Bruno et al, the incidence of aneurysmal SAH among Hispanic residents of New Mexico was approximately 2.5 times higher than among non-Hispanic whites, which suggests a higher prevalence or a greater tendency to rupture of berry aneurysms among Hispanics.

Sex: Gender influences the prevalence of aneurysms at certain anatomic locations. In females, the most common location of aneurysms is the supraclinoid segment of the internal carotid artery. In males, the most common site of ruptured aneurysms is the anterior communicating complex, while the most common reported site of unruptured aneurysms is the supraclinoid carotid. Females are more prone than males to developing aneurysms of the ophthalmic, cavernous, and posterior communicating segments of the internal carotid artery.

Age: Intracranial aneurysms are diagnosed more frequently during midlife. Fox documented a peak incidence of symptomatic aneurysms in the fourth decade, while two cooperative studies showed an age peak in the fifth decade. Intracranial aneurysms are rare in children and are more likely to be associated with vascular anomalies, trauma, infection, or systemic disease. Symptomatic aneurysms in children have a peculiar predilection for the carotid bifurcation.

Anatomy: The internal carotid artery enters the petrous portion of the temporal bone at the base of the skull through the carotid canal. Within the petrous bone, the carotid artery runs vertically and then turns horizontally at its genu to travel in an anteromedial direction, forming the carotid siphon. As the carotid artery passes above the foramen lacerum and under the Gasserian ganglion, it penetrates the lateral dural ring and turns medially, forming the lateral carotid loop, to enter the cavernous sinus. In the cavernous sinus (cavernous segment), the carotid artery proceeds in a superomedial direction toward the posterior clinoid process. At the level of the posterior clinoid, the carotid artery makes a forward turn, forming the medial loop. The meningohypophyseal trunk originates at this level. The carotid then exits the cavernous sinus and enters the subarachnoid space.

The ophthalmic segment of the internal carotid artery extends from the distal dural ring to the origin of the posterior communicating artery. This is the longest subarachnoid segment of the internal carotid artery, and it possesses two major bends that create areas of hemodynamic stress that predispose to aneurysm formation. The first bend, best seen on lateral angiographic views, occurs as the carotid artery ascends and bends sharply posteriorly after penetrating the dura. The second bend, best appreciated on a dorsal (or anterior-posterior) angiographic view, is a gentler, medial-to-lateral curve as the artery runs medial to the anterior clinoid process and arcs laterally to ascend toward the bifurcation.

The ophthalmic segment has two major branches. The ophthalmic artery usually arises immediately beneath the optic nerve. The superior hypophyseal artery arises from the medial or ventromedial surface of the carotid, below the anterior clinoid process. Ophthalmic aneurysms typically arise along the first bend of the internal carotid artery, distal to the origin of the ophthalmic artery, and project either dorsally or dorsomedially toward the optic nerve. Superior hypophyseal artery aneurysms usually arise from the inferomedial surface of the internal carotid artery and project superomedially. The posterior communicating artery originates from the posteromedial surface of the internal carotid artery and penetrates the membrane of Liliequist to join the posterior cerebral artery inside the interpeduncular cistern. Several perforators originate from the carotid or posterior communicating artery (anterior thalamoperforating arteries). Posterior communicating aneurysms project posteriorly and slightly inferiorly.

The choroidal segment of the internal carotid artery begins at the origin of the anterior choroidal artery and ends at the carotid bifurcation. The anterior choroidal artery arises distal and lateral to the posterior communicating artery. The internal carotid artery then bifurcates into the anterior and middle cerebral arteries.

The middle cerebral artery begins at the bifurcation of the internal carotid artery and runs along the sylvian fissure. It can be divided into the following 4 segments: An M1 segment located between the carotid bifurcation and the genu, an M2 segment that runs over the insular surface, an M3 segment that traverses the opercular surface of the sylvian fissure to reach the cortical surface, and a distal M4 segment consisting of its cortical branches.

The vertebral artery enters the subarachnoid space at the cranio-occipital junction. The first branch is the posterior spinal artery, which descends into the spinal cord. The vertebral artery then courses medially and superiorly around the medulla. The most important branch is the posterior inferior cerebellar artery, which travels in a posterior and lateral direction, just inferior to the olive.

The basilar artery begins at the vertebrobasilar junction and courses superiorly toward the interpeduncular fossa. The first major branch of the basilar artery is the anterior inferior cerebellar artery, which courses laterally and posteriorly, to supply the inferior surface of the cerebellum. The superior cerebellar artery originates just proximal to the basilar bifurcation and courses laterally to supply the superior cerebellar hemisphere. The basilar artery terminates in the interpeduncular fossa where it bifurcates into the posterior cerebral arteries.

The posterior cerebral artery consists of three segments as follows: The P1 segment, which extends from its origin at the basilar bifurcation to its junction with the posterior communicating artery and contains several posterior thalamoperforating arteries; the P2 segment, which courses through the crural and ambient cisterns, giving origin to the anterior temporal, hippocampal, medial posterior choroidal, and peduncular perforating arteries, middle and posterior temporal arteries, and lateral posterior choroidal arteries; and the P3 segment, which courses through the quadrigeminal cistern toward the calcarine fissure, where it divides into calcarine and parieto-occipital arteries.

Clinical Details: In a review of the literature, 89% of saccular intracranial aneurysms presented with SAH, 7% presented with mass effect, and 4% were incidental findings.
Warning signs, such as a sentinel leak or aneurysmal expansion, frequently precede aneurysm rupture.
The classic description of SAH resulting from a ruptured intracranial aneurysm is a sudden and explosive "worst headache of one's life." Patients experience different degrees of mental status change. A massive release of catecholamines accompanies SAH and, frequently, induces myocardial changes that can cause lethal arrhythmias, pulmonary edema, or heart failure.

Clinical findings in survivors of aneurysm rupture vary, depending on the origin, location, and severity of the hemorrhage. Bleeding confined to the subarachnoid space usually produces nonfocal symptoms and signs of increased intracranial pressure and meningeal irritation, including headache, confusion, photophobia, nausea, vomiting, blurred vision, nuchal rigidity, and cranial nerve palsies. Nuchal rigidity often arises within 6-24 hours. On examination, patients may show a positive Kerning sign (pain in the hamstrings when straightening legs) and Brudzinski sign (involuntary hip flexion on neck flexion).

Focal neurologic deficits often are indicative of a related ischemic infarct or mass effect from an intracranial hematoma. The type of deficit depends on the location and the size of the clot, which may cause cranial neuropathies, visual field cuts, or speech deficits. Although several clinical grading scales to assess SAH have been proposed, the Hunt and Hess classification is used most widely.

Table 1: Hunt and Hess Clinical Classification of Subarachnoid Hemorrhage

This clinical grading system correlates with treatment and patient outcome. It is generally accepted that a higher Hunt and Hess grade correlates with a higher incidence of vasospasm and poor outcome. However, although there are some statistics in the literature, establishing accurate percentages in relationship to the Hunt and Hess or Fisher grading is difficult. Intensive medical treatment of patients with aneurysmal subarachnoid hemorrhage has led to the improvement of perioperative management and subsequent significant improvement of the outcome of these patients. Traditionally, the outlook for patients presenting with a subarachnoid hemorrhage grades IV and V has been dismal, whereas numerous series of aneurysm patients with Hunt and Hess grades I to III have reported good neurologic recovery in 60-90%. In addition, the presenting Hunt and Hess grading, surgical morbidity also has been associated with aneurysm size, location, and patient's age. Regarding aneurysms' size, a study of a morbidity of
2.3% for aneurysms smaller than 5 mm, and 6.8% for aneurysms between 5 mm and 15 mm, and 14% for aneurysms between 16 mm and 25 mm. Morbidity also varied with aneurysm location, with a 4.8% morbidity for posterior communicating aneurysms, 8.1% for middle cerebral artery aneurysms, 11.8% for ophthalmic aneurysms, 15.5% for anterior communicating aneurysms, and 16.8% for carotid bifurcation aneurysms. Morbidity has been reported to be 6.5% for patients younger than 45 years, 14% for age 45-64, and 32% for patients older than 64.

Preferred Examination: A strong, clinical suspicion of aneurysm can be validated by several diagnostic studies, including computed tomography (CT), lumbar puncture, magnetic resonance imaging (MRI), and cerebral angiography. CT typically is the first diagnostic test ordered when the possibility of SAH exists. An unenhanced scan can confirm subarachnoid blood in more than 90% of acute patients. Diffuse severe SAH is seldom helpful in suggesting the specific site of the aneurysm. However, localized SAH can be highly indicative of the site of aneurysm rupture, as in the case of blood in the sylvian fissure caused by rupture of a middle cerebral artery (MCA) trifurcation aneurysm, or of blood interhemispherically between the frontal lobes anteriorly due to the rupture of an aneurysm of the anterior communicating artery (Acomm).

Limitations of Techniques: In patients with diffuse SAH, CT scan may not indicate the site of aneurysm rupture.

In severely anemic patients with a small hemorrhage, CT scan can be falsely negative, although rarely.