Saccular, or berry, aneurysms must be distinguished from other types of intracerebral aneurysms such as traumatic, dissecting, mycotic, and tumor-related aneurysms. Saccular aneurysms lack the normal muscular media and elastic lamina layers [7]. Eighty-five percent of saccular aneurysms are located in the anterior circulation; 15% are in the posterior circulation [8]. Common sites for aneurysms are at the junction of the anterior cerebral and anterior communicating arteries, the origin of the posterior communicating artery, the middle cerebral artery trifurcation, and at the top of the basilar artery. Less common are those located at the cavernous carotid, the internal carotid bifurcation, the distal anterior cerebral, and the proximal basilar arteries. Twelve percent to 31% of patients have multiple aneurysms. Nine percent to 19% have aneurysms located at identical sites bilaterally (mirror aneurysms), and multiple aneurysms may occur within families [9]. Systemic diseases such as polycystic kidney, Marfan’s syndrome, Ehlers–Danlos syndrome, pseudoxanthoma elasticum, fibromuscular dysplasia, and coarctation of the aorta are associated with an increased incidence of intracerebral aneurysms [10,11].

It is unclear at present whether aneurysms have a congenital/hereditary origin or result from subsequent degenerative mechanisms. Supporting a congenital theory for aneurysm occurrence, individuals with a single primary relative with an intracranial aneurysm are at a 1.8 fold increased risk of intracranial aneurysm; those with two primary relatives have a 4.2 fold increased risk. Supporting the degenerative theory, there is an increased incidence of intracranial aneurysms in patients with hypertension, cigarette abuse, and alcohol abuse, and in the majority of cases, a family history of aneurysms is absent [11,12,13,14].

The signs and symptoms of intracranial aneurysms result from their expansion or rupture. Aneurysmal expansion can lead to localized headache, facial pain, pupillary dilatation and ptosis from oculomotor nerve compression, and visual field defects from optic nerve or chiasm compression. Warning leak or “sentinel” hemorrhage occurs in approximately 20% of patients and is characterized by nuchal rigidity or meningismus that usually lasts at least 48 hours. The event is misdiagnosed in 20% to 40% as muscular-tension headache, migraine, sinusitis, viral syndrome, aseptic meningitis, or malingering [17]. Evidence of aneurysmal expansion or warning leak must be regarded with a high index of suspicion because such events precede major hemorrhage. Neurologic and functional outcomes are greatly improved if the patient is treated while neurologically intact before hemorrhage [18].

Aneurysmal rupture typically produces severe headache which is maximal at onset and is associated with neck pain, nausea, vomiting, photophobia, and lethargy. At the time of rupture, patients may lose consciousness and may demonstrate abducens nerve palsy, subhyaloid hemorrhages, or papilledema, reflecting the acute rise in intracranial pressure (ICP) that may transiently equal mean arterial pressure [19]. Other focal symptoms may also develop. Early seizures after SAH (8% to 11%) reflect a rise in ICP and are not indicative of the site or severity of rupture [20,21].

The clinical grading scale developed by Hunt and Hess [22] is useful in estimating the patient’s prognosis (Table 178.1). Grades I and II at presentation have a relatively good prognosis, whereas grades IV and V have a poor prognosis, and grade III an intermediate prognosis. The Glasgow Coma Scale is also useful in predicting outcome after early surgical intervention [23].

If SAH is suspected, an urgent noncontrast head CT should be obtained to identify, localize, and quantify the hemorrhage. CT imaging is 98% to 100% sensitive in the first 12 hours after SAH, declining to under 85% sensitive 6 days following a hemorrhage [6]. A lumbar puncture is indicated if the CT is nondiagnostic. CT scan may be negative in up to 35% of patients with sentinel leaks [24]. CT angiography (CTA) is the preferred study in the emergent surgical setting, and is often used when the presence of a large parenchymal clot makes delay for conventional arteriography unacceptable. CTA uses a contrast-enhanced high-speed spiral (helical) CT performed with reconstruction of the axially acquired data into angiographic images. CTA can demonstrate aneurysms of 2- to 3-mm size with sensitivities of 77% to 97% and specificities of 87% to 100% [25,26].

Traumatic lumbar puncture and SAH are distinguished by xanthochromia, demonstrated by spectrophotometric analysis of a centrifuged sample of the CSF [27]. Cell counts remain uniform in all tubes of CSF in a true SAH, and blood clots do not form. The CSF protein is usually elevated and glucose may be very slightly reduced. Opening pressure at the time of lumbar puncture may reflect the elevation of ICP.

Four-vessel cerebral angiography is necessary to localize the aneurysm, define the vascular anatomy, and assess vasospasm and the possible presence of multiple aneurysms. It should be performed within 24 hours after initial hemorrhage. If angiography does not reveal an aneurysm, magnetic resonance imaging and angiography can be performed to reveal aneurysms larger than 3 mm. If these studies are also negative, angiography is repeated in 1 to 3 weeks because acutely, intraluminal thrombus and vasospasm can interfere with angiographic visualization of aneurysms [6,28,29].

Complications of SAH are fatal in 25% of cases [15,27]. General preoperative medical management should include provisions for quiet bed rest, head elevation to improve cerebral
venous return, good pulmonary toilet to avoid atelectasis and pneumonia, and prophylaxis against thrombophlebitis with pneumatic boots. Patients should receive stool softeners. Nausea and vomiting can be controlled with antiemetics. Pain control is best accomplished with agents such as morphine or fentanyl. Mean arterial pressures higher than 100 mm Hg should be lowered gently until repair of the aneurysm can be achieved, but agents that can depress consciousness such as α-methyldopa should be avoided. Blood pressure is managed with beta-blocking agents; these agents may also reduce the risks of cardiac arrhythmias.

After SAH there may be a salt-wasting diuresis. Suggested mechanisms include an increase in circulating atrial natriuretic peptide. This syndrome is distinguished from the syndrome of inappropriate antidiuretic hormone by urine output and urine chemistry; both may result in hyponatremia. Accordingly, fluid input and output must be followed closely along with serum electrolytes and osmolality.

Seizures have been reported to occur in up to 18% of patients with SAH at onset, and are less common in hospitalized patients, recently reported at 4% [30]. The need for prophylactic anticonvulsants is controversial, and phenytoin remains the most common anticonvulsant used, though recent studies suggest a worse cognitive outcome with its use [31]. Levetiracetam is sometimes substituted if hepatic enzymes rise or suspected drug fever occurs, but data on its efficacy in this setting is as yet unavailable.

Elevation of ICP must be treated promptly with an agent such as mannitol. The use of dexamethasone for cerebral edema is restricted to patients with postoperative edema due to retractor manipulation, and is used to blunt headache caused by meningeal irritation; it has been reported anecdotally to shorten the course of hydrocephalus after SAH as well.

Cardiac dysrhythmias may complicate care following SAH; a variety of mechanisms have been proposed. Increased levels of circulating catecholamines influence the α-receptors of the myocardium and can result in prolonged myofibril contraction, eventually causing myofibrillar degeneration and necrosis. An alternative theory of myocardial injury suggests that coronary artery spasm is the mechanism for the myocytolysis. SAH is the most frequent neurologic cause for electrocardiographic changes, which include large upright T waves and prolonged QT intervals (on average, approximately 0.53 seconds). In addition, prominent U waves, inverted T waves, and minor elevation or depression of the ST segment can occur. Despite ST-T changes, the incidence of myocardial ischemia remains low [32,33]. Pathologic Q waves are not common in SAH and suggest the need for further investigations for myocardial infarction. Patients with coronary artery vasospasm have a worse prognosis [34]. Arrhythmias are very common: a prospective study of 120 patients performed by using Holter monitoring indicated a 90% incidence of ventricular and supraventricular arrhythmias in the first 48 hours of hospitalization [35]. These do not appear to account for significant mortality.

Aneurysmal rebleeding, hydrocephalus, and cerebral vasospasm with ischemia are the three major neurologic complications after SAH.

Rebleeding is a serious and frequent neurologic complication of SAH, carrying a mortality rate from 50% to 70% [5,6,9]. The peak incidence of rebleeding occurs during the first day after SAH, and a secondary peak occurs 1 week later. The rerupture risk for an untreated ruptured aneurysm is 23% at 2 weeks, 35% to 42% at 4 weeks, and 50% within 6 months [29]. Clinically, patients suffer with increasing headache, nausea, vomiting, depressed level of consciousness, and the appearance of new neurologic deficits. Occasionally, seizures occur, but they have not been shown to be a cause of rebleeding. Attempts to prevent rebleeding by drug-induced hypotension and bed rest have not been successful [36]. Antifibrinolytics decrease the rate of rebleeding, but older studies associate their use with increased incidence of ischemic insults from vasospasm [37,38]. Modern approaches including early aneurysm repair and intravascular therapy for vasospasm may ameliorate these issues, but antifibrinolytics are not strongly recommended [6].

Hydrocephalus can develop acutely within the first few hours after SAH because of impaired CSF resorption at the arachnoid granulations or intraventricular blood causing obstruction of CSF outflow. Clinically significant hydrocephalus developing subacutely over a few days or weeks after SAH is manifested by the loss of vertical gaze and progressive lethargy. Patients may appear to be abulic. Ventricular CSF drainage may be indicated if the clinical neurologic examination deteriorates or for any obtunded patient with hydrocephalus. CSF drainage is limited in patients with unprotected aneurysms because there is a danger of rerupture associated with abrupt decreases in ICP. A delayed form of hydrocephalus manifested by cognitive changes and gait disorders may be observed several weeks after the SAH; in these cases, a ventriculoperitoneal shunt may be indicated [5].

Stroke due to vasospasm is a major cause of morbidity and mortality in the postoperative period. Several controlled studies have shown an important role for the calcium antagonist nimodipine in ameliorating neurologic deficits caused by vasospasm. Beneficial effects are probably related to calcium channel–blocking properties, interfering with steps in the ischemic cascade [39,40,41]. The neurologic outcome and mortality rates of SAH patients prophylactically treated with nimodipine are improved 25% to 50% over control subjects. Fewer infarcts are noted in these patients, although there is no difference in the incidence or extent of arteriographic vasospasm [42,43,44]. The only adverse effect is mild transient hypotension. Current recommendations are to administer 60 mg of nimodipine orally every 4 hours for a 21-day course beginning at the onset of SAH.