Subarachnoid Hemorrhage SAH

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SAH is a common and often devastating condition. Despite considerable advances in diagnostic, surgical, and anesthetic techniques and perioperative management, the outcome for patients with SAH remains poor.

Pathogenesis and Pathophysiology. SAH is most often caused by leakage of blood from abnormal blood vessels on the surface of the brain resulting in aneurysms and vascular malformations. Aneurysms, often referred to as berry or congenital, are outpouchings on arteries probably caused by a combination of congenital defects in the vascular wall and degenerative changes. Aneurysms usually occur at branching sites on the large arteries of the circle of Willis at the base of the brain ( .Fig

4.5.-10. ). When an aneurysm ruptures, blood is released under arterial pressure into the subarachnoid space and quickly spreads through the CSF around the brain and spinal cord. Aneurysms are less often caused by arterial dissection through the adventitia of arterial walls, embolism of infected or myxomatous material to the vasa vasorum of distal cerebral arteries (mycotic aneurysms), and degenerative elongation and tortuosity of arteries (dolichoectasia).

Vascular malformations (AVMs) are the second most common identifiable cause of nontraumatic SAH, accounting for approximately 10 percent of SAHs. Rupture of AVMs often causes ICH and SAH. Bleeding of AVMs is usually less vigorous and under less pressure than aneurysmal bleeding. Other less frequent causes of SAH include bleeding diatheses, trauma, bleeding into meningeal tumors, and the use of sympathomimetic drugs such as methamphetamine and cocaine. Amyloid angiopathy is an important cause of SAH during the geriatric years.

Epidemiology and Risk Factors. SAH is a significant cause of worldwide morbidity and mortality, predominantly among young adults of both sexes. Population-based incidence rates for SAH vary from 6 to 16 per 100,000, with the highest rates reported in Finland and Japan. The annual prevalence of aneurysmal SAH in the United States probably exceeds 30,000 persons. Unlike other stroke types, the incidence of SAH has not declined over time.

Figure 45-10 Commonest sites of intracranial aneurysms: (a) posterior inferior cerebellar artery, (b) basilar artery, (c) posterior communicating artery (PCA), (d) internal carotid artery (ICA), (e) anterior communicating artery (ACA), and (f) bifurcation of the middle cerebral artery (MCA). (Adapted from Jones EF, Kalman JM, Calafiore P, et al: Proximal aortic atheroma. An independent risk factor for cerebral ischemia. Stroke 1995:26:218-224: with permission.)

The incidence of SAH increases with age (mean age of approximately 50 years) and is higher in women than in men. Blacks are at higher risk than whites. Population-based mortality rates for SAH have progressively declined, and the survival rate after SAH has improved since the 1970s. The risk of SAH is increased during the third trimester of pregnancy. SAH due to aneurysm rupture is a leading cause of maternal mortality, contributing to between 6 and 25 percent of maternal deaths.^ Significant risk factors for SAH include smoking, hypertension, and heavy alcohol use. Use of oral contraceptives, hormone replacement therapy, hypercholesterolemia, and physical activity are not significantly related. During pregnancy, there is also a greater risk of AVM rupture y , y

Clinical Features and Associated Disorders. A sudden increase in ICP and meningeal irritation cause sudden severe headache, cessation of physical and intellectual activity, vomiting, and alteration of consciousness. Drowsiness, restlessness, and agitation are especially common. Severe focal neurological signs such as hemiplegia and hemianopia are absent at onset unless the aneurysm also bleeds into the brain. Expanding aneurysms or focal surrounding collections of blood within the cisterns and sub-arachnoid space can affect the cranial nerves and adjacent brain structures, causing characteristic focal features that depend on the location of the aneurysm. Xa.ble..,.4.5-8, lists these common focal signs. SAH commonly causes various complications, which are discussed later in association with the management of patients with SAH.

Patients with fibromuscular dysplasia, polycystic kidney disease, and connective tissue diseases have a higher incidence of aneurysms. Embolization of bacteria, fungi, and tumor tissue to the adventitia of cranial arteries can cause mycotic aneurysms. Endocarditis and cardiac myxomas are the usual causes. About one fifth of patients with aneurysms have more than one vascular anomaly or other aneurysms.

Differential Diagnosis and Evaluation. Severe migraine and meningitis are the major differential diagnostic considerations. Sometimes only lumbar puncture can settle separation of these three disorders.

History taking and neurological examination are the essential core of the diagnosis of SAH and of grading the clinical status. A CT scan that is performed within the first 24 hours shows approximately 95 percent of all SAH cases

TABLE 45-8 -- FOCAL SIGNS IN PATIENTS WITH ANEURYSMS AT VARIOUS SITES

Site of Aneurysms

Clinical Finding

Internal carotid--post communicating

Third nerve palsy

Middle cerebral artery

Contralateral face or hand paresis

Aphasia (left side)

Contralateral visual neglect (right side)

Anterior communicating

Bilateral leg paresis

Bilateral Babinski's signs

Basilar artery apex

Vertical gaze paresis

Coma

Intracranial vertebral artery/posterior inferior cerebellar artery

Vertigo

Elements of lateral medullary syndrome

and is also useful in detecting increased intracerebral density in large AVMs. When the diagnosis of SAH is highly likely clinically but the CT scan is normal, a lumbar puncture to detect blood in the CSF is necessary. After the diagnosis of SAH has been made, cerebral angiography is performed to define and localize aneurysm(s).69]

Management. Management of patients with SAH is directed to prevent and manage relatively common complications of SAH, such as rebleeding, vasospasm, hydrocephalus, hyponatremia, and seizures.

Rebleeding may be related to variations or changes in blood pressure rather than to absolute blood pressure. Bed rest, analgesics to relieve headache, and stable maintenance of blood pressure using antihypertensive medications in hypertensive patients are generally recommended. Because antifibrinolytic therapy has been found to be associated with a higher risk of brain ischemia and no benefits in overall outcome, use of antifibrinolytic agents is usually recommended only in certain clinical situations, for example, patients with low risk of vasospasm or a beneficial effect of delaying surgery. Early surgical clipping of the aneurysm is the method of choice, but interventional endovascular occlusive procedures are occasionally used for surgically unclippable aneurysms. y

Cerebral vasospasm is the delayed narrowing of large capacitance arteries at the base of the brain after SAH, which is often associated with radiographic or cerebral blood flow evidence of diminished brain perfusion in the territory of the constricted arteries. About one half of patients with SAH have vasospasm, which may resolve or progress to cerebral infarction, and 15 to 20 percent of such patients die from vasospasm despite maximal therapy. y Angiographic vasospasm has a typical temporal course: onset between 3 to 5 days after hemorrhage, maximal narrowing at 5 to 14 days, and gradual resolution over 2 to 4 weeks. y Oral nimodipine is recommended to reduce poor outcome related to vasospasm. Other calcium antagonists administered orally or intravenously are of uncertain value. So-called triple H therapy composed of hypertension, hypervolemia, and hemodilution is recommended. Aneurysms should be clipped when possible, and patients receiving this therapy should be closely monitored in an intensive care setting for hemodynamic function using TCD. The value of intracisternal fibrinolysis and antioxidant and anti-inflammatory agents are uncertain. Transluminal angioplasty is recommended for treatment of vasospasm in patients in whom conventional therapy has failed.

Acute obstructive hydrocephalus after SAH complicates about 20 percent of cases. Ventriculostomy is recommended in severe cases, although there may be associated increased rebleeding and infection. Chronic communicating hydrocephalus also occurs frequently. Temporary or permanent CSF diversion is recommended in symptomatic patients. In many patients, hydrocephalus and increased subarachnoid fluid can be managed by repeated lumbar punctures.

Hyponatremia occurs in 10 to 34 percent of cases after SAH. Hypotonic fluids should be avoided, and fluid restriction should not be instituted to treat hyponatremia. Volume should be maintained using isotonic solutions.

Seizure-like episodes occur in 25 percent of patients after SAH. Because of the potential risk of rebleeding,

some recommend the administration of prophylactic anticonvulsants. The long-term use of anticonvulsants is not routinely recommended for patients with no seizure episodes and should be considered only for patients with risk factors such as prior seizure, hematoma, infarcts, or middle cerebral artery aneurysms.

During pregnancy, the management options after SAH are early clipping or delivery (spontaneous or by cesarean section), with a possible risk of rebleeding during delivery when aneurysms are unclipped. Cesarean section may be appropriate for patients with an acute hemorrhage who are near term, but management is otherwise similar to nonpregnant patients. Craniotomy and clipping have been successfully archived at all stages of pregnancy. No difference is present in prognosis between pregnant and nonpregnant patients with SAH.

Reduction of exposure to the risk factors for SAH might result in a decreased incidence of SAH. Treatment of hypertension with antihypertensive medication, cessation of smoking, and moderation of alcohol use reduces the risk of SAH. Screening of certain high-risk populations for unruptured aneurysms is of uncertain value. Advances in MRA may facilitate screening in the future. In patients with acceptable surgical risk, clipping of unruptured aneurysms larger than 5 to 7 mm is often recommended.y

Prognosis and Future Perspectives. At times, the initial bleeding is so severe that death or irreversible brain damage occurs. If the bleeding is limited, the patient survives but is at risk for rebleeding in the days and weeks after the initial SAH. For untreated, ruptured aneurysms, there is a 3- to 4-percent risk of rebleeding in the first 24 hours, 1- to 2-percent per day risk in the first month, and a long-term risk of 3 percent per year after 3 months. Urgent evaluation and treatment of patients with suspected SAH is strongly recommended.^

Many recent advances in endovascular treatment of aneurysms and AVMs may improve the outcome in patients with lesions that are inaccessible to surgery. The major problem is early recognition and referral to neurological centers for early definitive treatment.

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