Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) represents a small portion of cerebrovascular disease, but accounts for a significant amount of stroke morbidity and mortality. The annual incidence of nontraumatic SAH is estimated at 10 to 15 per 100,000, with over 30,000 cases per year in the United States. Acute mortality of SAH has been estimated at 25% to 50%, depending on allowances for the likelihood of underdiagnosis in cases of sudden death. Additionally, SAH represents about 4.5% of stroke mortality, but because it occurs at younger ages than ischemic stroke, it accounts for over 25% of all stroke-related years of potential life lost before age 65 (1). For the most part, the management of ruptured intracranial aneurysm is shared between neurosurgeons and neurointensivists and offers one of the most fruitful areas for clinical investigation in neurocritical care.

Traumatic head injury is the most common cause of SAH, with bleeding related to cortical contusions, hematomas, and vessel injury. Vascular malformations are responsible for a small number of SAH cases, with arteriovenous malformation (AVM) responsible for 5% to 10%. Studies have inconsistently associated hypertension with SAH (2), and 10% to 20% have no vascular lesion identified on angiography. A small number of these patients have SAH related to bleeding dyscrasias and malignancy.

Rarely, intracranial vertebral dissections can lead to dissecting aneurysms with subsequent rupture and SAH (3). The subject of this chapter, spontaneous SAH, is for all intents and purposes caused by rupture of an intracerebral aneurysm. Although developmental abnormalities of the vessel wall may be the fundamental cause of berry aneurysms, they are only rarely present at birth, but rather develop over time, increasing in prevalence with increasing age. It is estimated that the population prevalence among adults approaches 3% to 5% (4,5). Most saccular aneurysms occur at the bifurcations of the large arteries at the base of the brain and rupture into the subarachnoid space of the basal cisterns (Fig. 15.1). Less commonly, they rupture into the
brain or ventricular system or both, resulting in intracerebral hemorrhage or acute hydrocephalus. In contrast, mycotic aneurysms occur at distal branch points of the middle, anterior, posterior cerebral, vertebral, or basilar arteries and rupture into the subarachnoid space over the cortical surface rather than into the basal cisterns.

FIG. 15.1. Computed tomography without contrast demonstrates blood in the basal cisterns.

The sites of the aneurysm and subsequent subarachnoid, intraventricular, or intracerebral clot determine the clinical features of the rupture and to some degree, the risks of subsequent development of vasospasm and hydrocephalus. As is well known, the most common sites of saccular aneurysms are the junction of the anterior communicating artery and the anterior cerebral artery, the junction of the posterior communicating artery and the internal carotid artery, the bifurcation of the middle cerebral artery, and the top of the basilar artery. Approximately 85% of cases occur in the anterior circulation. Furthermore, 12% to 31% of patients have multiple aneurysms, and in some 10% to 20% the aneurysms have bilateral identical locations (6). Aneurysms are slightly more common in women, and smoking has been identified as a risk factor.

Current data suggest that many aneurysms remain asymptomatic throughout life. The natural history risk of these so-called “incidental aneurysms” has long been a topic of debate. A recent retrospective review of a large cohort of patients with unruptured aneurysms suggested that small, incidental aneurysms have a bleeding risk less than 0.1% per year (7). This study and a related prospective study demonstrated that larger aneurysms (over 7 to 8 mm in diameter), have higher risks of hemorrhage. In addition, patients with residual aneurysms following rupture of the first aneurysm have the highest risks of rupture of the second incidental one. These and other studies also have demonstrated that the complication rate for surgical treatment of unruptured aneurysm is higher than previously thought, ranging from 5% to 30% for combined morbidity and mortality depending on the age of the patient and aneurysm size and location (7,8). The recent development of aneurysm treatment with endovascular techniques may well be safer but the long-term prevention of rupture remains to be demonstrated.

Management of subarachnoid hemorrhage has become a complex issue, with numerous treatment options and putative benefits of various aspects of neurocritical care. It is apparent that centers that have more experience with the care of this group of patients appear to have significantly better outcomes as judged by in-hospital death and disability (9).

CLINICAL PRESENTATION, EVALUATION, AND MANAGEMENT

Prodromal Symptoms

Prodromal symptoms may betray the location of an unruptured aneurysm and, at times, suggest progressive enlargement. The onset of a third cranial nerve palsy—particularly when associated with pupillary dilation, loss of light reflex, and focal pain above and behind the eye—points to an expanding aneurysm at the junction of the posterior communicating artery and internal carotid artery (10). Involvement of the third cranial nerve usually signifies acute aneurysmal enlargement or a small focal hemorrhage. Sixth cranial nerve palsy suggests a cavernous sinus aneurysm and visual field defects can result from an expanding supraclinoid carotid aneurysm. Occipital and posterior cervical pain suggest a posterior inferior cerebellar artery or anterior inferior cerebellar artery aneurysm; pain in or behind the eye and in the low temple suggests an expanding middle cerebral aneurysm. Sudden severe headache may result from a small leakage of blood from an aneurysm, and has been termed a sentinel headache. Indeed, a sudden unexplained headache in any location should arouse suspicion of subarachnoid hemorrhage, although the majority of sudden headaches turn out to be benign. Many patients presenting with subarachnoid hemorrhage have sought medical attention for headache in the preceding days. Although this likely reflects “sentinel hemorrhage” pain related
to expansion of an aneurysm has been postulated. Whatever the mechanism, the importance of rapid recognition and intervention is clear. A review of referrals to tertiary centers that see large numbers of patients with aneurysms revealed that 25% of patients had been seen earlier and not diagnosed with subarachnoid hemorrhage (11). Not surprisingly, the risk of misdiagnosis was greatest (38%) in those with no or minimal neurological deficit at the time of evaluation.

Initial Clinical Presentation

Acute Major Subarachnoid Hemorrhage

For the brief moment of aneurysmal rupture, when acute major subarachnoid hemorrhage occurs, intracranial pressure (ICP) approaches the mean arterial pressure and cerebral perfusion pressure falls (12). These changes may account for the sudden but transient decrease in consciousness that occurs in most cases. Although the change in level of consciousness may be preceded by a brief moment of excruciating headache, most patients first complain of headache on regaining consciousness. In about 45% of patients, severe headache, usually associated with exertion, but without loss of consciousness, is the presenting complaint (13). The headache is often described by the patient as “the worst headache of my life.” Words such as explode or burst may be used. Often it is described as all over or in the back of the head and neck. Whatever the nature of the onset, vomiting is a prominent symptom, and vomiting with sudden headache, of course, should raise the question of acute subarachnoid hemorrhage.

Although sudden severe headache in the absence of focal neurological symptoms is the hallmark of aneurysmal rupture, not infrequently neurological deficits emerge. Unilateral third cranial nerve palsy strongly suggests a posterior communicating artery aneurysm. Sixth nerve palsy is common and does not have great significance as a localizing sign, although it often corresponds to an infratentorial aneurysmal rupture. A middle cerebral artery bifurcation aneurysm may rupture into the subdural space and present as a subdural hematoma. Anterior communicating artery aneurysms sometimes rupture into the basal cisterns of the subarachnoid space and form a clot that is large enough to produce localized mass effect. Any aneurysm can rupture into the brain parenchyma and result in intracerebral hemorrhage (14). The common resulting deficits include hemiparesis, aphasia, anosognosia, memory loss, and abulia. Cerebral edema often follows, resulting in progressive mass effect and deterioration, sometimes requiring surgical evacuation.

Occasionally, acute unilateral hemispheric swelling and associated focal neurological signs occur immediately after aneurysmal rupture. The reasons for such swelling are uncertain. Acute vasospasm has been proposed as an explanation for transient interruption of the cerebral circulation in an arterial territory. Unwitnessed hypotension or hypoxia may have accompanied the initial bleeding with secondary global brain injury. Acute hydrocephalus also may occur independently of acute cerebral edema and account for the persistence of a stuporous or comatose state. Often there is no adequate explanation for the initial neurological deficits, and in many cases they gradually improve over a matter of days.

Careful documentation of the initial neurological deficit, attempting to establish its cause, and closely following its course is of utmost importance for further decisions in the management of such patients. A clinical grading system devised by Hunt and Hess is widely used to categorize the clinical status of patients with acute subarachnoid hemorrhage (15). Although the scale (Table 15.1) is useful and used routinely in patient management, it does not adequately quantitate the clinical deficit, nor account for the pathophysiologic nature of the deficit. Restated, diagnostic and therapeutic decisions regarding these patients are best made with an accurate, serial, quantitative documentation of the neurological deficit and its pathophysiologic nature.

TABLE 15.1. Hunt and Hess Scale for clinical grading in subarachnoid hemorrhage

I	Asymptomatic, mild headache
II	Cranial nerve palsy, severe headache
III	Drowsy, confused, mild deficit
IV	Stupor, moderate to severe hemiparesis, early posturing
V	Coma, decerebrate posturing

Initial Evaluation

Computed Tomography Scan

Noncontrast computed tomography (CT) of the head has become the initial diagnostic study of choice for suspected subarachnoid hemorrhage. Approximately 95% of patients have evidence of subarachnoid blood on a plain CT scan obtained within the first 48 hours after aneurysmal rupture (16). Inexperienced radiologists frequently miss small amounts of subarachnoid blood and a “negative” scan in a suggestive case is worth reviewing. A plain CT scan should be performed first because contrast may show enhancement in the basal cisterns that may be mistaken for clotted blood. A later contrast CT scan including CT angiography, may demonstrate an aneurysm or an unsuspected arterial venous malformation (17). If the CT scan neither establishes the diagnosis of subarachnoid hemorrhage nor demonstrates a mass lesion or obstructive hydrocephalus, a lumbar puncture should be performed to establish the diagnosis of subarachnoid hemorrhage. Lumbar puncture may be indicated before CT scanning if the imaging study is not available at the time of the suspected subarachnoid hemorrhage and the patient has no lateralizing neurological deficits or evidence of papilledema. The extent and location of subarachnoid blood generally points to the location of the aneurysm and identifies the cause of an initial neurological deficit. The CT scan also has found great use in predicting which patients are destined to develop delayed ischemic neurological deficits caused by cerebral vasospasm (4,18,19).

Laboratory Evaluation

Routine laboratory studies should include electrolytes, blood urea nitrogen, and creatinine, as well as white blood count, hematocrit, and platelet count. Clotting studies of prothrombin time (INR) and partial thromboplastin time also should be checked. Toxicology screens may be helpful if cocaine and amphetamine use is suspected. Baseline electrolytes are of value because hyponatremia may develop, most commonly probably related to a salt wasting syndrome, which causes loss of salt and water in the urine with subsequent volume depletion and dilutional hyponatremia (Chapter 6) (20,21). Platelet count, bleeding time, and other clotting parameters should be documented again before invasive procedures. Serum viscosity increases significantly when the hematocrit is greater than 40% or when the serum fibrinogen levels are greater than 250 mg%. Adjustment of the serum viscosity becomes important in patients at risk for symptomatic cerebral vasospasm but its significance has not been studied systematically and it is not often attended to in most units.

A baseline electrocardiogram (ECG) is important and often shows ST changes similar or identical to ischemic abnormalities or a prolonged QRS complex or Q-T interval, and perhaps most characteristically, tall T waves (22). These changes have been linked to elevated blood catecholamine levels as a result of hypothalamic dysfunction that in turn stimulates the α-adrenergic receptors in the myocardium. Catecholamine excess, either via stimulation by norepinephrine-containing nerve terminals or circulating epinephrine, results in prolonged muscle fiber contraction, and leads to myofibrillar necrosis. This topic is reviewed extensively in Chapter 5. Serum markers of myocardial ischemia, creatine kinase, and troponin, are frequently elevated and found more frequently in larger hemorrhages. The distinction from an associated myocardial infarction is then difficult. Echocardiography is indicated in those patients presenting with hypotension and signs
of left ventricular failure. Hypokinesis in a diffuse global pattern or predominantly affecting the cardiac base is consistent with an initial catecholamine stress injury and suggests that recovery of cardiac function will occur over several days. Focal wall motion abnormalities or apical hypokinesis is more suggestive of coronary ischemia. Cardiac catheterization may be useful in the setting of continued and/or recurrent ischemic injury as indicated by ECG changes or serum markers.

Angiography

Cerebral angiography is usually planned as part of the acute evaluation to identify the source of the hemorrhage and localize and characterize the anatomy of any aneurysm. Angiography should also be performed without delay if an arteriovenous malformation or mycotic aneurysm is suspected because of the presence of intraparenchymal blood or subarachnoid blood located over the hemisphere rather than in the basal cisterns. Another possible indication for acute angiography is an intracerebral hematoma secondary to aneurysmal rupture presenting with mass effect, a combination that may make emergency surgical evacuation necessary. This most frequently occurs when a middle cerebral bifurcation aneurysm ruptures and produces a large intratemporal or sylvian fissure hematoma. Documenting the location and anatomy of the aneurysm before such surgery is imperative because it is almost always preferable to clip the aneurysm at the time of clot evacuation. Some centers now use CT and CT angiography in this scenario to shorten the evaluation time so that emergency surgical intervention can be more quickly carried out.

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