Intracranial Pressure Response

The volume of blood escaping during rupture of an aneurysm varies from a negligible amount constituting a “warning leak” to massive amounts (≥150 mL) associated with immediate death. The pathophysiologic consequences depend on the volume and location of the bleeding, as well as the preexisting size of the cerebrospinal fluid (CSF) space into which the aneurysm ruptures and the patient’s age and premorbid condition. A general correlation can be expected between the volume of SAH and clinical grade, risk for vasospasm and other complications (e.g., increased intracranial pressure [ICP], seizures, hydrocephalus), and the extent of the physiologic changes (e.g., reduced cerebral blood flow [CBF] and metabolism), systemic alterations (e.g., hyponatremia, hypovolemia, hypermetabolism), catabolic state, cardiac arrhythmia, and cardiac wall motion abnormalities.

The ICP response to rebleeding of aneurysms is known in the subset of patients with SAH who have ICP monitors in place during their rebleeding, but these changes may not be representative of those that occur with the first hemorrhage. During rebleeding, ICP rises to diastolic blood pressure and CBF occurs only during systole.^8,9 Temporary circulatory arrest may help stop the aneurysmal bleeding but may also be associated with transient global ischemia, which would cause loss of consciousness. Because many patients do not lose consciousness, however, normal clotting probably also contributes to arrest of the hemorrhage. In addition, animal experiments have shown that the rate of blood flowing into the subarachnoid space determines the volume of SAH.¹⁰ High flow rates, which would theoretically occur with large aneurysm tears, produce large-volume SAH in a short time, whereas low flow rates, which might result from a small hole in the aneurysm, lead to slow accumulation of a small volume of SAH.

The results of ICP monitoring in 52 patients for a mean of 8 days after SAH showed that mean ICP rose as clinical grade worsened.¹¹ Mean ICP was 10 mm Hg in patients with clinical grades 1 and 2, 18 mm Hg in patients with clinical grades 2 and 3, and 29 mm Hg in those with clinical grades 3 to 5. Vasospasm, which was more common in patients with a poor clinical grade and larger SAH, was associated with a significant rise in ICP from a mean of 16 mm Hg in those without vasospasm to 29 mm Hg in those with vasospasm. This fact should be considered carefully in patients experiencing deterioration from vasospasm days after SAH. Substantial improvement in cerebral perfusion pressure can be achieved by ventricular drainage. Cerebral perfusion pressure is equal to mean arterial blood pressure minus ICP. There are no specific data regarding optimal cerebral perfusion pressure in patients with aneurysmal SAH, but guidelines for head injury suggest that it be maintained at values higher than 70 mm Hg. ICP is related to outcome; 80% of patients with pressure below 15 mm Hg do well, as opposed to good outcomes in just 15% of patients with ICP in excess of 15 mm Hg.¹²

Cerebral Blood Flow, Volume, and Metabolism

Numerous studies of CBF, cerebral blood volume, and cerebral metabolism have been conducted in patients with ruptured aneurysms. Almost all studies agree that CBF is globally decreased after SAH.¹² For example, in 30 patients with SAH, regional CBF decreased from a mean of 54 mL/100 g per minute in normal individuals to 42 mL/100 g per minute in patients with grade 1 to 2 and no vasospasm, 35 mL/100 g per minute in patients with grade 3 to 4 and no vasospasm, 36 mL/100 g per minute in patients with grade 1 to 2 and vasospasm, and 33 mL/100 g per minute in patients with grade 3 to 4 and vasospasm.¹³ The cerebral metabolic rate of oxygen (CMRO₂) showed a similar pattern, with progressive reductions being associated with deteriorating clinical grade and worsening vasospasm. Cerebral blood volume was markedly increased in patients with severe neurological deficits associated with severe vasospasm. It was concluded that vasospasm produces narrowing of the large, angiographically visible arteries at the base of the brain and that this narrowing is accompanied by compensatory dilation of the distal, intracerebral arterioles. Other studies have shown a lack of increased cerebral blood volume after SAH, thus suggesting impaired autoregulatory vasodilation.¹⁴

Mean CBF decreases with time after SAH; it reaches a nadir in 10 to 14 days, after which it slowly increases toward normal.^12,15 A relative hyperemia in relation to the reduced CMRO₂ occurs immediately after SAH.^16,17 In patients with poor grades, CBF and cerebral metabolism may remain depressed for weeks. In addition to global reductions in CBF and CMRO₂, regional perfusion defects can develop after SAH and can be correlated with areas of angiographically demonstrated severe vasospasm and ventricular dilation. Areas of low CBF are also present around intracerebral hematomas, although their size and importance may be overestimated.¹⁸ Regions of brain irrigated by vasospastic arteries have elevated oxygen extraction fractions. Positron emission tomography shows that as long as the area is ischemic and infarction has not developed, CMRO₂ remains normal but flow is reduced. The development of infarction is heralded by a fall in CMRO₂ with relatively increased CBF (relative hyperemia).¹⁶ The degree to which the reduced blood flow after SAH is due to hypovolemia and hypotension is unclear, but there is some evidence that the alterations in flow can be prevented by maintenance of normovolemia or hypervolemia with or without induced hypertension.^19,20

Little information is available on the pathogenesis of CBF and the metabolic changes that occur after SAH. In patients without vasospasm, intracerebral clots, or hydrocephalus studied in the first 4 days after SAH, CMRO₂ is decreased without accompanying changes in the oxygen extraction fraction, thus suggesting that the primary alteration is a reduction in CMRO₂ and that CBF falls because of decreased demand.¹⁶ This is usually attributed to a toxic effect of the subarachnoid blood, but a neural mechanism or an effect of global ischemia may be important. A relative hyperemia is usually present and is postulated to be due to intracranial circulatory arrest, transient global cerebral ischemia, and lactic acidosis occurring at the time of rupture. Mitochondrial respiration, sodium-potassium adenosine triphosphatase activity, and extracellular potassium and calcium levels are altered in the brain tissue of experimental animals exposed to subarachnoid blood, although the relationship of these changes to CBF and CMRO₂ has not been fully clarified.^21–23

The relationship of CBF to blood pressure and PaCO₂ is also altered after SAH. The response of CBF to changes in blood pressure at different times after SAH was studied in 38 patients.²⁴ Autoregulation was intact in good-grade patients but became progressively impaired in poor-grade patients and with development of vasospasm. Autoregulation is not lost in an all-or-none fashion. The degree of impairment tends to be worse as consciousness is more impaired, as vasospasm becomes more severe, and 5 to 10 days after SAH. Loss of the CBF response to changes in PaCO₂ occurs with more severe brain damage than that required to disturb autoregulation, and the combination of loss of autoregulation and variation in CBF with changes in PaCO₂ is termed vasomotor paralysis. After SAH, vasomotor paralysis may be observed in patients with clinical grades 4 and 5, usually with severe vasospasm. Measurements of CBF with intra-arterial xenon 133 in 38 patients with aneurysmal SAH found that responses to alterations in PaCO₂ were generally preserved, although they were reduced.²⁴ Impaired CO₂ reactivity was associated with increased ICP and high lactate levels in CSF, and poor clinical grade and vasospasm were associated with impaired CO₂ responsiveness. Transcranial Doppler studies have demonstrated impairment in CO₂ reactivity after SAH, even in patients with a good clinical grade.²⁵ This tends to occur during vasospasm and then subsequently resolves. Hyperventilation should be used with caution in patients with SAH. It may be useful for reducing increased ICP and increasing CMRO₂, but it may also increase the risk for ischemia by causing vasoconstriction.²⁶

Symptoms and Signs of Subarachnoid Hemorrhage

The hallmark of SAH is a sudden, usually severe, headache, although at most about 80% of patients who can give a history will recount such a headache.¹² Challenges arise in assessing the minority of patients in whom an atypical manifestation occurs, and for this reason clinicians must remain vigilant for the possibility of SAH because a missed diagnosis can result in catastrophic sequelae. The classically described cardinal symptom of SAH as a sudden, severe headache or the “worst headache of my life” may be overemphasized as a reliable initial diagnostic symptom, but all patients with headaches that are unusually severe or sudden in onset should be investigated for SAH. Byyny and coauthors reported that 4 of 27 patients seen in an emergency department with a sudden severe headache were found to have SAH on computed tomography (CT).²⁷ An additional 19% had SAH detectable only by lumbar puncture. The positive predictive value of a sudden severe headache was just 93%. Linn and colleagues reported that it may be the initial symptom in only a third of patients with SAH. In the same series, just half of the patients reported their headache to reach maximum severity instantaneously, with a fifth of the patients reporting it to escalate over a period of 1 to 5 minutes and the remainder over a period greater than 5 minutes.²⁸ Other ominous features include vomiting, onset with exertion, altered level of consciousness, meningismus, or focal neurological deficit. Absence of these clinical findings, however, does not rule out SAH.

Premonitory symptoms (warning leaks or sentinel hemorrhages), typically consisting of an unusually severe headache of sudden onset, sometimes associated with nausea, vomiting, and dizziness, are usually attributed to small hemorrhages from the aneurysm. In 1752 patients with ruptured aneurysms from three series, 20% had a history of a sudden, severe headache before the event leading to admission.^29–31 Other possible mechanisms for these headaches include hemorrhage into the aneurysm wall, acute expansion of the aneurysm sac, or ischemia. The importance of recognizing warning leaks has repeatedly been emphasized because the diagnosis may be delayed until catastrophic SAH occurs, which almost certainly makes the outcome worse than if the diagnosis had been made promptly and correctly.³⁰ Some authors discourage the use of terminology such as “sentinel bleed” or ““warning leak” and instead encourage clinicians to have a high index of suspicion in the pursuit of an accurate diagnosis of SAH to foster the mindset that the patient either has or has not experienced SAH.²⁸

Many other symptoms and signs can develop before rupture of an aneurysm, including hemiparesis, dysphasia, extraocular muscle impairment, visual loss, visual field defects, and localized headache. They depend on the size and anatomic location of the aneurysm.¹²

Ruptured aneurysms may produce distinct clinical features at specific sites. Transient bilateral lower extremity weakness may be due to rupture of an anterior cerebral artery aneurysm. SAH from a middle cerebral artery aneurysm is more likely to produce hemiparesis, paresthesia, hemianopia, and dysphasia. Sarner and Rose did not find that any particular aneurysm site had a higher propensity to induce coma.³² Seizures occur more commonly with aneurysms of the anterior circulation and probably with middle cerebral artery aneurysms. Third nerve palsy or unilateral retro-orbital pain suggests an aneurysm arising at the junction of the internal carotid and posterior communicating artery. Third nerve lesions also occur with aneurysms at the origin of the superior cerebellar artery. Carotid-ophthalmic artery aneurysms may produce unilateral visual loss or visual field defects. Focal neurological deficits after SAH may be due to a mass effect from the aneurysm, vasospasm, seizures, or hematomas in the brain or subdural spaces.

Terson reported vitreous hemorrhage and hemiparesis in association with SAH.¹² Vitreous and other intraocular hemorrhages may be seen on ophthalmoscopic examination in 3% to 13% of patients with SAH and are associated with poor clinical grades.^33,34 Because the prognosis for visual recovery is good with no treatment, vitrectomy is generally reserved for patients who fail to improve after months.

Numerous exertional activities have been temporally associated with aneurysm rupture. A cooperative study reported that a third of 2288 aneurysm ruptures occurred during sleep, a third during unspecified circumstances, and a third during various exertional activities, including lifting, emotional strain, defecation, coitus, coughing, and parturition.³⁵ Schievink and associates found that SAH occurred during stressful events in 43% of patients, nonstressful events in 34%, rest or sleep in 12%, and uncertain circumstances in 11%.³⁶ If one takes into account the fact that exertional activities probably occupy a small percentage of one’s lifetime, it seems likely that the fluctuations in blood pressure and changes in venous and CSF pressure that may occur with these activities increase the risk for rupture of an aneurysm. Head injury has only rarely been associated with aneurysmal SAH.

Computed Tomography

Non–contrast-enhanced cranial CT is the first investigation in patients with suspected SAH. The probability of detecting the hemorrhage is proportional to the volume of blood in the subarachnoid space, the time after hemorrhage, and the quality of the scan (Fig. 363-1). In a cooperative study, 3% of 1553 patients were found to have normal scans within 24 hours of confirmed SAH.³⁷ The incidence is probably lower with current CT scanners, but CT still has only about 93% sensitivity for SAH, thus highlighting the need for lumbar puncture when clinically indicated in the context of normal CT findings.²⁷ CT on the day of the ictus showed SAH in 92%, intraventricular hemorrhage in 20%, intracerebral hemorrhage in 19%, hydrocephalus in 16%, mass effect in 8%, aneurysm in 5%, subdural hemorrhage in 2%, and hypodense areas in 1%. With time, the incidence of normal CT scans increases, as well as the presence of areas of hypodensity, whereas hydrocephalus and hemorrhage decrease. By 5 days after SAH, 27% of the scans were normal and 58% showed hemorrhage. Intracerebral hemorrhage takes longer to resolve than SAH. Alert patients are significantly more likely than drowsy patients to have a normal scan or a thin, local collection of blood, and all other abnormalities evident on CT are more common in patients with a poor clinical grade. Additional stigmata of SAH include enlargement of the temporal horns in the absence of increases in other parts of the ventricular system.³⁸

FIGURE 363-1 A, Changes on computed tomography (CT) in patients with a ruptured aneurysm in relation to time after subarachnoid hemorrhage (SAH). The incidence of abnormalities on CT is highest initially and decreases thereafter such that at 5 days about 27% of patients have normal findings. B, Changes in cerebrospinal fluid (CSF) in patients with a ruptured aneurysm in relation to time after SAH. Xanthochromia appears within hours and is found almost universally after 12 hours.

(From Weir B. Headaches from aneurysms. Cephalalgia. 1994;14:79-87.)

The volume and location of subarachnoid blood on CT give prognostic information about the risk for vasospasm and outcome after SAH. A widely used system of grading SAH on CT was proposed by Fisher and coworkers (Fig. 363-2).^39,40 In a prospective study, these authors reported good correlation between the location and volume of the blood and the subsequent development of vasospasm. The degree of SAH on CT was an independent risk factor for death and disability in the International Cooperative Study on the Timing of Aneurysm Surgery.³⁷ Subsequent studies have suggested that initial clot volume and percentage of clot cleared per day are significant predictors of vasospasm whereas Fisher grade and initial clot density are less important.⁴¹ The Fisher scale may not correlate well with vasospasm because the categories are broad and not defined with modern imaging techniques.

FIGURE 363-2 Computed tomography shows different grades of subarachnoid hemorrhage (SAH) according to the scale of Fisher and colleagues.³⁹ Grade 1 is a scan with no SAH. A, Grade 2 is a scan showing a thin layer of subarachnoid blood less than 1 mm thick. This measurement, however, was taken from scans printed at different magnification, so it is not actually 1 mm. B, Grade 3 is a scan showing focal or diffuse subarachnoid blood thicker than 3 mm. Grade 4 is a scan showing intracerebral (C) or intraventricular (D) blood with or without subarachnoid blood.

Studies evaluating CT angiography (CTA) for detection of intracranial aneurysms report sensitivities of 77% to 97% and specificities of 87% to 100%. Sensitivity diminishes significantly with aneurysms measuring less than 3 mm in maximal diameter, and in such cases sensitivities have been reported in the range of 40% to 91%.^42–47 CTA has been demonstrated to be useful in determining suitability of the aneurysm for endovascular treatment in more than 95% of cases.⁴⁸

We use CTA as the preliminary study for evaluation of patients with spontaneous SAH. Catheter-based angiography is indicated when contemplating endovascular treatment, when no source of hemorrhage is identified on CTA, when further anatomic information is required before surgery, and in some cases as the first investigation when there is concern about the administration of contrast material because of allergies or poor renal function.

Lumbar Puncture

Lumbar puncture is indicated for the diagnosis of SAH when findings on CT are normal. CT may show normal results if the SAH is very small or an inordinate amount of time has elapsed between hemorrhage and the CT scan. Contraindications to lumbar puncture include abnormal blood clotting, increased ICP as a result of a space-occupying lesion, suspected spinal arteriovenous malformation, and infection at the lumbar puncture site. When bedside lumbar puncture is not feasible, fluoroscopically assisted lumbar puncture is recommended. Risks associated with lumbar puncture include neurological deterioration from rebleeding of the aneurysm or cerebral herniation. Data from two studies reported that 17 (10%) of 165 patients with SAH who underwent lumbar puncture experienced deterioration within 24 hours.^49,50 It was thus recommended that CT always be performed before lumbar puncture in the setting of suspected SAH. Limited accessibility to a CT scanner and a high level of suspicion for infectious meningitis may make lumbar puncture the initial diagnostic test in patients who do not have focal neurological deficits or a depressed level of consciousness. A review of the literature on lumbar puncture and meningitis concluded that there was no evidence to recommend CT before lumbar puncture in patients with suspected acute meningitis unless atypical features or focal neurological findings were present.⁵¹

Interpretation of CSF results can sometimes be challenging. Theoretically, any erythrocytes in CSF represent hemorrhage. It is possible that a small hemorrhage from an aneurysm could occur directly into the brain parenchyma or into a loculated CSF space and that erythrocytes would not be detected in lumbar CSF, although this is very rare. During CSF access, however, erythrocytes may be introduced artifactually into the CSF sample (traumatic tap). There are many criteria for differentiating a traumatic tap from SAH (Table 363-2), but none are very reliable. A declining erythrocyte count in subsequent tubes is an unreliable indicator of a traumatic tap.⁵² Xanthochromia is a yellow discoloration in a centrifuged CSF sample caused by release of hemoglobin and its breakdown products from hemolysis of erythrocytes. It is a very reliable sign of SAH in CSF obtained more than 12 hours after SAH. The most sensitive test for detection of xanthochromia, however, is spectrophotometry, but most laboratories only visually inspect uncentrifuged CSF. If the CSF is not centrifuged, it may be discolored by erythrocytes that are present as a result of either SAH or a traumatic tap. Furthermore, when erythrocytes are introduced into the CSF sample during a traumatic tap, they will eventually lyse and produce xanthochromia. Therefore, CSF samples should be kept at 4°C, centrifuged immediately, and examined for xanthochromia in timely fashion. The time for xanthochromia to appear after SAH is variable, but it persists longer than intact erythrocytes do (see Fig. 363-1). The sensitivity of visual inspection for detecting xanthochromia in 81 patients more than 12 hours after SAH was less than 50%, thus highlighting the utility of spectrophotometry.⁵³ If spectrophotometry for hemoglobin and bilirubin is negative on CSF obtained more than a few hours after the onset of symptoms, angiography is probably not necessary except under unusual circumstances. If findings on CT are normal, erythrocytes are present but not xanthochromia, and 12 or more hours has elapsed after the ictus, we generally perform at least CTA or magnetic resonance angiography (MRA) and occasionally catheter angiography. About 70% of patients seen 3 or more weeks after suspected SAH have xanthochromia. CT will usually be normal, and if CSF is clear at this time, CTA or catheter-based angiography should be performed.

TABLE 363-2 Characteristics of Cerebrospinal Fluid after Subarachnoid Hemorrhage and Traumatic Lumbar Puncture*

* The presence of any erythrocytes or xanthochromia should lead to the tentative diagnosis of a ruptured aneurysm.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI; fluid-attenuated inversion recovery [FLAIR] and proton density sequences) has been shown to be as sensitive as CT in detecting acute SAH, but MRI remains impractical in most cases as an initial investigation.⁵⁴ It is, however, useful for investigating atypical hemorrhage patterns (e.g., craniocervical junction, parenchymal hemorrhage) or when there has been a delay from the onset of symptoms to initial imaging. For the detection of subacute hemorrhage, gradient echo T2 is the most sensitive sequence, with sensitivities of 94% in the acute phase and 100% in the subacute phase. The next most sensitive sequence is FLAIR, with values of 81% and 87% for the acute and subacute phases, respectively.⁵⁵

There is concern about performing MRI postoperatively in patients with aneurysm clips, and a fatality has been reported.⁵⁶ Modern aneurysm clips are alloys of cobalt, nickel, molybdenum, and chromium, with or without small amounts of iron.⁵⁷ They are not ferromagnetic and should not move in the magnet. Titanium clips are either pure titanium or alloys of titanium, vanadium, and aluminum and are not ferromagnetic. Some institutions test the clips by checking whether they move in the magnet before implantation. Stainless steel clips should not be used.

Catheter Cerebral Angiography

Catheter-based cerebral angiography remains the “gold standard” for the investigation of spontaneous SAH, but it is not always required. Technologic advances in cross-sectional imaging and the ability to create three-dimensional volume-rendered images from 64-slice or greater multidetector CT scanners make catheter angiography unnecessary in some cases. When the pattern of hemorrhage is consistent with the discovered aneurysm and no additional confounding factors are present, the surgeon may be confident in operating without performing catheter-based angiography. Complex aneurysms, endovascular treatment, and associated vascular lesions (i.e., arteriovenous malformation or dural arteriovenous fistula) mandate catheter angiography.

Catheter angiography is also indicated for spontaneous SAH with no underlying cause detected on CTA. A complete angiogram consists of a six-vessel study (including both external carotid arteries) and may include provocative maneuvers as clinically relevant (i.e., cross-compression to study the anterior communicating artery, Alcock’s maneuver to study the posterior communicating artery). A rapidly deteriorating neurological condition may preclude catheter angiography. If neck or back pain or a lower extremity neurological deficit is prominent, searching for a spinal arteriovenous malformation, aneurysm, or neoplasm with spinal MRI or angiography, or both, may be indicated. If the initial angiogram is negative and the clinical and CT patterns are not consistent with benign perimesencephalic hemorrhage, we usually obtain another angiogram about 7 days later. Angiogram-negative benign perimesencephalic hemorrhage is typically manifested as a severe headache without instantaneous onset, and the blood seen on CT is symmetrical about the midline and localized primarily to the prepontine, interpeduncular, crural, and ambient cisterns.

In a review of 2899 procedures, the rate of neurological complications with catheter angiography was 1.3%; 0.7% were transient, 0.2% were reversible, and 0.5% were permanent. Neurological complications were significantly more common in patients 55 years or older, in patients with cardiovascular disease, and when fluoroscopic times were 10 minutes or longer.⁵⁸ Allergic reactions to contrast medium occur in less than 1 in 50,000 studies, and about 1 in a million patients die as a result of such a reaction.⁵⁹

Rupture of an aneurysm during angiography is uncommon. In the first cooperative study, in which 5484 patients were studied by angiography, 7 patients (0.13%) rebled during angiography and 12 (0.22%) 10 minutes to 24 hours later.³⁵ Based on subsequent studies, it is estimated that 3% of patients show extravasation of dye when angiography is performed for investigation of SAH.⁶⁰ If extravasation was observed on an angiogram, the mortality was 70%. It has been suggested that the rate of rebleeding associated with cerebral angiography can be reduced by avoiding catheter angiography within the first 6 hours after SAH, but this remains unproven.^60,61 Because rebleeding is probably most common immediately after the first hemorrhage, whether angiography causes the rebleeding is unknown. We do not delay angiography because a patient is seen immediately after SAH has occurred.

Twenty percent to 30% of patients have multiple aneurysms.¹² A combination of clinical and radiologic features can identify the ruptured aneurysm in 90% to 95% of cases.^62–65 A review of 69 patients with multiple aneurysms generated the following algorithm to predict which aneurysms would bleed: (1) exclude extradural aneurysms, (2) study CT for the presence of focal SAH, (3) look for focal spasm or a mass effect on the angiogram, (4) pick the larger or more irregularly shaped aneurysm, (5) examine the patient for focal neurological signs, (6) consider repeating the angiogram at a later date to look for change in aneurysm size or for focal angiographic signs, and (7) choose the aneurysm that has the highest chance of rupture (anterior communicating artery aneurysm).⁶⁶ Overall, the most proximal and largest aneurysm usually ruptures. If there are two aneurysms on the same artery, it is generally the proximal one that is ruptured. In some cases, MRI has provided additional evidence of localizing value. In about two thirds of patients with multiple aneurysms, all lesions will be able to be clipped through a single craniotomy, and this may be advisable depending on the age and condition of the patient and the location of the aneurysms. In exceptional circumstances and despite the best diagnostic aids, it may not be possible to determine preoperatively which aneurysm bled. The literature contains cases in which recurrent SAH developed in patients with multiple aneurysms after the unruptured one was clipped.

No cause of SAH will be found in 9% to 30% of patients undergoing angiography for SAH, but there are numerous other causes of SAH (see Table 363-1). We perform cranial MRI and MRA in such patients, although the yield is low. In 15 series published between 1978 and 1988, 253 of 1218 patients underwent repeat angiography after an initially negative study, and an aneurysm was found in 11%.⁶⁷ The aneurysm may be missed initially if it thromboses totally after bleeding. Review of the initial studies by another neuroradiologist may be helpful. The anterior communicating artery complex probably harbors the most missed aneurysms. Studies have shown that there is a subgroup of patients with angiogram-negative SAH in whom blood is located predominately in the prepontine and perimesencephalic cisterns. Repeat angiography is probably unnecessary in this situation if a good-quality initial angiogram does not show a posterior circulation aneurysm.⁶⁸

Residual aneurysm was detected on 8% of postoperative angiograms obtained within days of surgery on 2416 patients reported in nine series.⁶⁹ Residual aneurysms hemorrhage at a rate of about 0.02%/yr, although the natural history of these rests is not known with certainty.^70,71 The advantage of knowing about an unexpected residual aneurysm intraoperatively is that an attempt can be made to obliterate it at the time. This must be weighed against the risk associated with further clip manipulation and angiography itself. The incidence of unexpected major arterial occlusion was about 6% in the series just reviewed.⁶⁹ Occlusion is also best detected by intraoperative angiography before permanent ischemia develops. Several series have identified characteristics that increase the yield of intraoperative angiography, such as giant aneurysms and those arising at the ophthalmic, anterior communicating, or middle cerebral arteries or at the basilar bifurcation.^69,72,73 Angiography is virtually always performed at the completion of endovascular aneurysm treatment, and residual aneurysms are seen frequently. Follow-up of residual aneurysms after surgery or endovascular treatment, usually with MRI/MRA, is indicated if treatment would be undertaken should growth occur.

Clinical Grading

Several clinical grading scales have been developed, including the Botterell, Hunt and Hess, and World Federation of Neurosurgical Societies (WFNS) scales (Table 363-3).^74–76 None are universally accepted despite numerous analyses.^77–79 Challenges in the development of a universal grading scale include significant interobserver and intraobserver variability and omission of important additional features that may be predictive of outcome but are too complex to include in a clinical grading scale.⁷⁹

Clinical grading is useful for estimating prognosis, for standardizing assessment to facilitate communication between physicians, and possibly for improving outcome measures in multicenter studies. Finally, repeated standardized assessment with some type of semiquantitative neurological scale is essential to detect deterioration in the patient’s condition. The neurological grade may best be determined after the patient is resuscitated and has undergone ventricular drainage if necessary. Neurological grade is an independent predictor of outcome after aneurysmal SAH.^37,80 Assessment of level of consciousness with the Glasgow Coma Scale (GCS), which is the basis of the WFNS scale, has less interobserver variability.^81,82 The WFNS scale was based on the observation that in a large clinical trial, the clinical features that best predicted outcome were the level of consciousness and the presence of a focal neurological deficit. The GCS is probably the most useful aspect of the grading scales.⁷⁹

General Care

Initial emergency care of a patient with SAH includes assessment of airway, breathing, and circulatory function. A brief neurological evaluation of the level of consciousness, cranial nerves, and motor function will determine whether emergency surgical interventions (placement of an external ventricular drain and evacuation of an intracerebral hematoma) are required. Intubation should be considered for patients with a GCS score of less than 8. Other than lifesaving procedures such as those to reduce severely increased ICP, repair of the aneurysm becomes the focus of treatment to reduce the risk for rebleeding. Secondary benefits of urgent aneurysm repair include safer use of treatments of vasospasm. The decision to treat and the modality used for aneurysm repair (endovascular or clipping) are based on multiple factors, including neurological grade, patient age, location and size of the aneurysm, aneurysm morphology, and the medical condition of the patient. The family history should be documented. Screening of other family members may be indicated if there are first-degree relatives with aneurysms. Diseases associated with aneurysms, such as coarctation of the aorta, polycystic kidney disease, fibromuscular dysplasia, and sickle cell disease, as well as cocaine use and smoking, should be elicited.

Typical admitting orders are shown in Table 363-4. Most patients are admitted to an intensive care or high-intensity observation unit. Bed rest in a dark room, limited visitors, and minimal stimulation are advocated by some practitioners but have not been proved to reduce rerupture rates. Once the aneurysm is repaired, early mobilization is encouraged as tolerated in an effort to minimize the complications associated with bed rest.⁸³ Adequate analgesia should be ensured and excessive painful stimuli avoided because pain can increase cerebral oxygen use by up to 30%.⁸⁴ Intermittent pneumatic compression devices are used routinely, as well as low-molecular-weight heparin prophylaxis, usually beginning 24 hours after aneurysm repair once a postoperative CT scan confirms no unexpected findings.

TABLE 363-4 Admitting Orders for Patients with Aneurysmal Subarachnoid Hemorrhage