Catastrophic Neurologic Disorders in the Emergency Department , 2nd Edition

Chapter 13. Aneurysmal Subarachnoid Hemorrhage

Contrary to common perception, many patients with aneurysmal subarachnoid hemorrhage (SAH) come to the emergency department with headache only, alert or drowsy, and minimal neurologic findings.1 The disastrous consequences for a patient with aneurysmal SAH thus may come later. Although the time spent in the emergency department is short, these patients need frequent neurologic assessment and close cardiopulmonary monitoring.

Recognition of SAH (Box 13.1) may seem straightforward in many cases, but errors may arise in the evaluation of patients with presumed normal findings on computed tomographic (CT) scans but typical onset of severe headache. The difficulties in assessment of patients with alleged SAH often can be traced back to misinterpretation of CT scans, failure to distinguish between bloody spinal fluid from needle trauma and true SAH, and, more simply but far more important, careless history-taking.

This chapter provides the necessary tools to appropriately assess these patients in the emergency department and transfer them to the intensive care unit.

Clinical Presentation

Fundamental in history-taking for a patient with acute headache is determination of the precise time of onset, quality of the headache, and whether the patient had similar earlier events. As described in Chapter 6, the headache in aneurysmal SAH is characteristic. A history of a severe “never experienced before,” “in the middle of a sentence,” “flash-like,” “explosive” acute headache is very suggestive of SAH.9 Many patients describe a brief sense of panic because they are stunned by the unexpected presentation. The often-quoted “worst headache of my life” in textbooks may not necessarily indicate acute onset or precisely define the severity of the headache (e.g., patients with chronic headaches or migraine have episodes that they commonly first classify as “the worst headache ever”). The headache usually is persistent, but resolution with the use of medication, such as nonsteroidal anti-inflammatory agents, aspirin, or even narcotics, should not be mistakenly interpreted as an argument against SAH.

When specifically asked, prior headaches may have been similar and shorter in duration. In 10%–20% of patients, an identical thunderclap headache is identified but ignored by the patient or by the consulted physician due to its rapid resolution or associated symptoms suggesting a more mundane viral infection or stress-related headache.10,11,12,13,14

Vomiting may occur several minutes into the ictus as a result of further distribution of blood throughout the subarachnoid space. It occurs in 50% of patients but is nonspecific. Profuse vomiting may override the headache and has been mistaken for a “gastric flu” by the patient or initially consulted physician. Clinical presentations have included acute paraplegia (anterior cerebral artery rupture into frontal lobes) and severe thoracic and lumbar pain caused by meningeal irritation. These presentations obviously have resulted in a delay in cranial CT scan imaging.1

Box 13.1. Aneurysmal Rupture

What causes aneurysms to rupture is puzzling. Risk factors have included recent documented enlargement (rupture of aneurysms less than 4 mm is very rare; most ruptured aneurysms are 7–8 mm, and risk of rupture increases significantly in aneurysms 10 mm or greater), hypertension, cigarette smoking, and family history of aneurysms and SAH.2,3,4 Aneurysmal rupture has been reported to have occurred during weight lifting, sexual orgasm, and brawling, events that suggest acute hypertensive stress on a thin aneurysmal wall. However, at least 50% of patients have SAH at rest.5,6

Intracranial pressure rises dramatically to at least the level of the diastolic blood pressure but may briefly increase to die level of the systolic blood pressure, causing a cerebral perfusion standstill.7 The increase in intracranial pressure decreases within 15 minutes but may persist if acute hydro-cephalus or shift from intracerebral hematoma has occurred. Rupture stops within 3–6 minutes after ejection of up to 15–20 mL/minute into the basal cistern8 (Fig. 13.1).

Clinical examination of patients with SAH includes grading of the severity of the SAH with use of the Glasgow Coma Scale and determining whether the patient has a motor deficit (World Federation of Neurological Surgeons [WFNS] scale, Table 13.1). However, stupor or coma in SAH (so-called poor-grade SAH) has many possible explanations. Impaired consciousness frequently is the result of a direct impact of the arterial jet and a massive increase in intracranial pressure, which significantly decrease cerebral perfusion pressure and thus result in global bihemispheric ischemia. Respiratory or cardiac arrest during the rupture followed by resuscitation may also result in an additional postanoxic-ischemic encephalopathy.15 Other causes of poorgrade SAH are intracranial hematoma with brain shift and brain stem compression and acute hydrocephalus.

Neck stiffness from cervical meningeal irritation may take some time to develop and is absent in coma. Nuchal rigidity can be demonstrated by failure to flex the neck in the neutral position and failure to retroflex when both shoulders are lifted. Flat-topped retinal hemorrhages (subhyaloid hemorrhages) are characteristic of aneurysmal SAH and indicate profound SAH. These hemorrhages occur when outflow in the optic nerve venous system is suddenly obstructed by the intracranial pressure wave. Visual loss may be severe, with perception of light or hand motion only, if the hemorrhage expands and ruptures into the vitreous (Terson's syndrome; see Color Fig. 13.2 in separate color insert).16,17,18

Figure 13.1 Gross pathology showing layer of sub-arachnoid hemorrhage at the basal part of the brain.

Table 13.1. World Federation of Neurological Surgeons (WFNS) Grading System for Subarachnoid Hemorrhage

WFNS Grade


Motor Deficit












Present or absent



Present or absent

GCS, Glasgow coma score (see Chapter 8 for full description).

Neuro-ophthalmologic signs can localize the site of the aneurysm. Rupture of a posterior communicating artery or carotid artery aneurysm can produce a third nerve palsy. The pupil is dilated and unreactive to light because of compression of the exteriorly located fibers that form the light reflex. However, up to 15% of posterior communicating artery aneurysms may occur with a pupilsparing third nerve palsy19 (see Chapter 3). Aneurysm of the basilar artery may produce unilateral or bilateral third or sixth nerve palsy. If the basilar artery aneurysm enlarges and progressively compresses the oculomotor nuclei of the pons, horizontal gaze paralysis, skew deviation, internuclear ophthalmoplegia, and nystagmus occur, commonly in association with long tract signs such as hemiparesis and ataxia. Occlusion of the proximal posterior cerebral artery, often encased in a giant aneurysm, may occur, causing either classic Weber's syndrome (see Chapter 15) due to mesencephalon infarction (third nerve palsy with opposite hemiparesis) or homonymous hemianopia due to occipital lobe infarction.

Hemiparesis that usually involves the face, arm, and leg in SAH should point to an intracranial hematoma. An anteriorly placed intracranial hematoma in the frontal lobe may not produce motor weakness but be associated with agitation and bizarre behavior. Many patients are confused, concoct bizarre stories, or ramble nonsensically. Korsakoff s syndrome with impaired recall and fabrications has been described in ruptured anterior communicating aneurysm. Abulia, a general sense of disinterest, and lackluster attention are also features, becoming apparent days later. Temporal lobe hematoma in the dominant hemisphere may produce aphasia, but often its associated brain shift decreases the level of consciousness and word output.

Generalized tonic-clonic seizures are accompanied by aneurysmal rupture in 10% of patients or appear during rebleeding. Nonconvulsive status epilepticus or epilepsia partialis continua is very uncommon in aneurysmal SAH. It is more common in patients with additional subdural hematoma and when delayed cerebral infarction occurs.20

Systemic manifestations, besides vomiting, may include respiratory failure and oxygen desaturation from aspiration, pulmonary edema, or obstruction of the airway by a foreign object (e.g., pieces of teeth broken during clenching of the jaws at the time of a seizure). Cardiac arrhythmias may involve the entire spectrum of supraventricular and ventricular arrhythmias. Most of the time they are associated with electrocardiographic changes, which may simulate or indicate anterior wall or subendocardial infarction. Elevated troponin I levels may occur in approximately 25% of the cases seen on the first day and indicate left, sometimes transient, ventricular dysfunction.21 Thus, with an incomplete medical history and no inquiry about acute headache, patients may be wrongly transferred to a medical intensive care unit (cardiac resuscitation and pulmonary edema), gastrointestinal service (vomiting), or coronary care unit (cardiac arrhythmias with new electrocardiographic changes).

The clinical state of the patient may suddenly change in the emergency department. We have seen several patients who soon after presentation had acute worsening of the headache and became significantly more drowsy, with a decrease of several points in the Glasgow coma score. Rebleeding could be demonstrated on CT scans in those instances. Other causes of further worsening in the emergency department are acute obstructive hydrocephalus and herniation from swelling surrounding a hematoma. These sequences of events should be recognized, particularly because re-bleeding is highly prevalent within the first 6 hours of initial rupture.

Interpretation of Laboratory Tests

Computed Tomographic Scanning

CT scanning has a very high sensitivity and specificity for SAH.22,23 The sensitivity of a noncontrast CT scan for SAH alone is 93% for patients seen within the first day, 84% for those seen on the second day, 50% after day 5, and 0 after day 10. The accumulation of subarachnoid blood on CT scans is characteristically diffuse, involving all basal cisterns, the interhemispheric and sylvian fissures, and the area along the convexity (Fig. 13.3). Additional lobar hematomas point to more certain localization of an aneurysm (Figs. 13.4, 13.5).24,25,26

Figure 13.3 Computed tomographic patterns of subarachnoid hemorrhage. Diffuse filling of basal cistern and fissures (arrows) produces a hyperdense cast.

Figure 13.4 Computed tomographic patterns of subarachnoid hemorrhage with associated hematomas indirectly localizing ruptured aneurysms. A: Sylvian fissure (middle cerebral artery). B: Frontal hematoma (anterior cerebral artery). C: Hematoma in cavum septum pellucidum. D,E: Medial temporal lobe with subdural hematoma (carotid artery). F: Corpus callosum (pericallosal artery). G–I: Thalamic hematoma with posterior cerebral artery (PI segment) aneurysm identified on magnetic resonance imaging. J,K: Premedullary hematoma with posterior inferior cerebellar artery aneurysm.


Hypodensity in both hemispheres and early loss of gray–white differentiation may develop in poorgrade SAH (Fig. 13.6). They reflect periodic acute arrest of cerebral flow caused by a very large increase in intracranial pressure at rupture. The CT scan findings are proof of early ischemic damage rather than cerebral vasospasm, which appears several days into the clinical course.

A clot in front of the brain stem with no extension beyond the suprasellar cisterns (so-called pretruncal SAH) highly predicts negative cerebral angiographic results,27,28,29 but it has been estimated that in 10% of cases a posterior circulation aneurysm (most commonly, basilar caput) can be found on cerebral angiograms. The typical CT and MRI patterns of pretruncal SAH should be recognized (Box 13.2, Figs. 13.7, 13.8).

Blood can be difficult to detect on CT scans and may be very subtle, particularly in patients seen several days after the onset. The most commonly encountered false-negative CT scans are from patients with blood in the posterior horns of the ventricles (Fig. 13.9A), sylvian fissure (Fig. 13.9B), or prepontine region, in which hemorrhage may be only a small layer on the pons (Fig. 13.9C). A tiny clot (involving a few pixels) may be localized in the interpeduncular cistern (Fig. 13.9D). It is easily missed, particularly if the CT scan slices through the posterior fossa and basal cisterns are 10 mm.

Figure 13.5 Prediction of hematoma for site of aneurysm in aneurysmal SAH. (Modified from Tokuda et al.25 By permission of Elsevier Science.) ACA, anterior cerebral artery; ACoA, anterior communicating artery; ICA, internal carotid artery; MCA, middle cerebral artery.

CT detection of aneurysms has improved with a new generation of scanners, but contrast enhancement is needed to demonstrate an aneurysm, which is visualized only if larger than 5 mm. Larger aneurysms (>1 cm in diameter) or giant aneurysms (>2.5 cm) (Fig. 13.10A,B) are disclosed on an unenhanced CT scan in most patients, although sometimes they are masked by an intracerebral hematoma. Magnetic resonance imaging (MRI) is most useful in further anatomic definition (Fig. 13.10C).

SAH may also indicate a nonaneurysmal source and has been described in central nervous system vasculitis, trauma, coagulopathy, and subacute bacterial endocarditis, but mostly with blood in sulci (Fig. 13.11).32,33 Typical CT scan features of traumatic SAH are shown in Figure 13.11C–G. It is important to consider other causes of coma and false SAH, most commonly due to anoxia and contrast for evaluation of multitrauma. False SAH in massive anoxic cerebral edema in a resuscitated patient most likely represents stagnation of flow in the dura.34,35Anoxic brain swelling may emerge within 1 day after cardiac resuscitation, and CT may show hyperintensity in the basal cistern, falx, and tentorium. CT scan signs of edema are usually very obvious (Fig. 13.12A,B). It is likely due to the combination of decreased attenuation from brain swelling, reduced cerebrospinal fluid (CSF) volume, and enlarged veins in the basal cisterns, all as a consequence of increased intracranial pressure. We have also noticed pseudosubarachnoid hemorrhage in bilateral subdural hematoma with obliteration of basal cisterns.36 In addition, contrast enhancement may significantly mimic SAH. A contrast-enhanced study may have occurred before CT scanning, and contrast material may still be visualized in patients with poor renal function or shock or both (Fig. 13.12C,D). In exceptional cases, elevated hematocrit (>20 g/dL) may cause hyperdensity if confined to the intravascular space.37 Both situations do somewhat more superficially mimic subarachnoid hemorrhage.

Figure 13.6 Development of bihemispheric ischemia (marked hypodensities, arrows) within 24 hours after subarachnoid hemorrhage.

Figure 13.7 Computed tomographic scan patterns of pretruncal nonaneurysmal subarachnoid hemorrhage in different patients. The spectrum includes complete filling of suprasellar cisterns and blood on the tentorium to more restricted clots and more subtle interpeduncular hematoma. The amount of blood is not critical in its recognition. The distribution of blood is limited and should not involve the entire lateral part of the sylvian fissure or the anterior hemisphere and ventricles.

Box 13.2. Pretruncal Nonaneurysmal Subarachnoid Hemorrhage

Pretruncal nonaneurysmal SAH (also called “perimesencephalic nonaneurysmal hemorrhage”) is a benign variant of SAH. The entity is defined by blood before or surrounding the brain stem. Blood may extend to the middle of the basal part of the sylvian fissure but not to the interhemispheric fissure, convexity, of third ventricle and frontal horns of the ventricular system. True perimesencephalic hemorrhage can also be due to trauma or SAH from a superior cerebellar artery or distal posterior cerebral artery or basilar tip aneurysm. Cerebral angiographic findings are normal, although cerebral vasospasm may occur and aneurysms may be found at far distant sites. Family members may harbor aneurysms as well. Patients do very well; rebleeding and cerebral Infarction do not occur. The underlying pathologic lesion is not known, although occasionally pontine capillary telangiectasias, focal dilatation of the basilar artery tip, anomalous veins, or a small bleb has been reported.30,31 It may represent a venous hemorrhage or intramural arterial dissection.

Magnetic Resonance Imaging

MRI is usually not sensitive for SAH.38,39 However, MRI may be able to show SAH when fluid attenuation inversion recovery (FLAIR) sequences are used. Recirculation of bloody CSF over the convexity is commonly seen as well (Fig. 13.13).40 MRI may be important in demonstrating an acute SAH in the posterior fossa, which, as mentioned previously, may be difficult to detect on CT scan because of beam-hardening artifacts.41,42 Often, in retrospect, CT scans showed a similar blood clot.43 Sometimes a small deposit of blood in the sylvian fissure not visualized on CT scans can be demonstrated on MRI.

Figure 13.8 A–C: Magnetic resonance imaging patterns of pretruncal nonaneurysmal subarachnoid hemorrhage. Blood may involve all or part of the cisterns in front of the brain stem.

Magnetic resonance angiography (MRA) is useful in demonstrating the aneurysm,44 and with three-dimensional time-of-flight MRA, aneurysms 3 mm in diameter and larger can be demonstrated (Fig. 13.14).45,46 CT angiography has become a very useful technique too. At this time, however, MRA or CT angiography is not a substitute for conventional cerebral angiography.

Cerebrospinal Fluid

As discussed in Chapter 6, the CSF should be examined for xanthochromia. If xanthochromia is found, absorption spectrophotometry could confirm oxyhemoglobin or bilirubin. This can be done hours later in stored, centrifuged CSF samples.

CSF xanthochromia is detected by spectroscopy in specimens from all patients up to 2 weeks after the onset of headache. Spectrophotometry is not commonly used in the United States and is more commonplace in the United Kingdom.47 Other tests that differentiate traumatic SAH from true SAH, such as measurements of CSF D-dimer and the sequential tube test that demonstrates the clearing of tubes tinged with blood, are all unreliable.

Figure 13.9 Subtle subarachnoid hemorrhage (false-negative computed tomographic scans). A: Dependent blood in posterior horns. B: Blood in sylvian fissure. C: Prepontine layer of blood. D: Small area of interpeduncular blood (see also Chapter 6).

First Priority in Management

Stabilization of a patient with aneurysmal SAH also includes early institution of pain medication (codeine 30–60 mg every 4 hours). Management of increased blood pressure in the emergency department is a delicate balancing act. Many of the earlier studies suggesting an increased risk of rerupture with sustained hypertension should be devalued by lack of strict criteria for the diagnosis of rebleeding. Conversely, marked reduction of postrupture hypertension may precipitate a further reduction of cerebral perfusion pressure and possibly induce more ischemia. The initial management of aneurysmal SAH is shown in Table 13.2, but there are several immediate concerns that could warrant action.

Figure 13.10 A: Computed tomographic scan showing giant middle cerebral artery aneurysm. B: Giant basilar tip aneurysm. C: Magnetic resonance imaging further delineates compression of the third ventricle causing obstructive hydrocephalus.

Acute hydrocephalus should be treated with a ventriculostomy ideally but only when clinical deterioration can be attributed to CSF obstruction. In one recent survey, almost one in four patients received ventriculostomy, demonstrating the uncertain criteria for placement.48 A prior perceived risk of inducing rebleeding was not found in a recent study.49 Preoperative ventriculostomy did not increase the risk when definitive therapy followed.

Nonetheless, the level of drainage in patients with rebleeding was significantly lower than that in patients without rebleeding (mean 2.5 cm H2O vs. 14 cm H2O). Drainage at a level of 10–15 cm H2O is preferred (see Chapter II).49

Figure 13.11 Typical nonaneurysmal locations of sub-arachnoid hemorrhage. A,B: Vasculitis. Arrows point to subarachnoid blood in a parietal sulcus and areas of segmental stenosis from vasculitis. C–G: Trauma (blood in fissure, cistern, and sulci or on tentorium).

Sudden deterioration in the emergency department often is due to rebleeding (Fig. 13.15), and emergency cerebral angiography is indicated. Placement of a platinum coil should be considered (Fig. 13.16) if the aneurysm is of sufficient size (4–10 mm). Neck size of the aneurysm should be less than 4 mm because anything larger may permit free herniation of the coil into the parent vessel, or the ratio of the largest diameter of the aneurysm to the size of its neck should be favorable; and patients should be poor surgical risks. However, the coil may become compacted after placement, increasing the risk of future rupture, in which case repeat cerebral angiography is needed in 6 weeks. A randomized study largely focused on good-grade (WFNS I or II) patients and small anterior cerebral artery and posterior communicating artery aneurysms and found equal benefit in coiling versus clipping of the aneurysm. Results in basilar artery aneurysms are still anecdotal but very promising.50,51 Two studies on poor-grade (WFNS V or Hunt and Hess grade 4 or 5) SAH patients found improved survival but at the expense of poor functional status.52,53 Whether platinum coil placement equals aneurysmal clipping in future risk of rupture remains to be investigated. Data from follow-up at 1–2 years are encouraging. However, rupture of a completely coil-occluded middle cerebral artery aneurysm after an 18-month interval has been reported.54Placement of coils in patients in poor neurologic state (WFNS III–IV) has been part of some aggressive protocols. Recurrent filling of the aneurysm occurred in 15% of 259 aneurysms treated by coil embolization. In some centers, annual rebleeding rates were 0.8% in the first year, 0.6% in the second year, and 2.4% in the third year after coil placement, with no rebleeding in 2 subsequent years.55

Figure 13.12 Pseudo–subarachnoid hemorrhage (SAH) (false-positive computed tomographic [CT] scan). A–C: Cerebral edema and pseudo-SAH. D,E:Intravascular contrast, 150 mL, from prior abdominal CT. Contrast may remain in vessels when the patient is in shock, which is often the reason for contrast CT scanning of the abdomen.

Figure 13.13 Magnetic resonance imaging with fluid attenuation inversion recovery (FLAIR) sequence: interpeduncular hemorrhage with subarachnoid blood over convexity. (From Wijdicks et al.41 By permission of the American Heart Association.)

Early endovascular management is also indicated if SAH is caused by a dissecting vertebral aneurysm (Fig. 13.17). Rebleeding is very common, and aggressive treatment with proximal (e.g. coiling) occlusion is warranted.56,57,58,59 Surgical management is indicated in a patient with an acute temporal lobe hematoma and early mass effect. Craniotomy with immediate clipping of the ruptured middle cerebral artery aneurysm is warranted, with deferral of cerebral angiography in most instances. Immediate surgical management of a frontal hematoma is rarely indicated. Neurosurgical management of most anterior cerebral artery aneurysms is more complex, requiring better definition by cerebral angiography.

Figure 13.14 Magnetic resonance angiographic view of 6 mm aneurysm of the internal carotid artery (posterior communicating artery aneurysm).

Outcome Predictors

Favorable clinical and CT scan features in aneurysmal SAH are absence of syncope at the onset, full awareness at presentation,60 lack of localizing neurologic signs, and subsequent early clipping of the aneurysm. Unfavorable signs are coma at ictus, older age, major comorbidity,61 rebleeding, large amounts of blood on CT scan, and intraventricular hemorrhage.60 The presence of intracerebral hematoma and retinal hemorrhage does not influence outcome. Basilar artery aneurysmal rupture has a worse outcome than rupture from other types of aneurysms.62 Visual loss from vitreous hemorrhage has a good outcome, but recovery may take up to 3 years (median, 9 months).18 Vitrectomy, at least in one eye, to remove the clot should be considered.

Table 13.2. Initial Management of Aneurysmal Subarachnoid Hemorrhage in the Emergency Department

Endotracheal intubation in patients with GCS <8 or hypoxemia
Maintenance fluid intake of 2 L of 0.9% NaCl
Accept mean arterial blood pressure ≤120 mm Hg and systolic blood pressure <180 mm Hg; treat with esmolol 500 µg/kg IV or labetolol 20 mg (both slow IV push, 1–2 minutes)
Nimodipine, 60 mg 6 times a day
Fosphenytoin, 20 mg/kg intravenously (only with documented seizures)
Ventriculostomy in patients with acute hydrocephalus and GCS ≤ 10
Emergency neurosurgical evacuation in patients with progressive drowsiness and temporal lobe hematoma

GCS, Glasgow coma score.

Figure 13.15 Massive subarachnoid hemorrhage with acute hydrocephalus and hemoventricle from dissecting vertebral aneurysm with fusiform dilatation. A: Computed tomographic scan. B: Cerebral angiogram.

Figure 13.16 Rebleeding in the emergency department. Computed tomographic scans at 2-hour intervals (left, right) in a patient with new headache followed by stupor.


·     Early surgical evacuation in patients with temporal lobe hematoma. Emergency coiling or clipping in any patient with CT scandocumented rebleeding and when due to a dissecting vertebral aneurysm.

·     In appropriate patients (WFNS grade I and II, small [<10 mm] anterior and posterior circulation aneurysms), placement of a platinum coil should be preferred in treatment of SAH to prevent rebleeding.63

·     Admission to a neurologic-neurosurgical intensive care unit, further observation for deterioration, and careful planning for cerebral angiography.

Figure 13.17 Successful endovascular coil placement in the patient in Figure 13.16. A: Before coil placement. B: After coil placement.


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No muscular contraction


Muscular contraction without joint involvement


Muscular contraction moves joint but not against gravity


Muscular contraction moves joint just overcoming gravity


Muscular contraction overcoming gravity and appreciable force


Muscular contraction not overcome by examiner

Source: Modified from Aids to the Examination of the Peripheral Nervous System. London: Bailltière Tindall, 2000. By permission of the Guarantors of Brain.