Hemorragia Subaracnoidea Aneurismatica

23/9/2019 Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis - UpToDate
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Aneurysmal subarachnoid hemorrhage: Clinical manifestations

and diagnosis
Authors: Robert J Singer, MD, Christopher S Ogilvy, MD, Guy Rordorf, MD
Section Editors: Jose Biller, MD, FACP, FAAN, FAHA, Jonathan A Edlow, MD, FACEP
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2019. | This topic last updated: Jul 26, 2019.
INTRODUCTION
In the United States, the proportion of stroke due to ischemia, intracerebral hemorrhage, and subarachnoid
hemorrhage (SAH) is approximately 87, 10, and 3 percent, respectively. Most nontraumatic SAHs are caused
by ruptured saccular aneurysms. This is often a devastating clinical event with substantial mortality, and high
morbidity among survivors.
The epidemiology, etiology, clinical manifestations, and diagnosis of aneurysmal SAH are reviewed here. Other
aspects are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and
pathogenesis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Unruptured
intracranial aneurysms" and "Overview of infected (mycotic) arterial aneurysm" and "Nonaneurysmal
subarachnoid hemorrhage" and "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".)
CLINICAL PRESENTATION
● Headache characteristics – The classic presentation of patients with aneurysmal SAH is a sudden-onset,
severe headache typically described as the "worst headache of my life" [1]. Every patient with this kind of
headache, often referred to as a "thunderclap headache" (see "Overview of thunderclap headache"),
should be evaluated for SAH. Headache is often an isolated finding. In neurologically intact patients with a
severe-onset headache peaking within one hour, three large sequential studies with a total of 5283 patients
found that 329 patients (6 percent) had SAH [2-5].
Importantly, the headache onset in SAH is not always noted as instantaneous, either because the patient
does not perceive it that way or because the physician does not elicit that information. In a study that
included 132 patients with SAH, the time to peak intensity was one hour in six (5 percent), and the
physician interobserver agreement for sudden onset was only moderate (kappa = 0.49) [2].
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Location is not useful since the headache can be localized or generalized.
● Associated symptoms – In addition to headache, common associated symptoms of SAH include a brief
loss of consciousness, vomiting, and neck pain or stiffness. In one series, these occurred in 9, 61, and 75
percent of patients, respectively, and each of these symptoms was more common in patients with SAH
compared with patients without SAH [3]. Meningismus and often lower back pain may not develop until
several hours after the bleed since they are caused by the breakdown of blood products within the
cerebrospinal fluid (CSF), which lead to an aseptic meningitis [6]. While many patients have an altered
level of consciousness, coma is unusual. Seizures occur during the first 24 hours in less than 10 percent of
patients but are a predictor of poor outcome [7]. SAH may also present as sudden death; as many as 22
percent of patients die before reaching the hospital [8].
● Prodromal symptoms – Some patients report a history of a sudden and severe headache (the sentinel
headache) that precedes a major SAH, occurring days to weeks prior to aneurysm rupture. Sentinel
headache may represent either a minor hemorrhage (a "warning leak") or physical changes within the
aneurysm wall (eg, acute dissection, thrombosis, or expansion), but supporting data are weak. A
systematic literature review of mainly retrospective studies through September 2002 found that 10 to 43
percent of patients with aneurysmal SAH reported a history of a sentinel or warning headache [9].
However, retrospective data may be confounded by recall bias, and a number of reports question the
existence of "warning leaks" as the cause of sentinel headaches, as reviewed separately. (See "Overview
of thunderclap headache", section on 'Sentinel headache'.)
● Clinical settings – While the onset of symptoms in the setting of physical exertion, activities associated
with a Valsalva maneuver, or emotional stress suggest SAH, aneurysmal SAH occurs most often during
nonstrenuous activity, rest, or sleep [10,11]. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology,
risk factors, and pathogenesis", section on 'Pathogenesis'.)
● Examination findings – Physical examination often shows hypertension and may show meningismus.
Terson syndrome (preretinal hemorrhages) may be seen and implies a poorer prognosis. In a systematic
review, patients with Terson syndrome had higher Hunt and Hess grades (table 1) and significantly higher
mortality than those without [12]. The preretinal hemorrhages of Terson syndrome may indicate a more
abrupt increase in intracranial pressure and must be distinguished from the more benign retinal
hemorrhages sometimes associated with SAH [13].
Nearly any neurologic sign may be present (table 2) and will depend on the location of the hemorrhage,
presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, infarction, or hematoma
[14].
Although a pupil-involving third nerve palsy is often cited as a finding of SAH, it is more common with an
expanding but unruptured aneurysm of the posterior communicating artery or superior cerebellar artery,
which is located close to where the third nerve exits the brainstem [15,16]. If present, this finding mandates
a work-up for an aneurysm including some form of cerebral angiography, but its absence does not
decrease the likelihood of SAH in patients with acute headache.
● Grading severity – A number of grading systems are used in practice to standardize the clinical
classification of patients with SAH based upon the initial neurologic examination. The grading system
proposed by Hunt and Hess (table 1) and that of the World Federation of Neurological Surgeons (WFNS)
(table 3) are among the most widely used. The WFNS system incorporates the Glasgow Coma Scale
(table 4) combined with the presence of motor deficit.
The Fisher grade is an index of vasospasm risk based upon a computed tomography (CT)-defined
hemorrhage pattern (table 5), and the Claassen grading system is a similar index of the risk of delayed
cerebral ischemia due to vasospasm (table 6). A system proposed by Ogilvy and Carter stratifies patients
based upon age, Hunt and Hess grade, Fisher grade, and aneurysm size (table 7). In addition to predicting
outcome, this scale more accurately substratifies patients for therapy.
Grading scales for SAH are discussed in greater detail separately. (See "Subarachnoid hemorrhage
grading scales".)
EVALUATION AND DIAGNOSIS
When to suspect SAH — The complaint of the sudden or rapid onset of severe headache is sufficiently
characteristic that SAH should always be considered in the evaluation. All patients with this complaint should
undergo immediate evaluation for SAH beginning with head computed tomography (CT), even those who are
alert and neurologically intact at the time of initial presentation [2,17]. Additional clues to the diagnosis of SAH,
such as preretinal hemorrhages, neck pain, or meningismus, may or may not be present. In a systematic review
and meta-analysis that included 22 diagnostic studies of emergency department patients evaluated for
spontaneous SAH, the presence of meningismus on physical examination had a positive likelihood ratio of 6.6
[18].
In neurologically intact patients, a clinical decision rule that included any of the following features had a
sensitivity of 100 percent and a specificity of 15 percent for the diagnosis of SAH [2]:
● Age ≥40 years

● Neck pain or stiffness
● Limited neck flexion on examination
● Witnessed loss of consciousness
● Onset during exertion
● Thunderclap headache (instantly peaking pain)
A subsequent validation study from the same investigators reported similar findings [3]. Limitations of these
studies include lack of independent validation and the fact that many patients did not have a head CT or lumbar
puncture and were classified as negative for SAH, including some who were lost to follow-up. Moreover,
application of this rule would have eliminated the need for evaluation in only 14 percent of patients [19].
Misdiagnosis and delayed diagnosis of SAH are common and can lead to delays in treatment and worse
outcomes [20,21]. Missed or delayed diagnosis of SAH usually results from three errors [16]:
● Failure to appreciate the spectrum of clinical presentation associated with SAH

● Failure to obtain a head CT scan or to understand its limitations in diagnosing SAH
● Failure to perform a lumbar puncture or correctly interpret the results
Perhaps the most important source of misdiagnosis results from the misconception that patients with
aneurysmal SAH always appear "sick" or have neurologic findings or altered mental status when in fact nearly
40 percent of patients are awake, alert, and neurologically intact [16]. Practitioners with the misconception may
not perform CT scans in such patients.
From a practice perspective, the vast majority of patients will be correctly diagnosed if all patients with
thunderclap headache undergo head CT (and lumbar puncture if the CT is done after six hours from headache
onset). Only an extremely small minority whose thunderclap headache is from a symptomatic but unruptured
aneurysm would be missed by this approach [22-24].
The frequency of SAH misdiagnosis may be decreasing but remains a problem. In four studies of patients
hospitalized with SAH published from 1980 to 1997, initial misdiagnosis rates ranged from 23 to 51 percent [1].
In contrast, a 2017 systematic review identified three studies published from 1996 to 2007 in emergency
department populations with a pooled misdiagnosis rate of 7 percent [25]. Included the systematic review was a
report of 482 patients admitted with SAH; initial misdiagnosis was independently associated with small SAH
volume, normal mental status at presentation, and right-sided aneurysm location [26]. Failure to obtain a head
CT scan at initial contact was the most common error, occurring in 73 percent of misdiagnosed patients. Among
patients with SAH and normal mental status at first contact (45 percent), the misdiagnosis rate rose to 20
percent and was associated with a nearly fourfold increase in mortality at 12 months as well as increased
morbidity among survivors.
Standard diagnostic approach — The first step in the diagnosis of SAH is noncontrast head CT [17]. A
lumbar puncture should be done if the head CT is negative [17]. If both tests are negative, they effectively
eliminate the diagnosis of SAH as long as both tests are performed within two weeks of the event [22,27]. In
cases presenting more than two weeks after headache onset (at such time when even xanthochromia may
have disappeared), additional testing with noninvasive CT angiography (CTA) or magnetic resonance
angiography (MRA) should be done. If diagnostic doubt remains, especially if the clinical context suggests other
causes of acute-onset severe headache, magnetic resonance imaging (MRI), catheter cerebral angiography, or
cerebral venography may be necessary (table 8) [17]. (See "Overview of thunderclap headache".)
The sensitivity of all diagnostic tests for SAH is time-dependent, measuring time from onset of the bleed. This is
due to the physiologic brisk flow of cerebrospinal fluid (CSF). Normally, there is approximately 150 mL of CSF
in a person's subarachnoid space at any point in time, but 450 to 500 mL are manufactured per 24 hours. This
is why CT scans and red blood cell (RBC) counts are very sensitive early but lose sensitivity with the passage
of time. RBCs present in the CSF undergo lysis, resulting in breakdown products such as bilirubin and
oxyhemoglobin, a process that takes time, accounting for the fact that xanthochromia is not sensitive early but
becomes increasingly sensitive with the passage of time.
Head CT scan — The cornerstone of SAH diagnosis is the noncontrast head CT scan [21,28]. The head CT
scan should be performed with thin cuts through the base of the brain to increase the sensitivity to small
amounts of blood [29].
● Sensitivity for SAH – The sensitivity of modern head CT for detecting SAH is highest in the first six hours
after SAH (nearly 100 percent when interpreted by expert reviewers), and then progressively declines over
time to approximately 58 percent at day 5 [23,28,30-32]. In the largest study of the relation of time and CT
sensitivity, the expert reviewers were attending-level general radiologists [33]. Clot is demonstrated in the
subarachnoid space in 92 percent of cases if the scan is performed within 24 hours of the bleed [28,33].
The sensitivity of head CT may be reduced with more minor bleeds. In one study, for example, a minor
SAH was not diagnosed by CT scan in 55 percent of patients; lumbar puncture was positive in all cases
[34] However, the time from SAH onset to head CT was not reported. Anemia with hematocrits of 30
percent or less and poor scan quality due to patient movement are other causes of ambiguous or false-
negative CT results. However, the most important factor that affects CT sensitivity is time from onset.
● Location of blood – Blood in SAH is generally found in the basal cisterns. Additional locations may
include the sylvian fissures, interhemispheric fissure, interpeduncular fossa, and suprasellar, ambient, and
quadrigeminal cisterns [14]. Intracerebral extension is present in 20 to 40 percent of patients and
intraventricular and subdural blood may be seen in 15 to 35 and 2 to 5 percent, respectively.
The distribution of blood on CT (performed within 72 hours after the bleed) is a poor predictor of the site of
an aneurysm except in patients with ruptured anterior cerebral artery or anterior communicating artery
aneurysms and in patients with a parenchymal hematoma [35]. However, the distribution of blood does
have implications about whether or not the cause of the SAH is aneurysmal (image 1). Blood localized to
the prepontine space suggests a nonaneurysmal perimesencephalic (also called prepontine) SAH.
Convexal SAH suggests reversible cerebral vasoconstriction syndrome (RCVS) or amyloid angiopathy,
whereas blood adjacent to bone in the frontal or middle fossae suggests traumatic SAH. (See
"Perimesencephalic nonaneurysmal subarachnoid hemorrhage".)
Lumbar puncture — Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal
head CT [21,36]. Although controversial, one possible exception involves select patients with isolated
headache, a normal examination, and a negative CT scan performed within six hours from onset of headache
and interpreted by an expert reviewer, as discussed below. (See 'Omitting lumbar puncture when CT is
negative' below.)
Lumbar puncture should include measurement of opening pressure, routine CSF analyses including cell counts,
and visual inspection for xanthochromia. The classic lumbar puncture findings of SAH are an elevated opening
pressure, an elevated RBC count that does not diminish from CSF tube 1 to tube 4, and xanthochromia. The
differential of RBC between tubes 1 and 4, and immediate centrifugation of the CSF can help differentiate
bleeding in SAH from that due to a traumatic spinal tap:
● Clearing of blood – Clearing of blood (a declining RBC count with successive collection tubes) is
purported to be a useful way of distinguishing a traumatic lumbar puncture from SAH. However, this is an
unreliable sign of a traumatic tap, since a decrease in the number of RBCs in later tubes can also occur in
SAH [37]. This method can reliably exclude SAH only if there is substantial RBC count in the first tube, and
the late or final collection tube is normal. One study found that the percent change in RBC count between
the first and last tubes was more useful than the absolute difference as a test for distinguishing traumatic
tap from SAH; the optimal test threshold based on this sample was a 63 percent reduction in the RBC
count [38]. These findings require independent confirmation. If the CSF is visibly bloody, one practical
method to increase the likelihood that the last tube of CSF will contain close to zero RBCs is to discard
CSF between the first and last tubes with a goal of visual clearing [17]. Given the brisk flow of CSF
(approximately 20 to 25 cc is produced every hour), even discarding 10 cc will take only 30 minutes for the
body to replace [39].
● RBC count – The greater the RBC count in the last tube, the more likely SAH is the cause. In one study
examining CSF results in 1739 patients with acute nontraumatic headache, fewer than 2000 RBC per
microL in addition to no xanthochromia excluded aneurysmal SAH with a sensitivity of 100 percent [40]. In
a retrospective report of over 4400 adults who had lumbar puncture in the emergency department, finding
fewer than 100 RBC per microL in the CSF greatly decreased the likelihood of a SAH [38]. These results
require independent prospective confirmation.
● Xanthochromia – Xanthochromia (pink or yellow tint) represents hemoglobin degradation products. An

otherwise unexplained xanthochromic supernatant in CSF is highly suggestive of SAH. Xanthochromia
may be visually detected by comparing a vial of CSF with a vial of plain water held side by side against a
white background in bright light [41]. The presence of xanthochromia indicates that blood has been in the
CSF for at least two hours. Therefore, if the CSF is analyzed quickly after a traumatic lumbar puncture or
SAH, there will not be xanthochromia; the absence of xanthochromia cannot be used as evidence of a
traumatic tap if a lumbar puncture is performed in a SAH of less than two hours duration. Over the course
of the ensuing hours, more patients will have xanthochromia, and by 12 hours post SAH, 100 percent of
patients will have xanthochromia, even when measured visually [42]. Xanthochromia lasts for two weeks or
more [43,44].
One retrospective study identified 117 adults with no known history of aneurysm or previous SAH who
presented to the emergency room with thunderclap headache [45]. All had a negative noncontrast head CT
followed by lumbar puncture. Xanthochromic CSF was found by visual inspection in 18 patients (15
percent). Those patients then had four-vessel catheter angiography, which detected a ruptured cerebral
aneurysm in 13 (72 percent). One patient with no xanthochromia had an elevated RBC count (≥20,000
RBC/microL) in four successive collection tubes and a ruptured aneurysm by angiography. In this series,
xanthochromia for the detection of cerebral aneurysms had a sensitivity and specificity of 93 and 95
percent.
Other conditions that can produce xanthochromia include increased CSF concentrations of protein (150
mg/dL), systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL), and traumatic lumbar puncture with
more than 100,000 RBCs/microL. (See "Cerebrospinal fluid: Physiology and utility of an examination in
disease states", section on 'Xanthochromia'.)
● Spectrophotometry — Spectrophotometry detects blood breakdown products as they progress from

oxyhemoglobin to methemoglobin and finally to bilirubin [43,46,47]. Bilirubin concentration peaks about 48
hours after SAH onset, and it may last as long as four weeks after major SAH [48]. While CSF
spectrophotometry is more sensitive than visual inspection for xanthochromia, it is not universally
recommended. As a practical matter, spectrophotometry of CSF is rarely available in North American
hospitals [49].
The sample of CSF to be tested by spectrophotometry should be the one that contains the least amount of
blood staining. It should be protected from light and sent immediately to the laboratory for analysis [43,48].
Spectrophotometry for detection of bilirubin is highly sensitive (>95 percent) when lumbar puncture is done
at least 12 hours after SAH [44]. Although xanthochromia is generally identified by visual inspection,
laboratory confirmation with CSF spectrophotometry is more sensitive and is recommended by some
experts, if available [43,48,50-52]. In one study, 11 analysts compared xanthochromic CSF samples using
visual and spectrophotometric analysis [51]. The spectrophotometric detection of bilirubin was significantly
higher than visual detection in conditions where CSF samples were contaminated by presence of
hemolyzed blood, or when CSF samples contained low levels of bilirubin. However, in a study comparing
visual inspection with spectrophotometry, CSF that was considered colorless by visual inspection was not
compatible with a diagnosis of SAH [53].
Despite a higher sensitivity than visual inspection for the detection of xanthochromia, CSF
spectrophotometry has only a low to moderate specificity for the diagnosis of SAH [54].
Alternative approaches — One alternative approach to the diagnosis of aneurysmal SAH is to follow a
negative head CT with CTA rather than lumbar puncture. Another involves omitting the lumbar puncture for
select patients who have a negative head CT performed within six hours of headache onset. The utility of MRI
in place of head CT for detecting SAH is supported by limited data.
CT followed by CTA — As CTA has become more available, some physicians have advocated the use of
CTA (rather than lumbar puncture) after a negative head CT for the diagnosis of aneurysmal SAH [55,56]. Chief
among the various potential downstream implications is finding an asymptomatic aneurysm, which occurs in
approximately 3 percent of the population [57,58]. Two cost-effectiveness studies concluded that the standard
approach with CT followed by lumbar puncture approach is equivalent or better than a CT/CTA approach
[59,60]. Therefore, we recommend the standard approach using CT, followed by lumbar puncture if CT is
negative, reserving CTA for patients with a positive noncontrast CT or CSF analysis.
Omitting lumbar puncture when CT is negative — Because the consequences of missing SAH are
potentially dire, we recommend a lumbar puncture when the CT scan is negative for blood, as do most
guidelines [36,56]. In contrast, some experts have argued that the sensitivity of CT when performed within six
hours of the onset of symptoms is sufficiently sensitive (100 percent) to make a follow-up lumbar puncture
unnecessary [33,61,62]. A meta-analysis published in 2016 found that less than 1.5 in 1000 patients with SAH
would be missed if no lumbar puncture was done in patients who met the following conditions: a normal head
CT using a modern scanner within six hours of headache onset (with a clear time of onset); CT interpretation by
an experienced radiologist; a normal neurologic examination; and presentation with an isolated thunderclap
headache [23]. There are important caveats (table 9) that suggest that this approach must be applied carefully
and cautiously [17]. One is that such studies are performed in centers where CT scans are generally interpreted
by expert reviewers (eg, at least the level of an attending radiologist). Another is that the sensitivity of CT may
be reduced when symptoms are atypical, such as isolated neck pain.
Other experts have questioned whether lumbar puncture is ever needed after a negative head CT in the
diagnosis of SAH, based upon both Bayesian analysis (the post-test likelihood after a negative CT is sufficiently
low to rule out SAH) and empiric data [18,63,64]. However, in a prospective study of patients with acute severe
headache, the diagnosis of SAH was missed by CT in 17 of 119 patients (14 percent) with SAH who had initial
CT performed more than six hours after the onset of headache [33]. We therefore continue to recommend
lumbar puncture after a negative CT, while other experts advise omitting the lumbar puncture for select patients
who meet all the criteria outlined in the table (table 9).
Brain MRI — Limited data suggest that proton density and fluid-attenuated inversion recovery (FLAIR)
sequences on brain MRI may be as sensitive as head CT for the acute detection of SAH [65]. In addition,
FLAIR and T2* sequences on MRI have a high sensitivity in patients with a subacute presentation of SAH (ie, 4
to 14 days from the onset of hemorrhage) [66]. However, due to logistical issues, MRI is seldom obtained as the
first study for suspected SAH [14].
As with a negative CT scan, lumbar puncture should follow a negative MRI if a patient is suspected to have
SAH [36,67].
DIFFERENTIAL DIAGNOSIS
Aneurysmal SAH is always the primary consideration when a patient presents with an abrupt onset headache.
However, a number of other conditions listed in the table can cause a similar presentation (table 8). These are
discussed in detail separately. (See "Overview of thunderclap headache".)
IDENTIFYING THE SOURCE OF BLEEDING
Choosing initial angiography — Once a diagnosis of SAH has been made, the etiology of the hemorrhage
must be determined with angiographic studies. We prefer conventional digital subtraction angiography (DSA)
because it has the best resolution for the detection of aneurysms and can facilitate endovascular treatment as
part of the same procedure. However, many centers use noninvasive imaging with computed tomography
angiography (CTA) or magnetic resonance angiography (MRA) as the initial study, reserving DSA for cases
when noninvasive imaging does not identify the cause of the SAH.
A major advantage of CTA over DSA is the speed and ease by which it can be obtained, often immediately after
the diagnosis of SAH is made by head computed tomography (CT) when the patient is still in the scanner. CTA
is increasingly used as an alternative to DSA in many patients with SAH, thereby avoiding the need for DSA in
a substantial number of cases [68,69], and is particularly useful in the acute setting in a rapidly declining patient
who needs emergent craniotomy for hematoma evacuation. Furthermore, CTA offers a more practical approach
to acute diagnosis than MRA, given the constraints of acute patient management.
Digital subtraction angiography — Of the available tests, DSA is believed to have the highest resolution to
detect intracranial aneurysms and define their anatomic features and remains the gold standard test for this
indication [36,70]. Most ruptured aneurysms can be readily identified using standard cross-sectional imaging
techniques coupled with DSA that includes injections of bilateral vertebral and internal carotid arteries, as well
as the external carotid circulation and deep cervical branches, which may supply a cryptic dural arteriovenous
fistula. Angiographic demonstration of key branch points, including the proximal posterior circulation, is
essential to definitively rule out aneurysm.
As an increasing number of aneurysms are treated endovascularly, another advantage of DSA is the ability to
both diagnose and then definitively treat the aneurysm in the same sitting. (See "Treatment of cerebral
aneurysms".)
The morbidity of DSA in patients with SAH is relatively low. In a meta-analysis of three prospective studies, for
example, the combined risk of permanent and transient neurologic complications was significantly lower in
patients with SAH compared with those with a transient ischemic attack (TIA) or stroke (1.8 versus 3.7 percent)
[71].
CT and MR angiography — CTA and MRA are noninvasive tests that are useful for screening and
presurgical planning. Both CTA and MRA can identify aneurysms 3 to 5 mm or larger with a high degree of
sensitivity [72], but they do not achieve the resolution of conventional angiography (ie, DSA). The sensitivity of
CTA for the detection of ruptured aneurysms, using DSA as the gold standard, is 83 to 98 percent [73-79].
Small aneurysms, in particular may not be reliably identified. Although small aneurysms rupture less frequently
than large aneurysms [80], they are more common, and rupture of small aneurysms (approximately 5 mm or
less) accounts for nearly one-half of SAH cases [81-83]. Therefore, DSA should be performed if CTA does not
reveal an aneurysm in a patient with SAH [36].
As technology improves, the sensitivity and specificity of noninvasive imaging is also likely to improve [84]. A
2011 meta-analysis of CTA diagnosis of intracranial aneurysms found that, compared with single-detector CTA,
use of multidetector CTA was associated with an overall improved sensitivity and specificity for aneurysm
detection (both >97 percent) as well as improved detection of smaller aneurysms ≤4 mm in diameter [85].
Another systematic review and meta-analysis restricted to patients with SAH had similar findings [86].
While a "spot sign" (ie, contrast extravasation) on CTA is associated with risk of hemorrhage expansion or
rebleeding in patients with intracerebral hemorrhage, this is not the case for SAH [87,88]. It is likely that this
sign, while appearing similar, actually reflects different processes when observed in SAH versus intracerebral
hemorrhage.
Patients with negative angiography
Repeat angiography — No angiographic cause of SAH is evident in 14 to 22 percent of cases. It is critical

to repeat the angiogram in 4 to 14 days if the initial angiogram is negative. The recommended follow-up test in
this setting is usually DSA. Up to 24 percent of all SAH patients with initial negative angiography have an
aneurysm found on repeat angiography [89-93]. This may increase to as much as 49 percent if patients with
perimesencephalic SAH and patients with normal CT scans are excluded [90].
Reasons for an initial false-negative angiogram include technical or reading errors, small aneurysm size, and
obscuration of the aneurysm because of vasospasm, hematoma, or thrombosis within the aneurysm
[89,90,94,95]. A third angiogram (DSA) at a period of two to three months is advocated by some, but is
probably not necessary if the initial two studies are felt to be well-performed and expertly reviewed (see
"Nonaneurysmal subarachnoid hemorrhage"). However, patients with SAH and a second negative angiogram
should have a brain and spine MRI to look for possible vascular malformation of the brain or spinal cord [14].
Nonaneurysmal SAH — An estimated 15 to 20 percent of SAH cases are nonaneurysmal. The causes of
nonaneurysmal SAH are potentially diverse, and include perimesencephalic hemorrhage, vascular
malformations, intracranial arterial dissection, and a variety of other etiologies. The mechanism of bleeding in
these cases is often not identified. (See "Nonaneurysmal subarachnoid hemorrhage".)
Some patients with an initially negative angiogram have blood in the cisterns around the midbrain on head CT,
which reflects a perimesencephalic pattern of hemorrhage (image 2). Perimesencephalic hemorrhage accounts
for about 10 percent of all cases of SAH and a majority of patients with nonaneurysmal SAH. Most patients with
perimesencephalic hemorrhage do not have an aneurysm or other defined etiology. The need for repeat
angiography in patients with perimesencephalic hemorrhage is discussed in detail separately. (See
"Perimesencephalic nonaneurysmal subarachnoid hemorrhage", section on 'Repeated testing'.)
COMPLICATIONS
A variety of early complications can occur with SAH, including rebleeding, hydrocephalus, cerebral edema,
vasospasm and delayed cerebral ischemia, seizures, hyponatremia, cardiopulmonary abnormalities, and
neuroendocrine dysfunction. These are discussed in detail separately. (See "Aneurysmal subarachnoid
hemorrhage: Treatment and prognosis", section on 'Early complications'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world
are provided separately. (See "Society guideline links: Stroke in adults".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics
patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the
four or five key questions a patient might have about a given condition. These articles are best for patients who
want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education
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pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade
reading level and are best for patients who want in-depth information and are comfortable with some medical
jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Hemorrhagic stroke (The Basics)" and "Patient education: Brain
aneurysm (The Basics)" and "Patient education: Subarachnoid hemorrhage (The Basics)")
● Beyond the Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond the Basics)"
and "Patient education: Hemorrhagic stroke treatment (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
● The overwhelming majority of patients with aneurysmal subarachnoid hemorrhage (SAH) present with a
sudden onset severe headache which may be associated with brief loss of consciousness, seizures,
nausea or vomiting, or meningismus. (See 'Clinical presentation' above.)
● Sudden onset of headache, regardless of severity or prior headache history, should raise the clinical
suspicion for SAH and compel a diagnostic evaluation. (See 'Evaluation and diagnosis' above.)
• Noncontrast head computed tomography (CT) reveals the diagnosis in more than 90 percent of cases
if performed within 24 hours of bleeding onset. (See 'Head CT scan' above.)
• Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT, with the
disputed exception of select patients with isolated headache and normal examination presenting early
and scanned within six hours of headache onset. The classic findings are an elevated opening
pressure, an elevated red blood cell count that does not diminish from cerebrospinal fluid (CSF) tube 1
to tube 4, and xanthochromia. Immediate centrifugation of the CSF can help differentiate bleeding in
SAH from that due to a traumatic spinal tap. (See 'Lumbar puncture' above.)
● Once a diagnosis of SAH has been made, the etiology of the hemorrhage must be determined with
vascular imaging. Of the available tests, digital subtraction angiography (DSA) is believed to have the
highest resolution to detect intracranial aneurysms and define their anatomic features and remains the gold
standard test for this but CT angiography is being increasingly used as a first-line test. (See 'Identifying the
source of bleeding' above.)
● Repeat angiography is necessary if the initial study is negative, unless the pattern of hemorrhage is
perimesencephalic. Additional testing is required for SAH that is nonaneurysmal. (See 'Patients with
negative angiography' above.)
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Topic 1130 Version 18.0
GRAPHICS
Hunt and Hess grading system for patients with subarachnoid hemorrhage
Grade Neurologic status
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
3 Drowsy or confused, mild focal neurologic deficit
4 Stuporous, moderate or severe hemiparesis
5 Coma, decerebrate posturing
Based upon initial neurologic examination.
Adapted from: Hunt W, Hess R. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968;
28:14.
Graphic 69179 Version 4.0
Focal physical findings in patients with subarachnoid hemorrhage
Findings Likely cause
Third nerve palsy Usually posterior communicating aneurysm; also posterior

cerebral artery and superior cerebellar artery aneurysms
Sixth nerve palsy Elevated intracranial pressure (false localizing sign)
Combination of hemiparesis and aphasia or visuospatial neglect Middle cerebral artery aneurysm, thick subarachnoid clots, or
parenchymal hematomas
Bilateral leg weakness and abulia Anterior communicating artery aneurysm
Ophthalmoplegia Internal carotid artery aneurysm impinging upon the cavernous

sinus
Unilateral visual loss or bitemporal hemianopia Internal carotid artery aneurysm compressing optic nerve or
optic chiasm
Impaired level of consciousness and impaired upward gaze Pressure on the dorsal midbrain due to hydrocephalus
Brainstem signs Brainstem compression by basilar artery aneurysm
Neck stiffness Meningeal irritation by the presence of subarachnoid blood
Retinal and subhyaloid hemorrhages Sudden increase of intracranial pressure
Preretinal hemorrhages (Terson syndrome) Vitreous hemorrhage due to severe elevations of intracranial
pressure
From: Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2015; 21:1263. DOI:
10.1212/CON.0000000000000217. Copyright © 2015 American Academy of Neurology. Reproduced with permission from Wolters Kluwer
Health. Unauthorized reproduction of this material is prohibited.
World Federation of Neurological Surgeons subarachnoid hemorrhage grading scale
Grade GCS score Motor deficit
1 15 Absent
2 13 to 14 Absent
3 13 to 14 Present
4 7 to 12 Present or absent
5 3 to 6 Present or absent
GCS: Glasgow Coma Scale.
Data from: Report of World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. J
Neurosurg 1988; 68:985.
Glasgow Coma Scale (GCS)
Score
Eye opening
Spontaneous 4
Response to verbal command 3
Response to pain 2
No eye opening 1
Best verbal response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No verbal response 1
Best motor response
Obeys commands 6
Localizing response to pain 5
Withdrawal response to pain 4
Flexion to pain 3
Extension to pain 2
No motor response 1
Total
The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed of three parameters: best eye response
(E), best verbal response (V), and best motor response (M). The components of the GCS should be recorded individually; for
example, E2V3M4 results in a GCS score of 9. A score of 13 or higher correlates with mild brain injury, a score of 9 to 12
correlates with moderate injury, and a score of 8 or less represents severe brain injury.
Fisher grade of cerebral vasospasm risk in subarachnoid hemorrhage [1]
Group Appearance of blood on head CT scan
1 No blood detected
2 Diffuse deposition or thin layer with all vertical layers (in interhemispheric fissure, insular cistern, ambient cistern) less
than 1 mm thick
3 Localized clot and/or vertical layers 1 mm or more in thickness
4 Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
CT: computed tomography.
Reference:
1. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT scanning.
Neurosurgery 1980; 6:1.
Claassen subarachnoid hemorrhage CT rating scale
Grade Head CT criteria
1 No SAH or IVH
2 Minimal SAH and no IVH
3 Minimal SAH with bilateral IVH
4 Thick SAH (completely filling one or more cistern or fissure) without bilateral IVH
5 Thick SAH (completely filling one or more cistern or fissure) with bilateral IVH
CT: computed tomography; SAH: subarachnoid hemorrhage; IVH: intraventricular hemorrhage.
From: Claassen J, Bernardini GL, Kreiter K, et al. Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after
subarachnoid hemorrhage: the Fisher scale revisited. Stroke 2001; 32:2012.
Ogilvy and Carter grading system to predict outcome for surgical management of
intracranial aneurysms
Criteria Points
Age 50 or less 0
Age greater than 50 1
Hunt and Hess grade 0 to 3 (no coma) 0
Hunt and Hess grade 4 and 5 (in coma) 1
Fisher scale score 0 to 2 0
Fisher scale score 3 and 4 1
Aneurysm size 10 mm or less 0
Aneurysm size greater than 10 mm 1
Giant posterior circulation aneurysm size 25 mm or more 1
The total score ranges from 0 to 5, corresponding to grades 0 to 5
Adapted from: Ogilvy CS, Carter BS. A proposed comprehensive grading system to predict outcome for surgical management of
intracranial aneurysms. Neurosurgery 1998; 42:959.
Etiologies of thunderclap headache
Most common causes of thunderclap headache:

Subarachnoid hemorrhage
Reversible cerebral vasoconstriction syndromes (RCVS)
Conditions that less commonly cause thunderclap headache:

Cerebral infection (eg, meningitis, acute complicated sinusitis)
Cerebral venous thrombosis
Cervical artery dissection
Spontaneous intracranial hypotension
Acute hypertensive crisis
Posterior reversible leukoencephalopathy syndrome (PRES)
Intracerebral hemorrhage
Ischemic stroke
Conditions that uncommonly or rarely cause thunderclap headache:

Pituitary apoplexy
Colloid cyst of the third ventricle
Acute myocardial infarction
Aortic arch dissection
Aqueductal stenosis
Brain tumor
Giant cell arteritis
Pheochromocytoma
Pneumocephalus
Retroclival hematoma
Spinal epidural hematoma
Varicella zoster virus vasculopathy
Vogt-Koyanagi-Harada syndrome
Disputed causes of thunderclap headache:

Sentinel headache (unruptured intracranial aneurysm)*
Primary thunderclap headache ¶
* Sentinel headache due to an unruptured intracranial aneurysm is a possible cause of thunderclap headache, but supporting data are
weak.
¶ There is controversy as to whether thunderclap headache can occur as a benign and potentially recurrent headache disorder in the
absence of underlying organic intracranial pathology.
Various radiologic patterns of subarachnoid hemorrhage on noncontrast computed tomography

(CT) of the head
(A) Obvious large SAH: hyperdense blood in all the basal cisterns, with some dilatation of the temporal horns of the lateral
ventricles, suggesting early hydrocephalus.
(B) More subtle, smaller SAH: small hyperdense collection of blood in the basal cistern adjacent to the left pons and suprasellar
cistern (short solid arrow).
(C) Perimesencephalic SAH: the long solid arrows indicate a perimesencephalic (sometimes called a pretruncal) SAH. These
hemorrhages represent approximately 10% of nontraumatic SAHs. They are thought to be caused by venous bleeding, will have a
negative CTA result, and usually have an excellent outcome. However, the radiographic pattern is also observed with posterior
circulation aneurysms, so all of these patients require neurosurgical consultation and vascular imaging.
(D) Convexal SAH: the arrowheads indicate a high convexal SAH. This pattern is observed in two groups of patients. In younger
patients, it is usually due to RCVS, but in older ones, it often indicates amyloid angiopathy. In a patient presenting with a severe rapid-
onset headache, RCVS would be the likely diagnosis.
(E) Traumatic SAH: the history usually suggests a traumatic SAH (the most common cause). However, if this pattern (dashed arrows
indicate small amounts of SAH abutting bone, often in the anterior frontal and temporal bones) is observed in a patient without a clear
history of trauma, the likely cause is a traumatic SAH.
SAH: subarachnoid hemorrhage; CTA: computed tomography angiography; RCVS: reversible cerebral vasoconstriction syndrome.
Reproduced from: Edlow JA. Managing Patients With Nontraumatic, Severe, Rapid-Onset Headache. Ann Emerg Med 2018; 71:400. Illustration
used with the permission of Elsevier Inc. All rights reserved.
Considerations for omitting the lumbar puncture in patients who have a negative CT within
six hours of headache onset in the evaluation for subarachnoid hemorrhage
Patient factors
The time of onset of the headache is clearly defined.
The CT is performed within six hours of headache onset.
The presentation is an isolated severe rapid-onset headache (no primary neck pain, seizure, or syncope at onset, or other
atypical presentations).
There is no meningismus and the neurologic examination result is normal.
Radiologic factors
The CT scanner is a modern, third-generation or newer machine with thin cuts through the brain.
The CT is technically adequate, without significant motion artifact.
The hematocrit level is >30%.
The physician interpreting the scan is an attending-level radiologist (or has equivalent experience in reading brain CT scans).
Radiologists should specifically examine the brain CTs for subtle hydrocephalus, small amounts of blood in the dependent
portions of the ventricles, and small amounts of isodense or hyperdense material in the basal cisterns.
Communication factors
The clinician should communicate the specific concern to the radiologist (eg, "severe acute headache; rule out SAH").
After a negative CT result, the clinician should communicate the posttest risk of SAH that persists (1 to 2 per 1000).
CT: computed tomography; SAH: subarachnoid hemorrhage.
Reproduced from: Edlow JA. Managing Patients With Nontraumatic, Severe, Rapid-Onset Headache. Ann Emerg Med 2018; 71:400. Table
used with the permission of Elsevier Inc. All rights reserved.
Perimesencephalic subarachnoid hemorrhage
CT scan demonstrates the typical findings of a nonaneurysmal

perimesencephalic subarachnoid hemorrhage. Note the predominance of
hemorrhage in the interpeduncular fossa (arrow).
CT: computed tomography.
Courtesy of Guy Rordorf, MD.
Contributor Disclosures
Robert J Singer, MD Nothing to disclose Christopher S Ogilvy, MD Consultant/Advisory Boards: Medtronic [Data Safety
Monitoring Board]. Guy Rordorf, MD Nothing to disclose Jose Biller, MD, FACP, FAAN, FAHA Nothing to
disclose Jonathan A Edlow, MD, FACEP Nothing to disclose John F Dashe, MD, PhD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by
vetting through a multi-level review process, and through requirements for references to be provided to support the content.
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Hemorragia Subaracnoidea Aneurismatica

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23/9/2019 Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis - UpToDate

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Aneurysmal subarachnoid hemorrhage: Clinical manifestations

Location is not useful since the headache can be localized or generalized.

EVALUATION AND DIAGNOSIS

● Age ≥40 years

● Failure to appreciate the spectrum of clinical presentation associated with SAH

● Xanthochromia – Xanthochromia (pink or yellow tint) represents hemoglobin degradation products. An

● Spectrophotometry — Spectrophotometry detects blood breakdown products as they progress from

IDENTIFYING THE SOURCE OF BLEEDING

Patients with negative angiography

Repeat angiography — No angiographic cause of SAH is evident in 14 to 22 percent of cases. It is critical

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

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6. Schievink WI. Intracranial aneurysms. N Engl J Med 1997; 336:28.

42. Walton J. Subarachnoid Hemorrhage, E & S Livingstone, Edinburgh 1956.

48. Cruickshank A, Beetham R, Holbrook I, et al. Spectrophotometry of cerebrospinal fluid in suspected

85. Menke J, Larsen J, Kallenberg K. Diagnosing cerebral aneurysms by computed tomographic

93. du Mesnil de Rochemont R, Heindel W, Wesselmann C, et al. Nontraumatic subarachnoid hemorrhage:

Topic 1130 Version 18.0

Grade Neurologic status

1 Asymptomatic or mild headache and slight nuchal rigidity

3 Drowsy or confused, mild focal neurologic deficit

4 Stuporous, moderate or severe hemiparesis

5 Coma, decerebrate posturing

Based upon initial neurologic examination.

Graphic 69179 Version 4.0

Focal physical findings in patients with subarachnoid hemorrhage

Findings Likely cause

Third nerve palsy Usually posterior communicating aneurysm; also posterior

Sixth nerve palsy Elevated intracranial pressure (false localizing sign)

Bilateral leg weakness and abulia Anterior communicating artery aneurysm

Ophthalmoplegia Internal carotid artery aneurysm impinging upon the cavernous

Brainstem signs Brainstem compression by basilar artery aneurysm

Neck stiffness Meningeal irritation by the presence of subarachnoid blood

Retinal and subhyaloid hemorrhages Sudden increase of intracranial pressure

Graphic 121321 Version 1.0

World Federation of Neurological Surgeons subarachnoid hemorrhage grading scale

Grade GCS score Motor deficit

GCS: Glasgow Coma Scale.

Graphic 65468 Version 2.0

Glasgow Coma Scale (GCS)

Response to verbal command 3

Best verbal response

Best motor response

Localizing response to pain 5

Withdrawal response to pain 4

Graphic 81854 Version 7.0

Fisher grade of cerebral vasospasm risk in subarachnoid hemorrhage [1]

Group Appearance of blood on head CT scan

3 Localized clot and/or vertical layers 1 mm or more in thickness

4 Intracerebral or intraventricular clot with diffuse or no subarachnoid blood

CT: computed tomography.

Graphic 81122 Version 3.0

Claassen subarachnoid hemorrhage CT rating scale

Grade Head CT criteria

2 Minimal SAH and no IVH