SA-CME credit is offered for this article.
Subarachnoid hemorrhage (SAH) is a medical emergency in which
radiologists play an important role in diagnosis and characterization to
optimize treatment. Prompt diagnosis is crucial, and knowledge of
underlying pathologic processes and potential complications guides the
diagnostic workup. This article reviews the imaging features and
relevant clinical characteristics of SAH.
As a result of this activity, the participant should be able to:
- Describe the criteria for diagnosis of SAH, including the
appropriate role of computed tomography (CT) and magnetic resonance (MR)
- Review the various etiologies of SAH, including ruptured aneurysmal and nonaneurysmal SAH, and SAH resulting from trauma.
- Explain the complications that can occur at the time of SAH ictus, as well as in the ensuing days and weeks.
The Institute for Advanced Medical Education is accredited by the
Accreditation Council for Continuing Medical Education (ACCME) to
provide continuing medical education for physicians.
The Institute for Advanced Medical Education designates this enduring material for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
These credits qualify as SA-CME credits.
Matthew D. Alexander, MD, Department of Radiology and Biomedical
Imaging, University of California, San Francisco, San Francisco, CA.
Nerissa U. Ko, MD, Department of Neurology, University of California, San Francisco, San Francisco, CA.
Steven W. Hetts, MD, Department of Radiology and Biomedical Imaging,
University of California, San Francisco, San Francisco, CA.
Cindy Schultz, Medical Writer, Monarch Medical Writing, LLC.
Radiologists and related medical physicians
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October 31, 2017
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Subarachnoid hemorrhage (SAH) is a medical emergency in which
radiologists play an important role in diagnosis and characterization to
optimize treatment. Incidence varies geographically, with reported
rates ranging from 2 to 32 per 100,000 individuals annually.1,2
SAH can inflict considerable morbidity and mortality, and the burden
imposed on society is significant given the relatively young age of many
affected individuals compared to other neurological pathologies.3,4
Prompt diagnosis is crucial, and knowledge of underlying pathologic
processes and potential complications guides the diagnostic workup. This
article will review imaging features and relevant clinical
Diagnosis and initial imaging
Patients with SAH present with severe headaches. While most patients
with a headache will not have SAH, computed tomography (CT) is typically
used to exclude SAH in the setting of severe headache.1-3
Headaches from SAH are classically described as the most severe of one’s
life, but acute onset within seconds is a more specific feature.3 CT is widely available, has short acquisition times, and is very accurate for diagnosis of SAH.1
CT correctly demonstrates hyperdense material within the subarachnoid
space in the setting of acute SAH 95% of the time (Figure 1).2
As cerebrospinal fluid (CSF) is resorbed by arachnoid granulations,
blood contents are also resorbed, causing dilution of the SAH and
resultant diminution of the density seen on CT and reduced sensitivity
in the subacute period.2 Given the potential for false negative CTs, lumbar puncture must be utilized to exclude occult hemorrhage after a negative CT.1,2
Computed tomography at diagnosis can also provide useful information
to guide treatment and determine prognosis. The Fisher scale is widely
used to grade SAH and is based on CT findings.5 Modifications have occurred as SAH thickness and presence of IVH were found to be additive in risk for ischemia.6
The Fisher and modified Fisher scales are summarized in Table 1.
Hemorrhage may be present in other intracranial compartments.
Intraventricular hemorrhage (IVH) may be found with varying severity; as
time passes blood is more likely to be found within the ventricular
system due to its contiguity with the subarachnoid space and the mobile
nature of CSF (Figure 2).2 However, larger hemorrhage volumes
can extend into the ventricles at the time of the initial insult, and
outcomes are likely to be poor when IVH is massive (Figure 3).2,7
Such a description is important prognostically because CSF diversion
in the setting of massive IVH has demonstrated no benefit, although some
centers have reported improved outcomes when used in conjunction with
fibrinolytic therapy.2,8,9 Epidural hemorrhage (EDH) and
intraparenchymal hemorrhage (IPH) can be seen, with severities varying
according to the underlying pathology (Figure 4).2 Subdural hemorrhage (SDH) rarely occurs but can be severe when present (Figure 5).2,10,11 CT can also identify concomitant soft tissue or osseous injuries of the head and neck (Figure 5 ).1
in 7 patients with SAH will develop intraocular hemorrhage, known as
Terson’s syndrome, which can be seen on CT, MR or fundoscopy and is a
sign of poor prognosis (Figure 6).12-14
CT is utilized to assess for SAH largely because of its accuracy,
efficiency and relative cost effectiveness. However, magnetic resonance
(MR) imaging offers comparable accuracy, and familiarity with SAH
appearances on these studies is crucial.2,15 MR characteristics of blood all relate to the paramagnetic properties of hemoglobin and the products of its degradation.16-18
As intracranial hemoglobin is degraded, it undergoes a well-described
sequence from oxygenated to deoxygenated states and then conversion to
methemoglobin, which can be present both intracellularly and
extracellularly as cells are lysed.16-18 Imaging characteristics of chronic blood products are due to ferritin and hemosiderin.16-19
Most understanding of the appearance and timeframe for the degradation
of intracranial blood is based on intraparenchymal hemorrhage.17
Due to higher levels of oxygen and free water in CSF, as well as
protein with which hemorrhage may interact, SAH has unique MR
characteristics.16,17 Early SAH is best visualized on fluid
attenuation inversion recovery (FLAIR) imaging, on which it appears
hyperintense; T1-weighted imaging may also demonstrate hyperintensity at
this stage but is frequently less well seen (Figure 7).2,15-17
Over the ensuing days, SAH remains visible on FLAIR, but gradient echo
(GRE) imaging becomes the best sequence for visualizing SAH (Fig-
ure 8).20,21 Degradation of hemoglobin progresses over a
longer time period compared to other intracranial compartments, and
resorption of products by arachnoid granulations may occur before
methemoglobin or hemosiderin accumulate.17 However, any of
the above-described degradation products can be seen, with typical
signal characteristics as seen elsewhere in the brain and summarized in
Table 2.16,17 Temporal descriptors such as hyperacute, acute,
and subacute are accepted based on understanding IPH degradation. Given
differences in temporal changes, such descriptors should be avoided in
describing SAH to prevent confusion. With repeated SAH, hemosiderin may
accumulate on the surface of the brain and cranial nerves, a condition
known as superficial siderosis, which appears hypointense on T2 weighted
images and GRE (Figure 8).17,22,23
Etiologies of subarachnoid hemorrhage
Numerous processes can cause subarachnoid hemorrhage, but a ruptured aneurysm is the origin in 85% of cases.2
Given the high likelihood of an aneurysm, further investigation is
warranted upon the diagnosis of SAH, particularly given the substantial
morbidity and mortality associated with them. Ten to thirteen percent of
patients with aneurysmal SAH die before reaching the hospital, and
overall mortality approaches 50%.3,24-32 Diagnostic cerebral
angiography (DSA) has long been considered the gold standard for
detection of cerebral aneurysms. (Figure 9) While techniques have been
optimized to maximize safety of cerebral DSA, risks still remain.33-37
Additionally, these procedures can require considerable resources and
coordination that may prohibit emergent performance in some centers. For
these reasons utilization of noninvasive CT or MR angiography has
increased, with sensitivities and specificities reported up to 97% and
100%, respectively (Figure 10).38-43 CT angiography is
typically preferred to MR angiography due to the time constraints and
clinical stability requirements of the latter.25 Diagnostic accuracy declines for aneurysms measuring less than 3mm, so DSA remains the gold standard.5,32,39-46
In addition to diagnosis of an aneurysm, high quality imaging is
necessary to plan appropriate treatment, with best characterization
occurring with both two- and three-dimensional DSA.2,3,25,47-49
Characteristics important to report include size, ratio of maximal
depth to neck width, morphology, direction of aneurysm projection, any
arteries arising from the aneurysm, and presence of an apical bleb
(Figures 9, 10).50,51
Aneurysms predominantly occur at arterial branching points, with the
majority occurring in the anterior circulation. They most commonly arise
from the anterior communicating (AComm, 30%), posterior communicating
(PComm, 25%), middle cerebral (MCA, 20%), and distal internal carotid
arteries (ICA, 7%). Seven percent of aneurysms occur at the distal
basilar artery, and 3% arise from the posterior inferior cerebellar
artery (PICA).25 Prevalence of cerebral aneurysms in the general population is 2%.52 In those individuals with a diagnosed aneurysm, an additional aneurysm is present in up to 35%.53-59
In the setting of SAH and multiple aneurysms, it is important to
identify the aneurysm that has ruptured. Certain characteristics are
suggestive of rupture, including length-to-neck ratio greater than 1.6,
increased volume to surface area, aneurysm angulation, and presence of
an apical bleb.60-63 Hemorrhage itself may aid identification of culprit aneurysms, although such clues are only reliable in the acute setting.64
Lateralized SAH typically indicates MCA, ICA, or PComm aneurysms, with
degree of lateralization of SAH corresponding to degree of
lateralization of aneurysms (Figure 11).64 Midline SAH occurs with basilar or AComm aneurysms (Figure 9).64
Posterior fossa SAH is associated with PComm and posterior circulation
aneurysms, whereas anterior circulation aneurysms typically cause
supratentorial SAH.64 When parenchymal hemorrhage occurs, the
aneurysm typically points at it, with AComm aneurysms bleeding into the
orbitofrontal gyrus or gyrus rectus and MCA aneurysms bleeding into the
operculum (Figure 12).64 Aneurysms causing compression
symptoms are more likely to rupture, and symptom localization can help
identify the offending aneurysm.50 Prompt treatment of the
ruptured aneurysm is imperative. 2-4% of aneurysms will rupture again
within the first 24 hours, and there is a 1-2% risk of rupture for each
day during the first month following initial rupture if the aneurysm is
SAH frequently occurs following trauma and can have multiple
appearances. Such SAH tends to be more peripheral and localized to the
site of injury (Figure 13).64 Hemorrhage often occurs in
other intracranial compartments, and important associated soft tissue or
osseous injuries can be seen as well (Figure 5).1 Worse
outcomes are associated with poor initial clinical state, larger volumes
of hemorrhage, EDH, midline shift, or obliteration of basal cisterns.1,66,67
Numerous other pathologic processes can cause SAH, including
nonaneurysmal vascular anomalies like arteriovenous malformations and
dural arteriovenous fistulae, dissection, inflammatory vasculitides,
idiopathic vasculopathy, reversible cerebral vasoconstriction syndrome,
coagulopathy, neoplasms, and illicit drugs, among many others.2,64,68
Approximately 10% of SAH cases will yield no clear diagnosis. Within
this group is a benign entity known as nonaneurysmal perimesencephalic
SAH (NAPSAH).2 This is a diagnosis of exclusion and has well-described characteristics that are important for radiologists to know well.69-71 NAPSAH is believed to result from venous rupture in the region of the mesencephalon.72 Its clinical presentation is distinctively different from most cases of SAH from aneurysm rupture and other etiologies.2
Headaches are less sudden in onset with development over minutes rather
than seconds, consciousness is never more than minimally altered, and
seizures do not occur with NAPSAH.2,64,69,73-79 This entity
demonstrates characteristic appearance on CT with hemorrhage isolated in
the cisterns anterior to and near the midbrain, at times located solely
in the quadrigeminal plate cistern (Figure 2).2,69,77,79-81 Trace hemorrhage layering dependently in the ventricles is allowable for this diagnosis, but frank IVH excludes NAPSAH.2,26,69,77,79
All patients with suspected NAPSAH must undergo evaluation with DSA
since small aneurysms or other etiologies not visible on noninvasive
angiography may be the source of SAH.2 2-5% of patients with a perimesencephalic SAH pattern on CT will subsequently be diagnosed with an aneurysm on DSA.2,69-71
Thrombosed aneurysms or very small aneurysms can elude detection on
DSA, so repeat DSA has historically been recommended several weeks after
an initial study.2,82-84 Some have questioned the utility of
repeat DSA, although no studies have been published demonstrating the
safety of foregoing a repeat study.82-85 NAPSAH does not
carry risk of repeat hemorrhage or ischemia, so patients given this
diagnosis do not require further surveillance beyond the time frame for
potential hydrocephalus.79,86 As such, it is important to
strictly follow requirements for this diagnosis of exclusion to avoid
false negatives and unwarranted cessation of surveillance following SAH.
Morbidity from SAH can arise from several complications that can
occur at the time of ictus or in the ensuing days and weeks. The most
pressing complication can be mass effect from hemorrhage. Increased
intracranial pressure from any source causes distinctive herniation
syndromes.87,88 Subfalcine herniation involves displacement of the cingulate gyrus under the falx, with midline shift and medial displacement
of a compressed ipsilateral ventricle (Figure 14).87
Descending transtentorial herniation involves medial displacement of the
temporal lobe into the incisura and effacement and eventual
obliteration of the basal cisterns, usually starting with the
suprasellar cistern.87 Ascending transtentorial herniation
occurs with increased pressure in the posterior fossa, and herniation of
the cerebellum effaces the quadrigeminal plate cistern.87 Finally, in tonsillar herniation the cisterna magna is obliterated by cerebellar tonsils descending into the foramen magnum.87
Mass effect is more common in cases of traumatic SAH with additional
intracranial hemorrhage, although herniation may be present with
isolated SAH and may be clinically unapparent.1,89,90
Herniation is typically a surgical emergency as ischemic damage occurs
from both physical compression of parenchyma and from reduced perfusion
due to arterial compression.88 Additionally, parenchymal
hemorrhage in the brainstem can occur in the setting of herniation, a
process termed Duret hemorrhage that can be seen on CT and MR and is
associated with poor outcomes (Figure 15).91
Ischemia can also occur following SAH in the absence of mass effect.2 This often occurs in the setting of vasospasm, although this is neither necessary nor sufficient for development of ischemia.2,92 Vasospasm occurs for unclear reasons on days 3 through 12 after SAH with risk peaking on day 7.25,65,92,93 Both vasospasm and infarct are more likely to occur with diffusely distributed SAH.6,94-96
If SAH has an arterial source, larger volumes of blood predict
subsequent ischemia, as does loss of consciousness at the time of ictus.2,92,97,98
These factors can prepare clinicians to have appropriate levels of
clinical suspicion in addition to providing recommended prophylactic
treatment with nimodipine and maintenance of euvolemia.99
Measures to prevent vasospasm are important because no clearly superior
means of screening have been identified, and treatment can be difficult.3 Neurological deficits progress slowly and typically refer to multiple arterial territories.92
Transcranial Doppler is employed for vasospasm screening at many
centers, but investigational results have been mixed, and no randomized
trials have been conducted.2,93,99,100 CT angiography is
sensitive and specific for severe vasospasm in proximal arteries, but
diagnostic accuracy plummets for mild to moderate vasospasm and distal
involvement.45,101 DSA is the best modality for diagnosing
vasospasm, and catheter-directed intra-arterial administration of
calcium channel blockers and angioplasty can be performed for vasospasm
refractory to noninvasive treatments (Figure 16).45,99,102 Treatment approaches vary between centers, but angioplasty is reserved for vasospasm in proximal arteries.102
Some treatment algorithms call for angioplasty only after failure of
intra-arterial calcium channel blocker infusion, while others primarily
treat proximal vasospasm with angioplasty primarily.102
Regardless of the presence of vasospasm, evaluation for ischemia and
infarct can be performed with CT or MR perfusion studies or diffusion
weighted MR imaging.99,101,103 More specifically, CT
perfusion studies have demonstrated excellent value of mean transit time
in the prediction of vasospasm on DSA and promise from blood-brain
barrier permeability imaging as a physiologic biomarker that may guide
treatments in the future (Figure 17).104,105
Hydrocephalus can occur with SAH of any etiology; it presents in up to 45% of SAH patients.25,65,86,106-110 It can be either acute or chronic and must be diverted when symptomatic.3 Symptoms are often subtle in onset with gradual progression, most commonly manifesting as a depressed level of consciousness.77
Hydrocephalus is more likely to occur in older patients, with diffuse
distribution of SAH, when SAH measures more than 5 mm thick, and when
IVH is present.106,111,112 Ventricular size on CT and MR is
variable between individuals and has poor accuracy for diagnosis of
hydrocephalus, although changes in size between different studies on the
same patient correlate with level of consciousness (Figure 18).111,112
Periventricular edema consistent with transependymal flow is a marker
of hydrocephalus, and this is better seen on MR than CT (Figure 18).113
SAH can occur from a variety of etiologies and result in a wide range
of outcomes. Radiologists play a key role in identifying the source of
SAH and providing information for planning the most appropriate
treatment, SAH features with implications for prognosis and
complications of the hemorrhage.
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