Nonaneurysmal subarachnoid hemorrhage

Authors

Farhan Siddiq, MD

David G Brock, MD, CIP Section Editor

Jose Biller, MD, FACP, FAAN, FAHA Deputy Editor

Janet L Wilterdink, MD

Last literature review version 16.2: May 2008 | This Topic Last Updated: June 13, 2008 (More)

INTRODUCTION — Subarachnoid hemorrhage (SAH) refers to bleeding within the subarachnoid

space, which lies between the arachnoid and pia mater and is normally filled with

cerebrospinal fluid. Most cases of subarachnoid hemorrhage are caused by rupture of an

intracranial aneurysm. Approximately 15 to 20 percent of patients presenting with SAH do not

have a vascular lesion on initial four-vessel cerebral angiography [1,2] . The causes of these

nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these

cases is often not identified.

This topic discusses nonaneurysmal subarachnoid hemorrhage. Aneurysmal SAH and

perimesencephalic SAH are discussed separately. (See "Etiology, clinical manifestations, and

diagnosis of aneurysmal subarachnoid hemorrhage" and see "Treatment of aneurysmal

subarachnoid hemorrhage" and see "Perimesencephalic nonaneurysmal subarachnoid

hemorrhage").

ETIOLOGIES

Perimesencephalic nonaneurysmal subarachnoid hemorrhage — A subtype of NASAH, so-

called perimesencephalic nonaneurysmal SAH is characterized by a specific pattern of localized

blood on computed tomography (CT), normal cerebral angiography, and a benign course that

distinguishes these patients not only from aneurysmal SAH, but also from other patients with

nonaneurysmal SAH [2-5] . In some case series, this makes up the majority, up to two-thirds, of

patients with NASAH [1] .

The CT findings that define perimesencephalic NASAH (PM-NASAH) include blood isolated to

the perimesencephalic cisterns anterior to the brainstem; there may be extension into the

ambient cisterns or basal parts of the sylvian fissures, but not into the lateral sylvian fissure,

anterior interhemispheric fissure, or lateral ventricles [1,5] .

Perimesencephalic nonaneurysmal subarachnoid hemorrhage is discussed separately. (See

"Perimesencephalic nonaneurysmal subarachnoid hemorrhage").

Occult aneurysm — Up to 24 percent of all SAH patients with initial negative angiography have

an aneurysm found on repeat angiography [6-10] . This may increase to as much as 49 percent

if patients with perimesencephalic SAH and patients with normal CT scans are excluded [7] .

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 [1,2,6,7] .

Even two negative angiograms do not exclude an aneurysmal source of bleeding. In some

cases, another angiogram or surgical exploration have revealed an aneurysmal bleeding

source, even after two negative angiograms [2,6,11,12] . Other case series suggest that the

similarities in rebleeding and other complication rates among patients with aneurysmal SAH

and patients with SAH and no identified bleeding source suggest that an occult aneurysm is

likely in these patients as well [2,4,7,13,14] .

Vascular malformations — Less than 10 percent of SAH are caused by vascular malformations

[6,13] . These can be intracranial or spinal in location.

Intracranial — Intracranial vascular malformations include both acquired and congenital

lesions; the latter are more common. These typically exist within the brain parenchyma and

produce intracerebral hemorrhage. However, depending on the location of the vascular lesion,

bleeding can be primarily or exclusively in the subarachnoid space [6,8,15-17] .

Rebleeding occurs in more than half of patients. Rebleeding from arteriovenous malformations

is less likely to be acute than with aneurysmal SAH; however, dural arteriovenous fistulae,

particularly those with cortical venous drainage, appear to be at higher risk for early

rebleeding [16,18] .

Most brain vascular malformations that produce SAH are either arteriovenous malformations

or dural arteriovenous fistulae. These are usually visualized on cerebral angiography [10,15,19]

. Catheterization of the external carotid artery may be required to image intracranial dural

arteriovenous malformations. Angiographically occult vascular malformations such as some

cavernous malformations, venous angiomas, and capillary telangiectasias are visualized on

brain MRI, but are less likely to be a source of SAH.

Vascular malformations associated with bleeding are usually managed surgically and/or with

endovascular interventions [20] . (See "Brain arteriovenous malformations" and see "Vascular

malformations of the central nervous system").

Spinal — Spinal vascular malformations can also be a source of NASAH. Up to 10 percent of

spinal vascular malformations present with SAH [8,21,22] . Dural arteriovenous fistulae are the

most common type of spinal vascular malformation [23] . Those that cause SAH are usually,

but not always, located in the cervical cord or craniocervical junction [24] . Prominent back or

neck pain or myelopathic signs at presentation can indicate this source, but these are often

absent and the clinical appearance can mimic that of intracranial aneurysm rupture [24-27] .

Vascular malformations in the spine can be difficult to visualize on neuroimaging modalities

[8,24,25] . Proximal vertebral artery angiography may reveal more rostral lesions. Often the

diagnosis is delayed until the patient presents with recurrent SAH. These lesions are generally

managed by neurosurgical and/or endovascular interventions. (See "Disorders affecting the

spinal cord", section on Vascular malformations).

Intracranial arterial dissection — Dissection of an intracranial artery can produce SAH; in one

case series, this accounted for 4.5 percent of SAH cases, but this high proportion likely reflects

referral or case-ascertainment bias [28] .

Dissection of an intracranial artery is usually initiated by a tear in the media producing an

intramural hemorrhage that dissects longitudinally between the adventitia and media [29] .

When the tear extends through (or is initiated in) the intima, a second, so-called false, lumen is

created. Usually, this leads to narrowing of the lumen, thrombus formation, and

thromboembolic stroke. However, if the dissection tears through the adventitia, a SAH occurs.

The latter scenario is more common with vertebrobasilar dissections.

If SAH occurs, bleeding is massive and often devastating [28,30,31] . If patients survive the

initial event, rebleeding occurs in 40 to 60 percent, often within the first 24 hours.

Many intracranial dissections are believed to occur in the setting of sudden or unusual

stretching of arteries, but such a history is often lacking. While connective tissue diseases such

as Ehler-Danlos syndrome and fibromuscular dysplasia are associated with intracranial arterial

dissection, most patients with dissection do not have these conditions [8,28,29] . Migraine and

hypertension may be risk factors.

Most cases of intracranial arterial dissection in the setting of SAH are diagnosed by

conventional cerebral angiography [2,29,30] . Magnetic resonance imaging (MRI) with fat

saturation is also a sensitive test, demonstrating intramural blood on cross-sectional images

[29] .

Vertebrobasilar dissections are generally treated surgically or with endovascular intervention

[30,31] . Management is individualized according to location and other anatomic features, and

can include ligation of the vertebral artery, trapping or wrapping of the pseudoaneurysm,

bypass, and stenting. These are complicated procedures that can incur additional morbidity in

these very sick patients.

Other causes: Cerebral venous thrombosis can rarely present with subarachnoid hemorrhage

as its primary manifestation [6,32-36] . Usually the presentation is somewhat less abrupt than

with aneurysmal rupture and the bleeding is localized and superficial. The thrombosis may be

visualized on venous phase of digital subtraction angiography and/or on MRI. (See "Etiology;

clinical features; and diagnosis of cerebral venous thrombosis"). Sickle cell disease can be

complicated by subarachnoid as well as intracerebral hemorrhage [1,8,37] . Most reported

cases occur in children with an established diagnosis. These children are often found to have

one or more aneurysms; in some cases SAH is believed to result from fragile collateral blood

vessels. Recent transfusion and treatment with corticosteroid therapy may be risk factors.

Case fatality rate was as high as 34 percent in one report [37] . Survivors appear to have a low

rate of recurrence. (See "Cerebrovascular disease in sickle cell disease", section on

Subarachnoid hemorrhage). Bleeding disorders and anticoagulant therapy can be complicated

by SAH, but this is a somewhat rare complication; intracerebral and subdural hemorrhages are

more common [4,8,38-40] . Systemic bleeding usually accompanies the SAH if this is the

primary cause; if it does not, the patient should be assumed to have an underlying aneurysm

or other vascular lesion until proven otherwise. Pituitary apoplexy often presents with sudden

onset of headache and vomiting, and there can be prominent subarachnoid blood on CT scan,

which may distract from or obscure the pituitary adenoma [41-44] . Pituitary apoplexy is

usually heralded by vision change and is accompanied by extraocular nerve palsy. If not

visualized on the initial CT scan, MRI will demonstrate the tumor [45,46] . Neurosurgical

decompression is indicated for visual loss. Patients also require endocrine evaluation for

potentially life-threatening, acute hypopituitarism. (See "Causes of hypopituitarism", section

on Pituitary apoplexy). Traumatic SAH is usually identified by the clinical setting. However, if a

clinical history is unavailable, radiologic clues of a traumatic origin include localized bleeding in

superficial sulci, adjacent skull fracture, and cerebral contusion as well as external evidence of

traumatic injury [8,40] . Cocaine abuse has been associated with both aneurysmal and

nonaneurysmal SAH [6,8,47,48] . The mechanism of bleeding in the latter is not known, but

may be related to acute blood pressure surges and/or an underlying hypertensive or toxic

vasculopathy [8,49] . Patients with SAH and cocaine abuse should be assumed to have an

underlying aneurysm or other vascular lesion until proven otherwise. Rare causes of SAH

include spinal aneurysms that can produce subarachnoid hemorrhage, usually with prominent

neck or back pain and myeloradicular symptoms [50,51] . Brain or cervical tumors have been

reported to produce SAH as the presenting manifestation [6,52] . Moyamoya disease is

associated with cerebral aneurysms which can rupture and produce SAH; rarely SAH occurs

due to rupture of the fragile transdural anastomotic vessels [53] . (See "Moyamoya disease").

DIAGNOSTIC EVALUATION — Subarachnoid hemorrhage (SAH) should be considered in any

patient complaining of a severe headache of sudden onset. Emergent computed tomography

(CT) of the head should immediately follow consideration of the diagnosis [40] . If the suspicion

is high and the CT scan fails to show blood in subarachnoid space, a lumbar must be obtained.

(See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid

hemorrhage", section on Diagnosis).

Patients with SAH should undergo basic laboratory testing including complete blood count,

serum chemistries, coagulation studies, and toxicology screen. A baseline electrocardiogram

should also be obtained.

Cerebral angiography — Most vascular lesions responsible for SAH are identified using

conventional digital subtraction cerebral angiography (DSA) that includes injections of 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. Proximal vertebral artery

angiography may reveal a vascular malformation in the cervical spine or cranio-cervical

junction. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid

hemorrhage").

The utility of CT angiography (CTA) is continuously improving [54] . A major advantage of CTA

over conventional angiography is the speed and ease by which it can be obtained, often

immediately after the diagnosis of SAH is made by head CT when the patient is still in the

scanner. CTA is increasingly used as a first test in many patients with SAH, avoiding the need

for conventional angiography in some patients [55-57] . In this setting, CTA is a more practical

approach to acute diagnosis than magnetic resonance angiography (MRA), given the

constraints of acute patient management. CTA has imperfect sensitivity for the detection of

cerebral aneurysms, particularly small aneurysms [57] . Even when an aneurysm is identified

by other technologies, DSA is often advocated to exclude multiple aneurysms and to better

plan surgical intervention [58] .

Repeat angiography — Up to 24 percent of all SAH patients with initial negative angiography

have an aneurysm found on repeat angiography [1,6-8,10,12,59] . This may increase to as

much as 49 percent if patients with perimesencephalic SAH and patients with normal CT scans

are excluded [1,7,9] . Repeat studies may also reveal an arterial dissection or a vascular

malformation not identified on the initial study [24,25,60] . Therefore, it is critical to repeat

DSA if the initial angiogram is negative. The appropriate timing of this study is unclear and

probably should be individualized according to the patient's condition and presence of other

complications. In reported case series, the repeat DSA has been performed between four days

and four weeks [1,6-10,61-63] . Repeat DSA may not be necessary in patients who have an

identified nonaneurysmal etiology of SAH and possibly perimesencephalic SAH [3,7] . (See

"Perimesencephalic nonaneurysmal subarachnoid hemorrhage", section on Repeated testing).

A third angiogram at a period of two to three months is advocated by some, but is probably

not necessary in most patients [2,6,8,59,60] . If the prior studies are technically inadequate, or

if rebleeding occurs, repeat angiography, if not surgical exploration, is warranted [2] . (See

"Further diagnostic study" below).

Magnetic resonance imaging — MRI may demonstrate angiographically occult vascular lesions

that can cause SAH. Such lesions include some vascular malformations in the brain or spinal

cord, tumors, including pituitary adenoma, and arterial wall hematoma suggesting arterial

dissection [27,64] . All patients with SAH and negative angiography should have gadolinium-

enhanced MRI of the brain and spinal cord [6,23] .

Further diagnostic study — Surgical exploration is not a routine aspect of the diagnostic

evaluation, but is reported to lead to a diagnosis of ruptured aneurysm, even after two or

more negative angiograms [2,6,11] . While in some cases this intervention was prompted by an

episode of rebleeding or a suspicious but not diagnostic finding on angiography, it is not always

certain in other cases why surgical exploration was performed.

Spinal angiography is also undertaken for diagnosis in some cases [24-27] . Usually this is

prompted by a specific clinical suspicion for a spinal vascular anomaly such as prominent back

or neck pain, radicular or myelopathic features on examination, or an abnormal, but not

diagnostic finding on other neuroimaging studies, such as MRI.

COMPLICATIONS — Common complications of SAH are: Rebleeding Vasospasm and cerebral

ischemia Hydrocephalus Increased intracranial pressure Seizures Hyponatremia Cardiac

abnormalities Hypothalamic dysfunction and pituitary insufficiency [60]

There is little specific information about the incidence or severity of these complications in

NASAH in comparison to aneurysmal SAH. Rebleeding risk is likely specific to the origin of SAH;

this is discussed above under the individual etiologies. Other complications, however, may be

expected to be somewhat similar across etiology.

The pathogenesis and clinical features of these complications are discussed separately. (See

"Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage",

section on Complications).

TREATMENT — The general care of patients with NASAH should be the same as aneurysmal

SAH patients. Patients are admitted to an intensive care setting for constant hemodynamic and

cardiac monitoring, given stool softeners, kept at bedrest, and given analgesia to diminish

hemodynamic fluctuations and lower the risk of rebleeding. Pneumatic compression stockings

to limit risk of deep vein thrombosis should be utilized while patients are immobile. (See

"Treatment of aneurysmal subarachnoid hemorrhage", section on General management).

Patients should receive other interventions to monitor, prevent, and treat complications of

SAH. These are discussed separately. (See "Treatment of aneurysmal subarachnoid

hemorrhage", sections on General management, Prevention of vasospasm, and Management

of complications).

Patients with perimesencephalic SAH may be managed somewhat differently once aneurysmal

SAH has been excluded. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage").

Interventions to prevent rebleeding and other etiologic-specific complications are

individualized to the underlying etiology. (See "Etiologies" above as well as other topic

reviews).

SUMMARY AND RECOMMENDATIONS — An estimated 15 to 20 percent of patients with

subarachnoid hemorrhage (SAH) are nonaneurysmal. The causes of nonaneurysmal SAH

(NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not

identified. Perimesencephalic NASAH make up the majority of NASAH in some case series.

These have a distinctive appearance on computed tomography and a benign course. (See

"Perimesencephalic nonaneurysmal subarachnoid hemorrhage"). Other causes of NASAH

include occult aneurysm, intracranial or spinal vascular malformations, and intracranial arterial

dissection. Less common etiologies include sickle cell disease, pituitary apoplexy, cocaine

abuse, cerebral venous thrombosis, and bleeding disorders. (See "Etiologies" above). The

diagnosis of SAH is usually made by computed tomography (CT) of the brain, which should

always be performed emergently in a patient with an abrupt onset of headache. A lumbar

puncture should follow a negative CT scan if the clinical suspicion is high. (See "Diagnostic

evaluation" above). All patients with SAH should be evaluated with basic laboratory testing

including complete blood count, serum chemistries, and coagulation studies and toxicology

screen. A baseline electrocardiogram should also be obtained. (See "Diagnostic evaluation"

above). We recommend that conventional digital subtraction cerebral angiography (DSA) be

performed in all patients with SAH, unless CT and/or CT angiography adequately defines the

pathogenesis. (See "Cerebral angiography" above). We recommend repeating DSA within 4 to

14 days after an initial negative study, because of the risk of a false negative. (See "Repeat

angiography" above). Patients with negative angiography should undergo gadolinium-

enhanced magnetic resonance imaging (MRI) of brain and spinal cord. (See "Magnetic

resonance imaging" above). Some patients will not have an etiologic diagnosis after DSA and

MRI. If rebleeding occurs in such patients, further diagnostic interventions may include further

angiographic study of the brain and/or spinal cord, and/or surgical exploration. (See "Further

diagnostic study" above). Complications of aneurysmal SAH, hydrocephalus, vasospasm and

cerebral ischemia, seizures, hyponatremia, and cardiac abnormalities also occur in NASAH. In

this regard, patients with NASAH should be managed similarly to aneurysmal SAH. (See

"Treatment of aneurysmal subarachnoid hemorrhage"). Patients may also require

interventions that are etiology-specific. (See "Etiologies" above, as well as other topic reviews).

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