Subarachnoid Hemorrhage

Dr.B.Ga n g a d h a r
 Subarachnoid Hemorrhage

 Excluding head trauma, the most common cause of SAH is

rupture of a saccular aneurysm.
 Other causes include
 bleeding from a vascular malformation
 (AV malformation or dural AV
fistula) and
 primary intracerebral hemorrhage extension into
the SA space.
 Idiopathic SAHs are localized to the perimesencephalic
cisterns and
o are benign
o they probably have a venous or capillary source, and
o angiography is unrevealing.

 Saccular ("Berry") Aneurysm

 2% of adults harbor intracranial aneurysms



 The aneurysm will rupture, producing SAH, in 25,000–30,000

cases per year in USA.


 Unruptured, asymptomatic aneurysms are much less

dangerous than a recently ruptured aneurysm.


 The annual risk of rupture for aneurysms <10 mm in size is

~0.1%, and
 for aneurysms >10 mm in size is
~0.5–1%.
 Saccular ("Berry") Aneurysm

 90 to 95 percent of SAs lie on the anterior part of COW.



 The most common sites are

 (1) the proximal portions of the ACoA,
 (2) at the origin of the PCoA from the stem of the IC,
 (3) at the first major bifurcation of the MCA, and
 (4) at the bifurcation of the IC into MCA & ACA.

Saccular ("Berry") Aneurysm
 Giant aneurysms( >2.5 cm) -5% of cases.
o Most common locations are the terminal internal carotid
artery, MCA bifurcation, and top of the basilar artery.
o Their risk of rupture is ~6% in 1ST year after identification
and may remain high indefinitely.
o They often cause symptoms by compressing the adjacent
brain or cranial nerves.


 Mycotic aneurysms –
o usually located distal to the 1ST bifurcation of major arteries
of COW.
o Most result from infected emboli due to bacterial endocarditis
causing septic degeneration of arteries and subsequent
dilatation and rupture.
 Pathophysiology
 Saccular aneurysms occur at the bifurcations of the large to
medium-sized intracranial arteries;
 Rupture is into the subarachnoid space in the basal cisterns
and often into the parenchyma of the adjacent brain
 As an aneurysm develops, it typically forms a neck with a
dome.
 The arterial internal elastic lamina disappears at the base of
the neck. The media thins, and connective tissue replaces
smooth-muscle cells.
 At the site of rupture (most often the dome) the wall thins,
and the tear that allows bleeding is often 0.5 mm long.
 Aneurysm size and site are important in predicting risk of
rupture.
o Those >7 mm in diameter and those at the top of BA and at
the origin of PCoA are at greater risk of rupture.
 Clinical Manifestations

Ø Most unruptured intracranial aneurysms - asymptomatic



Ø Symptoms are usually due to rupture and resultant SAH,

although some present with mass effect on cranial nerves
or brain parenchyma.


Ø At the moment of aneurysmalrupture with major SAH, the ICP

suddenly rises. This may account for the sudden transient
LOC that occurs in nearly half of patients.


Ø Sudden LOC may be preceded by a brief moment of

excruciating headache, but most patients first complain of
headache upon regaining consciousness.
Ø
 Clinical Manifestations
§ In 10% of cases, aneurysmal bleeding is severe enough to
cause loss of consciousness for several days.
§
§ In ~45% of cases, severe headache associated with exertion
is the presenting complaint.


§ The patient often calls the headache "the worst headache of

my life“


 The most important characteristic is sudden onset



 The headache is usually generalized, often with neck

stiffness, and vomiting is common.
 focal neurologic deficits may occur.
 Clinical Manifestations
 ACA or MCA bifurcation aneurysms may rupture and form a
hematoma large enough to produce mass effect. The
common deficits that result include hemiparesis, aphasia,
and abulia.


 Occasionally, prodromal symptoms suggest the location of a

progressively enlarging unruptured aneurysm.


 A 3RD cranial nerve palsy may occur with an expanding

aneurysm at the junction of the PCoA and the ICA.


 A 6th nerve palsy may indicate an aneurysm in the cavernous

sinus, and


 visual field defects can occur with an expanding supraclinoid

carotid or anterior cerebral artery aneurysm
 Clinical Manifestations

 Occipital and posterior cervical pain may signal a PICA or

AICA aneurysm.


 Pain in or behind the eye and in the low temple can occur
with an expanding MCA aneurysm.


 Aneurysms can undergo small ruptures and leaks of blood

into the subarachnoid space, so-called sentinel bleeds.


 Sudden unexplained headache at any location should raise

suspicion of SAH and be investigated, because a major
hemorrhage may be imminent
 Grading Scales for SAH

 Hunt-Hess Scale


o 1 Mild headache, normal mental status, no cranial nerve or

motor findings


o 2 Severe headache, normal mental status, may have cranial

nerve deficit


o 3 Somnolent, confused, may have cranial nerve or mild

motor deficit


o 4 Stupor, moderate to severe motor deficit, may have

intermittent
 reflex
posturing

 World Federation of Neurosurgical Societies (WFNS)
Scale


o 1 Glasgow Coma Scalea (GCS) score 15, no motor

deficits


o 2 GCS 13–14, no motor deficits



o 3 GCS 13–14, with motor deficits



o 4 GCS 7–12, with or without motor deficits



o 5 GCS 3–6, with or without motor deficits

o
 Delayed Neurologic Deficits

 4 major causes of delayed neurologic deficits:

ü rerupture,
ü hydrocephalus,
ü vasospasm, and
ü Hyponatremia


v Rerupture
 The incidence of rerupture of an untreated aneurysm in the
1st month
 following SAH is ~30%, with the peak in the
first 7 days.
 Rerupture is associated with a 60% mortality and poor
outcome.
 Early treatment eliminates this risk
 Delayed Neurologic Deficits

v Hydrocephalus
 Acute hydrocephalus can cause stupor and coma
 Subacute hydrocephalus may develop over a few days or
weeks and causes progressive drowsiness or slowed
mentation (abulia) with incontinence.
 Hydrocephalus is differentiated from cerebral vasospasm with
a CT scan, CT angiogram, transcranial Doppler (TCD)
ultrasound, or conventional x-ray angiography.
 Hydrocephalus may clear spontaneously or require temporary
ventricular drainage.
 Chronic hydrocephalus may develop weeks to months after
SAH and manifest as gait difficulty, incontinence, or
impaired mentation
 Delayed Neurologic Deficits
v Vasospasm
 Narrowing of the arteries at the base of the brain following
SAH causes symptomatic ischemia and infarction in ~30% of
patients
 is the major cause of delayed morbidity and death.


 Signs of ischemia appear 4–14 days after the hemorrhage,

most often at 7 days.


 The severity and distribution of vasospasm determine

whether infarction will occur.


 Delayed vasospasm is believed to result from direct effects of

clotted blood and its breakdown products on the arteries
within the subarachnoid space.

 Delayed Neurologic Deficits

 Vasospasm can be detected reliably with conventional x-ray

angiography( invasive ,expensive and carries the risk of
stroke).


 TCD ultrasound on a daily or every-other-day basis,

vasospasm can be reliably detected.


 CT angiography is another method that can detect

vasospasm.


 Severe cerebral edema in patients with infarction from

vasospasm may increase the ICP enough to reduce cerebral
perfusion pressure.



 Delayed Neurologic Deficits

v Hyponatremia.
 Hyponatremia may be profound and can develop quickly in
the first 2 weeks following SAH.


 There is both natriuresis and volume depletion with SAH, so

that patients become both hyponatremic and hypovolemic.
 Both ANP and BNP have a role in producing this "cerebral salt-
wasting syndrome.“


 Typically it clears over the course of 1–2 weeks and, in the

setting of SAH, should not be treated with free-water
restriction as this may increase the risk of stroke
 Laboratory Evaluation and Imaging

 The hallmark of aneurysmal rupture is blood in the CSF.

 More than 95% of cases have enough blood to be visualized
on a high-quality noncontrast CT scan obtained within 72 h.
 If the scan fails to establish the diagnosis of SAH and no mass
lesion or obstructive hydrocephalus is found, a lumbar
puncture should be performed to establish the presence of
subarachnoid blood.
 Lumbar puncture prior to an imaging procedure is indicated
only if a CT scan is not available at the time of the
suspected SAH.
 spinal fluid stained to yellow within 6–12 h, peaks in intensity
at 48 h and lasts for 1–4 weeks, depending on the amount
of subarachnoid blood.
 Sr .electrolytes- daily or twice daily
 ECG
 IMAGING FINDINGS
 General Features
 • Best diagnostic clue: Hyperdense CSF on NECT
 • Location: Interhemispheric SAH suggests ACoA aneurysm,
 sylvian correlates with MCA
 CT Findings
 • NECT: 95% positive in first 24 h, < 50% by 1 week
 • CTA: Multislice CTA 90-95% + for aneurysm > 2 mm
 MR Findings
 • T1WI: "Dirty" CSF (isointense to brain)
 • T2WI: Hyperintense CSF
 • FLAIR: Hyperintense (not pathognomonic for SAH)
 • T2* GRE: Hypointense hemosiderin deposition in
 70-75% of patients with prior SAH
 • DWI: May show multifocal restrictions
 • MRA: 85-95% sensitive
 IMAGING FINDINGS

 Angiographic Findings
 • Conventional
 o Negative in 15-20% of aSAHi , repeat positive < 5%
 o Considered "gold standard“


 Imaging Recommendations
 • Best imaging tool: NECT + multi slice CTA
 • Protocol advice: Thin slices, low pitch, arterial phase only
Anterior communicating artery aneurysm rupture
SAH due to rupture of a basilar artery aneurysm
 Axial TlWI MR  Axial FLAIR MR
 IMAGING FINDINGS

 DIFFERENTIAL DIAGNOSIS
 Nonaneurysmal SAH
 • Occult trauma, dissection
 • Perimesencephalic nonaneurysmal SAH
 • Vascular malformation, neoplasm (e.g., ependymoma)
 "PseudoSAH"
 • Low density brain (e.g., with diffuse cerebral edema)
 • High density CSF (e.g., following intrathecal contrast)
 NonSAH causes of high CSF signal on FLAIR
 • Meningitis (inflammatory, neoplastic )
 • High oxygen tension or gadolinium in CSF
 NONANEURYSMAL PERIMESENCEPHALIC SAH

 Clinically benign entity with SAH confined to

perimesencephalic , prepontine cisterns
 No identifiable source demonstrated at angiography


 IMAGING FINDINGS
 General Features
 • Best diagnostic clue: Hyperdense prepontine,
perimesencephalic CSF
 • Location: "Pretruncal" (anterior to pons, around midbrain)
 • CTA/MRA/DSA
 o Angiography negative in 90-95% of pnSAH
 o 5-10% prevalence of vertebrobasilar aneurysm in
pnSAH
 NONANEURYSMAL PERIMESENCEPHALIC SAH

 CT Findings
• NECT

 o High attenuation anterior to midbrain, in ambient cisterns

 o No extension into distal sylvian, interhemispheric fissures
• CTA: Posterior circulation aneurysm in 5-10%

 MR Findings
 • T1WI: "Dirty" CSF (iso-, not hypo intense)
 • T2WI: Acute pnSAH -hyperintense (difficult to see)
 • FLAIR: Hyperintense CSF in/around pons, midbrain
 • T2* GRE: Hypointense

 NONANEURYSMAL PERIMESENCEPHALIC SAH

 Angiographic Findings
 • Conventional
 o Considered "gold standard"
 o Saccular or blister-like aneurysm identified as cause of
pnSAH in 5-10%
 o Vasospasm, hydrocephalus rare « < aSAH)
 Imaging Recommendations
 • Best imaging tool: NECT scan = best screening for pnSAH
 • Protocol advice: If NECT scan positive, CTA +/- DSA
DIFFERENTIAL DIAGNOSIS

Aneurysmal SAH (aSAH)

Traumatic SAH (tSAH)

Meningitis

Artifact
Axial graphic shows
classic pnSAH.
Hemorrhage is confined

to the interpeduncular
fossa and ambient
(perimensencephalic)
cisterns (arrows).
Source is usually

venous.
NONANEURYSMAL PERIMESENCEPHALIC SAH

Axial TlWI MR shows "dirty"



 Axial NECT CSF in angio-negative pnSAH

 SUPERFICIAL SIDEROSIS

 Recurrent SAH causes hemosiderin deposition on surface of

brain, brain stem & cranial nerve leptomeninges.
 IMAGING FINDINGS
 General Features
 • Best diagnostic clue: Contours of brain & cranial nerves
outlined by hypointense rim on T2 or T2* GRE MRimages
 • Location: Cerebral hemispheres, cerebellum, brainstem,
cranial nerves & spinal cord may all be affected
 • Size: Linear low signal along CNS surfaces varies in
thickness but usually <2 mm
 CT Findings
 • NECT
 o Cerebral & cerebellar atrophy

 SUPERFICIAL SIDEROSIS

 o Especially marked in posterior fossa

 • Cerebellar sulci often disproportionately large
 o Slightly hyperdense rim over brain surface
 CECT: No enhancement typical


 MR Findings
 • T1WI: Hyperintense signal may be seen on CNS surfaces
 • T2WI
 o High-resolution, thin section T2 MR of CPA-lAC
 • Cranial nerves 7 & 8 appear darker & thicker than
normal
 • Adjacent cerebellar structures & brain stem show low
signal surfaces
 • Less easily seen than on T2* GRE images
 SUPERFICIAL SIDEROSIS
 FLAIR: Dark border on local surface of brain , brain stem,
cerebellum & cranial nerves


 T2* GRE
 o Most sensitive to hemosiderin deposition on CNS surfaces
 MR findings do not correlate with severity of disease
 Imaging Recommendations
 Best imaging tool
 o Brain MR
 • Once diagnosis of superficial siderosis is made,
search for
 cause of recurrent SAH must commence
 • Whole brain MR with contrast & MRA first
 • Total spine MR second if brain negative for underlying
lesion
S UP ERFICIAL S ID EROS IS

Axial graphic shows



darker brown
hemosiderin staining
on all surfaces of the
brain, meninges and
cranial nerves.
S UP ERFICIAL S ID EROS IS

Axial T2* GRE MR

reveals superficial
siderosis as dark
hemosiderin staining in
folia of cerebellum
(arrows).
In addition, the 7th &

8th cranial nerves in the

CPA-lAC are black (open
arrows)
S UP ERFICIAL S ID EROS IS

Axial T2* GRE MR in

patient with ataxia and
bilateral SNHL shows
intense hemosiderin
staining of the surface
of the cerebellum as
hypointense, blooming
stripes (arrows).
S UP ERFICIAL
S ID EROS IS

Coronal T2* GRE MR

in patient with
superficial siderosis
shows low signal
along all dural and
cerebellar surfaces in
the posterior fossa
(arrows).
 S UP ERFICIAL
S ID EROS IS

Axial T2WI MR reveals

juvenile pilocytic

astrocytoma (arrow)

causing
chronic SAH yielding

superficial siderosis of

adjacent brain surfaces

 SUPERFICIAL SIDEROSIS

 DIFFERENTIAL DIAGNOSIS
 MR sequence artifact
 Brain surface vessels
 Neurocutaneous melanosis
 Meningioangiomatosis (MA)
 SACCULAR ANEURYSM
 IMAGING FINDINGS
 Ruptured SAs have high density blood in basal cisterns, sulci
 Multi-slice CTA positive in 95% of patients with aSAH
 50% have "flow void" on T1WI
 Typically hypointense on T2WI
 Best imaging tool: NECT for aSAH + multislice CTA
DIFFERENTIAL DIAGNOSIS

 Vessel loop
 Infundibulum < 3 mm, conical, small PCoA arises directly
from apex
 Pseudoaneurysm -Often arises distal to COW
 "Flow void" mimic on MR -Aerated anterior clinoid or
supraorbital cell
 Short T1 on MRA- Lipoma
 Pituitary gland (contrast-enhanced MRA)
 Saccular aneurysm at the ICA bifurcation.

 Axial T2WI MR "flow void"

adjacent to COW DSA of the right ICA

DDx: Saccular Intracranial Aneurysm
 Treatment

 The medical management of SAH focuses on

 protecting the airway,
 managing BP before and after aneurysm
treatment,
 preventing rebleeding prior to treatment,
 managing vasospasm,
 treating hydrocephalus,
 treating hyponatremia, and
 preventing pulmonary embolus.
 Treatment
Intracranial hypertension


 Pts who are stuporous should undergo emergent

ventriculostomy to measure ICP and to treat high ICP in
order to prevent cerebral ischemia.
 Medical therapies- mild hyperventilation, mannitol , and
sedation
 High ICP refractory to treatment is a poor prognostic sign
 Care is required to maintain adequate cerebral perfusion
pressure while avoiding excessive elevation of arterial
pressure.
 If the patient is alert, it is reasonable to lower the BP to
normal using nicardipine, labetolol, or esmolol.
 If the patient has a depressed level of consciousness, ICP
should be measured and the cerebral perfusion pressure
targeted to 60–70 mmHg
 Treatment

Preventing Rebleeding


 Bed rest in a quiet room and

 Stool softeners to prevent straining.
 If headache or neck pain is severe, mild sedation and
analgesia are prescribed.
 Extreme sedation is avoided because it can obscure changes
in neurologic status.
 Adequate hydration is necessary to avoid a decrease in blood
volume predisposing to brain ischemia
 Phenytoin is often given as prophylactic therapy since a
seizure may promote rebleeding.
 Treatment

 Glucocorticoids may help reduce the head and neck ache

caused by the irritativeeffect of the subarachnoid blood.
Their routine use is not recommended.


 Antifibrinolytic agents are not routinely prescribed but may be

considered in patients in whom aneurysm treatment cannot
proceed immediately.
 They are associated with a reduced incidence of aneurysmal
rerupture but may also increase the risk of delayed cerebral
infarction and DVT


 Vasospasm

 Nimodipine (60 mg PO every 4 h) improves outcome, perhaps

by preventing ischemic injury rather than reducing the risk
of vasospasm.


 Symptomatic cerebral vasospasm -also treated by increasing

CPP by raising MAP through plasma volume expansion and
the judicious use of IV vasopressor agents, usually
phenylephrine or norepinephrine.


 Volume expansion helps prevent hypotension, augments

cardiac output, and reduces blood viscosity by reducing the
hematocrit. This method is called "triple-H"
therapy(hypertension, hemodilution, and hypervolemic).

 Vasospasm

 Intraarterial vasodilators and PTA are considered If

symptomatic vasospasm persists despite optimal medical
therapy
 Vasodilatation by direct angioplasty appears to be
permanent, allowing triple-H therapy to be tapered sooner
 Intraarterial papaverine (neurotoxic ) should be reserved for
refractory cases
 Free-water restriction is contraindicated in patients with SAH
at risk for vasospasm because hypovolemia and
hypotension may occur and precipitate cerebral ischemia
 Treatment

Acute hydrocephalus


 can cause stupor or coma.

 It may clear spontaneously or require temporary ventricular
drainage.
 When chronic hydrocephalus develops, ventricular shunting is

the treatment of choice.



Hyponatremia


 parenteral fluids containing normal saline.

 Frequently, oral salt supplementation coupled with normal
saline will mitigate hyponatremia, but often patients also
require hypertonic saline.
 Care must be taken not to correct serum sodium too quickly

 Treatment
Prevention of pulmonary embolism


 pneumatic compression stockings.



 Unfractionated heparin S/C for DVT prophylaxis can be initiated

immediately following endovascular treatment and within days
following craniotomy and surgical clipping.


 Systemic anticoagulation with heparin is contraindicated in

patients with ruptured and untreated aneurysms.
 It is a relative contraindication following craniotomy.


 Following craniotomy, use of IVC filters is preferred to prevent

further pulmonary emboli, while systemic anticoagulation with
heparin is preferred following successful endovascular
treatment.

 Early aneurysm repair
 Prevents rerupture and allows the safe application of
techniques to improve blood flow (e.g., induced
hypertension and hypervolemia) should symptomatic
vasospasm develop.
 An aneurysm can be "clipped" by a neurosurgeon or "coiled"
by an endovascular surgeon.
 Surgical repair involves placing a metal clip across the
aneurysm neck, thereby immediately eliminating the risk of
rebleeding.
 This approach requires craniotomy and brain retraction,
which is associated with neurologic morbidity.
 Endovascular techniques involve placing platinum coils, or
other embolic material, within the aneurysm via a catheter
that is passed from the femoral artery.
 The aneurysm is packed tightly to enhance thrombosis
and over time is walled-off from the circulation.
Refernces:


 Harrison's principles of internal medicine,17th e

 Diagnostic imaging: Brain by Anne 0. Osborn
 Adams & Victors' Principles of Neurology, 8th Edition
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