Download - Imaging in SAH
IMAGING IN SAHDR.SARATHMENON.R, MD(Med),DNB(Med),MNAMS
DM Resident
Dept.of .Neurosciences
Amrita Institute of Medical Sciences,Kochi
INTRODUCTION
Definition Epidemology Grading system Imaging modalities Differentials
IMAGING MODALITIES
NCCT/CTA MRI /MRA Angiography Nuclear imaging Neurosonography
SAH What is it?
Bleeding into the subarachnoid space (space between the pia & arachnoid meningeal layers) where blood vessels lie & CSF flows
Where does the blood come from?An aneursym on a blood vessel in the
subarachnoid space has ruptured (~70%)Unknown (~15%)AVM (~10%)Rare causes (e.g. tumour) (~5%)
Where does the blood go?Anywhere where CSF goes, may get
hydrocephalus if into ventricle & causes obstruction of CSF circulation
SAH Incidence = 1/7000 people
Higher chance if: Female
3rd trimester of pregnancy
Middle-aged
Abuse of stimulant drugs
Connective tissue disorder
Family history
PCKD
SAH – THE PROBLEM
80% in 40-65 year olds15% in 20-40 year olds
It can kill quickly25% die within 24 hours50% will be dead at 6 months
It causes significant disabilityCognitive impairmentNeurological disability depending on size of
bleed & complications encountered
GRADING OF SAH
WFNS Grading : Grade GCS Motor Deficit I 15 Absent II 13-14 Absent III 13-14 Present IV 7-12 +/- V 3-6 +/-
MODIFIED H & H GRADINGGrade Description Mortalit
y (%)
Grade 0 Unruptured aneurysm --
Grade I Asymptomatic or minimal headache with normal neurologic examination
2
Grade II Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy
5
Grade III Lethargy, confusion, or mild focal deficit 15 — 20
Grade IV Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity, vegetative disturbances
30 — 40
Grade V Deep coma, decerebrate rigidity, moribund appearance
50 — 80
CT GRADING SYSTEM OF FISHER
1 No subarachnoid blood detected 2 Diffuse or vertical layers < 1 mm thick 3 Localized clot and/or vertical layer > 1 mm 4 Intracerebral or intraventricular clot with
diffuse or no SAH
INVESTIGATIONS
CT scan without contrast
Lumbar puncture
CTA
Cerebral angiogram
MRI/MRA
98% sensitive @ 12 hours80% at day 350% at day 7
Also good to see if any associated ICH or hydrocephalus. May help localise the location of the aneurysm if there is more than 1 & may also see AVM
CT SCAN- NCCT Evident in the largest subarachnoid spaces- suprasellar
cistern and Sylvian fissures.
most conspicuous within 2-3 days of onset
Acute SAH is typically 50-60 Hounsfield units (HU).
The protein content of the hemoglobin molecule is predominantly responsible for the attenuating effect of blood; absolute measurement in HU varies with the hematocrit value
localizing the source of bleeding- - interhemispheric fissure,frontal lobe- Aco A - Sylvian fissure- I/L MCA - Posterior fossa- post.circulation aneurysm
NCCT- Sensitivity-93-100% in first 24 hrs
• Scrutinize these areas systematically for SAH – Perimesencephalic cisterns – Sylvian fissures Dilation of temporal horns suggestive of
hydrocephalus, which raises a possibility of SAH
CTA: Multislice CTA 90-95% + for aneurysm ~ 2 mm
CORTICAL SAH
SAH-CISTERNAL
A nonenhanced computed tomography scan of the brain that demonstrates an extensive SAH filling the basilar cisterns in a patient with a ruptured intracranial aneurysm
SAH & LP CT & LP are critical to diagnosing SAH
No need for LP if obvious blood in subarachnoid space on CT
If NCCT –ve, LP needed.
Blood may not be evident on CT, especially if it is performed > few days after bleed
LP should only be performed after 12 hours of headache onset
If NCCT,LP –VE, CTA to r/o saccular aneurysm
SAH & LP When blood enters the CSF (e.g. from SAH or during
LP) the red cells are broken down & oxyhaemoglobin is released
It then takes 12 hours for the oxyhaemoglobin to be converted into bilirubin – conversion is via an enzyme found in the brain.
Bilirubin in the CSF, therefore, tells us that blood must have been in the subarachnoid space for at least 12 hours
Blood which entered the CSF during the LP would not encounter the enzyme & could not produce bilirubin
The CSF will look xanthochromic (yellowish discolouration) if bilirubin is present which they will look for with spectroscopy in the lab
CTA
subarachnoid hemorrhage and contrast medium filling the right sylvian fissure, the interhemispheric fissure, and the lateral and third ventricles
CTA SPOT SIGN
MRI/MRA (FLAIR) is the most sensitive for the detection of
SAH FLAIR images, SAH appears as high signal-
intensity (white) in normally low signal-intensity (black) CSF spaces.
In acute SAH, FLAIR and CT scanning have similar findings.
T2- and T2*- low signal-intensity in normally high signal-intensity subarachnoid spaces.
T1-weighted - intermediate-intensity or high-intensity signal in the subarachnoid space
MRA may be useful for evaluating aneurysms > 5mm and other vascular lesions that cause SAH
LEVEL OF CONFIDENCE FLAIR MRI is as sensitive as or more sensitive
than CT scanning in the evaluation of acute SAH compared with LP, FLAIR MRI cannot exclude
SAH. MRI -valuable in the subacute phase of SAH, in
which the density of hemorrhage on CT scans decreases.
Magnetic field inhomogeneity - artifactual increase in signal intensity in sulci over the cerebral convexities on FLAIR images, which can mimic SAH.
Hyperintensity in the subarachnoid space on FLAIR images seen in meningitis or leptomeningeal carcinomatosis
SAH appears hyperintense on the T2-weighted and fluid-attenuated inversion recovery (FLAIR) images and isointense to hypointense on the T1-weighted (T1W) image. Marked blooming is observed on the gradient-echo (GRE) image. Findings in the right parietal region extend into cortical sulci and suggest hyperacute or acute hemorrhage.
Sagittal T1-weighted image shows a right SDH (fig a). Axial fluid attenuated inversion recovery image demonstrates SAH (arrows) in the right parietal region (fig b).
NUCLEAR IMAGING
not useful in the initial diagnosis of subarachnoid hemorrhage (SAH), role in the diagnosis of related vasospasm
(SPECT) scanning with the radiopharmaceutical technetium-99m (99m Tc) hexamethylpropyleneamine oxime (HMPAO).
semiquantitative and qualitative in that the cerebellum is generally considered as a control value for normal perfusion
Space-occupying lesions such as cerebral hematoma can cause perfusion defects on SPECT perfusion imaging
ANGIOGRAPHY standard imaging -intracranial aneurysms,
arteriovenous malformations (AVMs), and fistulae (AP), lateral, and one or more oblique views of
both carotid and vertebral artery contrast injection studies
submentovertical - the neck of a middle cerebral artery bifurcation aneurysm or anterior communicating artery aneurysm
aneurysm location, shape, neck size, and neck-to-maximal diameter ratio - the aneurysm is better treated with open craniotomy or with an endovascular technique.
LEVEL OF CONFIDENCE
high degree of accuracy false-negative rate in the range of 1-2% A repeat cerebral arteriogram at 10-14 - initial
angiogram negative B/l selective external and internal carotid artery
angiograms - exclude a dural arteriovenous fistula B/l vertebral arteriograms of the neck ( selective
thyrocervical trunk and/or careful injections of the right superior intercostal artery) demonstrate the arterial and venous circulation of the cervical spinal cord
If thorough arteriographic studies do not demonstrate a specific cause for an SAH, a presumptive diagnosis of idiopathic perimesencephalic hemorrhage is sometimes made
An angiogram showing a bilobed aneurysm of a posteroinferior cerebellar artery immediately before rupturing
onset of an aneurysmal rupture, with extravasation of contrast material into the subarachnoid space from the anterosuperior aspect of a bilobed aneurysm in a posteroinferior cerebellar artery
later-phase angiogram of a rupturing bilobed aneurysm of a posteroinferior cerebellar artery shows progressive opacification of the subarachnoid space in the posterior fossa
late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid spaces, including the ambient, prepontine, and perimedullary cisterns
NEUROSONOGRAPHY Echoencephalography is useful for diagnosing
germinal matrix and intraventricular hemorrhage in the newborn
transcranial Doppler USG - diagnosis and management of vasospasm in patients with SAH.
Serial transcranial Doppler USG - presence of vasospasm and allow for the maximization of medical therapy for vasospasm before the patient becomes symptomatic
Flow measured in the middle cerebral arteries, which have have flow velocities normally in the 30-80 cm/s range. Elevation to 120 cm/s indicates moderate vasospasm, and elevation to 200 cm/s indicates severe vasospasm
sensitivity of transcranial Doppler ultrasonographic imaging for the detection of vasospasm has been reported to be 85-90%
SAH: DIFFERENTIAL DIAGNOSIS
Aneurysmal Nonaneurysmal “Pseudo-SAH” Reversible cerebral vasoconstriction
syndrome (RCVS)
ANEURYSMAL SAH
• SAH caused by ruptured aneurysm • Worst headache of life • 40-60 years, M:F = 1:2 • 50% mortality, 20% rebleed within 1st 2
weeks • Outcome inversely proportional to Hunt and
Hess (H&H) grade and WFNS grade • Severity of vasospasm/ischemia correlates
with Fisher CT grading (amount) – 1 = no SAH visible – 2 = diffuse, thin layer (< 1 mm) – 3 = localized clot or thick layer (> 1 mm) – 4 = intraventricular blood
ANEURYSMAL SAH • NCCT: – May show culprit aneurysm as filling defect
within hyperdense SAH – Effaced cistern, hydrocephalus, +/- IPH • CTA: 90-95% positive if > 2 mm • MRA TOF: 85-95% sensitive for aneurysm > 3 mm • DSA: current gold standard • Highest amount of blood near site of rupture ACoA aneurysm anterior interhemispheric fissure MCA aneurysm Sylvian Basilar tip, SCA, PICA, VA prepontine cistern,
foramen magnum, 4th ventricle
Subarachnoid hemorrhage secondary to rupture of left superior cerebellar artery aneurysm
NON-ANEURYSMAL SAH-PERIMESENCEPHALIC
Hyperdense prepontine, perimesencephalic CSF Location: "Pretruncal" (anterior to pous, around midbrain) • CTA/MRA/DSA- Angiography negative in 90-95% of pnSAH- 5-10% prevalence of vertebrobasilar aneurysm in
pnSAH
- DSA Saccular or blister-like aneurysm identified as cause
of pnSAH in 5-10% Vasospasm, hydrocephalus rare « < aSAH)
NON-ANEURYSMAL (PMSAH)
Small SAH, localized to interpeduncular cistern• Presumed venous etiology with low recurrence
REVERSIBLE CEREBRALVASOCONSTRICTION SYNDROME (RCVS)
• Reversible, multifocal cerebral vasoconstrictions
• Clinical thunderclap headache +/- neurodeficit • NCCT often negative: 20% with small cortical
SAH +/- IPH • Vasculitic pattern on CTA, MRA and DSA – Segmental arterial constriction – Interval DSA may show rapid improvement with
vasodilator Rx
BEWARE: CORTICAL SAH FROM VENOUSSINUS THROMBOSIS
Small SAH with hyperdense clot of superior sagittal sinus on CT, absence of flow voids on T2WI and loss of venous signal on MRV image
PSEUDO-SAH
Increased density in basal cisterns, frequently related tocardiopulmonary arrest• Hypodense brain (severe edema): cisternal effacement, distension +/-thrombosis of vessels•
two images suggest subarachnoid hemorrhage along the cisterns with effacement of the quadrigeminal cisterns seen in meningitis
PSEUDO SAH
Other causes: intrathecal contrast, meningitis polycythemia Falx cerebri Tentorium cerebelli Streak artifact –bone from skull base Motion artifact hyperintensity of SAH is reported to range
between 60 and 70 Hounsfield units, whereas that of PSAH is reported to range between 29 and 33 Hounsfield units
SAH WITH INTRAVENTRICULARHEMORRHAGE
CONCLUSION • LP more sensitive than CT • Negative NCCT but still suspicious of SAH –
still need LP • MRI is sensitive to detect SAH using FLAIR, GRE
and SWI – But problematic in perimesencephalic cistern Persistent vasospasm – vessels can be
permanently narrow Etiologies of non-traumatic SAH – 80% ruptured aneurysm – 10% non-aneurysmal perimesencephalic SAH – 10% others (brain AVM, spinal AVM, DAVF,
venous infarct, tumor)
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