Imaging of Non-traumatic Intracranial Hemorrhage

www.RiTradiology.com


Non-traumatic
Intracranial Hemorrhage
Rathachai Kaewlai, MD
Emergency Radiology Minicourse 2014



Decisions To Make
in Emergency Head CT
Prior to the scan During the scan After the scan
To perform or not How to perform Diagnosis
or differential diagnosis
How fast to perform IV contrast Recommendations
Any preparation needed Technique: CTA, CTV,
post-contrast imaging
Urgent findings needing
communication
Neck CTA as well?



Scan Techniques
Non-contrast head CT
Acute stroke Trauma Trauma with spinal
board
Scan coverage Foramen magnum to vertex
Scan mode Conventional Helical Helical
Slice thickness 4 mm 3 mm 3 mm
kVp 120 120 120
mAs 300x0.75 200x0.75 220x0.75
Reformations Cor/sag 4 mm Ax/cor/sag bone 1 mm
Cor/sag 3 mm
Ax/cor/sag bone 1 mm
Cor/sag 3 mm
3D - Skull Skull
CTDIvol (mGy) 46.1 51.5 57
ACR CTDIvol upper limit (suggested): 75 mGy



ICH: When To Stop at NCCT
SAH SDH IPH Multi-compartment
ICH
- Trauma and SAH
predominantly in
superficial location
- Any - Hypertension AND
IPH in one of these
locations:
Basal ganglia
Thalamus (unilateral)
Pons
Cerebellar hemisphere
- Trauma
Definitely
trauma
Definitely
hypertensive



When Do We Need IV Contrast?
Clinical indications
•  First-onset seizure
•  R/O brain mass
•  (R/O infection)
Non-contrast images
•  Hemorrhage
–  Lobar
–  Non-traumatic SAH
–  Deep SAH in trauma
•  Hypodensity
–  Not following arterial territories
–  Vasogenic edema
•  Normal non-contrast scan
–  Hyperacute stroke <6 hr
–  Suspected venous thrombosis



Scan Techniques
Contrast-enhanced head CT
CT angiography/venography CT with IV contrast
Scan coverage Foramen magnum to vertex
Scan mode Helical Helical
Injection rate and
scan time
4 mL/s
CTA: trigger 120 HU at basilar artery
CTV: 25s after CTA or trigger 180 HU at sagittal sinus
1 mL/s, 70s
Slice thickness 1 mm 3 mm
kVp 120 120
mAs 280x0.75 200x0.75
Reformations MIP ax/cor/sag 5/3 mm
Small FOV at COW 0.5 mm
Cor/sag 3 mm
3D VRT -
CTDIvol (mGy) (no data) 51.5



ICH: When To Do CTA
ICH
- No trauma
- Trauma but SAH
predominantly in
deep location
- - Young patients
- Lobar Hemorrhage
in older patients
without known
malignancy
- No trauma
- No coagulopathy
Vascular diseases:
aneurysm, AVM
CTA spot sign
IPH = intraparenchymal hemorrhage



ICH: When To Do CTV
Dural sinus thrombosis
During the Scan
ICH
- - - Parasagittal, esp. if bilateral
- Bilateral thalamic
- Disproportionate surrounding
edema and no known malignancy



ICH: When to do just Post-contrast
•  IPH with known malignancy, suspicious for hemorrhagic metastasis



When Do We Need Neck CTA?
•  Stroke in the young (<40 yr)
–  To R/O carotid/vertebral dissection (can be non-traumatic)
•  Hyperacute stroke <6 hr if no bleeding seen on NCCT and
moderate/severe stroke
•  Trauma to R/O arterial injuries: do neck CTA (covering circle of Willis
down to aortic arch)
–  No need for head CTA



Hemorrhage
•  Extravasation of RBCs
–  Microscopic (microbleeds)
–  Macroscopic
•  By appearance
–  Petechial (punctate): cortical contusion, DAI, reperfusion injury/
hemorrhagic transformation
–  Coalescent: venous infarction
–  Membrane-limited: EDH, SDH, SAH, IVH
•  By location
–  Extraaxial: EDH, SDH, SAH
–  Parenchymal: white matter, gray matter, IVH



ICH: CT vs MRI
NCCT
•  Thought to be 100%
sensitive for detecing
“clinically relevant” acute
hemorrhage
•  Criterion standard
MRI (Gradient imaging)
•  GRE as sensitive as NCCT
for acute ICH
•  More accurate for acute
stroke because better
sensitivity for ischemia
•  Limited availability
•  Contraindication
•  Patient’s medical instability
•  Operating time
Limit MRI usage



CT Appearance of Hemorrhage
•  CT attenuation links
to atomic number and
physical density of
globin molecules, and
hematocrit
Timing CT attenuation
<12 h Isodense,
heterogeneous
12h – 7d Hyperdense
7d – 1m Isodense
> 1m Isodense to hypodense



Hematocrit Effect
35-45 HU
0-10 HU
60-90 HU
Whole blood = cells + plasma
55-65%
35-45%



MR Appearance of Hemorrhage
•  Serum around clot will be bright on T2W
Blood products T1W T2W
Oxyhemoglobin I B
Deoxy Hb I (1-3 hr) D (2 hr)
Met Hb (in cells) B (3-14 hr) D
Met Hb (in solution) B B
Hemosiderin D D
B = bright, D = dark, I = isointense
I Be
IdDy
BidDy
BaBy
Doo Doo



Clinical Diagnosis of ICH
•  Often difficult
–  Sudden onset focal neurological deficits, similar to patient with acute
ischemia
–  Certain findings are more likely a/w ICH: LOC, coma, neck
stifness, seizure accompanying neurologic deficit,
dBP greater than 110 mmHg, vomitting, headache
•  Many patients lack these features, neuroimaging is needed



CT Often Sufficient for ICH
•  Location of hemorrhage
•  Unicompartmental or multi-??
•  Secondary effect of hemorrhage
•  Cause of hemorrhage
–  Need IV contrast?
–  CTA, CTV or routine post-contrast?
–  MRI? MRA?



Diagnosis & Differentials
Location Intra- or extra-axial
Supra- or infra-tentorial
Grey matter, white matter, deep nuclei
Specific structures
Anatomy
Appearance Hypo-, iso- or hyperdense
Enhancement
Acuity Acute, subacute or chronic History
Older exams
Secondary effects Effects to surrounding tissues
Brain herniations
Anatomy
Nature (Congenital)
Trauma
Tumor
Infection/inflammation
Vascular
Toxic/metabolic
Location
Appearance
Acuity



Differentials by Location
SAH Aneurysm, trauma
Non-aneurysmal perimesencephalic SAH (pmSAH)
Brain AVM, DAVF, venous infarction, spinal AVM
EDH, SDH Trauma
For SDH in infants, consider non-accidental
IPH Hypertensive
Lobar
Vascular malformation
Tumor
Hemorrhagic venous infarct
Hemorrhagic transformation of ischemic infarct
Amyloid angiopathy
IVH Extension from IPH
Intraventricular tumor
Multicompartmental ICH Trauma, coagulopathy



Subarachnoid Hemorrhage (SAH)
•  Hemorrhage under the arachnoid membranes
•  Worst headache of life
•  Morbidity: vasospasm, mass effect (parenchymal
hematoma and hydrocephalus
•  NCCT is probably best in acute setting
–  Hyperdense sulci
•  Probability of detection proportional to
–  Amount of hemorrhage
–  Time from hemorrhage onset
•  NCCT sensitivity drops with time*
•  98-100% during first 12 hours
•  93% at 24 hours
•  57-85% at 6 days after onset
*Bederson JB, et al. Stroke 2009;40:994
SAH in cortical and cisternal
spaces. Arrow points to blood
reflux into ventricles



•  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)
Medscape.com
Cortical SAH on FLAIR (top) and
susceptibility (bottom) MR images
*Edlow JA, et al. J Emerg Med 2008;34:237



•  Scrutinize these areas systematically
for SAH
–  Perimesencephalic cisterns
–  Sylvian fissures
•  Dilation of temporal horns suggestive
of hydrocephalus, which raises a
possibility of SAH
Lamina terminalis
cistern*
Interpeduncular
cistern
Quadrigeminal
cistern*
Sylvian cistern
Crural cistern
Ambient cistern
*Median, unpaired cisterns



Subarachnoid Hemorrhage (SAH) and
Accompanying Hydrocephalus
•  Common and may occur early
•  May be obstructive or nonobstructive
–  Plugging of cerebral aqueduct
–  Plugging of arachnoid granulations  decreased
uptake of CSF
•  Earliest sign is dilation of temporal horns. must be
evaluated in all CTs
•  Other findings: IVH, IPH, SDH
* *
* *
*



SAH: Differential Diagnosis
•  Aneurysmal
•  Nonaneurysmal
•  “Pseudo-SAH”
•  Reversible
cerebral
vasoconstriction
syndrome
(RCVS)
Cohen-Gadol AA, Bohnstedt BN. Am Fam Phys 2013;88



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
abc.net.au



Aneurysmal SAH
•  Saccular much more common than
dissecting aneurysm
•  Saccular aneurysm:
–  90% anterior circulation: intradural ICA
bifurcation, circle of Willis, MCA bifurcation
(common)
–  10% posterior circulation
•  Dissecting aneurysm: intradural VA
neuroems.com
Medicinenet, Inc.



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
*



Non-aneurysmal pmSAH
•  Small SAH, localized to interpeduncular cistern
•  Presumed venous etiology with low recurrence
©Neuroradiology on the Net @blogspot



SAH: Reversible Cerebral
Vasoconstriction 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 Venous
Sinus Thrombosis
Venous sinus 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



BEWARE: Pseudo-SAH
•  Increased density in basal cisterns, frequently related to
cardiopulmonary arrest
•  Hyperdense brain (severe edema): cisternal effacement, distension +/-
thrombosis of vessels, adjacent brain hypodensity
•  Other causes: intrathecal contrast, meningitis
Pseudo-SAH from severe brain edema
©Neurology 2012; 78:e54.



Intraparenchymal Hemorrhage
HYPERTENSIVE
•  Classic locations AND
hypertension
NON-HYPERTENSIVE, LOBAR
•  Need to find etiologies
–  Vascular malformation
–  Tumor
–  Hemorrhagic venous infarct
–  Hemorrhagic
transformation of ischemic
infarct
–  Amyloid angiopathy



Hypertensive Hemorrhage
•  Rupture of small blood vessel that has
been damaged by chronic HTN
•  50% of primary nontraumatic ICH
•  Most common cause of spontaneous
ICH between 45-70 years
•  Elderly patients a/w systemic HTN
•  Predilection for areas supplied by
penetrating branches of MCA and
basilar arteries
–  Putamen and external capsule 60-65%
–  Thalamus 15-20%
–  Pons, cerebellum10%
–  Lobar 5-15%
*
Hypertensive hemorrhage of the right
putamen with mild surrounding edema



Hypertensive Hemorrhage
•  Neurologic deterioration common within 48 hr
–  Increasing hematoma
–  Edema
–  Development of hydrocephalus
–  Herniation syndromes
•  Recurrent in 5-10% of cases usually in
different location
•  80% mortality in massive ICH with IVH *
Hypertensive hemorrhage in the left
thalamus and posterior limb of the left
internal capsule



BEWARE: Some Basal Ganglia
Hemorrhage
•  Young patient + No hypertension
  Renovascular disease, pheochromocytoma, drugs, etc.
•  Vascular malformation, aneurysm
•  Hemorrhagic neoplasm
•  Need IV contrast!
Basal ganglia hemorrhage secondary to reninoma.
Images from Mao J, et al. J Clin Hypertension 2012;14:802.



Lobar Hemorrhage: Differentials
•  Vascular (AVM, cavernous malformation), aneurysm
•  Tumor
•  Amyloid angiopathy
•  Hemorrhagic venous infarct
•  Hemorrhagic transformation of ischemic infarct
Lobar Hemorrhage a/w
subarachnoid extension is
unlikely related to HTN –
think vascular abnormalities.
Underlying cause of lobar hemorrhage
is often difficult to determine



Arteriovenous Malformation (AVM)
•  Pial vascular malformation of brain, artery 
vein shunting. No intervening capillary bed
•  “Young adult with nontraumatic ICH”
•  All brain AVMs are potentially hazardous.
Majority becomes symptomatic
•  Hemorrhage (50%), seizure (25%), focal
deficit (25%)
*
Hematoma of the left
parietotemporal lobe with edema



Arteriovenous Malformation (AVM)
•  NCCT: may be normal if small
–  Iso-/hyperdense serpentine vessels
–  Calcification in 25-30%
–  If bleed, IPH, IVH >> SAH
•  CECT: strong enhancement of arterial
feeders, nidus and draining veins
•  CTA: enlarged feeders and draining veins
–  Look for intranidal aneurysms
–  Look for subtle early draining veins as a
clue to diagnose thrombosed AVM
•  Main DDx: High-grade glioma with AV
shunting and dAVF
*
*
Two cases of AVMs presenting as lobar
hemorrhage. Arrows = AVM nidus



Cavernous Malformation
•  Far less frequent than AVM
•  Lobulated collection of immature vessels,
hemorrhages of various stages without
normal intervening brain
•  Cumulative risk of hemorrhage = 0.5-1%
per year (usually without clinical)
•  40-60 years, M = F
•  Can enlarged, regress or occur de novo
•  Size: microscopic to giant (> 6 cm)
•  “Popcorn ball” on NCCT (neg in 30-50%)
•  Little/no enhancement.
•  CTA: usually negative
•  Look for associated DVA
Cavernous malformation



Bleeding Tumor
•  Extensive and abnormal tumor vascularity
•  Primary or metastatic tumors
•  Metastatic disease
–  Hemorrhage common with some mets
(melanoma, choriocarcinoma, lung, thyroid,
HCC, RCC)
–  “Spontaneous” ICH in elderly patient may be
caused by metastasis
–  Disproportionate surrounding edema
–  Almost all enhance on CECT, mostly at rim
•  High-grade glioma
–  Most have marked vascularity +/- gross hemorrhage
–  Necrotic core with thick, irregular enhancing tumor
most common in supratentorial white matter
–  Marked mass effect and surrounding edema/tumor
infiltration
Bleeding metastatic tumor



Hemorrhagic Venous Infarction
•  Parenchymal abnormalities common with cortical venous thrombosis
–  Petechial hemorrhage, edema
–  Hypodensity in affected vascular distribution
•  Many predisposing factors. No cause in 20-25%
•  M < F, Most common presentation = headache
•  Type 4 of venous ischemia (Type 1 = no abnormality, 2 = high T2/
FLAIR signal but no enhancement, 3 = high T2/FLAIR signal with
enhancement, 4 = hemorrhage or venous infarction)



Hemorrhagic Venous Infarction
•  Hyperdense cortical vein “cord” sign +/- dural sinus
thrombosis (DST)
•  Enlarged veins (distended with clot)
•  Linear, cigar-shaped thrombus
•  Collateral channels and DST seen on CECT/CTV
•  Negative CTV does not exclude CVT
–  Nonocclusive thrombus
–  Chronic thrombus (also enhances)
–  Need to optimize technique (0.6 mm slice thickness,
MPr 1-2 mm with thick-slice overlaps
•  NCCT is needed to exclude false-negative CTV
due to dense thrombus
–  Bright dural sinuses may also be due to high HCT,
dehydration, polycythemia Superficial, lobar hemorrhage with SAH
and “empty delta” sign of the superior
sagittal sinus on post-contrast image



Hemorrhagic Transformation of Ischemic
Infarct
•  15-20% of MCA occlusions
–  Petechial hemorrhages: Punctate, increased
attenuation resulting in cortex appearing
“near-normal”
–  Secondary hematoma: Discrete hematoma on
infarct, usually small component of
abnormal tissues
•  Reperfusion of infarcted tissues which have
weakened vessels
•  Usually by 48-72 hours after stroke onset
•  Common location = basal ganglia and cortex
•  Other signs of arterial ischemic infarct
–  Wedge-shaped hypoattenuation involving both
gray and white matter
Diagram from Khatri R et al. Neurology 2012; 79:S52
Punctate hemorrhages seen
within right MCA infarct



Cerebral Amyloid Angiopathy
•  Degenerative blood vessels weakned by
deposition of B-amyloid
•  Pathology: lobar hemorrhage, multiple
small cortical hemorrhages
•  10-20% localized form
•  Usually in elderly
•  “Normotensive demented patient with
lobar hemorrhage of different stages”
•  Usually multiple, recurrent hemorrhages
with progressive cognitive decline
•  Gray-white junction most commonly at
parietal and occipital lobes
•  Not common in brainstem, deep gray
nuclei, cerebellum and hippocampus
Large lobar hemorrhage of the left temporal lobe without abnormal vessels or
enhancement. Susceptibility MRI showing several other microhemorrhages
**
*
*



Unusual Causes of Lobar Hemorrhage
•  Ruptured berry aneurysm
•  Most intracranial aneurysm ruptures are a/w acute SAH but they
frequently have IPH
•  Temporal region (MCA bifurcation aneurysm)
•  Frontal region (AcoA aneurysm)
* *
MCA bifurcation aneurysm bleeds into the right temporal lobe



CTA Spot Sign
•  Prognostic sign in acute ICH suggesting
hematoma expansion
Findings
Appearance Serpiginous
Spot-like
Location Within margin of IPH
No connection to outside vessel
Size >1.5 mm diameter in maximal axial dimension
Density At least double the density (HU) compared to
background hematoma
Lesion number Multiple
Single
Thompson AL, Kosior JC, Gladstone DJ, et al. Can J Neurol 2009; 36:456.
*



Intraventricular
Hemorrhage
•  Blood in ventricular system
•  Significant morbidity 2/2 obstructive
hydrocephalus
•  Primary or secondary
–  Primary – dominant blood in ventricles
(little, if any, parenchymal blood)
•  Tumors or vascular malformations
–  Secondary – large extraventricular
component (e.g., IPH or SAH with
secondary extension into ventricles).
•  Far more common than primary
•  In adults, this is commonly 2/2 basal ganglia
hypertensive IPH or SAH with ventricular reflux
•  In children, this is a distinct entity SAH with ventricular reflux
*
*



Multicompartmental ICH
•  Trauma
•  Coagulopathy “presence of fluid-fluid level”
•  SAH-IVH
•  Extension of large IPH to other spaces
*
Coagulopathic ICH: IVH (blue arrow), parenchymal hemorrhage (star) and SAH
(red arrow). Note fluid-fluid level (green arrow)



Communication of Urgent Findings
•  Communication to referring physicians regarding “urgent” imaging
finding(s) is a standard of care
•  Documentation of communication must be routine
•  All ICHs are considered urgent findings – needing communication &
documentation
–  New, increasing
–  Except when it is known and stable from prior scan
•  Be aware that many times, secondary effects are more catastrophic
than hemorrhages themselves



Reading Emergency Head CT:
“Blood Can Be Very Bad”
Blood Evaluate for hemorrhage (bright white on CT)
Blood isodense around 1-2 weeks
Hypodense by 2-3 weeks
EDH, SDH, IPH, IVH, SAH and extracranial hemorrhage
Cisterns Four key cisterns examined for blood, asymmetry and effacement:
• Perimesencephalic
• Suprasellar
• Quadrigeminal plate
• Sylvian
Brain Look for symmetry, gray-white differentiation, shifting, hyper- or
hypodensity
Ventricles Hydrocephalus (first evident in dilation of temporal horns)
Compression/shift of ventricular system
Bone Fractures increase suspicion for intracranial injury
Perron AD. Emergency Medicine. Philadelphia, London: Saunders; 2008

Imaging of Non-traumatic Intracranial Hemorrhage

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