Imaging of Non-traumatic Intracranial Hemorrhage

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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

Def

inite

ly

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ma

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


- 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


- - -  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

* *

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*


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

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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

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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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