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Neuroimaging of

Intracranial Hemorrhage

Lee Madeline, MD

November 2, 2013

Much of this talk pilfered from

◦ The Net

Role of Imaging

To recognize the presence of blood

To localize and differentiate hemorrhages

◦ (SAH, SDH, EDH)

To determine the age of the hemorrhage

To identify the etiology

◦ Exclude stroke mimic (tumor, etc.)

To aid in ascertaining the patient's prognosis

Neuroimaging of ICH

Appearance on CT

Appearance on MRI

Etiology for ICH

◦ Intracerebral

◦ Extracerebral

All in just 30 minutes!

ICH: Appearance on CT

Density of Tissue Gray Scale • air black

• fat darker gray

• CSF gray

• brain lighter gray

• acute blood, contrast white

• bone very white

Hemorrhage on CT

IPH SAH SDH EDH

Mutifocal hemorrhagic contusions

Subacute: Isodense Subdural

ICH: Appearance on MRI

Depend on …

the age of the hematoma

imaging sequence or parameters

site of the hemorrhage (“faster” IPH)

local partial pressure of oxygen in the tissues (hypoxic)

the local pH (acidic)

pt’s hematocrit

local glucose concentration

hemoglobin concentration

integrity of the BBB

the patient's temp (hyper)

Stages of Hemorrhage

As a hematoma ages, hemoglobin changes

through several forms

◦ Oxyhemoglobin

◦ Deoxyhemoglobin

◦ Methemoglobin

◦ Then RBCs are broken down into

Ferritin

Hemosiderin

Stages of Hemorrhage

Phase Time Hemoglobin,

Location

Hyperacute < 24 h Oxyhemoglobin,

intracellular

Acute 1-3 d Deoxyhemoglobin,

intracellular

Early subacute >3 d Methemoglobin,

intracellular

Late subacute >7 d Methemoglobin,

extracellular

Chronic >14 d Ferritin and hemosiderin,

extracellular

Evolution of Hemorrhage on MRI

Phase Time

Hemoglobin,

Location

Appearance

T1-

Weighted

MRI

T2-

Weighted

MRI

Hyperacute < 24 h Oxyhemoglobin,

intracellular

Isointense or

hypointense

Hyperintense

Acute 1-3 d Deoxyhemoglobin,

intracellular

Isointense Hypointense

Early

subacute

>3 d Methemoglobin,

intracellular

Hyperintense Hypointense

Late subacute >7 d Methemoglobin,

extracellular

Hyperintense Hyperintense

Chronic >14 d Ferritin and

hemosiderin,

extracellular

Hypointense Hypointense

“I D / B D / B B / D D”

Hyperacute (<24h)

Right external capsule and insular cortex in a known hypertensive patient

T1 isointense to hypointense

T2 hyperintense

I “B”D / B D / B B / D D

Acute (1-3d)

T1 iso to hypodense

T2 hypointense

I D / B D / B B / D D

Early Subacute (>3d)

T1 hyperintense

T2 hypointense

I D / B D / B B / D D

Late Subacute (>7d)

Late Subacute hemorrhage bithalamic regions in a pt with known cerebral malaria.

T1 hyperintense

T2 hyperintense

T2 (and GRE) hypointense rim due to hemosiderin.

I D / B D / B B / D D

Chronic (>14d)

The hematoma shows a large medial subacute component and a small lateral chronic component.

The chronic component (arrow) is hypointense on both T1 and T2.

This hypointensity is enhanced due to the blooming effect of blood on GRE.

I D / B D / B B / D D

Cavernous Malformation

Characteristic “popcorn appearance” on MRI

Intracranial Hemorrhage

8-13% of all strokes

More likely to result in death or major

disability than ischemic stroke

Annually, more than 20,000 individuals in

the US die from ICH

ICH has a 30-day mortality rate of 44%

ICH: Categorize by Cause

Drug abuse

Moyamoya

Sickle cell disease

Eclampsia or postpartum

vasculopathy

Infection

Vasculitis

Hypertension

Vascular malformations

Aneurysmal SAH

Cerebral amyloid angiopathy

Intracranial neoplasm

Coagulopathy

Hemorrhagic transformation

of an ischemic infarct

Cerebral venous

thrombosis

Trauma (SDH/EDH) > Non Traumatic

Cerebral Hemorrhage Categorized by etiology

Intracranial Bleeds

◦ hypertensive bleeds

◦ hemorrhagic transformation of ischemic infarction

◦ cerebral amyloid angiopathy

◦ aneurysmal SAH

Extraaxial Fluid Collections

◦ EDH / SDH

Hypertensive Bleeds

most common cause of nontraumatic

intraparenchymal hemorrhage in the brain

Chang

Hypertensive Hemorrhage

Pathophysiology

◦ degenerative cerebral microangiopathy

characterized by hyalinization of the walls of small

arterioles and, ultimately, fibrinoid necrosis.

Charcot- Bouchard aneurysms

Hypertensive Bleeds

Location

◦ putamen/external capsule,

60-65%

◦ thalamus, 15- 25%

◦ pons and brainstem, 5-10%

◦ cerebellum, 2-5%

◦ cerebral hemispheres, 1-2%

IV extension in 50%

Men have 5-20% higher

incidence Osborn

HTN Bleed in Cerebellum

62 yo with HTN with acute onset of ataxia and confusion

CT T2

Acute = Dark on T2

47 yo with HTN bleed in BS

Cerebral Hemorrhage

Intracranial Bleeds

◦ hypertensive bleeds

◦ hemorrhagic transformation of ischemic infarction

◦ cerebral amyloid angiopathy

◦ aneurysmal SAH

Extraaxial Fluid Collections

◦ EDH / SDH

Hemorrhagic Transformation of

Brain Infarction

Infarcted brain has a propensity to bleed, particularly

when reperfused in the acute phase.

Hemorrhage due to brain infarction may be recognized

b/o assoc cytotoxic edema that conforms to an arterial

territory.

◦ assoc may be difficult to diagnose when early massive

bleeding obscures the underlying infarct.

Baseline CT < 3 hrs

Hemorrhagic Transformation of

Ischemic Infarction

Day 1 CT s/p TPA

Hemorrhagic Transformation of

Ischemic Infarction

Cerebral Hemorrhage

Intracranial Bleeds

◦ hypertensive bleeds

◦ hemorrhagic transformation of ischemic infarction

◦ cerebral amyloid angiopathy

◦ aneurysmal SAH

Extraaxial Fluid Collections

◦ EDH / SDH

Cerebral Amyloid Angiopathy

Pathophysiology

◦ Deposition of beta-amyloid in the arterial media and/or

adventitia of small arterioles

◦ Cerebrum > cerebellum

◦ Dissection into

SAS is common,

Ventricular extension is uncommon.

◦ In elderly, lobar ICH and multiple microbleeds are highly

suggestive of CAA.

◦ not associated with systemic amyloidosis

◦ although most cases are sporadic, familial forms exist

Amyloid Angiopathy

Amyloid is a protein that infiltrates vessel walls, replaces

smooth muscle cells in the media, and may make the vessel structurally

brittle.

Amyloid Angiopathy

20 months later 6 weeks later

65 yo with multiple intracerebral hemorrhages

Initial

Cerebral Amyloid Angiopathy

Prognosis

◦ Lobar ICH is assoc w a lower mortality rate (11-

32%) and a better functional outcome than

hypertensive deep ganglionic bleeds

◦ Of individuals with CAA-related hemorrhage, 25-40%

have a recurrence

highest risk in the first year

Merino

Cerebral Hemorrhage

Intracranial Bleeds

◦ hypertensive bleeds

◦ hemorrhagic transformation of ischemic infarction

◦ cerebral amyloid angiopathy

◦ aneurysmal SAH

Extraaxial Fluid Collections

◦ EDH / SDH

SAH Etiology

Overall, head trauma is the most common

cause of SAH

80% of nontraumatic SAH results from

ruptured aneurysms

Less common causes:

mycotic aneurysm

AVM

infection

hemorrhagic disease

SAH Presentation

sudden onset of the “worst headache of my life”

frequently followed by photophobia, nausea, and vomiting

most common in those aged 40-65 ◦ blacks have 2.1 times greater risk

◦ slightly higher in women than men

annual incidence of aneurysmal SAH is 6-25 per 100,000

>27,000 Americans suffer ruptured intracranial aneurysms each year

SAH from basilar tip aneurysm

Pattern of SAH:

“Aneurysmal”

SAH from ruptured MCA aneurysm

Pattern of SAH:

“Aneurysmal”

Pattern of SAH:

Perimesencephalic Low rate of re-hemorrhage

Lower rate of Sx vasospasm

Venous hemorrhage

SAH Morbidity/Mortality

10-15% of pts die before reaching hospital

mortality rate reaches as high as 40% within

the first week

Rebleed carries a mortality rate of 75%

about half die in the first 6 mo

> 1/3 have major neurologic deficits

25% multiple

SAH Pathophysiology

Aneurysms are acquired lesions related to

hemodynamic stress on the arterial walls at

bifurcation points and bends

Saccular aneurysms are specific to the

intracranial arteries b/c walls lack an external

elastic lamina and contain a very thin

adventitia—factors that may predispose to

the formation of aneurysms

lie unsupported in the SA space

Mycotic Aneurysms

any aneurysm that results from an infectious

process involving the arterial wall

Bacterial endocarditis 80%

2-4% of all intracranial aneurysms

occur with greater freq in children

often are found on vessels distal to CoW

fusiform morphology and are usually v friable

Peripheral and multiple

Mycotic Aneurysm

SAH

Intracranial aneurysms classified to

according to

◦ gross pathologic appearance

◦ location

3 types

◦ saccular or berry aneuryms

◦ fusiform

◦ dissecting aneurysms

Osborn

Fusiform Aneurysm

Elongated aneurysm caused by

atherosclerotic disease

Usually located in vertebrobasilar system

Present in older patients

Can contain thrombus and calcification

Saccular Fusiform

Dissecting Aneurysm

Following a dissection an intramural hematoma results

in a saclike outpouching

Etiology:

◦ trauma>vasculopathy (SLE, FMD)>spontaneous

dissection

Location: extracranial ICA, VA

High incidence of hemorrhage

Osborn

Dissecting Aneurysm

NANG: elongated contrast collection beyond vessel lumen

SAH and IVH

SAH and IVH differ from IPH, SDH and EDH in that

they are mixed with CSF.

Like EDHs and SDHs, SAHs have high oxygen levels;

therefore, they age more slowly than IPH.

In cases of mild SAH, RBCs may be resorbed by the

time notable methemoglobin formation occurs.

Therefore, T1 shortening is seldom seen.

… CT is advocated for the early diagnosis of SAH.

SAH and IVH

SAH and IVH on MRI

FLAIR is the most sensitive MRI sequence for detecting

SAH.

◦ SAH appears as high SI c/t normally hypointense CSF

T2- and T2* can potentially demonstrate SAH as an area

of low signal in normally hyperintense SA spaces.

On T1, acute SAH may appear as intermediate or high

signal in the SA space. (Less sensitive)

In chronic and repeated SAH, hemosiderin may stain the

leptomeninges, leading decreased signal known as

superficial siderosis.

Hemosiderosis from prior SAH on MRI

SAH and IVH

MRA useful in the evaluation of aneurysms and other

vascular lesions.

CTA may be adequate for identifying and characterizing

lesions without a need for catheter DSA in the acute

phase of the illness.

Primary IVH is rare

◦ HTN

◦ Acomm Aneurysm

◦ Anticoagulation

◦ Vascular malformation

◦ Moyamoya disease

◦ IV tumors

Cerebral Hemorrhage

Intracranial Bleeds

◦ hypertensive bleeds

◦ hemorrhagic transformation of ischemic infarction

◦ cerebral amyloid angiopathy

◦ aneurysmal SAH

Extraaxial Fluid Collections

◦ EDH / SDH

SDH and EDH

Because the dura is well vascularized and because O2 tension

remains high, progression from one stage to another is slower in SDH /

EDH than IPH.

First 4 stages same as those for IPH.

The chronic stage characterized by continued oxidative

denaturation of methemoglobin.

◦ No hemosiderin rim is seen in the surrounding hematoma and

no tissue macrophages are present.

EDHs are differentiated from SDH on the basis of their classic

biconvexity versus medially concavity

SDH dissecting

down from the

head

EDH from

Catheter

SDH – Late Subacute

isodense on CT Bright / Bright

Mimics for Hemorrhage

… hyperintensity on T1 Melanin:

◦ Mets from melanoma less commonly display susceptibility on GRE, and they

typically show some contrast enhancement.

Fat:

◦ Use of fat-suppression techniques can help differentiate fat from hemorrhage.

◦ Presence of a chemical shift artifact may also indicate a fatty lesion.

Hem Mets:

◦ Contrast enhancement, which is not seen in bland hematomas.

Calcification:

◦ Differences in the morphology

◦ CT may also help differentiate these entities

Gadolinium

Diffuse Cerebral Edema

SAH Mimic: Diffuse hypoxic ischemic brain

injury

Conclusion

As hemorrhage evolves, it passes through 5 well-defined and easily

identified stages, as seen on MRI.

◦ Knowledge of these stages may be useful for dating a single

hemorrhagic event or for ascertaining if multiple hemorrhagic

events occurred at different times.

CT more sensitive for detecting hyperacute parenchymal

hemorrhage or early SAH or IVH

MRI more sensitive after 12-24 hours.

MRI is also more specific than CT in determining the age of a

hemorrhage.

Both T1and T2 MRI used to adequately characterize and stage a

hemorrhage.

◦ I D / B D / B B / D D

Thank You!

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