Intracranial Intracranial spontaneous hemorrhage spontaneous - - PowerPoint PPT Presentation

Intracranial Intracranial Intracranial Intracranial spontaneous hemorrhage spontaneous hemorrhage spontaneous hemorrhage spontaneous hemorrhage mechanisms, imaging and mechanisms, imaging and mechanisms, imaging and mechanisms, imaging and management management management management

Dora Zlatareva Department of Diagnostic Imaging Medical University, Sofia, Bulgaria

Intracranial hemorrhage (ICH)

ICH

• 15% of strokes
• 25 per 100,000 pt/year
• Mortality - 40% in 1 mo
• Multiple intracranial

compartments

• By diverse pathology

Neuroimaging

• Identify the cause of

hemorrhage

• location and severity of

hemorrhage

• To guide patient

treatment

Mechanisms

• Hypertensive damage to blood vessels
• Rupture of an aneurysm
• Rupture of AVM
• Cerebral amyloid angiopathy
• Altered hemostasis (thrombolysis & anticoagulation)
• Hemorrhagic necrosis (like tumor and infection)
• Substance abuse (cocaine)

Location

• Basal ganglia
• Lobes of cerebrum
• Thalamus
• Pons
• Cerebellum
• Other brainstem sites

Causes

• Hypertension
• Cerebral amyloid angiopathy
• Hemorrhagic conversion of ischemic infarction
• Cerebral aneurysms
• Cerebral AVM
• Dural AV fistula
• Vasculitis
• Venous sinus thrombosis

Imaging

• CT – first modality- acute blood- hyperdense
• CTA - vascular underlying cause (SAH, IPH)
• CT venography –dural venous sinuses
• MRI –r/o tumour
• Depend on time, sequence, size, location
• Cerebral DSA – suspected vascular abnormality,

CTA is either normal or equivocal, or to treat

Recommendations for Neuroimaging in ICH

Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH Class I, Level of Evidence A (Unchanged from the previous) CT angiography and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion Class IIb, Level of Evidence B CTA, CT venography, CeCT, CeMRI, MRA and MRV can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiologic suspicion Class IIa, Level of Evidence B (New recommendation).

AHA/ASA Guideline (2010) Guidelines for the Management of Spontaneous Intracerebral Hemorrhage

ICH: CT appearance ICH: CT appearance ICH: CT appearance ICH: CT appearance

• Acute phase:
• Hyperdense mass (50-80 HU)
• Subacute phase (1-6 weeks)
• Peripheral edema
• Attenuation falls 1.5 HU / day

from the periphery

• chemical breakdown of globin

Hb < 8-10g/dl isodense hematoma

ICH: CT appearance

• Chronic phase
• Hypodense lesion
• Sequelae gliosis
• Hemosiderin!!

ICH: CT appearance

• Still bleeding hematoma
• “Swirl sign”
• Due to semiliquid unretracted clot

Parizel, Eur Radiol 2001

IPH – due to hypertension

• 60ies -70ies, 30-50% mortality
• Acute-BG, cerebellum, occipital lobes
• IPH cerebral cortex - consider other Dg
• Younger than 50 -?other causes -Tu or vascular

malformation

IPH – due to hypertension

• Complications
• Intraventricular hemorrhage
• Hydrocephalus
• Herniation
• Rebleeding
• Initial hemorrhage – different size
• NCCT - predict outcome
• Worse prognosis
• Initial size of the hematoma
• intraventricular extension of the hemorrhage
• expansion of the hematoma on serial imaging

IPH – due to hypertension

• Management
• Surgical treatment contoversial
• Hematoma >3cm
• Benefit of surgery??
• External drainage for hydrocephalus?
• Treatment of systemic HT

IPH- Cerebral amyloid angiopathy

• Cerebral microhemorrhages
• Sulcal SAH –DD from vasculitis
• AGE >60
• Other areas of ICH
• Large cerebral IPH -DD hypertensive
• Subcortical WM
• Spares BG, posterior fossa, brainstem

Linn, AJNR, 2008

Hemorrhagic transformation of ischemic stroke

• )HH99"99<I
• Phhmhgmg(HI1)
• CfuPHfdu(HI2)
• Phymhmm<30%fdu,gh

mff(PH1)

• >30%+gfmff(PH2)– 9gf

Antithrombotic or thrombolytic Th

Cerebral aneurysms

• CT -100% sensitivity for acute SAH in the first 6-24H
• SAH in basal cisterns or diffusely through SA space
• Ventricles and brain parenchyma (lobar hematoma)
• Surgical clipping, endovascular coiling/embolization

SAH

SAH

Cerebral AVM

• ICH - most common presentation of cerebral AVM
• IPH - (young pt or child suspect AVM)
• Intraventricular hemorrhage (IVH)
• SAH
• CTA, MRI,MRA, DSA

Heit et al, J stroke 2017

Management Embolization, Surgery, Radiosurgery

Dural AV fistula

Vasculitis

• Primary, SLE, Behcet
• ICH or ischemic lesion
• Sulcal SAH near convexity -most common
• CT -hyperdensity within cerebral sulci
• MRI - sulcal hyper FLAIR, hypo GRE or SWI
• Sulcal SAH +NO trauma - DSA in negative CTA to

r/o vasculitis or vasculopathy

• Immunosuppressive Th

• Multiple chronic

hemorrhages

• Perivascular

enhancement

• Irregular vessel walls

CNS vasculıtıs CNS vasculıtıs CNS vasculıtıs CNS vasculıtıs

Venous thrombosis

• Cortical vein or dural venous sinus
• Cord sign (hyperdense cortical vein on NCCT),

empty delta sign (CT venography)

• Cerebral edema, parenchymal hemorrhages,

ischemic and hemorrhagic infarcts

• SAH - uncommon, cerebral convexities or Sylvian

fissures, sparing the basal cisterns

Venous thrombosis

• Uncommon and often clinically confusing entity
• Imaging plays an essential role in Dg
• Secondary to skull base infections, dehydration,

hypercoagulable states, compression from meningiomas or other dural tumors

Superior sagittal sinus thrombosis

Underlying tumors

• Primary Tu- hemorrhage

inside the Tu

• Metastasis- at the periphery
• Management -Tu therapy,

surgery, Radio, Chemotherapy

Choi, ET AL., Glioma Mimicking a Hypertensive Intracerebral Hemorrhage, JKNS 2013

Tumors, cavernoma…

Substance abuse (cocaine)

• Hemorrhagic or ischemic strokes
• IPH or SAH -twice as common as ischemic strokes
• 40%–50% -an underlying AVM or aneurysm
• Hematoma in BG, thalamus

Management

• Initial medical stabilization
• Neuroimaging - establish Dg and elucidate etiology
• Neurologic exam - determine baseline severity
• Prevent hematoma expansion (BP management,

reversal of coagulopathy)

• Consideration of early surgical intervention
• Prevention of secondary brain injury

Management

• Hemostatic agents (factor VIIa) early-reduce hematoma

expansion, clinical effectiveness has not been shown

• Anticoagulation reversal with prothrombin

concentrates + Vit K - in VitK antagonist-related ICH

• Ongoing trials for minimally invasive approaches or

hemicraniectomy, role of surgery in ICH to be defined

• BP control, antithrombotic prevention after ICH -

consider the risk of recurrent bleeding and ischemia

Take home messages

• Elderly patient with HT, BG hematoma
• Hypertensive hemorrhage
• Do SWI to see other microbleeds
• Eldery normotensive patient, lobar hematoma
• Amyloid angiopathy / tumor
• Do +C MRI, SWI, MRA? DSA?
• Enhancing lesion Tm
• Subcortical microbleeds on SWI Amyloid angiopathy

Take home messages

Young patient with ICH (ALERT!!!)

Do +C MRI, MRA / CTA / DSA, SWI Angio abnormal Vasc. Malf, Vasculitis, DVST Enhancing single lesion Tm Enhancing multiple lesions Met, Vasculitis, Septic emboli Multiple “black dots” on SWI Vasculitis, Cavernomas Patient of any age with associated SAH Aneurysm Patient of any age with ICH, you still cannot decide the etiology Refer to the clinician, short time FUp scan

I would like to thank to Cem Calli for ideas and cases

Thank you for your kind attention!