imagingof cerebral redflags! hemorrhage when a … hemorrage...11.10.2019 7 subdural hematoma...
TRANSCRIPT
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Imaging of CerebralHemorrhage
Prof. Dr. E. Turgut TaliPresident, World Federation of Neuroradiological Societies
President, Turkish Society of NeuroradiologyPast CEO, European Board of Neuroradiology
Past President, European Society of Neuroradiology
Head, Division of NeuroradiologyGazi University School of Medicine
Ankara, [email protected]
When a patient • Focal neurological deficits• Severe headache• Vomiting• High systolic blood pressure greater than 220 mm. Hg• Decreased consciousness with a sudden onset• Symptoms progression over minutes-hours
Intracerebral hemorrhage (ICH) should be the first condition considered in the
diagnosis!
Red Flags!
ACR Appropriateness Criteria ACR Appropriateness Criteria
ACR Appropriateness Criteria ACR Appropriateness Criteria
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• Brain computed tomography (CT) • The gold standard for identifying acute
hemorrhage • Subacute and chronic stages may be occult
ICH Imaging•Magnetic resonance imaging (MRI) • An alternative with an advantage of being able to
differentiate between the acute and chronic stages of hemorrhage • Hyperacute stage • T2* and susceptibility-weighted (SWI) are as sensitive
as CT for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage
ICH Imaging
Blood = Plasma + Cells
35-45% 55-65%
35-45 HU 0-10 HU 60-90 HU
Hyperdense massCould be isodense; if hemoglobine < 8-10 g/dl or with bleeding diatheses (e.g., hemophilia)Attenuation decreases 1.5 HU/day Chronic stage; hypodense lesion, sequela gliosis, hemosiderin
Intracerebral Hemorrhage
Central hypodensity possible: Rapidly accumulating hematoma & unretractedsemiliquid clot; "swirl sign"
Enhancing spots inside thehematoma shows extravasation
Hemorrhagic sedimentationlevel; hematocrite effect, bloodserum-settled blood cells
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CECT: Intracerebral Hemorrhage
• No enhancement in the acute phase• May occur between 2-6 weeks
• Developing neovascularization aroundintracranial hemorrhage (ICH)
• Blood-brain barrier (BBB) breakdown in the vascularized capsule• DDx: Brain tumor / Abscess
Hematoma Volume MeasurementABC/2 method; A: Maximal hematoma diameter on the axial slice with largest hematoma areaB: Maximal hematoma diameter perpendicular to A C: The number of CT slices with hematoma multiplied by slice thickness (ignoring slices with <25% of hematoma area compared with the reference slice)
Alastair JS, Stroke 2015
Hematoma Volume Measurement
• ABC/2 scores are sufficiently accurate to categorize
ICH volume and assess eligibility for the CLEAR-III
and MISTIE III studies, and moderately accurate for
change in ICH volume
• Accuracy decreases with large, irregular, or lobar
clots. Attempts to improve the accuracy of volume
measurements could provide additional clinical
value.
MISTIE-II: Minimally Invasive Surgery Plus Recombinant Tissue-Type
Plasminogen Activator for Intracerebral Hemorrhage Evacuation
CLEAR-IVH: Clot Lysis Evaluation of Accelerated Resolution of
Intraventricular Hemorrhage
Hematoma Volume Measurement• Intracerebral hemorrhage volume is probably more
important than GCS score in determining treatment. GCS score of at least 13 or when ICH volume is less than 30 mL, regardless of GCS score.
Cho DY Surg Neurol 2008• Operation is to be the preferred choice of treatment
for the cases GCS≥6 and for large hematomas (>40ml volume)
Anik I, Turkish Neurosurg 2011
MRI in Intacranial HemorrhageT1 iso iso hyper hyper hyper hypo
T2 iso hypo hypo hypo hyper hypo
Oxy Hb Deoxy Hb Met Hb Hemosiderine
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T1
T2
Oxy Hb Edema Deoxy Hb
T1
T2
Edema Deoxy Hb Met Hb
T1
T2
Edema Deoxy Hb Met Hb
T1
T2
Edema Met Hb
Phacytes withhemosiderine and/or
ferritine
T1
T2
Phacytes withhemosiderine and/or
ferritine
Met HbHemosiderine
T1
T2
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SWI: Hyperacute & Acute Hematoma
Even at early stage, some transition to
deoxyhemoglobin formation may cause
rim hypointensity
Loss of signal due to T2* dephasing
from paramagnetic deoxy-Hb confined
to RBCs.
SWI: Subacute & Chronic HematomaMarked hypointensity at periphery of hematoma noted due to ferritin/hemosiderin accumulation.
Loss of signal due to T2* dephasing from paramagnetic met-Hb confined to RBCs. Even more hypointensity is seen at periphery due to accumulation of ferritin and hemosiderin.
SWI: Hematoma vs Calcification
Phase map shows bright signal of hemorrhage.
DWI: Hyperacute Hematoma
Restricted diffusion in the hematoma center due to reduced extracellular space and increased viscosity.
DWI: Acute Hematoma
Both have dark centers, due to strong paramagnetic artifacts and the T2-blackout effect. Susceptibility artifacts make accurate calculation of ADC values difficult.
DWI: Subacute Hematoma
Both have dark centers, due to strong paramagnetic artifacts and the T2-blackout effect. Brighter susceptibility artifacts is present at periphery of trace image.
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DWI: Chronic Hematoma
Hypointense on DWI and hyperintense on ADC map
• Extraaxial• Epidural• Subdural• Subarachnoid• Intraventricular
Intracerebral Hemorrhage
Lobar Thalamocapsular
Thalamic Caudate
• Intraaxial• Lobar• Thalamocapsular• Thalamic• Caudate
IntracerebralHemorrhage • Trauma -> fracture & concussion
• Tearing/stripping of both layers from inner table
• Because the dura is especially tightly attached to sutures, rarely cross suture lines
• Laceration of outer periosteal layer • Laceration of meningeal vessels artery
90%, venous 10%• Blood between naked bone and dura • Normal arterial pressure continues to
dissect periosteum from bone• Inner (meningeal dura) intact
Epidural Hemorrhage
•Usually acute clinical presentation •Young patients, usually < 40 •Dura firmly fixed in
older patients •Usually unilateral•85-95% associated with skull fracture
Epidural Hemorrhage• NECT is the procedure of choice • Soft tissue, bone, and multiplanar
reconstructions should be obtained (useful in identifying vertex epidural hematomas)
• Hyperdense (60-90 HU) lentiformextraaxial collection
• Hypodense component (“swirl” sign) is seen in about one-third of cases and indicates active, rapid bleeding with unretracted clot
• Air seen in 20% of cases
Epidural Hemorrhage
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Subdural Hematoma• Subdural hematoma > Epidural
hematoma • Acute, subacute, chronic presentation• May be bilateral• Causes• Trauma is common cause, 15% occur as
“Contre-coup” injuries, no particular association with fracture
• Aneurysm rupture, skull/dura-arachnoid metastases from vascular extracranial primary neoplasms, and spontaneous hemorrhage in patients with severe coagulopathy
• Rarely, an acute spontaneous SDH of arterial origin occurs in someone without any traumatic history or vascular anomaly
Subdural Hematoma• Tearing of bridging cortical veins (as they
cross the subdural space to enter a duralvenous sinus)
• Cortical vein lacerations (either a skull fracture or the sudden changes in velocity and brain rotation that occur during non-impact closed head injury
Subdural Hematoma• Tearing of bridging cortical veins (as they cross the subdural space to enter a
dural venous sinus) • Cortical vein lacerations (either a skull fracture or the sudden changes in
velocity and brain rotation that occur during non-impact closed head injury
Subdural Hematoma• Tearing of bridging cortical veins (as they cross the subdural space to enter a
dural venous sinus) • Cortical vein lacerations (either a skull fracture or the sudden changes in
velocity and brain rotation that occur during non-impact closed head injury
Subdural Hematoma• Isolated SDH in infants and
elderly• More atrophy more freedom
of movement• Larger subarachnoid space –
more movement – more SDH
Subdural Hematoma• Vast majority of SDHs are
associated with traumatic subarachnoid hemorrhage, significant parenchymal injuries; cortical contusions, brain lacerations, diffuse axonal injuries
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Subdural Hematoma• “Currant jelly” clot• Under bulging dura
• Spreads diffusely• Covers brain• Often spreads over tentorium• May cross sutures, not dura• Extends into interhemispheric fissure
• NECT• Crescent shape • 60% hyperdense, 40% mixed • Swirl sign• Dots and lines of CSF trapped• CECT are helpful in detecting small
isodense aSDHs. The normally enhancing cortical veins are displaced inward by the extraaxial fluid collection
Subdural Hematoma Stages
Acute < 3 days
Sulcal effacement, subfalcial herniation, Shift
Chronic>2 weeks
Subacute 3 days-2 weeks
Left frontoparietal hyperdense, homogeneous, crescent-shaped
extraaxial collection
Acute subdural hematoma
Asymmetric hyperdensity along the left tentorium SDH can be difficult to
differentiate from adjacent parenchyma
Effacement of adjacent sulci, an important clue for subtleSDHs (suggested “subdural”
window width 130 andwindow level of 30)
Isodense acute subdural hematoma: transition phase during from an acute SDH to
a chronic
Hemorrhagic sedimentationlevel; hematocrite effect, bloodserum-settled blood cells
• LP more sensitive than CT• Trauma is most common
cause for RBC’S in CSF • Not seen as easily or as often on
CT SAH on CT • Causes• Usually Aneurysm / AVM• Uncommon cause: neoplasm• Uncommon cause: spinal disease
• Morbidity• Vasospasm • Mass Effect (parenchymal
hematoma) • Hydrocephalus
Subarachnoid Hemorrhage
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• CTA, Angiography, MRA• Hyperdensities in sulci
• CTA, Angiography, MRA• Normal in 2 days• 2 days-2 weeks; vessel
narrowing, beading• MRI• Dirty sulci on T1, T2• Hyperintense sulci on FLAIR• Blooming hypointensity on
GRE, SWI
Subarachnoid Hemorrhage• Intraventricular hemorrhage is present
in nearly half of all patients with aSAH• The presence of intraventricular blood
together with thick SAH is designated a grade 4 bleed• Increases in modified Fisher grade have
a moderately linear relationship with the risk of vasospasm, delayed infarction, and poor clinical outcome
Intraventricular Hemorrhage
• CT• Initial imaging modality• Subacute and chronic stages may be occult
•MRI• T2* and/or susceptibility-weighted (SWI) are
as sensitive as CT
Imaging of Hemorrhage