14.10.2019 1 Intracerebral Hemorrhage Prof. Dr. E. Turgut Tali President, World Federation of Neuroradiological Societies President, Turkish Society of Neuroradiology Head, Division of Neuroradiology Gazi University School of Medicine Ankara, Turkey [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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IntracerebralHemorrhage
Prof. Dr. E. Turgut Tali
President, World Federation of Neuroradiological Societies President, Turkish Society of Neuroradiology
Head, Division of NeuroradiologyGazi University School of Medicine
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
• 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 60‐90HU
Hyperdense mass
Could be isodense; if hemoglobine < 8-10 g/dl or with bleeding diatheses (e.g., hemophilia)
• No enhancement in the acute phase• Enhancement may occur between 2-6
weeks• Developing neovascularization around
intracranial hemorrhage (ICH)• Blood-brain barrier (BBB) breakdown in
the vascularized capsule• DDx: Brain tumor / Abscess
Hematoma Volume Measurement
ABC/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 Volum Measurement
A: 4,27 B: 4,39 C: 0.5 x 10 =5ABC = 93,5 / 2 = 46,75 mL
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 EvacuationCLEAR-IVH: Clot Lysis Evaluation of Accelerated Resolution of Intraventricular Hemorrhage
Hematoma Volume Measurement• Intracerebral hemorrhage volume is probably more
important than Glascow Coma Scale score (GCS) in determining treatment
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 Intracerebral Hemorrhage
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Parenchymal Hemorrhage Stages Hemorrhagic infarct can be shown byMRI
Blood ageing or degradation can be followed by MRI
Non-EnhancedMRI
T1 iso iso hyper hyper hyper hypo
T2 iso hypo hypo hypo hyper hypo
Oxy Hb Deoxy Hb Met Hb Hemosiderine
T1
T2
Oxy Hb Edema Deoxy Hb
T1
T2
Edema Deoxy Hb Met Hb
T1
T2
Edema Deoxy Hb Met Hb
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T1
T2
Edema Met Hb
Phagocytes withhemosiderine and/or
ferritine
T1
T2
Phagocytes withhemosiderine and/or
ferritine
Met Hb
Hemosiderine
T1
T2
Siderosis
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 red blood cells (RBC).
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.
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SWI: Hematoma vs Calcification
Phase map shows bright signal of hemorrhage. Phase map shows signal void of calcification
SWI: Hematoma vs Calcification
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.
• 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 multiplanarreconstructions should be obtained (useful in identifying vertex epidural hematomas)
• 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
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Subdural Hematoma• Tearing of bridging cortical veins as they cross the subdural space to enter a duralvenous sinus most common etiology
• 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 (larger spaces) 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
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
Left frontoparietal hyperdense, homogeneous, crescent-shaped
extraaxial collection
Acute subdural hematoma
Asymmetric hyperdensity along the left tentorium
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SDH can be difficult to differentiate from adjacent
parenchymaEffacement of adjacent sulci, an important clue for subtle
SDHs (suggested “subdural” window width 130 and
window level of 30)
Isodense acute subdural hematoma: transition phase during from an acute SDH to
a chronic
Hypodense collection
Subdural Hematoma Stages
Acute < 3 days
Sulcal effacement, subfalcial herniation, Shift
Chronic>2 weeks
Subacute 3 days‐2 weeks
Utility of Multiplanar Reformats for Small Acute Subdural Hematoma
If Falx is too thick: Subdural Hematoma Iso-hypointense collection