brain haemorrhage. etiology non treated arterial hypertension amyloid angiopathy aneuryzms and avm...
TRANSCRIPT
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Brain haemorrhage
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Brain haemorrhage
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Brain haemorrhage
• Etiology • Non treated arterial hypertension • Amyloid angiopathy • Aneuryzms and AVM• Head injury• Complications of antikoagulant therapy • Bleeding to brain infarct or tumor
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Etiology• 80% - typical hypertonic brain haemorrhage -
thalamus and BG, cerebellum, midbrain
• 20% - other cause : atypical haemorrhage • AVM • Bleeding to brain tumor • angiomas • arterial aneurysms
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Pathogenesis
• Bleeding to brain tissue• compression of tissue• destruction of tissue• brain oedema• posthemorrhagic pseudocyst
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Clinical feature
• Very often very severe - focal signs, ICH, koma, epi.paroxysms, headache, vomitus,
• Prognosis depends on : • cause, localisation,• patient´s condition• compensation
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Dg.
• Brain CT
• Brain MRI
• In atypical haemorrhage - AG, DSA, MR-AG
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Brain haemorrhage
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Therapy
• Surgiical
• Conservative
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SAHSubarachnoid haemorrhage
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Subarachnoid haemorrhage
• Bleeding into the subarachnoid space surrounding the brain
• 5-10% of all strokes
• About 80% - rupture of an intracranial saccular aneurysm
• 20% - AVM, mycotic aneurysm
• Nonaneurysmal SAH
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Etiology SAH
1. Saccular - „berry“- with nech and bodythe most often
2. Fusiform - without neck not so often
3. Dissecans
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Etiology SAH - AVM
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Subarachnoid haemorrhage
• Sudden onset of excrutiating headache, sometimes accompanied by focal neurologic symptoms and signs or sudden coma
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Risk factors SAH
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The most often localisation
A. cerebri anterior, a. comunic.ant. Bifurcation ICA and art. communicans post. The origin of art. cerebri ant. The first bifurcation of MCA Bifurk. a.comm.post. and PCA Bifurcation of BA one aneurysm or more aneurysms (30%)
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The most often localisation
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Clinical feature
• Incidence: 6-24 / 100 000, women, age 50.-60
• Sudden onset of headache
• +- unconsciousness
• vomitus, defecation
• meningeal irritation
• +- focal neurological signs
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Hunt-Hess classification (grading system)
• Grade 1 - headache, slight nuchal rigidity• Grade 2 - cranial nerve palsy, severe
headache, nuchal rigidity• Grade 3 - mild focal deficit, lethargy,
confusion• Grade 4 - stupor, moderate-to-severe
hemiparesis, early decerebrate rigidity• Grade 5 - deep coma, decerebrate rigidity,
moribund appearance
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Dg. SAHBrain CT Lumbar punction
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Dg. SAH
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Etiology SAH
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Etiology SAH
Angiography 3D CT angiography
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Etiology SAH - AVM
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3D CT angiography
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Grading System of Fisher - CT
• 1. No subarachnoid blood detected
• 2. Diffuse vertical layers less than 1 mm
• 3. Localized clot and/or vertical layer more than 1 mm
• 4. Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
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Grading System of Fisher - CT
Grade 1 - normal CT
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Grading System of Fisher - CT
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Grading System of Fisher - CT
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Therapy SAH
• Conservative - without origin of SAH
• rest in bed 14-21 days
• blood presure
• prevention of vasospasms - blockers of Ca chanels - Nimodipin - iv. pump
• prevention of caughing
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Therapy SAH Clipping
Therapy SAHSTENT
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Therapy SAH
Clipping
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Therapy SAH - clipping
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Therapy SAH - Coiling
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Therapy SAH - coilling
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Therapy SAH - coilling
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Therapy SAH - coilling
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Coilling
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Complications of SAH
• Increased ICP (+ brain herniation), sudden death compression of brain
• Affected brain perfussion - focal ischemia of brain
• Hydrocephalus - affected resorbtion of CSF • Vazospasm (4.-14. day )- 40-70 % of patients• Rebleeding - 25% (first 24 hours.)• Complications of therapy
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SAH complications
• Vazospasm• Ca2+ channel
blockers• Nimodipin i.v.
pump • Blood presure
control
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SAH complications
• Hydrocephalus• Therapy –
ventriculoperitoneal shunt