Brain haemorrhage

Brain haemorrhage

Brain haemorrhage

• Etiology • Non treated arterial hypertension • Amyloid angiopathy • Aneuryzms and AVM• Head injury• Complications of antikoagulant therapy • Bleeding to brain infarct or tumor

Etiology• 80% - typical hypertonic brain haemorrhage -

thalamus and BG, cerebellum, midbrain

• 20% - other cause : atypical haemorrhage • AVM • Bleeding to brain tumor • angiomas • arterial aneurysms

Pathogenesis

• Bleeding to brain tissue• compression of tissue• destruction of tissue• brain oedema• posthemorrhagic pseudocyst

Clinical feature

• Very often very severe - focal signs, ICH, koma, epi.paroxysms, headache, vomitus,

• Prognosis depends on : • cause, localisation,• patient´s condition• compensation

Dg.

• Brain CT

• Brain MRI

• In atypical haemorrhage - AG, DSA, MR-AG

Brain haemorrhage

Therapy

• Surgiical

• Conservative

SAHSubarachnoid haemorrhage

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

Etiology SAH

1. Saccular - „berry“- with nech and bodythe most often

2. Fusiform - without neck not so often

3. Dissecans

Etiology SAH - AVM

Subarachnoid haemorrhage

• Sudden onset of excrutiating headache, sometimes accompanied by focal neurologic symptoms and signs or sudden coma

Risk factors SAH

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%)

The most often localisation

Clinical feature

• Incidence: 6-24 / 100 000, women, age 50.-60

• Sudden onset of headache

• +- unconsciousness

• vomitus, defecation

• meningeal irritation

• +- focal neurological signs

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

Dg. SAHBrain CT Lumbar punction

Dg. SAH

Etiology SAH

Etiology SAH

Angiography 3D CT angiography

Etiology SAH - AVM

3D CT angiography

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

Grading System of Fisher - CT

Grade 1 - normal CT

Grading System of Fisher - CT

Grading System of Fisher - CT

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

Therapy SAH Clipping

Therapy SAHSTENT

Therapy SAH

Clipping

Therapy SAH - clipping

Therapy SAH - Coiling

Therapy SAH - coilling

Therapy SAH - coilling

Therapy SAH - coilling

Coilling

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

SAH complications

• Vazospasm• Ca2+ channel

blockers• Nimodipin i.v.

pump • Blood presure

control

SAH complications

• Hydrocephalus• Therapy –

ventriculoperitoneal shunt