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Brain haemorrhage. Etiology Non treated arterial hypertension Amyloid angiopathy Aneuryzms and AVM Head injury Complications of antikoagulant therapy.

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Presentation on theme: "Brain haemorrhage. Etiology Non treated arterial hypertension Amyloid angiopathy Aneuryzms and AVM Head injury Complications of antikoagulant therapy."— Presentation transcript:

1 Brain haemorrhage

2

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

4 Etiology 80% - typical hypertonic brain haemorrhage - thalamus and BG, cerebellum, midbrain 20% - other cause : atypical haemorrhage AVM Bleeding to brain tumor angiomas arterial aneurysms

5 Pathogenesis Bleeding to brain tissue compression of tissue destruction of tissue brain oedema posthemorrhagic pseudocyst

6 Clinical feature Very often very severe - focal signs, ICH, koma, epi.paroxysms, headache, vomitus, Prognosis depends on : cause, localisation, patient´s condition compensation

7 Dg. Brain CT Brain MRI In atypical haemorrhage - AG, DSA, MR- AG

8 Brain haemorrhage

9 Therapy Surgiical Conservative

10 SAH S ubarachnoid haemorrhage

11 S ubarachnoid 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

12 Etiology SAH 1. Saccular - „berry“- with nech and body the most often 2. Fusiform - without neck not so often 3. Dissecans

13 Etiology SAH - AVM

14 S ubarachnoid haemorrhage Sudden onset of excrutiating headache, sometimes accompanied by focal neurologic symptoms and signs or sudden coma

15 Risk factors SAH

16 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%)

17 The most often localisation

18 Clinical feature Incidence: 6-24 / 100 000, women, age 50.-60 Sudden onset of headache +- unconsciousness vomitus, defecation meningeal irritation +- focal neurological signs

19 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

20 Dg. SAH Brain CTLumbar punction

21 Dg. SAH

22 Etiology SAH

23 Angiography 3D CT angiography

24 Etiology SAH - AVM

25 3D CT angiography

26 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

27 Grading System of Fisher - CT Grade 1 - normal CT

28 Grading System of Fisher - CT

29

30 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

31 Therapy SAH Clipping Therapy SAH STENT

32 Therapy SAH Clipping

33 Therapy SAH - clipping

34 Therapy SAH - Coiling

35 Therapy SAH - coilling

36

37

38 Coilling

39 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

40 SAH complications Vazospasm Ca 2+ channel blockers Nimodipin i.v. pump Blood presure control

41 SAH complications Hydrocephalus Therapy – ventriculoperitoneal shunt


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