haemorrhagic stroke Flashcards
describe the falx cerebri
major dura fold
dura mater between longitudinal fissuer
divides left + right hemisphers
describe tentoruim cerebelli
forms tent partition between cerebrum + cerebellum
above tentorium space, below infratentorial space
describe the dura mater
periosteal layer adheres to skull
meningeal layer adheres to aracnoid mater
loosely covers brain
subdural space
describe arachnoid mater
csf reabsoprtion
finger projections penetrate meningeal layer of dura
subarachnoid space = contains CSF
describe pia mater
closely adheres to surface of brain
name the common and non-spontaneous causes of intracerebral haemorrhage
common = long-standing hypetension non-spontaneous = TBI
describe the role of cerebral amyloid angiopathy in ICH
amyloid deposition on wallsof cerebral arteries
weakens wealls = haemorrhage
what type od rupture in iCH and where does bleed
arterioles
deep, non-corticol structures
bleed in periphery of cerebral hemi = better outcome
how do charcot-bouchard aneurysms occur and where
chronic hypertension => deposition lipid-hyaline substances in arteriole wall => weaken
minute aneurysms
deep brain where vessel diameter <300nm
what are the clinical features of ICH
normal stroke symptoms + severe headache vomiting rapid loss consciousness seizures
outcomes of ICH
death 24-48 = common
survivors = motor cognitive deficits
management BP -> effect on cerebral ischaemia
What is subarachnoic haemarrohage and why does it occur
blood in subarachnoid space => bloody CSF
commonly occur from berry aneurysms
what are the biggest risk factors for SAH and what can is result from
- smoking hypertension, alcohol, genetics
- from vascular malformations, trauma, rupture of ICH into ventricular system, malignant hypetension,
acute = shitting, orgasm
what are berry aneurysms, where do they occur and what are their cause
small
branch at circle of willis
developmental defects in elastic lamina/acquired defects in artery
cause = infection, immunolgical, inflam, atherosclerotic, vascular
hypertension exacerbates defecit
rupture => SAH, or ICH
what are the clinical features and outcomes of SAH
severe, sudden headache nausea, vomitingstiff neck (meningeal irritation) photophobia blurred/double vision loss consciousness/seizures
oucomess = 30-50% mortality
imapcted by haemorrhage severirt, sex, age, treatment, comorbidities
3 treatments for berry aneurysms
clip = blood cant pass through aneurysm
endovascular coiling = packed platinum coils via catheter = prevents passage blood => aneurysm
artery bypass = aneurysm blocked = blood diverted to new artery
what are the complications of ICH or SAH
acute/chronic hydrocephalus
cerebral oedema
blood pool effects = iscaemia + infarction of adjacent structures, increased ICP, dec CPP, herniation syndromes, compression resp centres of brain stem
what is a peri-haematomal oedema
complication of ICH swelling around haematoma (clot) worsens neuro outcomes expands quick treated by reduce cerebral oedema
describe hydrocephalus
complication stroke
abnormal inc in V of CSF in skill
30% SAH
treatment = extraventricular drain
describe vasospasm as a complication
its effects and treatments
decrease calibre of cerebral artery
effect of clotted blood and breakdown within brain
vasospasm => prog cerebral iscahemia/stroke -> cerebral oedema -> death
treatment = ca2+ blocker => prevent ichaemic injury, cause hypotension (need manage), volume expansions
how can we use tpa for ICH treatment
wait for bleed to stabilise
minimally invasive procedure
administer tpa through catheter directly into haematoma to dissolve over 3 days
