10- raised ICP Flashcards
(26 cards)
what does the monro-kellie doctrine say
increase in volume of either CSF, blood or brain must be offset by decrease in volume
what is reduced first to reduce ICP
CSF and venous blood
describe change in ICP and volume over time
- initially compensatory changes can buffer
- as they deplete then ICP rises rapidly
what can cause too much CSF (cause of raised ICP)
congenital
-hydrocephalus
acquired
-bleed/tumour obstructing drainage
what can cause too much blood (cause of raised ICP)
outside cerebral vessels
- intrcranial haemorrage
- haemorrhagic stroke
inside cranial vessels
- increased arterial pressure (malignant hypertension)
- increased venous pressure (SVC obstruction)
what can cause too much brain (cause of raised ICP)
cerebral oedema secondary to trauma, infection, ischemia and infarct
what is hydrocephalus
a buildup of CSF in ventricles
how to treat hydrocephalus
short term- extra ventricular device to drain CSF from lateral ventricle
long term- shunts from ventricular system to peritoneum or to right atrium
what can caused raised ICP
- tumour
- cerebral abscess
- idopathic intracranial hypertension
which cause of raised ICP can be treated with lumbar puncture
idiopathic intracranial hypertension
2 major consequences of raised intracranial pressure
- brain ischemia due to impaired cerebral perfusion
- compression and herniation of the brain
what determines cerebral blood flow
cerebral perfusion pressure
how to calculate cerebral perfusion pressure CPP
CPP= mean arterial pressure - ICP
role of cerebral autoregulation
keeps CPP and cerebral blood flow the same despite variations in MAP
what range can the brain autoregulate between
- can stabilise CPP and therefore CBF between 50 and 150 mmHg.
- below this it cannot dilate arterioles anymore (50mmHg is max vasodilation)
- above 150 it cannot vasoconstriction arterioles anymore (150mmHg is max vasoconstriction)
what happens if the brain cannot auto regulate and when does this occur
occurs when
- the brain tissue is damaged
- lower than 50 or higher than 150
without autoregulation the CPP and CBF is dependent and respnsive to changes in MAP
what is the response of the brain to increased ICP
- vasodilation of cerebral arterioles (autoregulation) increases cerebral blood flow to maintain CPP
- elevate MAP by increasing systemic BP
describe the effects of an expanding mass on ICP
- compensation by extrusion of CSF and venous blood
- rising ICP reduces CPP and so reduces CBF. so autoregulation causes cerebral vasodilation and increased MAP to oppose reduction in CPP
- ICP rises but brain cannot compensate further
- hypoxic brain
- compression on brain and brainstem
symptoms raised ICP
- reduced visual acuity
- papilloedema
- diplopia
- headache worsening in mornings and when leaning forwards
- vomiting
- seizures
- reduced GCS (confusion/drowsiness)
- Increased BP
- focal neurological signs
- difficulty concentrating
radiological features of raised ICP
midline shift (subfalcrine herniation), effacement of ventricles, loss of grey white matter differentiation
describe subfalcine herniation
cingulate guys under faux cerebri. causes compression pf anterior cerebral artery
describe transtentorial hernitation
uncal herniation
-causes CNIII lesion and compression on cerebellar peduncle causing motor signs
describe tonsillar herniation
cerebellar tonsils herniate through foramen magnum, compressing brainstem. terminal in final stages
late features of raised ICP
- brain herniation
- cushings triad- raised BP, bradycardia, irregular breathing (compression on cardio resp centres in medulla)
