2.3 raised icp and brain herniations Flashcards
common types of cerebral oedema 3
cytotoxic
ionic
vasogenic
cytotoxic oedema characteristics 4
occurs w ischemia
swelling of brain cells
due to failure of ion pumps, which fail to remove sodium resulting in osmosis into the cell
no increase in total brain volume
ionic oedema 3
due to a loss of ion balance between the brain and blood, resulting in brain having higher ion balance
hence water leaves blood to enter brain
follows cytotoxic oedema
vasogenic oedema 3
increase in extracellular fluid due to BBB breakdown
albumin and other proteins enter the brain resulting in water following
occurs hours after cerebral ischemia
monro-kellie doctrine
the skull is a rigid, fixed volume structure containing: blood, CSF and brain tissue
The total volume of these three components must stay contact.
If the volume of one increases the volume of one of the others must decrease or intracranial pressure will rise
what is the relationship between icp and cerebral perfusion
when icp is greater than blood pressure, cerebral perfusion pressure is zero
there will be no perfusion to the brain
what are the three compensatory mechanisms in response to raised icp 3
increase CSF reabsorption and decrease production
venous vasocronstriction
arterial vasoconstriction
what is bad about the compensatory mechanism of arterial vasoconstriction when there is raised icp
arterial vasoconstriction->decreased perfusion->arterial vasodilation->intracranial hypertension->increased ICP
complications of ICP 6
compressed blood vessels = reduced perfusion
cerebral perfusion pressure decreases = reduced perfusion
ischemia
loss of brain tissue function due to compression
brain tissue becomes hypercapnic
brain herniation
what happens when the brain becomes hypercapnic 3
acts as a further vasodilator which further increases ICP
ICP will then exceed BP resulting in a lack of CPP
death will ensure
clinical features of icp early 5
altered mental state
headache
nausea
dipoplia
pupillary changes
clinical features of late icp 6
decrease in consciousness
speech impairment
papiloedema
cushings triad
babinskis sign
brain herniation
common brain herniations
subfalcine
transtentorial
tonsilar
which brain herniation is the most common
subfalcine
subfalcine herniation characteristics 2
innermost part of fronal lobe pushes under the falx cerebelli
caused by swelling in one hemisphere
transtentorial herniation characteristics
innermost part of the temporal lobe pushes down towards the tentorium
puts pressure on midbrain and brainstem
what are specific clinical features of transtentorial herniation 4
eye becomes fixed and dilated
ptosis
ipsilateral loss of pupillary reflex
progressive deterioration of consciousness due to compression of midbrain
tonsilar herniation characteristics 3
cerebellum moves down through foramen magnum to compress lowerv brain stem and upper cervical of spinal cord
causes dysfunction to brainstem centres
life threatening
medications you can give in increased intracranial pressure
mannitol
hypertonic saline
barbituates
steroids
what does mannitol do? 3 two way it works and when it cant be done
increases osmolarity of the blood to draw water from the brain parenchyma
decreases blood viscosity
cannot be done in HF and if BB not intact
what does hypertonic saline do
draws water out of the brain parenchyma
what do barbituates do
decrease cerebral metabolic activity therefore less need for blood flow to provide nutrients and oxygen
what do steroids do
reduce BBB permeability, preventing vasogenic oedema which is commonly seen in diseases
what is the clinical guideline for ICP management 4 steps
- CSF drainage + hyperventilation
- Mannitol, hypertonic saline
- barbituates
- decompressive craniectomy
