Session 10 Raised ICP Flashcards
(19 cards)
What are the normal ranges for ICP?
What is ICP determined by?
Determined by volume of blood, brain and CSF all enclosed within a rigid box
Values
Adults = 5-15 mmHg
Children = 5-7 mmHg
Term infants = 1.5-6 mmHg
> 20 mmHg = raised!
Describe the Monro-Kellie doctrine
Any increase in the volume of one of the intracranial constituents (brain, blood or CSF) must be compensated by a decrease in the volume of one of the others
Is the case of an intracranial mass (e.g. brain tumour), the first components to be pushed out of the intracranial space are CSF and venous blood since they are at the lowest pressure
Calculation for cerebral perfusion pressure =
Normal values?
CPP = MAP - ICP
Normal CPP = >70 mmHg
Normal MAP = around 90 mmHg
Normal ICP = around 10 mmHg
What happens to CPP if MAP increases?
CPP increases, triggering cerebral auto regulation to maintain cerebral blood flow (vasoconstriction)
What happens to CPP if ICP increases
CPP decrease, triggering cerebral auto regulation to maintain cerebral blood flow (vasodilation)
what happens if CPP drops below 50 mmHg
Cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
ICP can be maintained at a coating level as an intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid and exponential rate
Damage to the brain can impair or abolish cerebral autoregulation
Describe Cushing’s triad (reflex or response)
A rise in ICP will initially lead to HYPERtension as the body increases MAP to maintain CPP
The increase in MAP is detected by baroreceptors which stimulate a reflex bradycardia via increased vagal activity (which can cause stomach ulcers as a side effect)
Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing
Causes of raised ICP? Refer to blood
Too much blood within the cerebral vessels
- raised arterial pressure - malignant hypertension
- raised venous pressure - SVC obstruction (e.g. external compression by a lung tumour)
Too much blood outside of cerebral vessels (haemorrhage)
- extramural
- subdural
- Haemorrhagic stroke
- intraventricular haemorrhage
Causes of too much CSF that leads to increased ICP?
Hydrocephalus - congenital or acquired - ref to notes
What are the clinical signs of hydrocephalus?
Bulging head with head circumference increasing faster than expected
Sunsetting eyes (due to direct compression of orbits as well as involvement of oculomotor nerve as it exits midbrain)
what are three ways of managing hydrocephalus?
- acute setting: tap fontanelle with a needle
- medium term drainage: external ventricular drain
- long term drainage: ventricular shunts
When would you use an external ventricular drain?
- risks and requirements?
Medium term drainage of CSF in hydrocephalus
Allows continuous pressure monitoring
Risk of infection due to direct communication between brain and outside world
Requires inpatient monitoring so not good as long term solution
Used if shunt fails or is contraindicated
Explain how a ventricular shunt works?
Long term drainage of CSF
A tube is placed from the ventricular system into the peritoneum (V-P) or right atrium (V-A)
VP is more common
Tube is tunnelled under the skin
A one way valve is incorporated to prevent backflip into ventricle
Extra length of tubing is provided to allow growth before revision is required
VP shunts vulnerable to infection (e.g. if abdominal infection - can track back up to brain) or kinking
What are some acquired causes of hydrocephalus?
Meningitis
Trauma
Haemorrhage (e.g. post subarachnoid)
Tumours (e.g. that compress cerebral aqueduct)
‘Too much brain’ can be a cause of increase ICP. What can cause cerebral oedema?
Vasogenic = breakdown of tight junctions
Cytotoxic = damage to brain cells
Osmotic - if ECF becomes hypotonic
Interstitial = flow of CSF across ependyma and damage to BBB
Idiopathic intracranial hypertension
Aka?
Presents with?
Typical in?
Diagnosis confirmed by?
Treatment?
Idiopathic intracranial hypertension
Aka = benign intracranial hypertension
Presents with = headache and visual disturbance
Typical in = obese middle aged females
Diagnosis confirmed by = raised opening pressure on an LP
NB: need to make sure there are no signs of pathology before doing an LP in a patient with suspected raised ICP as this can precipitate brain herniation
Treatment = Weight loss and BP control
Clinical features of raised ICP?
Headache
- constant
- worse in the morning
- worse on bending / straining
Nausea and vomiting
difficulty concentration or drowsiness (effect on daily life)
Double vision
- problems with accommodation (early sign)
- acuity
- visual field defects
- papilloedema
Focal neurological signs (depends where lesion is)
Seizures
One consequence of raised ICP is brain herniation (when brain ICP is very high!)
what are the different types and what happens?
Tonsillar herniation (Coning) * cerebellar tonsils herniate through foramen magnum, compressing medulla
Subfalcine herniation
- cingulate gyrus is pushed under the free edge of the flax cerebral
- can compress anterior cerebral artery as it loops over the corpus callosum
Uncal herniation
- uncus of temporal lobe herniated through tentorial notch compressing adjacent midbrain
- can cause third nerve palsy and maybe even contralateral hemiparesis (due to compression of cerebral peduncle)
Central downward herniation
* medial temporal lobe / other midline structures pushed down through tentorial notch
External herniation through skull fracture or therapeutic craniectomy
How would you manage raised ICP?
Brain protection measures:
- Airway and breathing - maintain oxygenation and removal of Co2
- Circulatory support - maintain MAP and hence CPP
- Sedation, analgesia and paralysis
- decrease metabolic demand
- prevents cough, shivering that might increase ICP further - Head up tilt
- improves cerebral venous drainage - Temperature
- prevents hyperthermia
- therapeutic hypothermia may be beneficial - Anticonvulsants
- prevent seizures, reduce metabolic demand - Nutrition and proton pump inhibitors
- improved heralding of injuries and prevent stomach ulcers use to increased vagal activity
Other treatments
- mannitol or hypertonic saline - osmotic diuretics
- ventricular drainage
- decompressive craniectomy as last resort
