S9) Pathophysiology and management of raised intracranial pressure Flashcards
What is intracranial pressure?
Pressure inside the neurocranium
What contributes to the ICP?
– brain
– blood
– CSF
All this fill the skull volume and therefore contribute to ICP (very little space left .: skull is pretty packed)
Determined by volume of blood, brain and CSF all enclosed within a rigid box
What is the narrow range of ICP?
5-15 mmHg (adults)
Values (wide range, can be difficult to define normality precisely)
Adults 5-15 mmHg
Children 5-7 mmHg
Term infants 1.5-6mmHg
A good rule of thumb is that a pressure >20 mmHg is raised
What is Monro-Kellie doctrine?
Idea that the sum of volumes- determined by brain,blood, CSF must remain constant to avoid increase in ICP.
Increase in one of the volumes must be offset by equal decrease of volume of others.
- 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
- In 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
In the presence of an intracranial mass (‘extra volume’) which will be the first to reduce in volume in an attempt to prevent ↑ICP?
Brain volume is typically fixed .: compensation is done initially through decrease of …
Decrease of CSF and venous blood
Describe the relationship between intracranial pressure and volume.
What can cause raised intracranial pressure? Identify 5 main ones.
- Too much CSF - hydrocephalus
- Too much blood
- Too much brain
- Mass lesion
- Other e.g. idiopathic intracranial hypertension
Identify the causes behind too much CSF that can lead to raised ICP.
Hydrocephalus:
– Congenital (more common than acquired types):
1. Obstructive
• Neural tube defects
- Aqueduct stenosis
- Frequently part of a larger syndrome
2. Communicating (i.e. drainage of CSF not impaired)
• Increased CSF production
• Decreased CSF absorption
vs
Acquired:
– Meningitis
– Trauma
– Haemorrhage (e.g. post subarachnoid haemorrhage) – Tumours (e.g. compressing cerebral aqueduct)
Identify the causes behind too much blood that can lead to raised ICP.
– Too much blood within cerebral vessels (rare):
• Raised arterial pressure
o Malignant hypertension
• Raised venous pressure
o SVC obstruction (e.g. external compression by a lung tumour)
– Too much blood outside of cerebral vessels (haemorrhage):
• Extradural
- Subdural
- Subarachnoid
- Haemorrhagic stroke
- Intraventricular haemorrhage
Identify the causes behind too much brain that can lead to raised ICP.
Cerebral oedema
o Four major pathophysiologies, but often multiple mechanisms at play in disorders such as stroke or trauma
1. Vasogenic (breakdown of tight junctions)
- Cytotoxic (damage to brain cells)
- Osmotic (e.g. if ECF becomes hypotonic)
- Interstitial (flow of CSF across ependyma and damage to BBB)
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)
Why adult/ acquired hydrocephalus compared to congenital hydrocephalus do we not see an expansion in the head circumference?
This is because in congenital hydrocephalus - the children’s fontanelles and sutures have still not be fused .: when there is an expansion within the skull, the head is able to expand as a result of it.
Whereas in adults, both the fontanelles and sutures are fused and mature .: can’t expand. The skull is much more rigid
How can we treat hydrocephalus?
Can be treated in acute setting by tapping the fontanelle with a needle
Medium term drainage can be achieved by external ventricular drain (EVD) - allows continuous pressure monitoring
Can be at risk of infection due to direct communication between brain and outside world
Requires inpatient monitoring so not good as a long term solution
Used if shunt fails or contraindicated
Long term drainage by ventricular shunts - long-term with shunts- tube placed from ventricular system to peritoneum or to right atrium
– V-P shunts performed most commonly
– Tube is tunnelled under skin
– A one way valve is incorporated to prevent backflow into ventricle
– Extra length of tubing is provided to allow growth before revision is required
– V-P shunts vulnerable to infection (e.g. if abdominal infection, can track back up to brain) or kinking
– Most shunts will require revision
Identify different mass lesions that can cause a raised ICP
Tumour
Cerebral abscess
Describe the idiopathic intracranial hypertension (one of the causes that can also result in raised ICP)
Idiopathic intracranial hypertension (IIH)
– Aka benign intracranial hypertension
– May present with headache and visual disturbance
– Usually obese middle aged females
– Poorly understood aetiology
– Diagnosis can be confirmed by raised opening pressure on an LP
→ Make sure there are no signs of intracranial pathology before doing an LP in a patient with suspected raised ICP as this can precipitate brain herniation!
– Treat with weight loss and blood pressure control
What are the two major consequences of rising ICP?
– Brain ischaemia [due to impaired cerebral perfusion (arterial supply)]
– Compression and herniation of the brain…. ………which eventually leads to death
(or severe brain neurological deficits due to irreversible damage from brain ischaemic infarct)
What is cerebral blood flow dependant on?
cerebral perfusion pressure (CPP)
Cerebral blood flow is dependant on cerebral perfusion pressure (CPP).
What is the equation that makes up CPP?
CPP = Mean arterial pressure - ICP
The mean arterial pressure - range of variability as it is influenced by systemic blood pressure
CPP = Mean arterial pressure - ICP
Explore this equation a bit
- CPP = mean arterial pressure (MAP) – ICP
- Normal CPP >70 mmHg
- Normal MAP ~90mmHg
- Normal ICP ~10 mmHg
- If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
- If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation)
- If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
- ICP can be maintained at a constant level as an intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid (exponential) rate
- Damage to the brain can impair or even abolish cerebral autoregulation
What mechanisms do we have to ensure that the CPP and .: the cerebral blood flow can be steadily maintained despite variations in MAP?
Autoregulatory mechanisms in the normal brain (cerebral autoregulation)
- these are compensatory mechanisms to ensure cerebral perfusion is steady by maintaining CPP
we don’t want a fluctuating BP in the brain
How does cerebral autoregulation maintain CPP and cerebral blood flow over a range of MAP?
In low MAP → maximal vasodilation
In high MAP → maximal vasoconstriction
But remember, this is limited! only so much we can vasoconstrict and vasodilate!
What are the problems with the cerebral autoregulation?
– Limits to this autoregulation (in a normal brain)!
– Damaged brain tissue= e.g. ischaemia or infarct
→ .: Any ability for cerebral autoregulation can be impaired or absence
– Without autoregulation CPP (and CBF) is directly dependent and responsive to changes in MAP
Cerebral blood flow is dependent on cerebral perfusion pressure.
If ICP increases, it will decrease CPP but there are mechanisms to mitigate this. What are they?
Also what is the catch with this i.e. what is the problem?
Increased ICP will decrease CPP but mechanisms occur to mitigate this:
i) cerebral arterioles vasodilate (cerebral autoregulation): ↑ cerebral blood flow to maintain CPP
ii) elevate MAP (by ↑ systemic BP)
….mechanisms problematic: ↑ cerebral blood volume will not help a rising ICP!
Describe the overall steps that occurs including compensatory mechanisms and consequences when there is a expanding mass e.g. tumour causing rise in ICP.
How can we recognised raised ICP?
– Early recognition and treatment reduces risk of
irreversible brain damage or death
inappropriate management e.g. lumbar puncture
– Preceding and presenting history, and clinical examination can be suggestive…
… but alone may be difficult to rule out ↑ ICP
– Imaging (usually CT) can provide additional evidence for presence of ↑ICP
What are the initial common presenting features of ICP?
• Headache
o Constant o Worse in the morning o Worse on bending / straining
• Nausea and vomiting
• Difficulty concentrating or drowsiness
o Effect on daily life • Confusion • Double vision
o Problems with accommodation (early sign, pupillary dilatation a late sign)
o Maybe effects on acuity
o Visual field defects
o Papilloedema (swelling of optic disc)
What are the presenting features as ICP continues to rise?
Focal neurological signs
o Depends on where lesion is
Seizures
Spot the signs … - as seen in raised ICP
Identify some radiological findings that can be seen in raised ICP
– Midline shift (indicates subfalcine herniation)
– Evidence of other brain herniation types
– Effacement (squashed) of ventricles (& other CSF spaces)
– Loss of grey-white matter differentiation
Untreated and continuing to rise ICP can lead to brain herniation.
Identify 3 main types.
- Subfalcine herniation
- Transtentorial herniation
- Tonsillar herniation (coning)
Describe the three types of brain herniation that can arise due to raised ICP.
– Tonsillar herniation aka coning
o Cerebellar tonsils herniate through foramen magnum, compressing medulla
– Subfalcine herniation
o Cingulate gyrus is pushed under the free edge of the falx cerebri
o Can compress anterior cerebral artery as it loops over the corpus callosum
– Uncal herniation
o Uncus of temporal lobe herniates through tentorial notch compressing adjacent midbrain
o Can cause third nerve palsy and maybe even contralateral hemiparesis (due to compression of cerebral peduncle)
– Central downward herniation
o Medial temporal lobe / other midline structures pushed down through tentorial notch
– External herniation through skull fracture or therapeutic craniectomy
Identify the late features of raised ICP.
– Brain herniation
– Cushing’s triad
What is Cushing’s triad? Describe it.
– Blood pressure: attempting to maintain CPP in face of high ICP
– Bradycardia: inc BP detected by baroreceptors-inc vagal tone (?compression on brainstem)
– Irregular breathing: compression on cardio-resp centres in medulla
Explain the signs seen in Cushing’s triad AKA Cushing’s reflex.
– 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 dangerous side effect)
– Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing
How do we manage a patient with acutely raised ICP?
– Resuscitate and stabilise patient (ensure ABC - airways, breathing and circulation…before D, disability!)
– Recognise raised ICP early and possible cause
History and clinical examination findings
Imaging (usually CT)
– Begin measures to prevent worsening of ↑ICP and secondary brain injury (from ischaemia and compression)
– Consult +/- referral to neurosurgeons
What are some brain protection measures?
– Elevate head of bed (10-15 degrees)
→ maximises cerebral venous return from the brain
– Adequate oxygenation and avoid hypo- or hyperventilation
→ maximises oxygen delivery to brain and prevents cerebral vasoconstriction
– Maintain normal blood pressure: avoid hypotension (remember CPP is dependant on systemic BP - don’t want brain to be deprived of oxygen) to ensure adequate CPP
- If BP high do not attempt to lower (may be directly driving perfusion to ischaemic areas of brain)
– Decrease cerebral metabolic rate
- Sedation, analgesia, paralysis (of muscles) , avoiding hyperthermia (to decrease metabolic rate), treating seizures (give anticonvulsants)
What is the further ongoing management of a patient with raised ICP?
– Drug therapies e.g. osmotherapies like hypertonic saline or mannitol
– Regularly re-evaluate and monitor neuro-observations
Further steps that may be required for some patients
– Invasive monitoring of ICP e.g. placement of “bolt” or external ventricular drain which can provide continuous pressure monitoring
What is the aim to maintain ICP at, esp when managing a patient with raised ICP?
aim to maintain ICP <20-25 mmHg
Overall management … student notes
What does a neuro observation chart look like?
Depending on clinical presentation/ CT findings +/- ICP measurement, may still be able to monitor and treat medically.
When would we consider surgical intervention? Give examples
– Surgical intervention depending on underlying cause
e.g. evacuation of haemorrhage
external ventricular drain → can allow for therapeutic CSF drainage
decompressive craniectomy (controversial? may not confer favourable outcomes/no benefit)
What does invasive ICP monitoring involve?
Invasive monitoring of ICP e.g. placement of “bolt” or external ventricular drain which can provide continuous pressure monitoring
Summary 1
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