Raised ICP

Question 1

What contributes to ICP?

Answer 1

Brain - 80%
Blood - 10%
CSF - 10%

Question 2

Normal ICP

Answer 2

5-15mmHg
If over 20mmHg = raised as varies between ages

Question 3

What is the Monro-Kellie Doctrine?

Answer 3

Sum of volumes (brain, blood and CSF) must remain constant to avoid raised ICP

Increase in volume of one or volume addition eg tumour, means other ones must decrease in volume

Question 4

What will be first to reduce in an attempt to avoid raised ICP?

Answer 4

1. CSF
2. Venous blood

Question 5

What is the relationship between ICP and volume?

Answer 5

Not linear, can get a large increase in volume before start seeing pressure changes due to the compensatory mechanisms of CSF and venous blood reducing in volume

But gets to a point where cannot be compensated anymore and then pressure rises rapildy

Question 6

What can cause raised ICP?

(5)

Answer 6

1. Too much CSF - congenital or acquired
2. Too much blood - haemorrhagic stroke/haemorrhage, malignant HTN, SVC obstruction rising venous pressure
3. Cerebral oedema - secondary to trauma, infection, ischaemia and infarct
4. Mass lesion - space occupying lesion eg tumour, cerebral abscess
5. Other - idiopathic intracranial hypertension

Question 7

What occurrs in appearance when infants get hydrocephalus?

Answer 7

Larger circumferance of head - unfused bones within skull allow expansion (fontanelles can bulge, cannot happen in adults as bones have fused)
Sunsetting sign - eyes are displaced downwards

Question 8

How is hydrocephalus treated acutely and long term?

Answer 8

Acute - removal of ventricular CSF or external ventricular drain

Long term - shunts from ventricular system to peritoneum or right atrium

Question 9

CT sign of hydrocephalus

Answer 9

Dilation of lateral ventricles - filled with CSF

Question 10

Who does idiopathic intracranial HTN often affect?

Answer 10

Women childbearing age who are overweight
= headache, blurred vision, but they are alert and conscious

Question 11

What are the two major consequences of raised ICP?

Answer 11

Brain ischaemia - due to impaired cerebral arterial supply
Compression and herniation of brain

—> death

Question 12

What is cerebral flow dependent on?

Answer 12

Cerebral perfusion pressure

Question 13

Normal CPP, MAP and ICP

Answer 13

CPP >70mmHg
MAP - 90mmHg
ICP - 10mmHg

CPP = MAP - ICP

Question 14

What is the equation for cerebral perfusion pressure?

Answer 14

CPP = Mean arterial pressure - ICP

Question 15

How does the body ensure CPP is kept constant to ensure cerebral blood flow?

Answer 15

Cerebral autoregulation - ensures CPP and cerebral blood flow is maintained despite variations in MAP

Question 16

What does cerebral autoregulation do if MAP decreases or increases?

Answer 16

If MAP decreases:
Maximal vasodilation of cerebral arterioles occur to ensure blood flow is maintained

If MAP increases:
Maximal vasoconstriction of cerebral arterioles occurs to protect brain from high pressures of MAP

Question 17

What happens if MAP goes way too high or low?

Answer 17

There are limits to cerebral autoregulation - sometimes CPP cannot be maintained and cerebral blood flow is reduced

Question 18

What happens to cerebral autoregualtion on damagaed brain tissue?

Answer 18

Can be impaired or absent

Question 19

What happens if autoregulation wasn’t present?

Answer 19

CPP is directly dependent and responsive to changes in MAP - high pressures and low pressures are transmitted straight to brain perfusion

Question 20

What happens to cerebral perfusion pressure when ICP rises?

Answer 20

CPP = MAP - ICP
CPP decreases if ICP increases but to try and help this:
* Cerebral arterioles vasodilate = increased cerebral blood flow to maintain CPP
* Elevate MAP by increasing systemic BP

Question 21

Problem with vasodilation of cerebral arterioles and increasing MAP when ICP rises

Answer 21

Increases in cerebral blood volume will not help rising ICP

Question 22

What are the 5 steps which occur when a tumour causes raised ICP?

Answer 22

1. Compensation by decreasing volume of CSF and venous blood
2. Rising ICP reduces CPP which reduces cerebral blood flow so cerebral vasodilation and increase MAP occurs to maintain CPP
3. ICP continues to rise, CPP cannot compete = brain hypoxia
4. Cerebral hypoxia = oedema = more raised ICP
5. Eventually compression on brain and brainstem

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Question 23

What is needed when recognising raised ICP?

Answer 23

Early recognition and treatment as this reduces risk of:
* Irreversible brain damage/death
* Inappropriate management eg LP - can cause brain herniation in raised ICP

Question 24

What imaging can be used to provide additional evidence (with history) for raised ICP?

Answer 24

CT - can also provide reason for raised ICP

Question 25

Common presenting features of raised ICP

Answer 25

• Headache - constant, worse in morning
• Vomitting
• Visual distrubances - impaired acuity, pailloedema (swollen optic disc), dipoplia (CN VI can be compressed with raised ICP due to vertical course)
• Focal neurological signs
• Seizures

Question 26

What features present as ICP continues to rise and worsens?

Answer 26

Perfusion of brain is impaired so:
* Difficulty concentrating
* Reduced GCS - confusion, drowsy, unconscious
* Focal neurologiccal signs
* Seizures
* Increased BP

Question 27

Radiological features of raised ICP

(3)

Answer 27

• Midline shift - sulfalcine herniation
• Effacement ventricles - squished
• Loss of grey and white matter differentiation

Question 28

5 types of herniation that can occur in untreated raised ICP

Answer 28

Subfalcine - cingulate gyrus under falx cerebri, anterior cerebral artery vulnerable, runs in midline

Transtentorial herniation (uncal) - CN III vulnerable, compression of cerebellar peduncle = motor signs

Tonsillar herniation (coning) - cerebellar tonsils go through foramen magnum, = compression of brainstem, final stages = terminal

Central downward herniation - medial temporal lobe/other midline structures pushed through tentorial notch

External herniation - if through craniotomy or skull fracture

Question 29

Late features of raised ICP

Answer 29

Brain herniation

Cushings triad:
* Blood pressure high - attemp to maintain CCP in face of high ICP
* Bradycardia - high BP detected by baroreceptors = increased vagal stimulation (or compression of brainstem)
* Irregular breathing - compression of cardio/resp centre in medulla

Question 30

Managing patient with acute raised ICP

Answer 30

Resuscitate and stabilse - ABCs
Recognise raised ICP early - history and exam
Image - CT
Measures to prevent more rise in ICP - mentioned in another card
Consult/refer to neuro

Question 31

Brain protection measures to do for raised ICP

Answer 31

• Elevate head of bed 10-15 degrees = maximal cerebral venous drainage to heart
• Adequate oxygenation - avoid hyper/hypoventilation = maximises O2 delivery to brain and prevents cerebral vasoconstriction
• Maintain normal BP - avoid hypotension to ensure adequate CPP, if BP high do not try to lower - this is allowing CPP to be maintained, lowering may = brain hypoxia
• Decreased cerebral metabolic rate which decreases demands for O2 of brain - sedate, analgesia, paralysis, avoid hyperthermia, treat seizures

Question 32

Ongoing management for raised ICP

Answer 32

• Drugs - osmotherpaies eg hypertonic saline or mannitol = osmotic diuresis
• Regularly re-evaluate and monitor neuro obs

Invasive:
* Placement of bolt/external ventricular drain which can provide continious pressure monitoring - try to keep lower than 20-25mmHg
* Surgery depending on cause - haemorrhage? external ventricular drain? decompressive craniotomy? - LAST RESORT