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Clinical Neuroscience > Session 10: Intracranial Pressure > Flashcards

Session 10: Intracranial Pressure Flashcards

1
Q

What is ICP determined by?

A

Volume of blood

Volume of brain

Volume of CSF

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2
Q

Normal ICP in:

Adults

Children

Term infants

A

Adults : 5-15 mmHg

Children: 5-7 mmHg

Term infants: 1.5-6 mmHg

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3
Q

What mmHg is raised ICP?

A

>20 mmHg

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4
Q

Explain the Monro-Kellie doctrine.

A

Any increase in the volume of one of the intracranial constituents (brain, blood, CSF) must be compensated by a decrease by one of the others.

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5
Q

In the case of an intracranial mass like a brain tumour, what is the first constituent to compensate?

A

CSF and venous blood are pushed out since they are at the lowest pressure.

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6
Q

What is cerebral perfusion pressure (CPP)?

A

Mean arterial pressure (MAP) - ICP = CPP

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7
Q

What is normal CPP?

A

>70 mmHg

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8
Q

Normal MAP

A

Around 90 mmHg

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9
Q

Normal ICP.

A

Around 10 mmHg

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10
Q

What happens to CPP if MAP increases?

A

CPP will increase.

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11
Q

What happens if CPP increase?

A

Cerebral autoregulation will take place to maintain cerebral blood flow by vasoconstriction.

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12
Q

What happens to CPP if ICP increases?

A

CPP will decrease

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13
Q

What happens if CPP decrease?

A

Cerebral autoregulation will once again be triggered and cause vasodilation in order to maintain cerebral blood flow.

This vasodilation will also occur if MAP decrease.

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14
Q

When does cerebral autoregulation fail?

A

When CPP <50 mmHg

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15
Q

Why does cerebral autoregulation fail at CPP <50 mmHg?

A

Because cerebral arterioles are maximally dilated.

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16
Q

Briefly explain the ICP rising as an intracranial mass expands.

A

At first the ICP can be maintain by compensation up to a point. After this the ICP will rise rapidly.

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17
Q

Explain Cushing’s reflex.

A

A rise in ICP will initially lead to hypertension as the body increases MAP to maintain the decrease in CPP.

The increase in MAP leads to detection by baroreceptors. This stimulate a reflex bradycardia via vagal activity.

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18
Q

What is a complication of the increased vagal activity due to Cushing’s reflex?

A

Can cause stomach ulcers

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19
Q

What is a complication of continuing compression of the brainstem?

A

Damage to respiratory centres and irregular breathing.

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20
Q

Causes of raised ICP

A

Too much blood within cerebral vessels

Too much blood outside of cerebral vessel (haemorrhage)

Too much CSF

Too much brain

Other

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21
Q

Give examples of raised ICP due to too much blood within cerebral vessels.

A

This is a rare cause of raised ICP.

It can be either raised arterial pressure like in malignant hypertension.

Or raised venous pressure like in SVC obstruction.

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22
Q

Give examples of raised ICP due to too much blood outside of cerebral vessels.

A

Extradural

Subdural

Subarachnoid

Haemorrhagic stroke

Intraventricular haemorrhage

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23
Q

Another word for too much CSF.

A

Hydrocephalus

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24
Q

Types of hydrocephalus.

A

Congenital

Acquired

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25
Q

Give causes of congenital hydrocephalus

A

The most common one.

Obstructive such as neural tube defects and aqueduct stenosis.

or

Increased CSF production

Decreased CSF absorption

26
Q

Clinical signs of congenital hydrocephalus.

A

Bulging head with head circumference increasing faster than expected.

“Sunsetting eyes” due to the direct compression of orbits as well as involvment of CN III as it exits midbrain.

27
Q

Management of congenital hydrocephalus.

A

Acutely by tapping the fontanelle

External ventricular drain (medium term)

Ventricular shunt (long term)

28
Q

Issues with external ventricular drain.

A

Allows continuous pressure monitoring but can be a risk of infection since there is direct communication between brain and exterior.

Requires inpatient monitoring.

29
Q

If there are so many issues with external ventricular drain, why is it used?

A

It is only used if shunt fails or contraindicated.

30
Q

Explain ventricular shunts.

A

Either tube from ventricular system into peritoneum or into right atrium.

A tube that is tunneled under the skin with a one-way valve.

There is also extra length of tubing to allow growth of the patient.

31
Q

Problems with ventricular shunts.

A

Vulnerable to infection.

An example is if there is an abdominal infection it can track its way up to the brain.

The tube can also kink.

This means that most shunts will require revision.

32
Q

Causes of acquired hydrocephalus.

A

Meningitis

Trauma

Haemorrhage

Tumours (e.g. compressing cerebral aqueduct)

33
Q

What is too much brain?

A

Cerebral oedema

34
Q

Four major pathophysiologies of cerebral oedema.

A

Vasogenic due to breakdown of tight junctions

Cytotoxic by damage to brain cells

Osmotic if ECF becomes hypotonic.

Interstitial where there is flow of CSF across ependyme and damage to BBB.

35
Q

Give other causes of hydrocephalus.

A

Tumour

Cerebral abscess

Idiopathic

36
Q

Give an idiopathic cause of hydrocephalus (sounds stupid).

A

Idiopathic intracranial hypertension also called benign intracranial hypertension.

37
Q

CP of IIH.

A

Headache and visual disturbances

38
Q

Which patients are most commonly affected by IIH?

A

Obese middle aged females.

39
Q

How is diagnosis confirmed of IIH?

A

Checking the opening pressure on an LP.

40
Q

Why is it important to rule out and other intracranial pathology before performing an LP in IIH patient?

A

Because it can precipitate the brain to herniating if you don’t.

41
Q

Treatment of IIH.

A

Weight loss

BP control

42
Q

Consequences of raised ICP.

A

Headache

Nausea and vomiting

Concentration problems

Drowsiness

Diplopia

Focal neurological signs

Seizures

Brain herniation

43
Q

Features of headache due to raised ICP.

A

A constant headache that is worse in the morning and worse on bending/straining.

(This is due to raised ICP in morning or on bending)

44
Q

Explain the issues with vision in raised ICP

A

Problems with accommodation reflex (early sign)

Pupillary dilation (late sign)

Can affect acuity

Visual field defects

Papilloedema

45
Q

Give types of brain herniation.

A

Tonsillar herniation

Subfalcine herniation

Uncal herniation

Central downward herniation

46
Q

Explain tonsillar herniation.

A

Cerebeller tonsils herniate through the foramen magnum.

This will compress the medulla

47
Q

Explain subfalcine herniation.

A

Cingulate gyrus is pushed under the free edge of falx cerebri.

This can compress the ACA when it loops over corpus callosum.

48
Q

Explain uncal herniation.

A

Uncus of temporal lobe herniates through the tentorial notch compressing the adjacent midbrain. Often causes a midline shift.

This can lead to CN III palsy and even contralateral hemiparesis due to compressing of cerebral peduncle.

49
Q

Explain central downward herniation.

A

Medial temporal lobe or other midline structures are pushed down through the tentorial notch.

50
Q

What is external herniation?

A

Through skull fracture or therapeutic craniectomy.

51
Q

Give brain protection management of increased ICP.

A

Airway and breathing

Circulatory support

Sedation, analgesia and paralysis.

Head up tilt

Temperature

Anticonvulsants

Nutrition and PPis.

52
Q

What is done in airway and breathing management?

A

Maintenance of oxygenation and removal of CO2.

53
Q

What is done in circulatory support.

A

Maintenance of MAP and therefore also CPP.

If MAP drops too low then the cerebral autoregulation cannot compensate for the decreased CPP.

54
Q

Why are patients with raised ICP sedated?

A

To decrease metabolic demand and to prevent coughs or shivering which might exacerbate the ICP.

55
Q

Why is a head up tilt performed?

A

To improve cerebral venous drainage (less blood in brain -> lower ICP)

56
Q

Why is temperature manipulated in raised ICP?

A

To prevent hyperthermia but also because therapeutic hypothermia may be beneficial (apart from the shivering)

57
Q

Why are anticonvulsants given?

A

To prevent seizures.

58
Q

Why are PPis given?

A

Due to the Cushing’s reflex leading to increased vagal activity and risk of peptic ulcers.

59
Q

Other less common treatments of raised ICP.

A

Mannitol or hypertonic saline

Ventricular drainage

Decompressive craniectomy as a last resort if everything else fails.

60
Q

Explain the pathophysiology of anoxic brain injury.

A

Decreased cerebral blood flow leads to less O2 delivery.

This leads to failure of ATP-driven ion pump.

There is efflux of K+, and influx of Na+ into cell.

This leads to depolarisation of the neurones as well as leading to the water following Na+ and cause oedema.

Mitochondrial anoxia causes metabolic failure and activates nitric oxide synthase (NOS) which produces NO.

Toxic oxygen radicals are also produced.

61
Q

Why are sedatives given for intubation in raised ICP?

A

To stop bucking in confused patients.

Bucking can lead to even more raised ICP

Clinical Neuroscience (22 decks)

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