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Clinical neuroscience > L15 - ICP > Flashcards

L15 - ICP Flashcards

1
Q

What can causes raised intracranial pressure?

A

Blood
Tumour
CSF
Brain inflammation

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2
Q

Normal intracranial pressure

A

Adults - 5 - 17 mmHg
Children - 5- 7 mmHg
Term infants - 1.5 - 6 mmHg

Pressure over 20mmHg is high

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3
Q

How to assess oxygenation and haemodynamics non invasive

A

NIRS - near infrared spectroscopy

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4
Q

ICP waveform

A

P1 - arterial pulsation
P2 - brain tissue compliance
P3 - dicrotic wave with aortic valve closure

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5
Q

Acute brain injury waveform

A
  • compliance decreases

- p1:p2 reversed

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6
Q

Monroe - Kellie doctrine

A

Any increase in the volume of intracranial:

  • blood
  • CSF
  • brain

Must be compensated for by a decrease in the others.

As volume increases, pressure increases exponentially as skull acts as rigid box

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7
Q

Intracranial Monroe - Kellie doctrine

A

Brain tumour increases the volume of the brain therefore CSF and venous blood are pushed out of the intracranial space as they are at low pressure.

  • sum of intracranial volumes remains constant
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8
Q

Cerebral perfusion pressure

A

CPP= MAP - ICP

Normal - above 70mmHg

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9
Q

Auto regulation of cerebral blood flow

A
  • If mean arterial pressure (MAP) increases, CPP increases which triggers intracranial vasoconstriction to preserve the cerebral blood flow
  • If ICP increases, CPP decreases triggering intracranial vasodilation
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10
Q

CPP less than 50 mmHg

A

Cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated

If ICP rises enough to cause CPP to decrease below 50 mmHg, ICP will rise exponentially and not compensated for

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11
Q

Why does raised ICP cause death

A

Brain ischaemia

Brain shifting

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12
Q

Symptoms and signs of raised ICP

A

Symptoms:

  • headaches - constant and worse in the morning and straining
  • Diplopia
  • nausea and vomiting
  • drowsy - and difficulty concentrating

Signs:

  • irregular breathing
  • decreased heart rate - slow pulse
  • hypertension (due to vasodilation)
  • Cheyne stokes respiration
  • confusion
  • non reactive pupils
  • loss of consciousness
  • papilloedema
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13
Q

Cushing’s reflex

A
  • bradycardia - increased MAP detected by baroreceptors therefore increased vagal activity (can causes stomach ulcers)
  • hypertension - vasoconstriction and increase in MAP to compensate for high ICP and maintain CPP
  • irregular breathing pattern - compression of brainstem damages the respiratory centres
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14
Q

Causes of raised ICP

A

Blood:

  • malignant hypertension (Rapid high BP that causes organ damage)
  • raised venous pressure - SVC obstruction
  • haemorrhage

CSF:

  • obstructive hydrocephalus E.g aqueduct stenosis
  • communication hydrocephalus - too much CSF production

Brain:

  • encephalitis
  • meningitis
  • Reye’s syndrome

Other:

  • drowning
  • craniosynostosis
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15
Q

Clinical signs of raised ICP

A
  • Bulging head with head circumference increasing more than expected
  • sunsetting eyes - direct compression of orbits and occulomotor nerve damage
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16
Q

When is an urgent CT done

A

GCS below 13
GCS below 14 -2 or more hours after the injury

Neurological abnormalities:

  • seizure
  • loss of consciousness
  • focal neurological deficit

Other:
- suspected skull fracture of basal skull fracture

17
Q

Management of raised intracranial pressure

A
  • tapping the fontanelle with a needle
  • medium term external ventricular drain (allows continuous pressure monitoring)
  • long term ventricular shunts
18
Q

Disadvantages of medium term external ventricular drains

A
  • increased risk of infection as there is a direct communication between the brain and external environment
  • inpatient monitoring (not good long term)
19
Q

When is an external ventricular drain used

A

When shunt fails or is contraindicated

20
Q

Ventricular shunts

A
  • Tube placed form the ventricular system to the peritoneum or right atrium
  • Has a valve to prevent back flow
  • extra length to compensate for child’s growth
21
Q

How does cerebral oedema cause damage to the brain

A

Vasogenic - break down of tight junctions
Cytotoxic - damage to brain cells
Osmotic - ECF becomes hypotonic
Interstitial - damage to blood brain barrier and CSF flow into ependyma

22
Q

Ependyma

A

Made up of ependyma cells which are a type of glial cell that line the ventricles

23
Q

Sites of herniation

A

Subfalcine
Transtentorial
Uncal
Tonsillar

24
Q

Subfalcine herniation

A

The cingulate gyrus herniates underneath the falx cerebri
Loss of ventricle on affected side

Can compress the anterior cerebral artery

25
Q

Uncal herniation

A

Uncus herniates through the tentorium cerebellum notch compressing CN III and midbrain

  • can compress the cerebral peduncle and cause contralateral hemiparesis
26
Q

Tonsillar herniation

A

Brain pushed down through the foramen magnum
The cerebellar tonsils can compress the medulla
- Coning

27
Q

Transtentorial herniation

A

Central downward herniation

Medial temporal lobe and other midline structures pushed down through the tentorial notch

28
Q

Management of brain herniation tier 0

A
  • maintains O2 and remove CO2 - maintain airways and breathing
  • maintain MAP and CPP - circulatory support
  • sedation, analgesics and paralysis - decreases metabolic demand and coughing which would increase ICP
  • head up tilt - improves venous drainage
  • Temperature - therapeutic hypothermia
  • fever control - potent vasodilation
  • anti convulsants - prevents seizures to decreases metabolic demand
  • nutrition and proton pump inhibitors - prevents stomach ulcers from vagal activity
29
Q

Tier 1 management

A
  • mannitol (osmotic agent) - osmotic diuresis
  • hypertonic saline
  • ventricular drainage
  • hyperventilation - decrease CO2 which acts as a vasodilator
30
Q

Tier 3

A

Barbiturate coma - avoid epilepsy
Hyperventilation
Hypothermia
Decompressive craniectomy

31
Q

Budd Chiari malformation

A

Cerebellum is too big

Protrudes down the foramen magnum

32
Q

Anoxic brai.

A

Absence of oxygen causes:

  • failure of Na+/K+ ATPase
  • efflux of K+
  • influx of Na+
  • depolarisation of neurones
  • water follows Na+ influx causing oedema

Mitochondrial anoxia activates nitric oxide synthase producing motor is oxide which is a vasodilator
- toxic oxygen radicals are also produced

Clinical neuroscience (20 decks)

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