3.8 Intracranial Pressure Monitoring Flashcards

1
Q

What are the clinical features of raised intracranial pressure (ICP)?

A
  • Headache
  • Nausea and vomiting
  • Confusion
  • Personality or behavioural changes
  • Visual disturbances due to papilloedema
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2
Q

Describe the headache with a raised ICP

A

Headache is worse in the morning
as cerebral oedema is worse in the
lying position and there is a

relative increase in hypoxia of the brain due to
hypoventilation during sleep.

It is also worse when bending down, coughing, and sneezing.

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3
Q

Severe Rises - Clinical Features

A

Acute severe increase in ICP leads to a decrease in GCS,

Cushing’s reflex; as ICP continues to rise,

it leads to fixed and dilated pupils,

Cheyne Stokes breathing pattern, and eventually hypotension and death.

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4
Q

What are the causes of increased intracranial pressure?

A

Raised ICP may be due to an increase in the
blood, tissue, or CSF components of the brain.

    • Blood—
      Increased blood flow or
      impaired venous drainage
      (e.g. venous sinus thrombosis)
    • Tissue—
      Tumour, brain abscess,
      haematoma, and cerebral oedema
    • CSF—Hydrocephalus or increase in CSF production,
      which happens in meningitis
      or choroid plexus tumour
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5
Q

What is the Monroe-Kellie theory?

A

The cranial cavity is a rigid closed container;

thus, any change in intracranial blood volume

is accompanied by the opposite change in

CSF volume if ICP is maintained.

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6
Q

can you draw the ICP elastance curve? see Figure 3.5.

A
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7
Q

Explain ICP eleastance curve

A
  1. Stage 1/2 = compensation phase.

As the volume of one of the intracranial
constituents increases,

the other two constituents decrease in volume in
order to keep the intracranial pressure constant.

  1. Stage 3/4 = decompensated phase.
    When compensatory mechanisms are exhausted,
    small increases in the volumes of intracranial constituents
    cause large increases in ICP
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8
Q

What changes the slop of ICP Curve

A

The slope of the curve is dependent on
which intracranial constituent is increasing.

The curve is steeper with blood and CSF as they are
incompressible and less steep with brain tissue as it is compressible.

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9
Q

What is the cushing’s reflex?

A

A hypothalamic response to brain ischaemia

wherein the sympathetic nervous system is activated,

which causes increased peripheral vascular resistance
with a subsequent increase in blood pressure.

The increased BP then activates
the parasympathetic nervous system

via carotid artery baroreceptors,
resulting in vagal-induced bradycardia.

The brain ischaemia that leads to Cushing’s reflex
is usually due to the poor perfusion
that results from increased ICP
due to haematomas or mass lesions.

Cushing’s reflex leads to the clinical manifestation of Cushing’s triad:

  1. hypertension,
  2. bradycardia,
  3. irregular respirations
    (Cheyne-Stokes breathing).
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10
Q

How do you manage raised icP?

A

This can be described as a reduction in blood, tissue, and CSF.

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11
Q

Blood

A
  • Ventilation
    Both hypoxia and hypercapnia can increase cerebral blood flow,

and hypoxia of the brain can increase lactic acid,
which further causes vasodilatation.

Hence, to prevent this,
mechanical ventilation is preferred.

Hyperventilation can be employed as a method to decrease the PCo2,
and this in turn causes vasoconstriction.

This can be used in an acute setting,
but its efficacy is limited.

If controlled ventilation is used, adequate
muscle relaxation and sedation should be used.

  • Positioning:
    Patients should be nursed in the head-up position,
    and
    jugular compression should be avoided to encourage venous drainage

Hypothermia and barbiturate therapy may
be used to decrease cerebral blood flow.

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12
Q

Tissue

A
  • Surgical decompression or removal of tumour and haematoma
  • Cerebral oedema can be treated with
    mannitol/frusemide or hypertonic saline
  • Corticosteroids may be used for
    oedema secondary to mass lesions
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13
Q

CSF

A

Shunts via the lateral ventricle to drain CSF in hydrocephalus.

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14
Q

How do you measure ICP?

A
  1. Noninvasive
  • From history and symptoms of
    headache,
    nausea/vomiting,
    confusion,
    behavioural changes
  • Papilloedema on eye examination
  • CT scan or MRI of the head
  1. Invasive
  • External ventricular drain placement:
    catheter is placed in the lateral
    ventricle at the level of foramen of Munro
  • Intraparenchymal fibre optic catheter placement:
    monitor is placed in the prefrontal area
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15
Q

How do you interpret the ICP waveforms?

see Figures 3.6
and 3.7.

A

There are four kinds of waves

  1. Normal
  2. A waves
  3. B waves
  4. C Waves
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16
Q
  1. Normal
A
  • Normal waves have a systolic upstroke (P1) and a diastolic
    downstroke (P3) with a dicrotic notch (P2)
17
Q
  1. A waves
A
  • Lundberg A waves, ‘or plateau waves’,

are steep increases in ICP lasting for 5 to 10 minutes.

They are always pathological and
represent reduced intracranial hypertension

indicative of early brain herniation

  • Steep ramp up to 50–80 mmHg, over 2–15 minutes
  • Peak is followed by an abrupt fall to baseline
  • Reflect extreme compromise of intracranial compliance
18
Q
  1. B waves
A
  • Lundberg B waves

oscillations of ICP at a frequency of
0.5 to 2 waves/min
are associated with an unstable ICP.

Lundberg B waves are possibly the result of cerebral vasospasm

19
Q
  1. C waves
A

Lundberg C waves

oscillations with a
frequency of 4–8 waves/min

are probably caused by interaction
between the cardiac and respiratory cycles

20
Q

Lundberg Waves

A

Lundberg A waves:
* Steep ramp up to 50–80 mmHg, over 2–15 minutes
* Peak is followed by an abrupt fall to baseline
* Reflect extreme compromise of intracranial compliance

Lundberg B
* Pressure pulses of 10–20 mmHg, over 0.5 to waves per minute
* Also reflect intracranial non–compliance but to a lesser degree

Lundberg C
* These waves represent diminished compliance in a qualitative fashion