Raised ICP Flashcards

1
Q

What are the normal intracranial pressures (CSF pressure) for Adults, children and term infants?

A
  • Adults: <10-15 mmHg
  • Children: 3-7 mmHg
  • Term infants: 1.5-6 mmHg
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2
Q

How can you measure ICP?

A
  • Lumbar puncture
  • Subdural ICP monitor
  • Subarachnoid ICP monitor
  • Epidural ICP monitor
  • many more…
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3
Q

What is NIRS?

A

Near Infra-Red Spectroscopy

  • Meaures ICP indirectly by measuring cerebral perfusion
  • Relies on the transparency of tissue for light int he NIR range and O2 dependent light absorbance of Hb
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4
Q

What is the normal ICP wave? What kind of things will increase ICP normally?

A

Usually P1> P2

Normally increased by; cough, respiration, valsalvar manouvre

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5
Q

How can the ICP wave change in acute brain injury?

A

A change in brain injury compliance causes the reversal of P1:P2 and P2> P1

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6
Q

What are some of the immediate compensatory mechanisms that kick in when ICP is raised?

A
  • Decrease in CSF volume → fluid moves into lumbar area
  • Reduced CSF production
  • Decreased blood volume → blood squuezed out of the sinuses
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7
Q

What delayed mechanism acts to reduce raised intracranial pressure?

A

Decrease in extracellular fluid

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8
Q

What is the Monro-Kellie doctrine?

A

The sum of intracranial volumes within brain and CSF and other components (tumour, haemaotoma) is constant

Intracranial volume rises gradually then rapidly to the point where the brain can b squeezed out of the foramen magnum

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9
Q

How does ICP relate to cerebral perfusion?

A

Cerebral perfusion pressure = MAP - ICP

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10
Q

What are the 2 major consequences of increased ICP?

A
  • Brain shifts
  • Brain ischemia
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11
Q

What are some of the symptoms and signs of rICP?

A

Symptoms

  • Headache
  • Nausea and vomting
  • Double vision
  • Neurological symptoms

Signs

  • Bradycardia
  • Systolic hypertension
  • Irregular respiration
  • Cheyne Stokes respirations
  • Decreased mental abilities
  • Confusion
  • Non-reactive pupils
  • Loss of conciousness
  • Pappiloedema
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12
Q

What is Cushing’s reflex?

A
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13
Q

What is craniosynotosis?

A

Early fusion of the sutres of the skull → not enough rough for the expanding brain

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14
Q

What should you not do to patients who have raised ICP?

A

Do not push in lots of fluids!

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15
Q

Explain what happens due to ICP in extradural haemorrhage?

A
  • Patient presents with loss of conciousness on initial injury
  • followed by transient recovery‘lucid interval’ (in 40% patients)
  • As haematoma enlarged, ICP rises compressing the brain → deteriorating conciousness
  • May see cranial nerve palsies as brain structures start to herniate
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16
Q

How do extradural haemorrhages occur?

A
  • collection of blood between the inner surface of the skull and the periosteal dura mater
  • Nearly always secondary to trauma
  • 90% of cases involved in a severed artery - commonly middle meningeal artery
17
Q

What happens in subdural haemorrhage?

A
  • Usually occurs in older patients where the brain shrinks and bridging beins under more tension
  • More fragile → vulnerable to break
18
Q

How can you reduce ICP?

A
  • Start by standard measures; airways control, ABC, ventilation
  • Tier 2; sedation, fever control, glucocorticoids and try hyperosmolar & diversion therapy, diuretics
  • Tier 3; barbituate coma (avoids epilepsy and rests the brain)
  • Eventually may need decompressive craniectomy or burr hole surgery
19
Q

Why can you get a fixed and dilated pupil in rICP?

A
  • Increased ICP can compress the occulomotor nerve
  • Responsible for pupil dilation and eye movements
20
Q

What can cause communicating hydrocephalus?

A
  • Abnormalities of the arachnoid granules that absorb CSF mean CSF isn’t absorbed → ICP rises
  • Impaired CSF reabsorbtion in the absence of any obstruction
21
Q

What can cause non-communicated hydrocephalus?

A
  • Due to CSF flow obstuction
  • Blockage of:
    • ​Foramen of Monro
    • Aqueduct of sylvius
    • 4th ventricle obstruction
    • Foramen of luschka and magendie
22
Q

What is Budd Chiari malformation?

A
  • Structural anatomical defect where the cerebellum tonsils are displaced downwards through the foramen magnum
  • More extremely can involve cerebellum, brainstem and 4th ventricle
23
Q

Why do you get oedema in an anoxic brain injury?

A
  • Decreased cerebral blood flow
  • Decreased O2
  • Na/K ATPase cannot function
  • Efflux K+ out of cell
  • Influx Na+ into the cell
  • Neurones become depolarised
  • Water will follow Na into the cell → oedema