Raised ICP Flashcards

1
Q

What is normal ICP

A

5-15mmHg

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2
Q

What is raised ICP?

A

> 20mmHg for more than 5 minutes

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3
Q

Describe the normal variation in ICP

A

ICP varies with HR due to arterial pressure, breathing, coughing, laughing, straining, sneezing, body position.
Either within normal limits or not sustained.

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4
Q

Monro Kellie theory - describe

A

Body compensates for space occupying lesions.
Skull is fixed closed space so has constant volume (brain, blood and CSF) - mostly water which is non-compressible.
The total volume = brain +arterial blood volume + venous volume + CSF
If one volume increases or there is a SOL mass you need to compensate with a decrease in the other volumes.
CSF and blood volumes can decrease.
When they can no longer compensate the brain has reached critical volume.
Any further increase in SOL mass results in increase in ICP.

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5
Q

How does a rise in ICP lead to brain death?

A

Eventually the ICP rises above cerebral perfusion pressure, which stops the blood supply to the brain leading to ischaemia.
Brain arterial vessels vasodilate and BP increases to improve cerebral perfusion. This raises ICP further forming a positive feedback loop.

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6
Q

Why should you avoid Lumbar puncture in someone with raised ICP?

A

Risk of coning because of dramatic change in pressure
Coning - cerebellar tonsillar herniation - sudden drop in pressure around the spinal cord creates a pressure gradient drawing the cerebellar tonsils down through the foramen magnum which can lead to brainstem death.

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7
Q

What are the symptoms of raised ICP

A

Headache:
Site = generalised and bilateral
Onset = varies depending on cause
Character = ache
Radiation = none
Associated symptoms = nausea, vomiting, mono-ocular vision loss (transient), altered mental state
Timing = worse first thing in morning, may wake patient
Exacerbating factors = worse when lying down, with raised intrathoracic pressure, on bending forward
Relieved by sitting forwards
Scale = varies

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8
Q

What are the signs of raised ICP? Why do these occur?

A

Papilloedema on fundoscopy (blurred optic disc margins) - due to impaired axoplasmic flow from the retina proximally
3rd nerve palsy - due to uncle herniation (ptosis, dilated pupil, down and out gaze)
6th nerve palsy - inability to abduct affected eye
Loss of vestibulo-occular reflex (no movement of eyes when putting cold or warm water into ears - following brainstem death
Confusion
Irritability
Impaired cognition
Reduced GCS
UMN signs (if there is subfalcine herniation compressing motor cortex or uncal herniation compressing crus cerebri of midbrain)
Decorticate posturing (flexion of elbows) if herniation causes compression of brain stem above the red nucleus.
Decerebrate posturing (elbow extension) if herniation causes compression below the red nucleus.
Biot’s respiration - due to pons compression (quick shallow inspiration followed by period of apnea)
Cushing’s reflex - ischaemia leads to hypertension, increased parasympathetic tone causes bradycardia, and irregular respiration

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9
Q

What might cause UMN signs in RICP?

A

Subfalcine herniation compressing the motor cortex or uncle herniation compressing the crus cerebri of the midbrain.

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10
Q

What is decorticate posturing? why does it occur?

A

Flexion of the elbows

If herniation causes compression of the brainstem above the red nucleus

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11
Q

What is decerebrate posturing?

A

Extension of elbows

If herniation causes compression below the red nucleus

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12
Q

Describe the Cushing’s reflex.

A

Raised ICP leads to ischaemia as arterioles become compressed when intracranial pressure > arterial pressure.
Sympathetic activation causes vasoconstriction –> hypertension. (It also causes raised HR and increased CO)
The hypertension is detected by baroreceptors in the aortic arch and carotid sinus, which cause parasympathetic stimulation to slow the heart rate and induce bradycardia.
Changes in homeostasis of the brainstem where the respiratory centre is leads to irregular breathing and apnea.

Thus Cushing’s reflex to raised ICP and brain ischaemia is:
Hypertension
Bradycardia
Irregular breathing

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13
Q

What are some causes of raised ICP?

A

Blood:
Increased intravascular volume - venous sinus thrombosis
Increased extravascular volume: extradural/subdural/subarachnoid/intracerebral haemorrhage

Brain:
Tumour
Oedema due to surgery/trauma, infarct, malignancy, infection, water intoxication

CSF:
Hydrocephalus: acquired, congenital, normal pressure

Other: meningioma, abscess idiopathic intracranial hypertension.

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14
Q

What is hydrocephalus and what can cause it?

A

Accumulation of CSF in the brain
Excess CSF production
Disruption of CSF flow: Alnorld chair malformation, spina bifida, aqueduct stenosis, clot post intraventricular haemorrhage, SOL)
Disruption of absorption at the arachnoid granulations (trauma)

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15
Q

What is the difference between congenital and acquired hydrocephalus?

A

Acquired hydrocephalus is any hydrocephalus that develops after birth.

Congenital hydrocephalus is any hydrocephalus that is present at birth (doesn’t follow the Monro-Kellie theory as the neonatal skull isnt a rigid closed box – soft fontanelles and unclosed sutures).

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16
Q

What is normal pressure hydrocephalus? How does it present? How is it treated?

A

Normal pressure hydrocephalus is a condition common in the elderly. There is a classical triad of dementia, urinary incontinence and abnormal gait. You treat with diuretics, lumbar punctures (since pressure is normal) or shunts.

17
Q

What is idiopathic intracranial hypertension? Presentation? Treatment?

A

Idiopathic intracranial hypertension (pseudotumour cerebri) is raised intracranial pressure without an underlying cause. It is common in overweight females aged 20-40. It presents with a typical RICP headache and is treated with diuretics or surgery.

18
Q

What investigations for RCIP?

A
  • Observations – to ensure Cushing’s syndrome and avoid pyrexia (which worsens ICP by vasodilation)
  • GCS monitoring
  • BM monitoring (hypoglycaemia worsens ICP by vasodilation)
  • Bloods
  • Blood gases (acidosis worsens ICP by vasodilation)
  • Head CT, MRI if inconclusive
  • Continuous ICP monitoring
19
Q

What is the management for RICP?

A

Stabilise

Treat cause

20
Q

What are medical treatments?

A

o Induce coma (keeps intrathoracic pressure low)
o Osmotherapy (mannitol/hypertonic saline)
o Hyperventilation – blow off CO2 leading to hypocapnic vasoconstriction, reduces blood portion of brain (but can worsen ischaemia)
o Maintain euglycaemia
o Antipyretics
o Therapeutic hypothermia
o Elevate head of bed
o Dexamethasone (if oedema is present)
o Acetazolamide (reduces CSF production)

21
Q

What are surgical treatments?

A

o Burr holes
• Drain subdural haematomas or insert ICP monitoring catheters
o Decompressive craniectomy – remove bone flap to relieve pressure
o Shunts
• Ventriculoperitoneal
• Ventriculoatrial

22
Q

Why might coma be induced

A

Keep intrathoracic pressure low

23
Q

How can hyperventilation help?

A

Blow off CO2 leading to hypocapnic vasoconstriction, this reduces blood portion of the brain but can worsen ischaemia

24
Q

What does dexamethasone do?

A

Corticosteroid - helps prevent cerebral oedema

25
Q

What does acetazolamide do?

A

Reduces CSF production