15. Raised ICP Flashcards

1
Q

What determines normal ICP?

A

Determined by volume of blood, brain and CSF all enclosed within a rigid box

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2
Q

What is the normal ICP?

A
  • Adults 5-15 mmHg
  • Children 5-7 mmHg
  • Term infants 1.5-6mmHg
    A good rule of thumb is that a pressure >20 mmHg is raised
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3
Q

What is the Monro-Kellie doctrine?

A

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

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4
Q

In the case of an intracranial mass(e.g. brain tumour), what does the monro-kielle doctorine say?

A

the first components to be pushed out of the intracranial space are CSF and venous blood, since they are at the lowest pressure

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5
Q

How is cerebral perfusion pressure calculated?

A

CPP = mean arterial pressure (MAP) - ICP

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6
Q

What is the normal value of MAP, ICP and therefore what is the normal CPP?

A
  • Normal CPP >70 mmHg
  • Normal MAP ~90mmHg
  • Normal ICP ~10 mmHg
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7
Q

What happens to CPP if MAP increases, and what occurs in response?

A

If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)

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8
Q

What happens to CPP if ICP increases, and what occurs in response?

A

If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation)

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9
Q

what would happen if ICP increased without cerebral autoregulation

A

if ICP increased, perfusion of the brain decreases (without cerebral autoregulation)

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10
Q

Below what CPP can cerebral blood flow not be maintained and why?

A

If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated

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11
Q

how does expansion of intracranial mass affect ICP?

A

• ICP can be maintained at a constant level as an

intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid (exponential) rate

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12
Q

WHat can damage to the brain do to cerebral autoregulation?

A

can impair or even abolish cerebral autoregulation

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13
Q

CPP explained in numbers

A
1) Normal:
○ CPP=MAP-ICP
○ CPP=90-10=80
○ >70 => normal CPP
2) Uncompensated SOL:
○ CPP-MAP-ICP
○ CPP=90-30=60
○ <70=> abnormal CPP
3) Compensated SOL:
○ CPP=MAP-ICP
○ CPP=110-35=75
○ >70=> normal CPP
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14
Q

what is the Cushing’s triad?

A

The three primary signs that indicate raised intracranial pressure:
• hypertension
• bradycardia
• irregular breathing

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15
Q

explain the Cushing’s reflex/triad?

A
  • A rise in ICP will initially lead to hypertension as the body increases MAP to maintain CPP
  • The increase in MAP is detected by baroreceptors which stimulate a reflex bradycardia via increased vagal activity
  • Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing (due to tonsilar herniation)
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16
Q

What may occur as a side effect of increased vagal activity in cushings reflex?

A

can cause stomach ulcers as a dangerous side effect

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17
Q

What are the causes of raised ICP?

A
  • too much blood within cerebral vessels (rare)
  • too much blood outside cerebral vessels (haemorrhage)
  • too much CSF
  • too much brain
  • something else
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18
Q

how can Too much blood within cerebral vessels be split?

A
  • Raised arterial pressure

* Raised venous pressure

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19
Q

What can cause raised arterial pressure within cerbral vessels?

A

Malignant hypertension

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20
Q

what is Malignant hypertension

A
○ Systolic >180mmHg or Diastolic >120mmHg
○ Signs of target organ damage
■ Retinal haemorrhages
■ Encephalopathy
■ Left ventricular hypertrophy
■ Reduced renal function
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21
Q

management of malignant hypertension?

A

○ Urgent referral
○ Goal is to decrease BP gradually in order to avoid
ischaemic events. - hypertension is prothrombotic state - increase risk of MI and strokes - if reduced too quickly can cause hypotension
○ High mortality rate

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22
Q

What can cause raised venous pressure in the skull?

A

SVC obstruction (e.g. external compression by a lung tumour)

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23
Q

how might patients with SVC obstruction present?

A

○ localised oedema of face and upper limbs
○ dilated veins over arms chest and face
○ SOB
○ difficulty swallowing

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24
Q

What are the different types of intracranial haemorrhages?

A
  • Extradural
  • Subdural
  • Subarachnoid
  • Haemorrhagic stroke
  • Intraventricular haemorrhage
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25
Q

describe Extradural haemorrhage

A

○ Between skull and dura
○ Most common cause=trauma
○ Unconscious Patient vs Patient with a ‘Lucid Interval’
○ CT-Biconvex shape

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26
Q

describe Subdural haemorrhage

A
○ Between Dura and Arachnoid mater
○ CT-Concave/Crescent
○ Note:
■ Acute vs Chronic
■ Acute: occurs suddenly, progresses quickly
■ Chronic: Slow progression
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27
Q

describe describe Extradural haemorrhage haemorrhage

A

○ Between arachnoid and pia mater
○ ‘Thunderclap’ headache
○ 85% rupture of intracranial aneurysm

28
Q

What can too much CSF cause?

A

Hydrocephalus

29
Q

What are the 2 division of hydrocephalus?

A
  • Congenital (more common)

- acquired

30
Q

What are the 2 causes of congenital hydrocephalus?

A
Obstructive
Communicating (i.e. drainage of CSF not impaired)
31
Q

What are the clinical signs of congenital hydrocephalus?

A
  • Bulging head with head circumference increasing faster than expected
  • Sunsetting eyes (due to direct compression of orbits as well as involvement of oculomotor nerve as it exits midbrain)
32
Q

effect of genetic on congenital hydrocephalus?

A

Genetic and non-genetic factors

■ Eg. mutation in L1CAM gene linked to aqueductal stenosis

33
Q

what are Obstructive causes of congenital hydrocephalus?

A
● Neural tube defects
• Leakage of CSF
• Causes fourth ventricle to push
downward 
● Aqueduct stenosis
● Dandy-Walker Syndrome
• Enlargement of fourth ventricle
• Outlets of ventricle partially blocked
• Cerebellum not fully developed
34
Q

what are Communicating causes of congenital hydrocephalus?

A

○ Overproduction of CSF
○ Reduced absorption of CSF
• Choroid plexus papilloma
• Infection and inflammation leading to scarring at subarachnoid space

35
Q

What is the management of congenital hydrocephalus?

A
  • Can be treated in acute setting by tapping the fontanelle with a needle
  • Medium term drainage can be achieved by external ventricular drain (EVD)
  • Long term drainage by ventricular shunts
36
Q

What is an external ventricular drain?

A

Flexible plastic catheter placed inside ventricle draining the CSF into a collecting bag

37
Q

What are the good/bad with EVD?

A
  • Allows continuous pressure monitoring
  • Can be at risk of infection due to direct communication between brain and outside world
  • Requires inpatient monitoring so not good as a long term solution - Used if shunt fails or contraindicated
38
Q

What is a ventricular shunt?

A

Tube is placed from the ventricular system into the peritoneum (V-P)(most common) or right atrium (V-A)

  • tunnelled under the skin
  • one way valve
39
Q

What are the issues with ventricular shunts?

A
  • V-P shunts vulnerable to infection (e.g. if abdominal infection, can track back up to brain) or kinking
  • Most shunts will require revision
40
Q

What are the causes of acquired hydrocephalus?What are the causes of acquired hydrocephalus?

A
  • Meningitis
  • Trauma
  • Haemorrhage (e.g. post subarachnoid haemorrhage)
  • Tumours (e.g. compressing cerebral aqueduct)
41
Q

What causes too much brain?

A

Cerebral oedema (brain swells)

42
Q

What are the 4 causes of cerebral oedema?

A

Four major pathophysiologies, which occur in disorders such as stroke or trauma:

  • Vasogenic (breakdown of tight junctions)
  • Cytotoxic (damage to brain cells)
  • Osmotic (e.g. if ECF becomes hypotonic)
  • Interstitial (flow of CSF across ependyma and damage to BBB)
43
Q

describe vasogenic cause of cerebral oedema

A

● Disruption of blood brain barrier

● Breakdown of tight junctions=increased permeability

44
Q

describe Cytotoxic cause of cerebral oedema

A

● Injury to cells of the brain (neurones,
glial cells, axons)
● Derangements in ATP-dependent transmembrane pumps-intracellular accumulation of fluid

45
Q

describe Osmotic cause of cerebral oedema

A

● Usually osmolarity of extracellular fluids
is equal on both sides of BBB
● If there is a change-osmotic gradient

46
Q

describe Interstitial cause of cerebral oedema

A

● Increased pressure within ventricles, eventual damage to their linings.
● CSF can now be found in brain parenchyma

47
Q

What else can cause a rise in ICP? (4)

A
  • Tumour
  • Cerebral abscess
  • Idiopathic
  • Craniosynostosis
48
Q

What is craniosynostosis?

A

premature closure of cranial sutures

49
Q

What does idiopathic intracranial hypertension present with?

A

May present with headache (worse in morning and night and relieves on standing) and visual disturbance
- Usually obese middle aged females

50
Q

How is a diagnosis of raised idiopathic intracranial hypertension made?

A

• CT/MRI
• By raised opening pressure on an LP (lumbar puncture)
- Make sure there are no signs of intracranial pathology before doing an LP in a patient with suspected raised ICP as this can precipitate brain herniation! - Contraindicated in raised ICP!

51
Q

How is idiopathic intracranial hypertension treated?

A

Treat with weight loss and blood pressure control

52
Q

what is cerebral abscess and what causes it?

A

○ Localised pus formation with capsulation within brain parenchyma.
○ Causes: Spread of infection (direct vsdistance), trauma, or unknown

53
Q

how can brain tumours be classified?

A

○ Primary
○ Metastatic
○ Intra vs Extra- axial

54
Q

WHat are the clinical features of raised ICP?

A
  • Headache
  • Nausea and vomiting
  • Difficulty concentrating or drowsiness (effect on daily life)
  • Confusion
  • Double vision
  • Focal neurological signs
  • Seizures
  • Non-reactive pupils
  • Loss of consciousness
55
Q

Describe the headaches that occur with raised ICP?

A
  • Constant
  • Worse in the morning
  • Worse on bending / straining (coughing, sneezing etc)
  • precipitated by exercise
56
Q

vision problems that present with raised ICP?

A

Problems with accommodation (early sign, pupillary dilatation a late sign)
o Maybe effects on acuity
o Visual field defects
o Papilloedema (swelling of optic disc)

57
Q

What are the different types of herniations? (5)

A
  • tonsillar (or coning)
  • subfalcine
  • uncal
  • central downward
  • external (through skill fracture/therapeutic craniotomy)
58
Q

WHat is a tonsillar herniation, what is at risk of compression?

A

Cerebellar tonsils herniate through foramen magnum, compressing medulla

59
Q

What is a subfalcine herniation, what is at risk of compression?

A
  • Cingulate gyrus is pushed under the free edge of the falx cerebri
  • Can compress anterior cerebral artery as it loops over the corpus callosum
60
Q

What is a uncal herniation, what is at risk of compression?

A
  • Uncus of temporal lobe herniates through tentorial notch compressing adjacent midbrain
  • Can cause third nerve palsy and maybe even contralateral hemiparesis (due to compression of cerebral peduncle)
61
Q

WHat is a central downward herniation?

A

Medial temporal lobe / other midline structures pushed down through tentorial notch

62
Q

What is involved in management of raised ICP?

A
  • Airway and breathing: Maintain oxygenation and removal of CO2
  • Circulatory support: Maintain MAP and hence CPP
  • Sedation, analgesia and paralysis
  • Head up tilt: Improves cerebral venous drainage
  • Temperature: Prevent hyperthermia, Therapeutic hypothermia may be beneficial
  • Anticonvulsants: Prevent seizures, reduce metabolic demand
  • Nutrition and proton pump inhibitors - Improved healing of injuries and prevent stomach ulcers due to increased vagal activity
63
Q

Why may sedation, analgesia and paralysis be useful?

A
  • Decrease metabolic demand

- Prevents cough / shivering that might increase ICP further

64
Q

What are some other treatments?

A
  • Mannitol or hypertonic saline: Osmotic diuresis
  • Ventricular drainage
  • Decompressive craniectomy as a last resort
65
Q

investigations for raised ICP?

A
● Bedside
○ Vital signs, ECG, fundoscopy
● Bloods:
○ FBC, U+E’s, CRP, Clotting, Group & Save, Crossmatch, Blood culture
● Imaging:
○ CT scan
○ MR
66
Q

divide management of ICP into simple measures, specific and surgical

A
Simple measures
● Elevate head of bed
● Avoid pyrexia
● Analgesia
Specific medical measures:
● Anticonvulsants
● Sedation or neuromuscular blockade
● Mannitol or hypertonic saline
Surgical:
● Ventriculostomy
● Decompressive craniectomy