S10 L2 Pathophysiology and management of raised intracranial pressure Flashcards

1
Q

What is intracranial pressure?

A

The pressure within the cranium of the skull

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2
Q

What is the normal range for intracranial pressure?

A

Adults: 5-15mmHg
Young children: 3-7mmHg
Infants: 1.5-6mmHg
Pressure >20mmHg is raised (good rule of thumb)

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3
Q

What contributes to the intracranial pressure?

A

CSF volume = 150ml (10%)
Blood volume = 150ml (10%)
Brain parenchyma = 1400ml (80%)

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4
Q

What is the Monro-Kellie doctrine?

A

Proposed that sum of volumes of brain, CSF and intracranial blood is constant
↑volume in any one compensated by ↓in others
e.g. intracranial mass, first components pushed out are the CSF and intracranial venous blood (lowest pressure)

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5
Q

What is important about blood and the brain?

A

15-20% of CO goes to the brain

  • Need oxygenated blood→ neurones need nourishment
  • Rising ICP
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6
Q

What is the cerebral perfusion pressure?

A

Represent the cerebral blood flow
Calculated:
- CPP = Mean Arterial Pressure (MAP) - ICP
Therefore if ↑ICP then ↓CPP unless the MAP decreases - autoregulation
MAP= DBP + 1/3(SBP-DBP)

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7
Q

How does autoregulation in the brain work?

A

↑MAP the ↑CPP triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
↑ICP then ↓CPP triggering cerebral autoregulation to maintain cerebral blood flow (vasodilation)

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8
Q

What happens if the ICP too big?

A

If CPP <50mmHg
Cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
ICP an be maintained at a constant level up to a point when the ICP will rise at a exponential rate
Damage to the brain can impair or even abolish cerebral autoregulation

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9
Q

What is CSF?

A

CSF produced by the choroid plexus
Around 500mls produced each day
Homeostasis, protection, buoyancy and waste clearance

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10
Q

What type of brain herniation is there?

A
  1. Subfalcine herniation → Cingulate gyrus from cerebral hemisphere, shifts across midline under falx cerebri, can compress anterior cerebral artery as it loops over the corpus callosum
  2. Tonsillar herniation (aka coning)→ cerebellar tonsils through foramen magnum, compressing medulla
  3. Uncal herniation → Herniation of uncus, medial temporal lobe through tentorial notch, compressing midbrain, cause third nerve palsy, maybe even contralateral hemiparesis (compression of cerebral peduncle)
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11
Q

What are clinical features of raised ICP?

A
  1. Headaches → constant, worse in the morning, worse on bending/straining
  2. Nausea and vomiting
  3. Visual disturbances e.g. double vision → problems with accommodation (early signs, pupillary dilation a late sign), visual field defects, papilloedema (swelling of optic disc)
  4. Confusion
  5. Seizures
  6. Amnesia
  7. Focal neurological signs e.g. CNIII palsy (depend where lesion is)
  8. Difficulty concentrating or drowsiness → effect on daily life
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12
Q

What is Cushing’s triad?

A

aka Cushing reflex

  1. Rise in ICP → Hypertension - compensatory autoregulation mechanism → ↑MAP to maintain CPP
  2. ↓HR- baroreceptors detect ↑BP ↑vagal activity results in bradycardia
  3. Irregular breathing → ↑ICP leads to tonsillar herniation resulting in compression of the brainstem leading to damage to respiratory centres resulting in irregular breathing
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13
Q

What are the caused of raised ICP?

A
  • Too much blood
  • Too much CSF
  • Too much brain tissue
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14
Q

What can cause there to be too much blood?

A
Too much in the cerebral vessels
- Raised arterial pressure 
→ Malignant hypertension 
- Raised venous pressure 
→ SVC obstruction 
Too much outside the cerebral vessels (haemorrhage)
- Extradural 
- Subdural 
- Subarachnoid
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15
Q

What is malignant hypertension?

A
Accelerated hypertension
- Systolic >180mmHg or diastolic >120mmHg
- Signs of target organ damage 
→ Retinal haemorrhages 
→ Encephalopathy 
→ Left ventricular hypertrophy 
→ Reduced renal function 
- Urgent referral is require (same day)
- Goal to decrease BP gradually to avoid ischaemic events (hypertension= prothrombotic state, ↑CVS/cerebrovascular events risk)
- High mortality rate
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16
Q

What is superior vena cava obstruction?

A
  • Intraluminal obstruction or extrinsic compression
  • Reduction in venous return from head and neck and upper limbs
  • Most common cause is malignancy (some intravascular devices- clot formation around device)
  • Oncology emergency
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17
Q

How would a patient with SVC obstruction present?

A

Localised oedema of face and upper limbs
Dilated veins over arms, neck, anterior chest wall
SoB, swallowing difficulties
Symptoms worse on lifting of arms

18
Q

What is an extradural haemotoma?

A

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

19
Q

What is a subdural haemorrhage?

A
Between dura and arachnoid mater 
CT-concave/crescent 
Note:
- Acute vs chronic 
- Acute: occurs suddenly, progresses quickly 
- Chronic: slow progression
20
Q

What is a subarachnoid haemorrhage?

A

Between arachnoid and pia mater
Thunderclap headache - worse headache, sudden onset
85% rupture of intracranial aneurysm

21
Q

What are the reasons for too much CSF?

A

Congenital
Acquired
Non communicating (flow of CSF block in ventricular system) vs communicating (passageway remains open, increased CSF due to ↑production or ↓removal)

22
Q

What is congenital hydrocephalus?

A
  • Present a birth
  • Genetic and non-genetic factor → e.g. mutation in L1CAM gene linked to aqueduct stenosis
  • Fluid build up in the ventricles within the brain
  • Present with:
    → Enlargement of head circumference- sutures bot fused
    → Downwards gaze -‘sunsetting gaze’
    → Delay in neurological development
23
Q

What is obstructive hydrocephalus?

A

A blockage to the flow of the CSF

  1. Aqueduct stenosis → most common, blockage/narrowing of the cerebral aqueduct
  2. Neural tube defects → leakage of CSF, causes fourth ventricle to push downward
  3. Dandy-Walker syndrome→ enlargement of fourth ventricle, outlets of ventricle partially blocked, cerebellum not fully developed
24
Q

What is communicating hydrocephalus?

A

Overproduction of CSF
Reduced absorption of CSF
→ Choroid plexus papilloma - uncommon, intraventricular tumours, cauliflower like appearance on imaging
→ Infection and inflammation leading to scarring at subarachnoid space

25
Q

What are the acquired causes of too much CSF?

A

Intraventricular haematoma
Tumour
Infection - meningitis
Trauma

26
Q

What are the causes of too much brain?

A
  • Cerebral oedema - swelling of the brain
  • Brain tumour
  • Cerebral abscess- localised pus formation with capsulation
27
Q

What are the causes of cerebral oedema?

A
  1. Vasogenic → disruption of BBB, breakdown of tight junctions= ↑permeability
  2. Osmotic → usually osmolarity of ECF is equal across BBB, if there is a change it alters the osmotic gradient
  3. Cytotoxic → Injury to cells of the brain (neurones, glial cells, axons), derangements in ATP-dependent transmembrane pumps- intracellular accumulation of fluid
  4. Interstitial → ↑pressure within the ventricles, eventual damage to their linings, CSF can now be found in brain parenchyma
28
Q

What are the causes of a brain tumour?

A

Primary
Metastatic
Intra (within brain tissue) vs extra-axial (outside brain tissue e.g. meninges)

29
Q

What are the causes of a cerebral abscess?

A

Spread of infection (direct -through bone otomastoiditis vs distance- through blood)
Trauma
Unknown (30%)

30
Q

What is idiopathic intracranial hypertension?

A

↑ICP absence of cause

Present with headache and visual disturbances

31
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Gender F>M

Increased BMI

32
Q

How is idiopathic intracranial hypertension diagnosed?

A

CT/MRI

Raised opening pressure on a lumbar puncture - contraindicated in raised ICP due to risk of herniation

33
Q

How is idiopathic intracranial hypertension treated?

A

Weight loss and blood pressure control

34
Q

How is the cause of ICP estabished?

A

History and examination

Investigations

35
Q

What investigations can be done?

A
  1. Bedside - vital signs, ECG, fundoscopy
  2. Bloods- FBC, U+Es, CRP, clotting, group and save, cross match blood cultures
  3. Imaging- CT scan, MRI
36
Q

When is a CT head scan required?

A

Acute presentation

Chronic presentation

37
Q

What is the management for raised ICP?

A
  1. Primary survey using ACBDE approach
    (A,B- airways and breathing→ maintain oxygenation and removal of CO2, C- circulatory support→ maintain MAP and hence CPP)
    - Stabilise patient
  2. Simple measures
    - Elevate head of bed → improves cerebral venous drainage
    - Avoid pyrexia → prevent hyperthermia, therapeutic hypothermia might be beneficial
    - Analgesia → ↓ metabolic demand
  3. Specific medical measures
    - Anticonvulsants → prevent seizures ↓metabolic demand
    - Sedation or neuromuscular blockade → prevent cough/ shivering that might ↑ICP
    - Nutrition and PPI → improve healing of head injuries and prevent stomach ulcers due to increased vagal activity
    - Mannitol or hypertonic saline - ↑diuresis
  4. Surgical
    - Ventriculostomy - drain CSF from ventricles
    - Decompressive craniectomy - last resort, remove part of the skull to relieve the pressure
38
Q

What is the long term management for hydrocephalus?

A

VP shunt or VA shunt

  • Tubes from ventricles in the brain to the peritoneum or atria to drain CSF from skull to ↓ICP
  • Contains one way valve to prevent backflow into the ventricles
  • VP shunts vulnerable to infection, can track back up into the brain
  • Most shunts require revision at some point
39
Q

What is the acute management for hydrocephalus?

A

Tapping the fontanelle with a needle

40
Q

What is the medium term management for hydrocephalus?

A
  • External ventricular drain (EVD)
  • Allows continuous pressure monitoring
  • Risk of infection due to direct communication between brain and outside world
  • Requires in patient monitoring- not good as long term solution
  • Use if shunt fails or contraindicated
41
Q

Why is the Glasgow coma scale useful in these patient?

A

Changes in the score can indicate deterioration
Normal- 15
Lowest- 3
Below 8 - consider airway!