Intracranial SOL

Question 1

Types of SOL?

Answer 1

Tumours
Infection (e.g. brain abscess, subdural empyema)
Vascular (acute haemorrhages extradural/subdural, spontaneous subarachnoid haemorrhage)
Hydrocephalus (excess accumulation of CSF)

Question 2

How do primary brain tumours present?

Answer 2

Symptoms due to raised ICP
Symptoms of neurological deficits due to compression/damage of adjacent structures
Symptoms of cortical/meningeal irritations
Hormonal effects
Systemic effects/generally unwell

Question 3

How are brain tumours diagnosed?

Answer 3

Complete neurological examination - VERY ESSENTIAL
Scans and other radiological investigations - CT & MRI
CSF studies
Bloods

Question 4

How is brain tumours managed?

Answer 4

Surgery 
Steroids
Radiotherapy 
Chemotherapy 
Treatment of any associated problems

Question 5

What is normal vs pathological ICP?

Answer 5

ICP is normally <15 mmHg in adults

Pathological ICP is persistent pressures >20 mmHg

Question 6

What are causes of ICP?

Answer 6

Increase in brain/tissue/mass volume (cerebral oedema, SOL - tumour, haematoma, abscess)
Increase in CSF volume: obstruction to CSF circulation, reduced CSF absorption, increased CSF production
Increase in blood volume: raised arterial PCO2, venous obstruction, raised temperature

Question 7

How is CPP (cerebral perfusion pressure) calculated?

Answer 7

CPP = ABP - ICP

When auto regulation is deranged, increased ABP is required to maintain CPP with increased ICP

Question 8

Symptoms of raised ICP?

Answer 8

Depends on rate and degree of increase
Headache 
Decreased level of consciousness
Nausea and vomiting
Visual problems
Hypertension and bradycardia
Respiratory depression

Question 9

What are the general ‘routine’ measures to control ICP?

Answer 9

Head up tilt, 30-45º - promotes venous outflow and CSF movement
Keep neck straight and avoid tight ETT tapes (endotracheal tube) - obstruction to jugular venous outflow increases ICP
Avoid hypotension - to maintain cerebral blood flow
Maintain adequate sedation - reduces metabolic demands
Maintain euvolaemia and normo-hyperosmolar state - reduces cerebral oedema
Maintain normal PCO2 - raised PCO2 causes cerebral vasodilation and increases cerebral blood volume

Question 10

What are the options to manage a acute rise in ICP?

Answer 10

Heavy sedation +/- paralysis
CSF drainage
Osmotic therapy (mannitol)
Hyperventilation
Barbiturate therapy
Decompressive craniectomy

Question 11

Why is hyperventilation done?

Answer 11

Reducing PaCO2 causes cerebral vasoconstriction and reduces intracranial blood volume
Results in a rapid reduction in ICP - however effect is short lived

Question 12

What is involved in osmotic therapy?

Answer 12

Mannitol - osmotic diuretic
• MOA of reducing ICP controversial - reduces brain volume by drawing free water out of tissue into circulation (dehydrates brain parenchyma)
• 20% solution (200 grams per litre)
• Usual bolus dose 100ml

Question 13

How does barbiturate therapy work?

Answer 13

Reduce brain metabolism and cerebral blood flow - lowering ICP

Question 14

What is an extradural haematoma (EDH)?

Answer 14

Bleed between skull and dural layer of meninges
- Most common in young adult males

Causes

• EDHs are usually the result of an arterial bleed (for example from the middle meningeal artery ) which is vulnerable to trauma to the side of the head (temporo-parietal area)
• Trauma
• Venous cause

Question 15

What are the clinical features of an EDH?

Answer 15

Patients may regain consciousness following a brief period of impaired/loss of consciousness at time of injury - due to cerebral concussion
Level of consciousness beings to deteriorate
Fixed and dilated ‘blown’ pupils

Managed with decompressive craniectomy

Question 16

What is a subdural haematoma (SDH)?

Answer 16

Collection of blood between dural and arachnoid meninges
Seen in the elderly or those with alcohol misuse
Cause
- Rupture of bridging of veins
- Trauma to temporal region of head

Question 17

Why is there a latent period between injury and clinical presentation in SDH?

Answer 17

Haematoma develops very slowly (a venous ooze) - may be weeks or even months

• So gradual deficits are seen
• Headache, drowsiness and confusion are common in the late stages
• Fluctuating level of consciousness for a variable period is typical of SDHs as the haematoma contracts and expands due to osmotic effects

Question 18

How is SDH managed?

Answer 18

• Surgical - decompressive craniotomy
• Optimise venous outflow and reduce ICP – elevate head, hyperventilation, IV mannitol
• Prophylactic anti-epileptics

Question 19

What is Giant Cell Arteritis?

Answer 19

Inflammation of walls of medium/large arteries

Usually occurs in over 50s and more common in Caucasian women

Question 20

What are the clinical features of giant cell arteritis?

Answer 20

Headache
Visual disturbances
Polymyalgia rheumatica features in 40% (inflammatory disease of muscle)
Scalp tenderness
Jaw claudication
Mono-neuropathy of limbs (damage to single nerve)
Loss of temporal artery pulsation

Question 21

How is giant cell arteritis diagnosed?

Answer 21

ESR (>20 mm/hr is high) and CRP
Refer to secondary care - where they can do temporal artery biopsy or ultrasound scan
Refer to ophthalmology if visual loss

Question 22

How is giant cell arteritis treated?

Answer 22

Oral prednisolone (60 mg OD) with gastro-protection
Regular monitoring