Intracranial SOL Flashcards
Types of SOL?
Tumours
Infection (e.g. brain abscess, subdural empyema)
Vascular (acute haemorrhages extradural/subdural, spontaneous subarachnoid haemorrhage)
Hydrocephalus (excess accumulation of CSF)
How do primary brain tumours present?
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
How are brain tumours diagnosed?
Complete neurological examination - VERY ESSENTIAL
Scans and other radiological investigations - CT & MRI
CSF studies
Bloods
How is brain tumours managed?
Surgery Steroids Radiotherapy Chemotherapy Treatment of any associated problems
What is normal vs pathological ICP?
ICP is normally <15 mmHg in adults
Pathological ICP is persistent pressures >20 mmHg
What are causes of ICP?
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
How is CPP (cerebral perfusion pressure) calculated?
CPP = ABP - ICP
When auto regulation is deranged, increased ABP is required to maintain CPP with increased ICP
Symptoms of raised ICP?
Depends on rate and degree of increase Headache Decreased level of consciousness Nausea and vomiting Visual problems Hypertension and bradycardia Respiratory depression
What are the general ‘routine’ measures to control ICP?
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
What are the options to manage a acute rise in ICP?
Heavy sedation +/- paralysis CSF drainage Osmotic therapy (mannitol) Hyperventilation Barbiturate therapy Decompressive craniectomy
Why is hyperventilation done?
Reducing PaCO2 causes cerebral vasoconstriction and reduces intracranial blood volume
Results in a rapid reduction in ICP - however effect is short lived
What is involved in osmotic therapy?
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
How does barbiturate therapy work?
Reduce brain metabolism and cerebral blood flow - lowering ICP
What is an extradural haematoma (EDH)?
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
What are the clinical features of an EDH?
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
What is a subdural haematoma (SDH)?
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
Why is there a latent period between injury and clinical presentation in SDH?
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
How is SDH managed?
- Surgical - decompressive craniotomy
- Optimise venous outflow and reduce ICP – elevate head, hyperventilation, IV mannitol
- Prophylactic anti-epileptics
What is Giant Cell Arteritis?
Inflammation of walls of medium/large arteries
Usually occurs in over 50s and more common in Caucasian women
What are the clinical features of giant cell arteritis?
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
How is giant cell arteritis diagnosed?
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
How is giant cell arteritis treated?
Oral prednisolone (60 mg OD) with gastro-protection Regular monitoring
