Intracranial bleeding

Background/Epidemiology

• Can be classified as
  • Extradural (epidural)
  • Subdural
  • Intracerebral
  • Subarachnoid
• Intracranial bleeding can act as a mass lesion (associated with rise in ICP and focal deficits)
  • If left untreated can cause ‘coning’, which can often be fatal

Extradural

• Epidemiology/Aetiology
  • Occurs in ~2% of head injury- but up to 15% of fatal cases
  • Around 30% are acute, 30% subacute and 10% chronic
  • More common in males
  • Most commonly due to damage to the middle meningeal artery, often with fractured temporal/parietal bones (lateral blow to the head)
• Presentation immediately after injury can be normal but later develops worsening headache and then change in conscious level, third nerve palsy, and nausea/vomiting (i.e. raised ICP)
• Appearance on CT (Immediate CT in these patients is the investigation of choice in patients with altered conscious level, focal neurological signs or suspected fracture)
  • Lentiform (convex) shaped ‘bleed’ (/lesion)
• Management
  • ABCDE with C-spine and full injury assessment
  • Surgical decompression (burr holes or craniotomy) should be considered in patients with impaired conscious level
  • Any patients with evidence of a fracture should be considered for surgery
  • Even in patients who appear normal, close observation is required to watch for any deterioration

Subdural

• Epidemiology/Aetiology
  • Occurs in 1-2% of head injury
  • More common in older patients
  • Most commonly due to damage of bridging veins between the cortex and venous sinuses
    • these are fragile and can tear easily
    • alternatively from vessel of the brain cortex which run along the surface of the brain
  • Can be acute or chronic (after injury)
• Appears as a crescent shaped bleed on CT
• Acute SDH
  • Usually present after trauma (lucid period is relatively less common than with EDH); loss of consciousness is probably most common
• Chronic SDH
  • Can present weeks after trauma (which may be trivial, particularly in the elderly on blood thinning drugs including aspirin)
  • usually presents with focal neurological signs, chronic headache or impaired consciousness
• Again, the management is principally surgical, although this is difficult in acute cases (mini-burr holes/mini craniotomy; success rate is less than in EDH)
  • Other management to consider (as with all ICBs) include mannitol (diuretic) and hyperventilation (to reduce osmotic pressure in the head)
  • Conservative management

Intracerebral haemorrhage and Contusions

• Bleeding/bruising within the cerebrum itself
• Not uncommon to complicate SDH

Presentation

• Late signs include
  • An enlarging, unresponsive pupil
  • Central respiratory depression
  • Cushing’s reflex :  Falling pulse rate and rising blood pressure