Subdural Haematoma

Definition, Aetiology and Pathophysiology

  • Subdural haematoma/haemorrhage (SDH) is a collection of blood in the the potenital space between the dura mater and arachnoid mater of the meninges surrounding the brain.
  • Can occur in any age group
    • Children – non-accidental injuries (‘shaken-baby’ syndrome)
    • Young adults – trauma e.g. road traffic accidents
    • Older adults – falls (not always obvious from history)
      • Note in older patients, brain atrophy increases the subdural space and the tension of bridging veins, making them more susceptible to injury and subsequent SDH
    • Occasionally can occur in any age group without injury (secondary to AV malformations/haemangiomas/dural AV fistulas)
  • Can be defined as
    • Acute – within 72 hours (usually of trauma/injury)
    • Subacute – 3-7 days
    • Chronic – >7 days, often weeks (may not have a clear history of trauma)
  • Usually caused by tearing of the ‘bridging’ veins which originate from the cortex and traverse the subdural space to drain into the venous sinuses
    • usually due to rapid acceleration/deceleration of the head
    • bleeding from a damaged cortical artery may also occur
  • Note that acute symptomatic SDH carried a very high mortality/morbidity (50-90%).


  • Acute
    • Usually present following a moderate-severe head injury
      • Often co-existing cerebral contusions/bleeds (i.e. complex SDH)
    • Reduced level or loss of consciousness is the most common presentation (note that this may not be immediate)
    • Pupillary abnormalities (anisocoria or ‘blown pupil’) may be seen in up to 40%
  • Chronic
    • May have a vague history or progressive symptoms
      • Falls/injury may or may not be a feature but if present, may have occurred weeks ago and/or may not be severe
      • Anorexia, nausea and vomiting are not uncommon
      • Gradually worsening focal neurology e.g. limb weakness, loss of sensation, vision or speech disturbances
      • Gradually deteriorating headaches
    • Anticoagulant use and alcohol excess are both significant risk factors.

Differential Diagnosis

  • Extradural or intracerebral haemorrhages
  • Meningitis or Encephalitis
  • Cerebral tumour
  • Stroke
  • Dementia
  • Other causes of reduced consciousness e.g. sepsis, DKA, hepatic encephalopathy


  • Blood tests may be normal
    • Abnormal (low) platelets or coagulation screens (including high INR) may be present
    • Group and save may be appropriate
  • CT scan
    • Acute
      • Crescent shaped homogeneously hyperdense extra-axial collection diffusely spread across the affected hemisphere
        • Note some areas may be more/less dense depending on fresh vs clotted vs liquefied blood.
    • Subacute
      • Can be hard to identify on CT as the density begins to drop with clot liquefication.  Clues include
        • CSF filled sulci do not reach the skull but rather fade into the subdural space
        • mass effect (sulcal effacement/distortion i.e. flattening; midline shift)
        • apparent thickening of the cortex
        • MRI/contrast CT may be useful
    • Chronic
      • Same as acute but hypodense (the SDH becomes the same density as CSF i.e. dark as in the ventricles)
    • Important features include size and mass effect


  • Treatment depends on the size (mass effect) and symptoms caused by the SDH
    • Small, asymptomatic SDH (especially chronic SDH) can be managed conservatively with repeat CT scans.
    • In acute symptomatic SDH, a craniotomy is usually required to evacuate the clot (once the patient is stable for theatre)
    • In chronic/subacute symptomatic SDH, burr hole drainage is often preferred (liquefied blood more easily drained)

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