Subdural haemorrhage

Pathophysiology

Tearing of bridging veins draining the surface of the brain to the dural sinuses, usually secondary to trauma. Blood collects between the dura and arachnoid mater, slowly raising ICP.

Can be spontaneous, especially in anti-coagulated patients. Risk increases with atrophy, high falls groups (epileptics, alcohol).

Parenchymal lacerations, usually involving arterial tears account for 20-30%.

Classic presenting complaint

Headache, fluctuating consciousness with developing hemiparesis in older patient on warfarin. Fall/trauma may have been minor or weeks ago such that they forget it happened.

On examination

Impaired cognition, reduced GCS.

As ICP increases, localising signs such as hemiparesis, unequal pupils (uncal herniation) and eventual respiratory arrest (coning).

Clinical approach & differential

  • Stroke
  • Delirium/dementia
  • CNS tumour or space-occupying lesion

Classic findings

Chronic subdural (hypodense) – taken from Radiopaedia

Chronic subdural (isodense) – taken from Radiopaedia

Acute subdural (hyperdense) – taken from Radiopaedia

Crescent-shaped hemorrhage that crosses suture lines (as opposed to extradural).

Acute:Ž hyperdense on CT, oedema, midline shift

Chronic: iso/hypodense on CT, obliteration of sulci, midline shift. See isodense examples above – this can be less obvious than hypodense.

Bloods takes about 14 days to become isodense, then >21 days to be hypodense.

Prognosis

Acute: 50-90%, depending on admitting GCS and time to surgery

Chronic:

Treatments

Check anti-coagulation – can this be reversed?

Is there a current need for AEDs?

Neurosurgery referral

  • If >10mm OR >5mm midline shift – evacuate, ideally within 4 hours
  • If <10mm and <5mm midline shift, evacuate if
    • GCS dropping
    • asymmetric pupils

Treat cause of falls