Key Facts

SDH is one of the commonest neurosurgical conditions. Acute SDH carries high mortality due to associated primary brain injury. Chronic SDH is increasingly common due to aging populations and widespread anticoagulant use.

Epidemiology

Acute SDH: incidence ~5-25 per 100,000 per year; most common in young males (trauma) and elderly (falls). Chronic SDH: incidence ~5-14 per 100,000 per year; incidence rising (aging population, anticoagulant use); mean age >70 years.

Aetiology

• Acute: head trauma (RTC, falls, assaults) — high-velocity injury; may also have associated contusion, DAI, skull fracture
• Chronic: minor or forgotten head trauma (weeks-months prior); risk factors: elderly (cerebral atrophy), anticoagulation, antiplatelet therapy, alcohol excess, CSF shunts (over-drainage), coagulopathy
• Subacute (3 days-3 weeks): transitional phase

Pathophysiology

Acute: trauma causes acceleration-deceleration injury → tearing of bridging veins (crossing from cortical surface to dural venous sinuses) → blood accumulates in subdural space. The blood spreads diffusely over the hemisphere (crescent shape). Associated parenchymal injury determines outcome more than the SDH itself.

Chronic: initial minor bleed organises → fibrous membrane formation (outer and inner) → neomembranisation with fragile capillaries → repeated micro-haemorrhages into collection → gradual enlargement → mass effect. The osmotic gradient of degrading blood products draws in fluid, further expanding the collection.

Acute SDH

• History of significant head trauma
• Reduced GCS (often from the outset — due to associated brain injury)
• Focal neurological deficit (contralateral hemiparesis)
• Ipsilateral fixed dilated pupil (uncal herniation → CN III compression)
• Rapid deterioration

Chronic SDH

• Insidious onset (weeks-months after trivial trauma)
• Fluctuating confusion/drowsiness (often mistaken for dementia or delirium)
• Headache (often mild)
• Personality/behavioural change
• Gait disturbance, falls
• Focal weakness (contralateral hemiparesis)
• Speech disturbance
• Seizures (~10%)

Red Flags

• Decreasing GCS (expanding haematoma, herniation)
• Fixed dilated pupil (uncal herniation)
• Progressive neurological deficit in elderly patient ("treatable dementia")
• Bilateral SDH (5-20% — may present without lateralising signs)

Imaging

• CT head (non-contrast): first-line
  • Acute SDH: crescent-shaped hyperdense (bright) collection; may cross suture lines; look for midline shift, mass effect
  • Subacute SDH (1-3 weeks): isodense (may be hard to see — look for effaced sulci, midline shift)
  • Chronic SDH: hypodense (dark) or mixed density collection; crescent; may be bilateral
  • Measure: maximum thickness, midline shift, mass effect on ventricles
• MRI head: more sensitive than CT (especially for isodense subacute SDH and bilateral collections)

Bloods

• Coagulation (INR, APTT, fibrinogen): URGENT if on anticoagulants
• FBC: platelet count
• U&Es, LFTs: baseline
• Group and save: for potential surgery

Additional

• GCS monitoring: serial neurological observations (neurosurgical chart)
• CT angiography: if vascular malformation suspected (young patient without trauma history)

Acute SDH

• Neurosurgical emergency: craniotomy and evacuation if: GCS ≤8, pupil abnormality, midline shift >5 mm, haematoma thickness >10 mm
• Reverse anticoagulation: PCC for warfarin; idarucizumab for dabigatran; andexanet alfa/PCC for anti-Xa agents
• Manage raised ICP: head elevation 30°, sedation, osmotherapy (mannitol 20% 0.5-1 g/kg or hypertonic saline)
• Supportive: ITU care, neuroprotection, seizure prophylaxis if concern

Chronic SDH

• Conservative: for small, asymptomatic collections; serial CT monitoring; stop/reverse anticoagulation; consider dexamethasone (Dex-CSDH trial — no benefit shown; NOT routinely recommended)
• Surgical: burr hole drainage (1-2 burr holes + irrigation ± subdural drain): first-line for symptomatic chronic SDH; performed under LA or GA; post-op: lie flat for 24-48 hours; subdural drain for 24-48 hours
• Mini-craniotomy: for organised/septated collections not amenable to burr holes
• Middle meningeal artery embolisation: emerging treatment for recurrent chronic SDH (EMBOLISE trial, STEM trial); reduces recurrence
• Recurrence rate: ~10-20% after initial burr hole drainage; risk factors: anticoagulant use, bilateral SDH, recollection on post-op imaging

Referral Criteria

• All acute SDH: immediate neurosurgical referral
• Chronic SDH with symptoms: neurosurgical referral
• All patients on anticoagulants with SDH: urgent anticoagulant reversal + neurosurgical input

Acute SDH: mortality ~50-90% (poor prognosis due to associated primary brain injury); outcome depends more on associated parenchymal injury than the SDH itself. GCS on admission is the strongest prognostic factor. Chronic SDH: excellent prognosis with surgical treatment — ~80-90% good outcome after burr hole drainage. Recurrence rate ~10-20%. Bilateral chronic SDH has higher recurrence. Early mobilisation and rehabilitation improves functional outcomes.

SDH CT Density Over Time

Subdural vs Extradural Haematoma