Subdural haematoma

🩸 A Subdural Haematoma (SDH) is bleeding into the potential space between the dura mater and arachnoid mater. 🧠 Classically venous in origin (torn bridging veins), producing a slower and often insidious presentation compared with extradural haematoma. ⚠️ Always suspect SDH in elderly, alcohol-dependent, anticoagulated, or cognitively declining patients after even minor trauma.

💡 Pathophysiology (What is really happening)

• Acceleration–deceleration forces tear bridging veins traversing from cortex to dural sinuses.
• Venous pressure is low → gradual accumulation → delayed neurological decline ⏳.
• Cerebral atrophy (ageing, alcohol misuse) increases vein length and fragility.
• In chronic SDH, inflammatory membranes form and become vascularised (often via middle meningeal artery branches), predisposing to recurrence.
• Mass effect → midline shift → raised intracranial pressure (ICP) and risk of herniation.

🧬 Classification by Time Course

• Acute: <72 hours (hyperdense on CT).
• Subacute: 3–21 days (may appear isodense).
• Chronic: >3 weeks (hypodense; liquefied).

📌 Risk Factors

• Falls (especially >65 years) 👴
• Alcohol misuse 🍺
• Anticoagulants (warfarin, DOACs) and antiplatelets 💊
• Coagulopathy or thrombocytopenia
• Low CSF pressure (post-LP, VP shunt)
• Epilepsy or high-impact trauma 🚗

🩺 Clinical Features

Presentation varies with bleed rate and cerebral reserve. Acute SDH often mimics severe TBI; chronic SDH frequently masquerades as delirium or dementia.

• Acute: ↓ GCS, severe headache 🤕, vomiting, seizures, focal deficit.
• Chronic: Progressive confusion, personality change, gait disturbance, falls.
• Focal signs: hemiparesis, aphasia, visual field deficit.
• Unilateral dilated pupil (CN III compression) → impending herniation 🚨.
• Cushing response: bradycardia + hypertension + irregular breathing.

📷 Imaging

CT Head (First-line)

• Crescent-shaped extra-axial collection.
• Crosses suture lines but limited by dural reflections (falx, tentorium).
• Assess thickness, midline shift, basal cistern effacement.

Large Subacute SDH with Midline Shift

Large Acute SDH

MRI is helpful when CT is equivocal (isodense collections, posterior fossa, chronic cases).

🔬 Investigations

• Bloods: FBC, U&E, clotting screen, group & save.
• Urgently check INR if on warfarin.
• Platelets ideally >100 × 10⁹/L for surgery.
• CT cervical spine in trauma.

⚠️ Complications

• Raised ICP and transtentorial herniation 🧠
• Recurrent chronic SDH (10–20%)
• Seizures
• Infarction from vascular compression
• Subdural empyema (rare)

⚡ Management

All moderate or large SDHs require early neurosurgical discussion. Management is guided by neurological status and imaging findings.

• Initial (ABC): Airway protection if GCS ≤8; maintain normoxia and normocapnia.
• Reverse anticoagulation:
  • Warfarin → IV vitamin K + PCC.
  • DOAC → specific reversal agents if available.
• Surgical Indications:
  • Thickness >10 mm OR midline shift >5 mm.
  • Neurological deterioration.
• Acute SDH: Craniotomy ± decompressive craniectomy.
• Chronic SDH: Burr-hole drainage ± subdural drain.
• Conservative: Small, asymptomatic SDH with close observation and repeat imaging 👀.
• Consider MMA embolization in recurrent chronic SDH.

🆘 Red Flags (Call Neurosurgery Immediately)

• Deteriorating GCS
• New pupillary asymmetry
• Progressive focal deficit
• Significant midline shift on imaging

📋 EDH vs SDH Comparison

🟥 EDH: Arterial (middle meningeal), biconvex, does NOT cross sutures, lucid interval possible. 🟦 SDH: Venous, crescent-shaped, CAN cross sutures, often delayed presentation.

⚠️ Confusion + fall + anticoagulation = SDH until proven otherwise.