Subdural Hematoma (SDH) — Clinical Brief

What Is It?

Pathophysiology

• No direct trauma required in the elderly or anticoagulated patients — acceleration forces alone (e.g., whiplash) can be sufficient
• Elderly and cerebral atrophy: the brain shrinks away from the skull, stretching bridging veins further and making them more susceptible to minor trauma
• Anticoagulants / antiplatelets: dramatically increase risk and severity

Classification by Time Course

The blood evolves: fresh clot is hyperdense → proteins lyse → becomes isodense → liquefies to hypodense. This is critical for dating the injury.

Clinical Presentation

Acute SDH

• Most patients are drowsy or comatose from the moment of injury
• Up to one-third have a lucid interval (minutes to hours) before deterioration
• Unilateral headache on the side of the hematoma
• Ipsilateral pupil dilation (CN III compression from uncal herniation)
• Contralateral hemiparesis (or ipsilateral if Kernohan's notch phenomenon)
• Stupor, coma, and bilateral pupillary changes = late/impending herniation

Subacute SDH

• Gradual neurological decline over days
• Headache, confusion, personality change

Chronic SDH

• Often presents insidiously: mild cognitive decline, gait disturbance, headache
• Easily mistaken for dementia, stroke, or normal pressure hydrocephalus
• Patient (or family) may not recall a trauma — "minor fall a few weeks ago"

Imaging

CT Head (Non-Contrast) — First-Line

Acute SDH: crescent-shaped hyperdense (bright) collection along the right inner table of the skull, conforming to the brain surface. Note the midline shift — this reflects the disproportionate mass effect. (Harrison's, p. 12566)

• Shape: crescent/concave (follows brain contour) — contrast with epidural which is lenticular/biconvex
• Location: crosses suture lines (epidurals do not)
• Midline shift: measured at the level of the septum pellucidum/foramen of Monro
• Sulcal effacement: compression of cortical gyri
• Subfalcine herniation: cingulate gyrus shifts under the falx
• Uncal herniation: medial temporal lobe herniates over the tentorium

MRI

• Superior for subacute/isodense SDH where CT may miss it
• Better for detecting underlying cortical contusions or diffuse axonal injury

Differentiating SDH from EDH

Management

Medical (Conservative) Indications

• Small SDH, neurologically intact, no significant midline shift
• Chronic SDH in asymptomatic patients
• Key interventions:
  • Reverse anticoagulation immediately (Vitamin K, FFP, PCC, or idarucizumab depending on agent)
  • ICP management: HOB 30°, osmotherapy (mannitol or hypertonic saline), avoid hypoxia/hypotension
  • Seizure prophylaxis (especially acute SDH — Levetiracetam or Phenytoin)
  • Serial CT monitoring

Surgical Indications (Neurosurgeon's Domain)

• Clot thickness >10 mm
• Midline shift >5 mm
• ICP >20 mmHg refractory to medical management
• Neurological deterioration regardless of clot size
• GCS drop of ≥2 points from injury

Prognosis

• Acute SDH: mortality 40–60% in large series; survivors often have significant disability. Outcomes correlate with GCS at presentation, age, and time to surgery.
• Chronic SDH: generally good prognosis with drainage; most elderly patients return to baseline.
• Poor prognostic signs: bilateral fixed dilated pupils, GCS 3, age >65, significant cerebral atrophy, coagulopathy, midline shift >10 mm.

Things That Will Impress a Neurosurgeon

1. Know the 4-5-10 rule for surgical criteria: clot >10 mm or shift >5 mm = operate; GCS drop >2 = operate regardless.
2. Ask about membrane formation in chronic SDH — the outer and inner membranes that form around the collection are vascularized and contribute to re-accumulation (hence recurrence risk).
3. Mention Markwalder grading scale — a 0–4 neurological grading scale for SDH severity.
4. Recognize that isodense SDH on CT can be bilateral and the midline may appear deceptively normal because the shift cancels out — but sulci will still be effaced.
5. Ask about the role of dexamethasone in chronic SDH — controversial, used in some centers to reduce membrane inflammation and aid resorption in non-surgical cases.