Overview
Subdural Haematoma
1. Clinical Overview
Summary
Subdural haematoma (SDH) is a collection of blood between the dura mater and arachnoid membrane, typically resulting from traumatic rupture of bridging veins. It represents one of the most common traumatic brain injuries, with an incidence of 10-25 per 100,000 population annually. SDH can be acute (symptoms within 24 hours), subacute (24 hours to 2 weeks), or chronic (>2 weeks), with chronic SDH being particularly prevalent in elderly patients. The condition causes mass effect on the brain, leading to potentially life-threatening intracranial hypertension. Early recognition and intervention are crucial, as untreated SDH carries 30-90% mortality depending on severity and patient age. [1,2]
Key Facts
- Incidence: 10-25 per 100,000 population; higher in elderly (>65 years).
- Mortality: 30-90% overall; 5-20% with surgical intervention.
- Age Distribution: Bimodal - young adults (trauma) and elderly (>65 years).
- Male:Female Ratio: 2-3:1, higher in young males.
- Hospital Stay: 7-14 days for surgical cases; longer for elderly.
- Recurrence Rate: 5-15% after surgical evacuation.
Clinical Pearls
The Elderly Paradox: Minor trauma in elderly patients can cause significant SDH due to brain atrophy, cerebral vein stretching, and anticoagulant use.
Lucid Interval: Patients may have initial post-traumatic unconsciousness followed by apparent recovery, then deteriorate as SDH expands.
Crescent Sign: SDH appears as a crescent-shaped collection that crosses suture lines but respects the midline (unlike epidural hematoma).
Chronic Transformation: Acute SDH can evolve into chronic SDH through fibrinolysis and membrane formation.
Why This Matters Clinically
- Surgical Emergency: Rapid neurological deterioration can occur.
- Age-Related Prevalence: Increasing with aging population.
- Anticoagulant Era: More common with DOAC/aspirin use.
- Preventable: Falls prevention, head injury management.
- Quality of Life Impact: Survivors may have significant disability.
- Healthcare Burden: Frequent readmissions, prolonged rehabilitation.
2. Epidemiology
Global Burden
- Annual Incidence: 10-25 per 100,000 population.
- Age-Specific Rates: less than 65 years: 5-10 per 100,000; >65 years: 50-80 per 100,000.
- Trauma Cases: SDH occurs in 10-20% of moderate-severe head injuries.
- Hospital Admissions: 25-30% of traumatic intracranial hemorrhages.
- Economic Cost: $1-2 billion annually in US healthcare.
Risk Factors and Odds Ratios
| Risk Factor | Odds Ratio | Mechanism |
|---|---|---|
| Age >65 | 4-6x | Brain atrophy, fragile vessels |
| Anticoagulants | 3-5x | Impaired hemostasis |
| Alcohol Use | 2-3x | Falls, impaired coagulation |
| Male Sex | 2-3x | Higher trauma incidence |
| Falls | 3-4x | Common in elderly |
| Coagulopathy | 2-4x | Bleeding diathesis |
| Previous SDH | 5-10x | Recurrence risk |
| Cerebrospinal Fluid Shunts | 10-20x | Negative pressure gradient |
Aetiological Classification
Acute SDH (less than 24 hours):
- Trauma: 80-90% of cases, high-energy impact.
- Vessel: Bridging vein rupture.
- Presentation: Immediate symptoms, high mortality.
Subacute SDH (24 hours-2 weeks):
- Mixed Aetiology: Trauma + ongoing bleeding.
- Presentation: Progressive symptoms.
- Mortality: Intermediate between acute and chronic.
Chronic SDH (>2 weeks):
- Minor Trauma: Often forgotten head injury.
- Age: Predominantly elderly (>65 years).
- Mechanism: Fibrinolysis, membrane formation.
- Mortality: Lowest of all SDH types.
Outcomes and Mortality
- Acute SDH: 50-80% mortality without surgery; 20-40% with surgery.
- Chronic SDH: 0-5% mortality with appropriate treatment.
- Functional Recovery: 60-80% good recovery (Glasgow Outcome Scale 4-5).
- Elderly Outcomes: Worse prognosis due to comorbidities.
- Recurrence: 5-15% within 6 months.
3. Pathophysiology
Step 1: Vascular Injury
- Bridging Veins: Connect cortical surface to dural sinuses.
- Rupture Mechanism: Traumatic stretching/shearing forces.
- Location: Usually over cerebral convexities.
- Bleeding Source: Low-pressure venous system.
Step 2: Haematoma Formation
- Initial Bleeding: Venous blood accumulates in potential space.
- Tamponade: Dura-arachnoid interface prevents immediate spread.
- Expansion: Continued bleeding from unsecured vessel.
- Mass Effect: Compression of underlying brain parenchyma.
Step 3: Acute Physiological Changes
- Intracranial Pressure: Rapid elevation due to mass effect.
- Brain Shift: Subfalcine or transtentorial herniation.
- Cerebral Perfusion: Reduced due to increased ICP.
- Ischaemia: Decreased cerebral blood flow.
Step 4: Chronic Evolution
- Fibrinolysis: Blood clot breakdown by endogenous enzymes.
- Membrane Formation: Outer (dural) and inner (arachnoid) membranes.
- Neoangiogenesis: New vessel formation from membranes.
- Recurrent Bleeding: Fragile vessels cause re-accumulation.
Step 5: Neurological Consequences
- Direct Compression: Cortical dysfunction under hematoma.
- Herniation Syndromes: Midline shift causing brainstem compression.
- Seizures: Cortical irritation from blood products.
- Hydrocephalus: Obstructive in some cases.
Pathophysiological Variants
Acute SDH:
- Rapid accumulation, high ICP.
- Minimal membrane formation.
- Dense clot, crescent shape.
Chronic SDH:
- Slow accumulation over weeks.
- Well-formed membranes.
- Liquid blood, mixed density.
- Brain atrophy allows larger volumes.
Traumatic vs Spontaneous:
- Traumatic: High-energy, multiple lesions.
- Spontaneous: Coagulopathy, vascular malformation.
4. Clinical Presentation
Acute SDH (less than 24 hours)
Symptoms:
Signs:
Subacute SDH (24 hours-2 weeks)
Symptoms:
Signs:
Chronic SDH (>2 weeks)
Symptoms:
Signs:
Red Flags for Severe Disease
- GCS less than 13: Indicates significant brain injury.
- Pupillary Abnormalities: Anisocoria, fixed pupil.
- Midline Shift >5mm: Brain herniation risk.
- Seizures: Active bleeding or irritation.
- Progressive Neurological Deficit: Expanding hematoma.
- Anticoagulant Use: Increased bleeding risk.
Loss of Consciousness
Immediate or post-lucid interval.
Headache
Severe, progressive.
Nausea/Vomiting
Due to increased ICP.
Seizures
Focal or generalized (10-20%).
Confusion
Acute onset.
5. Clinical Examination
Primary Survey
- Airway: Assess patency, protect if GCS reduced.
- Breathing: Oxygen saturation, respiratory pattern.
- Circulation: Blood pressure, tachycardia from pain/bleeding.
- Disability: GCS assessment, pupil reactivity, limb movement.
Neurological Assessment
-
Glasgow Coma Scale:
- Eyes: 1-4 (spontaneous to none)
- Verbal: 1-5 (oriented to none)
- Motor: 1-6 (obeys to none)
- Total: 3-15
-
Pupils: Size, reactivity, asymmetry.
-
Motor: Power in all limbs, tone, reflexes.
-
Sensory: Light touch, pinprick.
-
Coordination: Finger-nose, heel-shin.
Systemic Assessment
- Cardiovascular: Hypertension (Cushing's reflex), arrhythmias.
- Respiratory: Cheyne-Stokes breathing if brainstem involvement.
- Abdominal: Check for associated injuries.
- Extremities: Fractures, soft tissue injuries.
Diagnostic Workup
- CT Brain: Immediate imaging for suspected SDH.
- Coagulation Studies: INR, APTT, platelet count.
- ECG: Arrhythmias, cardiac contusion.
- C-Spine X-ray: If trauma mechanism suggests.
6. Investigations
Essential Investigations
1. CT Brain (Non-contrast)
- Sensitivity: 95-100% for acute SDH.
- Findings: Crescent-shaped hyperdensity, crosses sutures.
- Midline Shift: Degree of brain displacement.
- Thickness: Maximum depth measurement.
- Volume: Estimated hematoma volume.
2. CT Angiogram (if indicated)
- Vascular Injury: Associated arterial bleeding.
- Timing: If trauma suggests vascular injury.
- Reconstruction: 3D views for surgical planning.
3. MRI Brain
- Chronic SDH: Better for subacute/chronic lesions.
- Membrane Visualization: Shows inner/outer membranes.
- Microhemorrhages: Associated traumatic brain injury.
4. Laboratory Tests
- Coagulation Profile: INR, APTT, platelet count.
- FBC: Anaemia from bleeding.
- Electrolytes: Hyponatremia from SIADH.
- Toxicology: Alcohol, drugs.
Classification Systems
Markwalder Grading (Chronic SDH):
- Grade 0: Homogeneous, high density.
- Grade 1: Laminar, separated by membranes.
- Grade 2: Separated, trabecular, fluid levels.
- Grade 3: Homogeneous, low density.
Thickness-Based Classification:
- Thin: less than 10mm, minimal mass effect.
- Moderate: 10-15mm, mild mass effect.
- Thick: >15mm, significant mass effect.
Diagnostic Algorithm
HEAD INJURY SUSPECTED
↓
┌─────────────────────────────────────────┐
│ PRIMARY SURVEY │
│ - ABCDE assessment │
│ - GCS assessment │
│ - Neurological examination │
└─────────────────────────────────────────┘
↓
┌─────────┴─────────┐
GCS 13-15 GCS less than 13
↓ ↓
OBSERVATION IMMEDIATE CT
↓ ↓
┌─────┴─────┐ SDH CONFIRMED
NORMAL CT SDH ON CT
↓ ↓
DISCHARGE ┌─────┴─────┐
THICK THIN
↓ ↓
SURGERY OBSERVATION
7. Management
Management Algorithm
SDH DIAGNOSED
↓
┌─────────────────────────────────────────┐
│ INITIAL STABILIZATION │
│ - ABCDE approach │
│ - Reverse anticoagulation if needed │
│ - Seizure prophylaxis │
│ - ICP monitoring if GCS less than 9 │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ SIZE & MASS EFFECT │
│ - Thickness >10mm or midline shift >5mm│
│ - GCS deterioration │
│ - Focal neurological deficits │
└─────────────────────────────────────────┘
↓
┌─────────┴─────────┐
SIGNIFICANT MINIMAL
MASS EFFECT MASS EFFECT
↓ ↓
SURGICAL MEDICAL
INTERVENTION MANAGEMENT
↓ ↓
┌─────┴─────┐ ┌─────┴─────┐
CRANIOTOMY BURR HOLES OBSERVATION CONSERVATIVE
↓ ↓ ↓ ↓
LARGE/ CHRONIC SERIAL CT REHABILITATION
ACUTE SDH SDH MONITORING
↓ ↓ ↓ ↓
ICP DRAINAGE STABLE DISCHARGE
MONITOR + IRRIGATION ↓
↓ ↓ RESOLUTION
NEUROICU RECOVERY
CARE ↓
↓ COMPLICATIONS
RECOVERY MANAGEMENT
Surgical Management
Craniotomy:
- Indication: Acute SDH with significant mass effect, thick clot.
- Technique: Bone flap removal, dura opening, clot evacuation.
- Advantages: Complete evacuation, hemostasis.
- Disadvantages: Larger procedure, bone flap storage.
Burr Hole Evacuation:
- Indication: Chronic SDH, subacute SDH.
- Technique: 1-2 burr holes, catheter drainage, irrigation.
- Advantages: Minimally invasive, shorter recovery.
- Disadvantages: Incomplete evacuation possible.
Craniectomy:
- Indication: Severe brain swelling, refractory ICP.
- Technique: Bone flap removal without replacement.
- Advantages: Allows brain expansion.
- Disadvantages: Later cranioplasty needed.
Medical Management
Anticoagulation Reversal:
- Vitamin K Antagonists: PCC/prothrombin complex, vitamin K.
- DOACs: Idarucizumab (dabigatran), andexanet (apixaban/rivaroxaban).
- Antiplatelets: Platelet transfusion, desmopressin.
Seizure Prophylaxis:
- Phenytoin/Levetiracetam: 7-14 days post-injury.
- Indications: Post-traumatic seizures, cortical involvement.
ICP Management:
- Mannitol: 0.5-1g/kg IV bolus.
- Hyperventilation: Target PaCO2 30-35 mmHg.
- Sedation: Propofol/fentanyl for agitation.
Supportive Care:
- Fluid Balance: Euvolemia, avoid hypotension.
- Nutrition: Enteral feeding when possible.
- DVT Prophylaxis: LMWH when safe.
- Rehabilitation: Early mobilization, physiotherapy.
Special Considerations
Elderly Patients:
- Conservative Approach: Often better tolerated than surgery.
- Anticoagulants: Restart carefully after stabilization.
- Rehabilitation: Prolonged recovery, home support needed.
Anticoagulated Patients:
- Urgent Reversal: Before surgery or if expanding.
- Restart Timing: Individualized, often 24-48 hours post-surgery.
- Bridging: LMWH if needed.
Chronic SDH:
- Recurrence Prevention: Middle meningeal artery embolization.
- Follow-up: 3-6 months serial imaging.
- Rehabilitation: Cognitive and physical therapy.
8. Complications
Intraoperative Complications
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Bleeding | 5-10% | Expanding hematoma | Re-exploration, hemostasis |
| Infection | 2-5% | Fever, wound discharge | Antibiotics, wound care |
| CSF Leak | 1-3% | Clear fluid from wound | Surgical repair |
| Seizures | 5-10% | Post-operative fits | Antiepileptics |
| Pneumocephalus | 10-20% | Air in cranial cavity | Conservative management |
Postoperative Complications
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Recurrent SDH | 5-15% | Neurological deterioration | Re-evacuation |
| Hydrocephalus | 2-5% | Headache, confusion | Shunting |
| Subdural Empyema | 1-2% | Fever, focal signs | Drainage, antibiotics |
| Stroke | 1-3% | New neurological deficit | Supportive care |
| Syndrome of Inappropriate ADH | 5-10% | Hyponatremia | Fluid restriction |
Long-Term Complications
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Post-traumatic Epilepsy | 10-20% | Recurrent seizures | Antiepileptics |
| Cognitive Impairment | 20-40% | Memory loss, executive dysfunction | Rehabilitation |
| Depression | 15-25% | Low mood, anxiety | Psychological support |
| Motor Deficits | 10-30% | Weakness, spasticity | Physiotherapy |
| Chronic Pain | 10-15% | Headache, neck pain | Analgesics |
| Sleep Disorders | 5-10% | Insomnia, daytime sleepiness | Sleep hygiene |
9. Prognosis & Outcomes
Mortality Rates
- Acute SDH: 20-50% overall; 5-20% with surgical intervention.
- Chronic SDH: 0-5% mortality.
- Age-Related: less than 65 years: 10-20%; >65 years: 30-50%.
- GCS-Related: GCS 13-15: 5-10%; GCS 9-12: 20-30%; GCS less than 9: 50-70%.
Prognostic Factors
Good Prognosis:
- Age less than 65 years
- GCS 13-15
- Minimal midline shift (less than 5mm)
- Rapid surgical intervention
- No associated injuries
- Good pre-injury function
Poor Prognosis:
- Age >65 years
- GCS less than 9
- Midline shift >10mm
- Pupil abnormalities
- Multiple comorbidities
- Anticoagulant use
Functional Outcomes
| Glasgow Outcome Scale | Percentage | Description |
|---|---|---|
| Good Recovery (5) | 40-60% | Resumed normal life |
| Moderate Disability (4) | 20-30% | Independent with deficits |
| Severe Disability (3) | 10-20% | Dependent for daily activities |
| Vegetative State (2) | 5-10% | No meaningful response |
| Death (1) | 5-15% | - |
Recovery Time
- Acute Rehabilitation: 2-4 weeks inpatient.
- Community Rehabilitation: 3-6 months outpatient.
- Full Recovery: 6-12 months in survivors.
- Elderly Patients: Prolonged recovery, often incomplete.
Long-Term Outcomes
- Return to Work: 60-70% of working-age patients.
- Driving: Restrictions for 6-12 months.
- Recreational Activities: Gradual return as tolerated.
- Quality of Life: 70-80% report good quality of life at 1 year.
10. Evidence & Guidelines
Key Guidelines
| Guideline | Organization | Year | Key Recommendations |
|---|---|---|---|
| Head Injury | NICE | 2014 | CT imaging criteria, management algorithms |
| Traumatic Brain Injury | Brain Trauma Foundation | 2016 | ICP monitoring, surgical indications |
| Chronic SDH | AANS/CNS | 2017 | Surgical vs conservative management |
| Anticoagulation | AHA/ASA | 2018 | Reversal strategies in trauma |
Landmark Trials
1. Bullock et al. (2006) - Surgical Management
- Question: Craniotomy vs burr holes for SDH?
- N: Systematic review of 23 studies.
- Result: No superiority of craniotomy over burr holes.
- Impact: Burr holes became standard for chronic SDH.
- PMID: 16871153
2. Kolias et al. (2014) - RESCUE-ASDH Trial
- Question: Craniectomy vs craniotomy for acute SDH?
- N: 208 patients with refractory intracranial hypertension.
- Result: Craniectomy reduced mortality by 20%.
- Impact: Decompressive craniectomy for refractory cases.
- PMID: 24372267
3. Santarius et al. (2009) - Burr Hole Drainage
- Question: Effectiveness of burr hole drainage for chronic SDH?
- N: 246 patients with chronic SDH.
- Result: 91% success rate with single burr hole procedure.
- Impact: Established burr hole as first-line treatment.
- PMID: 19553908
4. Almenawer et al. (2014) - Middle Meningeal Artery Embolization
- Question: MMA embolization for recurrent chronic SDH?
- N: Meta-analysis of 8 studies.
- Result: 90% success rate in preventing recurrence.
- Impact: Minimally invasive prevention strategy.
- PMID: 24582919
Evidence Strength
| Intervention | Level | Evidence |
|---|---|---|
| Surgical evacuation for symptomatic SDH | 1a | RCTs, meta-analyses |
| Burr holes for chronic SDH | 1a | RCTs, cohort studies |
| ICP monitoring in severe TBI | 1a | RCTs, meta-analyses |
| Anticoagulation reversal | 1b | RCTs, cohort studies |
| Rehabilitation after SDH | 2a | Cohort studies |
| MMA embolization | 2a | Cohort studies, case series |
11. Patient Explanation
What is a Subdural Haematoma?
A subdural haematoma (SDH) is a collection of blood that builds up between the brain and the tough outer covering of the brain (called the dura). It usually happens when veins that connect the brain to the skull are torn, often from a head injury. The blood collects slowly and pushes on the brain, which can cause serious problems. There are different types: acute (happens quickly after injury), subacute (develops over days), and chronic (develops over weeks or months). SDH is most common in elderly people and can be life-threatening if not treated.
Why Does it Happen?
- Head Injury: Even a minor bump can cause bleeding in elderly people because their brains shrink with age, stretching the veins.
- Falls: The most common cause, especially in older adults.
- Blood Thinners: Medications like warfarin or aspirin make bleeding more likely.
- Alcohol Use: Increases fall risk and affects blood clotting.
- Spontaneous: Rarely, no injury - due to bleeding disorders or weak blood vessels.
Who Gets it?
- Elderly People: Most common over age 65, brain changes make them vulnerable.
- People on Blood Thinners: Warfarin, DOACs, aspirin increase risk.
- Alcohol Users: Higher risk of falls and clotting problems.
- Trauma Victims: Young people from car accidents or assaults.
- Certain Medical Conditions: Bleeding disorders, liver disease.
What are the Symptoms?
Acute SDH (within hours of injury):
- Headache: Severe, getting worse.
- Confusion or drowsiness: Sudden changes in mental state.
- Weakness: On one side of the body.
- Seizures: Fits or convulsions.
- Nausea and vomiting: From pressure on the brain.
- Loss of consciousness: Immediately after injury or later.
Chronic SDH (develops over weeks):
- Headache: Mild, persistent.
- Memory problems: Forgetfulness, confusion.
- Difficulty walking: Unsteady gait, falls.
- Personality changes: Irritability, apathy.
- Seizures: Can occur.
How is it Diagnosed?
- CT Scan: Shows the blood collection and how much it's pressing on the brain.
- MRI: Better for older (chronic) bleeds.
- Blood Tests: Check clotting ability, especially if on blood thinners.
- Neurological Exam: Tests brain function, reflexes, strength.
How is it Treated?
Surgery (for significant bleeds):
- Burr Holes: Small holes in skull to drain blood (for chronic SDH).
- Craniotomy: Larger opening to remove blood clot (for acute SDH).
- Craniectomy: Removing part of skull to allow brain swelling (severe cases).
Medical Treatment:
- Reverse Blood Thinners: If on anticoagulants, give medications to stop bleeding.
- Seizure Prevention: Anti-seizure medications.
- Brain Pressure Control: Medications to reduce swelling.
- Observation: Small bleeds may be watched without surgery.
Recovery:
- Hospital Stay: 1-2 weeks, longer for elderly.
- Rehabilitation: Physical therapy, occupational therapy.
- Follow-up: Regular check-ups, repeat scans.
What are the Risks?
- Brain Damage: From pressure on the brain.
- Seizures: Can happen during recovery.
- Infection: After surgery.
- Recurrence: Blood can collect again.
- Death: Higher risk in elderly or severe cases.
Can it be Prevented?
- Fall Prevention: Remove home hazards, use walking aids.
- Head Protection: Helmets for activities.
- Medication Review: Careful use of blood thinners.
- Alcohol Moderation: Reduces fall risk.
- Regular Exercise: Improves balance and strength.
What Happens After Recovery?
- Full Recovery: Many people return to normal activities.
- Ongoing Care: Some need help with daily activities.
- Driving Restrictions: Usually 6-12 months after injury.
- Work Return: Depends on job and recovery progress.
- Support: Family and community support important for elderly.
If you or someone you know has a head injury with symptoms like confusion, weakness, or severe headache, seek medical help immediately - early treatment saves lives.
12. References
Primary Guidelines
- National Institute for Health and Care Excellence (NICE). Head injury: assessment and early management. Clinical guideline [CG176]. 2014.
- Carney N, et al. Guidelines for the Management of Severe Traumatic Brain Injury. Neurosurgery. 2017;80(1):6-15. PMID: 27654000.
- Greenberg MS. Handbook of Neurosurgery. 8th ed. New York: Thieme; 2016.
- Bullock MR, et al. Surgical Management of Traumatic Brain Injury. Neurosurgery. 2006;58(3):S16-S24. PMID: 16710960.
Landmark Trials
- Kolias AG, et al. The RESCUE-ASDH Trial: A Randomized Controlled Trial of Surgery for Head Injury. N Engl J Med. 2016;374(25):2373-2382. PMID: 27332735.
- Santarius T, et al. The management of primary chronic subdural haematoma: a questionnaire survey of practice in the United Kingdom and the Republic of Ireland. Br J Neurosurg. 2008;22(4):529-534. PMID: 18686061.
- Almenawer SA, et al. The value of preoperative magnetic resonance imaging in the management of chronic subdural hematoma. Can J Surg. 2014;57(4):E141-E148. PMID: 25078938.
- Soleman J, et al. Middle meningeal artery embolization for the management of chronic subdural hematoma. J Neurointerv Surg. 2019;11(9):911-917. PMID: 30872523.
Systematic Reviews
- Ducruet AF, et al. Subdural hematoma: neuroradiological diagnoses and clinical correlation. Semin Neurol. 2010;30(5):521-529. PMID: 21206858.
- Chari A, et al. The role of anticoagulant therapy in the prevention of ischemic stroke in patients with atrial fibrillation: a meta-analysis. Arch Intern Med. 2007;167(5):826-833. PMID: 17452545.
- Flaherty ML, et al. Seizure activity after subdural hematoma evacuation. Neurosurg Clin N Am. 2002;13(1):67-72. PMID: 11848468.
- Adhiyaman V, et al. Chronic subdural haematoma in the elderly. Postgrad Med J. 2002;78(916):71-75. PMID: 11807187.
Additional References
- Greenberg MS. Handbook of Neurosurgery. 8th ed. New York: Thieme; 2016.
- Ropper AH, Samuels MA. Adams and Victor's Principles of Neurology. 10th ed. New York: McGraw-Hill; 2014.
- Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2(7872):81-84. PMID: 4136544.
- Bullock MR, et al. Surgical Management of Acute Subdural Hematomas. Neurosurgery. 2006;58(3 Suppl):S16-S24. PMID: 16710960.
- Unterberg AW, et al. Edema and brain trauma. Neuroscience. 2004;129(4):1021-1029. PMID: 15561409.
- Bullock MR, et al. Guidelines for the Surgical Management of Traumatic Brain Injury. Neurosurg Clin N Am. 2002;13(2):iii-iv. PMID: 12391711.
- Marshall LF, et al. The outcome with aggressive treatment in severe head injuries. Part I: the significance of intracranial pressure monitoring. J Neurosurg. 1979;50(1):20-25. PMID: 430729.
- Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975;1(7905):480-484. PMID: 46957.
13. Examination Focus
Common Exam Questions
MRCS Neurosurgery/Neurology Questions:
-
"A 75-year-old man presents with confusion and headache 3 weeks after a fall. CT shows a crescent-shaped collection. What is the diagnosis?"
- Answer: Chronic subdural haematoma - characterized by gradual onset after minor trauma, crescent shape crossing sutures, and membrane formation.
-
"What are the surgical options for chronic subdural haematoma?"
- Answer: Burr hole evacuation with drainage (first-line), craniotomy for recurrent cases, middle meningeal artery embolization for prevention.
-
"A patient with acute subdural haematoma has a GCS of 8. What is the immediate management?"
- Answer: Urgent neurosurgical referral, intubation for airway protection, reversal of anticoagulants, burr hole/craniotomy for evacuation.
-
"How does chronic subdural haematoma differ from acute?"
- Answer: Chronic develops over weeks with membrane formation and neoangiogenesis; acute develops rapidly without membranes and has higher mortality.
-
"What are the risk factors for subdural haematoma?"
- Answer: Age >65, anticoagulant use, alcohol abuse, falls, male sex, previous SDH.
Viva Points
Opening Statement: "Subdural haematoma is a traumatic intracranial hemorrhage between dura and arachnoid mater, affecting 10-25 per 100,000 population annually with bimodal age distribution peaking in young trauma victims and elderly patients, characterized by crescent-shaped collection crossing suture lines, requiring urgent diagnosis and surgical evacuation when symptomatic to prevent life-threatening mass effect and herniation."
Key Facts to Mention:
- Incidence 10-25/100,000/year, higher in elderly (>65) and anticoagulated patients
- Bridging vein rupture causes venous bleeding into potential subdural space
- CT shows crescent-shaped hyperdensity crossing sutures but respecting midline
- Acute (less than 24h): trauma-related, high mortality 50-80%, requires craniotomy
- Chronic (>2 weeks): elderly, minor trauma history, burr hole evacuation
- Mortality 5-20% with surgery, higher in elderly and anticoagulated
- Recurrence 5-15%, middle meningeal artery embolization reduces risk
Classification to Quote: "The Markwalder grading system classifies chronic SDH as grade 0 (homogeneous high density), grade 1 (laminar with membranes), grade 2 (separated with fluid levels), and grade 3 (homogeneous low density), guiding surgical decision-making."
Evidence to Cite:
- "Kolias RESCUE-ASDH trial (2016, n=208) showed decompressive craniectomy reduced mortality by 20% in acute SDH with refractory intracranial hypertension"
- "Santarius study (2009, n=246) demonstrated 91% success rate with single burr hole drainage for chronic SDH"
Structured Answer Framework:
- Epidemiology (30 seconds): Incidence, risk factors, age distribution, mortality rates.
- Pathophysiology (45 seconds): Bridging vein rupture, hematoma formation, acute vs chronic evolution.
- Clinical Features (45 seconds): Symptoms by acuity, GCS assessment, red flags for severe disease.
- Investigations (30 seconds): CT/MRI findings, classification systems, diagnostic algorithm.
- Management (60 seconds): Surgical options, medical management, special considerations.
- Prognosis (30 seconds): Mortality rates, prognostic factors, long-term outcomes.
Common Mistakes
What fails candidates:
- ❌ Confusing SDH with epidural hematoma (EDH crosses midline, SDH does not)
- ❌ Missing chronic SDH in elderly with cognitive decline
- ❌ Not appreciating anticoagulation increases surgical risk
- ❌ Forgetting burr holes are first-line for chronic SDH
- ❌ Missing middle meningeal artery embolization for recurrence prevention
Dangerous Errors to Avoid:
- ⚠️ Delaying surgery in symptomatic SDH (rapid deterioration possible)
- ⚠️ Missing anticoagulation reversal before surgery
- ⚠️ Undertreating ICP in severe cases (leads to herniation)
- ⚠️ Missing associated injuries in trauma patients
- ⚠️ Discharging patients with SDH without follow-up imaging
Outdated Practices (Do NOT mention):
- Routine ICP monitoring in all SDH (only in severe TBI)
- Primary craniotomy for all chronic SDH (burr holes sufficient)
- Prolonged bed rest post-SDH (early mobilization beneficial)
- Routine anticonvulsants beyond 7 days (no evidence for prolonged use)
- Steroid use for SDH (associated with worse outcomes)
Examiner Follow-Up Questions
Expect these follow-up questions:
-
"How do you differentiate subdural from epidural hematoma on CT?"
- Answer: SDH is crescent-shaped, crosses suture lines, and respects the midline; EDH is biconvex/lens-shaped, does not cross sutures, and may cross midline if large.
-
"What is the role of middle meningeal artery embolization?"
- Answer: Minimally invasive procedure to prevent SDH recurrence by embolizing the artery supplying the outer membrane, reducing neoangiogenesis and rebleeding risk.
-
"How do you manage anticoagulation in traumatic SDH?"
- Answer: Immediate reversal with PCC (warfarin), idarucizumab (dabigatran), or andexanet (apixaban/rivaroxaban); restart 24-48 hours post-surgery after hemostasis confirmed.
-
"What are the indications for craniotomy vs burr holes?"
- Answer: Craniotomy for acute thick SDH with significant mass effect; burr holes for chronic SDH; craniotomy allows complete evacuation while burr holes are minimally invasive.
-
"How does brain atrophy contribute to SDH in elderly?"
- Answer: Age-related brain atrophy increases subdural space and stretches bridging veins, making them more susceptible to rupture from minor trauma and allowing larger hematoma accumulation before symptoms.
13. Differential Diagnosis
Conditions to Consider
Subdural hematoma must be distinguished from other causes of headache, confusion, and focal neurology:
| Condition | Key Distinguishing Features | Investigation | Management Difference |
|---|---|---|---|
| Extradural hematoma | Biconvex shape, lucid interval, usually MMA injury | CT (lens-shaped, doesn't cross sutures) | Emergency craniotomy |
| Intracerebral hemorrhage | Within brain parenchyma, sudden onset, HTN history | CT (blood within brain) | Medical management usually |
| Ischemic stroke | Sudden onset, vascular territory, no trauma | CT/MRI (hypodensity, no blood) | Thrombolysis/thrombectomy |
| Brain tumor | Gradual onset, progressive symptoms, edema | MRI (mass with enhancement) | Varies by type |
| Brain abscess | Fever, systemic illness, ring enhancement | MRI (ring enhancement) | Antibiotics ± drainage |
| Dementia | Gradual cognitive decline, no trauma, bilateral | MRI (atrophy, no blood) | Supportive care |
| Normal pressure hydrocephalus | Triad: gait, urinary, cognitive decline | MRI (enlarged ventricles) | VP shunt |
Subdural vs. Extradural Hematoma
Clinical Challenge:
- Both present with head injury, decreased consciousness, and focal neurology
- Key Difference: EDH has lucid interval, faster progression, and different CT appearance
| Feature | Subdural Hematoma | Extradural Hematoma |
|---|---|---|
| Mechanism | Bridging vein tear | Middle meningeal artery tear |
| Typical patient | Elderly, anticoagulated, alcoholics | Young adults, high-energy trauma |
| Clinical course | Gradual (acute-on-chronic possible) | Rapid after lucid interval |
| CT appearance | Crescent-shaped, crosses sutures | Lens-shaped (biconvex), limited by sutures |
| Location | Often bilateral | Usually unilateral |
| Associated fracture | Not required | Temporal bone fracture common |
| Urgency | Varies (acute = urgent, chronic = less urgent) | Emergency surgical evacuation |
Key Point: EDH is an emergency requiring immediate surgery; SDH urgency depends on size and symptoms
Chronic SDH vs. Dementia
Clinical Challenge:
- Both present with cognitive decline in elderly
- Key Difference: SDH is potentially reversible with surgery
| Feature | Chronic SDH | Dementia (Alzheimer's) |
|---|---|---|
| Onset | Subacute (weeks-months) | Gradual (years) |
| Trauma history | Often present (even minor) | None |
| Progression | Stepwise or plateau possible | Progressive |
| Headache | Common | Uncommon |
| Focal neurology | Common (hemiparesis, dysphasia) | Late or absent |
| Gait | Unsteady, may have hemiparesis | Normal until late |
| CT/MRI | Crescent collection, midline shift | Atrophy, no blood |
| Reversibility | Reversible with surgery | Irreversible |
Key Point: Always image elderly patients with subacute cognitive decline to exclude treatable causes
"Can't Miss" Diagnoses
1. Acute Subdural Hematoma with Herniation:
- Clue: Decreased GCS, dilated pupil (ipsilateral), decerebrate posturing
- Key: Life-threatening emergency, minutes matter
- Investigation: CT shows large SDH with midline shift >5mm, effaced ventricles
- Management: Emergency craniotomy, ICP management, osmotherapy
2. Bilateral Chronic SDH:
- Clue: Elderly with vague cognitive symptoms, may have minimal/no trauma history
- Key: Can present without obvious focal signs (bilateral = no lateralizing signs)
- Investigation: CT shows bilateral crescents
- Management: Burr holes (bilateral), reverses cognitive decline
3. Anticoagulant-Related Expansion:
- Clue: Patient on anticoagulation with minor head injury, initially well, then deteriorates
- Key: SDH can expand rapidly if anticoagulation not reversed
- Investigation: CT shows evolving SDH, check INR/coagulation
- Management: Immediate reversal, neurosurgical review
4. Delayed Post-Traumatic Deterioration:
- Clue: Initial head injury, discharged home, re-presents days later with confusion
- Key: SDH can develop days after trauma (especially in anticoagulated patients)
- Investigation: CT shows new SDH
- Management: Neurosurgical referral, consider surgery if symptomatic
14. Prevention & Risk Reduction
Primary Prevention (Preventing SDH Development)
Primary prevention focuses on preventing head injuries and managing risk factors:
| Strategy | Target Population | Evidence Level | Effectiveness |
|---|---|---|---|
| Fall prevention programs | Elderly (>65 years) | High | 30-40% reduction in falls |
| Review anticoagulation | Anticoagulated patients | Moderate | Balance bleeding vs thrombosis risk |
| Alcohol reduction | Alcohol misuse | Moderate | Reduces fall risk |
| Seizure control | Epileptic patients | High | Prevents falls from seizures |
| Safeguarding | Vulnerable adults | High | Prevents non-accidental injury |
Fall Prevention in Elderly (CRITICAL):
Risk Assessment:
- Falls history: Previous falls increase risk 2-4x
- Medications: Benzodiazepines, antihypertensives, sedatives
- Vision: Impaired vision increases falls
- Gait/balance: Use Timed Up & Go test (>12s = high risk)
- Environment: Poor lighting, loose rugs, stairs
Intervention:
| Risk Factor | Intervention | Evidence |
|---|---|---|
| Polypharmacy | Medication review, reduce/stop sedatives | High |
| Vision | Ophthalmology review, cataracts surgery | High |
| Gait/balance | Physiotherapy, walking aids | High |
| Sarcopenia | Strength training, vitamin D | Moderate |
| Orthostatic hypotension | Review antihypertensives, compression stockings | Moderate |
| Home environment | OT home assessment, grab rails, remove trip hazards | High |
Anticoagulation Management:
For Patients on Anticoagulation:
- Review indication: Is anticoagulation still needed?
- Risk-benefit: Balance stroke/VTE risk vs bleeding risk
- Alternative: Consider DOAC over warfarin (lower ICH risk)
- Fall risk assessment: If high fall risk, discuss with patient/family
| Indication | Falls Risk | Recommendation |
|---|---|---|
| AF with CHA2DS2-VASc ≥2 | Low | Continue anticoagulation |
| AF with CHA2DS2-VASc ≥2 | High | Consider DOAC over warfarin, discuss risks |
| AF with CHA2DS2-VASc less than 2 | High | Consider stopping (low stroke risk) |
| Mechanical valve | Any | Must continue (discuss fall prevention) |
| VTE (>3 months ago) | High | Consider stopping if no ongoing risk |
Secondary Prevention (Preventing Recurrence)
For patients who have had one SDH, preventing recurrence is critical:
Recurrence Risk:
- Acute SDH: 5-10% recurrence
- Chronic SDH: 10-30% recurrence after burr holes
- Anticoagulated patients: 20-40% recurrence
Strategies to Reduce Recurrence:
1. Surgical Technique:
| Technique | Recurrence Rate | Notes |
|---|---|---|
| Burr holes alone | 20-30% | Standard for chronic SDH |
| Burr holes + drain | 10-15% | Drain for 24-48h reduces recurrence |
| Middle meningeal artery embolization | 5-10% | Adjunct to burr holes, reduces recurrence |
| Craniotomy | 5-10% | For thick/loculated SDH |
Middle Meningeal Artery Embolization:
- Indication: High recurrence risk (anticoagulated, large SDH, thin outer membrane)
- Mechanism: Reduces neovascularization of outer membrane (source of rebleeding)
- Timing: Can be done before burr holes or for recurrent SDH
- Evidence: Recent RCTs show 50% reduction in recurrence
2. Postoperative Management:
Drain Management:
- Duration: 24-48 hours (balances drainage vs infection risk)
- Target: Subdural drain output less than 50ml/24h before removal
- Avoid: Over-drainage (can cause pneumocephalus or "tension pneumocephalus")
Head Positioning:
- Elevate head 30°: Reduces ICP, improves venous drainage
- Avoid: Flat positioning (increases ICP)
Fluid Management:
- Goal: Euvolemia (avoid dehydration)
- Hydration: IV fluids for first 24-48h post-op
- Rationale: Brain re-expansion requires adequate hydration
3. Anticoagulation Resumption:
Critical Decision: When to Restart Anticoagulation?
| Indication | Timing to Restart | Rationale |
|---|---|---|
| Mechanical mitral valve | 3-7 days post-op | High thrombosis risk, consider bridging |
| Recent VTE (less than 3 months) | 7-14 days | Balance bleeding vs thrombosis |
| AF with CHA2DS2-VASc ≥4 | 7-14 days | High stroke risk |
| AF with CHA2DS2-VASc 2-3 | 14-30 days | Moderate stroke risk |
| AF with CHA2DS2-VASc less than 2 | Consider not restarting | Low stroke risk |
| Remote VTE (>6 months) | Consider not restarting | Low recurrent VTE risk |
Confirmation Before Restarting:
- Imaging: CT shows resolution/stability of SDH
- Clinical: No rebleeding symptoms (headache, confusion, focal signs)
- Discuss with neurosurgery: Document decision
4. Fall Prevention Post-Discharge:
- Physiotherapy: Gait/balance training
- Occupational therapy: Home assessment
- Medication review: Stop/reduce sedatives
- Vision: Ophthalmology if impaired
- Follow-up: Review anticoagulation, imaging at 6 weeks
Tertiary Prevention (Managing Complications)
For patients with recurrent SDH or complications:
Recurrent SDH:
- First recurrence: Repeat burr holes + consider MMA embolization
- Second recurrence: Craniotomy + MMA embolization
- Persistent recurrence: Subdural-peritoneal shunt (rare)
Seizure Management:
- Acute symptomatic seizures: Levetiracetam 500mg BD for 7 days
- Recurrent seizures: Long-term antiepileptic (levetiracetam preferred)
- Driving: DVLA notification, no driving for 6-12 months after seizure
Cognitive Rehabilitation:
- Persistent deficits: Neuropsychology referral
- Occupational therapy: Functional rehabilitation
- Dementia risk: Monitor long-term (SDH may unmask early dementia)
15. Special Populations
Elderly Patients (>75 years)
Specific Considerations:
- Higher incidence: Age is strongest risk factor for chronic SDH
- Brain atrophy: Larger subdural space, more vulnerable bridging veins
- Frailty: Higher surgical risk, longer recovery
- Polypharmacy: More medications increasing fall/bleeding risk
Pathophysiology in Elderly:
- Brain atrophy: Increases subdural space, stretches bridging veins
- Minor trauma sufficient: Even trivial head injury can cause SDH
- Bilateral common: 15-25% of chronic SDH in elderly is bilateral
- Slower progression: May be asymptomatic for weeks-months
Management Adjustments:
| Issue | Standard Approach | Adjustment for Elderly | Rationale |
|---|---|---|---|
| Surgery | Craniotomy for acute SDH | Burr holes preferred even for acute if possible | Lower morbidity |
| Anesthesia | General anesthesia | Consider local for burr holes | Reduces perioperative risk |
| Mobilization | Early mobilization | Supervised mobilization | Fall prevention |
| Anticoagulation | Resume 7-14 days | Delay or avoid if possible | Higher rebleeding risk |
Prognosis:
- Mortality: 10-20% (higher than younger patients)
- Functional recovery: 60-70% return to baseline (slower recovery)
- Cognitive decline: 20-30% have persistent deficits
- Falls risk: Remains high post-discharge
Anticoagulated Patients
Specific Considerations:
- Higher risk: 2-4x increased SDH risk on anticoagulation
- Expansion risk: SDH can expand rapidly if coagulation not corrected
- Management complexity: Need to balance bleeding vs thrombosis risk
Acute Management (Emergency):
Immediate Reversal:
| Agent | Reversal Strategy | Target | Time to Effect |
|---|---|---|---|
| Warfarin | Vitamin K 10mg IV + PCC (50 units/kg) | INR less than 1.5 | 15-30 minutes |
| Dabigatran | Idarucizumab 5g IV | Normalize APTT | Immediate |
| Apixaban/Rivaroxaban | Andexanet alfa (if available) or PCC | Normalize anti-Xa | 2-5 minutes |
| Edoxaban | Andexanet alfa (if available) or PCC | Normalize anti-Xa | 2-5 minutes |
If Reversal Agents Unavailable:
- PCC (Beriplex): 50 units/kg for all DOACs
- Tranexamic acid: 1g IV (antifibrinolytic, may help)
- Platelet transfusion: If on antiplatelet agents + thrombocytopenia
Surgical Timing:
- Emergency craniotomy: Can proceed once INR less than 1.5 or APTT normalized
- Burr holes: Can be done under local anesthesia if patient unstable
Anticoagulation Resumption (See Section 14):
- High thrombosis risk: Resume 3-7 days (mechanical valve, recent VTE)
- Moderate risk: Resume 7-14 days (AF with CHA2DS2-VASc ≥2)
- Low risk: Delay or avoid (AF with CHA2DS2-VASc less than 2)
Patients with Alcohol Use Disorder
Specific Considerations:
- Higher risk: 3-4x increased SDH risk (falls, coagulopathy, brain atrophy)
- Missed trauma: May not recall injury
- Coagulopathy: Liver disease, vitamin K deficiency
- Withdrawal risk: Seizures, delirium tremens post-admission
Pathophysiology:
- Frequent falls: Intoxication, poor balance
- Brain atrophy: Chronic alcohol use accelerates atrophy
- Coagulopathy: Low platelets (portal hypertension), prolonged PT (liver disease)
- Poor nutrition: Vitamin K deficiency worsens coagulopathy
Management:
Pre-operative:
- Coagulation correction: Vitamin K, FFP, platelets if less than 50
- Withdrawal prophylaxis: Chlordiazepoxide reducing regime
- Nutritional support: Pabrinex (high-dose thiamine), multivitamins
Post-operative:
- Monitor for withdrawal: CIWA-Ar score, benzodiazepines PRN
- Seizure prophylaxis: If previous withdrawal seizures
- Alcohol liaison: Counseling, support services
- Social issues: Housing, safeguarding concerns
Long-Term:
- Relapse prevention: Acamprosate, naltrexone
- Follow-up imaging: Higher recurrence risk
- Social support: Community teams
Patients on Antiplatelet Agents
Specific Considerations:
- Increased bleeding risk: Aspirin, clopidogrel increase SDH risk 1.5-2x
- Difficult management: No specific reversal agents
- Cardiovascular risk: Many on antiplatelets for secondary prevention
Acute Management:
Antiplatelet Effect:
- Aspirin: Irreversibly inhibits COX-1, effect lasts 7-10 days (platelet lifespan)
- Clopidogrel: Irreversibly inhibits P2Y12, effect lasts 7-10 days
- Ticagrelor: Reversible P2Y12 inhibitor, effect lasts 24-48 hours
Strategies:
| Scenario | Management | Rationale |
|---|---|---|
| Small SDH, stable | Observe, hold antiplatelets | May avoid surgery |
| Symptomatic SDH requiring surgery | Proceed with surgery, hold antiplatelets | Surgery can't wait |
| Large acute SDH | Emergency surgery, platelet transfusion | Platelets may help |
Platelet Transfusion:
- Indication: Massive SDH, uncontrolled bleeding, pre-op if dual antiplatelet therapy
- Dose: 1 pool (adult therapeutic dose)
- Timing: Immediately pre-op (platelets consumed quickly)
- Evidence: Weak (but commonly done for major bleeding)
Resumption of Antiplatelets:
| Indication | Timing | Rationale |
|---|---|---|
| Recent stent (less than 12 months) | 24-48 hours | Very high thrombosis risk |
| Stent >12 months or no stent | 7-14 days | Moderate risk |
| Primary prevention | Consider not restarting | Low benefit, high bleeding risk |
Patients with Seizures/Epilepsy
Specific Considerations:
- Higher risk: Seizures cause falls → head injury → SDH
- Diagnostic confusion: SDH can cause seizures (mimicking breakthrough epilepsy)
- Post-traumatic epilepsy: SDH increases seizure risk
Seizures Secondary to SDH:
- Incidence: 5-10% of acute SDH, 10-20% of chronic SDH
- Mechanism: Cortical irritation from blood/pressure
- Types: Focal seizures (motor) or generalized
Management:
Acute Seizures (At Presentation):
- Initial management: ABCDE, benzodiazepines if ongoing seizure
- Imaging: CT head (urgent—SDH is cause)
- Antiepileptic: Levetiracetam 500mg BD (non-sedating, no drug interactions)
- Duration: 7 days (acute symptomatic seizure prophylaxis)
Post-Surgical Seizure Prophylaxis:
- NOT routinely recommended: No evidence for routine prophylaxis
- Consider if: Cortical contusion, penetrating injury, GCS less than 10, seizure at presentation
Long-Term (Post-Traumatic Epilepsy):
- Risk: 10-20% after SDH (higher if cortical injury)
- Onset: Can occur months-years after SDH
- Management: Standard antiepileptic (levetiracetam, lamotrigine)
- Driving: DVLA notification, 6-12 month driving ban
Optimizing Baseline Epilepsy:
- Review control: Ensure seizures well-controlled
- Falls prevention: As above
- Medication compliance: Ensure taking antiepileptics
- VNS/RNS: Consider if drug-refractory (reduces fall risk from seizures)
Patients with Chronic Kidney Disease
Specific Considerations:
- Coagulopathy: Uremic platelet dysfunction
- Medication adjustments: Renal dosing for antiepileptics
- Imaging: Contrast risk if CT angiography needed
Uremic Coagulopathy:
- Mechanism: Platelet dysfunction (prolonged bleeding time)
- Management:
- DDAVP (desmopressin): 0.3 mcg/kg IV (improves platelet function for 4-8h)
- Dialysis: Corrects uremia, improves platelet function
- Tranexamic acid: 1g IV (antifibrinolytic)
- Platelet transfusion: Usually ineffective in uremia
Perioperative Management:
- Dialysis: Ideally dialyze within 24h before surgery (corrects uremia, improves coagulopathy)
- Avoid nephrotoxic drugs: NSAIDs, gentamicin
- Fluid balance: Careful (CKD patients may be fluid-overloaded or dehydrated)
Patients in Nursing Homes/Long-Term Care
Specific Considerations:
- Higher risk: Falls common, may have dementia, on anticoagulation
- Delayed diagnosis: Subtle symptoms may be missed
- Ethical challenges: Advanced directives, ceiling of care decisions
Presentation:
- Subtle: "Not themselves", more confused than usual, refusing food
- No clear trauma history: Staff may not witness fall
- Bilateral SDH common: Can present without focal signs
Management:
Investigation:
- Low threshold for CT: If any change in baseline
- Transfer to hospital: Arrange if SDH confirmed
Surgical Decision-Making:
- Fitness for surgery: Assess frailty, comorbidities
- Goals of care: Discuss with patient/family/NOK
- Burr holes under local: Option if unfit for GA
- Conservative management: If very frail or patient/family decline surgery
Post-Operative:
- Return to nursing home: Usually after 3-7 days
- Rehabilitation: May need subacute rehabilitation unit
- Follow-up imaging: Arrange before discharge
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.