Subdural Hemorrhage Clinical Overview

I. The "On-Call" Snapshot

  • Clinical Significance in Malaysia: This is a bread-and-butter neurosurgical emergency, primarily driven by road traffic accidents in younger adults and falls in our aging population.

  • High-Yield Definition: A subdural haemorrhage (SDH) is a collection of blood in the potential space between the dura mater and the arachnoid mater.

  • Clinical One-Liner: Basically, it's a bleed from torn bridging veins, often from a head knock, that slowly or quickly squashes the brain.

II. Etiology & Risk Factors

  • Etiology: Tearing of the cortical bridging veins as they cross the subdural space to drain into the dural venous sinuses. This is usually caused by sudden acceleration-deceleration forces.

  • Risk Factors:

    • Non-Modifiable:

      • Cerebral atrophy (the elderly, chronic alcoholics): The brain shrinks, stretching the bridging veins and making them more susceptible to tearing from minor trauma. This is the classic profile for chronic SDH.

      • Age > 65 years.

    • Modifiable:

      • Anticoagulant / Antiplatelet use (Warfarin, Aspirin, Clopidogrel).

      • Coagulopathies (e.g., chronic liver disease).

      • Recurrent falls.

III. Quick Pathophysiology

Head movement causes the brain to move within the skull, but the venous sinuses are fixed. This shear force tears the bridging veins. Venous blood leaks into the subdural space. In an acute SDH, the bleeding is rapid and acts as a fast-growing mass lesion, causing a sharp rise in intracranial pressure (ICP) and potential for herniation. In a chronic SDH, the initial bleed is slow. The blood breaks down, creating an osmotic gradient that draws CSF into the hematoma cavity, causing it to gradually expand over weeks, leading to insidious symptoms.

IV. Clinical Assessment

  • Red Flags & Immediate Actions:

    • GCS drop of ≥ 2 points: Alert senior immediately, re-assess ABCs, prepare for urgent CT.

    • Pupil changes (unilateral dilation - the "blown pupil"): Signifies uncal herniation. This is a neurosurgical emergency. Alert senior & neurosurgery registrar, consider starting IV Mannitol after discussion.

    • Cushing's Triad (Hypertension, Bradycardia, Irregular Respirations): Late sign of critically high ICP. Stabilise airway, alert seniors from both your team and anaesthesia.

    • Post-traumatic seizure: Secure airway, give IV benzodiazepine (e.g., Diazepam 5-10mg slow push), load with an anticonvulsant as per local protocol (usually IV Levetiracetam).

  • History:

    • Common (>50%): History of head trauma (may be trivial or forgotten in cSDH), headache, fluctuating level of consciousness.

    • Less Common (10-50%): Focal neurological deficits (e.g., unilateral weakness), nausea/vomiting, cognitive changes (confusion, memory loss - especially in cSDH).

    • Pertinent Negatives: Ask about anticoagulant use, history of falls, alcohol abuse, and seizures. The absence of a clear traumatic event does not rule out a cSDH, especially in the elderly.

  • Physical Examination:

    • General: Check for scalp lacerations, bruising (Battle's sign, raccoon eyes).

    • Neurology:

      • GCS: This is your baseline and trend. Do it yourself, don't just copy the last entry.

      • Pupils: Size, symmetry, and reaction to light. Document it clearly.

      • Focal Deficits: Check for hemiparesis, pronator drift.

      • Gait: In ambulatory patients with suspected cSDH, gait disturbance is a key sign.

  • Clinical Pearl: The classic "lucid interval" is more famous in extradural haemorrhage, but you can see it in acute SDH too. A patient talks to you and then rapidly deteriorates. Never trust a head injury.

V. Diagnostic Workflow

  • Differential Diagnosis:

    • Extradural Hemorrhage (EDH):

      • Points For: Typically a younger patient after direct trauma (e.g., RTA, assault), classic history of brief LOC, a lucid interval, then rapid decline. Associated with a skull fracture.

      • Points Against: Slower onset, elderly patient, no clear high-impact trauma.

      • How to Differentiate: Non-contrast CT Brain. EDH shows a biconvex (lens-shaped) hyperdense collection that does not cross suture lines.

    • Subarachnoid Hemorrhage (SAH):

      • Points For: Sudden onset "thunderclap" headache ("worst headache of my life"), neck stiffness, photophobia.

      • Points Against: Clear history of trauma leading to progressive neurological signs rather than an abrupt, explosive headache.

      • How to Differentiate: Non-contrast CT Brain shows blood in the basal cisterns and sulci.

    • Ischemic Stroke:

      • Points For: Focal neurological deficit, risk factors (hypertension, diabetes).

      • Points Against: History of trauma, headache, fluctuating GCS are less typical for stroke.

      • How to Differentiate: Non-contrast CT Brain will be normal in early ischemic stroke but will clearly show an SDH.

  • Investigations Plan (as per Malaysian CPG - Early Management of Head Injury in Adults):

    • Bedside / Initial (First 15 Mins):

      • Fingerprick Glucose: To rule out hypoglycemia as a cause for altered mental status.

      • ECG: Especially in older patients, to check for arrhythmias that may have caused a fall.

    • First-Line Labs & Imaging:

      • FBC, RP, Coagulation Profile (PT/INR, aPTT): Essential, especially if the patient is on warfarin or has liver disease.

      • Group & Screen (G&S): If surgery is a possibility.

      • Non-Contrast CT Brain: This is the gold standard.

        • Acute SDH: Crescent-shaped, hyperdense (bright) collection along the cerebral convexity.

        • Subacute SDH (3-21 days): Isodense (similar density to brain parenchyma), can be subtle. Look for effacement of sulci or midline shift.

        • Chronic SDH (>21 days): Hypodense (dark) collection. May see acute-on-chronic bleed with mixed densities.

    • When to Scan (Criteria from MOH CPG):

      • Immediate Scan: GCS <13 initially, GCS <15 at 2 hours post-injury, suspected open/depressed skull fracture, basal skull fracture signs, post-traumatic seizure, focal deficit, ≥2 episodes of vomiting.

      • Urgent Scan (even with GCS 15): Age ≥65, on anticoagulants/antiplatelets, dangerous mechanism of injury, >30 mins retrograde amnesia.

VI. Staging & Severity Assessment

  • Severity is based on the Glasgow Coma Scale (GCS) on presentation:

    • Mild Head Injury: GCS 13-15

    • Moderate Head Injury: GCS 9-12

    • Severe Head Injury: GCS ≤ 8

  • Radiological Severity (Surgical Indications): This is what the neurosurgeons will ask for.

    • Acute SDH thickness > 10 mm OR

    • Midline shift > 5 mm

    • These are indications for surgical evacuation regardless of GCS.

  • Chronic SDH - Markwalder Grading Scale: Useful for assessing cSDH patients.

    • Grade 0: Asymptomatic.

    • Grade 1: Alert, oriented, mild symptoms (e.g., headache).

    • Grade 2: Drowsy/disoriented with variable neurological deficits.

    • Grade 3: Stuporous but responds to stimuli, severe focal signs.

    • Grade 4: Comatose.

    • Impact: Patients in Grade 0-1 may be managed conservatively; Grade 2-4 usually require surgery.

VII. Management Plan

  • Immediate Stabilisation (The ABCDE Plan):

    • Airway: Secure with cervical spine protection. Intubate if GCS ≤ 8 or if airway is compromised.

    • Breathing: Administer high-flow oxygen (e.g., via non-rebreather mask at 15L/min) to maintain SpO2 > 95%.

    • Circulation: Secure two large-bore IV cannulas. Maintain systolic BP > 110 mmHg. Use isotonic crystalloids (Normal Saline). Avoid hypotension at all costs.

    • Disability: Assess GCS and pupils. If signs of raised ICP:

      • Elevate head of bed to 30 degrees.

      • IV Mannitol 20%: 0.5-1.0 g/kg over 15-20 mins. Discuss with senior/neurosurgery before giving.

      • Consider hyperventilation to a PaCO2 of 30-35 mmHg as a temporary measure if intubated.

    • Exposure: Log-roll patient to check for other injuries, prevent hypothermia.

  • Definitive Treatment (The Ward Round Plan):

    • Reversal of Anticoagulation:

      • Warfarin: Give IV Vitamin K 10mg. For emergency reversal, give Prothrombin Complex Concentrate (PCC). If unavailable, use Fresh Frozen Plasma (FFP).

      • Antiplatelets (Aspirin/Clopidogrel): Discuss with senior/haematology. May require platelet transfusion if actively bleeding and surgery is planned. Give IV Tranexamic acid (brand: Transamin) 1g.

    • Seizure Prophylaxis: Prophylactic anticonvulsants are recommended for severe TBI to prevent early post-traumatic seizures.

      • First-Line: IV Levetiracetam (brand: Keppra) 500mg-1g BD.

    • Surgical Intervention: The definitive treatment for significant acute SDH.

      • Craniotomy: For acute SDH to evacuate the clot.

      • Burr Hole Craniostomy: The standard for most chronic SDHs.

    • Conservative Management: For small, asymptomatic acute SDH or Grade 0 cSDH with minimal mass effect. Involves close observation, serial GCS charting, and repeat imaging.

  • Long-Term & Discharge Plan:

    • Requires neuro-rehabilitation (physiotherapy, occupational therapy).

    • Follow-up in neurosurgery clinic.

    • Careful re-introduction of anticoagulants must be decided by the neurosurgical and primary team.

    • Provide clear head injury advice to patient and family.

VIII. Complications

  • Immediate:

    • Cerebral Herniation: Management: Emergency decompression, ICP management.

    • Seizures: Management: Benzodiazepines, loading with anticonvulsants.

  • Short-Term:

    • Hematoma Expansion/Recurrence (esp. cSDH): Management: May require repeat surgery.

    • Cerebral Edema: Management: Medical ICP management, decompressive craniectomy.

  • Long-Term:

    • Post-traumatic Epilepsy: Management: Long-term anticonvulsant therapy.

    • Cognitive and Motor Deficits: Management: Neuro-rehabilitation.

    • Hydrocephalus: Management: May require ventriculoperitoneal (VP) shunt.

IX. Prognosis

Prognosis depends heavily on the initial injury severity. The Glasgow Outcome Scale (GOS) is used to classify outcome.

  • Top 3 Prognostic Factors:

    1. Admission GCS: The single most powerful predictor. GCS 3-5 has a very high mortality.

    2. Pupillary response: Bilaterally fixed and dilated pupils are an extremely poor sign.

    3. Age: Older patients have worse outcomes.

X. How to Present to Your Senior

"Dr, for review please. This is Patient [Name/Bed], a [age]-year-old [man/woman] with a background of [e.g., hypertension, on warfarin], who presented after a [mechanism, e.g., fall].

On assessment, his GCS is [score E_V_M_], pupils are [size, reactive/unreactive]. He has a [focal deficit, e.g., right hemiparesis].

My main differential is an acute subdural haemorrhage. CT brain shows a [e.g., large left-sided acute SDH with significant midline shift].

I have already done ABCs, sent bloods including coags and G&S, and I have contacted the neurosurgery registrar on-call at [Hospital Name]. I would like to ask about starting IV Mannitol as his right pupil is starting to dilate."

XI. Summary & Further Reading

  • Top 3 Takeaways:

    1. Suspect SDH in any elderly patient with a fall and confusion, or any patient with trauma and a fluctuating GCS.

    2. The Non-Contrast CT Brain is your most important diagnostic tool. Know the surgical indications: thickness >10mm or midline shift >5mm.

    3. Your immediate job is ABCDEs, GCS monitoring, reversing any coagulopathy, and making a timely and clear referral to neurosurgery. Hypotension is the enemy.

  • Key Resources:

    • Malaysian CPG: Ministry of Health, "Early Management of Head Injury in Adults" (2015/2016). You should have a copy of this.

    • UpToDate: Search for "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Management of acute subdural hematoma".

    • Amboss: Search for "Subdural hemorrhage".

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