Acute Subdural Haematoma

Also known as: Acute SDH

Acute subdural haematoma is accumulation of acute blood between dura and arachnoid, usually from:

Torn bridging veins
Cortical vessel injury
Lacerated brain associated with high energy trauma

Unlike EDH, acute SDH frequently accompanies major underlying parenchymal injury.

CT classically demonstrates a crescentic collection that can cross cranial sutures but is limited by dural reflections such as the falx and tentorium.

Outcome depends not only on haematoma size but also on:

Primary brain injury
Age
GCS
Pupillary status
Hypotension
Associated contusions

Reverse anticoagulation

For life threatening intracranial bleeding, reverse anticoagulation rapidly.

Warfarin

Give:

4 factor prothrombin complex concentrate according to INR and body weight

plus:

Vitamin K 10 mg IV

Dabigatran

Use:

Idarucizumab 5 g IV

Apixaban or rivaroxaban

Use:

Andexanet alfa where available and appropriate, or 4 factor PCC according to institutional emergency reversal protocol.

Do not delay life saving surgery waiting for complete laboratory normalisation when reversal has been initiated and neurological deterioration is ongoing.

Surgical thresholds

Evacuate an acute SDH when:

Thickness is greater than 10 mm

Midline shift is greater than 5 mm

regardless of GCS.

A comatose patient with:

GCS below 9
SDH thickness below 10 mm
Shift below 5 mm

still requires surgery when one or more of the following occur:

GCS has fallen by at least 2 points
New asymmetric or fixed dilated pupils
ICP is persistently elevated.

Severe TBI patients with acute SDH and coma require ICP focused monitoring and treatment.

Procedure

Perform a large trauma craniotomy.

Evacuate clot.

Control:

Cortical bleeding
Bridging veins where accessible
Contused bleeding surfaces

Inspect for significant underlying parenchymal injury.

If the brain remains swollen beyond the inner table or ICP remains dangerously high, leave the bone flap off and perform decompressive craniectomy with duraplasty.

The decompression should be large rather than a small restrictive window.

Nonoperative management

A small SDH without significant shift or neurological deficit can be observed with:

Frequent examination
Repeat CT
Correction of coagulopathy
ICP surveillance in severe injury

Any deterioration requires immediate reassessment.

Seizures

Use 7 day early seizure prophylaxis in significant acute SDH unless there is a specific contraindication.

Do not continue prophylaxis long term unless a seizure occurs or another indication develops.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Concussion

Concussion is a mild traumatic brain injury producing transient disturbance of neurological function after biomechanical force.

Loss of consciousness is not required.

Conventional CT and MRI are usually normal because concussion is primarily a functional and microscopic neuronal injury rather than a macroscopic structural lesion.

The typical GCS is 13 to 15, although most uncomplicated concussion patients are GCS 15 by assessment.

Symptoms can affect:

Cognition
Balance
Vision
Sleep
Mood
Headache pathways

The clinical task is first to ensure that the patient does not have a more dangerous structural head injury.

Symptoms include:

Headache
Dizziness
Nausea
Photophobia
Phonophobia
Blurred vision
Difficulty concentrating
Slowed thinking
Memory disturbance
Fatigue
Irritability
Sleep disturbance

There may be:

Brief loss of consciousness
Retrograde amnesia
Anterograde amnesia
Confusion
Imbalance

Red flags

Urgent reassessment and usually CT are required with:

Declining GCS
Repeated vomiting
Worsening severe headache
New focal neurological deficit
Seizure
Unequal pupils
Significant anticoagulant use with concerning injury
Suspected skull fracture
Progressive confusion
Severe behavioural change
Significant mechanism plus concerning examination

Diagnosis is clinical.

Do not obtain CT simply to diagnose concussion.

CT is used to exclude intracranial haemorrhage or fracture when clinical decision rules and patient factors indicate imaging.

In an adult taking anticoagulants who has a normal neurological examination and a negative initial CT, routine admission solely for repeat imaging is generally unnecessary when the patient remains neurologically stable and reliable follow up exists.

MRI is not routinely required for uncomplicated acute concussion.

Consider MRI or specialist evaluation when:

Focal deficit persists
Symptoms are unusually prolonged
Structural injury remains suspected despite CT
Another diagnosis is likely

First 24 to 48 hours

Use relative rest, not prolonged complete sensory deprivation.

Allow:

Light daily activity
Short walks
Simple cognitive activity

provided symptoms do not increase substantially.

Most adults should begin gradual return to ordinary activity after approximately 1 to 2 days, rather than remaining completely inactive until every symptom disappears.

Avoid:

Alcohol
Driving while attention or reaction time remains impaired
Contact sport
Activities with substantial risk of a second head injury

Headache treatment

A practical initial option is:

Paracetamol 1 g orally every 6 to 8 hours as required

maximum 4 g daily in adults without significant hepatic risk.

NSAIDs can be used after clinically important intracranial bleeding has been excluded when there is no other contraindication.

Avoid routine opioids because:

Sedation interferes with neurological assessment
Dependence can develop
They often worsen dizziness and nausea

Return to work and study

Return progressively according to symptom tolerance.

Temporary modifications can include:

Shorter working hours
Frequent breaks
Reduced screen exposure
Reduced complex multitasking
Temporary avoidance of driving or safety critical work

Persistent symptoms should trigger targeted assessment for:

Vestibular dysfunction
Migraine phenotype
Cervicogenic headache
Sleep disorder
Mood disturbance
Oculomotor dysfunction

Return to sport

Do not allow same day return to contact sport after suspected concussion.

After return to normal daily function and appropriate clinical clearance, use graded progression:

Normal daily activity
Light aerobic exercise
Moderate activity
Heavy noncontact exercise
Full contact practice after medical clearance
Return to competition

Each stage generally lasts at least 24 hours. If symptoms return, step back to the previous asymptomatic stage.

Persistent symptoms

Most patients improve within days to several weeks.

Symptoms persisting beyond approximately 2 to 4 weeks deserve reassessment rather than repeated instructions simply to rest.

Management should target the dominant deficit.

For example:

Vestibular rehabilitation for persistent dizziness
Graded aerobic rehabilitation for exertional intolerance
Migraine directed therapy for post traumatic migraine
Sleep intervention for insomnia
Psychological support where mood or anxiety symptoms contribute

Acute Subdural Haematoma

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management