Acute Subdural Haematoma

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

Presentation ranges from headache to coma.

Findings include:

• Reduced GCS
• Focal weakness
• Pupillary asymmetry
• Seizures
• Posturing
• Progressive intracranial hypertension

In older adults, an acute SDH can follow apparently modest trauma because cerebral atrophy places greater tension on bridging veins.

Anticoagulation substantially increases expansion risk.

Noncontrast CT: determine:

• Maximum haematoma thickness
• Midline shift
• Basal cistern compression
• Associated contusion
• Traumatic SAH
• Skull fracture

Repeat CT immediately with neurological deterioration.

Reverse anti coagulation

For life threatening intracranial bleeding, reverse anti coagulation 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

or

• 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.