Traumatic Subarachnoid Haemorrhage

Traumatic subarachnoid haemorrhage is blood within the subarachnoid space caused by traumatic disruption of small cortical or leptomeningeal vessels.

It commonly accompanies:

• Cerebral contusions
• Subdural haematoma
• Skull fracture
• Diffuse brain injury

Small isolated convexity tSAH in a neurologically intact patient behaves very differently from aneurysmal subarachnoid haemorrhage.

The main clinical priorities are:

• Identify associated traumatic lesions
• Ensure the pattern is truly traumatic
• Detect deterioration from cerebral oedema or evolving haemorrhage
• Prevent secondary brain injury

Symptoms include:

• Headache
• Nausea
• Vomiting
• Confusion
• Reduced GCS
• Seizure
• Focal deficit when associated lesions exist

Severe tSAH is a marker of greater injury severity and is associated with worse outcome in severe TBI.

Noncontrast CT: shows blood within cortical sulci, fissures or basal cisterns.

A small amount of blood immediately adjacent to a contusion or over the cerebral convexity in a clear traumatic mechanism is usually traumatic.

Consider CT angiography when:

• Blood is predominantly within basal cisterns
• Haemorrhage pattern is disproportionate to the trauma
• Mechanism is uncertain
• There is no convincing traumatic lesion
• Aneurysmal rupture could have caused the fall or crash

Do not label every subarachnoid haemorrhage after a fall as traumatic without considering whether spontaneous aneurysmal SAH preceded the trauma.

Mild isolated tSAH

A neurologically intact patient with a small isolated tSAH can generally be managed with:

• Observation
• Serial neurological examination
• Analgesia
• Correction of anticoagulation where clinically appropriate
• Repeat CT according to neurological course and local protocol

Routine neurosurgical operation is not required.

Deterioration

Repeat CT urgently with:

• Falling GCS
• New focal deficit
• New pupillary abnormality
• Repeated seizure
• Increasing headache with vomiting

Look for:

• Expanding contusion
• Acute SDH
• Hydrocephalus
• Diffuse swelling

Nimodipine

Do not routinely prescribe nimodipine for isolated traumatic SAH simply by extrapolating from aneurysmal SAH.

The delayed cerebral ischaemia pathway that drives routine nimodipine therapy after aneurysmal rupture is not established in the same way after isolated traumatic SAH.

ICP management

Severe tSAH with coma is treated as severe TBI.

Use:

• ICP monitoring when indicated
• ICP threshold above 22 mmHg for treatment
• CPP 60 to 70 mmHg
• Hyperosmolar therapy
• Ventilation and oxygenation targets
• Surgery for associated mass lesions

Seizure prophylaxis

A small isolated tSAH in an awake neurologically intact patient does not automatically require prophylaxis.

Use 7 day prophylaxis when overall TBI severity or associated cortical injury creates substantial early seizure risk.