Initial management

Timely treatment of moderate to severe traumatic brain injury (TBI) can reduce the risk of death and improve patient outcomes.

Many of these treatments aim to prevent secondary brain injury, which is a further injury to the brain after the primary injury (original brain trauma). This may occur immediately after the primary injury (e.g. resulting from hypoxia or hypotension) or over the following hours and days, e.g. resulting from hyperthermia, intracranial hypertension or nutritional deficits.

On this page:

• Avoid hypoxia
• Avoid hypotension and manage causes of shock
• Control and avoid spikes in intracranial pressure
• Manage antithrombotics
• Prevent and manage seizures
• Avoid hyperthermia
• Maintain normal blood glucose levels
• Physiological targets for initial management

Avoid hypoxia

Hypoxia is associated with increased mortality following TBI.

Maintain oxygenation within recommended physiological targets.

Perform early endotracheal intubation and mechanical ventilation when indicated, including in patients with:

• reduced consciousness (GCS ≤ 8)
• severe agitation
• loss of airway protective reflexes
• GCS ≥ 9 with thoracic and abdominal injuries.

During intubation, maintain spinal precautions until spinal injury has been excluded.

Maintain normal carbon dioxide (CO₂) levels.

Avoid hypotension and manage causes of shock

Hypotension is significantly associated with increased mortality following a TBI. Maintain adequate blood pressure to support cerebral perfusion pressure and reduce secondary ischemic injury.

Identify the cause of hypotension and resuscitate accordingly.

The most common causes of hypotension are:

• shock – look for other injuries and consider:
  • haemorrhagic shock due to blood loss
  • obstructive shock due to tension pneumothorax, tamponade or pulmonary embolism
  • neurogenic, septic or cardiogenic shock
  • brain injury-associated shock.
• Iatrogenic causes – mannitol and induction or anaesthetic drugs may cause hypotension.

Manage shock according to the underlying cause

• Haemorrhagic shock: control haemorrhage, resuscitate with blood products, and escalate via local pathways.
• Neurogenic shock: commence isotonic crystalloid resuscitation (e.g. compound sodium lactate, or 0.9% sodium chloride) to maintain tissue perfusion while avoiding fluid overload. Consider early vasopressors such as noradrenaline or adrenaline infusions titrated to target blood pressure. Consider central vascular access if vasopressors are initiated.
• Haemodynamic effects of induction or anaesthesia: carefully consider drug choice and dosing, and ensure senior clinician involvement in planning, drug administration and airway management for rapid sequence intubation.
• Effects of mannitol: restore intravascular volume with isotonic crystalloid.

More about management of traumatic haemorrhagic shock.

Follow recommended blood pressure thresholds

• Maintain systolic blood pressure (SBP) at:
  • ≥ 100 mmHg for patients aged 50–69 years
  • ≥ 110 mmHg for patients aged 15–49 years or over 70 years.
• In patients with haemorrhagic shock and confirmed or suspected severe TBI, aim for a systolic blood pressure of 100–110 mmHg.

For ongoing monitoring and greater accuracy, start invasive arterial monitoring when indicated.

Control and avoid spikes in intracranial pressure

Patients with raised baseline ICP following TBI may have impaired autoregulation, and acute spikes in ICP can worsen secondary brain injury.

ICP is not usually directly measured. Focus management on preventing factors that increase ICP and maintaining adequate cerebral perfusion:

• Provide adequate analgesia and sedation.
• Use hyperosmolar therapy and hyperventilation only when indicated.
• Elevate the head of bed to 30–45° to reduce ICP by 5–6 mmHg.
• Keep the head in a neutral midline position.
• Ensure cervical collars are not too tight and remove them when no longer required, as tight collars may increase ICP by 4–5 mmHg.
• Avoid circumferential cloth or surgical tape for securing endotracheal tubes. Use fixation methods that do not constrict the neck or impair venous outflow.

Hyperosmolar therapy

Hyperosmolar therapy lowers ICP by creating an osmotic gradient that shifts water out of swollen brain tissue, reducing cerebral oedema and supporting cerebral perfusion.

Use hyperosmolar therapy as an emergency temporising treatment for life-threatening raised ICP following TBI or intracranial bleeding with brainstem compression.

Administer hypertonic saline (preferred) or mannitol when indicated:

• Hypertonic saline dosing options include:
  • 3%: 3 mL/kg bolus over 10 minutes
  • 7.5%: 250 mL bolus over 10 minutes
  • 20%: 10–20 mL bolus over 10 minutes
• Mannitol dosing:
  • 0.25–1 g/kg bolus over 15 minutes

Use mannitol with caution, as it may cause hypotension.

Support intravascular volume with isotonic crystalloid (e.g. compound sodium lactate, or 0.9% sodium chloride) and maintain recommended blood pressure targets.

Hyperventilation and carbon dioxide management

Hyperventilation temporarily lowers ICP by reducing arterial carbon dioxide (CO₂), causing cerebral vasoconstriction and reduced cerebral blood volume.

Maintain PaCO₂ within the normal range (35–45 mmHg) and pressure of end-tidal carbon dioxide (PETCO₂) 30–40 mmHg, where available.

Use hyperventilation only as an emergency temporising measure for acute intracranial hypertension or impending brain herniation. Consider it a bridge to additional interventions (e.g. repeat CT scan, osmotic therapy, definitive decompressive surgery) when clinical signs of intracranial hypertension or brain herniation are present, including:

• asymmetric, dilated or non-reactive pupils
• motor exam with extensor posturing
• Cushing reflex (hypertension plus bradycardia)
• decline in Glasgow Coma Scale (GCS) score of more than 2 points.

When using hyperventilation, always:

• consult a senior clinician and/or neurosurgeon before instigating hyperventilation therapy
• obtain an early arterial or venous blood gas to ensure accuracy of ventilation settings and adjust accordingly
• use hyperventilation for the shortest duration possible
• maintain PaCO₂ above 30 mmHg.

Do not use prolonged prophylactic hyperventilation, particularly with PaCO₂ of ≤ 25 mmHg, because it may worsen outcomes.

Manage antithrombotics

Anticoagulant reversal

Pre-injury anticoagulant use, including vitamin K antagonists and direct oral anticoagulants (DOACs), is associated with a higher risk of intracranial haemorrhage (ICH), haemorrhage progression, neurosurgical intervention, and poorer outcomes following TBI compared with non-anticoagulated patients.

Coagulopathy is also common in severe TBI and is associated with worse outcomes. Correction of coagulopathy is associated with improved outcomes after isolated TBI.

Carefully assess patients taking vitamin K antagonists or DOACs on arrival.

Consult your networked neurosurgical service and haematologist early for advice regarding reversal treatments available locally.

Initiate drug-specific reversal therapy when indicated, particularly for patients with life-threatening bleeding or requiring emergency surgery, as per the following guidelines from the Clinical Excellence Commission:

• Periprocedural management of anticoagulant and antiplatelet agents guideline (PDF)
• DOACs guideline (PDF)

Antiplatelet therapy

The role of platelet transfusion to reverse antiplatelet therapy in patients with intracranial haemorrhage is uncertain. Emerging evidence suggests platelet transfusion may not improve outcomes and some studies suggest potential harm.

Do not commence platelet therapy routinely for TBI patients taking antiplatelet medication.

Consult your neurosurgical service before considering platelet transfusion in this setting.

Prevent and manage seizures

Patients with TBI are at increased risk of early (< 7 days) post-traumatic seizures. Early seizures are more common in severe TBI and penetrating injury, and are associated with increased morbidity and mortality; longer ICU and hospital stays; increased mechanical ventilation; and a higher risk of developing post-traumatic epilepsy.

In high-risk patients, prophylactic anti-convulsant therapy reduces the incidence of early post-traumatic seizures compared with no anti-convulsant therapy.

Take immediate steps to control seizures when they occur.

Consider prophylactic anti-convulsant therapy (e.g. phenytoin or levetiracetam) during the first 7 days after injury in patients with severe TBI, when the anticipated benefit outweighs the potential harms.

Do not continue prophylactic anti-convulsant medications beyond 7 days unless there is another clinical indication.

There is insufficient evidence to recommend levetiracetam over phenytoin, or vice versa, for the prevention of early post-traumatic seizures on the basis of efficacy or toxicity alone.

Consider anti-convulsant therapy for patients who develop late (> 7 days) post-traumatic seizures.

Avoid hyperthermia

Hyperthermia worsens secondary brain injury by increasing metabolic demand, reducing cerebral oxygenation, and promoting inflammation, oxidative stress and neuronal death.

Maintain normothermia (36–37.9°C).

Treat fever > 38.0°C promptly.

Maintain normal blood glucose levels

Blood glucose levels outside of the normal range may worsen secondary brain injury and are associated with poorer outcomes. Hyperglycaemia in particular has been associated with increased mortality.

Maintain blood glucose between 5.6 and 10 mmol/L.

Physiological targets for initial management