Airway and oxygenation
Treat life threatening extracranial injuries simultaneously.
Intubate when there is:
- GCS 8 or lower with inadequate airway protection
- Hypoxaemia despite oxygen
- Ventilatory failure
- Severe agitation preventing safe resuscitation
- Impending herniation requiring controlled ventilation
Maintain adequate oxygenation and avoid SpO₂ below 90%. In practice, target normal arterial oxygenation rather than accepting borderline hypoxaemia.
Use rapid sequence intubation with strict avoidance of:
- Hypoxia
- Hypotension
- Prolonged apnoea
- Excessive hyperventilation
Maintain PaCO₂ approximately 35 to 40 mmHg during routine ventilation.
Do not routinely hyperventilate a TBI patient to PaCO₂ 25 mmHg or lower.
In acute impending herniation, temporary controlled hyperventilation to approximately PaCO₂ 30 to 35 mmHg can reduce ICP while definitive treatment is being organised. This is a bridge, not definitive therapy.
Blood pressure
Hypotension substantially worsens outcome.
Practical minimum systolic pressure targets are:
- Age 15 to 49 years: at least 110 mmHg
- Age 50 to 69 years: at least 100 mmHg
- Age 70 years or older: at least 110 mmHg.
Use isotonic crystalloid for initial resuscitation where appropriate, while actively identifying haemorrhage elsewhere.
Avoid routine hypotonic fluids.
If blood pressure remains inadequate after appropriate volume resuscitation, use vasopressor support, commonly:
Norepinephrine IV infusion approximately 0.05 to 1 microgram/kg/min, titrated to systemic and cerebral perfusion targets.
Position
Elevate the head approximately 30° when haemodynamics permit.
Keep:
- Head midline
- Neck free of constriction
- Cervical collar appropriately fitted
Avoid excessive hip flexion or other positions that impair cerebral venous return.
Intracranial pressure monitoring
ICP monitoring is particularly appropriate in salvageable severe TBI with significant CT abnormalities and in selected severe patients at high risk of intracranial hypertension.
Treat sustained ICP above 22 mmHg.
Target cerebral perfusion pressure:
CPP 60 to 70 mmHg
where:
CPP = MAP minus ICP
Avoid routinely driving CPP substantially above 70 mmHg with excessive fluids and vasopressors because pulmonary complications increase.
Initial ICP treatment
Correct reversible causes first:
- Head position
- Hypoxaemia
- Hypercapnia
- Fever
- Seizures
- Pain
- Agitation
- Ventilator dyssynchrony
Provide adequate analgesia and sedation.
A practical regimen can include:
Propofol IV infusion 5 to 50 micrograms/kg/min
titrated according to haemodynamics and ICP.
or
Midazolam IV infusion 0.02 to 0.1 mg/kg/hour
where propofol is unsuitable.
High dose propofol requires caution because of hypotension and propofol infusion syndrome.
Hyperosmolar therapy
For acute intracranial hypertension or herniation:
3% sodium chloride 2 to 5 mL/kg IV bolus
or a fixed adult bolus such as:
3% sodium chloride 250 mL IV
can be used according to local neurocritical protocol.
In immediately life threatening herniation, concentrated hypertonic saline such as 23.4% sodium chloride 30 mL IV through secure central access is used in some specialist units.
Monitor:
- Sodium
- Chloride
- Serum osmolality
- Renal function
Avoid uncontrolled severe hypernatraemia.
An alternative is:
Mannitol 0.25 to 1 g/kg IV bolus
provided systemic blood pressure and intravascular volume can be maintained.
Mannitol can cause:
- Osmotic diuresis
- Hypotension
- Renal injury
- Electrolyte abnormalities
Hypertonic saline is often favoured when hypotension is a major concern.
CSF drainage
An external ventricular drain can both:
- Measure ICP
- Drain CSF therapeutically
Continuous CSF drainage can reduce ICP burden in selected severe TBI patients.
Seizure prophylaxis
Early post traumatic seizures occur within the first 7 days.
Antiseizure prophylaxis is appropriate in higher risk injuries such as:
- Severe TBI
- Cortical contusion
- Acute SDH
- EDH
- Intracerebral haematoma
- Depressed skull fracture
- Penetrating injury
A traditional evidence based regimen is:
Phenytoin 20 mg/kg IV loading dose
followed by approximately:
100 mg IV or orally every 8 hours
with level and toxicity monitoring.
A widely used practical alternative is:
Levetiracetam 1 to 1.5 g IV loading dose
followed by:
500 to 1000 mg IV or orally every 12 hours
for 7 days in a patient without seizures.
Levetiracetam is frequently preferred operationally because it has fewer drug interactions and does not require serum level monitoring, although superiority over phenytoin for prevention of early seizures has not been established.
Do not continue prophylactic antiseizure medication indefinitely simply to prevent late post traumatic epilepsy when no seizure has occurred.
Steroids
Do not use corticosteroids to treat traumatic brain injury or traumatic cerebral oedema.
High dose corticosteroids increase mortality in moderate and severe TBI.
Temperature
Treat fever aggressively.
Aim for normothermia.
Routine prophylactic therapeutic hypothermia is not used simply to improve neurological outcome after diffuse TBI.
Refractory intracranial hypertension
When ICP remains elevated despite first line treatment:
- Reassess CT for a new surgical lesion
- Increase sedation
- Drain CSF if possible
- Repeat hyperosmolar therapy when safe
- Consider neuromuscular blockade in selected ventilator or ICP crises
- Consider barbiturate therapy in highly selected refractory cases with haemodynamic support
- Consider decompressive craniectomy
Secondary decompressive craniectomy for late refractory intracranial hypertension can reduce mortality and improve overall outcome, although survival with severe disability must be discussed in appropriate cases.
When performed, use a large frontotemporoparietal decompression at least approximately 12 × 15 cm, rather than a small bone window.
VTE prophylaxis
Use mechanical prophylaxis early unless contraindicated.
Begin pharmacological prophylaxis when repeat imaging demonstrates stable intracranial haemorrhage and neurosurgical bleeding risk is acceptable.
A practical regimen is:
Enoxaparin 30 mg subcutaneously every 12 hours
or institution specific trauma dosing adjusted for renal function and anti Xa monitoring where used.
Do not start pharmacological prophylaxis blindly before determining whether the intracranial haemorrhage is stable.
