Initial stabilisation of major paediatric head injury — formative SAQs

1. Airway management

A Glasgow Coma Scale of 8 or below is the threshold for definitive airway protection, because the child cannot reliably protect the airway or maintain adequate ventilation. I intubate using rapid sequence induction with preoxygenation, a neuro-friendly induction agent that avoids hypotension, and a muscle relaxant. I avoid coughing, bucking and prolonged laryngoscopy because each raises intracranial pressure. I confirm tube placement with waveform capnography immediately and secure the tube before transport. Manual in-line cervical stabilisation is maintained throughout. [1]

2. Ventilation target

The ventilation target is normocapnia: I aim for a partial pressure of carbon dioxide in the normal range for age, guided by waveform capnography and confirmed by blood gas. Prophylactic hyperventilation is contraindicated because lowering the partial pressure of carbon dioxide below the normal range causes cerebral vasoconstriction, reduces cerebral blood flow, and risks cerebral ischaemia. I reserve temporary mild hyperventilation for the acute signs of impending herniation, such as a unilateral dilated pupil, while hyperosmolar therapy and neurosurgical escalation are prepared. [1]

3. Fluid strategy

I give isotonic crystalloid, such as 0.9 percent saline or a balanced solution, in aliquots of approximately 10 mL per kilogram, reassessing after each. I avoid hypotonic fluids because hyponatraemia worsens cerebral oedema. Even a single episode of hypotension after severe traumatic brain injury is associated with a doubling of mortality, so I maintain an age-appropriate systolic blood pressure aggressively. If shock persists despite fluid resuscitation, I consider blood products and vasoactive support and escalate to critical care. [1] [7]

4. Disability assessment and positioning

I record the Glasgow Coma Scale score, the time and the trend. I check pupils for size and reactivity and look for abnormal posture. I check bedside glucose immediately because hypoglycaemia worsens outcome and is immediately treatable; I correct any dangerous low now. I position the head of the bed 30 degrees up and keep the head midline, with the cervical spine protected, because this promotes jugular venous drainage and reduces intracranial pressure without compromising cerebral perfusion, provided the child is normovolaemic. [1]

5. Imaging and referral timing

I arrange urgent CT of the head and cervical spine once the child is stable enough for transport to the scanner. I never send an unstable child to CT without monitoring, escort and a rescue plan. I call neurosurgery and retrieval at the point of recognising severe traumatic brain injury, in parallel with resuscitation, not after the CT confirms an operable lesion. Early referral allows planning for transfer, operating theatre readiness and ongoing intensive care. [8] [11]

1. Hyperosmolar therapy and evidence

The two first-line agents are 3 percent hypertonic saline and mannitol. 3 percent saline is given as a bolus, typically in the range of 2 to 5 mL per kilogram, with monitoring of serum sodium to avoid exceeding approximately 155 to 160 mmol per litre. Mannitol is given as a bolus of 0.25 to 0.5 g per kilogram intravenously, with monitoring of serum osmolality to avoid exceeding approximately 320 mOsm per litre. The JAMA Network Open comparison found that both agents reduce intracranial pressure, with hypertonic saline showing a numerically greater reduction, and a 2025 outcome study found no statistically significant difference in mortality between the two. A systematic review confirmed comparable efficacy, so either agent is acceptable based on local protocol. Mannitol can cause hypovolaemia through its diuretic effect, so I monitor the circulation and replace intravascular volume with isotonic fluid. [2] [3]

2. Cerebral perfusion pressure

Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure. This means hypotension is doubly dangerous because it lowers the driving pressure at the same time as the intracranial pressure may be rising from the haematoma or oedema. After traumatic brain injury, cerebral autoregulation is often impaired, so cerebral blood flow becomes passively dependent on systemic blood pressure with no safety margin. Maintaining an age-appropriate blood pressure is therefore a direct neuroprotective act, not merely supportive care. [7]

3. Seizure prophylaxis

Post-traumatic seizures worsen secondary brain injury by raising metabolic demand, intracranial pressure and oxygen consumption. Early seizure prophylaxis is recommended for children at high risk, typically those with severe traumatic brain injury and an abnormal CT scan, for the first seven days after injury. Levetiracetam or phenytoin are the common agents, chosen with local protocol. Prophylaxis is not indefinite: seven days covers the period of highest early seizure risk. I treat any actual clinical seizure with first-line benzodiazepine and investigate the cause. [1]

4. Escalation and retrieval

I call neurosurgery and retrieval at the point of recognising the unilateral dilated pupil and the haematoma with midline shift, in parallel with hyperosmolar therapy, not after local options fail. I discuss the child's physiology, the treatment underway, the expected response, the escort and equipment, the transport time and weather, the safest destination and the contingency if transfer is delayed. The neuroprotection bundle continues throughout transfer with continuous monitoring and a named owner for the next escalation. I keep the family informed and document objectively. [8] [11]