Traumatic brain injury with hypotension: the induction plan is the danger
A 34-year-old man is brought to the emergency department after a high-speed motorcycle collision. He opens his eyes to pain, makes incomprehensible sounds and withdraws from pain (GCS 7). Both pupils are 3 mm and reactive. He is supine in a rigid cervical collar, breathing spontaneously at 24/min with SpO2 92% on a non-rebreather mask, heart rate 122/min and blood pressure 96/54 mmHg. There is a scalp laceration with active bleeding and the left leg is deformed. FAST scan is negative. CT shows a left frontal contusion with 6 mm midline shift and effaced basal cisterns. The intensive care unit has one bed and the operating theatre is busy with another emergency. A trainee is preparing to induce anaesthesia with propofol 2 mg/kg and suxamethonium 1.5 mg/kg and to ventilate to a PaCO2 of 30 mmHg.
1. Critique the trainee's plan and describe how you would modify it.
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The plan has three serious flaws. First, propofol 2 mg/kg in a hypovolaemic patient with a blood pressure of 96/54 mmHg will almost certainly cause profound hypotension, and hypotension is one of the strongest avoidable causes of secondary brain injury. Second, prophylactic hyperventilation to a PaCO2 of 30 mmHg is not recommended: it reduces cerebral blood volume and can cause ischaemia in injured brain. Third, preoxygenation is inadequate, with SpO2 92% on a reservoir mask, and the cervical collar, scalp bleeding and full stomach have not been addressed in the plan.
I would optimise before induction: apply direct pressure to the scalp, establish large-bore access, give a balanced crystalloid or blood bolus as indicated, and have push-dose or infusion vasopressor ready. Preoxygenate with a tight-fitting mask and consider apnoeic oxygenation; maintain manual in-line stabilisation and remove the front of the collar to allow mouth opening. For induction, ketamine 1–2 mg/kg or etomidate, plus an opioid and rocuronium 1.2 mg/kg, with immediate laryngoscopy and prompt confirmation of tube position. Aim for normocapnia of about 35–38 mmHg, not 30, unless there are signs of herniation. Keep the head up 30 degrees once the airway is secure and maintain systolic pressure at or above 110 mmHg.
2. What physiological targets would you set for the first 24 hours, and why?
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The aim is to prevent secondary injury. For a 34-year-old, the Brain Trauma Foundation recommends a systolic blood pressure of at least 110 mmHg; in practice I would target a mean arterial pressure of 70–80 mmHg to support a cerebral perfusion pressure of about 60–70 mmHg, guided by intracranial pressure monitoring if it is available. Fluids should be isotonic; avoid hypotonic solutions and glucose-containing fluids that can worsen cerebral oedema. Noradrenaline is appropriate to support pressure after volume resuscitation.
Oxygenation should keep SpO2 above 94% and PaO2 above about 10 kPa, avoiding both hypoxia and hyperoxia. Ventilation should target a PaCO2 of 35–38 mmHg. Temporary hyperventilation to 30–35 mmHg is a bridge for signs of herniation, not a routine target.
Control temperature and avoid hyperthermia; treat seizures if they occur but do not use routine prophylaxis. Nurse with the head up 30 degrees and the neck neutral, avoiding tight collar straps and obstruction of venous drainage. Correct coagulopathy and anaemia, check electrolytes, and sedate and ventilate adequately to prevent coughing and rises in intrathoracic pressure. Repeat imaging if the neurological examination deteriorates, and arrange transfer to a neurosurgical centre if the CT findings warrant it.
3. The patient becomes bradycardic with a rising blood pressure and a dilated left pupil during transfer. What is your immediate management?
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This is the Cushing response and suggests raised intracranial pressure with possible herniation. Immediate steps are to secure the airway if not already done, give 100% oxygen and check the tracheal tube position, then briefly hyperventilate to a PaCO2 of about 30–35 mmHg as a temporising measure while definitive treatment is arranged. Elevate the head to 30 degrees and ensure the neck is neutral with no tight collar or tape obstructing venous drainage.
Give hyperosmolar therapy: hypertonic saline 3% in a 250 mL bolus, or mannitol 0.5–1 g/kg if there is no hypovolaemia or renal contraindication. Maintain blood pressure: do not allow the bradycardia and hypertension to be treated as a primary cardiac problem, because the priority is cerebral perfusion. Atropine may be needed if bradycardia is severe, but the underlying cause must be addressed. Ensure sedation and analgesia are adequate and consider a bolus of neuromuscular blocker to prevent coughing, which raises intracranial pressure.
Urgent neurosurgical review and repeat CT are needed; if theatre is unavailable, the patient should be transferred to a neurosurgical centre after stabilisation. The episode and all interventions should be documented, and the possibility of a delayed extradural or subdural haematoma considered.