Haemorrhagic Shock with a Small Subdural Haematoma: Which Pressure Target Wins?
A 32-year-old man is brought in after a high-speed motorcycle collision. GCS is 9 (E2 V2 M5), pupils 3 mm and reactive, heart rate 138/min, blood pressure 78/40 mmHg, temperature 35.1 °C, pelvic binder in place, and the abdomen is distended. FAST is positive in Morison's pouch. Haemoglobin is 6.8 g/dL, lactate 6.2 mmol/L, base deficit −8, and INR 1.6. Trauma CT shows a grade IV liver laceration with active contrast extravasation, an unstable pelvic ring injury, and a 5 mm frontal subdural haematoma with no midline shift. He was intubated in the emergency department with ketamine 100 mg and rocuronium 100 mg and is being ventilated with tidal volumes of 550 mL, PEEP 5, FiO2 1.0, EtCO2 31 mmHg. The massive transfusion protocol has been activated and he is booked for emergency laparotomy with interventional radiology on standby.
1. State your target blood pressure for this patient and explain how you reconcile the competing goals of haemorrhagic shock and traumatic brain injury.
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The two doctrines pull in opposite directions. Hypotensive resuscitation (target systolic 80–90 mmHg) limits clot disruption and bleeding until surgical control, and is supported by trauma guidelines for uncontrolled haemorrhage. Traumatic brain injury guidance wants systolic ≥110 mmHg and MAP ≥80 mmHg to preserve cerebral perfusion pressure. Applying brain-injury targets blindly will exsanguinate him; applying haemorrhage targets blindly will produce secondary ischaemic brain injury.
My resolution is staged and time-based:
- From now until haemorrhage is controlled: target systolic 90 mmHg (MAP ~65), accepting that this is a compromise. The absolute floor is systolic 80 mmHg - I will not allow any episode below that.
- Once the liver and pelvis are controlled: move the target up to systolic ≥110 mmHg / MAP ≥80 mmHg and keep it there for at least 24–48 hours.
- How the pressure is achieved matters as much as the number: raise pressure with blood products in a balanced ratio, not crystalloid. A 500 mL crystalloid bolus raises pressure briefly, dilutes clotting factors, disrupts clot and worsens oedema - it is the worst way to hit a number.
- Vasopressors are a rescue, not a strategy, while he is actively bleeding; they raise pressure without replacing lost volume and can drive more bleeding.
- Note that a 5 mm subdural with no midline shift is not, on its own, an indication for hyperventilation or aggressive cerebral resuscitation. The immediately lethal problem is the liver.
2. The anaesthetic trainee asks for etomidate 20 mg for induction in theatre. Justify your induction plan, including drug choice, dose and the monitoring you would insist on.
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Etomidate 20 mg is too much. That is roughly 0.25 mg/kg for an 80 kg man - a normal-dose induction. In shock, reduced cardiac output and prolonged arm–brain circulation time mean a standard dose produces profound, prolonged hypotension. Dose requirements fall by 30–50%.
Induction plan:
- Arterial line and large-bore access first. At least two wide-bore cannulae, rapid infuser primed with blood products, fluid warmer, and a vasopressor drawn up and connected before any drug is given.
- Preoxygenate (already intubated, so check the circuit and confirm the tube position and cuff).
- Drug: ketamine 1–1.5 mg/kg (roughly 50–75 mg here) or etomidate 0.1–0.15 mg/kg (8–12 mg). Either is defensible. Ketamine preserves sympathetic tone but is less predictable in the catecholamine-depleted patient; etomidate is the more haemodynamically stable agent but causes adrenal suppression, which matters little after a single dose even in trauma. My choice would be a reduced-dose ketamine with a vasopressor running, because the patient is already volume- and catecholamine-driven.
- Muscle relaxant: he has already had rocuronium 100 mg; confirm paralysis with a peripheral nerve stimulator rather than assuming it. If further relaxation is needed, rocuronium is appropriate - suxamethonium is contraindicated with a crush injury and hyperkalaemia risk.
- Monitoring: arterial line, capnography, pulse oximetry (accepting poor peripheral perfusion - use the ear or a forehead probe), temperature probe, urinary catheter, blood gas and thromboelastometry at intervals, and cardiac output monitoring.
3. List the intraoperative measures you would use to prevent secondary brain injury without worsening bleeding, and explain the rationale for each.
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Oxygenation and ventilation
- Keep SpO2 ≥94% and PaO2 >60 mmHg - a single hypoxic episode measurably worsens outcome.
- Target normocapnia, EtCO2 35–38 mmHg. Hypocapnia causes cerebral vasoconstriction and ischaemia; hypercapnia raises intracranial pressure. Avoid prophylactic hyperventilation.
Pressure and perfusion
- As above: systolic ≥90 mmHg during active bleeding, ≥110 mmHg afterwards, achieved with blood products.
- Head-up 15–30° with the neck neutral and the collar loosened once the spine is cleared radiologically - improves cerebral venous drainage without a big haemodynamic penalty.
- Keep PEEP modest (5–8 cmH2O). Higher PEEP raises intrathoracic pressure, impedes cerebral venous drainage and can raise intracranial pressure.
Temperature, glucose and coagulation
- Avoid hypothermia (currently 35.1 °C) but do not over-warm to the point of increasing bleeding; use forced-air warming and warmed fluids, targeting 36–37 °C.
- Glucose 6–10 mmol/L; avoid both hypoglycaemia and hyperglycaemia.
- Correct coagulopathy guided by thromboelastometry, give calcium replacement with massive transfusion, and give tranexamic acid 1 g if within three hours of injury.
- Haemoglobin ≥7–8 g/dL, since anaemia reduces cerebral oxygen delivery further.
Drugs and fluids
- Avoid hypotonic fluids such as 5% dextrose, which worsen cerebral oedema; use balanced crystalloid or blood.
- Adequate sedation and analgesia to reduce cerebral metabolic demand, and treat any seizure activity.
Communication - a clear plan with the surgeon about how much bleeding is anticipated, when interventional radiology is called, and what constitutes futility.