A 32-year-old motorcyclist with an unstable pelvis, positive FAST and the lethal triad at 4 units of blood
A 32-year-old man is brought in 25 minutes after a high-speed motorcycle collision. He is confused, groaning, and localises pain; the airway is patent and breath sounds are equal. Blood pressure is 84/48 mmHg, pulse 132/min, respiratory rate 28/min, temperature 34.7 °C. The pelvis is unstable on gentle compression, with bruising over the perineum and a fixed, shortened right leg; there is tenderness across the lower abdomen. A pelvic binder is applied and 4 units of packed red cells with 4 units of fresh frozen plasma are running through a rapid infuser. FAST shows free fluid in Morison's pouch and in the pelvis. Arterial blood gas: pH 7.18, base deficit −12 mmol/L, lactate 6.4 mmol/L; INR 1.8, fibrinogen 1.1 g/L, ionised calcium 0.92 mmol/L, haemoglobin 7.4 g/dL. He remains hypotensive after the fourth unit. The hospital has a hybrid theatre with in-house interventional radiology and a 24-hour operating team; CT is next door.
1. List, in order, what you will do in the next 20 minutes and justify the sequence.
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The airway and cervical spine are clinically clear, so move on.
- Two large-bore cannulae; activate the massive haemorrhage protocol with a 1:1:1 ratio of red cells, plasma and platelets (or whole blood if the blood bank supplies it) and keep the rapid infuser running. Empirical balanced resuscitation, given before laboratory results, treats the coagulopathy already visible in his INR of 1.8 and fibrinogen of 1.1 g/L.
- Tranexamic acid 1 g over 10 minutes plus 1 g over 8 hours. The mortality benefit is time-dependent and confined to administration within 3 hours of injury.
- Correct the ionised calcium of 0.92 mmol/L with 10 mL of 10% calcium chloride or 30 mL of calcium gluconate. Citrate in stored blood chelates calcium; hypocalcaemia worsens both coagulopathy and myocardial contractility.
- Warm him: forced-air blanket, warmed fluids, raised theatre temperature. At 34.7 °C he is coagulopathic, and the lethal triad is already established.
- Check the pelvic binder sits at the level of the greater trochanters, not the iliac crests, and add a second binder if the ring is still mobile.
- Permissive hypotension to a systolic of 80–90 mmHg until haemorrhage is controlled. His GCS is normal, so there is no head injury to argue against it.
- Decide the destination: he is a transient responder with a positive FAST. Do not send him to CT. Move to the hybrid theatre for laparotomy with immediate access to angioembolisation.
- Antibiotics, tetanus prophylaxis, and a documented secondary survey once haemorrhage is controlled.
2. Explain how you decide whether the bleeding is pelvic or intra-abdominal, and what you would do if the pelvis turns out to be the dominant source.
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The pelvic fracture and the positive FAST are both plausible sources, and the common error is to assume it is one or the other.
- Pattern of response: a transient or non-responder to 4 units suggests an arterial bleeder rather than capillary ooze, and in an unstable pelvic ring injury that is classically a branch of the internal iliac artery.
- FAST: fluid in Morison's pouch suggests intraperitoneal blood. Fluid confined to the pelvis is far less reliable, because a retroperitoneal haematoma can track and a full bladder mimics free fluid.
- Radiograph and examination: an open-book or vertical shear pattern with a widened symphysis points to pelvic bleeding; a distended, tender abdomen points to the abdomen.
- The pragmatic sequence: an unstable patient with a positive FAST goes to laparotomy. If at laparotomy you find an expanding retroperitoneal haematoma from the pelvis with no intraperitoneal source, do not open it - pack it, close temporarily and go straight to angioembolisation, because opening a pelvic haematoma releases the tamponade and the patient exsanguinates on the table.
- If the abdomen is clean and he stays unstable, the pelvis is the source: angioembolisation of the internal iliac branches is definitive, with external fixation added for mechanical stability.
- Repeat FAST and haemoglobin trends are adjuncts and never a reason to delay.
3. The decision is made for a damage-control laparotomy. State the operative principles, the endpoints that allow you to stop, and the mistakes to avoid.
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Damage control has three phases: control haemorrhage and contamination quickly, correct physiology in intensive care, then return for definitive repair.
Operative principles. Rapid midline laparotomy and four-quadrant packing to identify the bleeding point; then ligate, repair or temporarily shunt a major vessel. Pack the liver, or perform splenectomy if the spleen is unsalvageable. Control contamination with staples or clips and leave bowel ends in discontinuity - no anastomosis and no stoma in an unstable, cold, coagulopathic patient. Do not explore a stable retroperitoneal haematoma related to a pelvic fracture. Close temporarily with a negative-pressure dressing and no fascial sutures, because the bowel will swell. Aim for a total operating time under 60–90 minutes.
Endpoints for stopping: temperature above 35–36 °C; base deficit improving or better than −8; lactate falling or below 4 mmol/L; INR below 1.5; fibrinogen above 1.5 g/L; platelets above 50 × 10⁹/L; and no surgical bleeding. If any endpoint is unmet, stop anyway and go to intensive care.
Mistakes to avoid: performing a definitive anastomosis; closing fascia under tension and causing abdominal compartment syndrome (monitor bladder pressure, abnormal above 20 mmHg with organ dysfunction); chasing the pelvis while missing a second bleeding site; and forgetting calcium, temperature and coagulopathy. Plan a re-look at 24–48 hours, earlier if he deteriorates.