The Borderline Responder: Pelvic Fracture, Free Fluid, and a Head Injury
A 34-year-old man arrives 40 minutes after a high-speed motorcycle collision. He is pale and agitated. Blood pressure 88/50 mmHg, heart rate 138/min, GCS 13 (E3 V4 M6), pupils equal and reactive. Breath sounds are equal; the abdomen is distended and tender; the pelvis is unstable on gentle compression despite a binder applied by paramedics. Femoral pulses are weak but palpable bilaterally. One litre of warmed crystalloid has been given with no change in blood pressure. Point-of-care lactate is 5.8 mmol/L with a base deficit of -9. FAST shows free fluid in Morison's pouch and in the pelvis. The CT scanner is 20 minutes away; the operating theatre is ready now. The blood bank has issued four units of packed red cells and four units of plasma.
1. State your resuscitation targets and the first products you would give in the next 10 minutes. Explain how the GCS of 13 changes the usual strategy for an unstable trauma patient.
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Fluids and targets. This is class III–IV haemorrhagic shock with two competing imperatives: stop the bleeding and protect the brain.
- Give blood, not crystalloid. The litre already given has done nothing but dilute clotting factors and cool him. Start a balanced massive transfusion ratio of approximately 1:1:1 (red cells, plasma, platelets), given through a rapid infuser and warmer.
- Calcium and temperature. Give 1 g calcium gluconate for every 3–4 units; hypocalcaemia worsens both coagulopathy and myocardial contractility.
- Tranexamic acid 1 g over 10 minutes (then 1 g over 8 hours) - the benefit is time-dependent and largely lost beyond 3 hours.
Why the head injury matters. In an isolated pelvic or abdominal bleed the standard is permissive hypotension (systolic ~80–90 mmHg) until haemostasis. That calculus changes here: a GCS of 13 raises the possibility of traumatic brain injury, and even one episode of systolic pressure below about 110 mmHg substantially worsens secondary brain injury. I would therefore target a systolic pressure of roughly 100–110 mmHg - higher than permissive hypotension, but still not normalised to 120 in a patient actively exsanguinating - while treating the abdomen and pelvis as the priority source of that hypotension. The two goals are not truly in conflict: definitive haemorrhage control is the most effective way to restore cerebral perfusion.
Do not forget. Avoid hyperventilation, keep the head neutral, and check that the pelvic binder is at the level of the greater trochanters, not the iliac crests.
2. The patient is taken to theatre. The theatre team asks whether CT should be done first to define the bleeding source. Justify your decision and outline the operative strategy.
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No CT. He is haemodynamically unstable with a positive FAST and a mechanically unstable pelvis. In that combination CT is a diagnostic luxury that converts an operable patient into a dying one on the scanner table. CT is appropriate for the stable or transiently responding patient in whom the source of bleeding is genuinely unclear; here there are two obvious sources and one obvious destination.
Operative sequence:
- Laparotomy first, because intraperitoneal free fluid with shock is the fastest-kill lesion. Rapid four-quadrant packing; look for retroperitoneal haematoma patterns indicating pelvic bleeding - a lateral haematoma is usually venous and managed by packing, whereas a central haematoma is surgical.
- Damage control, not definitive repair. No time-consuming anastomoses or complex vascular repairs in an acidotic, coagulopathic, hypothermic patient. Pack, control obvious bleeding, temporary abdominal closure with a negative-pressure dressing.
- Address the pelvis in parallel. Keep the binder on; call interventional radiology for angioembolisation of pelvic arterial bleeding while you are still operating, and involve orthopaedics for external fixation.
- Resuscitate in the ICU, correct calcium, temperature and coagulopathy using viscoelastic testing, then plan a re-look laparotomy in 24–48 hours.
The key judgement is recognising that this patient cannot tolerate a single long definitive operation, so the correct decision is a staged one.
3. After four units of blood his heart rate is still 130/min and systolic pressure 85 mmHg, with a tense abdomen and blood soaking through the temporary dressing. What is your next move, and what findings would make you decide the abdomen is no longer the primary problem?
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Interpretation. Persistent tachycardia and hypotension after four units, in a patient whose abdomen has become tense and is bleeding through the dressing, indicates either an uncontrolled intra-abdominal source or ongoing pelvic bleeding, or both. This is not the moment for more tests.
Immediate actions:
- Return to theatre for repacking and re-exploration rather than accepting the loss. Reassess the liver, spleen, mesentery and retroperitoneum; look specifically for a missed major retroperitoneal haematoma.
- Simultaneous escalation: activate massive transfusion, correct calcium and temperature, give fibrinogen concentrate or cryoprecipitate if viscoelastic testing shows a fibrinogen deficit, and give platelets if the count is falling.
- Get the pelvis treated definitively. If the pelvic binder is adequate and the abdomen is packed and dry, the remaining bleeding is likely pelvic - push for urgent angioembolisation, or preperitoneal packing if angio is unavailable and the patient is crashing.
Findings that would shift the problem away from the abdomen: an abdomen that is soft with a dry dressing, a distended rigid pelvis with an enlarging thigh haematoma, or a rapidly expanding flank mass. In those cases the abdomen is controlled and the pelvis or a retroperitoneal vessel is the driver - angioembolisation or preperitoneal packing becomes the priority. Repeating the same operation without changing the diagnosis is the common failure mode here.