Pelvic Fracture, Class III Shock, and a Low Ionised Calcium
A 28-year-old motorcyclist is brought in after a high-speed collision. He is pale and agitated with a GCS of 14 (E3 V5 M6). A pelvic binder is in place, the right leg is shortened and internally rotated, and the abdomen is distended. Observations: blood pressure 78/44 mmHg, heart rate 138/min, respiratory rate 30/min, SpO2 94% on 15 L via reservoir mask, temperature 35.3°C. He has already received 2 L of crystalloid pre-hospital and 4 units of packed red cells in the resuscitation room. Arterial gas: pH 7.18, lactate 6.8 mmol/L, base deficit −10, haemoglobin 72 g/L, ionised calcium 0.86 mmol/L, INR 1.4. The massive haemorrhage protocol has been activated and a balanced 1:1:1 regimen is running. The trauma surgeon is in the CT scanner and asks you to 'keep him alive and get him to interventional radiology'.
1. What are your priorities in the first 20 minutes, and what would you deliberately avoid?
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Priorities: stop the bleeding, keep the brain perfused, and do not dilute or cool the patient further.
- Airway and C-spine: he is talking with a GCS of 14, so I do not rush to intubate; but if his conscious level falls, or he needs transfer with unstable physiology, I pre-oxygenate and perform an RSI with ketamine 1–2 mg/kg (haemodynamically neutral) and rocuronium, assuming a difficult airway and a full stomach. Intubation removes the ability to use the patient's own respiratory compensation and can precipitate collapse in severe hypovolaemia - so it is done on my terms, with drugs and fluid ready, not in a panic during transfer.
- Haemorrhage control: confirm the pelvic binder is at the level of the greater trochanters (not the iliac crests), apply traction to the shortened leg, and get the surgeon to consider a pre-peritoneal pelvic pack or external fixation. Do not remove the binder to 'look'.
- Damage-control resuscitation: continue balanced blood products rather than crystalloid; the 2 L of crystalloid already given is part of why the ionised calcium and pH are where they are. Tranexamic acid 1 g is indicated if within 3 hours of injury. Active warming (forced air, warmed fluids, raise the theatre temperature).
- Calcium: ionised calcium 0.86 mmol/L is true hypocalcaemia from citrate chelation and it worsens coagulopathy and myocardial contractility. Give calcium chloride 10% 10 mL or calcium gluconate 10% 30 mL peripherally, and recheck after each 4 units.
- Perfusion target: permissive hypotension (systolic ~80–90 mmHg) is acceptable for the pelvic bleeding, but with a GCS of 14 and a possible head injury I would target a systolic of at least 100 mmHg to avoid a second hit to the brain.
Avoid: large crystalloid boluses, vasopressors as a substitute for volume while the pelvis is unsecured, and any delay for a full trauma series if the patient is physiologically unstable.
2. After 8 more units of red cells the ionised calcium is 0.78 mmol/L, fibrinogen 1.1 g/L, INR 1.6, and viscoelastic testing shows a low functional fibrinogen. How do you correct this, and in what order?
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Correct calcium first, then fibrinogen, then consider plasma - and reassess after each step.
- Calcium is the rate-limiting step. Citrate in stored blood chelates ionised calcium; at 0.78 mmol/L there is both coagulopathy (calcium is a cofactor for the coagulation cascade) and impaired myocardial contractility, which will make every other resuscitation measure less effective. Give calcium chloride 10% 10 mL via a central line or calcium gluconate 30 mL peripherally, and repeat the ionised calcium after every 4 units of blood.
- Fibrinogen next. Fibrinogen 1.1 g/L in an actively bleeding trauma patient is inadequate; target ≥1.5–2.0 g/L. Give cryoprecipitate (typically 2 pools of 5 units) or fibrinogen concentrate 3–4 g, guided by viscoelastic testing, and recheck.
- Plasma if there is ongoing bleeding with an INR >1.5 and no better explanation; a balanced ratio is already running, so this is a top-up rather than a new strategy. Avoid giving plasma purely to correct a number in a patient who is not bleeding.
- Platelets if the count is below 50 × 10⁹/L with ongoing haemorrhage, or if there is evidence of platelet dysfunction (head injury, antiplatelet drugs).
- Whole blood is a reasonable alternative to component therapy if available and the patient is still bleeding massively; it delivers fibrinogen and platelets in a physiological ratio and reduces the citrate load per unit of red cells.
- Do not forget the non-haematological variables: keep the patient warm (temperature 35.3°C is enough to impair enzymatic clotting), correct pH where possible, and recheck lactate and base deficit as markers of ongoing bleeding rather than as numbers to chase.
3. The patient remains hypotensive at 82/50 mmHg with a rigid abdomen and a pelvic haematoma on FAST, and interventional radiology has a 40-minute wait. The surgeon asks about resuscitative endovascular balloon occlusion of the aorta (REBOA). How do you reason through that?
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REBOA is a bridge, not a treatment, and the decision hinges on whether the bleeding is pelvic arterial, abdominal, or both, and whether the patient will arrest before definitive control.
Reasoning for:
- He is in class IV shock with a pelvic haematoma and remains hypotensive despite products; if he arrests, his mortality is extremely high. Zone III REBOA (below the renal arteries, above the aortic bifurcation) can raise afterload and cerebral/coronary perfusion while the pelvis is embolised.
Reasoning against:
- A rigid abdomen with a positive FAST suggests intra-abdominal bleeding, and there may be a liver, spleen, or mesenteric injury. Zone III occlusion will not control that; Zone I (descending thoracic aorta) would, but it causes severe visceral and renal ischaemia and is only justified for a few minutes while moving to the operating theatre for a laparotomy.
- REBOA does not stop bleeding; it raises pressure and can increase bleeding from unoccluded collateral vessels. It also risks limb ischaemia, access complications, and requires a team who do it regularly.
- Angioembolisation is definitive for pelvic arterial haemorrhage and is only 40 minutes away.
My decision: do not place REBOA as a substitute for angioembolisation. Escalate the transfer - pre-alert the angio suite, keep the pelvic binder, keep products running, and if he becomes peri-arrest, a resuscitative thoracotomy or Zone I REBOA with immediate laparotomy becomes the conversation, decided jointly with the surgeon. The most useful thing I can do in the next 40 minutes is to correct calcium, fibrinogen and temperature so that he survives to be embolised, and to have the airway and a massive transfusion line ready for the moment he deteriorates.