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Gen Surg SAQssurgical-critical-care

Gen Surg SAQs · surgical-critical-care

Blunt polytrauma with hypotension and hypocalcaemia — activate, ratio, clock, calcium and whole-blood choice

Fellowship SAQ on damage control resuscitation: DCR-versus-DCS definition, ABC activation with the PROPPR humbling, EAST ratios, TXA clock with PATCH 90-minute refinement, calcium check-and-replace with counter-evidence, neutral whole-blood RCTs, CRYOSTAT-2 restraint, ITACTIC limits and the TBI exception.

10 marks12 min2 min readVerification in progress

Target exams

FRACSFRCS(Gen Surg)ABSFRCSC
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Target exams

FRACSFRCS(Gen Surg)ABSFRCSC
Prompt
A 41-year-old man arrives 55 minutes after blunt polytrauma: systolic pressure 82 mm Hg, heart rate 134, positive FAST, lactate 6.4 mmol/L, temperature 34.9 degrees C, ionised calcium 0.98 mmol/L, 2 units of red cells running. (A) Define damage control resuscitation versus damage control surgery, justify activation with the ABC variables and state your ratio plan with PROPPR and EAST numbers. (4 marks) (B) State your TXA dose and window with the timing gradient and 90-minute refinement, and your calcium plan with the trial thresholds and the honest counter-evidence. (3 marks) (C) Choose whole blood versus components using the 2026 randomised trials, state your fibrinogen and viscoelastic positions, and name what changes with concomitant severe brain injury. (3 marks)

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Model answer

(A) Resuscitation-first doctrine, activated on physiology, run at equal ratios (4 marks). Damage control resuscitation focuses on initial hypotensive resuscitation and early blood products to prevent the lethal triad of acidosis, coagulopathy and hypothermia — while DCS is abbreviated laparotomy prioritising physiology over anatomy — and DCR may let borderline patients who previously needed DCS undergo early definitive surgery instead.[47] He meets activation on physiology alone: penetrating-or-blunt mechanism with positive FAST, systolic at or below 90 and heart rate at or above 120 score the four ABC variables, with lactate 6.4 and temperature 34.9 completing the bleeding picture — never wait for laboratory coagulation, which arrives normal while lactate already screams shock.[32] Run equal amounts of red cells, plasma and platelets in the early empiric phase per EAST (protocol OR 0.61, high plasma OR 0.60, high platelets OR 0.44), accepting PROPPR's honesty — no 24-hour or 30-day mortality difference (12.7 versus 17.0%, 22.4 versus 26.1%), fewer exsanguinations (9.2 versus 14.6%), more haemostasis (86 versus 78%), complications equal across all 23 prespecified.[8][5] Formalise the score but distrust its negative: applied to PROPPR bleeders an ABC of 2 managed only 66.8% sensitivity and 37.0% specificity, and a third of trial patients entered by gestalt below threshold — so a low score never vetoes blood in a bleeding patient.[35]

(B) TXA now by the clock, calcium by the level (3 marks). Give 1 g over 10 minutes then 1 g over 8 hours immediately: at 55 minutes he sits in the best band — within-1-hour bleeding-death RR 0.68, 1-to-3-hour RR 0.79, beyond-3-hour RR 1.44 — with PATCH-TXA refining the window to 90 minutes (inside aRR 0.64, beyond aRR 1.04).[16][17][18] His ionised calcium of 0.98 meets verified hypocalcaemia (1.0 or less): prehospital plasma pushed lows from 36% to 53% with severe lows predicting worse survival — so measure ionised calcium with every round and replace under citrate load.[21] Then state the counterweight that separates pass from distinction: in 346 protocol activations 83.2% were hypocalcaemic yet neither first calcium nor citrate-corrected dose touched mortality — so check-and-replace is defended, fixed-dose mortality claims are not, and no milligram dose is stated on this evidence.[22]

(C) Components by default, whole blood by logistics, fibrinogen and VHA with restraint (3 marks). Two 2026 prehospital randomised trials were neutral — TOWAR 30-day death 25.9% whole blood versus 20.5% components, English composite 48.7% versus 47.7% — so choose whole blood where it simplifies the chain (prehospital, single-bag logistics, proven LTO-WB safety with identical 73 versus 74% survival) and balanced components where the bank runs equal ratios well.[12] Give no empiric cryoprecipitate: 3 pools early changed 28-day death not at all (25.3 versus 26.1%) — replace documented hypofibrinogenaemia with bleeding only.[28] Use viscoelastic assays as early-warning adjuncts, quoting ITACTIC neutrality (alive free of massive transfusion 67 versus 64%, mortality 25 versus 28%) — never a superiority claim, never a cutoff this evidence lacks.[25] With concomitant severe brain injury everything shifts: no permissive hypotension (the 84.3%-except-TBI professional consensus), TXA by the coma-scale rule with benefit possibly persisting past 2 hours when GCS sits below 9, and pressure targets set for the brain, not the clot.[1]

References14ShowHide
  1. [47]Lamb CM, MacGoey P, Navarro AP, et al. Damage control surgery in the era of damage control resuscitation. Br J Anaesth, 2014.PMID 25038156
  2. [1]Ribeiro Junior MAF, Pacheco LS, Duchesne JC, et al. Damage control resuscitation: how it's done and where we can improve. A view of the Brazilian reality according to trauma professionals. Rev Col Bras Cir, 2025.PMID 39813417
  3. [5]Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA, 2015.PMID 25647203
  4. [8]Cannon JW, Khan MA, Raja AS, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg, 2017.PMID 28225743
  5. [16]Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet, 2010.PMID 20554319
  6. [17]Roberts I, Shakur H, Afolabi A, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet, 2011.PMID 21439633
  7. [18]Ali A, Gruen RL, Bernard SA, et al. Tranexamic Acid Timing and Mortality Impact After Trauma. Ann Emerg Med, 2026.PMID 40751727
  8. [32]Nunez TC, Voskresensky IV, Dossett LA, et al. Early prediction of massive transfusion in trauma: simple as ABC (assessment of blood consumption)? J Trauma, 2009.PMID 19204506
  9. [35]Baird EW, Lammers DT, Abraham P, et al. Diagnostic performance of the ABC score in the PROPPR trial. Injury, 2024.PMID 38852527
  10. [21]Moore HB, Tessmer MT, Moore EE, et al. Forgot calcium? Admission ionized-calcium in two civilian randomized controlled trials of prehospital plasma for traumatic hemorrhagic shock. J Trauma Acute Care Surg, 2020.PMID 32317575
  11. [22]Chanthima P, Yuwapattanawong K, Thamjamrassri T, et al. Association Between Ionized Calcium Concentrations During Hemostatic Transfusion and Calcium Treatment With Mortality in Major Trauma. Anesth Analg, 2021.PMID 33646983
  12. [12]Sperry JL, Guyette FX, Cotton BA, et al. Prehospital Resuscitation with Type O Whole Blood for Trauma and Hemorrhage. N Engl J Med, 2026.PMID 42150044
  13. [28]Davenport R, Curry N, Fox EE, et al. Early and Empirical High-Dose Cryoprecipitate for Hemorrhage After Traumatic Injury: The CRYOSTAT-2 Randomized Clinical Trial. JAMA, 2023.PMID 37824155
  14. [25]Baksaas-Aasen K, Gall LS, Stensballe J, et al. Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomized, controlled trial. Intensive Care Med, 2021.PMID 33048195
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