Major trauma and damage control

10 min read Last updated April 8, 2026

Surgical approach

  • Overall aim: prioritise rapid haemorrhage and contamination control over definitive repair; accept temporary measures to restore physiology
    • Trigger: ongoing bleeding/physiological exhaustion (acidosis, hypothermia, coagulopathy), multiple injuries, prolonged definitive surgery unsafe
  • Damage control surgery (DCS) phases
    • Phase 0 (pre-op/ED): haemorrhage control (tourniquet, pelvic binder, haemostatic dressings), activate MHP, rapid imaging/decision (CT vs theatre)
    • Phase 1 (OR): abbreviated surgery: pack bleeding surfaces, clamp/ligate vessels, temporary shunts, stapled bowel ends, control contamination, temporary abdominal closure
    • Phase 2 (ICU): rewarming, correction of coagulopathy, acidosis, calcium; ventilatory and haemodynamic optimisation
    • Phase 3 (return to OR): definitive repair/reconstruction once physiology restored (often 24–72 h)
  • Common damage control procedures
    • Trauma laparotomy: packing (liver/spleen), Pringle manoeuvre, splenectomy, stapled bowel, temporary closure (vacuum dressing/Bogota bag)
    • Pelvic haemorrhage: binder, preperitoneal packing, external fixation, angioembolisation (if stable enough)
    • Thoracic: resuscitative thoracotomy (selected), lung tractotomy, hilar clamping, packing
    • Extremity: tourniquet, vascular shunt, fasciotomy, external fixation

Anaesthetic management (damage control / major trauma theatre)

  • Type of anaesthesia: GA with controlled ventilation; regional techniques usually deferred in unstable/coagulopathic trauma
    • Ketamine/etomidate commonly used for induction in shocked patients; avoid large propofol doses
  • Airway device: cuffed ETT (RSI with cervical spine precautions if indicated); SGA generally inappropriate
    • Anticipate difficult airway: blood/vomit, facial trauma, immobilisation, reduced FRC, agitation/intoxication
  • Duration: typically 30–120 min for abbreviated DCS (can be longer if multiple cavities/ongoing haemorrhage)
    • Goal is speed: stop bleeding/contamination then ICU; avoid prolonged definitive surgery
  • How painful: very; high opioid requirements but titrate to haemodynamics; consider ketamine infusion; regional/neuraxial usually contraindicated early
    • Post-op analgesia often via IV opioids +/- ketamine; consider regional blocks later when stable/coagulation corrected
  • Key intra-op priorities: haemorrhage control + balanced transfusion + temperature + calcium + coagulation-guided therapy
    • Early MHP, rapid infuser, blood warmer, active forced-air warming, frequent labs/ABGs/TEG/ROTEM

Definitions and concepts

  • Major trauma: injury/combination of injuries that is life-threatening or life-changing; often defined by ISS >15 (system dependent)
  • Damage control: strategy to prevent death from physiological exhaustion by limiting operative time and prioritising haemorrhage/contamination control
  • Lethal triad / diamond: hypothermia + acidosis + coagulopathy (± hypocalcaemia)
  • Trauma-induced coagulopathy (TIC): early endogenous coagulopathy (shock, tissue injury, endothelial dysfunction) worsened by dilution, hypothermia, acidosis

Initial approach: ED/Resus (team-based)

  • Use structured approach (ATLS-style): A (with C-spine), B, C, D, E with early haemorrhage control
    • Simultaneous actions: call for help, activate trauma team, early MHP if suspected major haemorrhage
  • Catastrophic external haemorrhage: direct pressure, haemostatic dressings, tourniquet, pelvic binder, splintage
  • Airway: early ETT if GCS ≤8, airway compromise, hypoventilation, severe shock, anticipated deterioration; RSI with C-spine precautions
    • Pre-oxygenation may be difficult; consider apnoeic oxygenation and gentle BVM with two-person technique if needed
  • Breathing: treat tension pneumothorax immediately; chest drains for significant pneumothorax/haemothorax; ventilate lung-protectively
  • Circulation: permissive hypotension in uncontrolled haemorrhage (except TBI/pregnancy); early blood products; minimise crystalloids
    • Targets (typical): SBP ~80–90 mmHg until haemorrhage control; if TBI aim SBP ≥100–110 mmHg (age dependent) and avoid hypoxia
  • Disability: assess GCS, pupils, glucose; early analgesia and sedation where appropriate
  • Exposure: full examination, prevent hypothermia (warm room, blankets, forced-air warmer, warmed fluids)

Massive haemorrhage and damage control resuscitation (DCR)

  • Principles of DCR: early haemorrhage control, balanced transfusion, minimise crystalloids, treat coagulopathy early, rewarm, correct calcium
  • Major haemorrhage protocol (MHP): predefined packs (RBC, FFP, platelets) + rapid delivery + clear leadership/communication
    • Balanced ratios often approximating 1:1:1 (RBC:FFP:platelets) until lab/viscoelastic-guided therapy available
  • Tranexamic acid: give early in suspected major haemorrhage (best within 3 h of injury); typical regimen 1 g IV then 1 g over 8 h (local protocols vary)
  • Fibrinogen replacement: cryoprecipitate or fibrinogen concentrate guided by labs/TEG/ROTEM; fibrinogen often first factor to fall
  • Calcium: citrate in transfused blood binds calcium → myocardial depression/coagulopathy; monitor ionised Ca and replace (e.g., calcium chloride via central line)
  • Temperature: aim normothermia; hypothermia worsens coagulopathy and acidosis; use active warming and warmed blood/fluids
  • Acidosis: indicates shock and poor perfusion; treat by haemorrhage control, oxygen delivery, ventilation; bicarbonate rarely primary solution
  • Vasopressors: not a substitute for volume/haemorrhage control; may be used as a bridge in profound vasoplegia after adequate transfusion/bleeding control

Anaesthetic technique: practical conduct in theatre

  • Preparation: brief with surgical/trauma team; confirm plan (DCS vs definitive), anticipated blood loss, access, imaging, ICU bed
  • Monitoring: standard + invasive arterial line early; large-bore IV access; consider central access for rapid infusion/vasoactive drugs; temperature monitoring; urinary catheter if feasible
    • Point-of-care: ABG, lactate, Hb, ionised Ca, glucose; TEG/ROTEM if available
  • Induction: haemodynamically cautious RSI; anticipate precipitous hypotension; have blood running before induction if shocked
    • Drug choices: ketamine or etomidate; rocuronium/suxamethonium as appropriate; consider fentanyl in small aliquots once perfusion improved
    • C-spine: manual in-line stabilisation; avoid hypotension/hypoxia (especially if TBI)
  • Ventilation: avoid hypoxia/hypercapnia; lung-protective strategy; consider permissive hypercapnia only if not contraindicated (e.g., severe TBI)
  • Maintenance: volatile or TIVA; often opioid-sparing with ketamine infusion; depth tailored to physiology and rapid surgical stimulation
  • Haemostasis/coagulation: follow MHP; give TXA; correct fibrinogen/platelets guided by labs/viscoelastic tests; avoid dilutional coagulopathy
  • Documentation/communication: running total of blood products, estimated blood loss, urine output, temperature, key lab values; communicate triggers for pack changes

Special situations

  • Traumatic brain injury (TBI): avoid hypoxia and hypotension; maintain CPP; avoid hyperventilation unless signs of herniation; consider hypertonic saline/mannitol per protocol
    • Analgesia/sedation: prevent coughing/straining; smooth intubation and ventilation; maintain normocapnia
  • Pelvic fracture haemorrhage: binder early; consider preperitoneal packing/ex-fix; angioembolisation if stable enough; large concealed blood loss common
  • Chest trauma: tension pneumothorax, massive haemothorax, cardiac tamponade; consider one-lung issues, pulmonary contusion; cautious PEEP
  • Pregnancy: left uterine displacement, higher aspiration risk, maintain uteroplacental perfusion (avoid hypotension), early obstetric involvement; Rh prophylaxis as indicated
  • Anticoagulants/antiplatelets: identify early; reverse where indicated (e.g., PCC for warfarin; specific DOAC reversal per agent/local policy)

Postoperative care (ICU focus)

  • Most DCS patients require ICU: ongoing haemodynamic support, ventilation, temperature control, coagulation correction, and planned re-look surgery
  • Key goals: normothermia, normal ionised Ca, improving lactate/base deficit, haemostasis, adequate oxygen delivery, avoid secondary brain injury
  • Analgesia/sedation: multimodal; consider ketamine, opioid infusions; regional techniques later when stable and coagulation normal
  • Complications to anticipate: ARDS, AKI, abdominal compartment syndrome, ongoing bleeding, sepsis, thromboembolism, transfusion reactions
You are called to ED for a 25-year-old with polytrauma after an RTC: hypotensive, tachycardic, confused, cold peripheries. Talk through your immediate management.

Structure your answer around team activation, catastrophic haemorrhage control, ABCDE, early blood, and preventing the lethal triad/diamond.

  • Call for help: activate trauma team, senior anaesthetist, ODP, blood bank; activate MHP early if suspected major haemorrhage
  • Catastrophic haemorrhage: direct pressure/haemostatic dressings, tourniquet, pelvic binder, splint long bones
  • Airway: assess; if threatened or GCS ≤8/intubation indicated → RSI with C-spine precautions; prepare suction and difficult airway plan
  • Breathing: high-flow O2; treat tension pneumothorax immediately; chest drains if needed; ventilate to avoid hypoxia
  • Circulation: large-bore IV/IO; send bloods incl. group & save/crossmatch, ABG/lactate, coag; start warmed blood products; minimise crystalloids; consider permissive hypotension unless TBI
  • Give TXA early (within 3 h) per protocol; monitor and replace ionised calcium
  • Prevent hypothermia: warm environment, forced-air warming, warmed fluids/blood
  • Decide destination: CT vs theatre vs IR based on physiology and suspected bleeding source; communicate and document
Define damage control surgery and damage control resuscitation. When would you choose this approach?

Examiners want definitions, rationale (physiological exhaustion), and triggers.

  • Damage control surgery (DCS): abbreviated operation to control haemorrhage and contamination with temporary closure, deferring definitive repair
  • Damage control resuscitation (DCR): resuscitation strategy to prevent/correct coagulopathy, hypothermia, acidosis using early balanced blood products, haemorrhage control, minimal crystalloids, TXA, calcium, warming
  • Choose when: ongoing haemorrhage, profound shock, hypothermia/acidosis/coagulopathy, multiple injuries, anticipated long definitive surgery, limited resources/time
  • Aim: restore physiology first (ICU), then definitive surgery once stabilised (often 24–72 h)
Talk through your anaesthetic plan for an emergency trauma laparotomy for haemorrhage.

Cover preparation, induction, monitoring/access, transfusion/coagulation, temperature, ventilation, and ICU handover.

  • Preparation: brief with surgeons; confirm MHP active; rapid infuser/blood warmer ready; difficult airway kit; vasopressors drawn up; plan for ICU
  • Monitoring/access: arterial line early; 2 large-bore IVs/IO; consider central access; temperature probe; urinary catheter if feasible
  • Induction: haemodynamically cautious RSI (ketamine/etomidate); have blood running; minimise induction dose; treat hypotension promptly
  • Maintenance: volatile/TIVA; ketamine infusion useful; titrate opioids carefully; muscle relaxation to facilitate surgery
  • Resuscitation: balanced transfusion; TXA; frequent ABGs/lactate; viscoelastic-guided products; replace fibrinogen/platelets; maintain ionised Ca
  • Temperature: aggressive warming; warmed fluids/blood; avoid exposure where possible
  • Post-op: ICU transfer intubated; structured handover with totals of products, labs, ongoing concerns, and re-look plan
Explain trauma-induced coagulopathy and how you would manage coagulopathy during major haemorrhage.

Mention early endogenous coagulopathy plus iatrogenic contributors; then a practical, protocolised management plan.

  • Mechanism: shock + tissue injury → endothelial activation, anticoagulant pathways, platelet dysfunction, hyperfibrinolysis; worsened by dilution, hypothermia, acidosis
  • Management: early haemorrhage control + DCR; activate MHP; balanced RBC/FFP/platelets; early TXA; fibrinogen replacement; avoid excessive crystalloids
  • Use labs/TEG/ROTEM to target therapy; repeat frequently
  • Correct contributors: rewarm, correct ionised Ca, optimise perfusion/oxygenation to treat acidosis
What is permissive hypotension? When is it contraindicated?

Define it, give typical targets, and list key contraindications.

  • Definition: deliberately accepting lower-than-normal BP until haemorrhage control to reduce bleeding and dilution from fluids
  • Typical target: SBP ~80–90 mmHg (or palpable radial pulse) in uncontrolled haemorrhage (local protocols vary)
  • Contraindications/relative contraindications: TBI (avoid hypotension), pregnancy (uteroplacental perfusion), prolonged transport time, spinal cord ischaemia concerns
A trauma patient has received multiple units of blood. Why do they become hypocalcaemic and why does it matter? How do you manage it?

This is a common FRCA viva thread during major haemorrhage discussions.

  • Cause: citrate anticoagulant in blood products chelates calcium; risk increased with rapid transfusion, liver dysfunction, hypothermia
  • Why it matters: reduced myocardial contractility, vasodilation, arrhythmias; worsens coagulation and hypotension
  • Management: measure ionised calcium on ABG; replace with calcium chloride (central line) or calcium gluconate (peripheral) per local dosing; recheck frequently
In major trauma, when would you take the patient straight to theatre rather than CT?

Answer in terms of physiology and suspected bleeding source; CT is for those stable enough to benefit from it.

  • Immediate theatre if haemodynamically unstable with suspected surgically correctable haemorrhage (e.g., positive FAST with shock, peritonitis, penetrating torso injury with instability)
  • CT if sufficiently stable to tolerate transfer and scan, and results will change management (e.g., define bleeding source for IR vs surgery)
  • Hybrid approaches: resus in ED + immediate haemorrhage control measures (binder/tourniquet) while deciding; consider IR for pelvic bleeding if stable enough
Describe the phases of damage control surgery and the anaesthetist’s priorities in each phase.

Organise by Phase 0–3 and link to anaesthetic actions.

  • Phase 0 (ED): airway/oxygenation, haemorrhage control measures, activate MHP, TXA, warming, rapid decision-making
  • Phase 1 (OR abbreviated): rapid induction with blood ready, invasive monitoring, balanced transfusion, coagulation/temperature/calcium management, facilitate rapid surgical control
  • Phase 2 (ICU): ongoing correction of coagulopathy/acidosis/hypothermia, ventilatory support, organ support, plan re-look
  • Phase 3 (definitive surgery): optimise physiology, plan analgesia (regional options may open up), anticipate adhesions/bleeding, ensure blood availability
What are the key complications of massive transfusion and how do you mitigate them?

Give a structured list: metabolic, coagulation, temperature, respiratory, immunological, and logistical.

  • Hypothermia → coagulopathy: use active warming and warmed blood/fluids
  • Hypocalcaemia (citrate): monitor ionised Ca and replace
  • Coagulopathy/dilution: balanced transfusion, fibrinogen replacement, platelets, viscoelastic guidance
  • Hyperkalaemia/acid-base disturbances: ABG monitoring, treat as required
  • Transfusion reactions/TRALI/TACO: vigilance, appropriate product use, haemovigilance reporting
  • Hypomagnesaemia and hypoglycaemia/hyperglycaemia: monitor and correct

0 comments