Trauma: initial management and damage control
Stem
A 34-year-old man, 80 kg, is brought straight to the operating room 50 minutes after a high-speed motorcycle crash. He is in a cervical collar, anxious but answering questions, with blood pressure 84/50 and heart rate 132. The FAST exam shows free fluid in the abdomen, and breath sounds are equal. He ate a large meal two hours before the crash. Two 16-gauge IVs are in place.
Question
How will you secure his airway and resuscitate him for the laparotomy?
Ideal answer
HeadlineHemorrhagic shock, full stomach, uncleared neck: primary survey in order; before I touch the airway, massive transfusion activated, warmed blood running.
- Manual in-line stabilization, collar front off, video laryngoscope: RSI with succinylcholine or rocuronium; reduced-dose ketamine, as induction will unmask the shock.
- Breathing: look for tension pneumothorax and flail chest, before and after positive pressure, even with equal breath sounds, because ventilation can turn a simple pneumothorax into tension.
- Circulation: 1:1:1 red cells, plasma, platelets, not crystalloid, with tranexamic acid because he is within 3 hours, and calcium.
- Systolic 80–90 mmHg until the bleeding is controlled;1 with a brain injury, cerebral perfusion instead. Disability and exposure follow; hypothermia prevention from the first minute.
- Support abbreviating the operation when the triad appears, because hypothermia, acidosis and coagulopathy are the enemy.
Watch for: arterial line, end-tidal CO2, temperature, serial gases.
Breaking down the answer
- Induction drug and dose — ketamine 0.5–1 mg/kg or etomidate 0.2 mg/kg, because hypovolemia contracts the volume of distribution and full-dose propofol stops the heart. I halve my usual dose, pressor and blood running before I push.
- Cervical spine — every blunt trauma patient has an unstable neck until cleared; the video laryngoscope needs less neck extension. I accept a slightly worse view for a stable spine.
- Permissive hypotension — limits clot disruption and dilution before surgical hemostasis. Changes if: brain or spinal cord injury, MAP at least 80 mmHg in severe brain injury,1 because one hypotensive episode worsens neurologic outcome; the elderly, in whom I target higher.
- Blood, not crystalloid — crystalloid dilutes clotting factors, cools the patient and worsens acidosis. Early protocol activation with blood products,2 then viscoelastic testing as soon as available to direct fibrinogen and platelets.
- Tranexamic acid, never late — in CRASH-2, starting it after 3 hours increased death from bleeding.3
- Calcium — citrate in every unit chelates ionized calcium, and low calcium on admission is associated with increased mortality;1 I check ionized calcium every 30 minutes and give calcium chloride, in practice about 1 g every few units.
- Damage-control surgery — shock with ongoing bleeding and coagulopathy, or hypothermia, acidosis, an inaccessible injury or a long procedure ahead,1 the surgeon packs, controls contamination and stops; definitive repair in a dying patient is an autopsy finding. ICU, rewarm, correct, return in 24–48 hours.
Follow-up question
The surgeon opens the abdomen, the pressure falls to 60 systolic and the end-tidal CO2 drops from 32 to 18.
What are you thinking, and what do you do?
Follow-up answer
HeadlineA sudden loss of venous return: decompressed abdominal tamponade, massive hemorrhage, or air embolism through an open hepatic vein. I say it out loud.
The surgeon packs and compresses the aorta; blood goes through the rapid infuser with calcium, and epinephrine in 10–50 mcg boluses while volume catches up. I check the chest for a tension pneumothorax that positive pressure has now created; if the end-tidal CO2 keeps falling, an echo for right-ventricular filling and air. I tell the surgeon the numbers that mean we are losing: a temperature of 34 °C, a base deficit of 12 and oozing from every surface. That is the moment to abbreviate, pack, and go to the ICU.
Pitfalls that cost points
- Chasing a normal blood pressure before the surgeon has clamped anything.
- Resuscitating with 3 L of crystalloid and then being asked why the patient is coagulopathic and cold.
Rapid-fire
Q: Why does hypothermia cause coagulopathy? A: Enzyme kinetics of the clotting cascade and platelet function fall with temperature, about 10% of factor activity per degree,1 and the laboratory does not see it because the sample is warmed to 37 °C.
Q: Why not succinylcholine in a burn or a crush injury? A: In the first 24 hours it is safe; after the acute phase, upregulated extrajunctional receptors release enough potassium to arrest the heart, with the risk peaking at 7–10 days.4
Q: Why is ketamine acceptable with a head injury? A: In a ventilated patient with controlled CO2 the intracranial pressure effect is small, and its preservation of blood pressure protects cerebral perfusion better than the hypotension of other agents.
Q: What is the acute coagulopathy of trauma? A: Tissue injury and shock activate protein C and fibrinolysis within minutes, before any dilution; that is why early plasma and tranexamic acid matter.
Numbers to know
| Item | Value |
|---|---|
| Permissive systolic target | 80–90 mmHg (MAP 50–60); MAP ≥ 80 in severe brain injury1 |
| Tranexamic acid | 1 g over 10 min, then 1 g over 8 h, within 3 h of injury1 |
| Product ratio | 1:1:1 plasma : platelets : red cells; ACS TQIP accepts plasma:RBC 1:1 to 1:22 |
| Calcium | Keep ionized Ca 1.1–1.3 mmol/L; calcium chloride preferred1 |
| Damage-control triggers | Shock with ongoing bleeding, coagulopathy, hypothermia, acidosis, inaccessible injury1 |
| Succinylcholine after burn or crush | Avoid beyond 24 h; risk peaks at 7–10 days4 |
Links
- Massive hemorrhage and transfusion, Perioperative hypothermia and coagulopathy, Airway management with cervical spine injury, Traumatic brain injury, Pneumothorax and tension pneumothorax
- Atlas: Volume status, IVC and fluid responsiveness; Lung ultrasound: pleura, A/B-lines, effusion, pneumothorax
- ATLS (American College of Surgeons); ASA practice guidelines for perioperative blood management; European trauma bleeding guideline (2023)
Sources
- 1.The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition · European multidisciplinary task force (Crit Care), 2023 · pmc.ncbi.nlm.nih.gov
- 2.ACS TQIP Massive Transfusion in Trauma Guidelines · American College of Surgeons, 2014 · ww2.facs.org
- 3.The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial · The Lancet, 2011 · researchonline.lshtm.ac.uk
- 4.QUELICIN (succinylcholine chloride) injection prescribing information · FDA / DailyMed · dailymed.nlm.nih.gov
Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.