Trauma: initial management and damage control

Why examiners ask this

Trauma compresses every attribute into one stem: organization (the ABCDE sequence delivered without fumbling), judgment (full stomach, unstable cervical spine and a falling pressure at the same time), and adaptability when the chest tube drains 1.5 L. It lets the examiner move seamlessly from the airway to hemorrhagic shock to the coagulopathy of trauma, and then ask why the surgeon wants to pack the abdomen and leave.

The 60-second answer

Decision points and the "why"

• Induction drug and dose — ketamine 0.5–1 mg/kg or etomidate 0.2 mg/kg, because the hypovolemic patient has a contracted volume of distribution and a full dose of propofol stops the heart. I halve what I would normally give and have a pressor and blood running before I push.
• Cervical spine — every blunt trauma patient has an unstable neck until cleared; manual in-line stabilization with the front of the collar removed, and a video laryngoscope because it needs less neck extension. I accept a slightly worse view for a stable spine.
• Permissive hypotension — a systolic of 80–90 mmHg limits clot disruption and dilution before surgical hemostasis; I abandon it with brain or spinal cord injury, holding a MAP of at least 80 mmHg in severe brain injury,¹ because even one episode of hypotension worsens neurologic outcome, and in the elderly, in whom I target higher.
• Blood, not crystalloid — crystalloid dilutes clotting factors, cools the patient and worsens acidosis. I activate the massive transfusion protocol early and start blood products rather than crystalloid,² give plasma, platelets and red cells in a 1:1:1 ratio, and move to viscoelastic testing as soon as it is available to direct fibrinogen and platelets.
• Tranexamic acid — 1 g over 10 minutes then 1 g over 8 hours, started within 3 hours of injury;¹ in CRASH-2, starting 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 to keep it in the normal range, in practice about 1 g every few units.
• Damage-control surgery — in hemorrhagic shock with ongoing bleeding and coagulopathy, or with hypothermia, acidosis, an inaccessible injury or a long procedure ahead,¹ the surgeon packs, controls contamination and stops. I support the decision because a definitive repair in a dying patient is an autopsy finding. I take the patient to the ICU to rewarm, correct and return in 24–48 hours.

The complication they will inject

The surgeon opens the abdomen, the pressure falls to 60 systolic and the end-tidal CO2 drops from 32 to 18. I say what I am thinking out loud: this is a sudden loss of venous return from decompression of the abdominal tamponade, massive hemorrhage, or an air embolism through an open hepatic vein. I ask the surgeon to pack and compress the aorta, give blood through the rapid infuser with calcium, and push epinephrine in 10–50 mcg boluses while the volume catches up. I check the chest for a tension pneumothorax that positive pressure has now created. If the end-tidal CO2 keeps falling I ask for an echo to look at 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 get out to the ICU.

Pitfalls that cost points

• Starting with "I would intubate" before confirming that the airway is the problem and the chest is not.
• Giving a full induction dose because "the patient is young."
• Resuscitating with 3 L of crystalloid and then being asked why the patient is coagulopathic and cold.
• Chasing a normal blood pressure before the surgeon has clamped anything.
• Forgetting the lethal triad: hypothermia, acidosis and coagulopathy, and what each does to the others.

Rapid-why

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

Links

• Massive hemorrhage and transfusion, Perioperative hypothermia and coagulopathy, Airway management with cervical spine injury (coming), Traumatic brain injury (coming), 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)