Advanced Trauma Life Support (ATLS): Major Haemorrhage Protocol & Anatomical Management
Key Takeaway
The Major Haemorrhage Protocol (MHP) within ATLS is a systematic approach to rapidly identify and manage severe trauma bleeding. It targets the lethal triad of coagulopathy, acidosis, and hypothermia, ensuring early intervention, haemostatic resuscitation, and definitive control across five anatomical compartments for improved patient survival.
A 32-year-old male is brought to the Major Trauma Centre following a high-speed motorcycle accident. He is tachycardic (HR 130 bpm) and hypotensive (SBP 85 mmHg). A pelvic binder has been applied. His FAST scan is negative, but a plain radiograph reveals an unstable pelvic ring injury. What are the key components of the "Major Haemorrhage Protocol" (MHP) you would initiate, and what is your priority in terms of surgical stabilization?
Candidate: I would immediately activate the MHP. I'd give tranexamic acid, warm the patient to prevent the 'lethal triad', and start a balanced transfusion (1:1:1 ratio). Since he has an unstable pelvic fracture, I need to stabilize the pelvis with an external fixator to reduce the volume. If he remains hypotensive, I would consider interventional radiology for angioembolization or possibly REBOA if the haemorrhage is non-compressible.
Candidates often focus solely on the pelvic fracture while ignoring the systemic physiological state. They fail to mention the "Lethal Triad" (acidosis, hypothermia, coagulopathy), omit the importance of calcium supplementation to counter citrate toxicity, or suggest aggressive fluid resuscitation, which actually worsens coagulopathy (dilutional effect).
A structured response is required: 1. Resuscitation: Activate MTP, permissive hypotension (target SBP 80-90 mmHg), TXA administration, and aggressive warming. 2. Correction of Physiology: Address hypocalcaemia and acid-base status. 3. Mechanical Control: Emphasize that the pelvic binder is a temporizing measure; urgent external fixation reduces the pelvic volume and "pelvic haematoma space," acting as a biological tamponade. 4. Definitive/Adjunctive: If hemodynamically unstable despite stabilization, advocate for angioembolization (for arterial sources) or REBOA (as a bridge to definitive control). Mention that CT scan is for stable patients; unstable patients go to the OR/Angio-suite.
The patient has been stabilized temporarily. You notice that despite a 1:1:1 transfusion ratio and surgical fixation, the patient continues to ooze from all raw surfaces, and your rotational thromboelastometry (ROTEM) shows a prolonged clotting time. How do you manage this?
Candidate: This indicates Trauma-Induced Coagulopathy (TIC). I would review the temperature and pH, ensure we are not over-resuscitating with crystalloids, and use the ROTEM to guide targeted therapy—likely fibrinogen concentrate or cryoprecipitate if fibrinogen levels are low, and potentially prothrombin complex concentrate (PCC) if factor levels are depleted.
Candidates often suggest "more blood" blindly or request FFP without justifying the need for specific factor replacement. They frequently overlook the physical state of the patient (hypothermia and acidosis) as the primary drivers of this dysfunction, focusing only on the laboratory result.
State that TIC is multifactorial (dilution, consumption, acidosis, hypothermia). The "Gold Standard" approach is viscoelastic-guided resuscitation. Address the physiological drivers first: "Warm the patient, correct the acidosis." Then, treat the specific ROTEM deficiency: if the A5/MCF is low, replace fibrinogen (the first factor to fall); if the CT (clotting time) is prolonged, consider PCC; and ensure TXA has been given to block hyperfibrinolysis.
