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Lethal Triad of Trauma

Lethal Triad of Trauma: Pathogenesis and clinical findings Severe tissue injury & polytrauma Traumatic brain injury Major hemorrhage & tissue hypoperfusion Severe burns (>20% total body surface) Unbalanced resuscitation (uneven ratios of blood products & fluids) Cerebral metabolic dysfunction leads to circulatory acidification Tissue hypoperfusion favors anaerobic metabolism (energy production in absence of oxygen) & lactic acidosis Aggressive crystalloid resuscitation causes non-anion gap metabolic acidosis Disseminated intravascular coagulation (DIC) causes tissue hypoxia & lactic acidosis Resuscitation hemodilutes (↓ concentration of blood components) clotting factors Clotting factors, fibrinogen & platelets are consumed Injury activates protein C (anticoagulant) & hyperfibrinolysis (↑ breakdown of blood clots) Histone-mediated thrombin production bypasses normal coagulation checkpoints Tissue factor leaks through injured blood- brain barrier into systemic circulation Cold IV fluids & blood products ↓ body temperature Environmental exposure & open body cavities predispose to inadequate thermoregulation Evaporation leads to body water loss Inadequate oxygen delivery leads to ↓ metabolic heat production Injury leads to peripheral vasoconstriction & ↓ shivering capacity Trauma directly injures the hypothalamus Authors: Steven Bigam Reviewers: Catherine R Jarvis Amanda Roze des Ordons* *MD at time of publication **See corresponding Calgary Guide slide(s) Acidosis (pH<7.2) Hypothermia (<35°C) Coagulopathy Lethal triad of trauma Baroreceptors stimulate the medulla & activate the sympathetic nervous system ↓ Mean arterial pressure (MAP) causes cerebral hypoperfusion & dysfunction Massive transfusion protocol** is activated Perfusion cannot be restored & causes refractory shock Clotting factors, fibrinogen & platelets are consumed Tachycardia (heart rate >100) Tachypnea (resp rate >25) Confusion Lethargy Citrate in stored blood binds free calcium Hypotension that is not restored with hemodynamic support ↓ Fibrinogen ↓ Platelets ↑ Demand on respiratory muscles causes fatigue ↓ Respiratory muscle tone & brainstem depression cause loss of respiratory drive Hypocalcemia (ionized calcium <0.90mmol/L)** ↓ MAP causes renal hypoperfusion ↓ Fibrin formation causes microvascular thrombosis Severe hyperkalemia (>6.5mmol/L)** Acute kidney injury** DIC** Respiratory failure ↓ Ventilation causes hypoxia (↓ oxygen delivery to tissues) & hypercarbia (↑ carbon dioxide in tissues) Heart contractility is impaired & can ↓ Intracellular potassium causes impaired electrical signaling in the heart lead to pulseless electrical activity Ventricular fibrillation Cell death causes cytokine- mediated organ destruction ↑ International normalized ratio (INR) & partial thromboplastin time (PTT) ↑ Norepinephrine vasoconstricts & ↓ bloodflow to extremities Traumatic cardiac arrest Multi-organ failure Cool, clammy, mottled (red-blue blotches) skin Absent myocardial contractions halts systemic circulation ↓ Oxygen supply & inflammation cause mitochondrial toxicity & energy failure Death Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Aug 30, 2026 on www.thecalgaryguide.com