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2025 PACUPrep BCCCP Preparatory Course Hemorrhagic Shock, Massive Transfusion, and Trauma‐Induced Coagulopathy Foundational Principles and Epidemiology of Hemorrhagic Shock and Trauma‐Induced Coagulopathy

Lesson 97, Topic 1

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Foundational Principles and Epidemiology of Hemorrhagic Shock and Trauma‐Induced Coagulopathy

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Hemorrhagic Shock and Trauma-Induced Coagulopathy

Foundational Principles and Epidemiology of Hemorrhagic Shock and Trauma-Induced Coagulopathy

Learning Objective

Understand the incidence, pathophysiology, risk factors, social determinants, and early recognition of hemorrhagic shock and trauma-induced coagulopathy (TIC).

1. Epidemiology and Mortality Impact

Hemorrhagic shock is a leading cause of preventable death in trauma, responsible for 30–40% of fatalities, with most occurring within the first two hours. Trauma-induced coagulopathy (TIC), a critical complication, is present on hospital arrival in up to one-third of major trauma patients and independently predicts poor outcomes.

Early Mortality: 30–40% of trauma fatalities are due to uncontrolled hemorrhage, with exsanguination often occurring within the “golden hour.”
Coagulopathy Burden: TIC is identified on admission in approximately 30% of severely injured patients and is a strong independent predictor of mortality.
Resource Utilization: Massive transfusion (defined as ≥10 units of red blood cells in 24 hours) is required in about 3% of civilian trauma admissions but accounts for a disproportionately large share of blood product utilization and early deaths.

Clinical Pearl: The Impact of Rapid Diagnostics

The implementation of early point-of-care coagulation assessment, such as thromboelastography (TEG) or rotational thromboelastometry (ROTEM), within 30 minutes of hospital arrival has been shown to reduce hemorrhage-related mortality by enabling faster, goal-directed transfusion strategies.

2. Risk Factors and Patient-Level Determinants

The risk and severity of hemorrhagic shock and TIC are influenced by a combination of the injury itself, the patient’s underlying health, pre-existing medications, and physiologic reserve.

Mechanism of Injury

Injury Mechanisms and Associated Bleeding Patterns
Blunt Trauma	Penetrating Trauma
Characterized by diffuse, often occult bleeding (e.g., retroperitoneal, pelvic).	Typically involves focal vascular disruption with a high risk of rapid exsanguination.
Associated with significant tissue injury and shear-induced endothelial activation, promoting early TIC.	May have less systemic tissue damage but more profound initial volume loss.

Chronic Comorbidities & Medications

Liver Disease: Impairs the synthesis of both pro-coagulant and anti-coagulant factors, leading to a fragile and unpredictable hemostatic state.
Antiplatelet/Anticoagulant Therapy: Directly impairs hemostasis. Early identification and consideration of reversal agents or targeted transfusions (e.g., platelets) are critical.

Age and Frailty

Elderly patients possess diminished physiologic reserve and cardiovascular compliance. They tolerate smaller absolute volume losses poorly and are more susceptible to the adverse effects of hypoperfusion.

Clinical Pearl: Guiding Platelet Transfusion

In trauma patients on antiplatelet agents (e.g., aspirin, clopidogrel), using TEG with platelet mapping or other functional platelet assays can guide therapy. It helps determine whether platelet transfusion is likely to be effective or if an alternative agent like desmopressin (DDAVP) might be beneficial to boost endogenous von Willebrand factor release.

3. Social Determinants of Health

Outcomes from hemorrhagic shock are not solely dependent on clinical factors. System-level and societal variables, including geography and public education, play a significant role.

EMS Response Time: Delays in reaching definitive care are detrimental. Studies indicate that each 10-minute increase in the pre-hospital interval can raise mortality by approximately 5% in patients with hemorrhagic shock.
Trauma System Access: Patients treated at designated Level I trauma centers have better outcomes. Bypassing these specialized centers is associated with higher rates of death from exsanguination and coagulopathy.
Bystander Interventions: Community training programs like “Stop the Bleed” empower the public to provide immediate hemorrhage control with tourniquets and hemostatic dressings, effectively bridging the gap until professional help arrives and blunting the progression of shock.

4. Pathophysiology of Hemorrhagic Shock

Acute hypovolemia triggers a cascade of compensatory mechanisms. When these fail, the body transitions to a state of decompensated shock, characterized by anaerobic metabolism, profound acidosis, endothelial injury, and progressive organ dysfunction.

Figure 1: The Pathophysiologic Cascade of Hemorrhagic Shock. Initial blood loss reduces cardiac output, triggering a compensatory sympathetic response to maintain perfusion to vital organs. As shock progresses, this compensation fails, leading to systemic hypoperfusion, lactic acidosis, and end-organ damage.

Initial Compensation: Sympathetic activation (tachycardia, vasoconstriction) preserves cerebral and cardiac perfusion at the expense of splanchnic (gut, liver, kidneys) and peripheral circulation.
Metabolic Derangement: Inadequate oxygen delivery forces cells into anaerobic glycolysis, leading to lactate accumulation and metabolic acidosis. Acidosis directly impairs both thrombin generation and platelet function, worsening bleeding.
Endothelial Injury: Systemic inflammation and ischemia damage the endothelial glycocalyx, leading to increased vascular permeability (“leaky capillaries”), interstitial edema, and microcirculatory collapse, a phenomenon known as “no-reflow.”

Clinical Pearl: Monitoring Resuscitation Adequacy

Serial lactate and base deficit measurements are crucial for guiding resuscitation. A failure to clear lactate by at least 10% per hour is a strong indicator of ongoing, inadequately treated shock and is associated with increased mortality.

5. Mechanisms of Trauma-Induced Coagulopathy (TIC)

Early TIC is a complex biological process, not simply a result of dilution. It is driven by shock-induced endogenous anticoagulation, factor consumption, platelet dysfunction, and excessive clot breakdown (hyperfibrinolysis).

Figure 2: The Lethal Triad of Trauma. This vicious cycle is central to TIC. Hypothermia and acidosis both severely impair platelet function and the enzymatic activity of clotting factors, which worsens coagulopathy. Ongoing bleeding (coagulopathy) leads to further heat loss and worsens shock-induced acidosis.

Protein C Activation: Severe tissue trauma and shock cause upregulation of endothelial thrombomodulin. This complex binds thrombin, leading to the activation of protein C, which in turn inactivates key clotting factors Va and VIIIa, creating an anticoagulated state.
Dilution and Consumption: Massive hemorrhage consumes clotting factors and platelets. Resuscitation with crystalloid or colloid fluids further dilutes the remaining factors.
Hyperfibrinolysis: Major injury triggers a surge in tissue plasminogen activator (tPA) release from the endothelium, leading to premature breakdown of any clots that do form.

Clinical Pearl: The Role of Tranexamic Acid (TXA)

Tranexamic acid (TXA) is an antifibrinolytic agent that works by blocking lysine-binding sites on plasminogen, preventing it from binding to and degrading fibrin clots. Landmark trials have shown that administering TXA within 3 hours of injury significantly reduces mortality from bleeding.

6. Clinical Presentation and Early Signs

Early in hemorrhagic shock, vital signs and physical exam findings can be deceptively normal. A high index of suspicion and a multimodal assessment combining clinical signs with point-of-care labs and ultrasound are essential for timely recognition.

Vital Sign Changes

Early Signs: Tachycardia and a narrowed pulse pressure (the difference between systolic and diastolic pressure) are often the first indicators.
Late Sign: Hypotension is typically a late and ominous sign, often not appearing until more than 30% of blood volume has been lost.
Mental Status: Reflects cerebral hypoperfusion and can progress from anxiety and agitation to confusion and ultimately lethargy or coma.

Physical Exam

Key signs of hypoperfusion include pallor, cool and clammy skin, and a delayed capillary refill time (>2-3 seconds).

Bedside Ultrasound (eFAST)

The eFAST (Extended Focused Assessment with Sonography for Trauma) exam can rapidly detect free fluid (presumed to be blood) in the peritoneum, thorax, and pericardium within minutes of arrival.

Clinical Scenario: The Unstable Patient with a Negative eFAST

An unstable patient with blunt abdominal trauma and a negative eFAST exam presents a diagnostic challenge. A negative eFAST does not exclude major hemorrhage, particularly in the retroperitoneum or from pelvic fractures. In this situation, the clinician must maintain a high suspicion for these injuries and proceed rapidly to pelvic binder placement, CT scanning, or direct operative exploration based on the degree of instability.

7. Summary and Clinical Pearls

Effective management of hemorrhagic shock and TIC hinges on rapid recognition, early hemorrhage control, and protocolized resuscitation strategies.

Key Takeaways

Combine rapid clinical assessment, vital sign trends (especially tachycardia and pulse pressure), point-of-care lactate/base-deficit, and eFAST for the earliest possible recognition of shock and TIC.
Pre-hospital hemorrhage control with tourniquets, hemostatic dressings, and permissive hypotension (targeting a palpable radial pulse or SBP of 80-90 mmHg) is crucial to blunting shock progression before arrival.
The cornerstones of modern damage control resuscitation are balanced component transfusion (approximating a 1:1:1 ratio of RBCs:FFP:platelets) and early administration of TXA.

Ongoing Controversies and Research

Several areas in trauma resuscitation remain subjects of active debate and research. These include defining optimal blood pressure targets for permissive hypotension in different patient populations (e.g., blunt vs. penetrating trauma, presence of traumatic brain injury), the role of crystalloid versus colloid fluids in initial resuscitation, and refining the specific clinical and laboratory thresholds for activating massive transfusion protocols.

References

Cotton BA, Harvin JA, Kostousouv V, et al. Trauma-Induced Coagulopathy: An Institution’s 35,000-Foot View. Anesth Analg. 2014;118(4):813-821.
Brohi K, Singh J, Heron M, Coats T. Early Coagulopathy Predicts Mortality in Trauma. J Trauma. 2003;55(1):39-44.
Holcomb JB, Jenkins D, Rhee P, et al. Impact of Hemorrhage on Trauma Outcome. J Trauma. 2006;60(6 Suppl):S3-S11.
Cap J, Kubisz P. Trauma-Induced Coagulopathy: Overview of an Emerging Medical Problem. Med Sci Monit. 2021;27:e929957.
Holcomb JB, Moore EE, et al. Prevalence and Association with Mortality Persist 20 Years After Landmark Study of Early Trauma-Induced Coagulopathy. Shock. 2024;61(3):e1-e7.
Cannon JW, Khan MA, Raja AS, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2017;82(3):605–617.
Mock CN, Jurkovich GJ, nii-Amon-Kotei D, Arreola-Risa C, Maier RV. Trauma mortality patterns in three nations at different economic levels: implications for global trauma system development. J Trauma. 1998;44(5):804–812.
Hayter MA, Pavenski K, Baker J. Massive transfusion in the trauma patient: Continuing Professional Development. Can J Anesth. 2012;59:1130–1145.
Schöchl H, Schmitt FC, Maegele M. Pathophysiology of Trauma-Induced Coagulopathy. Hamostaseologie. 2024;44(1):31-39.
Simmons JW, Powell MF. Acute traumatic coagulopathy: pathophysiology and resuscitation. Br J Anaesth. 2016;117(suppl_3):iii31-iii43.
Kawasaki T, et al. Pathophysiology of Trauma-Induced Coagulopathy and Its Management. J Intensive Care. 2016;4:30.
Pavoni V, Gianesello L, et al. Trauma-Induced Coagulopathy Management. AboutOpen. 2022.

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