Trauma remains a leading cause of potentially preventable death in modern warfare. While advances in haemorrhage control, resuscitation strategies, and evacuation platforms have significantly improved survival, a substantial proportion of casualties still deteriorate due to physiological failure rather than anatomical injury. Central to this failure is the Trauma Triad of Death – hypothermia, metabolic acidosis, and trauma-induced coagulopathy, a self-reinforcing cycle strongly associated with increased morbidity and mortality (Remondelli et al., 2025).
In contemporary and future operating environments – defined by dispersed forces, contested evacuation, and prolonged field care (PFC) – management of the trauma triad is no longer confined to Role 2 or Role 3 facilities. This article describes how prevention of the triad is a core Role 1 responsibility, embedded within correct execution of Tactical Combat Casualty Care (TCCC) and the MARCH algorithm (Massive Haemorrhage, Airway, Respiration, Circulation, and Hypothermia/Head injury).
The Trauma Triad of Death: A Contemporary Understanding
Modern trauma research demonstrates that hypothermia, acidosis, and coagulopathy develop early and concurrently, often within minutes of injury, particularly in the presence of uncontrolled haemorrhage and shock (Moore et al., 2021). These processes do not occur in isolation; each worsens the others, accelerating physiological collapse.
Crucially, the trauma triad is not something treated after MARCH, it is prevented through the disciplined application of MARCH from the first intervention.
Hypothermia
Trauma-related hypothermia is frequently shock-driven and iatrogenic (meaning accidental hypothermia because of interventions such as medication administration including but not limited to anaesthetics, beta-blockers and clonidine as well as cold fluid administration), rather than purely environmental. Haemorrhage reduces metabolic heat production, while exposure during assessment, wet clothing, wind, and unwarmed fluids accelerate heat loss. Even mild hypothermia impairs platelet function and coagulation enzyme activity, increasing bleeding and mortality risk (Bennett et al., 2020).
Prevention and Treatment (MARCH / TCCC)
Although listed last in the MARCH sequence, hypothermia prevention must occur throughout all phases of care:
M (Massive Haemorrhage): Early haemorrhage control limits shock-related heat loss.
A/R (Airway / Respiration): Rapid, exposure-minimising airway and respiratory interventions.
C (Circulation): Avoidance of excessive crystalloid. Use of warmed blood products where available.
H (Hypothermia / Head Injury): Immediate insulation from ground and wind, hypothermia prevention kits or thermal blankets, minimised exposure, and active warming where possible.
TCCC doctrine identifies hypothermia prevention as life-saving treatment, not comfort care, and mandates early intervention in all climates (Committee on Tactical Combat Casualty Care, 2024).
Metabolic Acidosis
Metabolic acidosis results from inadequate tissue perfusion and oxygen delivery, leading to anaerobic metabolism and lactate accumulation. Persistent acidosis reduces myocardial contractility, diminishes catecholamine responsiveness, and directly impairs coagulation factor activity (Moore et al., 2021). Acidosis is therefore a marker of unresolved shock, not a primary biochemical disorder.
Simply put, when the body doesn’t receive enough blood flow and oxygen, its cells are forced to produce energy in an inefficient way. This causes acids to build up in the bloodstream. If this acidic state continues, it weakens the heart’s ability to pump, makes the body’s stress responses less effective, and interferes with normal blood clotting.
As a result of this, acidosis should be seen as a warning sign that shock or poor circulation has not yet been fixed, rather than a problem on its own.
Prevention and Treatment (MARCH / TCCC)
Preventing acidosis is about fixing blood flow and oxygen delivery to the body, not about trying to “neutralise” the acid with chemicals:
M (Massive Haemorrhage): Tourniquets, haemostatic dressings, and pelvic stabilisation preserve circulating volume.
A/R (Airway / Respiration): Effective airway management and treatment of thoracic injury optimise oxygen delivery.
C (Circulation): Permissive hypotension (where appropriate), avoidance of excessive crystalloid, and early use of blood or blood products.
Pharmacological buffering has no Role 1 application without correction of perfusion deficits (Remondelli et al., 2025).
Trauma-Induced Coagulopathy
Trauma-induced coagulopathy (TIC) is the body’s early reaction to serious injury, where the normal ability of the blood to clot is disrupted. It is triggered by damage to tissues, poor blood flow, injury to blood vessels, and problems with the body’s system for controlling bleeding.
When the body also becomes cold or too acidic, clotting works even less effectively, which increases bleeding and makes shock worse (Moore et al., 2021).
Prevention and Treatment (MARCH / TCCC)
Prevention of TIC begins at the point of injury:
M (Massive Haemorrhage): Immediate haemorrhage control prevents clot consumption.
C (Circulation): Damage Control Resuscitation principles. Minimal crystalloid, early blood or whole blood, balanced component therapy where available.
C/H (Circulation / Hypothermia): Aggressive hypothermia prevention preserves enzymatic clotting function.
C (Circulation): Early administration of tranexamic acid (TXA) within guideline timeframes.
These interventions directly target the physiological drivers of TIC and are achievable, at least in part, even in austere Role 1 environments (Committee on Tactical Combat Casualty Care, 2024; Remondelli et al., 2025).
Teaching Aid: MARCH and the Trauma Triad of Death (Role 1 Quick Reference)
Key Principle: The trauma triad is not treated later; it is prevented through disciplined MARCH execution.
M – Massive Haemorrhage: Stops the driver of shock, limits acidosis, preserves clotting, reduces heat loss.
A – Airway: Maintains oxygen delivery, preventing hypoxic acidosis.
R – Respiration: Corrects hypoxia, supporting cardiac and coagulation function.
C – Circulation: Preserves physiology through permissive hypotension, blood-based resuscitation, and TXA.
H – Hypothermia: Continuous insulation and warming prevent clotting failure and physiological decline.
Role 1 Vignette: Preventing the Triad Forward
A dismounted infantry patrol sustains an IED strike during limited visibility operations. One soldier presents with a traumatic lower-limb amputation and suspected pelvic injury. Enemy activity delays evacuation.
Role 1 Actions: A tourniquet is applied immediately, followed by pelvic stabilisation and haemostatic dressings. Recognising early shock, the team avoids unnecessary exposure, deploys a hypothermia prevention kit, and insulates the casualty from the ground.
Crystalloid use is avoided. Permissive hypotension is maintained while monitoring mental status and pulse quality. Active warming continues throughout.
Outcome: When evacuation becomes available hours later, the casualty arrives normothermic, with haemorrhage controlled and shock partially mitigated. Demonstrating how Role 1 prevention of the trauma triad directly influences survivability.
Key Lesson: Role 1 clinicians are not passive stabilisers but active preventers of physiological collapse. Early, disciplined interventions can halt progression into the full trauma triad long before surgical care is available.
Prolonged Field Care (PFC) Implications
In PFC scenarios, early interruption of the trauma triad may be temporary. Hypothermia, acidosis, and coagulopathy can recur if warming, perfusion, and haemostasis are not sustained (Remondelli et al., 2025). This reinforces the need for ongoing reassessment and sustained physiological support at Role 1 and Role 2.
Conclusion
The trauma triad of death remains a dominant mechanism of battlefield mortality. Hypothermia, acidosis, and coagulopathy are early, interdependent threats, best prevented (not reacted to) through disciplined application of TCCC and the MARCH algorithm.
In future conflicts characterised by delayed evacuation and prolonged care, the ability of Role 1 teams to recognise and prevent the trauma triad will remain a decisive determinant of combat survivability.
The omission of the “trauma diamond of death” is particularly noticeable. Current literature increasingly recognises hypocalcaemia as a critical fourth factor, especially in the context of massive transfusion and prolonged care. Failing to address this risks presenting an incomplete picture of modern trauma physiology and resuscitation priorities.
Further, the article simplifies the Role 1 contribution by implying that prevention of the triad is sufficient. In reality, under dispersed, contested, and extended evacuation timelines, Role 1 elements are increasingly required to manage ongoing physiological deterioration over time. This introduces complex considerations—logistics, access to blood products, rewarming capability, and monitoring—that are not explored.
Ultimately, while this is a useful entry-level overview, it does little to progress the professional discourse toward the realities of prolonged care and LSCO.
Recent literature (e.g. Remondelli et al., 2025) already positions trauma care in large-scale combat operations as a continuum—spanning prehospital, en route, and prolonged phases. Within that, Prolonged Casualty Care (PCC) is not a niche concept but a central requirement driven by contested evacuation, dispersion, and operational friction.
In that context, Role 1 is not simply preventing the triad—it is increasingly responsible for managing evolving physiology over extended periods, often with constrained resources. That has implications well beyond MARCH:
calcium management in transfusion
sustained warming capability
monitoring and reassessment
logistical endurance of treatment teams
These are not edge cases—they are foreseeable conditions in LSCO.
There is also value in being precise with language. The shift from PFC to PCC reflects an understanding that prolonged care is not confined to “the field,” but extends across joint environments, including maritime settings. That distinction matters as we think about how health support integrates across the force.
None of this invalidates the trauma triad—it remains foundational. But if we stop there, we risk preparing for a version of casualty care that assumes conditions we may not have.
The point on the trauma diamond of death fair. The trauma diamond is physiologically valid and increasingly relevant in practice but the evidence hasn’t yet displaced the triad as the core predictive model. Expanding into that space would definitely help bridge foundational knowledge with current trauma thinking.
I also agree that the Role 1 reality is shifting, especially in dispersed and prolonged care environments. As junior medics, understanding that we may need to manage deterioration over time and not just initial stabilisation is an important mindset shift.
Balancing simplicity with evolving practice is always difficult, but discussions like this help connect the fundamentals to the realities we’re likely to face.