Halloween may have come and gone, but for trauma patients, some true horrors linger year-round. Still lurking in the shadows are silent killers—hypothermia, acidosis, and coagulopathy—the dreaded ‘Trauma Triad of Death.' Just when things seem like they couldn't get any worse, hypocalcemia and hypotension creep in, presenting their own sinister twist. In this post, we’ll delve into these hidden terrors that haunt trauma patients and uncover how we can break the curse of poor outcomes.
The Trauma Triad
The Trauma Triad is comprised of three interplaying clinical phenomena: acidosis, hypothermia, and coagulopathy. The concept of the Trauma Triad has been around since the 1980s. It was first dubbed the “bloody vicious cycle” by the American Trauma Society and was correlated with increased hemorrhage and death. Today, increased mortality rates, higher transfusion requirements, and lengthened ICU stays are recognized as proximate effects of the Trauma Triad. However, as trauma research continues, other factors such as hypocalcemia and hypotension have been identified as contributors to poor outcomes.
Acidosis
Existing literature demonstrates mortality rates up to three times higher in trauma patients presenting with extreme acidosis (pH <7.0) compared to patients with mild acidosis or normal pH. Acidosis can worsen coagulopathy and hypothermia, and vice versa. Preventing or minimizing acidosis relies on restoration of tissue perfusion, ideally via volume replacement with whole blood or packed red blood cells.
In trauma patients, acidosis (pH < 7.35) is usually caused by lactic acid. Hemorrhagic shock causes shunting of the remaining blood volume to vital organs like the heart, lungs, and brain. While necessary to keep the patient alive, shunting deprives the peripheral tissues and end-organs of perfusion and thereby starves those cells of oxygen. In the absence of oxygen, the cells resort to anaerobic metabolism which produces lactic acid as a byproduct. Lactic acid collects in the blood stream leading to metabolic acidosis. If all of that sounded like nonsense, you can read more about it in my ABG blog.
Administration of crystalloid solution can exacerbate acidosis for two main reasons. Both 0.9% normal saline (NSS) and lactated ringers (LR) have a lower pH than human blood: around 5.5 and 6.5, respectively. In large volumes, these solutions will lower blood pH. Beyond their direct contribution to acidosis, crystalloids will increase overall circulating volume but at the expense of diluting important blood components such as hemoglobin. This reduces the patient’s already-compromised oxygen carrying capacity, further starving cells of vital oxygen.
Hypothermia
Hypothermia, defined as core temperature less than 35oC (95oF) has been identified in up to 2/3 of trauma patients upon arrival to the emergency department. Hypothermia is classified by severity as mild, moderate, or severe, with mortality and other complications increasing as core temperature decreases. In addition to being individually associated with increased mortality, larger blood transfusion requirements, and longer ICU stays, hypothermia also contributes to the severity of the other Triad components.
Decreased body temperature causes a leftward shift on the oxyhemoglobin dissociation curve, which means that hemoglobin-bound oxygen molecules are less likely to offload at the tissue level. This worsens tissue ischemia and acidosis. Additionally, many vital enzymatic reactions are hindered in (relatively) cold environments; without these reactions, cellular metabolism and clotting mechanisms cannot function normally.
Hypothermia arises from many sources in trauma patients. In hypovolemic states, the body begins to lose its intrinsic ability to regulate temperature; therefore, the ambient air temperature will be contributory, even on a warm summer day. Increasing cabin temperatures in your aircraft or ambulance might be uncomfortable for you, but important to your patient’s survival. Additional heat loss occurs through evaporation of water, so ensuring wet clothing is not just cut away, but completely removed from underneath the patient can help limit heat loss. Utilize warm fluids to prevent iatrogenic cooling and consider placing hot packs around the patient. Finally, cover the patient with multiple warm blankets and expose only one portion of the body at a time during physical exam.
Coagulopathy
Trauma patients incur distinct coagulation abnormalities ranging from uncontrolled hemorrhage to thrombotic conditions collectively known as trauma-induced coagulopathy (TIC). While the underlying pathophysiologies are complex and not fully understood, TIC is recognized as a separate condition from disseminated intravascular coagulopathy and is thought to be directly related to vascular and tissue trauma, shock physiology, and inflammatory processes. Acidosis and hypothermia can intensify coagulopathy as activation of the clotting cascade is stalled in acidotic environments and cold temperatures prevent key metabolic processes within the cascade from occurring normally.
Coagulopathy is identified through lab work in the emergency department and is correlated in current literature with significantly worse patient outcomes. Current literature suggests that patients with INR > 1.2 (normal value is between 0.8 and 1.2) upon ED arrival incur mortality rates of up to 3-5x that of patients without coagulopathy. In the prehospital environment, prudent blood administration and minimizing additive causes may help mitigate or lessen the development of coagulopathy.
The Trauma Diamond - Hypocalcemia
In more recent years, the role of hypocalcemia (ionized calcium level of <1.0mmol/L) in poor trauma outcomes has been recognized, morphing the Trauma Triad into the Trauma Diamond. Causes of hypocalcemia in patients with severe traumatic injuries are believed to be both iatrogenic and intrinsic. Blood products contain a preservative known as citrate, which binds calcium ions and renders them unusable to the cells. Moreover, tissue ischemia secondary to hemorrhagic shock and subsequent reperfusion is theorized to cause a cellular influx of calcium ions, reducing serum calcium availability; although the exact mechanism is not fully understood, hypocalcemia has been identified in patients PRIOR to blood product administration, indicating the presence of a pathophysiological cause.
Calcium plays a key role in many physiologic functions, including maintenance of vascular tone, cardiac contractility, and clot activation/durability. Hypocalcemia has been demonstrated to contribute significantly to increased mortality in trauma patients, regardless of injury severity. Many current trauma protocols include the administration of calcium in conjunction with blood transfusion; Various protocols accessible online suggest 1-2g of calcium per 2-4 units of blood.
No consensus recommendation for dose or frequency has been established. Research is active and ongoing. Interestingly, a recent study performed using Department of Defense Trauma Registry data yielded a higher association with hypercalcemia and mass transfusion, but overall worse outcomes and increased mortality with hypocalcemia.
The Trauma…Star? - Hypotension
Hypotension doesn’t seem to be commonly included in the shapely cohort of really-bad-trauma-patient-symptoms, but a clear association with mortality does exist. One study out of Taiwan observed mortality rates of 100% when patients met all three trauma triad criteria and had a systolic blood pressure <60mmHg upon arrival to the ED. In the absence of severe hypotension, patients who met all Triad criteria demonstrated a mortality rate of roughly 47%. From this, we can appreciate hypotension as a strong predictor of mortality.
Whole blood is the ideal volume replacement in hemorrhagic shock, and packed red blood cells are a worthy alternative. If blood products are not available, conservative use of crystalloids should be used to restore perfusion. You may have heard the term “permissive hypotension” used in these instances. Permissive hypotension is the maintenance of systolic blood pressures (SBP) or mean arterial pressures (MAP) below normal physiological values in order to maximize perfusion while minimizing deleterious effects of crystalloids. It has been linked to decreased mortality and faster recovery. Ideal targets are still somewhat debated, but largely range between 70-90mmHg for systolic blood pressure goals. As always, follow your local protocols.
Summary
The Trauma Triad includes acidosis, coagulopathy, and hypothermia and the more recently proposed Trauma Diamond adds hypocalcemia
Hypotension is also a data-supported predictor of mortality
Targeting your treatment towards avoidance of these complications can give your patient their best chance at long term survival
References
Casella, Joshua, and Matthew Perry. “EMS Tactical Paramedic Lethal Triad.” PubMed, StatPearls Publishing, 5 May 2024, www.ncbi.nlm.nih.gov/books/NBK603758/. Accessed 10 Oct. 2024.
Jessica Dawkins Mills BSN, et al. “Trauma Diamond of Death: Adding Calcium to the Lethal Triad.” Journal of Emergency Nursing, Elsevier, 3 May 2024, www.sciencedirect.com/science/article/abs/pii/S0099176723003471.
Tzeng W-J, Tseng H-Y, Hou T-Y, Chou S-E, Su W-T, Hsu S-Y, Hsieh C-H. From Death Triad to Death Tetrad—The Addition of a Hypotension Component to the Death Triad Improves Mortality Risk Stratification in Trauma Patients: A Retrospective Cohort Study. Diagnostics. 2022; 12(11):2885. https://doi.org/10.3390/diagnostics12112885
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Brohi, K.; Singh, J.; Heron, M.; Coats, T. Acute traumatic coagulopathy. J. Trauma 2003, 54,1127-1130.
Vasudeva M, Mathew JK, Groombridge C, Tee JW, Johnny CS, Maini A, Fitzgerald MC. Hypocalcemia in trauma patients: A systematic review. J Trauma Acute Care Surg. 2021 Feb 1;90(2):396-402. doi: 10.1097/TA.0000000000003027. PMID: 33196630; PMCID: PMC7850586.
Woodward L, Alsabri M. Permissive Hypotension vs. Conventional Resuscitation in Patients With Trauma or Hemorrhagic Shock: A Review. Cureus. 2021 Jul 19;13(7):e16487. doi: 10.7759/cureus.16487. PMID: 34430103; PMCID: PMC8372825.
