Calcium in hemorrhagic trauma

Reviewing the trauma lethal triad: hypothermia, acidosis and coagulopathy


By Darien LaGoy; Jordan Anderson; Casey Patrick, MD, FAEMS; Xavier De La Rosa, BS, LP, NRP, FP-C

Trauma is consistently a leading cause of death in the U.S. and is the No. 1 cause of death for people under 45 years of age [1]. Preventable traumatic deaths are often hemorrhagic in nature and a majority occur in the prehospital setting [2]. EMS trauma education focuses on the lethal triad of trauma:

  1. Acidosis
  2. Hypothermia
  3. Coagulopathy
Calcium plays a vital role in the lethal triad of trauma and is of significant interest as a potential adjunct treatment for traumatic hemorrhagic shock.
Calcium plays a vital role in the lethal triad of trauma and is of significant interest as a potential adjunct treatment for traumatic hemorrhagic shock. (Photo/Xavier de la Rosa)

These three conditions are interrelated, compound each other and, if not reversed, universally result in death. Calcium plays a vital role in each of the three triad components and is of significant interest as a potential adjunct treatment for traumatic hemorrhagic shock.

Trauma lethal triad

Trauma patients are hypothermic secondary to blood loss, associated heat loss, as well as slowed metabolism. Potential environmental exposure and relatively cold fluid/medication administration also can contribute. Despite hypothermia being a known predictor for poor outcomes in trauma patients, one study found that 37% of trauma patients presented to the ICU hypothermic [3]. The same study found that almost half of the patients who died within 28 days presented to the ICU in a hypothermic state. It is vital that we not neglect warming our trauma patients while performing other advanced treatments and procedures.

Acidosis is a result of blood loss leading to poor perfusion. A central shift of circulating blood volume leaves the extremities in a state of anerobic metabolism. This results in lactic acid accumulation and a drop in pH. Administration of 0.9% saline can further contribute to this process as well. For this reason, crystalloid should be minimized with maintenance of a mean arterial pressure (MAP) from 50 mmHg to 70 mmHg, recognizing the exact value and acceptable range for permissive hypotension is not yet determined [4].

Coagulopathy describes impaired physiologic clotting. In the hemorrhagic shock trauma patient, coagulopathy occurs due to both clotting factor and platelet loss, calcium loss and because the clotting cascade requires normothermia and normal pH. This constellation of derangements inhibits the body’s ability to clot, contributing to further hemorrhage until hemorrhage is controlled.

Hypothermia, acidosis and coagulopathy worsen each other, forming the lethal triad. The more hypothermic the patient, the more acidotic they become, the more coagulopathic, and so on in a vicious cycle.

Hypocalcemia in hemorrhagic trauma

There are four major reasons that hemorrhagic trauma results in hypocalcemia: hemorrhage, hypothermia, hyperkalemia and eventually, blood transfusion.

  • Hemorrhage. Just like clotting factors and platelets, the loss of blood volume also represents a loss of total volume of calcium. This leaves less calcium available for critical metabolism, including cardiac contractility and essential clotting cascade functions.
  • Hypothermia. A rapid decrease in blood volume along with exposure and resuscitation leads to profound hypothermia in hemorrhagic shock. In cases where patients become hypothermic, ionized calcium shifts intracellularly where it can be utilized for action potential inducing muscle contraction/shivering. A shivering trauma patient is a hypothermic patient and therefore hypocalcemic. As calcium declines muscle contractions cease, and the patient’s temperature drops further.
  • Hyperkalemia. In all patients (medical and trauma), excessive serum potassium (extracellular) causes cardiac conduction abnormalities and can be fatal. Thus, the treatment goal for hyperkalemia focuses on shifting the potassium intracellularly. In the trauma patient, tissue damage causes potassium to leak extracellularly, resulting in hyperkalemia. Potassium, once extracellular, is bound in the serum plasma by ionized calcium to maintain homeostasis. This increased potassium/ionized calcium binding results in further hypocalcemia [5].
  • Blood transfusion. If the patient requires large volume transfusion, either 1:1:1 component or whole blood, it is accepted standard practice to co-administer calcium. Hypocalcemia is a known complication of blood transfusion secondary to preserving agents, mainly citrate, which binds calcium exacerbating hypocalcemia. In theory, citrate can undergo rapid hepatic metabolisim reducing this hypocalcemic effect. However, as the typical trauma patient is hypoperfused, hypothermic and acidotic, citrate metabolism is slowed, resulting in a significant drop in calcium [6].

Hypocalcemia and mortality

Hypothermia, acidosis and coagulopathy all contribute to increased trauma mortality and each process results in hypocalcemia. Recent evidence is conflicting on whether hypocalcemia may be an independent predictor of mortality in trauma.

One systematic review found that trauma patients who were hypocalcemic prior to blood transfusion experienced a 10% increase in mortality [7]. Other recent evidence suggests no evidence for hypocalcemia as an independent predictor of increased mortality [8]. As with any retrospective data, correlation and/or causation can be murky at best.

It is reasonable to assume that hypocalcemic trauma patients on ED arrival were likely farther along the lethal triad compared to the survivors. Therefore, calcium status should be closely monitored as a component of ED trauma resuscitation. Further prospective studies are needed to better investigate hypocalcemia as a mortality predictor in traumatic shock along with when and how to best replace calcium in traumatic resuscitation.

Bleeding control

The prehospital treatment for traumatic shock must focus on external bleeding control, prevention of hypothermia and acidosis, along with rapid hemorrhage source control. Especially as EMS blood transfusion data evolves, emergency providers must also closely monitor hypocalemia as a potential key treatment component as well.


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About the authors

Darien LaGoy, NRP

Darien LaGoy has 7 years’ experience in emergency medicine with experience in both military combat medicine and civilian EMS. He is currently serving as an attendant paramedic for Harris County ESD11 Mobile Healthcare.

Jordan Anderson, NRP, CCP-C

Jordan Anderson has over 15 years’ experience as a paramedic and is currently the clinical practice manager at Harris County ESD11 Mobile Healthcare

Casey Patrick , MD, FAEMS

Dr. Casey Patrick is medical director for Harris County ESD11 Mobile Healthcare and assistant medical director for the Montgomery County Hospital District EMS service in Greater Houston, where he helped develop and produces the MCHD Paramedic Podcast.  Dr. Patrick is board certified in both Emergency and EMS Medicine and works as a community emergency physician in multiple states. Additionally, he is an active member of the Texas NAEMSP State chapter and the national association, and serves as an EMS1 Editorial Advisory Board member.

Xavier A. De La Rosa, BS, LP, NRP, FP-C

Xavier A. De La Rosa is chief clinical officer for Harris County ESD 11 Mobile Healthcare. He has held multiple roles including for-profit EMS, 911 EMS, flight medicine and EMS-based fire service, and as a lieutenant in the Training Division of Fort Bend County EMS in Texas. 

He has a degree in Emergency Health Sciences from the University of Texas Health Science Center San Antonio and a Master's of Business Administration from Johns Hopkins with concentrations in Private and Public Sector Leadership; and Health Innovation, Technology and Management.

References

1. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. (Jan. 24, 2014.) Injury Prevention & Control: Data & Statistics (WISQARS). Retrieved March 30th 2022, from www.cdc.gov/injury/wisqars/

2. Eastridge BJ, Holcomb JB, Shackelford S. Outcomes of traumatic hemorrhagic shock and the epidemiology of preventable death from injury. Transfusion. 2019 Apr;59(S2):1423-1428. doi: 10.1111/trf.15161. PMID: 30980749.

3. Balvers, K., Van der Horst, M., Graumans, M., Boer, C., Binnekade, J. M., Goslings, J. C., & Juffermans, N. P. (2016). Hypothermia as a predictor for mortality in trauma patients at admittance to the Intensive Care Unit. Journal of emergencies, trauma, and shock9(3), 97–102.

4. M Das J, Anosike K, Waseem M. Permissive Hypotension. [Updated 2021 Nov 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558915

5. Takaaki Ookuma,corresponding author Koji Miyasho, Nobuhiro Kashitani, NobuhikoBeika, Naoki Ishibashi, Takahiro Yamashita, and Yoshihito Ujike. (2015, August13). The clinical relevance of plasma potassium abnormalities on admission in trauma patients: a retrospective observational study. Journal of intensive care.

6. Hall C, Nagengast AK, Knapp C, Behrens B, Dewey EN, Goodman A, Bommiasamy A, Schreiber M. Massive transfusions and severe hypocalcemia: An opportunity for monitoring and supplementation guidelines. Transfusion. 2021 Jul;61 Suppl 1:S188-S194. doi: 10.1111/trf.16496. PMID: 34269436.

7. Vasudeva, Mayank MBBS; Mathew, Joseph K. MBBS, FACEM; Groombridge, Christopher MBBS, FACEM et al. (2021, February). Hypocalcemia in trauma patients: A systematic review. Journal of Trauma and Acute Care Surgery, 90(2).

8. Chanthima P, Yuwapattanawong K, Thamjamrassri T, Nathwani R, Stansbury LG, Vavilala MS, Arbabi S, Hess JR. Association Between Ionized Calcium Concentrations During Hemostatic Transfusion and Calcium Treatment With Mortality in Major Trauma. Anesth Analg. 2021 Jun 1;132(6):1684-1691. 

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