Trauma’s Lethal Triad of Hypothermia, Acidosis & Coagulopathy Create a Deadly Cycle for Trauma Patients

 

 
 
 

Ryan Gerecht, MD, CMTE | From the April 2014 Issue | Wednesday, April 2, 2014


It’s 11 p.m. on a Saturday night when you’re dispatched to a local nightclub for reports of a young male who’s suffered multiple gunshot wounds. En route, police notify you the scene is safe and there’s a single patient bleeding profusely from multiple extremity wounds. On arrival you find a 25-year-old male lying on the street in a rapidly expanding pool of blood. He’s nearly unconscious but breathing spontaneously. His skin is cool, moist and pale. His pulse is rapid and barely palpable. As you and your partner begin your rapid trauma assessment, obtain vital signs, and prepare for rapid packaging and transport to the trauma center 20 minutes away, you know this young man is on the brink of death.

Trauma & the Triad
Despite great advancements in trauma care over the past 30 years, trauma is still one of the leading causes of death in any age group. This is especially apparent in the young—for those aged 1–44 years old, trauma is the No. 1 cause of death in the United States.1 Of these deaths, hemorrhage accounts for up to 40% and remains as the leading preventable cause of trauma-related death.2,3

The lethal triad of hypothermia, acidosis and coagulopathy has been recognized as a significant cause of death in patients with traumatic injuries. In 1982, a study described a “bloody vicious cycle” in which hemorrhage and tissue injury cause this predictable triad of complicating factors.4 Ultimately, this triad resulted in worsening hemorrhage and eventual death. Authors of the research suggested treatment of hypothermia, acidosis and coagulopathy in trauma requires as much attention as the traditionally emphasized surgical management of injuries.4

Today, we recognize that to successfully resuscitate the critically ill trauma patient, all emergency providers must have a firm understanding of the lethal triad. This understanding should serve as the cornerstone for all interventions provided to the bleeding trauma patient. Left untreated, hypothermia, acidosis and coagulopathy bring about and propagate each other, eventually resulting in a predictable but irreversible progression toward death.

Hypothermia
Normal human body temperature is 35.6–37.8 degrees C with hypothermia being defined as a core temperature < 35 degrees C.5 In one study, it was found that almost half of EMS-transported trauma patients had a temperature < 36 degrees C on arrival to the ED.6 Important to note is that there was no association between season of the year and frequency of hypothermia. At highest risk were those patients older than 65 and those who had been entrapped.6 In addition, hypothermia in trauma has been associated with a significantly increased mortality compared to patients with the same body temperature from environmental exposure alone. In a study of 71 trauma victims, a core temperature < 32 degrees C was associated with 100% mortality independent of the presence of shock, injury severity or volume of fluid resuscitation.7 Because hypothermia in a trauma patient predicts such a poor outcome, the traditional classification system of hypothermia has been revised for use in this vulnerable patient population. (See Table 1--below.)

Even mild hypothermia in a trauma patient can result in devastating physiologic consequences. (See Table 2.) Of particular concern is the effect of hypothermia on the coagulation system.8 The coagulation system is a temperature- and pH-dependent series of complex enzymatic reactions that result in the formation of blood clots to stop both internal and external hemorrhage.

Coagulopathy is the term used to describe a broad group of disease states in which there is an impaired ability of this coagulation system to synthesize blood clots.5 It’s been repeatedly demonstrated that as a patient’s core temperature decreases, so does the body’s ability to stop bleeding. This is a result of impaired platelet function, inhibition of the clotting factors, and inappropriate activation of clot breakdown.8

Hypothermia in trauma patients is caused by a multitude of factors. Hemorrhagic shock, traumatic brain injuries, and alcohol intoxication impair the body’s ability to regulate its core temperature.8 In addition, patients at the extremes of age and those with certain medical conditions such as diabetes or thyroid disease are at higher risk to develop hypothermia after trauma.8 Furthermore, those patients with prolonged exposure to the environment as during an extrication and those with severe burns are at risk for rapid heat loss causing profound hypothermia.

Lastly, an important care consideration for a trauma patient is the temperature of the fluids and blood products we infuse as well-intentioned therapy. Room temperature normal saline (20–25 degrees C) is very hypothermic relative to the desired normal body temperature. Thus, large volume resuscitations with even room temperature IV fluids can significantly contribute to this arm of the lethal triad.

Acidosis
A pH level is a measure of the blood’s acidity on a scale of 0–14; water has a “neutral” pH of 7.0. A healthy individual maintains a physiologically normal pH of 7.35–7.45 through a complex balance of hydrogen ions (acids) and buffers predominately controlled by the pulmonary and renal systems.

Acidosis is defined as an arterial pH < 7.35 and can result from a variety of disease states. However, in trauma patients the major contributor is poor perfusion to the tissues. Anemia from acute blood loss, peripheral vasoconstriction in response to hypothermia and blood loss, and overall decreased cardiac output severely impair oxygen delivery to the tissues. This results in tissue oxygen demand far exceeding oxygen delivery. Thus, to make functional energy, the body’s cells are forced to utilize anaerobic metabolism instead of the normal aerobic metabolism, resulting in the production of lactic acid as a byproduct.9

As a trauma patient’s perfusion worsens, lactic acid rapidly accumulates in the tissues. This causes the body’s pH to drop, resulting in a severe metabolic acidosis. It’s important to note that this process frequently occurs in the presence of normal or only slightly abnormal vital signs.

An additional cause of acidosis in the trauma patient is excessive resuscitation using unbalanced crystalloid solutions such as normal saline.10 With a pH around 5.5, normal saline is far more acidic than the desired normal blood pH. In large-volume resuscitations, normal saline predictably causes its own metabolic acidosis as a result of the high chloride content.11 This hyperchloremic metabolic acidosis only serves to compound the existing lactic acidosis of trauma. Furthermore, there’s evidence that excessive use of normal saline with its high chloride content may increase systemic tissue inflammation and thereby contribute to the coagulopathy of trauma.11 Lactated Ringers (LRs) is an imperfect substitution: Although its pH is 6.5, LR contains lactate and is incompatible with many medications and blood products.

Lastly, a trauma patient may also have respiratory acidosis. This is a result of hypoventilation due to respiratory depression or obstruction resulting in hypercapnia (increased CO2 levels). Common causes of a respiratory acidosis in trauma include narcotic or alcohol use, traumatic brain injuries, flail chest or preexisting medical conditions such as chronic obstructive pulmonary disease.

With severe acidemia (pH < 7.20), disastrous consequences can occur.12 (See Table 3.) For the trauma patient, one of the most harmful effects is that their coagulation system can become severely impaired. In one study, the function of part of the coagulation system was reduced by 55–70% when the pH dropped from 7.4 to 7.0.13

Coagulopathy
Coagulopathy can occur for a number of reasons; however, regardless of the specific cause, coagulopathy results in the potential for continued hemorrhage in the bleeding trauma patient.

Coagulopathy in trauma is a common occurrence, present in nearly one in four severely injured patients arriving at the ED. Furthermore, its presence is associated with a four-fold increase in mortality.14–16 The coagulopathy of trauma occurs not only because of hypothermia and acidosis as previously discussed, but also as a result of losing clotting factors through hemorrhage and hemodilution, and the body’s use and subsequent depletion of both platelets and clotting factors.9

Dilutional coagulopathy occurs when we resuscitate a bleeding trauma patient with fluid or blood products that don’t contain the same clotting factors lost in the acutely hemorrhaged whole blood.10 Crystalloids such as normal saline and packed red blood cells dilute the remaining clotting factors circulating in the trauma victim’s blood. Furthermore, in the critically injured, through a complex series of enzymatic reactions, the clotting cascade can become abnormally activated, causing excessive clot formation and subsequent breakdown (fibrinolysis) out of proportion to the injury.9 This abnormal and excessive activation of the coagulation system rapidly consumes the body’s remaining clotting factors, resulting in a further deficiency of the essential factors needed to achieve hemorrhage control.

Lastly, EMS providers should be aware of those trauma patients who have a baseline coagulopathy because of preexisting medical conditions. Examples include those patients on anticoagulant therapy such as warfarin (Coumadin) or a novel oral anticoagulant such as dabigatran for stroke prevention in the setting of atrial fibrillation. These patients and those with chronic liver or renal failure have an increased risk of developing a truly life-threatening coagulopathy and hemorrhage after trauma.17

EMS Management of the Lethal Triad
There are several simple steps providers can and should follow to battle the lethal triad.

1. The triad begins and ends with bleeding, so find the bleeding and stop it. Hold pressure, use combat gauze, apply a tourniquet, bind the pelvis, etc. (See the article “Training & speed are crucial: Options, issues & training to prevent death from massive blood loss,” by Joe Holley, MD, FACEP, in the JEMS December 2013 supplement, Putting the clamp on hemorrhage: How a simple, effective point-of-injury tool will transform the way bleeding is controlled in the field.)
2. Do not stop your search for bleeding with the first source you find, as others may exist.
3. Always assume your patient’s temperature is dropping right before your eyes, because it is, and much faster than you’d expect.
4. “Strip ‘em and flip ‘em,” but not with reckless abandon. Make every effort to expose only those body parts you’re examining in the moment and keep the remainder of the patient covered.
5. Patients can and will become hypothermic in conditions you consider warm. Prioritize limiting a patient’s exposure to the environment, especially during prolonged extrications.
6. Place a warm blanket between the newly extricated patient and your cold, hard backboard.
7. Turn up the heat in your ambulance. If you aren’t sweating, it’s certainly not warm enough. (Ideally, 27 degrees C.)
8. Promptly remove wet or bloody clothes and replace with a warm blanket. Shivering wastes valuable cellular energy and oxygen in an attempt to stay warm while producing more lactate, contributing to acidosis.
9. We don’t bleed normal saline, so limit crystalloid infusion as much as possible. It contributes to the patient’s acidosis and dilutes the remaining clotting factors in your patient’s blood. IV fluids may improve a number, but may actually hurt your patient in the long run.
10. Except in those patients with a traumatic brain injury, utilize a permissive hypotension resuscitation strategy. Our goal should be to maintain tissue perfusion typically defined as the presence of a radial pulse or normal mental status. We should avoid overly aggressive fluid administration to normalize blood pressure, which can “pop the clot” and worsen hemorrhage. (See “Vital pathways: Detect & treat symptoms related to hemorrhagic shock,” by Peter Taillac, MD, FACEP and Chad
Brocato, DHSC, CFO, JD, from the JEMS October 2012 issue and “Add a little salt: Permissive hypotension in trauma resuscitation,” by Jeff Beeson, DO, FACEP, EMT-P and Trenton Starnes, NREMT-P in the JEMS April 2013 issue.)
11. Whenever possible, administer only warmed fluids. (Ideally 40 degrees C.)
12. Measure prehospital lactate levels when available to more accurately detect cryptic shock in trauma patients with normal vital signs. End-tidal carbon dioxide may also be a useful marker.
13. Monitor and maximize oxygenation.
14. Treat causes of hypoventilation to prevent a respiratory acidosis.
15. Identify high-risk patients with a baseline coagulopathy due to medications or preexisting medical conditions.
16. Administer tranexamic acid (TXA)—an antifibrinolytic that prevents clot breakdown and thus decreases blood loss—if your system permits its use. TXA has been shown to decrease mortality in two large trauma studies. (See “TXA: A difference-maker for trauma patients? Role of tranexamic acid in EMS & preoperative trauma management,” by Jeffrey M. Goodloe, MD, NREMT-P, FACEP; David S. Howerton, NREMT-P; Duffy McAnallen, NREMT-P and Howard Reed, NREMT-P, in the JEMS April 2013 issue.)

Case Conclusion
As you rapidly assess your patient lying in the street, your partner simultaneously obtains a set of vital signs: blood pressure of 72/40, heart rate of 118, respiratory rate of 24 and an O2 saturation of 94% on room air. On your rapid trauma exam his lungs are clear and his abdomen is soft and non-tender. Inspection of the lower extremities reveals two seemingly large caliber projectile wounds to the right upper leg and one to the left upper leg. From these wounds flows bright red blood. You immediately direct a responding firefighter to place direct pressure to these wounds and the patient is promptly moved to your waiting ambulance.

In the back of your preheated ambulance, you place the patient on high-flow oxygen by a non-rebreather mask, your partner successfully places a 16-gauge IV, and you begin to strip the young man of his wet and bloody clothes. Knowing the importance of preventing hypothermia in trauma patients, you’re careful to keep the young man covered with warm, dry sheets and a space blanket as you perform a more detailed exam.

You find no other sources of bleeding but the patient continues to have an altered level of consciousness with only palpable central pulses, and significant tachypnea. You know these findings are a result of severe hemorrhagic shock causing poor perfusion to your patient’s brain and peripheral tissues. You also recognize that, because of this poor perfusion, the patient is likely becoming severely hypothermic, acidotic and coagulopathic, given the amount of blood loss, his vital signs, and the exposure to the cold rain while lying in the street. There’s no question in your mind; the lethal triad of trauma is fully present in your patient.

On reassessment of the leg wounds you note they continue to bleed despite direct pressure. You quickly decide to place proximal tourniquets to both legs, as you know that the most important intervention to prevent progression of the lethal triad is to aggressively control hemorrhage. Your partner administers a 500 cc bolus of warmed normal saline in an attempt to increase tissue perfusion but not dilute the patient’s remaining clotting factors or worsen his acidosis. In addition, you administer one gram of TXA per protocol to help combat the coagulopathy of trauma. Your partner notifies the receiving trauma center of your patient’s critical condition.

On arrival to the trauma center, with tourniquets in place, there’s no active hemorrhage from the leg wounds. After the fluid bolus, your patient has a weak but palpable radial pulse, and repeat vital signs are a blood pressure of 90/60, heart rate 106, respiratory rate 20 and an oxygen saturation of 100%. The awaiting trauma surgeons rush your patient to the operating room to repair his vascular injuries. While you’re restocking your ambulance, the emergency physician approaches you and compliments your exceptional efforts to stop the bleeding and prevent hypothermia and acidosis, use of a permissive hypotension resuscitation strategy, and administration of TXA.

Final Thoughts
When faced with the unique challenge of resuscitating a critically ill trauma patient in a dynamic and austere prehospital environment, knowledge of and respect for the lethal triad is mission critical. Simply stated, hemorrhage in trauma causes acidosis, hypothermia and coagulopathy. Hypothermia results in worsening acidosis, which both contribute to the severity of coagulopathy. A worsening coagulopathy results in continued hemorrhage, beginning a truly self-sustaining and deadly cycle.

With the exception of hypothermia, EMS is not routinely capable of knowing exactly which arms of the lethal triad are present in real time for a given trauma patient—the degree of acidosis or severity of coagulopathy is usually determined by lab testing. Despite this, EMS is uniquely positioned to combat this silent cycle of death before it spirals out of control.

At the end of the day, recognition and prevention of this lethal triad can be more effective than treatment. A variety of seemingly simple but truly significant actions and inactions by EMS at both the scene and during transport can directly prevent or slow the progression of the lethal triad. As time passes, the three arms of the triad become so tightly interwoven that it becomes nearly impossible to stop and reverse the cycle. Thus, EMS personnel on the front lines of our nation’s trauma system have the very real opportunity to improve the outcomes for the millions of people injured annually. jems

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 Feb. 11, 2014, from www.cdc.gov/injury/wisqars/.
2. Sauaia A, Moore Fa, Moore EE, et al. Epidemiology of trauma deaths: A reassessment. J Trauma. 2007;62(2):307–310.
3. Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome: An overview of epidemiology, clinical presentations, and therapeutic considerations. J Trauma. 2006;60(Suppl. 6):S3–S11.
4. Kashuk JL, Moore EE, Millikan JS, et al. Major abdominal vascular trauma—A unified approach. J Trauma. 1982;22(8):672–679.
5. Moffatt SE. Hypothermia in trauma. Emerg Med J. 2013;30(12):989–996.
6. Helm M, Lampl L, Hauke J, et al. Accidental hypothermia in trauma patients. Is it relevant to preclinical emergency treatment? Anaesthesist. 1995;44(2):101–107.
7. Tsuei BJ, Kearney PA. Hypothermia in the trauma patient. Injury. 2004;35(1):7–15.
8. Soreide E, Smith CE. (2005.) Hypothermia in trauma victims—friend or foe? Trauma Care International. Retrieved Feb. 10, 2014, from www.itaccs.com/traumacare/archive/05_01_Winter_2005/friendorfoe.pdf .
9. Weingart S, Meyers CM. (March 1, 2008.) Thoughts on the resuscitation of the critically ill trauma patient. EMCrit Blog. Retrieved Feb. 10, 2014, from www.emcrit.org/podcasts/trauma-resus-part-i/.
10. Ho AM, Karmakar MK, Contardi LH, et al. Excessive use of normal saline in managing traumatized patients in shock: A preventable contributor to acidosis. J Trauma. 2001;51(1):173–177.
11. De Backer D, Cortes DO. Characteristics of fluids used for intravascular volume replacement. Best Pract Res Clin Anaesthesiol. 2012;26(4):441–451.
12. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders first of two parts. N Engl J Med. 1998;338(1):26–34.
13. Meng ZH, Wolberg AS, Monroe DM, et al. The effect of temperature and pH on the activity of factor VIIa: Implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma. 2003;55(5):886–891.
14. Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma. 2003;54(6):1127–1130.
15. McLeod JB, Lynn M, McKenney MG, et al. Early coagulopathy predicts mortality in trauma. J Trauma. 2003;55(1):39–44.
16. Maegele M, Lefering R, Yucel N, et al. Early coagulopathy in multiple injury: An analysis from the German Trauma Registry on 8,724 patients. Injury. 2007;38(3):298–304.
17. Lewis AM. Trauma triad of death emergency. Nursing. 2000;30(3):62–64.

Learning Objectives

  • List the individual components of the lethal triad of trauma.
  • Understand the pathophysiology that makes the lethal triad a deadly self-propogating cycle in critically ill trauma patients.
  • Learn simple interventions EMS providers can perform to help prevent or slow the rapid progression of the lethal triad.

Table 1: Traditional classification of hypothermia & revised classification for trauma patients

Degree of hypothermia

Traditional classification (°C)

Trauma classification (°C)

Mild

32–35

34–36

Moderate

28–32

32–34

Severe

20–28

< 32

Profound

14–20

 

Deep

< 14

 

KEY Terms

Acidosis: Lower than normal pH due to increased hydrogen ion concentration.
Coagulation system: A temperature- and pH-dependent series of complex enzymatic reactions that result in the formation of blood clots to stop both internal and external hemorrhage.
Coagulopathy: Any disorder of the blood that makes it difficult for blood to coagulate.
Hypothermia: Lowered body core temperature.
Lethal triad: A combination of acidosis, coagulopathy and hypothermia that usually leads to death in a patient experiencing trauma.

 

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Related Topics: Patient Care, Trauma, trauma, Lethal triad, hypothermia, hemorrhage, coagulopathy, coagulation system, acidosis, Jems Features

 

Ryan Gerecht, MD, CMTE

Ryan Gerecht, MD, CMTE, started his career in EMS over 10 years ago as an EMT. Today he’s a flight physician with University of Cincinnati Air Care & Mobile Care and is the assistant medical director for Colerain Township Department of Fire and EMS. He’s the inaugural NAEMSP/Physio-Control EMS medicine medical director fellow, and will begin his EMS fellowship with the University of Cincinnati and Cincinnati Fire Department in July.

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