BY ROMMIE L. DUCKWORTH
Firefighters play a critical role in the initial care of victims of severe trauma. First responders, emergency medical technicians, and paramedics can ensure positive patient outcomes by stopping the subtle but vicious cycle of hypothermia, acidosis, and bleeding. We must stop this cycle, known as the “Trauma Triad of Death” (TTD) or the “Lethal Triad” before it kills the patient.
Our understanding of trauma care has advanced as new tools and techniques for field providers have helped improve care, generally leading to better patient outcomes. Yet, the TTD remains a significant contributor to morbidity and mortality.1 First identified in 1982, this deadly combination of hypothermia, acidosis, and coagulopathy (bleeding problems) often begins with one of these three problems, which aggravates the other two.2 Each leg of the triad feeds into the others, resulting in a downward spiral toward death. This process can easily go unrecognized and uninterrupted when providers focus on only a single, obvious concern without identifying and stopping the cycle as a whole.(2)3
Hypothermia occurs any time the body’s normal mechanisms for temperature regulation are overwhelmed and heat loss exceeds heat generation, causing body temperature to fall below 35°C (95°F).4 In trauma patients, hypothermia is common, especially during prolonged rescues, and can easily occur at temperatures that feel quite comfortable to rescuers.5
Hypothermia is even more likely to occur in patients who have difficulty maintaining body temperature such as the very young, the very old, the alcohol-impaired, those with head injuries, and those with chronic diseases (e.g., diabetes, renal insufficiency, or heart failure). (5)
Some traumas accelerate heat loss. For example, patients may find themselves unexpectedly exposed to a cold environment following a winter car crash on an icy road; falling while hiking in the mountains during a rain storm; or suffering a diving-related injury in a cold lake. Trauma-associated hypothermia can even occur at room temperatures. For example, a patient who falls down stairs, landing on a cool tile floor where he may lie for an extended period of time, is at risk for significant temperature loss. In one study, almost half of emergency medical service (EMS)-transported trauma patients had a body temperature less than 36°C (96.8°F) on arrival at the emergency department. Consequences of hypothermia can be lethal. In another study, trauma victims with a core temperature lower than 32°C (89.6°F) had 100-percent mortality independent of their injury severity, degree of shock, or fluid resuscitation.6,7
Hypothermia will accelerate as a patient develops shock and heat production slows. EMS providers may inadvertently worsen hypothermia by administering fluids at temperatures below normal body temperature. (1,3,4)8
Normal body temperature is maintained by the hypothalamus, a structure in the brain that produces hormones that influence numerous body functions including the production of heat through muscle contractions and shivering. When body temperature falls, skeletal muscles work to produce heat, drastically increasing oxygen consumption.9 This high metabolic demand can place vital organs at risk of becoming ischemic.
In limited situations such as near-drownings and post-cardiac arrest resuscitations, hypothermia may be beneficial. For trauma victims, hypothermia contributes to a rapid physiological spiral toward death.10 Hypothermia decreases cardiac output, reduces cardiovascular response to catecholamines such as epinephrine, and contributes to myocardial ischemia. (8) Perhaps most significantly, hypothermia can reduce the function of clotting factors, making it harder to stop bleeding while at the same time contributing to acidosis through ischemia, impairing the blood’s ability to deliver oxygen. (10)
Acidosis is an increase in the acidity of blood and body tissues. The chemical processes for normal body function typically require a pH range between 7.35 and 7.45.11 The development of acidosis, an arterial pH below 7.35, can occur because the body is making too much acid, not getting rid of enough acid, or both. (11)
Just because we can’t do a field measurement of arterial blood pH doesn’t mean that we can’t anticipate, identify, and work to correct acidosis. When the body goes into shock, acidosis can worsen as tissues, starved for oxygen, begin using anaerobic metabolism to meet their needs for energy, producing waste acids.
If the body’s bicarbonate buffering system is overwhelmed, the kidneys will attempt to excrete more acid in the urine and the respiratory system will increase rate and depth of breathing to exhale more carbon dioxide. This can be identified by patient presentation, including declining mental status, increasing respiratory rate, and increasing heart rate. (11) If these mechanisms are unable to compensate, severe acidosis will develop and cause the following:
- Decreased cardiac output.
- Decreased arterial blood pressure.
- Decreased ability for hemoglobin to bind with and carry oxygen.
- Decreased threshold for ventricular fibrillation.
- Decreased ability for the blood to coagulate and stop hemorrhage.
A coagulopathy is a bleeding disorder; either blood clots form where they should not or fail to form where they should. Coagulopathy is relatively common in trauma and is associated with a fourfold increase in mortality.12
Normally when blood vessels are torn, small blood cells called platelets sense the damage, activate, and begin to stick to the injury site. Chemical signals are released from the platelets, attracting other cells to the area and causing them to clump together to form a “platelet plug,” which works to slow bleeding. On the surface of these activated platelets, chemicals in the blood, called clotting factors, undergo a series of complex reactions known as the coagulation cascade, forming a mesh-like fibrin clot. When this clot is no longer needed, the body will break it down and replace the clotting factors that have been used.13
Responders should seek to identify patients with preexisting conditions such as chronic liver or renal failure that might make it more difficult for blood to clot. Victims of trauma may also be taking anticoagulant medications to help reduce the chance of clot formation. Anticoagulants increase blood clotting times and also make it much more difficult to control bleeding.
A clotting disorder called “disseminated intravascular coagulation” (DIC) can also occur as a result of traumatic injury. (8,9) DIC is an improper series of chain reactions in the clotting cascade that cause unwanted clots to form throughout the body. (8,9) These clots can occlude blood vessels and cut off blood supply to vital organs as well as trigger an inflammatory response throughout the body. (8,9) Even worse, DIC uses up clotting factors and platelets, making it more difficult to form clots at sites of hemorrhage. (8,9)
As already mentioned, coagulopathy can also result from hypothermia and acidosis through loss of clotting factors as the patient bleeds out or by the dilution of clotting factors from overzealous administration of intravenous fluids. (8)
The Vicious Cycle
Essentially, this cycle can begin with any leg of the TTD. Massive hemorrhage decreases oxygen delivery, leading to hypothermia, which can disrupt the coagulation cascade, worsening the hemorrhage. With less blood to deliver oxygen and nutrients, the body’s cells switch to anaerobic metabolism, which is less efficient, producing less heat and releasing lactic and other acids leading to acidosis. This acidosis disrupts the blood’s ability to carry oxygen; reduces myocardial performance; and can damage other tissues and organs, again worsening both coagulopathy and hypothermia.
Field management of the TTD should focus on stopping bleeding, thwarting hypothermia, and preventing shock.
- Stop the bleed. Address massive hemorrhage first. Make note of minor bleeding that you find, but don’t let it distract you from life-saving interventions including correction of hypothermia and prevention of shock.
- Manage airway/breathing. You must maintain the patient’s airway and respirations. If the patient cannot maintain his own airway or is not breathing adequately, then it needs to be managed.
- Correct hypothermia. When you have identified the potential for hypothermia, the first and arguably most important step is to stop the heat loss. Remove the patient from what is cooling him or remove the thing that is cooling. Aggressive fluid resuscitation may be necessary; but unless fluids are warmed. they will significantly contribute to hypothermia. Rewarming patients in the field is not typically recommended because of the challenges of accurate temperature measurement during field trauma management.
- Prevent shock. Patients in hypovolemic shock need blood products. Although some prehospital systems can administer blood or blood products, such facilities are not widely available. The most common fluids available for resuscitation are crystalloid solutions such as normal saline and Ringer’s lactate solution.14 Normal saline has a pH of approximately 5.5, markedly more acidic than normal blood pH of 7.4. (14) When used for a large volume of fluid resuscitation, normal saline can worsen acidosis because of its high chloride content. (14) With a pH of 6.5, Ringer’s lactate is arguably a better solution, but it is incompatible with simultaneous administration of blood products (through the same intravenous line). (14)
It all begins with an awareness and understanding of the TTD. Without this, these subtle but fatal processes will go unnoticed, especially in the presence of more traumatic external injuries; but they will ultimately be major contributors to or the cause of death in victims of multisystem trauma.
ROMMIE L. DUCKWORTH is a past volunteer chief officer and current career fire captain, a technical rescue team coordinator, and an EMS coordinator for the Ridgefield (CT) Fire Department. He has 30 years of experience working in career and volunteer fire agencies, public and private emergency services, and hospital-based health care systems. He is an award-winning educator, an author, and a frequent speaker at international conferences including FDIC International.