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Mistakes in Trauma Care: Cold Fluids and Cold Ambulances
It is a hot day, 105ºF in the shade, and the humidity is 85% when you get the call. You and your partner give thanks for your new ambulance that has a separate gasoline generator to run the air conditioning system, which you have set at 65ºF in the patient compartment.
Your patient, a 72-year-old woman, fell in her kitchen last night and lay there all night, unable to move because of an obvious right hip fracture. A neighbor checked on her around noon, found her and called 9-1-1. On arrival you find the patient confused and unable to give many details of her fall except that it was “yesterday.” She has been incontinent of urine and feces and moans in pain as you examine her. You decide to give her 100 mcg of fentanyl before moving her, so you start a line with normal saline and, because her blood pressure is 82/50, decide to administer 500 mL of fluid. Your IV bag is cold, having been in the patient compartment all morning with the air conditioning running.
After the woman’s pain abates, you place her on a scoop stretcher and then on your ambulance stretcher. As you struggle to make your way down the steep stairs from her front porch to the sloping sidewalk, sweat pours off both you and your partner, and you silently curse both dispatch for not sending fire to help and yourselves for not calling for additional assistance. But once in the back of the ambulance, the cool air feels refreshing, and you set off for the Level III hospital 30 minutes away. Because the patient’s BP has not responded well to the initial bolus, you quickly run in another 500 mL of fluid and then cut back to a rate of 1,000 mL/hour. You hand her over to the ED staff without further incident.
Two weeks later one of the ED nurses says, “Remember that patient you brought in a couple of weeks ago with the fractured hip? That was my great-aunt, and she just died in the ICU. She got DIC and ARDS, and they couldn’t save her.”
“DIC and ARDS?” you say. “How did that happen?”
The Triad of Death
The link between poor survival in trauma patients and the so-called triad of death—coagulopathy, hypothermia and metabolic acidosis—is well known.1 Once it occurs, hemorrhage control and prevention of acidosis are difficult. If a patient arrives in an emergency department in this condition, their odds of survival are diminished.2
Much has been written about the so-called Golden Hour in trauma, yet there is scant, if any, evidence supporting the notion that prehospital times affect survival.3 Conversely, while there is much evidence that hypothermia leads to complications relating to poor survival—literally dozens of studies have traced its role in the other two aspects of the triad, acidosis and coagulopathy—little has been written about the role of prehospital care in the prevention of the triad of death. In this article we will examine the role of hypothermia in the development of the triad and its sequelae, disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS) and acidosis.
Hypothermia
We know hypothermia increases fluid requirements and independently increases acute mortality after major injury.4 Moreover, it can be a consequence of severe exsanguinating injury, and subsequent fluid administration during resuscitation efforts can lead to tissue hypoperfusion, diminished oxygen delivery, reduced heat generation, cardiac dysrhythmias, decreased cardiac output, increased systemic vascular resistance, and a leftward shift of the oxygen-hemoglobin dissociation curve.4
Some of this seems counterintuitive unless one recalls that patients compensating for hypovolemic shock are vasoconstricted, and addition of saltwater provides no oxygen-carrying capacity. A combination of administering fluids that are far below normal body temperature and a large volume of infusions can lead to events that are not survivable. Hypothermia in trauma is an ominous sign by itself, but when it’s combined with massive fluid administration, mortality increases. Administration of fluids that are 30ºF below normal body temperature can quickly lower core temperature to devastating levels. In one study of 71 adult trauma patients, no patient whose core temperature fell below 32ºC (89.6ºF) survived.5
Coagulopathy
Coagulation depends upon a cascade of enzymatic reactions that are adversely affected by hypothermia. Hypothermia prolongs coagulation times.6 A team led by Andrea Ferrara, MD, found that patients who were hypothermic and acidotic developed clinically significant bleeding despite adequate blood, plasma and platelet replacement in the hospital.7 If hypothermia can be avoided with simple prehospital measures, it may avert coagulation problems.
Acidosis
Metabolic acidosis is implicated in coagulopathy, but the mechanism is poorly defined. Physician Brian Murray reported a case of a 49-year-old woman with severe hypothermia (87.0ºF) and metabolic acidosis (pH 6.67) in 1961, and speculated that her acidosis was secondary to hypothermia.8 Surgeon Walter Ballinger and colleagues found in an experiment with dogs that lactate produced by hypoxic metabolism increased during cooling, indicating a metabolic acidosis.9 Acidosis, in turn, impairs coagulation.10,11 Although one study found acidosis alone produced no significant coagulopathy, when coupled with hypothermia it had a profound effect.12
Disseminated Intravascular Coagulation
DIC is a complex condition involving the coagulation process. It has many causes, among them trauma, infections, obstetrical complications and cancer. It begins with release of clotting factors, followed by formation of microclots in the circulation and eventual consumption of all reserve clotting factors, resulting in uncontrolled bleeding from multiple sites such as gums, wound sites and even IV sites.13
In the case of trauma, the clotting process is activated with traumatic damage to the tissues. Hypothermia and acidosis, however, interfere with normal clotting, leading to tissue hypoxia, production of lactic acid and toxic byproducts of cellular necrosis that promote agglutination of blood cells, eventual sludging of the blood, further interference with tissue perfusion, production of more toxins, more interference with clotting, more microclot formation, and eventual depletion of clotting factors.14,15 Hypothermia and acidosis contribute to further coagulation problems and more bleeding. DIC can be an explosive and life-threatening disorder, although it may also be mild, depending upon underlying causes.15
Acute Respiratory Distress Syndrome
As early as 1821, British physician Rene Laennec described a condition known as pulmonary edema without heart failure, and to this day ARDS is also described as non-cardiac pulmonary edema.16
ARDS is characterized by increased permeability of the pulmonary capillaries, resulting in fluid leaking into the interstitial and alveolar space—a different mechanism entirely from cardiogenic pulmonary edema, which involves increased hydrostatic pressures in the pulmonary circulation.
This leaking in turn leads to decreased blood volume, decreased ventilation, increased tissue perfusion and worsening shock.14 At one time, patients with ARDS were almost certain to die, but with today’s ventilatory techniques and improved ICU care, mortality has dropped to between 30%–60%. Patients with underlying medical conditions such as chronic liver disease, cirrhosis, chronic alcohol abuse, chronic immunosuppression, sepsis, chronic renal disease and non-pulmonary organ failure are at greater risk.17
Like DIC, ARDS is not a “stand-alone” process; rather it develops after another insult to the body. Contributing factors include trauma, severe sepsis, multiple transfusions, aspiration of gastric contents and drug overdose. Among trauma patients, those with multiple fractures are at greater risk.18
DIC, ARDS and the triad of death are intertwined. One leads to the other in a spiral. Shock states contribute to both DIC and ARDS, and one may contribute to the other. The triad of death contributes to both.
Prevention and Treatment
Current strategies in treating trauma patients are aimed at preventing the triad of death, DIC and ARDS from happening.19
Earlier this year in EMS World, Paul Murphy and associates wrote of the triad of death: While the prehospital treatment of hypothermia, acidosis and coagulopathy is predominantly supportive, it is important for prehospital providers to be familiar with the individual components of this condition; care given in the prehospital setting can help reduce the likelihood a patient succumbs to the trauma triad of death.20
Medics must be proactive in maintaining body temperature, and this is particularly important when administering fluids. When treating and transporting trauma patients, the patient compartment should be warm enough that the attendants are uncomfortable, and IV fluids should be kept at 105–113ºF. This can be accomplished with a simple heating pad on the “action area” of the ambulance or, if preferred, a commercially manufactured IV fluid warmer. Cold IV fluids can lower body temperature rapidly. This can be useful in certain cases, such as with post-cardiac arrest patients, but not for trauma patients.
Even though the outside temperature was hot, the patient was cold from lying motionless on the floor of an air-conditioned house overnight. In addition to her intertrochanteric femur fracture, her pelvis was also fractured, leading to serious hemorrhage into her peritoneal cavity. Her hypothermia was further exacerbated by the cool temperature of the patient compartment and administration of IV fluids that were at least 30ºF cooler than normal body temperature. Because of their own discomfort on the hot day, the medics overlooked the patient’s hypothermia, which led her into the triad of death and from there to DIC and ARDS. She also had a history of alcohol abuse that, coupled with her age, made her extremely vulnerable to the conditions that eventually killed her.
Summary
Do not be misled into thinking that because the weather is warm, a patient cannot become hypothermic. Keep your patient warm, give warm fluids, and you will increase their chances of surviving serious trauma. The triad of death can be prevented if you recognize its dangers and act proactively.
References
1. Mitra B, Tullio F, Cameron, Fitzgerald M, Trauma patients with the ‘triad of death.’ Emerg Med J 2011 Jul 23.
2. Brohi K. Damage control surgery. Trauma.org 5:6, June 2000, www.trauma.org/archive/resus/DCSoverview.html.
3. Newgard CD et al. Emergency medical services intervals and survival in trauma: Assessment of the ‘golden hour’ in a North American prospective cohort. Ann Emerg Med 2010 Mar; 55(3): 235–246.
4. Gentilello LM, Jurkovich GJ, Stark, MS, Hassantash SA, O’Keefe GE. Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study. Ann Surg 1997 Oct; 226(4): 439–449.
5. Jurkovich GJ, Greiser WB, Luterman A, Curreri PW. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma 1987; 27(9): 1,019–24.
6. Rohrer MJ, Natale AM. Effect of hypothermia on the coagulation cascade. Crit Care Med 1992 Oct; 20(10): 1,402–5.
7. Ferrara A, MacArthur JD, Wright HK, Modlin IM, McMillen MA. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg 1990 Nov; 160(5): 515–8.
8. Murray BJ. Case report: Severe lactic acidosis and hypothermia. West J Med 1961 Feb; 134(2): 162–166.
9. Ballinger WF, Vollenweider H, Templeton III JY, Pierucci Jr. L. Acidosis of hypothermia. Ann Surg 1961 Oct; 154(4): 517–523.
10. Ramaker AJ, et al. Effects of acidosis, alkalosis, hyperthermia and hypothermia on haemostasis: Results of point of care testing with the thromboelastography analyzer. Blood Coag & Fibrin 2009 Sept; 20(6):436–439.
11. Engstrom M, et al. Acidosis impairs the coagulation: A thromboelastographic study. J Trauma 2006 Sept; 61(3): 624–628.
12. Dirkmann D, Hanke AA, Gorlinger K, Peters J. Hypothermia and acidosis synergistically impair coagulation in human whole blood. Anesth Analg 2008 Jun; 106(6): 1,627–32.
13. Kirkpatrick AW, Chun R, Brown R, Simons RK. Hypothermia and the trauma patient. Can J Surg Oct 1999; 42(5): 333, 335.
14. Hall JE. Guyton and Hall Textbook of Medical Physiology, 12th ed., p. 277. Philadelphia: Saunders Elsevier, 2011.
15. Kasper DL, et al. Harrison’s Principles of Internal Medicine, 16th ed., p. 683–684. McGraw-Hill, 2008.
16. Laennec RTH. A treatise on the diseases of the chest: In which they are described according to their anatomical characters, and their diagnosis established on a new principle by means of acoustic instruments. Translated by Forbes. Birmingham, AL: Classics of Medicine Library, 1979.
17. Op. cit., Kasper, p. 1,595.
18. Op. cit., Kasper, p. 1,592.
19. Martini WZ. Coagulopathy by hypothermia and acidosis: Mechanisms of thrombin generation and fibrinogen availability. J Trauma 2009; 67(1): 202–209.
20. Murphy P, Colwell C, Gilbert P. Understand the Trauma Triad of Death. EMS World Feb 2012; 41(2): 44–51, www.emsworld.com/article/10565011/understand-the-trauma-triad-of-death.
William E. (Gene) Gandy, JD, LP, NREMT-P, has been a paramedic and EMS educator for more than 30 years. He has implemented a two-year associate degree paramedic program for a community college, served as both a volunteer and paid paramedic, and practiced in both rural and urban settings and the offshore oil industry. He has testified in court as an expert witness in a number of cases involving EMS providers and lectures on medical/legal aspects of EMS. He lives in Tucson, AZ.
Steven “Kelly” Grayson, NREMT-P, CCEMT-P, is a critical care paramedic for Acadian Ambulance in Louisiana. He has spent the past 14 years as a field paramedic, critical care transport paramedic, field supervisor and educator. He is a former president of the Louisiana EMS Instructor Society and board member of the Louisiana Association of Nationally Registered EMTs. He is a frequent EMS conference speaker and the author of the book En Route: A Paramedic’s Stories of Life, Death, and Everything In Between, and the popular blog A Day in the Life of An Ambulance Driver.
