‘AACN Clinica! asus Volume 10, Number 1 pp. 65-94 ©1000, AACN The Trauma Triad of Death: Hypothermia, Acidosis, and Coagulopathy Judy Mikhail, RN, MSN, CCRN, CEN [With the organization of trauma aysterns, the development of trauma centers, the application of standardized methods of fesuscitation, and improvements in modern blood banking techniques, the ability to aggressively resuscitate patients in extremis has evolved, The concept of the "golden hour" has translated into unprecedented speed and efficiency of trauma resuscitation with the ultimate goal of short injury-to-incision times. As the shift in care of patients in extremis has continued to move from the street to the emergency department and beyond, the focus of trauma resuscitation has shifted to the operating room and ultimately to the intensive care unit, The “new” golden hour may well be the time in the operating ream before the patient reaches the physiologic limit, defined as the onset of the triad: hypothermia, acidosis and coagulopathy, Critical care ‘nurses must understand this triad, because It forms the basis and underlying logic en which the damage control philosophy has been bull, This article explores the pathogenesis and treatment of acidosis, hypothermia, and coagulopathy as it applies to the ‘exsanguinating trauma patient. (KEYWORDS: acidosis, coagulopathy, damage control, hypothermia, nursing, shook, trauma) 85 OWhy We Are Where We Are ‘As American society has become more vio- lent, trauma centers have had to adjust cor- respondingly. The concept of trauma centers emerged in the 1960s and 1970s and contin- ued to expand throughout the 1980s, At the same time, the incidence and level of pen trating injury from violence reached epi- demic proportions in the United States, peaking in the mid to late 1980s.! There was an increase in the number of patients with multiple wounds from semiautomatic, large caliber weapons resulting in greater energy wansfer, cavitation effect, and tissue disrup- tion. With the organization of trauma sy: tems, the development of trauma centers, the application of standardized methods of resuscitation, and improvements in modern blood banking techniques, the ability to 2 gressively resuscitate patients in extremis has evolved. The concept of the “golden hour” has translated into unprecedented speed and efficiency of trauma resuscitation with the ultimate) goal of short injury-to-incision times, Trauma centers g @ substantial volume of patients with penetrating trauma have become especially adept at aggressive resuscitation, AS a result, patients who in From the Hurley Medical Center, Plint, Michigan, Reprint requests to Judy Mikhail, RN, MSN, CCRN, Trauma Clinical” Nurse Specialis/Coordinator, Hurley Medical Center, One Hurley Phiza, Plint, Mi 48503.86 = MIKHAIL years past would have died at the scene or in the emergency department are now arriv- ing in the operating room with vital signs. As the shift in care of patients in extremis has continued to move from the street to the emergency department and beyond, the fo- cus has shifted to the operating room and u timately to the intensive care unit The new golden hour may well be the lime in the operating room before the p: tient reaches the physiologic limit, defined as the onset of the triad: hypothermia, aciclo- sis and coagulopathy? Rontondo and Zonies! describe this lethal triad as the phys- jologic perturbations in death by exsar guination (Fig. 1). Kashuk et al.4 and Moore et al’ have referred to this triad as “the bloody vicious cycle” (Fig. 2). The metabolic derangements of the triad that build on and reinforce each other in an already extremely fragile patient require that the critical care nurse take an active role in trauma resuscit tion. The goal of trauma resuscitation is to abort the traditional exploratory laparotomy, where all injuries are identified and dealt with in a definitive manner, and instead to perform damage control or staged laparo- tomy. Damage control surgery entails initial laparotomy, abbreviated in duration, ir tended to control hemorrhage and contami- nation, pack the abdomen, and temporarily close the skin of the abdominal wall. The p: tient is then moved quickly to the intensive care unit for stabilization and rewarming b fore subsequent reoperations «tre performed cl until definitive care is rendleredl, Damage control surgery is discussed in further detail elsewhere in this issue. The speed by which the exsanguinating trauma patient moves from prehospital 10 the emergency department, operating room, and intensive care unit has been significantly compressed in today's trauma system. There ACIDOSIS <—_,> HYPOTHERMIA AACN Clinical Issues is a blurring and merging as never before of the roles of nursing from prehospital, to emergency department, to operating room, anesthesia, and the intensive unit. Nurses who care for trauma victims must be knowledgeable and skilled in managing pa- tients with challenging, complex conditions This article explores the pathogenesis «and treatment of hypothermia, acidosis, and co- agulopathy as it applies to the exsanguinat- ing trauma patient. Critical care nurses must understand the concepts of this triad, be- cause it forms the basis and underlying logic ‘on which the damage control philosophy has been built, OMetabolic Acidosis The predominate physiologic deficit result- ing from inadequate perfusion is metabolic acidosis, When tissue hypoxia is. present, normall cell physiology is altered, and a shift from aerobic to anaerobic metabolism oc- curs, resulting in kictic acidosis. The amount of kictate produced is believed to correlate with the total oxygen debt, the magnitude of hypoperlusion, and the severity of shock. The association between high lactate levels and hypovolemic shock was first described by Huckabee 40 years ago.5 In 1964 Broader and Weil® showed the association between high lactate levels and increasing tisk of death, Since then, several investigators have demonstrated increasing risk of death with metabolic acidosis as demonstrated by arter- pH, lactate, and base deficit clearance.7-" The deleterious effects of acidosis on the cardiovascular system include decreased ca diac contractility and cardiac output, vasodi- lation and hypotension, decreased hepatic and renal blood flow, bradycardia, and in- creased susceptibility to ventricular dys rhythmias.%*16 These adverse effects are gen- Figure 1. The lethal triad: Physio- logic perturbations in death by exsanguination. Reprinted, with permission, from Flotondo M, Zonies M. The damage control se~ quence and underlying logic. Surg Clin North Am 1997:77:761-777.6 COAGULOPATHY +997 We Saunders Co.Vol. 10, No. 1 February 1999 ‘THE TRAUMA TRIAD OF DEATH = 87 “THE BLOODY VICIOUS CYCLE" Hemorrhage Cellular latrogenicl] Shock Factors. Ape ‘Coagulopathy creas (oon Contact Activation Massive Transfusion Clotting Factor] ~~ i Deficiencies Pre-existing Diseases Figure 2, The pathogenesis of the bloody vicious cy- cle" after severe injury is multifactorial, but progres sive core hypothermia and persistent metabolic aci- dosis are pivotal. Reprinted with permission, from Moore E, Laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg 1996:172: 405-410. © 1996 Excerpta Medica Inc. erally not seen until pH decreases below 7.2.15 The metabolic acidosis of hemorrhagic shock is exacerbated by aortic clamping, va- sopressors, massive transfusions, «and. im paited myocardial performance.!7 The exact role that acidosis plays in the triad remains ill defined. In preliminary work in animals, Dunn et al.! have demonstrated impaired hemostasis at pH 7.2. Djaldetti et al. have implicated pHi as directly affecting platelet function. Watts et «120 analyzed 112 trauma patients during the immediate posti jury period for the effect of hypothermia and severity of trauma on coagulation, Tempera lure accounted for six times more variation in acidosis than did injury severity. Acidosis therefore appears to be a sequela of hy- pothermia rather than of injury severity. This, is the only stucly to date that shows that aci- dosis within the triad contributes 10 coague lopathy primarily as a result of hypothermia, not independent of it ‘Therapy for metabolic acidosis remains directed toward correcting the underlying cause, that of hypoperfusion. A major goal continues to be optimizing oxygen delivery with adequate cardiac index and oxygen- curying capacity through volume loading and transfusions to achieve « hematocrit of more than 22%, Inotropic support is added when necessary. Resuscitation endpoints in clude normalization of arterial pH, base deficit, lactate, and gastric tonometry (pHi). In clinical trials, researchers have failed to demonstrate any clear advantage of bicar- bonate administration, whereas the potential adverse effets are well documented! Wile son? advocates deferring bicarbonate ad- ministration until pH persists below 7.1, de- spite optimal fluid loading and inowopic support. OHypothermia Hypothermia is an frequent pathophysio- logic consequence of severe injury and sub>- sequent resuscitation.2? Hypothermia results from heat loss that exceeds the body's ability to generate heat. It is estimated that as many 66% of trauma patients arrive in the em gency department with hypothermia.2! Gre- gory et al.2 found that hypothermia de oped at some point in 57% of the trauma patients studied, and that temperature loss was most severe in the emergency depart- nent. Predisposing factors include heat loss in the field, resuscitation maneuvers, injury severity, age, elevated alcohol level, expo: sure of body cavities during. surgery, im- paired thermogenesis, and degree of transfu- sion?" Gentiletio¥ classified the severity of hy- pothermia in the trauma patient as mild (36°C to 34°C), moderate (33.9°C to 32°C), and severe (below 28°C). Adverse clinical ef- fects such as cardiac dysthythmias, reduction in cardiac output, increase in systemie vase lar resistance, and a left shift in the oxygen- hemoglobin saturation curve have been de- cribed.2 Predicted mortality rates as high as 100% are seen in patients with severe hy-88 = MIKHAIL pothermia and severe injury.225 Clinical studies®0 have also shown that there is ex- cess lactic acid production in the presence of hypothermia, further enhancing the tad correlation. The most significant effect of hy- pothermia in trauma is coagulopathic bleed- ing. Hypothermic coagulopathy is attributed to prolonged clotting cascade enzyme reac- tions, dysfunctional platelets, and fibrinoly- sis.31 Hypothermia: A Double Edged Sword? The exact association between hypothermia and clinical morbidity remains elusive. Hy- pothermia has both protective and harmful clinical effects. During hypothermia, meta- bolic and oxygen demands are reduced? and multiple temperature-dependent enzy- matic reactions are simultaneously dis- rupted." Beneficial outcomes of hypother- mia have been demonstrated in brain injuries, cardiac arrest, and ischethic renal failure? Beneficial effects have also been seen in studies in animal models with in- duced hemorrhagic shock. Kim et al.3 using an uncontrolled hemorthagic shock model in rats recently demonstrated that moderate hypothermia prolongs survival time. No clinical trials of intentional hy- pothermia in patients with hemorrhagic shock have been performed to date. In the trauma patient, the question re- mains whether it is hypothermia, per se, or the severity of the injury producing the hy- pothermia that causes death, Researchers have shown that trauma patients with hy- pothermia have a higher mortality rate than do patients with a similar injury severity score who remain warm. However, the process of dying is normally characterized by a progressive decline in oxygen con- sumption and heat production, Therefore, hypothermia may not be the cause but the expected result of severe injury. Most stuclies analyzing the affect of hypothermia on out- comes to date have been retrospective. Gen- tilello et al.,#? in a prospective randomized study of 57 patients with major trauma and hypothermia, demonstrated that_hypother mia increases fluid requirements and inde- pendently increases the rate of death after major tauma, The need is apparent for a prospective multi-institutional study to inves- AACN Clinical Issues tigate this complex research question. The primary goal in atrisk patients is to avoid the onset of the triad of hypothermia, acido- sis, and coagulopathy, which is rapidly fatal if uninterrupted. Rewarming Strategies ‘The critical care nurse is responsible for init ating, maintaining, and monitoring the pa tient’s response to rewarming technique Rewarming strategies initiated in the emer- gency department and operating room are continued and extended aggressively in the intensive care unit, Strategies include passive and active external rewarming and active core rewarming, Passive external rewarming involves removing blood- or saline-soaked dressings or blankets, increasing ambient room temperature, and decreasing air flow over the patient by keeping the room doors shut. Active external rewarming devices in- clude fluid-circulating, convective-air, and Aluminum space blankets and overhead radi- ant warmers. Conductive rewarming with fluid-filled heating blankets placed under the patient is relatively inefficient because of minimal body-blanket contact, estimated to be Jess than 30%. Convective-air and alu- minum space blankets placed over the pa- tient provide greater heat exchange by creat- ing « 43°C microenvironment around the patient, which effectively stops heat loss. Su- perior warming is achieved when standard cotton blankets are placed over these blan- kets and the edges secured, although this limits patient access, Head covering is of prime importance: Because significant vaso- constriction does not occur in scalp vessels, as much ais 50% of radiant heat loss occurs from the neck up.23 Aluminized caps are ef fective warmers because they reflect emitted photons back to the scalp. Plastic bags or shower caps are an inexpensive and readily available alternative. The effectiveness of overhead radiant warmers is unclear, When aimed directly onto vasoconstricted skin, these warmers may cause inadvertent burn: yet when directed over a blanket, they pro- vicle no direct heat exchange to the patient. During laparotomy, it is recommended that covering exposed bowel with moist towels be avoided, because it can increase evapora- tive heat loss by nearly 250%. Dry towelslo. 1 February 1999 ‘THE TRAUMA TRIAD OF DEATH #89 or plastics bags «re superior, The nurse must remember that all of these strategies are more effective in preventing hypothermia than in treating it. ‘The hypothermic trauma patient requires active core rewarming which may include airway rewarming, heated body cavity lavage, heated intravenous Auids, continu- ous arteriovenous rewarming (CAVR), and extracorporeal circulatory rewarming. Hu- miclified ventilator circuits can be warmed to 41°C. Heated gastric, bladder, or colonic lavage is relatively ineffective because of the small surface area for heat transfer.28 Peri- toneal lavage is generally not feasible in most trauma patients undergoing laparo- tomy. Rarely, pleural lavage has been used with the plicement of two ipsilateral chest tubes enabling continuous flow of heated water. Use of warmed intravenous fluids is one of the simplest and most effective means of providing heat to the core in patients requir- ing massive fluid resuscitation. Current fluid warmer technology allows large volumes of warmed fluids to be infused quickly and to the current American Association of Blood. Bank standard of 42°C.*! Blood-warming, methods include surface-contact warmers, counter-current warmers, and heated-saline admixture.2-" In-line microwave blood- warming technology (in development) has been shown to heat blood safely to 49°C and shows great promise for the future.54® Cardiopulmonary bypass has limited ap- plicability in trauma patients because of the need for systemic anticoagulation. An alter- native is CAVR, developed by Gentilello et als? In CAVR, percutancously placed 8.5 French femoral arterial and venous catheters, and the patient's blood pressure, create an extracorporeal arteriovenous cir- cuit that uses the heating mechanism of a counter-current fluid warmer. Early studies have shown the greater effectiveness of CAVR in comparison with traditional warm ing techniques in rapidly rewarming trauma patients with severe hypothermia. “© How- ever, widespread use of this clevice has been limited because of the obligatory learning curve for involved personnel and infre- quency of use at many trauma centers in the country. Recently, CAVR use has been que: tioned for its negligible effect on long-term survival and associated increase in respira- tory distress syndrome, length of hospital stay, and ultimate cost, raising the possibility that rewarming only postpones, but does not prevent, death? Venovenous bypass, al- though more complex than arteriovenous systems, can also be performed by using a conventional roller pump to drive blood through a heat exchanger, which requires the constant attention of qualified person- nel.s459 Rewarming strategies tre summa- rized in Table 1 Despite implementation of aggressive re- warming strategies, patients often experi- ence the triad of hypothermia, coagulopa- thy, and acidosis during " exploratory laparotomy. The ultimate rewarming tech- nique is immediate packing, clecontamina- tion, and closure of the abdomen known as damage control surgery. The use of damage control surgery has evolved only in the past decade. Closing the “hostile” abdomen quickly and moving to the intensive care unit for rewarming is a lifesaving maneuver and in some institutions is performed within minutes. Using a mathematical model, Burch et al.!7 have estimated that the minimum pre: dicted heat loss of « trauma patient in shock who is subjected to exploritory laparotomy, despite state-of-the. dition, is 4.6°C per hour. This finding emphasizes the signif- icance of evaporative heat loss from an open peritoneal cavity with eviscerated bowel as a major contributor to hypothermia and re forces the need to terminate the operation quickly by temporary closure of the abdomi- nal cavity to prevent further heat loss. Good communication between the emer gency department, operating room, and in- tensive care unit should enable the critical care nurse to be prepared to receive the crit- ically ill patient with hypothermia, coagu- lopathy, and acidosis on short notice, to con- tinue all rewarming strategies initiated in the operating room, and to initiate other sti gies as technology allows OCoagulopathy Hemorthage after trauma is the result of two mechanisms: mechanical bleeding, also known as surgical bleeding, and coagulopa-90 = MIKEIATL AACN Clinical Issues TABLE 1 = Rewarming Strategies by Department Emergency department ‘Tum up heat in trauma resuscitation room ‘+ Minimize draft in trauma room, keep doors closed ‘Perform intubation with caution and by the most experienced provider + Administer warmed humicified oxygen to 41°C to ventilator circuit ‘+ Remove all wet clothing upon patient arrival + Apply head covering + Apply blankets (convective air heating or aluminum space blankets preferred) * Minimize body exposure when possible for examination and procedures + Monitor teriperature continuously, preferably via bladder or rectal + Administer all fluids and blood through a warmer to 42°C. Operating room + Tum up room temperature * Cover head and use heating blankets permitting surgical exposure + Drape effectively ‘= Monitor continuous core temperature via bladder or esophageal monitoring + Ventilate with warmed humidified oxygen at 41°C + Administer all luids and blood through a warmer to 42°C, + Perform pleural and or peritoneal warmed lavage as indicated + Apply dry towels or plastic bags to exposed bowel (avoid moist towels) ‘Assess for the onset of hypothermia, acidosis and coagulopathy + Anticipate employment of damage control surgery techniques + Prepare for immediate temporary closure of the abdomen using alternative techniques (towel clips, slo's, mariex, vicry, ete). Critical care unit + Tur up room temperature and keep room door closed * Continue head covering and convective warring blanket use + Coordinate and minimize exposure forall procedures * Monitor continuous core temperature via pulmonary artery catheter or bladder + Administer all fluids and blood through a warmer to 42°C + Ventilate with warmed humidified oxygen to 41°C + Implement continuous arterio venous rewarming (CAVA) thy, also defined as nonsurgical bleeding. sis.s! In several studies, investigators have in- Whereas mechanical damage may be treated dicated that hypothermia is related to the re- effectively by rapid surgical control, coagu- sultant shock state rather than merely to lopathy in the trauma patient isa more insid- blood volume loss.%2736053 Others have ious process. Developing in the operating shown that coagulation is unrekwted to the room andl intensive care unit, it may account severity of injury. Fluid resuscitation is for as many as half of all hemorrhagic deaths.5! Coagulopathy in the trauma patient is usually caused by hypothermia, massive transfusion, or both.? The mechanism by which hypothermia affects clotting is not clearly understood and continues to be de- bared.*!52 Suggested theories include enzyme inhibition, platelet alteration, and fibrinoly- commonly believed to ctuse or exacerbate hypothermia if the patient is not sufficiently warmed, Gubler et al.,% however, demon- strated that simultaneous hypothermia and hemodilution have «in independent additive effect on coagulopathy. Watts et al2? at tempted to determine a dose-response asso- ciation between hypothermia and coagu-Vol. 10, No.1 February 1999 ‘THE TRAUMA TRIAD OF DEATH = 91 TABLE 2 # Conditional Probability of Developing Life Threatening Coagulopathy 1S8>25 SBP<70mmHg Temp<34°C pH<7.10 Probability 1% x 10% x x 39% x x 49% x x 58% x x x 85% x x x x 98% ISS = injury severity score; SBP Reprintad from Cosqrlf N, Moore systolic blood pressure. ‘Sauaia A, Kenny-Maynihan M, Burch J, Galloway B. Predicting Ife threatening coagulopa- Ihy in the massively iransfused trauma pationt: Hypothermia and acidosis visited. J Trauma 1997;42:857-862, lopathy. ‘They found that those patients whose temperatures were higher than 33°C had significant hypercoagulability that is ac- wally common in trauma patients from the release of tissue thrombopkistin. When core temperatures dropped below 34°C, a distinct slowing of enzyme activity and decreased platelet function occurred, associated with hypothermic coagulopathy. This correlates with the trauma classification of hypothermia advanced by Gentilello et a.28 with core tem- peratures below 34°C and 32°C correspond- ing to moderate and severe hypothermia, respectively. Aggressive rewarming with on- going component therapy is required for ade- quate treatment. Suggested endpoints include prothrombin time «ind partial thromboplastin ne less than 1.25 times control levels, « platelet count higher than 100,000/mm®, and fibrinogen more than than 100 mg percent! Oldentification of Patients At Risk Despite the recognized deleterious effects of the triad—acidosis, hypothermia, and coagu: lopathy—the early identification of patients at risk remains elusive. Garrison et al.7 found the presence of early postinjury acido- sis, hypothermia, «and coagulopathy dlistin- guished nonsurvivors from survivors in a blunt trauma population with prolonged transport times. They suggested that key risk factors were transfusion of more than 15 units, injury severity score higher than 35, pH less than 7.2, and hypotension for longer than 70 minutes. Morris et al.5* found that tisk factors for the development of coagu- lopathy included temperatures fess than 35°C and base deficit less than or equal t0 15 iff et al. performed a pros- pective analysis of patients over t 2-year pe riod who received massive transfusions (greater than 10 units packed erythrocytes), to identify risk factors for the development of coagulopathy. Significant risk factors in- clude: pH less than 7.1, temperature le: than 34°C, injury severity’ score higher than 25, and systolic blood pressure less than 70 mmllg. Cosgriff et al. have calculated the conditional probability of development of coagulopathy with these risk factors (Table 2). Note that probability increase: tors increase, OThe Triad The multifactorial interactions between act- dosis, hypothermia, and coagulopathy in the exsanguinating trauma patient remain com- plex and formidable. The triad is not initi- ated by injury severity alone, or number of blood products transfused, but rather by the degree of hypoperfusion (Le. shock state).2627.4653-55 Progressive core hypother- mia with persistent metabolic acidosis is the precursor to severe and recalcitrant cougu- lopathy, The causal association of core hy- pothermia and coagulopathy has been demonstrated by numerous investigators, and the pathophysiology is multifactor- |.172028-8149-8052 ‘The role of metabolic aci- losis in the pathogenesis of impaired coagu- lation is less defined but is clearly implicated.\7-20290 Finally, it is known that92 = MIKHAIL the trauma patient with hypoperfusion who requires massive transfusion is at risk for the triad and that early recognition and use of damage control surgery offers the optimum, treatment for arresting this vicious cycle. OConclusion Nursing is pivotal to this ultimate resuscita- tion, of “pushing back the edge of death” in possibly the most demanding trauma patient to be confronted. Patients who previously died at the scene, in the emergency depart- ment, or operating room are now surviving to arrive in the intensive care unit in ex- tremis, thrusting the critical care nurse to the forefront of resuscitation. Critical care nurses’ understanding, prevention, and co- ordination of treatment of the trauma triad is the ultimate nursing challenge. References 1. Rotonclo MF, Zonies DH. The damage control sequence and underlying logic. Surg. Clin North Am 1997:77:761-777. Mattox KL, Hitshberg A, Wall M, Alternate ap- proaches to resuscitation, In: Ivatury RR, Gayten CG, eds. The Textbook of Penetrating Trauma, Balimore: Williams & Wilkins; 3 , Moore JB, Major abdomin: A unified approach. J 672-679, 4, Moore EE, Staged laparotomy for the hy- pothermia, acidosis, and coy drome, Am J Surg 1996;172:40: 5. 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