ourniquets are indicated when direct pressure is unable to establish bleeding control
You and your partner are dispatched to the scene of a rural motor vehicle collision. After a 35-minute response, you arrive on scene to find a single patient who was involved in a vehicle rollover on a state highway. The driver is unrestrained and still in the vehicle.
The vehicle shows a large amount of external damage. The patient is awake and alert but complaining of abdominal pain. Volunteer fire department personnel have placed him in a C-collar prior to your arrival and are extricating him on a long backboard to ease movement from the roadside ditch to your gurney.
As the patient is removed from the backboard, you begin your assessment. You find a 19-year-old male who shows no signs of serious head trauma and reports the accident occurred when he "swerved to miss a bunny rabbit."
The young man's chest is clear to auscultation. His chest wall is stable but mildly tender to palpitation. His heart sounds tachycardic. He has a strong carotid pulse.
As you finish your primary assessment, your partner reports vitals: heart rate of 115, blood pressure 100/65 mmHg, pulse oximeter 98%, temperature 37 degrees C. Your partner sets the blood pressure cuff to cycle every five minutes and establishes IV access.
Upon physical examination you find the patient's abdomen is rigid with marked tenderness in the left upper quadrant. His extremities show abrasions to his left upper leg and left forearm. No other apparent injury is noted.
The patient moves all four extremities on command. His pelvis is stable. He denies any loss of consciousness and reports that he thinks he hit the steering wheel with his abdomen. He takes no medications daily. He has no allergies. He denies any drug or alcohol use.
Trauma remains a major cause of death and disability globally.1,2 Damage control resuscitation is a strategy that focuses on attempting to maintain or restore homeostasis intrauma patients.
The name "damage control" references the naval tactics employed to keep a damaged ship as combat-capable as possible until definite repair can take place. The concept goes hand in hand with damage control surgery. However, for prehospital care, surgery is clearly beyond the scope of practice and won't be discussed here.
First described in the late 1970s and early 1980s, damage control resuscitation has continued to evolve and is primarily focused on mitigating the life threats of trauma.3
The main threats concentrated on in damage control resuscitation are acidosis, coagulopathy and hypothermia. Ideally, these pathologies are all addressed in a simultaneous and balanced manner. These three abnormalities form a forward feedback loop that leads to progressive worsening of a patient's hemodynamic status and will eventually lead to death.
This instability is due to the fact that the human body is designed to function within a very narrow set of physiologic parameters. The enzymes that dictate cellular metabolism function best at a pH of 7.4 and temperature of 37 degrees C.
These enzymes allow the chemical reactions the body relies upon to occur at a lower energy input than would be chemically required without them. Deprived of the actions of these enzymes, the body's ability to perform basic functions is severely impaired.
Lactic acid formation is a result of tissue hypoxia. Tissue hypoxia can occur because not enough blood is getting to the tissues (hypoprofusion) or the blood that is being supplied is very poorly oxygenated.
The end result at the cellular level is a switch from oxidative phosphorylation to anaerobic metabolism yielding lactic acid as a byproduct. Whatever the cause, lactic acid lowers the pH of the body when it exceeds the body's physiologic buffering capacity.
Coagulopathy occurs when the enzymes that cause blood to clot are unable to function, or the body is out of clotting factors. Bleeding from trauma causes consumption of clotting factors.
Additionally, infusion of fluid deficient of clotting factors exacerbates this by causing dilution. A low pH due to lactic acidosis or a low body temperature also causes coagulopathy. Hypothermia results when the body loses more heat to the environment than it is able to produce.4
Metabolism is a large source of body heat production. As the body's temperature drops, all enzymes become less efficient.3 This results in worsening coagulopathy, and decreased metabolism, including decreased lactic acid breakdown. The decrease in metabolism not only results in impaired lactic acid clearance but impaired ability to produce heat. This worsens coagulopathy and hypothermia.
Worsening coagulopathy leads to continued bleeding, worsening tissue hypoprofusion and lactic acid production. Thus, the forward feedback cycle is perpetuated. (See Figure 1, p. 36.)
Figure 1: The forward feedback cycle following traumatic injury
Patients in Need
Identifying which patients are in need of damage control resuscitation is similar to identifying which patients need the highest level of trauma care. Since prehospital care is often limited by resources and time (vs. in-hospital care), historic and physiologic findings are most helpful to identify these patients. These objective findings can be relatively quick and easy to identify on scene.
Anatomic parameters for damage control resuscitation consideration include: injury severity score > 36, penetrating abdominal or chest injuries, unstable pelvic fracture, long bone fracture with head injury, truncal hemorrhage or amputation.3
Physiologic parameters include: weak or absent radial pulse, core body temperature < 35 degrees C, systolic blood pressure < 100 mmHg, and heart rate > 100.3
These criteria are similar to, although not quite the same as, the guidelines for field triage of injured patients from the American
College of Surgeons Committee on Trauma (ACS-COT). The ACS-COT physiologic guideline include Glasgow coma scale < 13, systolic blood pressure < 90, respiratory rate < 10 or > 29 breaths per minute (< 20 if under age 1 year), or need for respiratory support.5
The ACS-COT anatomic guidelines include all penetrating injuries to the head, neck, torso and extremities proximal to the elbow or knee; chest wall instability or deformity; two or more proximal long bone fractures; crushed, degloved, mangled or pulseless extremity; amputation proximal to the wrist or ankle; pelvic fracture; open or depressed skull fracture; or paralysis.5
Damage control resuscitation is a strategy that
focuses on attempting to maintain or restore
homeostasis in trauma patients. Photo Andrew Klein
The mainstay of breaking the pathophysiologic cycle is to achieve hemorrhage control. In circumstances where only definitive surgery is capable of stopping bleeding, getting the patient to the operating room in a timely fashion is of the utmost importance. There are, however, tools available to EMS that can temporize bleeding until an operating room can be reached.
The first-line treatment for bleeding is direct pressure. Direct pressure results in superior measurements of wound pressure when compared to standard and elastic dressings. One study showed average pressures of 180 mmHg with direct pressure, 88 mmHg with elastic bandages, and 33 mmHg with standard bandages.6
The amount of pressure applied is important because in order to stop the bleeding, the pressure must exceed the blood pressure at the wound. Although it's labor intensive, direct pressure achieves higher pressures than either elastic or standard bandages.
Tourniquets are indicated when direct pressure is unable to establish bleeding control.7 The tourniquet has been around in various iterations for hundreds of years. When indicated, the tourniquet should be applied as soon as possible. There's a decrease in mortality when tourniquets are applied in the field vs. the ED.8 Once applied, the tourniquet should be left on until definitive care is reached.
Another option for bleeding that's not controllable with direct pressure is hemostatic dressings. Hemostatic dressings generally have high success rates for controlling bleeding that's resistant to direct pressure.9
These dressings are broadly divided into three categories: intrinsic pathway activators, factor concentrators and mucoadhesive agents.
Intrinsic pathway activators directly signal the blood to clot. Examples of intrinsic pathway activators include kaolin and smectite.
Factor concentrators work by absorbing the liquid component of the blood, leaving concentrated clotting factors to form a clot. An example of factor concentrators includes mucopolysaccharide hemispheres.
Mucoadhesive agents work by forming an electron bond to cell walls. Examples of mucoadhesive agents include chitosan-
Pelvic and femur fractures can result in significant bleeding.10,11 The bleeding associated with unstable pelvic fractures is usually from the sacral venous plexus.12 It can often be temporized with some sort of pelvic binder, be it improvised or commercial.13,14
Traction splints may decrease the bleeding associated with femur fractures. No good modern data exists regarding traction splints; however, anecdotal evidence from World War I shows a significant decrease in mortality for isolated femur fracture after instating a traction splinting program.15 Therefore, splinting is important to keep in mind and accomplish as soon as possible after other serious sources of bleeding have been addressed.
Appropriate fluid administration might help to maintain homeostasis. Inappropriate fluid administration will do just the opposite.16
In penetrating trauma to the torso, in particular, research shows that withholding isotonic IV fluid had a mortality benefit.17 This data came from an urban EMS system where transport times were presumed to be relatively short. Only patients with a systolic blood pressure of 90 mmHg or less were included. This would seem to suggest that there may be a role for restrictive isotonic fluid administration.
There's additional data to support this and even extrapolate it to blunt trauma. Large data from a national trauma data bank suggest that IV fluid administration is associated with increased mortality for all types of trauma.18 Although the absolute difference in the results is low (0.3%), it's statically significant given the large study size of 776,000 patients. There's of course some disagreement in the literature with some studies showing no harm from IV fluid.19
ED data from a large Level 1 trauma center showed an increase in mortality associated with IV fluid volumes of greater than 1.5 L but no increase in mortality with 1 L of fluid or less.20
It's postulated that the benefit may come from decreased dilatational coagulopathy and hemostatic maintenance.20 There appears to be no benefit from using hypertonic saline compared to normal saline in the prehospital setting.21 Although there's no perfect prehospital study, these studies did attempt to control for severity of injury and other confounding factors. Current evidence, however, doesn't support the strategy of allowing a low blood pressure and restricting fluid in patients with head injuries.22
Hypotensive head trauma patients have increased mortality compared to patients resuscitated to a normal blood pressure. The takeaway message is that the minimum amount of isotonic fluid needed to maintain mental status or mean arterial pressure of 65 mmHg is probably the best strategy for patients without significant head injury.3,23
Blood & Plasma Transfusion
Transfusion of blood products is a potentially lifesaving intervention for patients with severe trauma. The ideal initial ratio for the massive transfusion of blood products is generally accepted to be one unit of fresh frozen plasma to one unit of platelets to one unit of packed red blood cells (PRBCs) (1:1:1).24
Recent research has looked at a lower ratio of platelets and plasma to packed cells 1:1:2. It showed that though the absolute all-cause mortality rate was lower in the 1:1:1 group, there was no statistical difference in mortality at 24 hours or 30 days. Notably, the 1:1:1 group did have statistically significant higher rates of hemostasis and lower rates of death due to exsanguination at 24 hours. Additionally, the complication rate was the same for both groups.25
A study of trauma patients transported by a helicopter EMS system that carried blood found that early transfusion in trauma patients with hemorrhagic shock results in decreased mortality.26
There was a correlation between shorter time to transfusion and survival for patients who received blood within one hour of arrival to the ED. This benefit wasn't found for all patients who received blood in the first 24 hours. This suggests a confounding factor: that this subset of patients was different than the patients who were not transfused with in the first hour of ED admission.26
Early transfusion with blood products is more beneficial than high volume isotonic fluid.3,27
Another component available to some EMS agencies is plasma. Plasma is the liquid component of the blood and contains many proteins including clotting factors. Although the exact mechanisms are unknown, plasma does decrease the damage to the lining of the blood vessels, the endothelium. This results in less fluid leaking out into the tissues.
Early plasma transfusion appears to have a favorable impact on mortality in trauma patients and is an integral part of balanced transfusion as noted above. Prehospital trauma trials investigating its efficacy are ongoing, and recent changes in logistical considerations may make plasma more feasible for prehospital use in the near future.28
Transfusion of blood products is a potentially lifesaving intervention for
patients with severe trauma. Photo courtesy North Memorial Ambulance Service
Pharmacologic treatments that may have a role in treating trauma-induced coagulopathy include: prothrombin complex concentrate (PCC), cryopricpate, calcium and tranexamic acid (TXA).
PCC is used to reverse pharmaceutical anticoagulation. It's a mix of vitamin K-dependent clotting factors and isn't typically used in the prehospital setting.
Cryopricpiate contains clotting factors VIII and XIII in addition to fibrinogen and von Willebrand factor. It isn't generally used in prehospital care in the United States.
Calcium is essential in the clotting cascade for the conversion of factor X to factor Xa and for the conversion of prothrombin to thrombin. Both of these reactions are critical for formation of a blood clot. Low calcium is a predictor of trauma mortality.29
Calcium is chelated, or captured by citrate. Citrate is used to keep donated blood from clotting. Thus, when PRBCs are transfused so is some citrate. This leads to calcium chelation and lowering of serum calcium.
In one study's sample of 156 massive transfusion patients, 97% developed hypocalcemia. Those who developed severe hypocalcemia had significantly lower pH, lower platelets, higher lactic acid and higher mortality (49% vs 24%).29
Another study found that 55% of major trauma patients arrived to the ED with hypocalcemia and 89% developed hypocalcemia after receiving one unit of blood. The authors concluded that, "With increasing early blood product use, trauma victims being at risk of hypocalcemia and receiving any amount of blood product further worsening this state, prompt recognition of hypocalcaemia and early targeted therapy is needed from arrival." 30
Additionally, calcium helps to increase myocardial contractility, countering the effect of hyperkalemia caused by acidosis. This results in increased blood pressure. It would seem reasonable for prehospital providers to begin replacing calcium after one unit of blood is transfused, or in anticipation of massive transfusion.
TXA is FDA approved for the treatment and prevention of dental bleeding in hemophilia and heavy menstrual bleeding and has seen "off-label" use to reduce blood loss during cardiac and orthopedic surgery as well as for trauma patients. TXA appears to stabilize blood clots by competitively binding to the lysine binding site on plasminogen and preventing its conversion to plasmin. This stops clot breakdown and is thought to result in less bleeding. As there's less clot turnover, TXA is theorized to reduce depletion of clotting factors and reduce consumptive coagulopathy. Since TXA is a lysine analog, it may have other physiologic effects that are not fully understood.
There's a large amount of data showing that TXA reduces bleeding associated with cardiac and orthopedic surgery. In a study of over 800,000 orthopedic cases that TXA reduce the needs for transfusion (7.7% vs 20.1%) and had no increase in complications.31 TXA is also used routinely in pediatric cardiac surgery, though it's infrequently used in pediatric trauma.32 In a small trial of 776 trauma patients, TXA appeared to significantly reduce pediatric trauma mortality.33
Following the publication of two seminal studies, MATTERS and CRASH-2, TXA was received enthusiastically in the U.S with multiple prehospital systems adding it to their formulary.27 This has resulted in significant controversy, largely due to the fact that the above studies aren't the most robust in design, resulting in concern about the true benefits of TXA in trauma.
The role of TXA in head trauma is unclear and currently being studied. Although there are multiple ongoing, more robustly designed prehospital studies, in the current literature it does appear that TXA may offer a benefit to trauma patients receiving massive transfusion, and regardless of benefit, causes no increase in complications.27 Since there appears to be a time-dependent component to the benefit of TXA, it would seem reasonable to continue TXA prehospital use in patients who meet transfusion criteria.3,27
Prehospital awareness of hypothermia is important for its management. After all, the mechanism by which patients become hypothermic is due to the movement of heat from hot (e.g., the patient) to cold (e.g., the environment).
If patients are insulated from heat loss, they'll be better able to maintain their temperature. This becomes particularly important when the patient has impaired heat production due to acidosis-the forward feedback cycle can be hard to break once it starts. An additional intervention is the use of hot packs or heated wraps, but extreme care must be taken not to cause burns.
The next blood pressure reading on the patient is 87/62 mmHg, and his heart rate is 120. He states that he "feels a little dizzy." Your partner starts a 250 mL bolus of normal saline.
Dispatch states that the helicopter that was activated and launched will arrive at the off-hospital helipad a few minutes before you'd arrive at the critical access hospital, so you make the decision, following local protocol, to bypass that hospital.
Despite the infusion of normal saline, the patient's blood pressure is still 88/60 mmHg, but his heart rate is 113 and he feels less dizzy. Your partner decreases the rate to keep the line open.
On arrival, the helicopter flight crew evaluates the patient. His heart rate is again in the 120 range. They start a second large-bore IV and begin to transfuse PRBCs and initiate transport to the nearest trauma center.
After transiently responding to the PRBCs, the patient receives 1 gram of calcium chloride, 1 gram of TXA and 1 unit of plasma inflight. He survives because of the joint efforts of the on scene responders and flight crew as a result of clear, well-defined trauma protocols, advanced hemorrhage control care, and rapid transport to the appropriate trauma center.
1. Peden M, McGee K, Krug E, eds.: Injury: A leading cause of the global burden of disease, 2000. World Health Organization: Geneva, 2002.
2. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet.2012;380(9859):2095-2128.
3. Giannoudi M, Harwood P. Damage control resuscitation: Lessons learned. Eur J Trauma Emerg Surg. 2016;42(3):273-282.
4. Kaafarani HM, Velmahos GC. Damage control resuscitation in trauma. Scand J Surg. 2014;103(2):81-88.
5. Sasser SM, Hunt RC, Faul M, et al. Guidelines for field triage of injured patients: Tecommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012;61(RR-1):1-20.
6. Naimer SA, Anat N, Katif G, et al. Evaluation of techniques for treating the bleeding wound. Injury. 2004;35(10):974-979.
7. Welling DR, Burris DG, Hutton JE, et al. A balanced approach to tourniquet use: Lessons learned and relearned. J Am Coll Surg. 2006;203(1):106-115.
8. Kragh JF Jr, Walters TJ, Baer DG, et al. Survival with emergency tourniquet use to stop bleeding in major limb trauma. Ann Surg. 2009;249(1):1-7.
9. Littlejohn L, Bennett BL, Drew B. Application of current hemorrhage control techniques for backcountry care: Part two, hemostatic dressings and other adjuncts. Wilderness Environ Med. 2015;26(2):246-254.
10. Grotz MR, Allami MK, Harwood P, et al. Open pelvic fractures: Epidemiology, current concepts of management and outcome. Injury. 2005;36(1):1-13.
11. Lieurance R, Benjamin JB, Rappaport WD. Blood loss and transfusion in patients with isolated femur fractures. J Orthop Trauma. 1992;6(2):175-179.
12. Gänsslen A, Giannoudis P, Pape HC. Hemorrhage in pelvic fracture: Who needs angiography?
Curr Opin Crit Care. 2003;9(6):515-523.
13. Routt ML Jr, Falicov A, Woodhouse E, et al. Circumferential pelvic antishock sheeting: A temporary resuscitation aid. J Orthop Trauma. 2006;20(1 Suppl):S3-S6.
14. Pizanis A, Pohlemann T, Burkhardt M, et al. Emergency stabilization of the pelvic ring: Clinical comparison between three different techniques. Injury. 2013;44(12):1760-1764.
15. Jones R. Crippling due to fractures: Its prevention and remedy. Br Med J. 1925;I:909-913.
16. Cotton BA, Guy JS, Morris JA Jr, et al. The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock. 2006;26(2):115-121.
17. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331(17):1105-1109.
18. Haut ER, Kalish BT, Cotton BA, et al. Prehospital intravenous fluid administration is associated with higher mortality in trauma patients: A National Trauma Data Bank analysis. Ann Surg. 2011;253(2):371-377.
19. Sharpe JP, Magnotti LJ, Croce MA, et al. Crystalloid administration during trauma resuscitation: Does less really equal more? J Trauma Acute Care Surg. 2014;77(6):828-832.
20. Ley EJ, Clond MA, Srour MK, et al. Emergency department crystalloid resuscitation of 1.5 L or more is associated with increased mortality in elderly and nonelderly trauma patients. J Trauma. 2011;70(2):398-400.
21. Bulger EM, May S, Kerby JD, et al. Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: A randomized, placebo controlled trial. Ann Surg. 2011;253(3):431-441.
22. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34(2):216-222.
23. Chang R, Holcomb J. Optimal fluid therapy for traumatic hemorrhagic shock. Crit Care Clin. 2017;33(1):15-36.
24. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63(4):805-813.
25. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets and red blood cells in a 1:1:1 vs. a 1:1:2 ratio and mortality in patients with severe trauma: The PROPPR randomized clinical trial. JAMA. 2015;313(5):471-482.
26. Powell EK, Hinckley WR, Gottula A, et al. Shorter times to packed red blood cell transfusion are associated with decreased risk of death in traumatically injured patients. J Trauma Acute Care Surg. 2016;81(3):458-462.
27. Ramirez RJ, Spinella PC, Bochicchio GV. Tranexamic acid update in trauma. Crit Care Clin. 2017;33(1):85-99.
28. Watson JJ, Pati S, Schreiber MA. Plasma transfusion: History, current realities, and novel improvements. Shock. 2016;46(5):468-479.
29. Giancarelli A, Birrer KL, Alban RF, et al. Hypocalcemia in trauma patients receiving massive transfusion. J Surg Res. 2016;202(1):182-187.
30. Webster S, Todd S, Redhead J, et al. Ionised calcium levels in major trauma patients who received blood in the emergency department. Emerg Med J. 2016;33(8):569-572.
31. Poeran J, Rasul R, Suzuki S, et al. Tranexamic acid use and postoperative outcomes in patients undergoing total hip or knee arthroplasty in the United States: Retrospective analysis of effectiveness and safety. BMJ.2014;349:g4829.
32. Nishijima DK, Monuteaux MC, Faraoni D, et al. Tranexamic acid use in United States children's hospitals. J Emerg Med. 2016;50(6):868-874.
33. Eckert MJ, Wertin TM, Tyner SD, et al. Tranexamic acid administration to pediatric trauma patients in a combat setting: The pediatric trauma and tranexamic acid study (PED-TRAX). J Trauma Acute Care Surg.2014;77(6):852-858.