Advances in Trauma Care: Lessons from the Wars in Iraq and Afghanistan

While I was in Afghanistan (2014-2015), I researched and wrote an article regarding the advances in trauma care that have resulted in our wars in Iraq and Afghanistan.  I intended to publish this in Advance for PA's and NP's when I came home, but neglected to pursue submission due to other priorities and my inability to contact Mike at Merion Publishing.   I'm going to post the article here on my blog site, if for nothing else than to show I did actually write it and maybe someone will still get some practical benefit.   I would also like to point out that some of these lessons were instrumental in the phenomenal work of the Trauma staff in Las Vegas who were able to save many lives in the 2017 mass shooting there.

Lessons from the Battlefield: Damage Control Surgery, Resuscitation and

Tranexamic Acid (TXA) in Trauma Care

Roger S. Best, EMPA-C, MPAS

If anything beneficial has ever come from modern warfare, it has been the improvements in the survival rate of severely injured combat casualties.  These benefits eventually ring down to traumatically injured patients in the civilian world.  The wars in Iraq and Afghanistan have brought several major advances in trauma care¹: damage-control surgery (DCS), damage-control resuscitation (DCR), and the use Transexamic acid (TXA) in patients with massive hemorrhage. This article addresses these modalities, beginning with damage control surgery.

The concept of DCS^2,3 has been evolving since the 1990’s, but with lessons learned during the wars in Iraq and Afghanistan, the concept and practice of damage-control surgery has rapidly advanced in the war-time theater.  These practices are now gaining acceptance in civilian trauma care settings as well.  In DCS, patients are initially evaluated and receive any indicated emergent life-saving interventions (LSIs), i.e. definitive airway management, thoracostomy, initial resuscitation for hypovolemia, etc.  Once these have been performed, the patient is then taken to the operating suite for initial surgical interventions that are specifically designed to: 1) control hemorrhage; 2) prevent or mitigate contamination, and 3) protect the patient from further injury.

It is now well-established that trauma patients surviving their initial injuries are more likely to die from severe metabolic derangements than from the failure to complete the surgical repair(s) of their injuries.  These derangements, referred to as the “lethal triad,” include coagulopathies, which impair hemorrhage control, hypothermia and metabolic acidosis.^* Once these derangements are established, their management becomes problematic. Ironically, prolonged surgical procedures to complete repairs of injuries are major contributors to these derangements and to the corresponding increase in delayed patient mortality.  This realization requires a shift in the surgical mindset, where conventional surgical wisdom dictated that surgery is best provided as a single definitive procedure to one of staged surgical intervention(s).

Our collective wartime experience now shows that the best patient outcomes result from initial life-saving interventions, followed by abbreviated, staged surgical procedures, particularly laparotomy, to control hemorrhage, prevent further contamination and protect the patient from further injury.  Once these initial goals are accomplished, the patient is then transferred to the intensive care setting for management of coagulopathy, hypothermia and metabolic acidosis.  Once the patient’s physiologic condition has been optimized, they can be returned to the OR for completion of surgical care.  Best practices in trauma care now dictate a continuum of staged surgical interventions, interspersed with ICU care in order to optimize the patient’s medical condition between interventions.

Damage Control Resuscitation (DCR)^3,4, is emergent medical care provided to treat or mitigate the impact of coagulopathies, hypothermia and metabolic acidosis, either in concert with DCS, or while the patient is awaiting surgical intervention.  The initial, and most important aspect of DCR, is to optimize the control of hemorrhage.  Death from hemorrhage accounts for 30-45% of trauma deaths, but paradoxically is the most preventable cause of death among combat casualties. 

In contrast to previous approaches initially using direct pressure, elevation and proximal arterial pressure points for the control severe bleeding, the methods best proven for the control of potentially life threatening hemorrhage should be limited to direct pressure to compressible bleeding sites, the use of hemostatic dressings, and the effective use of tourniquets.

Direct pressure remains the mainstay of initial hemorrhage control measures. Hemostasis can be achieved quickly with a compressible wound.  Hemostatic dressings used in conjunction with pressure are highly effective.  In cases where an extremity injury results in severe bleeding and these techniques will not quickly bring this under control, then proximal application of a tourniquet is the intervention of choice. In the wartime experience, the use of tourniquets have shown several advantages, where the prehospital time is under six (6) hours, including:

·         Improved hemorrhage control

·         Decreased incidence of shock

·         Improved survival

·         Acceptably low rate of tourniquet-related complications

Non-traditional tourniquets (junctional tourniquets) have also been developed and have shown success in controlling hemorrhage from typically non-compressible sites, such as the iliac and axillary arteries⁵.  In areas of hemorrhage where bleeding is occurring from inaccessible sites, i.e. Pelvic fractures, non-compressible injuries not amenable to tourniquet application, therapies such as pelvic binders and also hemostatic dressings (i.e. Combat Gauze) have shown some benefit.  Ultimately, the goal of using more aggressive methods of hemorrhage control are intended to reduce the need for massive transfusion and address the resultant risk of coagulopathy.

Predictive indicators of the need for transfusion therapy include penetrating injuries to the trunk, systemic hypotension (SBP<90 and="" core="" hg="" hypothermia="" mm="">36°C or 96°F).  However, data from the National Trauma Data Bank has shown increased mortality with SBP of <110 10mm="" 4.8="" a="" abnormalities.="" absent="" altered="" are="" as="" at="" base="" begin="" combination="" deaths="" deficits="" defined="" drop="" early="" every="" following="" for="" heart-rate="" helpful="" heralding="" hg.="" hg="" hypotension="" identifying="" in="" increase="" injured="" is="" laboratory="" loss="" massive="" mental="" mm="" nbsp="" o:p="" of="" onset="" or="" patients="" perfusion="" pulse="" radial="" requiring="" sbp.="" sbp="" sbps="" severely="" status="" studies="" the="" therapy.="" this="" tissue="" transfusion="" trauma="" variability="" weak="" with="">

·         Base deficit > 6 or pH < 7.25

·         INR > 1.5

·         Hemoglobin <11 hematocrit="" o:p="" or="">

Even with what would have previously been considered “stable” levels of SBP (90-118 mm/hg), the insidious onset of the shock state can be seen in the increasing base deficit, declining pH, declining H&H values, and the early onset of coagulopathy. 

The next component of DCR is the prevention of hypothermia, which increases the risk of life-threatening hemorrhage and associated mortality, with a death rate of 100% in severe cases.  Strategies to combat the incidence and degree of hypothermia in the prehospital setting by focusing on hemorrhage control, limiting the amount of clothing removed, instituting passive warming techniques such as the use of wool, solar and warming blankets and the infusions warmed IV fluids.  Passive and active anti-hypothermic measures should be continued in the emergency and intensive care settings.

The final component of DCR is the management of hypotension, transfusion considerations and the mitigation of metabolic derangements.  Ideally, the goal would be to address all of these derangements simultaneously.  In prehospital settings, or at facilities where appropriate surgical services are not readily available, consideration should be given to “hypotensive resuscitation” in selected cases.

In hypotensive resuscitation, aggressive hemorrhage control of active bleeding is the focus, along with vascular access and conservative intravenous fluid administration, while a lower-then-normal SBP is permitted.  The intention is to avoid rebleeding and dilutional coagulopathy until surgical control of hemorrhage can be accomplished. This approach uses the body’s natural coagulation cascade, vascular spasm secondary to injury, and a degree is hypotension (SBP <90 1="" 2="" a="" and="" animal="" are="" b="" be="" beneficial:="" by="" care.="" cases="" clearly="" cns="" combat="" controlled="" current="" delayed="" felt="" field="" further="" hemorrhage="" hg="" hospitals="" however="" hypotension="" hypotensive="" immediately="" in="" indicated="" is="" mitigate="" mm="" nbsp="" non-compressible="" not="" of="" only="" operations="" operative="" or="" patient="" permissive="" practices="" quickly="" reaching="" reflects="" resuscitation="" s="" situations="" studies="" support="" surgical="" taken="" teams="" the="" there="" to="" trauma="" two="" war="" well-supported="" where="" will="" with="" zones.="">⁶

or in cases of impending vascular collapse. 

Where hypotensive resuscitation is not indicated, intravenous therapy may be instituted to support circulation.  Traditionally, crystalloid solutions such and normal saline (NS) or lactated ringer’s solution (LR) have been used for initial resuscitation.  In animal studies of these fluids in the treatment of traumatic shock, NS was shown to contribute to metabolic acidosis and worsening coagulopathy, whereas this was not observed using LR. Theoretically, either fluid in significant volume (>20 mL/kg) may result in dilutional coagulopathy, and while LR has been shown to be superior in animal models for trauma resuscitation, neither fluid is ideal and the administration of greater than 20 mL/kg is of dubious benefit.  Colloidal solutions, such as HES (Hetastarch) also contribute to dilutional coagulopathy, but has the added disadvantage of impairing the plasma activity of von Willebrand factor⁷.  These effects would make such solutions undesirable for resuscitation in the setting of continuing hemorrhage.

Vasopressor agents, though widely used in medical shock states, are generally eschewed in the case of acute hemorrhagic shock.   However, an exception may be the use of low-dose vasopressin, which apparently becomes deficient in advanced stages of hemorrhagic shock.  Theoretically, vasopressin may lower overall resuscitation volumes is hemorrhagic shock, reducing morbidity and mortality, but there are currently no studies to support its use.  Promising studies thus have shown enhanced survival from lethal hemorrhage in porcine subjects⁸ and reduced fluid resuscitation volumes in human subjects. More extensive human trials are planned involving the use of vasopressin in trauma.

The resuscitation fluids of choice for hemorrhagic shock include whole blood, or combination blood component therapy.  Whole blood has the advantage of volume replacement with an equivalent oxygen-carrying substitute, while concomitantly addressing coagulation deficiencies.  In the absence of whole blood, component therapy at a 1:6:6* ratio of platelets, PRBCs and fresh-frozen plasma respectively is the currently preferred option until patient stabilization has been obtained⁹.

*Concentrated platelets are equivalent to the number of platelets contain in 6 units of whole blood.  Administration of a unit of concentrated platelets per 6 units of PRBCs and FFP is equal to a blood component transfusion ratio of 1:1:1.

Massive transfusion is generally considered as the administration of 10 or more units of blood within a 24-hour period.  During massive transfusion, the patient will need to be under continuous surveillance for associated transfusion-related complications, including potential hyperkalemia and hypocalcemia, and treated accordingly¹⁰.

In patients who receive massive transfusion therapy, the early use of Transexamic acid (TXA) has been shown to improve survival¹¹.  TXA is an Antifibrinolytic agent that exerts a protective effect against the onset of coagulopathies (i.e. DIC). Studies using TXA in the setting of combat trauma have demonstrated improvements in long-term patient survival, despite higher injury severity scores in TXA-treated casualties requiring massive transfusion if TXA is administered within 3 hours following an injury¹².

Advances in the care of trauma victims continue to evolve from our dynamic experiences with combat casualties.   Simply getting the patient into the surgical suite is no longer the gold standard of care, but rather a part of a balanced multi-disciplinary approach that includes life-saving pre-hospital and emergency department therapies, staged surgical interventions, and intensive care optimization that will provide more substantial reductions in mortality and morbidity than seen previous decades.

1. Howell SJ. Advances in trauma care: a quiet revolution. British Journal of    Anaesthesia (2014) 113 (2): 201-202

2.       Wyrzykowski AD, Feliciano DV: Trauma damage control. In Trauma. 6th edition. 2008: 851-870. 

3.       Lenhart MK., Savitsky E., Eastridge B., Combat Casualty Care: Lessons Learned from OEF and OIF. Office of the Surgeon General, U.S. Army. Borden Institute, Fort Detrick MD. 2014.

4.    McLamb CM, MacGoey P, Navarro, AP, Brooks AJ. Damage control surgery in the era of damage control resuscitation. British Journal of Anaesthesia; (2014) 113 (2): 242-249.

5.       Kotwal, Russ S., et al. Management of Junctional Hemorrhage in Tactical Combat Casualty Care: TCCC Guidelines–Proposed Change 13-03. Journal of Special Operations Medicine; 13.4 (2013): 85-93.

6.  Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; et al. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. Journal of Neurotrauma 2007; 24 (1 Supplement): S7-13.

7.       Treib J, Haass A, Pindur G. Coagulation disorders caused by hydroxyethyl starch. Thromb Haemost; 1997; 78(3): 974-983.

8.       Karl H. Stadlbauer, M.D., Horst G. Wagner-Berger, M.D., et al. Vasopressin, but Not Fluid Resuscitation, Enhances Survival in a Liver Trauma Model with Uncontrolled and Otherwise Lethal Hemorrhagic Shock in Pigs. Anesthesiology; 2003; 98: 699–704

9.       Ho AM, Dion PW, Cheng CA, et al. A mathematical model for fresh frozen plasma transfusion strategies during major trauma resuscitation with ongoing hemorrhage. Canadian Journal of Surgery 2005; 48(6): 470-478.

10.   Kristen C. Sihler, MD, MS; Lena M. Napolitano, MD. Complications of Massive Transfusion. Chest; 2010; 137(1): 209-220.

11.   Rappold JF, Pusateri AE. Tranexamic acid in remote damage control resuscitation. Transfusion. 2013 Jan; 53 (Supplement 1): 96S-99S.

12.   Olldashi F, Kerci M, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: An exploratory analysis of the CRASH-2 randomised controlled trial. The Lancet 2011; 377 (9771) 

Roger Scott Best, EMPA-C, MPAS

Emergency Medicine Physician Assistant

Bagram Air Field, Afghanistan - Providing medical services in support of 401st Army Field Support Brigade

Lives in Garner, North Carolina.