The Crashing Trauma Patient

Author: Bryant Allen, MD (@bryantkallen, Assistant Profess of Emergency Medicine, Carolinas Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021, Senior Staff Physician, Henry Ford Hospital)

ABCDE: General principles for the resuscitation and treatment of the unstable trauma patient

Case 1: A 35-year-old male presents after a high-speed motor vehicle collision. He was the restrained driver of a vehicle traveling approximately 70 mph when it struck a tractor-trailer stopped in the roadway. First responders found him slumped in his seat, airbags deployed, with the seat fractured from the vehicle. The car had severe front-end damage. He was placed in a cervical collar by EMS and after a prolonged extraction was placed on a spine board. Obvious injuries included an open deformity to his right femur, a tender and distended abdomen, and multiple facial and scalp injuries. Vital signs per EMS included a maximum heart rate of 139 bpm, lowest blood pressure of 84/40 mmHg, respiratory rate of 30 bpm, and GCS of 6.

Introduction

Accidental and traumatic injuries remain one of the leading causes of death worldwide, accounting for 5.8 million deaths annually and a large percentage of ED evaluations.¹ Increasing disease severity creates an environment that makes patient care difficult. The American College of Surgeons has created a protocol driven framework, Advanced Trauma Life Support, in order to overcome this challenge and achieve success in the “Golden Hour”.

Management of the crashing trauma patient can be hectic and challenging. The primary role of the traumatologist is to create a calm environment in the trauma bay in order to effectively designate roles and provide cohesive, structured care. Preparing the trauma team prior to arrival can be helpful in order to obtain appropriate equipment, including an airway cart, RSI drugs, tube thoracostomy, ED thoracotomy tray, or a Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) catheter. Managing the room and all members of the trauma team can be difficult, but can often make a sloppy and potentially unsuccessful resuscitation more organized. As the Boy Scouts of America motto states, “Be prepared.”

After preparation for the resuscitation is complete, initial evaluation and management of the unstable trauma patient can be framed using the ATLS Primary Survey mnemonic ABCDE.

A – Airway maintenance and cervical spine precaution

Cervical spine precautions

Patients presenting with debilitating traumatic injury have been found to have a high prevalence of cervical spine injuries, with between 4-34% of polytrauma patients suffering from cervical spine injury.² Given this high likelihood of injury, care should be taken with initial evaluation, transport and bed transfer of these patients, with use of appropriately sized and fitted cervical collars. Manual in-line stabilization methods during intubation are important as well, given stabilization with a cervical collar during intubation can limit jaw movement, increasing the difficulty of intubation.² However, when such interventions limit laryngoscopic views, as has been seen in the setting of direct laryngoscope usage, relaxation of aggressive immobilization may be necessary to facilitate successful intubation.³ Efforts to limit flexion and extension, including usage of a supraglottic airway, gum-elastic bougie or video laryngoscopy, should be considered for every polytrauma patient requiring airway management.

Intubation

In many cases, the unstable and crashing trauma patient will require securement of the airway through intubation. An extensive deep dive into this topic was covered recently (here). The trauma airway is an inherently difficult airway and should never be taken for granted. Patients present un-fasted and with pathology that often makes standard intubation approaches impossible. Additionally, they present with pathology that suffers greatly from even small periods of hypotension or hypoxia. As such, practitioners should have a well thought out airway management plan, with multiple backups and airway adjuvants available for immediate use at the bedside, including materials for a surgical airway.⁴

B – Breathing and ventilation

Pneumothorax

Traumatic pneumothorax may quickly develop tension physiology, resulting in devastating preload elimination, hypotension and hypoxia. As such, rapid identification and reversal are key to preventing decompensation or cardiac arrest. Several methods for decompression of pneumothorax are described. Needle decompression has been described and is still taught as part of ATLS; however, this method is often unsuccessful and has frequent complications, requiring the provider to be prepped for rapid conversion to finger thoracostomy.⁵ Recent literature has identified lack of appropriate placement of needle for decompression and inadequate angiocatheter length as potential causes of needle decompression failure.⁶ Given the timely need for reversal of tension physiology in the unstable trauma patient, efforts should be directed instead at performance of finger thoracostomy, a procedure used in the initial stages of tube thoracostomy placement.⁷  As resuscitation proceeds, immediate placement of a chest tube is reasonable over finger thoracostomy.

Several methods may be used to rapidly identify a pneumothorax, including X-ray, point-of-care ultrasound and auscultation of breath sounds. In the unstable trauma patient, auscultation of lung sounds can be extremely difficult with standard stethoscopes.⁸ Other components of the physical exam may point toward pneumothorax with tension physiology, such as tracheal deviation, subcutaneous emphysema with crepitus, and penetrating trauma. Supine radiographs of the chest certainly demonstrate large pneumothoraces, but there is growing literature to support improved identification of this pathology and other lung pathology with ultrasound.^9-11 Examination of the intercostal spaces on the anterior chest wall with linear array probe may illustrate lack of lung sliding as evidence of pneumothorax, and in the setting of traumatic instability, should be acted upon.

In setting of rapid decompensation and pending cardiac arrest, many algorithms recommend immediate bilateral decompression in blunt, and ipsilateral decompression in penetrating trauma.^5,12 Vigilance should be maintained in the post-intubation patient, given the propensity for worsening pneumothorax in the setting of positive-pressure ventilation.

C – Circulation with hemorrhage control

Hemorrhage identification and control

The most common etiology of hemodynamic collapse in the trauma patient is hemorrhagic shock. Given this, the trauma practitioner should quickly identify the shock state and determine the source of hemorrhage. ATLS teaches practitioners to look to “blood on the floor and then four more (chest, abdomen, pelvis/retroperitoneum, long bones)” as sources for major blood loss.

Superficial injuries

Blood from superficial and deep lacerations is often the most obvious source for blood loss. Despite the frequent overestimation of blood lost at the scene of a trauma, large volume exsanguination can occur without correction. Direct pressure to venous and arterial bleeding is often sufficient to prevent additional blood loss, but care should be made not to overpad dressings. Big, bulky dressings can be less effective that those that provide direct, pointed pressure to the site of hemorrhage. In the setting of continued blood loss despite pressure, the practitioner should be prepared to ligate bleeding vessels, either though whip-stitching of the vessel or closure of the wound with sutures/staples to provide tamponade. The key to a successful trauma resuscitation is exposure; a missed scalp laceration can result in severe hemorrhage that would have been easily addressed if the patient was rolled and scalp explored.

Hemothorax

Large volume blood loss into the chest can result from both blunt and penetrating trauma, and can potentially result in tension physiology. After identification of hemopneumothorax in the unstable trauma patient, a chest tube should be placed on the affected side. ATLS recommends placement of large bore chest tubes in the setting of any traumatic hemothorax large enough to be identified on chest radiograph.¹ Often hemothorax is secondary to a lung laceration or intercostal vessel injury, and decompression with placement of chest tube may be the definitive management, with patients often not requiring further intervention. However, should the patient have massive output (see below), further surgical intervention is necessary.

With large volume hemorrhage, early initiation of auto-transfusion of the patient’s own whole blood should be attempted. Patient’s with suspected diaphragmatic injury, concomitant gastric injury with violation into the thorax or associated chest malignancy are potential contraindications for autotransfusion.¹³ Commercially available devices can be used to ensure adequate filtration when used in-line with chest tube suction devices.

Intra-abdominal hemorrhage

Damage to intra-abdominal organs, both solid and hollow, can result in large volume blood loss without significant changes to the external appearance of the patient.¹ Gross examination of the abdomen and review of the mechanism of injury can lend some information as to the presence of an abdominal injury. In the absence of obvious signs of injury, the addition of the Focused Assessment Sonography in Trauma (FAST) exam can help to identify presence of intra-abdominal free fluid suggestive of traumatic hemorrhage. Given the high sensitivity and specificity, FAST examination carries an EAST Level II recommendation as the initial study for identifying intra-abdominal free fluid. Diagnostic peritoneal lavage may also be employed to identify hemorrhage in this setting. Many algorithms exist for the use of these procedures in the unstable patient instead of CT imaging. Positive studies should result in immediate surgical intervention, unless a contraindication is present.

Pelvic fractures

The pelvis also serves as a large cavity for blood loss, with a substantial increase in volume in the setting of acute pelvic ring fractures. In one cadaveric study, fracture of the pelvis resulting in a pelvic diastasis of 5cm resulted in a 20% increase in pelvic volume, with a high association of venous injury.¹⁴ As a result, large volumes of blood can rapidly accumulate in the pelvis. Binding the pelvis, either with commercially-available devices or with an appropriately fitted sheet, has been found to decrease the volume of the pelvis, but has not been shown to have a statistically significant decrease in blood loss.¹⁵ Given the potential for decreasing pelvic volume and blood loss, placement of a temporary pelvic binder is recommended in the setting of a potential pelvic source of hemorrhage. In the patient who has no other identifiable source for hemorrhage, pelvic angiography is the EAST recommended intervention over surgical intervention.

Extremity

The compartments containing long bones can serve as a large vacuum for blood loss in the setting of acute fracture, in addition to blood lost externally in the setting of open fractures. One study illustrated an average blood loss of greater than 1,200cc in the setting of isolated femur fractures in adults.¹⁶ Rapid identification of and splinting of fractures can result in improved pain control and decreased blood loss.¹⁷ For most fracture related external hemorrhage, external direct pressure is sufficient to prevent additional hemorrhage. Some devices exist for rapid wound packing which may be of benefit in this patient population. However, in the setting of massive hemorrhage with suspected arterial source, placement of a tourniquet may be indicated. Tourniquet use has illustrated decreased hemorrhage rates and improved morbidity and mortality, even when placed by first responders in the out-of-hospital environment.^18,19 If placing such devices, carefully document placement location and specific time of placement to prevent prolonged tourniquet times.

General hemorrhage

One intervention proven to decrease death from bleeding and all-cause mortality at 30-days is the early administration of an antifibrinolytic agent tranexamic acid.²⁰ This medication has shown great success when administered in the first hour after injury, though it did illustrate a slight association with increased risk of bleeding death if administered after 3 hours post-injury.²⁰ As such, this medication is recommended in the setting of transfusion-requiring severe traumatic injury and should be given early in the evaluation, potentially in the pre-hospital setting.²¹ Recommended dosing is 1g administered IV over 10 minutes, with additional infusion of 1g over 8 hours. For further details, go here:

http://www.emdocs.net/ed-crash-course-txa-matters/
http://www.emdocs.net/txa-use-trauma-update/

Anticoagulant reversal

Use of anticoagulants and antiplatelet agents complicate the management of traumatic hemorrhage.²² Often the hemodynamically stable patient will be unable to provide medication history, and additional data may be necessary to know of concomitant anticoagulant use. Elderly patients, patients with history or evidence of atrial fibrillation and those with history of CVA should be considered at risk for usage of either anticoagulant or antiplatelet agents. Point-of-care PT/INR may help if the patient is using warfarin, but will otherwise be of little help to the practitioner.

In the setting of anticoagulant use, efforts should be made to reverse the anticoagulated state in the setting of life-threatening hemorrhage. Use of these agents has an associated increased injury severity and mortality in elderly patients, so rapid reversal of their effects is paramount.²³ Several protocols exist for reversal in the trauma patient, but consensus statements do not exist. With the addition of new reversal agents, more work should be done to create reversal protocols.

The use of anti-platelet agents also creates an unfavorable environment for hemostasis. Some protocols call for the transfusion of platelets to reverse effects. In the hemodynamically unstable patient, platelets should be added as part of standardized massive transfusion protocols, making this intervention less important for the specific reversal of the anti-platelet agent.

Resuscitative Thoracotomy

A third subset of shock that may present in the unstable and crashing trauma patient is that of cardiogenic shock. In the setting of blunt traumatic injury, this may be related to direct cardiac contusion or free wall rupture, resulting in pericardial tamponade. In the penetrating trauma patient, this may also be due to cardiac injury resulting in pericardial tamponade. As discussed in a prior post on traumatic cardiac arrest, emergency department thoracotomy can be considered in certain situations for correction of potentially reversible causes. Pericardiocentesis, though temporizing, may only have short-lived effects, given the nature of injuries that lead to pericardial tamponade in the setting of trauma. As such, rapid transition to thoracotomy is recommended.

New therapies

REBOA: A relatively new therapy for the management of traumatic hemorrhage of the trunk and torso is the use of resuscitative endovascular balloon occlusion of the aorta (REBOA). A technique initially described in 1950s, REBOA has been used in multiple arenas related to hemorrhage, from abdominal aortic aneurysm rupture to post-partum hemorrhage.²⁴ Through the strategic placement of a balloon catheter in various zones of the aorta, a provider can selectively prevent distal blood flow to sites of hemorrhage, hopefully temporizing the patient until more definitive management can be performed. Several protocols have been proposed for initiation of REBOA in the ED, with more facilities introducing REBOA programs.²⁵ Despite expanding its use, one review of REBOA use illustrated no improvement in hemorrhage-related mortality.²⁶ REBOA remains a viable option in the age of damage control resuscitation of the patient with massive traumatic torso hemorrhage, though more research is needed to identify the best populations for usage.

Resuscitation

After identifying the potential source of exsanguination, efforts should be directed at resuscitation. “Damage control resuscitation” protocols have been developed to reduce the dangers of the “lethal triad” of trauma: acidosis, hypothermia, and coagulopathy.²⁷ Infusion of crystalloid in large volumes has been linked to worsening acidosis and hemodilution. After initial field resuscitation with crystalloid, the unstable patient should be transitioned to blood product. The Eastern Association for the Surgery of Trauma guidelines give Level I recommendation for the transfusion of packed red blood cells in the setting of trauma and hemodynamic compromise, with less emphasis placed on hemoglobin directed transfusion.²⁸ Combat literature has shown that the ideal transfusion product would be whole blood, though this resource is not often held in supply. The PROMMTT study found that practitioners attempted to replicate whole blood in their transfusion patterns, approaching a 1:1:1 or 1:1:2 ratio of plasma to platelets to packed red blood cells. Further investigation into ideal transfusion ratios by the PROPPR trial showed similar outcomes with these ratios, but noted a slight improvement in achievement of hemostasis and 24-hour mortality related to exsanguination in the 1:1:1 group.²⁹

Given that hemorrhage is the most common etiology of shock in the trauma patient, little emphasis should be placed on vasopressor agents. Blood product replacement remains the gold standard in management of traumatic hemorrhagic shock. An exception to this rule involves patients with traumatic spinal cord injuries presenting with hypotension secondary to neurogenic shock.³⁰ While guidelines recommend aggressive reversal of hypotension with fluid resuscitation, there is no one specific vasopressor agent for additional support recommended.³¹ Norepinephrine, phenylephrine or dopamine are all mentioned as potential agents, though phenylephrine should be avoided in those patients presenting with simultaneous bradycardia secondary to neurogenic shock.³²

D – Disability; neurologic status

GCS/neurologic examination

After initial assessment, efforts should be made to perform a neurologic examination and determine the Glasgow Coma Scale of the patient. In the unstable patient, efforts may often proceed quickly to rapid sequence intubation, which can prevent adequate neurologic examination. Though protection of the patient’s airway is paramount, a neurologic exam should be performed and short-acting paralytics should be considered for RSI if possible.

Spinal cord injuries

Spinal column and cord injuries may complicate the poly-traumatized patient, leading to further injury load and potential source for hemodynamic instability. Patients will often present in a cervical collar and on spinal immobilization boards, though recent review of the literature suggests that spinal motion restriction methods may be more beneficial than immobilization boards. Efforts to minimize spinal manipulation should be attempted, with knowledge that life-saving measures may limit the ability to do so. During initial resuscitation, some elements of the physical exam may suggest spinal cord injury: focal neurologic deficit, priapism, or shock refractory to standard transfusion methods. Careful attention should be made to prevent hypoxia and hypotension, which increase morbidity and mortality.

Intracranial hemorrhage (ICH) management

Traumatic intracranial injury can complicate the course of the poly-traumatized patient. Though CT examination may be performed after the patient reaches a more hemodynamically stable state, suspicion of severe ICH should remain high so that early intervention can occur. The practitioner should look for signs of expanding ICH: palpable skull crepitus/obvious skull fracture, signs of basilar skull fracture, scalp hematoma, and facial bone fractures. Additionally, patients with diminished GCS without obvious signs of head injury should be considered high risk for ICH.

Progressively worsening ICH and associated edema can quickly progress, resulting in herniation of intracranial contents. This is often heralded by a combination of vital sign changes and lateralizing physical exam findings. Cushing’s response is the combination of bradycardia and hypertension in the herniating patient. Additionally, a unilateral dilated and unreactive pupil may be observed. Hemodynamic instability due to severe ICH and herniation requires rapid intervention. Hypertonic saline or mannitol may be used in an effort to decrease intracranial pressure, though guidelines do not exist for preferential use. The practice of hyperventilation should be avoided, unless rapid surgical decompression is possible, given the associated cerebral vasoconstriction and decreased oxygen delivery. Neurosurgical consultants should be involved as early as possible. Please go here for further details: http://www.emdocs.net/icp-management-update/

E – Endpoints/Markers (ATLS uses “Exposure/environmental control” here)

The ultimate goal in the resuscitation of the unstable and crashing trauma patient is to preserve life and return the patient to a normal physiologic state. However, the severity of injury may require prolonged resuscitation and multiple interventions before an external sign of response is noted by the practitioner. Surrogate markers for injury severity are the serum lactate level and base deficit. Severely elevated base deficit has been linked to increased mortality and blood product requirements, while the rate at which the base deficit is corrected in the resuscitation is associated with improved survival.^33-35 Base deficit may be slightly better than lactate at this prediction, but lactate has also shown utility.³⁶ Both are recommended as markers of resuscitation response by the most recent EAST Guidelines. Hemoglobin measurement is known to be inherently flawed in the acutely hemorrhaging patient and should not be used as an initial risk stratifying tool or resuscitation goal. Aggressive efforts to improve oxygen delivery, through prevention of further hemorrhage, application of supplemental oxygen and transfusion of blood product may be linked to more rapid correction of these physiologic markers and improved outcomes.³⁷

Ultimately, the crashing trauma patient may require definitive surgical intervention. The initial resuscitation should be aimed at rapid identification of potentially reversible causes of hemorrhage, protection of the airway, and aggressive resuscitation. If the facility does not have the potential for surgical intervention, then the patient should quickly be prepped for transfer. Intubation, placement of chest tubes, and fracture splinting can be performed quickly in most emergency departments; however, a “stay-and-play” approach to the trauma patient is often detrimental to the patient and transport should not be delayed if available.

Case Recap

35-year-old male presents after a high speed MVC. Patient unresponsive on scene, placed in cervical collar and on spinal board by EMS after prolonged extrication. 5 minutes prior to patient arrival, EMS alerts EM providers to current vital signs and mechanism of injury. Trauma surgery paged to ED, lead EM physician briefs nursing and support staff in trauma bay prior to arrival, assures adequate procedural supplies are present and alerts blood bank to likely massive transfusion protocol event. Airway setup prepped.

Primary Survey:

A: Airway intact and without obvious obstruction

B: Spontaneous but sonorous respirations, left chest wall crepitus with diminished lung sounds

C: Thready pulses in bilateral radial locations and left dorsalis pedis; absent pulse in right DP; large volume hemorrhage from posterior scalp wound; open right femur fracture with continued hemorrhage; distended abdomen

D: GCS 6 (Eye – 1, Verbal – 2, Motor – 3)

E: Cool to touch, worse in distal right lower extremity

Vitals: HR 139 bpm, BP 84/40 mmHg manual, RR 30 bpm, SpO2 78%

Patient identified as having multiple potential sources for shock on arrival. After initial assessment, he underwent endotracheal intubation using ketamine and rocuronium. Video laryngoscope was used primarily, and intubation was successful on first attempt with no worsening hypoxia. Lack of breath sounds with associated crepitus to the left chest wall raised concern for left hemopneumothorax, and a left chest tube was placed with return of air and 500cc blood immediately. An autotransfuser device was employed, and the massive transfusion protocol was initiated at 1:1:1 ratio with 1g TXA IV. Given an open deformity to the right femur, a tourniquet was requested, but after the patient was placed in a traction splint, hemorrhage ceased. The scalp laceration was stapled for rapid hemostasis. Chest radiograph confirmed appropriate ETT placement, chest tube placement with small residual hemothorax, and left sided rib fractures. Pelvic radiograph demonstrated a sacral fracture with associated anterior diastasis, resulting in the placement of a pelvic binder. FAST examination was performed, illustrating presence of anechoic fluid collection in Morison’s pouch and peri-splenic views. After interventions and blood product administration, vital signs were notable for persistent hypotension and minimal improvement in tachycardia, resulting in immediate transit to operating room for exploratory laparotomy.

Discharge problem list following 15-day hospitalization:

Right-sided subdural hematoma, status post surgical decompression
Right maxillary, frontal sinus fractures
Rib fractures (R 3-5, L 3-8)
Left hemopneumothorax
Liver laceration
Splenic laceration, status post splenectomy
Sacral fracture
Pelvic ring fracture
Right open femoral shaft fracture, status post ORIF

References / Further Reading

1. ATLS Student Course Manual, 10^th edition
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3. Manoach S, Paladino L. Manual in-line stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Ann Emerg Med 2007; 50(3): 236-45.
4. Stephens CT, Kahntroff S, Dutton RP. The success of emergency endotracheal intubation in trauma patients: a 10-year experience at a major adult trauma referral center. Anesth Analg. 2009 Sep;109(3):866-72.
5. Leigh-Smith S. Tension pneumothorax – time for a re-think? Emerg Med J 2005; 22:8-16.
6. Chang SJ, Ros SW, Kiefer DJ, Anderson WE, Rogers AT, Sing RF, Callaway DW. Evaluation of 8.0cm needle at the fourth anterior axillary line for needle chest decompression of tension pneumothorax. J Trauma Acute Care Surg 2014; 76(4):1029-34.
7. Aylwin CJ, Brohl K, Davies GD, et al. Pre-hospital and in-hospital thoracostomy indications and complications. Ann R Coll Surg Engl 2008; 90:54-7.
8. Gaydos S. Clinical auscultation in noisy environments. J Emerg Med. 2012; 43(3): 492-3.
9. Zanobetti M, Poggioni C, Pini R. Can chest ultrasonography replace standard chest radiography for evaluation of acute dyspnea in the ED? Chest. 2011; 139(5):1140-7.
10. Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, Jiang GY. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Crit Care. 2006; 10(4): R112.
11. Tasci O, Hatipoglu ON, Cagli B, Ermis V. Sonography of the chest using linear-array versus sector transducers: Correlation with auscultation, chest radiography, and computed tomography. J Clin Ultrasound. 2016 Feb 11 [Epub ahead of print]
12. Sherren PB, Reid C, Habig K, Burns BJ. Algorithm for the resuscitation of traumatic cardiac arrest patients in a physician-staffed helicopter emergency medical service. Crit Care 2013; 17(2): 308.
13. Salhanick M, Corneille M, Higgins R, Olson J, Michalek J, Harrison C, Stewart R, Dent D. Autotransfusion of hemothorax blood in trauma patients: is it the same as fresh whole blood? Am J Surg 202(6):817-822, 2011
14. Baque P, Trojani C, Delotte J, et al. Anatomical consequences of “open-book” pelvic ring disruption: a cadaver experimental study. Surg Radiol Anat. 2005;27:487–490.
15. Sadri H, Nguyen-Tang T, Stern R, Hoffmeyer P, Peter R. Control of severe hemorrhage using C-clamp and arterial embolization in hemodynamically unstable patients with pelvic ring disruption. Arch Orthop Trauma Surg. 2005;125:443–447.
16. Lieurance R; Benjamin JB; Rappaport WD. Blood loss and transfusion in patients with isolated femur fractures. J Orthop Trauma. 1992; 6(2):175-9.
17. Wood SP, Vrahas M, Wedel SK. Femur fracture immobilization with traction splints in multisystem trauma patients. Prehosp Emerg Care, 2003 Apr–Jun; 7(2): 241–3.
18. Kragh JF, Littrel ML, Jones JA, et al. Battle casualty survival with emergency tourniquet use to stop limb bleeding. J Emerg Med 2011;41:590-597.
19. Callaway DW, Robertson J, Sztajnkrycer MD. Law enforcement-applied tourniquets: a case series of life-saving interventions. Prehosp Emerg Care. 2015 Apr-Jun;19(2):320-7.
20. Roberts I, Shakur H, Coats T, et al. The CRASH-2 trial: a randomized controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013; 17(10).
21. Napolitano J. et al. Tranexamic acid in trauma: how should we use it? J Trauma Acute Care Surg. 2013 Jun;74(6):1575-86.
22. Pieracci FM, Eachempati SR, Shou J, Hydo LJ, Barie PS. Use of long-term anticoagulation is associated with traumatic intracranial hemorrhage and subsequent mortality in elderly patients hospitalized after falls: analysis of the New York State Administrative Database. J Trauma. 2007 Sep;63(3):519-24.
23. Boltz MM, Podany AB, Hollenbeak CS, Armen SB. Injuries and outcomes associated with traumatic falls in the elderly population on oral anticoagulant therapy. Injury. 2015 Sep;46(9):1765-71.
24. Stannard A, Eliason JL, Rasmussen TE. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011; 71(6): 1869-72.
25. Biffl WL, Fox CJ, Moore EE. The role of REBOA in the control of exsanguinating torso hemorrhage. J Trauma Acute Care Surg. 2015; 78(5): 1054-8.
26. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhage shock. J Trauma Acute Care Surg. 2016; 80(2): 324-34.
27. http://www.ahcmedia.com/articles/135668-damage-control-resuscitation
28. EAST Guidelines Napolitano LM, Kurek S, Luchette FA, et al. Red Blood Cell Transfusion in Adult Trauma and Critical Care. J Trauma. 2009; 67(6): 1439-42.
29. Holcomb JB, Tilley BC, Baraniuk S, Fox EE, et al; PROPPR Study Group. 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 Feb 3;313(5):471-82.
30. Atkinson PP, Atkinson JL. Spinal shock. Mayo Clin Proc. 1996 Apr;71(4):384-9.
31. Stein DM, Roddy V, Marx J, Smith WS, Weingart SD. Emergency neurological life support: traumatic spine injury. Neurocrit Care. 2012 Sep;17 Suppl 1:S102-11.
32. Wing PC, et al. Early Acute Management in Adults with Spinal Cord Injury. J Spinal Cord Med. 2008; 31(4): 403–479.
33. Davis JW, Kaups KL, Parks SN: Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma 1998;44:114-118.
34. Davis JW, Shackford SR, MacKersie RC, Hoyt DB: Base deficit as a guide to volume resuscitation. J Trauma 1988;28:1464-1467.
35. Rixen D, Raum M, Bouillon B, et al: Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the Deutsche Gesellschaft für unfallchirurgie. Shock 2001;15:83-89.
36. Shoemaker WC, Appel P, Bland R: Use of physiologic monitoring to predict outcome and to assist in clinical decisions in critically ill postoperative patients. Am J Surg 1983;146:43-38.
37. Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J: Lactate clearance and survival following injury. J Trauma 1993;35:584-589.

Additional FOAMed resources:

https://www.east.org/education/practice-management-guidelines/
http://lifeinthefastlane.com/
http://blog.ercast.org/
http://emcrit.org/