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Official reprint from UpToDate www.uptodate.com ©2016 UpToDate

Initial evaluation and management of shock in adult trauma

Author: Christopher Colwell, MDSection Editor: Maria E Moreira, MDDeputy Editor: Jonathan Grayzel, MD, FAAEM

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Sep 2016. | This topic last updated: Dec 11, 2015.

INTRODUCTION — Shock refers to inadequate tissue perfusion, which manifests clinically as hemodynamicdisturbances and organ dysfunction. At the cellular level, shock results from insufficient delivery of requiredmetabolic substrates, principally oxygen, to sustain aerobic metabolism.

In the setting of trauma, loss of circulating blood volume from hemorrhage is the most common cause ofshock. Inadequate oxygenation, mechanical obstruction (eg, cardiac tamponade, tension pneumothorax),neurologic dysfunction (eg, high­spinal cord injury), and cardiac dysfunction represent other potential causesor contributing factors [1]. Shock is a common and frequently treatable cause of death in injured patients andis second only to traumatic brain injury as the leading cause of death from trauma [2,3].

This topic review will discuss the evaluation and initial management of shock in the trauma patient. The initialmanagement of the trauma patient, a general overview of shock, including pathophysiology and differentialdiagnosis, and discussions of the management of shock in other clinical circumstances are presentedelsewhere. (See "Initial management of trauma in adults" and "Definition, classification, etiology, andpathophysiology of shock in adults" and "Evaluation and management of suspected sepsis and septic shock inadults" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

PATHOPHYSIOLOGY AND CLASSIFICATION — The pathophysiology of shock primarily relates to animbalance in oxygen supply and demand. Patients in shock suffer from a critical reduction in the oxygenavailable to the mitochondria. Adenosine triphosphate (ATP) can still be synthesized by anaerobic glycolysisbut at only 5 to 10 percent of the normal rate [4]. Anaerobic glycolysis results in the accumulation of pyruvate,which is converted to lactate [5]. (See "Definition, classification, etiology, and pathophysiology of shock inadults".)

The compensatory physiologic responses to acute hemorrhage attempt to maintain adequate oxygen deliveryto tissues. Stimulation of the sympathetic nervous system results in an increased heart rate, vasoconstriction,and increased ventricular contractility. As the shock state progresses, vital organ (eg, brain and heart)perfusion can only be maintained at the expense of nonvital organs. If the process is not reversed,progressive lactate production leads to worsening systemic metabolic acidosis, which along with hypoxemiaultimately causes the loss of peripheral vasoconstriction and cardiovascular collapse.

The Advanced Trauma Life Support (ATLS) manual describes four classes of hemorrhage to emphasize theearly signs of the shock state [3]. Clinicians should note that significant drops in blood pressure are generallynot manifested until class III hemorrhage develops, and up to 30 percent of a patient's blood volume can belost before this occurs:

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Class I hemorrhage involves a blood volume loss of up to 15 percent. The heart rate is minimally elevatedor normal, and there is no change in blood pressure, pulse pressure, or respiratory rate.

Class II hemorrhage occurs when there is a 15 to 30 percent blood volume loss and is manifestedclinically as tachycardia (heart rate of 100 to 120), tachypnea (respiratory rate of 20 to 24), and a

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DIFFERENTIAL DIAGNOSIS — Hemorrhage is the most common cause of shock in the trauma patient.Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from major external wounds.The thigh can hold up to approximately 1 to 2 L of blood. Scalp lacerations can bleed profusely and are oftenoverlooked if significant thoracic or abdominal injuries are present.

A number of other potential causes of traumatic shock must also be considered, including (table 1):

In penetrating trauma, diaphragmatic rupture complicated by incarceration of abdominal organs and bowelperforation can lead to septic shock.

PREHOSPITAL MANAGEMENT — The prehospital management of patients in traumatic shock is focused onrecognition, rapid transport, and stabilization of the airway, breathing, and circulation. Prehospital cliniciansmust be diligent about looking for signs of hypoperfusion, ideally recognizing traumatic shock beforehypotension develops, and providing appropriate management according to their level of skill. Delayed fluidresuscitation for penetrating trauma remains controversial. (See "Prehospital care of the adult trauma patient"and 'Delayed fluid resuscitation/controlled hypotension' below.)

EVALUATION AND MANAGEMENT

Recognition — Recognition is the first step in managing traumatic shock. Ideally, shock is recognized beforehypotension develops [6]. The clinical presentation of traumatic shock depends on the rate, volume, andduration of bleeding, the patient's baseline physiology, and the presence of other acute pathologic processes(eg, tension pneumothorax, myocardial ischemia).

Obvious and immediately detectable manifestations of the shock state include:

decreased pulse pressure, although systolic blood pressure changes minimally if at all. The skin may becool and clammy, and capillary refill may be delayed.

Class III hemorrhage involves a 30 to 40 percent blood volume loss, resulting in a significant drop in bloodpressure and changes in mental status. Any hypotension (systolic blood pressure less than 90 mmHg) ordrop in blood pressure greater than 20 to 30 percent of the measurement at presentation is cause forconcern. While diminished anxiety or pain may contribute to such a drop, the clinician must assume it isdue to hemorrhage until proven otherwise. Heart rate (≥120 and thready) and respiratory rate aremarkedly elevated, while urine output is diminished. Capillary refill is delayed.

Class IV hemorrhage involves more than 40 percent blood volume loss leading to significant depressionin blood pressure and mental status. Most patients in class IV shock are hypotensive (systolic bloodpressure less than 90 mmHg). Pulse pressure is narrowed (≤25 mmHg), and tachycardia is marked(>120). Urine output is minimal or absent. The skin is cold and pale, and capillary refill is delayed.

Cardiac tamponadeTension pneumothoraxPulmonary contusion with resulting pulmonary dysfunctionHemothorax with resulting pulmonary dysfunctionMyocardial infarction or contusion (ie, cardiogenic shock)Spinal cord injury (ie, neurogenic shock)Effects of pharmacologic or toxicologic agentsFat or air embolism

TachycardiaHypotensionCool extremitiesWeak peripheral pulsesProlonged capillary refill (>2 seconds)

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Large­scale bleeding occurs at five possible locations:

When the cause of shock is not obvious, evaluation and treatment occur in tandem. A trauma ultrasoundexamination, or Focused Assessment with Sonography for Trauma (FAST), is performed to look forhemopericardium and intraabdominal bleeding. The three standard initial trauma radiographs include thechest, pelvis, and lateral cervical spine, although depending upon the hospital and the clinical scenarioclinicians may forego plain radiographs in favor of computed tomography (CT). Of the standard plainradiographs, the portable chest radiograph is most likely to reveal an injury requiring immediate intervention.Remember that the presence of one injury in no way excludes the possibility of other, more serious injuries. Insome centers, clinicians may forego plain radiographs if CT scanners are immediately available and adjacentto the trauma bay.

Shock may exist even in the setting of "normal" vital signs, making diagnosis difficult. Young patients withoutunderlying comorbidities can maintain a blood pressure within the normal range despite substantial blood lossby compensatory vasoconstriction and increases in heart rate. A bradycardic response to penetratingintraperitoneal injury, which may be vagally mediated, has been described [7]. In addition, a paradoxical orrelative bradycardia has been described in hypoperfusing trauma patients [8]. A retrospective review of morethan 1700 trauma patients that compared presenting heart rate with base deficits and lactate concentrationsreported that the absence of tachycardia in the presence of hypoperfusion is associated with a poor prognosisindependent of injury severity, systolic blood pressure, and head injury.

Recognizing shock in its early stages is more difficult, but provides clinicians the opportunity for early reversalof end­organ hypoperfusion. Serial examinations and serial ultrasound studies can help to identify occultinjuries [9].

Alterations in mental status caused by hypoperfusion may be subtle initially and can be difficult to distinguishfrom drug or alcohol intoxication or associated head injury. Altered mental status on presentation or asubsequent decline in mental status, particularly in patients without obvious evidence of head injury, shouldraise suspicion for cerebral hypoperfusion. In young, otherwise healthy patients, subtle alterations, such asagitation, confusion, irritability, indifference to surroundings, or inattention to instructions, may be the only signof early shock. A patient who is aggravating you or your staff may be showing early signs of shock, notintoxication.

Subtle examination findings may provide evidence of early shock. Pallor or poor capillary refill may representperipheral vasoconstriction. Diaphoresis may indicate physiologic stress and appear before vital signabnormalities. Mild tachypnea may reflect compensation for metabolic acidosis. Low­urine output may indicateinadequate visceral perfusion. Patients who are unable to maintain a urine output greater than 0.5 mL/kg/hourand have a high­urine specific gravity may be compensating for hypovolemia.

Elderly patients are more likely to take medications (eg, beta blockers) that affect the hemodynamic responseto injury and are more likely to have baseline hypertension. It is important to interpret vital signs with thepatient's baseline in mind [10]. The emergency clinician may need to predict this physiologic baseline basedon age and other available information (eg, medication list). As an example, a systolic blood pressure of 110mmHg may be dangerously low in a patient with underlying hypertension. (See "Geriatric trauma: Initialevaluation and management".)

Narrowing of the pulse pressure (<25 mmHg)Altered mental status not due to head injury

External hemorrhageThoracic cavityPeritoneal cavityRetroperitoneal space (often from a pelvic fracture)Muscle or subcutaneous tissue (usually from a long­bone fracture)

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Nonhemorrhagic causes of traumatic shock may demonstrate typical presentations, but often do not. As anexample, pericardial tamponade is classically described as exhibiting Beck's triad of hypotension, distendedneck veins, and muffled heart sounds, but these are late findings when present. If significant, ongoinghemorrhage exists or the pericardium periodically decompresses by emptying blood into the pleural space,tamponade can occur without distended neck veins. Ultrasound examination (and possibly re­examination) iscritical. (See 'Management of nonhemorrhagic shock' below.)

A large pneumothorax or hemothorax may be detected clinically by the appearance of respiratory distress,unilateral diminished breath sounds, or air crepitus on palpation. In the stable patient with suspectedpneumothorax, confirmation by chest radiograph is prudent; in the unstable patient, immediate treatment withneedle decompression or rapid chest tube placement is necessary and must not be delayed for radiography.The classic description of a tension pneumothorax includes ipsilateral absent breath sounds, deviation of thetrachea away from the affected side, and hypotension from inadequate preload due to compression of theinferior vena cava. Tracheal deviation and hypotension occur late. Animal studies suggest hypoxemia may bean earlier sign of tension pneumothorax than hypotension [11].

Neurogenic shock may develop in the patient with a high­spinal cord injury. Neurologic deficits may not beapparent in the unresponsive patient, but are usually obvious otherwise. Hypotension, which may be mild inthese patients, results from the loss of peripheral vascular resistance. Tachycardia is absent because of theloss of sympathetic tone. Hypotension associated with neurologic deficits and the absence of peripheralvasoconstriction (these patients often have warm extremities and good urine output) raises suspicion forneurogenic shock. Volume status must be closely monitored because excess fluid administration may bedetrimental. Hypotension should not be attributed solely to neurologic injury until hemorrhagic shock has beenruled out. (See "Acute traumatic spinal cord injury".)

Initial management — Management of the patient in traumatic shock is focused on:

Assessment and treatment are performed simultaneously in the seriously injured patient (algorithm 1). Theemergency clinician evaluates the airway and hemodynamic status and looks for hemorrhage whileperforming the following immediate interventions listed in order of priority:

Direct pressure is the primary and preferred means for controlling external hemorrhage. While clampingbleeding vessels under direct visualization is acceptable when necessary, blind clamping should NOT beperformed. Scalp lacerations can bleed profusely and are often overlooked if significant thoracic or abdominalinjuries are present. Scalp lacerations can be managed with clips (eg, Raney clips) (picture 1) or by closingthe wound with running (ie, noninterrupted) stitches (ie, whip­stitch) using heavy suture. A whip­stitch mayalso be used to control severe bleeding from extremity wounds when direct pressure is inadequate and thefew available clinicians must perform other important interventions for an unstable trauma patient.

Use of a tourniquet is acceptable to stop hemorrhage in cases of amputation or severe extremity injury whenother measures have not successfully controlled bleeding. Tourniquets must be released periodically (eg,every 45 minutes) to avoid prolonged ischemia and possible tissue loss. (See "Severe extremity injury in theadult patient", section on 'Control of hemorrhage'.)

Restoring intravascular volumeMaintaining adequate oxygen deliveryLimiting ongoing blood loss

Establishing a patent and protected airway while protecting the cervical spineMaximizing oxygenationGaining intravenous access and initiating fluid resuscitationControlling hemorrhageObtaining blood for laboratory and blood bank testing

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Vascular access is obtained as rapidly as possible. Two large­bore (16 gauge or larger) intravenous (IV) linesplaced in the antecubital region are ideal, but not always possible. Intraosseous devices can be placed rapidlyand offer an effective alternative when there is difficulty placing an IV catheter. (See "Peripheral venousaccess in adults" and "Intraosseous infusion".)

Placement of a central venous catheter (size 8 French) can be performed when adequate peripheral accesscannot be obtained, and allows measurement of central venous pressure. Central line placement underultrasound (US) guidance offers high success rates with fewer complications than procedures performedwithout US [12,13]. Some experts advocate use of distal saphenous vein cutdowns due to ease of access andconsistency of anatomy [14]. (See "Principles of ultrasound­guided venous access" and "Overview of centralvenous access".)

Traumatic shock occurs most often from hemorrhage, generally from an intraabdominal injury in blunt trauma.Ultrasound (US) is an integral part of the initial evaluation of the trauma patient, and reliably identifies freeintraabdominal fluid in the hands of proficient ultrasonographers [15]. During the initial resuscitation, theFocused Assessment with Sonography for Trauma (FAST) exam, is performed to assess first for pericardialeffusion and then for intraperitoneal bleeding. (See "Emergency ultrasound in adults with abdominal andthoracic trauma".)

Ultrasound has largely replaced diagnostic peritoneal lavage (DPL) in the initial assessment of the traumapatient, although DPL retains an important role in specific circumstances. If ultrasound is unavailable or itsfindings are equivocal or inconsistent with the clinical picture, a DPL or diagnostic peritoneal tap (DPT) canprovide important information. An example of such a scenario would be an unstable patient with major pelvictrauma in whom the ultrasound cannot determine whether intraabdominal free fluid is blood or urine. (See"Initial evaluation and management of blunt abdominal trauma in adults", section on 'Diagnostic peritoneallavage (DPL)' and "Pelvic trauma: Initial evaluation and management", section on 'Diagnostic tests'.)

Unstable pelvic fractures and associated vascular injuries can cause hemorrhagic shock. Preliminarystabilization of the pelvis by applying a circumferential pelvic binder or tying a sheet firmly around the pelviscan reduce bleeding. Such interventions are most important with "open­book" pelvic fractures (in which thesymphysis pubis is disrupted (≥2.5 cm), the pelvis opened, and the retroperitoneal space enlarged) (image 1).(See "Pelvic trauma: Initial evaluation and management", section on 'Management'.)

Intravenous fluid resuscitation — Fluid resuscitation in trauma, including the optimal type and volume, isthe subject of considerable debate. We suggest that initial fluid resuscitation for trauma patients inhemorrhagic shock consist of 2 L of isotonic saline (ie, normal saline, abbreviated as NS) given as rapidly aspossible through short, large gauge (16 or larger) peripheral IVs. Central venous catheters are used whenperipheral IVs are not available.

Many hospitals have blood products immediately available in the emergency department. In such hospitals,immediate transfusion of blood products, rather than fluid resuscitation, can be performed for patients withsevere hemorrhage in obvious need of transfusion. (See 'Transfusion for severe ongoing hemorrhage' below.)

Infusions of large volumes of NS can lead to the development of a nonanion gap hyperchloremic metabolicacidosis. On the other hand, large volume resuscitation using lactated ringers (LR) can cause a metabolicalkalosis, as lactate metabolism generates bicarbonate. The typical volumes of either NS or LR used during atrauma resuscitation do not appear to have significant clinical consequences. However, harm can ensue incases when excessive amounts (eg, 10 L) of either fluid are given to a patient at increased risk (eg, patientwith acute renal injury caused by hypoperfusion during a period of hemorrhagic shock). LR and blood must beinfused through separate IV tubing because of the risk of clotting, which may be problematic in the setting oftrauma.

Debate over the best approach to fluid resuscitation in traumatic shock is likely to continue. A systematicreview of prehospital fluid resuscitation in trauma found insufficient evidence for the superiority of anyparticular fluid type [16]. Some researchers claim LR is superior to NS in the resuscitation of uncontrolled

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hemorrhagic shock, stating that patients who receive large volumes of NS experience increased blood lossand greater hypercoagulability; other researchers argue just the opposite [17,18]. We prefer NS for the initialresuscitation fluid, but feel it is reasonable to change to LR (L­isomer if available) after the initial resuscitation(ie, once 50 mL/kg of NS has been infused) in patients requiring additional IV fluid.

Clear end­points for fluid therapy remain undefined [19]. Further resuscitation is based on the patient'sresponse to initial IV fluids and overall condition. A mean arterial pressure (MAP) around 65 mmHg or asystolic blood pressure (SBP) around 90 mmHg is a reasonable goal in penetrating trauma (MAP = [(2 xdiastolic) + systolic]/3). The reasons for this are described separately. (See 'Delayed fluidresuscitation/controlled hypotension' below.)

In blunt trauma patients, particularly those with possible traumatic brain injury (TBI), a MAP above 105 mmHgor a SBP above 120 mmHg is reasonable. These goals may need to be adjusted upward in patients with aknown history of uncontrolled hypertension.

The ideal MAP or SBP for the multiple trauma patient remains unclear. Some authors advocate strictly limitingthe amount of IV fluid used for trauma resuscitation in the absence of hypotension or obvious injury [20].Packed red blood cells are given if the goal blood pressure is not maintained following initial IV fluidresuscitation. (See 'Transfusion of red blood cells' below.)

Hypertonic saline has been evaluated extensively, and may provide benefit through osmotic movement ofinterstitial fluid into the vascular compartment and modulation of the inflammatory response to injury [21].While some clinical trials have shown improved outcomes [22], others have failed to do so, even in patientswho would seem most likely to benefit (eg, patients with hypotension and severe TBI) [23,24]. Further study isneeded to clarify the role of hypertonic saline.

The value of colloids (albumin solution, dextran) for resuscitation of traumatic shock is unproven [25,26].Colloids effectively increase intravascular volume and may maintain plasma oncotic pressure at more normallevels compared with crystalloids. However, a systematic review of trials comparing resuscitation fluids foundthat use of colloids did not improve mortality or morbidity among trauma patients [26]. (See "Treatment ofsevere hypovolemia or hypovolemic shock in adults", section on 'Colloid versus crystalloid'.)

Research continues into oxygen­carrying resuscitation fluids that can serve as alternatives to PRBCs. Theideal replacement fluid would transport oxygen effectively, expand intravascular volume, exhibit few or no sideeffects, and demonstrate great durability. Potential replacement fluids are discussed elsewhere. (See "Oxygencarriers as alternatives to red cell transfusion".)

Delayed fluid resuscitation/controlled hypotension — Questions remain whether reversal of hypovolemiaor control of hemorrhage should take priority in trauma resuscitation. Some researchers describe aggressivefluid administration as ineffective and potentially harmful [27­30], and suggest that limited volume replacementthat maintains minimally adequate organ perfusion may improve outcomes [31]. This strategy is often referredto as delayed fluid resuscitation or controlled hypotension, an approach which targets early fluid resuscitationonly to a systolic blood pressure of 70 mmHg.

Controlled hypotension may be beneficial in patients with hemorrhagic shock due to torso injuries fromgunshot or stab wounds. However, it may be detrimental to blunt trauma patients with brain injury, ashypotension reduces cerebral perfusion and increases mortality [32]. The rationale for improved outcomeswith delayed fluid resuscitation is that aggressive fluid administration might, via augmentation of bloodpressure, dilution of clotting factors, and production of hypothermia, disrupt thrombus formation and enhancebleeding [33,34].

In one widely cited prospective study of 598 patients with penetrating chest injuries treated at a major traumacenter, delayed fluid resuscitation until operative intervention to control bleeding was associated with astatistically significant improvement in patient survival (70 versus 62 percent in those given immediate fluidrepletion) [35]. Care must be taken when extrapolating the results of this trial. Stratification was not performed

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to identify which patients might benefit from delayed therapy, subjects were primarily young and healthy, andthe mean time from injury to operation was two hours, results that are not attainable in most circumstances.

In a preliminary analysis of a trial conducted at another major trauma center, 90 young adults with penetrating(n = 84) or blunt (n = 6) trauma resulting in at least one systolic blood pressure reading below 90 mmHg, andhemorrhage requiring immediate laparotomy or thoracotomy, were randomly assigned upon arrival to theoperating theater to resuscitation using a low­goal mean arterial pressure of 50 mmHg (LMAP group) or ahigh­goal mean arterial pressure of 65 mmHg (HMAP) [36]. Among the patients excluded were those withtraumatic brain injury. Anesthesiologists did not intervene to lower the blood pressure of patients in the LMAPgroup whose MAP exceeded 50 mmHg. Patients in the LMAP group had lower postoperative mortality (6versus 10 deaths), received fewer blood products (1594 versus 2898 mL), and did not develop coagulopathyor multiple organ failure (MOF), compared to seven cases of coagulopathy and two cases of MOF in theHMAP group. However, there was no significant difference between the groups in overall mortality at 30 days.

Other results favoring delayed fluid resuscitation or controlled hypotension have been reported in small clinicaltrials and a variety of animal models of hemorrhagic shock [33,37­44].

The results of these studies notwithstanding, adoption of the strategy of delayed fluid resuscitation orcontrolled hypotension into clinical practice must be undertaken cautiously [45]. Factors that should beconsidered when determining whether this strategy is appropriate include the patient’s mental status andlikelihood of intracranial injury, type of injury (penetrating versus blunt), severity of injury (eg, ongoinghemorrhage), and proximity to a trauma center. Delayed fluid administration and controlled hypotensionshould probably not be implemented unless emergent surgical exploration with rapid control of the bleedingsource can be performed [39]. Further research is needed in this area [45].

Transfusion of blood products

Transfusion for severe ongoing hemorrhage — For trauma patients with severe, ongoing hemorrhagethat is unlikely to be controlled quickly or adequately, we suggest immediate transfusion of blood products in a1:1:1 ratio of packed red blood cells (PRBC), fresh frozen plasma (FFP), and platelets. In other words, assoon as the treating clinician recognizes that the patient will require 4 or more units of PRBCs over one hour(or 10 or more units over 12 to 24 hours), he/she should begin transfusing 6 units of PRBCs, 6 units of FFP,and 6 units of random donor platelets (or 1 unit of apheresis platelets). Note that 1 unit of apheresis plateletsis equivalent to 6 units of non­apheresis (ie, random donor or whole­blood derived) platelets. Hypothermiamust be controlled during transfusions. Evidence to support this approach of transfusing components in a1:1:1 ratio is presented separately. (See "Massive blood transfusion", section on 'Trauma'.)

A massive transfusion protocol should be in place for any hospital that manages trauma. This protocol shouldbe activated in anticipation of the need for large­scale transfusion as soon as the clinician treating the patientrecognizes the presence or likelihood of severe, ongoing hemorrhage.

Excessive infusion of crystalloid (ie, ratio of crystalloid to PRBCs >1.5:1) has been associated with worseoutcomes in patients with severe hemorrhage, according to observational data, and should be avoided[30,46]. (See 'Intravenous fluid resuscitation' above.)

Transfusion of red blood cells — When to begin blood transfusion remains an important, unansweredquestion in trauma research, and often depends on clinical circumstances. As an example, immediatetransfusion of packed red blood cells (PRBC) is needed when exsanguination is imminent, such as a patientwith a thoracic injury whose chest tube releases over 2 L of blood upon placement. Another patient with a self­inflicted wrist laceration may not require any blood, despite being hypotensive, because hemorrhage ispromptly controlled, the wound is easily repaired, and comorbidities are absent.

In most trauma patients with hemorrhagic shock, we suggest 2 units of packed red blood cells (PRBC) betransfused if hemodynamics fail to improve after the administration of 2 to 3 L (or greater than 50 mL/kg) ofcrystalloid. Further transfusions are given based upon the patient's injuries and response to the initial

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transfusion. Transfusion in patients with massive hemorrhage is discussed above. (See 'Transfusion forsevere ongoing hemorrhage' above.)

Typed and cross­matched PRBCs are best, but can require considerable time to prepare. If the patient'scondition warrants, clinicians can transfuse immediately using type O Rh­positive or type O RH­negative formales and type O Rh­negative for girls and women of child­bearing age, until type­specific or typed and cross­matched blood is available.

In most instances, preparation of fully typed and cross­matched blood requires at least 20 minutes, and morelikely 30 to 45 minutes. Type­specific blood can usually be obtained within 15 to 20 minutes. In general, type Oblood is available immediately, depending on transport time from the blood bank to the emergency department(ED). Trauma centers often store type O blood in refrigerators in the ED.

The safety of the blood supply continues to improve, and although some risk of transmitting infectious agentspersists, such events are rare. Transfusion­associated infection is discussed separately. (See "Transfusion­transmitted bacterial infection" and "Risk of HIV from blood transfusion" and "Blood donor screening:Laboratory testing".)

Research continues into oxygen­carrying resuscitation fluids that can serve as alternatives to PRBCs. Theideal replacement fluid would transport oxygen effectively, expand intravascular volume, exhibit few or no sideeffects, and demonstrate great durability. Potential replacement fluids are discussed elsewhere. (See "Oxygencarriers as alternatives to red cell transfusion".)

Transfusion of clotting factors — Treatment of hemorrhage with IV crystalloid and packed red bloodcells (PRBCs) increases the risk of coagulopathy from dilution of clotting factors and platelets, and possiblyhypothermia [47]. Prevention of coagulopathy with early transfusion of plasma and platelets is critical in thepatient with severe hemorrhage [20]. (See "Massive blood transfusion" and "Coagulopathy associated withtrauma".)

There remain no clear answers to the questions when and how much to transfuse clotting factors in traumapatients requiring massive transfusion. If bleeding is severe, clinicians cannot wait for laboratory values toguide transfusion, and such measurements may be inaccurate in the setting of massive hemorrhage [48]. Ourapproach to the transfusion of clotting factors for patients with severe, ongoing bleeding is described above.(See 'Transfusion for severe ongoing hemorrhage' above.)

For patients with bleeding that is not massive but is ongoing and significant (eg, more than 4 units of PRBCstransfused in the first few hours or chest tube continues to drain >200 mL of blood per hour), we suggestusing the same transfusion ratios used for patients with severe hemorrhage: a 1:1:1 ratio of packed red bloodcells (PRBC), fresh frozen plasma (FFP), and random donor platelets. If apheresis platelets are used, thisbecomes a 6:6:1 ratio of PRBCs, FFP, and apheresis platelets respectively. Hypothermia must be controlledduring transfusions. Where available, thromboelastography provides a faster and more accurate assessmentof coagulopathy in the trauma patient, and can help guide ongoing treatment with clotting factors. (See"Coagulopathy associated with trauma", section on 'Thromboelastography' and "Coagulopathy associated withtrauma", section on 'Thromboelastography­based transfusion'.)

Several retrospective studies have reported higher survival rates among patients with severe bleeding whoare treated with higher plasma to PRBC transfusion ratios [49­60]. As an example, a retrospective study usingdata from a United States combat support hospital during the second Iraq war assessed the mortality of 246severely wounded soldiers that required massive blood transfusion and found that patients given a higher ratioof plasma to PRBCs had significantly lower mortality rates [50]. Patients were divided into three groups basedon the plasma to RBC ratio: high ratio (1 to 1.14), medium ratio (1 to 2.5), and low ratio (1 to 8). Injury severityscores were identical in all groups, although the low­ratio group had more thoracic wounds and a loweraverage initial hemoglobin and blood pressure. Group survival was 65 percent, 34 percent, and 19 percentrespectively. Logistic regression analysis found that the plasma to RBC ratio was independently associated

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with survival (odds ratio [OR] 8.6; 95% CI 2.1­35.2). Improved survival with more aggressive plasmatransfusion is consistent with the results of other studies in both military and civilian populations [52­60].

Fewer studies of have assessed the effect of higher plasma to PRBC transfusion ratios in patients withsignificant, but not massive bleeding. Authors of one retrospective study reported lower mortality anddecreased use of blood products among patients treated with higher ratios [61].

The determination of the optimal plasma to PRBC transfusion ratio awaits prospective study [62,63].Nevertheless, in the civilian setting, individual trauma centers have developed effective transfusion protocols[64]. Some advocate 2 units of FFP for every 6 units of PRBCs transfused. Other centers advocate moreaggressive approaches [65]. At one of the largest United States trauma centers, 6 units of FFP are givenonce 6 units of PRBCs are transfused [20]. Another major urban trauma center transfuses 1 unit of FFP foreach unit of PRBCs [52].

Some authors advocate using fibrinogen levels to determine when to transfuse cryoprecipitate [66]. Afibrinogen concentration below 100 mg/dL is generally treated with 10 units of cryoprecipitate (each unit ofcryoprecipitate comes from 1 unit of whole blood, and raises the fibrinogen level by about 5 mg/dL). Providedmassive, ongoing hemorrhage is not present, using laboratory measurements to guide transfusion is areasonable approach.

Transfusion of platelets — Treatment of hemorrhage with IV crystalloid and PRBCs increases the risk ofcoagulopathy from dilution of platelets and clotting factors, and possibly hypothermia [47]. Prevention ofcoagulopathy with early transfusion of plasma and platelets is critical in the patient with severe hemorrhage[20]. (See "Massive blood transfusion" and "Coagulopathy associated with trauma".)

There remain no clear answers to the questions when and how much to transfuse platelets in trauma patientsrequiring massive transfusion. If bleeding is severe, clinicians cannot wait for laboratory values to guidetransfusion, and such measurements may be inaccurate in the setting of massive hemorrhage [48]. Ourapproach to the transfusion of platelets for patients with severe, ongoing bleeding is described above. (See'Transfusion for severe ongoing hemorrhage' above.)

Note that 1 unit of apheresis platelets is equivalent to 6 units of nonapheresis (ie, random donor or whole­blood derived) platelets. Hypothermia must be controlled during transfusions.

For patients with bleeding that is not massive but is ongoing and significant (eg, more than 4 units of PRBCstransfused in the first few hours or chest tube continues to drain >200 mL of blood per hour), we suggestusing the same transfusion ratios used for patients with severe hemorrhage: a 1:1:1 ratio of packed red bloodcells (PRBC), fresh frozen plasma (FFP), and random donor platelets. If apheresis platelets are used, thisbecomes a 6:6:1 ratio of PRBCs, FFP, and apheresis platelets respectively.

A retrospective study, using data from a large trauma database of 657 patients requiring massive bloodtransfusion, reported a stepwise improvement in survival with higher platelet to PRBC transfusion ratios [67].After controlling for such factors as injury severity, initial blood pressure, and transfusion of other bloodproducts, the researchers found that patients receiving the highest apheresis platelet to PRBC ratio (≥1:6) hada 14.5 percent mortality rate while those with the lowest ratio (<1:18) had a 48.2 percent mortality rate. Otherretrospective studies have reported similar results [51,56,60].

Some authors advocate using platelet counts to determine when to transfuse platelets [66]. A platelet count ofless than 100,000/microL is treated with 6 units of random donor platelets or 1 unit of apheresis platelets.Provided massive, ongoing hemorrhage is not present, using laboratory measurements to guide transfusion isa reasonable approach.

Reversal of anticoagulation — Some trauma patients, particularly elders with comorbidities, may be takinganticoagulants. Provided below are several tables outlining methods for reversing particular anticoagulants in

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cases of life­threatening bleeding, as well as links to more detailed discussions of how to manage bleedingassociated with these medications:

Vasopressors — No human studies exist to support the use of vasopressors in the resuscitation of the adultwith multiple trauma [68]. Their use early in the management of hemorrhagic shock may be harmful [69].

Laboratory tests — Hematology and chemistry laboratory tests are of limited use in the acute managementof the trauma patient. Clinicians should consider them adjuncts to diagnosis and not substitutes for clinicalassessment. (See "Initial evaluation and management of blunt abdominal trauma in adults", section on'Laboratory tests'.)

The following laboratory studies are obtained in all patients with traumatic shock:

The emergency clinician should order a blood type and cross­match for any victim of significant trauma inanticipation of the need for transfusion. The blood bank should be notified directly (ie, by telephone or inperson) of the need for packed red blood cells, and other blood products, should a trauma victim present withlife­threatening hemorrhage.

The hematocrit can be useful as a baseline value, but must be interpreted in light of the clinical context,including the extent of hemorrhage, time since the injury, premorbid hematocrit, and the amount of exogenousfluid administration. As an example, the clinician should not be reassured by a normal hematocrit in the acutetrauma victim with hypotension. The hematocrit is most helpful when measured serially to assess ongoinghemorrhage.

Hemorrhagic shock may create a metabolic acidosis with a base deficit (ie, decreased serum bicarbonate) orincreased serum lactate. While such findings suggest shock, clinicians must interpret them in the context ofthe patient's clinical appearance. Typically, laboratory values lag behind clinical improvement after aggressiveresuscitation.

Coagulation studies, a platelet count, and serum electrolytes are helpful to determine the need for bloodproducts and electrolyte replacement, if hemorrhage is ongoing. Additional testing may be needed dependingon clinical circumstance.

Management of nonhemorrhagic shock

Pneumothorax — Pneumothorax occurs often in both blunt and penetrating trauma, and may be delayed(image 2 and image 3). Traumatic pneumothorax or hemothorax is managed by the placement of a largethoracostomy tube (36 French or larger) in the lateral chest. (See "Placement and management of

Warfarin (see "Management of warfarin­associated bleeding or supratherapeutic INR", section on'Serious/life­threatening bleeding'). Initial emergency treatment to reverse anticoagulation due to warfarinin patients with severe hemorrhage is outlined in the following table (table 2).

Direct thrombin inhibitors (eg, dabigatran) and factor Xa inhibitors (eg, rivaroxaban, apixaban, edoxaban)(see "Management of bleeding in patients receiving direct oral anticoagulants"). Initial emergencytreatment to reverse anticoagulation due to direct oral anticoagulants in patients with severe hemorrhageis outlined in the following table (table 3).

Heparin (see "Heparin and LMW heparin: Dosing and adverse effects", section on 'Bleeding').

Low molecular weight heparin (see "Heparin and LMW heparin: Dosing and adverse effects", section on'Bleeding').

Type and cross­match several units of packed red blood cellsBaseline hemoglobin or hematocritSerum bicarbonate (base deficit) and serum lactate

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thoracostomy tubes".)

If the clinician suspects a tension pneumothorax and the patient is hypotensive, a needle thoracostomy can beperformed, as a temporizing measure, using a long, large (eg, 12 or 14 gauge) angiocatheter or needleinserted above the rib at the second intercostal space in the mid­clavicular line or the fifth intercostal space inthe mid­axillary line. The ideal length is unclear, but a 4.5 cm (2 inch) needle is a reasonable first choice.Studies of chest wall thickness using CT scan suggest this length may be inadequate in some patients, butlonger needles increase the risk of injuring the subclavian vessels or other structures [70,71]. Should a 4.5 cmneedle fail to decompress a tension pneumothorax and a tube thoracostomy be delayed, clinicians should usea longer needle.

Pericardial tamponade — Pericardial tamponade can occur with penetrating or major blunt chest trauma.Immediate ultrasonography (US) or echocardiography offers the best opportunity for rapid, early, andaccurate diagnosis. Pericardiocentesis is performed if pericardial tamponade is suspected and the patient ishypotensive and worsening despite volume resuscitation. If pericardiocentesis recovers blood and improvesthe patient's clinical status, emergent thoracotomy is indicated. If thoracotomy cannot be performed,pericardiocentesis can be repeated as necessary or a J­shaped catheter can be inserted into the pericardialspace to allow continual drainage of the hemopericardium. (See "Emergency pericardiocentesis".)

Pericardiocentesis is "classically" performed using the subxiphoid approach [72]. However, some researchersand a large observational study support the use of the paraapical or parasternal approach under ultrasoundguidance [73]. Use of the parasternal approach allows the needle entry site to be closer to the pericardiumand eliminates the risk of liver injury. No controlled trials have compared these approaches in trauma patients.(See "Cardiac tamponade".)

Emergency thoracotomy — In trauma patients who are profoundly hypotensive despite aggressive fluidresuscitation, or have lost discernible blood pressure for only a few minutes, an emergency left lateralthoracotomy to enable decompression of pericardial tamponade, vascular or pulmonary clamping, and directsuture repair, may be life­saving. The indications, contraindications, and performance of emergencythoracotomy are discussed in detail separately. (See "Initial evaluation and management of penetratingthoracic trauma in adults", section on 'Emergency department thoracotomy (EDT)' and "Resuscitativethoracotomy: technique", section on 'Preparation'.)

Pregnancy — Hypotensive pregnant trauma patients are placed in the left lateral decubitus position or theright side of their backboard is tilted up about 15 degrees in order to move the gravid uterus off of the inferiorvena cava. These maneuvers improve venous return and may increase the blood pressure. (See "Initialevaluation and management of pregnant women with major trauma".)

Monitoring and endpoints for prolonged resuscitation — Clear end­points for initial fluid therapy remainundefined [19]. A mean arterial pressure (MAP) around 65 mmHg or a systolic blood pressure around 90mmHg is a reasonable goal in penetrating trauma. In blunt trauma patients, particularly those with possibletraumatic brain injury (TBI), a mean arterial pressure above 105 mmHg or a systolic blood pressure above120 mmHg is reasonable. Some authors advocate strictly limiting the amount of IV fluid used for traumaresuscitation in the absence of hypotension or obvious injury [20]. Packed red blood cells are transfused,along with appropriate replacement of coagulation products, if the goal blood pressure is not maintainedfollowing the initial IV fluid resuscitation. (See 'Transfusion of red blood cells' above.)

Some trauma patients, particularly in community hospitals, must be managed in the emergency departmentfor prolonged periods when surgical resources or transport is unavailable. It remains unclear which endpointsare most useful for guiding such prolonged resuscitations. Those emergency clinicians without access tosophisticated noninvasive technologies rely on standard physiologic and laboratory measurements todetermine whether resuscitation is adequate. An approach modeled on goal­directed therapy for septic shock,with the important caveat that greater emphasis be placed on blood transfusion and coagulation factor

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replacement, may be helpful [74]. (See "Evaluation and management of suspected sepsis and septic shock inadults" and 'Transfusion of red blood cells' above.)

The following parameters may be used to guide prolonged resuscitation of traumatic shock [74,75]:

Transfusion of blood products in patients without massive bleeding undergoing prolonged resuscitation oftrauma­related shock may be performed using the following guidelines:

If bleeding is massive and ongoing, laboratory measurements can be inaccurate. Empiric guidelines fortransfusion of blood products in this setting are provided above. (See 'Transfusion for severe ongoinghemorrhage' above.)

Some researchers advocate using the lactate concentration to assess the adequacy of resuscitation [77­79].Lactate levels may lag behind clinical improvement following aggressive resuscitation if rapid analyzers areunavailable. Other authors suggest that the magnitude of metabolic acidosis has prognostic value [80] andthat the admission base deficit (ie, serum bicarbonate) may be superior to plasma lactate in predicting injuryseverity and death [81]. Both endpoints may provide useful feedback about tissue oxygen debt and theadequacy of resuscitation [82,83].

Studies have compared noninvasive and invasive (eg, pulmonary artery catheter) monitoring started in theemergency department for resuscitation of critical trauma patients. Enhanced noninvasive monitoring appearsto be feasible, safe, inexpensive, and equivalent to invasive monitoring [74,84]. Noninvasive monitoring inthese studies included such technologies as thoracic electrical bioimpedance, esophageal Doppler monitoring,and orthogonal spectral imaging, in addition to standard measures, such as MAP, heart rate, pulse oximetry,and carbon dioxide tension. Many emergency clinicians do not have access to these technologies, and theirrole in ED management of trauma awaits further study.

DISPOSITION — Definitive management of the patient with traumatic shock often requires emergencysurgery. Emergency clinicians should consult a trauma surgeon as soon as possible for all victims ofsignificant trauma who may require operative or critical care interventions. If the patient must be transferredfor definitive care, early communication with a trauma center and preparation for transfer is performed

Blood pressure: Maintain MAP above 65 mmHg for penetrating trauma, and above 105 mmHg for blunttrauma

Heart rate: Maintain between 60 and 100 beats per minute

Oxygen saturation: Maintain above 94 percent

Urine output: Maintain above 0.5 mL/kg/hour

Central venous pressure: Maintain between 8 and 12 mmHg

Lactate and base deficit: Monitor serum lactate and serum bicarbonate every four hours to ensure end­organ perfusion is adequate or improving with resuscitation

Mixed central venous oxygen saturation: Monitor every four hours to ensure end­organ perfusion isadequate or improving with resuscitation; goal is to maintain above 70 percent

Hemoglobin: Transfuse 2 units PRBCs if hemoglobin falls below 8 g/dL for patients without risk for acutecoronary syndrome (ACS), or below 10 g/dL for patients at risk for ACS [76]

Platelets: Transfuse 1 unit of apheresis platelets, or 6 units of random donor platelets, if the serumconcentration falls below 50,000/microL

International normalized ratio (INR): Transfuse 2 units of FFP if INR rises above 2

Fibrinogen: Transfuse 10 units of cryoprecipitate if the fibrinogen concentration falls below 100 mg/dL

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concurrently with assessment and stabilization. The lack of adequate resources to manage a patient's injuries,including specialty and subspecialty care, is an indication for transfer to a trauma center. In cases involving ahypotensive patient with an identified injury (eg, high­grade splenic laceration), but no trauma surgeon isavailable, emergent consultation with a general surgeon may be necessary for possible laparotomy prior to atime­consuming transfer that would put the patient at risk.

DEVELOPING TREATMENTS FOR HEMORRHAGE

Hemostatic agents — In some circumstances, external hemorrhage cannot be controlled using directpressure and standard dressings. A number of hemostatic products are being developed to control suchbleeding, including chitosan dressing, QuickClot powder, and fibrin sealant dressing. Although some of theseproducts have been used by military personnel in combat, few controlled studies with civilians have beenperformed and it remains unclear how these products should be used by civilian emergency clinicians. Theseagents are discussed separately. (See "Fibrin sealant".)

Antifibrinolytic agents — Several antifibrinolytic agents have been shown to be safe and effective atreducing bleeding during elective surgery; these agents may also be of benefit in controlling bleeding followingtrauma. Antifibrinolytic agents are discussed separately. (See "Early noncardiac complications of coronaryartery bypass graft surgery", section on 'Antifibrinolytic agents'.)

In CRASH­2, a trial spanning 274 hospitals in 40 countries, over 20,000 trauma patients with or at risk ofsignificant hemorrhage were randomly assigned within eight hours of injury to treatment with the antifibrinolyticagent tranexamic acid (n = 10,096) or placebo (n = 10,115) [85]. Overall mortality was lower in the tranexamicacid group (14.5 versus 16 percent; relative risk [RR] 0.91, 95% CI 0.85­0.97), as was death from hemorrhage(4.9 versus 5.7 percent; relative risk [RR] 0.85, 95% CI 0.76­0.96). No differences in complications fromvascular occlusion (eg, pulmonary embolism, myocardial infarction) were noted between the two groups.

A follow­up analysis of the CRASH­2 trial confirmed the benefit of tranexamic acid in reducing mortality frombleeding [86]. The relative risk of bleeding to death was 0.68 (95% CI 0.57­0.82), a 32 percent reduction inmortality, when the drug was given within one hour of injury and 0.79 (95% CI 0.64­0.97) when given betweenone and three hours. However, tranexamic acid appeared to increase the risk of fatal hemorrhage when it wasadministered after three hours.

In the United States, experience using tranexamic acid in trauma patients is growing but remains limited.Based upon the results of the CRASH­2 trial and a subsequent systematic review, we believe tranexamic acidis a reasonable early intervention (within three hours of injury) in patients with signs of significant hemorrhagefollowing trauma [87,88]. The best place to administer tranexamic acid may be the prehospital environmentbecause early administration is important and storage and administration are simple. However, no publishedstudies have examined prehospital use.

Recombinant factor VIIa — Off­label use of recombinant factor VIIa (Factor VIIa) is widespread, includinguse by the military for injured soldiers with severe hemorrhage. The use of Factor VIIa in this and other clinicalscenarios is discussed separately. (See "Therapeutic uses of recombinant coagulation factor VIIa in non­hemophiliacs", section on 'Managing post­traumatic hemorrhage'.)

Red blood cell substitutes — Red blood cell substitutes (eg, hemoglobin­based oxygen carriers,perfluorocarbons) continue to be studied in both animal and human trials. This subject is discussed separately.(See "Oxygen carriers as alternatives to red cell transfusion", section on 'Surgery'.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics”and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5 to 6grade reading level, and they answer the four or five key questions a patient might have about a givencondition. These articles are best for patients who want a general overview and who prefer short, easy­to­readmaterials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed.

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These articles are written at the 10 to 12 grade reading level and are best for patients who want in­depthinformation and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e­mailthese topics to your patients. (You can also locate patient education articles on a variety of subjects bysearching on “patient info” and the keyword(s) of interest.)

SUMMARY AND RECOMMENDATIONS

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Basics topic (see "Patient education: Shock (The Basics)")

Hemorrhagic shock comprises the majority of cases of traumatic shock and is commonly divided into fourclasses based on clinical presentation (described in detail above). Significant drops in blood pressure aregenerally not manifested until class III hemorrhage develops, and up to 30 percent of a patient's bloodvolume can be lost before this occurs. (See 'Pathophysiology and classification' above.)

Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from major externalwounds. The thigh can hold up to approximately 1 L of blood. Scalp lacerations can bleed profusely andare often overlooked. Other potential causes of traumatic shock may include cardiac tamponade andtension pneumothorax. A detailed list of potential causes of traumatic shock is provided (table 1). (See'Differential diagnosis' above.)

Obvious and immediately detectable manifestations of the shock state include: tachycardia, hypotension,cool extremities, weak peripheral pulses, prolonged capillary refill (>2 seconds), narrowing of the pulsepressure (<25 mmHg), and altered mental status. (See 'Recognition' above.)

Shock may exist even in the setting of "normal" vital signs. Young otherwise healthy patients can maintaina blood pressure within the normal range despite substantial blood loss; subtle alterations, such asagitation, confusion, irritability, or inattention, may be their only signs of early shock. Altered mental statusfrom inadequate cerebral perfusion can be difficult to distinguish from drug or alcohol intoxication orassociated head injury. Altered mental status on presentation or a subsequent decline in mental status,particularly in patients without obvious evidence of head injury, should raise suspicion for cerebralhypoperfusion. Other subtle presentations of traumatic shock are described above. (See 'Recognition'above.)

Initial management of the patient in traumatic shock is focused on restoring intravascular volume,maintaining adequate oxygen delivery, and limiting ongoing blood loss. The essential tasks includeestablishing a patent and protected airway (while protecting the cervical spine), maximizing oxygenation,gaining intravenous access and initiating fluid resuscitation, controlling hemorrhage, and obtaining bloodfor laboratory and blood bank testing (ie, blood typing and cross­matching). Ultrasound (US) reliablyidentifies free intraabdominal fluid in the hands of proficient ultrasonographers. Management is discussedin detail above and an algorithm is provided (algorithm 1). (See 'Initial management' above.)

The best approach to fluid resuscitation remains controversial. We suggest that initial fluid resuscitationfor trauma patients in hemorrhagic shock consist of 2 L of normal saline (NS) (Grade 2C). The infusion isgiven as rapidly as possible through short, large gauge (16 or larger) peripheral IVs. (See 'Intravenousfluid resuscitation' above.)

The best approach to blood transfusion in trauma is unknown. For patients with signs of ongoingbleeding, but without massive hemorrhage, we suggest 2 units of packed red blood cells (PRBC) betransfused if hemodynamics fail to improve after the administration of 2 to 3 L (or greater than 50 mL/kg)of crystalloid (Grade 2C). Further transfusions are given based upon the patient's injuries and responseto the initial transfusion. Treatment of hemorrhage with IV crystalloid and PRBCs increases the risk ofcoagulopathy from dilution of platelets and clotting factors, and possibly hypothermia. (See 'Transfusionof red blood cells' above and 'Transfusion of clotting factors' above and 'Transfusion of platelets' above.)

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For trauma patients with severe, ongoing hemorrhage that is unlikely to be controlled quickly oradequately, we suggest immediate transfusion of blood products in a 1:1:1 ratio of packed red blood cells(PRBC), fresh frozen plasma (FFP), and platelets (Grade 2B). Appropriate quantities of either randomdonor or apheresis platelets may be used. (See 'Transfusion for severe ongoing hemorrhage' above.)

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The key to management of nonhemorrhagic causes of shock, primarily tension pneumothorax andpericardial tamponade, is early recognition based on clinical, radiograph, and US findings. Emergentthoracotomy may be indicated for pericardial tamponade, particularly in the setting of penetrating thoracictrauma. (See 'Management of nonhemorrhagic shock' above.)

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59. Dente CJ, Shaz BH, Nicholas JM, et al. Improvements in early mortality and coagulopathy are sustainedbetter in patients with blunt trauma after institution of a massive transfusion protocol in a civilian level Itrauma center. J Trauma 2009; 66:1616.

60. Shaz BH, Dente CJ, Nicholas J, et al. Increased number of coagulation products in relationship to redblood cell products transfused improves mortality in trauma patients. Transfusion 2010; 50:493.

61. Wafaisade A, Maegele M, Lefering R, et al. High plasma to red blood cell ratios are associated withlower mortality rates in patients receiving multiple transfusion (4≤red blood cell units<10) during acutetrauma resuscitation. J Trauma 2011; 70:81.

62. Kashuk JL, Moore EE, Johnson JL, et al. Postinjury life threatening coagulopathy: is 1:1 fresh frozenplasma:packed red blood cells the answer? J Trauma 2008; 65:261.

63. Sperry JL, Ochoa JB, Gunn SR, et al. An FFP:PRBC transfusion ratio >/=1:1.5 is associated with alower risk of mortality after massive transfusion. J Trauma 2008; 65:986.

64. Cotton BA, Gunter OL, Isbell J, et al. Damage control hematology: the impact of a traumaexsanguination protocol on survival and blood product utilization. J Trauma 2008; 64:1177.

65. Hirshberg A, Dugas M, Banez EI, et al. Minimizing dilutional coagulopathy in exsanguinatinghemorrhage: a computer simulation. J Trauma 2003; 54:454.

66. Faringer PD, Mullins RJ, Johnson RL, Trunkey DD. Blood component supplementation during massivetransfusion of AS­1 red cells in trauma patients. J Trauma 1993; 34:481.

67. Inaba K, Lustenberger T, Rhee P, et al. The impact of platelet transfusion in massively transfusedtrauma patients. J Am Coll Surg 2010; 211:573.

68. Sperry JL, Minei JP, Frankel HL, et al. Early use of vasopressors after injury: caution before constriction.J Trauma 2008; 64:9.

69. Plurad DS, Talving P, Lam L, et al. Early vasopressor use in critical injury is associated with mortalityindependent from volume status. J Trauma 2011; 71:565.

70. Zengerink I, Brink PR, Laupland KB, et al. Needle thoracostomy in the treatment of a tensionpneumothorax in trauma patients: what size needle? J Trauma 2008; 64:111.

71. Wax DB, Leibowitz AB. Radiologic assessment of potential sites for needle decompression of a tensionpneumothorax. Anesth Analg 2007; 105:1385.

72. Vayre F, Lardoux H, Pezzano M, et al. Subxiphoid pericardiocentesis guided by contrast two­dimensional echocardiography in cardiac tamponade: experience of 110 consecutive patients. Eur JEchocardiogr 2000; 1:66.

73. Tsang TS, Enriquez­Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic echocardiographicallyguided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. MayoClin Proc 2002; 77:429.

74. Bilkovski RN, Rivers EP, Horst HM. Targeted resuscitation strategies after injury. Curr Opin Crit Care2004; 10:529.

75. Garcia A. Critical care issues in the early management of severe trauma. Surg Clin North Am 2006;86:1359.

76. Napolitano LM, Kurek S, Luchette FA, et al. Clinical practice guideline: red blood cell transfusion in adulttrauma and critical care. J Trauma 2009; 67:1439.

77. Baue AE. Physiology of shock and injury. In: Shock and Resuscitation, Gelder ER (Ed), McGraw­Hill,New York 1993.

78. Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med 1992; 20:80.

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79. Mikulaschek A, Henry SM, Donovan R, Scalea TM. Serum lactate is not predicted by anion gap or baseexcess after trauma resuscitation. J Trauma 1996; 40:218.

80. Bannon MP, O'Neill CM, Martin M, et al. Central venous oxygen saturation, arterial base deficit, andlactate concentration in trauma patients. Am Surg 1995; 61:738.

81. Davis JW, Parks SN, Kaups KL, et al. Admission base deficit predicts transfusion requirements and riskof complications. J Trauma 1996; 41:769.

82. Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring of hemorrhagic shock during the initialresuscitation of multiple trauma patients: a review. J Emerg Med 2003; 24:413.

83. Tisherman SA, Barie P, Bokhari F, et al. Clinical practice guideline: endpoints of resuscitation. J Trauma2004; 57:898.

84. Shoemaker WC, Wo CC, Chien LC, et al. Evaluation of invasive and noninvasive hemodynamicmonitoring in trauma patients. J Trauma 2006; 61:844.

85. CRASH­2 trial collaborators, Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascularocclusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH­2): arandomised, placebo­controlled trial. Lancet 2010; 376:23.

86. CRASH­2 collaborators, Roberts I, Shakur H, et al. The importance of early treatment with tranexamicacid in bleeding trauma patients: an exploratory analysis of the CRASH­2 randomised controlled trial.Lancet 2011; 377:1096.

87. Napolitano LM, Cohen MJ, Cotton BA, et al. Tranexamic acid in trauma: how should we use it? J TraumaAcute Care Surg 2013; 74:1575.

88. Ker K, Roberts I, Shakur H, Coats TJ. Antifibrinolytic drugs for acute traumatic injury. CochraneDatabase Syst Rev 2015; :CD004896.

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GRAPHICS

Differential diagnosis of shock in trauma

I. Low CVP

A. Hypovolemia

1. Hemorrhage

a. External (compressible)

i. Lacerations

ii. Contusions

iii. Fractures (partly compressible)

b. Internal (noncompressible)

i. Intrathoracic

ii. Intraperitoneal

iii. Retroperitoneal (partly compressible)

c. Fractures (partly compressible)

2. Third spacing (eg, burns)

B. Neurogenic (high cervical cord injury)

II. High CVP

A. Pericardial tamponade

B. Tension pneumothorax

C. Myocardial contusion

III. Other diagnoses to consider

A. Pharmacologic or toxicologic agents

B. Myocardial infarction (severe)

C. Diaphragmatic rupture with herniation

D. Fat or air embolism

CVP: central venous pressure.

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Traumatic shock: Initial management

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Raney clips

Scalp lacerations can sometimes bleed profusely. In such cases, scalp clips (likethe Raney Clips® pictured above) can tamponade bleeding.

Reproduced with permission from: Aesculap® Raney Clips. Copyright © 2010 B.Braun Aesculap.

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Open book fracture: Pubic symphysis diastasis

This anterior­posterior (AP) x­ray of the pelvis reveals significant diastasis at thesymphysis pubis of this trauma patient. Such fractures can cause significanthemorrhage. Emergent treatment consists of closing the fracture and stabilizing thepelvis by applying a pelvic binder or tying a sheet tightly around the lower pelvis.

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Emergent reversal of anticoagulation from warfarin for life­threateninghemorrhage in adults: Suggested approaches based upon available resources

A. 4­factor prothrombin complex concentrate (4F PCC) is available (preferred approach):

1. Give 4F PCC* 1500 to 2000 units IV over 10 minutes. Check INR 15 minutes after completion of theinfusion. If INR is not ≤1.5, give additional 4F PCC (refer to topic or drug reference for details).

2. Give vitamin K 10 mg IV over 10 to 20 minutes.

B. 3­factor prothrombin complex concentrate (3F PCC) is available but 4F PCC is not available:

1. Give 3F PCC* 1500 to 2000 units IV over 10 minutes. Check INR 15 minutes after completion of theinfusion. If INR is not ≤1.5, give additional 3F PCC (refer to topic or drug reference for details).

2. Give Factor VIIa 20 mcg/kg IV OR give FFP 2 units IV by rapid infusion. Factor VIIa may be preferred ifvolume overload is a concern.

3. Give vitamin K 10 mg IV over 10 to 20 minutes.

C. Neither 3F PCC nor 4F PCC is available:

1. Give FFP 2 units IV by rapid infusion. Check INR 15 minutes after completion of infusion. If INR ≥1.5,administer 2 additional units of FFP IV rapid infusion. Repeat process until INR ≤1.5. May wish to administerloop diuretic between FFP infusions if volume overload is a concern.

2. Give vitamin K 10 mg IV over 10 to 20 minutes.

These products and doses are for use in life­threatening bleeding only. Evidence of life­threatening bleeding andover­anticoagulation with a vitamin K antagonist (eg, warfarin) are required. Anaphylaxis and transfusion reactionscan occur.It may be reasonable to thaw four units of FFP while awaiting the PT/INR. The transfusion service may substituteother plasma products for FFP (eg, Plasma Frozen Within 24 Hours After Phlebotomy [PF24]); these products areconsidered clinically interchangeable. PCC will reverse anticoagulation within minutes of administration; FFPadministration can take hours due to the volume required; vitamin K effect takes 12 to 24 hours, butadministration of vitamin K is needed to counteract the long half­life of warfarin. Subsequent monitoring of thePT/INR is needed to guide further therapy. Refer to topics on warfarin reversal in individual situations for furthermanagement.

PCC: unactivated prothrombin complex concentrate; 4F PCC: PCC containing coagulation factors II, VII, IX, X, protein Sand protein C; 3F PCC: PCC containing factors II, IX, and X and only trace factor VII; FFP: fresh frozen plasma; PT:prothrombin time; INR: international normalized ratio; FEIBA: factor eight inhibitor bypassing agent.* Before use, check product label to confirm factor types (3 versus 4 factor) and concentration. Activated complexes andsingle­factor IX products (ie, FEIBA, AlphaNine, Mononine, Immunine, BeneFix) are NOT used for warfarin reversal.¶ PCC doses shown are those suggested for initial treatment of emergency conditions. Subsequent treatment is based onINR and patient weight if available. Refer to topic and Lexicomp drug reference included with UpToDate for INR­baseddosing.

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Direct oral anticoagulant­associated bleeding reversal strategies

Type of bleeding Agent Possible interventions

Major bleeding (eg,intracranial,retroperitoneal,compartment syndrome,massive gastrointestinal)

Dabigatran (Pradaxa) Idarucizumab Activated PCC* (eg, FEIBA)

Antifibrinolytic agent (eg, tranexamic acid, epsilon­aminocaproic acid)Oral activated charcoal (if last dose within prior twohours)HemodialysisRBC transfusions if needed for anemiaPlatelet transfusions if needed for thrombocytopeniaor impaired platelet function (eg, due to aspirin)Surgical/endoscopic intervention if appropriate

Rivaroxaban (Xarelto),apixaban (Eliquis),edoxaban (Lixiana)

4­factor unactivated PCC* (eg, Kcentra)Antifibrinolytic agent (eg, tranexamic acid, epsilon­aminocaproic acid)

Oral activated charcoal (if last dose recent enough)RBC transfusions if needed for anemiaPlatelet transfusions if needed for thrombocytopeniaor impaired platelet function (eg, due to aspirin)Surgical/endoscopic intervention if appropriate

Minor bleeding (eg,epistaxis, uncomplicatedsoft tissue bleeding, minor[slow] gastrointestinalbleeding)

Dabigatran (Pradaxa) Local hemostatic measuresPossible anticoagulant discontinuation

Half­life (normal renal function ): 12 to 17 hoursPossible antifibrinolytic agent (eg, tranexamic acid,epsilon­aminocaproic acid)

Rivaroxaban (Xarelto),apixaban (Eliquis),edoxaban (Lixiana)

Local hemostatic measuresPossible anticoagulant discontinuation

Half­lives (normal renal function ):Rivaroxaban 5 to 9 hoursApixaban 8 to 15 hoursEdoxaban 6 to 11 hours

Possible antifibrinolytic agent (eg, tranexamic acid,epsilon­aminocaproic acid)

The table describes measures that may be used to manage bleeding associated with direct oral anticoagulants(DOACs). Clinical judgment is essential in all cases of DOAC­associated bleeding in order to assess the risks ofbleeding and weigh these against the risks of thrombosis if anticoagulation is discontinued or reversed. Refer toUpToDate topics on the use of direct thrombin inhibitors and direct factor Xa inhibitors, and management of DOAC­associated bleeding for further details and dosing. The onset of all of the agents discussed herein is approximately2 to 4 hours.

DOAC: direct oral anticoagulant; PCC: prothrombin complex concentrate; FEIBA: factor eight inhibitor bypassing activity;RBC: red blood cell.* Use PCC product only if continued bleeding is reasonably likely to be fatal within hours.¶ The anticoagulant effect of these agents (especially dabigatran) will dissipate more slowly as renal function declines.Severe hepatic failure may also prolong the half­life for rivaroxaban, apixaban, and edoxaban.

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¶

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Pneumothorax

This posterior­anterior (PA) radiograph of the chest reveals a left pneumothorax.The lateral border of the lung (arrows) no longer lies adjacent to the chest wall andthe lung parynchema is contracted accounting for the lung's abnormal appearance.Note the air and absence of lung markings along the left lateral border of the heart(small arrowheads) and the inferior and medial displacement of the left mainstembronchus. The border of the scapula (large arrowheads) is sometimes mistaken fora pneumothorax.

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Chest radiograph of a pneumothorax after stab wound

This plain chest radiograph shows a left apicolateral pneumothorax with typicalconvex white visceral pleural line (yellow arrows).

Courtesy of Paul Stark, MD.

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Normal chest radiograph

Posteroanterior view of a normal chest radiograph.

Courtesy of Carol M Black, MD.

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Contributor Disclosures

Christopher Colwell, MD Nothing to disclose Maria E Moreira, MD Nothing to disclose Jonathan Grayzel,MD, FAAEM Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multi­level review process, and through requirements for references to beprovided to support the content. Appropriately referenced content is required of all authors and must conformto UpToDate standards of evidence.

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