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Diagnosis and Management of Shock in the Injured Patient

April 12, 2022 - read ≈ 15 min



Patrick Heindel, MD.

Brigham and Women’s Hospital, Department of Surgery, Harvard Medical School, Boston, Massachusetts


Anupamaa J. Seshadri, MD.

Beth Israel Deaconess Medical Center, Department of Surgery, Harvard Medical School, Boston, Massachusetts



Shock is defined by inadequate tissue perfusion leading to end-organ dysfunction. Fundamentally, shock is a physiologic state where metabolic demands of cellular processes are not met. In a state of shock, tissue oxygen delivery is impaired and toxic metabolites build up in tissued leading to cellular injury, and ultimately, cellular death. The trauma patient is particularly at risk for development of shock throughout the course of their injury. Shock is the second most common cause of trauma-related death, surpassed only by brain injury[1,2]. Herein, we broadly describe shock in the trauma patient and provide resources for diagnosis and initial management.

Clinical Presentation

Hypovolemic / Hemorrhagic

The trauma patient presenting with evidence of shock is bleeding until proven otherwise. Classically, the earliest vital sign change in hemorrhagic shock is decreased pulse pressure, followed by progressive tachycardia and eventually hypotension as the shock state transitions from compensation to decompensation. It may take up to 1500-2000 cc blood loss for hypotension to occur, and therefore hypotension is not the most reliable sign of ongoing bleeding. Ongoing blood loss may be clearly visible, or require ultrasonography, cross-sectional imaging, or surgical exploration to identify. Body cavities which can hold a blood volume significant enough to produce hemorrhagic shock include the chest, abdomen, retroperitoneum, pelvis, and thighs.


Obstructive shock is the result of impairment of venous return to the heart. In the trauma patient, typical causes of obstructive shock include tension pneumothorax and cardiac tamponade, which are immediately life threatening and reversible with timely intervention. Long bone fracture can result in fat embolus syndrome with obstruction of pulmonary artery capillary beds.

Tension pneumothorax should be diagnosed clinically with evidence of respiratory distress in an awake patient, hypotension, absent or diminished breath sounds, hyperresonance of the chest to percussion, jugular venous distension, and mediastinal shift (including the trachea) away from the affected side. Cardiac tamponade can be identified with ultrasound as part of the FAST exam, and clinically with Beck’s triad of hypotension, muffled heart tones, and jugular venous distension, as well as dyspnea, orthopnea, tachycardia, and elevated central venous pressure. Accumulation of small volumes of blood acutely, due to a penetrating myocardial injury for example, can produce rapid circulatory collapse.


Neurogenic shock is a loss of vasomotor tone seen in a patient with severe cervical or high thoracic spinal cord injury, typically in the setting of high energy blunt trauma. Neurogenic shock may present with hypotension, an inappropriately normal heart rate or bradycardia due to underlying sympathetic dysregulation, and warm extremities (in contrast to hypovolemic shock). Evaluation of neurogenic shock can be challenging in a patient with polytrauma, but should be considered in patients with predisposing injury burdens after addressing other causes of shock.


Cardiogenic shock is not commonly seen in the initial presentation of the trauma patient, although can be important particularly in patients with critical care needs and underlying cardiovascular comorbidities. Rarely, myocardial infarction can occur as a consequence of severe blunt myocardial injury or injury to coronary vessels. Atrial or ventricular rupture can also lead to shock, but often these patients do not survive to the treatment facility. A comprehensive review of cardiogenic shock as a result of myocardial infarction is beyond the scope of this article, but may be recognized in a patient with relevant electrocardiogram changes and/or serum markers of cardiac injury.

Distributive (Septic)

Septic shock is the key form of distributive shock encountered in the injured patient. Like cardiogenic shock, initial presentation with septic shock is rare in the trauma patient, but important to consider later in the hospital course in patients with predisposing injuries and critical care needs. Sepsis refers to life-threatening organ dysfunction caused by a dysregulated host response to infection, and septic shock is the most severe manifestation of sepsis. The 2016 Society of Critical Care Medicine (SCCM)/European Society of Intensive Care Medicine (ESICM) definition of septic shock includes meeting criteria for sepsis (Sequential Organ Failure Assessment [SOFA] Score increase ≥2 due to the presence of infection) as well as requiring vasopressors to maintain a mean arterial pressure ≥65 mmHg and with a serum lactate >2 mmol/L (>18 mg/dL)[3].

Evaluation of Shock in the Trauma Patient

Evaluation of an injured patient presenting with undifferentiated shock should be focused on ruling out and treating immediately life-threatening and reversible causes of shock. Advanced Trauma Life Support (ATLS) principles should be followed in the initial diagnosis and management of the injured trauma patient. Early recognition of shock is critical in prevention of morbidity and mortality, and ideally occurs prior to a transition from compensated shock to decompensated shock with hemodynamic collapse. Typical clinical manifestations of shock in the injured patient include narrow pulse pressure, tachycardia, tachypnea, hypotension, cool extremities, diminished pulses, delayed capillary refill, pallor, oliguria, and altered mental status in the absence of head injury.

Diagnostic imaging should be pursued when clinically appropriate. The extended Focused Assessment with Sonography for Trauma (eFAST) can be performed rapidly as an adjunct to the primary survey to assess for intraperitoneal free fluid, hemopericardium, and pneumothorax. eFAST is particularly useful in the hemodynamically unstable blunt trauma patient to rapidly ascertain shock etiology. Plain radiographs of the chest and pelvis are standard adjuncts to the primary survey that can additionally identify sources of shock which may not be easily identified with clinical exam or ultrasonography, e.g. retroperitoneal bleeding due to pelvic fracture. Radiographs can also help with operative planning (triage of body cavities) in a patient too unstable to proceed to cross-sectional imaging. Cross-sectional imaging should only be used in the hemodynamically stable trauma patient.

Laboratory studies can help identify shock etiology and severity, and all patients with trauma-related shock should have initial assessment with blood typing and crossmatch, complete blood count, coagulation studies, serum electrolytes, and serum lactate. Importantly, hematocrit should be interpreted in the context of any resuscitation prior to obtaining the lab, as a patient in hemorrhagic shock may have a normal hematocrit prior to resuscitation, and should not necessarily be reassuring. Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are useful adjuncts to guide resuscitation when available[4].


Management of shock is centered on reversing the underlying causes of shock while providing supportive care to improve tissue perfusion. To that end, identifying the etiology of shock is critical to provide the appropriate treatment. Hemorrhage is the most common cause of shock in the injured patient, and therefore undifferentiated shock should be treated as hemorrhagic shock while other causes of shock are investigated[1]. Key principles of the management of hemorrhagic shock include preventing or limiting ongoing blood loss, intravascular volume resuscitation, and maintenance of oxygen delivery to vital organs [2].

The best initial management of external hemorrhage is direct pressure, with tourniquet use if necessary and applicable [5]. Pelvic bleeding can be controlled initially with pelvic binder stabilization, which is particularly important and effective in injuries resulting in widening of the pubic symphysis (“open book” or Young-Burgess anteroposterior compression pelvic ring fractures) [6].

Vascular access must be prioritized, and ideally consists of two large-bore peripheral IV’s above the level of the diaphragm [1]. Secondary options for vascular access include intraosseous lines and central venous catheters, although both will limit resuscitation flow volume.

A strategy of permissive hypotension should be used in suspected hemorrhagic shock, with avoidance of all crystalloid resuscitation if possible [7]. Crystalloid has been shown to potentiate coagulopathy and hypothermia, and should only be used when blood products are unavailable in patients with a systolic blood pressure (SBP) <100 [8]. Lower SBPs may be tolerated to avoid crystalloid if there is evidence of organ perfusion, such as no altered mental status, or when hospital transport time is short (<20 minutes) [7,8]. Patients with concomitant traumatic brain injury (TBI) may need more aggressive blood pressure goals to maintain cerebral perfusion pressure and minimize secondary brain injury. Bleeding patients with TBI or spinal cord injury (SCI) present a particularly challenging clinical problem. Goal MAPs should be maintained ≥85-90 mmHg in the setting of SCI or severe TBI, but achievement of these goals with ongoing hemorrhage may be unrealistic until definitive hemorrhage control [9,10]. Transfusion should be prioritized, and if needed, vasopressors (e.g. norepinephrine) can be initiated concomitantly to achieve target MAP goals. If crystalloid must be used to resuscitate the bleeding patient, balanced solutions such as Lactated Ringers are preferred to normal saline, as saline can potentiate acidosis (non-anion gap hyperchloremic metabolic acidosis) [11].  

As soon as availability permits, resuscitation with balanced blood products (1:1:1 ratio of red blood cells, platelets, and plasma) or whole blood should commence [12]. Uncrossmatched blood (O-positive for males and females without the potential for child-bearing, O-negative for all other females) can be used until a blood type and crossmatch is performed. Anticoagulation reversal should occur concomitantly with resuscitation [13].

Massive transfusion protocol (MTP) should be initiated as soon as the treating physician recognizes severe ongoing hemorrhage [14]. The Assessment of Blood Consumption (ABC) score is a simple validated tool to guide decision making in activation of MTP, but should not be used as the exclusive criteria for activation of MTP [15]. If a patient has any two of the following on presentation, activation of MTP should be strongly considered: (1) penetrating mechanism of injury, (2) positive FAST exam, (3) SBP of ≤90 mmHg, (4) heart rate of ≥120 bpm. Resuscitation endpoints should be guided by the physiologic status of the patient and the degree of ongoing bleeding, and can be informed by focused ultrasound and laboratory markers of perfusion and coagulopathy [14,16].

If available, tranexamic acid (TXA) can be administered within 3 hours of injury to counteract trauma coagulopathy, and has been demonstrated to improve survival in certain patient populations [14,17–20].

Tissue oxygen delivery can be improved through the optimization of any of three parameters: serum hemoglobin, hemoglobin oxygen saturation (SpO2), and cardiac output. To that end, in addition to transfusion of blood products, supplemental oxygen should be used to maintain adequate SpO2.

Vasopressors should be avoided in the treatment of hemorrhagic shock [21]. Neurogenic shock can be treated with norepinephrine and/or phenylephrine to counteract peripheral vasoplegia [9,10] Septic shock should be treated according to the Surviving Sepsis guidelines, targeting a MAP of ≥65 with norepinephrine and the addition of vasopressin if necessary [3,22].

Heat loss should be avoided, and warming measures initiated as soon as feasible, included removal of all wet clothing, warming blankets applied, and forced air warming employed if available. 

Ultimately, definitive management of the trauma patient presenting with refractory shock occurs in the operating room. The disposition of the trauma patient in shock should be determined rapidly after initial assessment and treatment, and proceeding to the operating room should not be delayed by interventions or studies which will not change the patient’s disposition. In patients requiring a definitive airway, careful consideration should be given to the appropriate venue for endotracheal intubation, as induction of anesthesia can precipitate rapid circulatory collapse, and may be best performed in the operating room after prepping and draping has occurred.

The concept of “damage control” has revolutionized trauma care in the past decades and the principles of damage control should be considered in all critically ill trauma patients [23]. Damage control surgery (DCS) and damage control resuscitation (DCR) are primarily concerned with rapidly addressing life-threatening injuries and minimizing the risk of the “lethal triad” of coagulopathy, acidosis, and hypothermia. Transition from a “definitive therapy” paradigm to a DCS paradigm must be determined on a case-by-case basis and informed by the patient’s physiology. For a patient in extremis, DCS is the correct approach. Fundamentally, DCS involves controlling hemorrhage, minimizing contamination, and avoiding prolonged and physiologically demanding definitive reconstruction. DCS encompasses a large spectrum of potential operative strategies, and may include preferentially leaving bowel in discontinuity, leaving packing to control bleeding, ligation of venous structures, arterial shunting, and temporary wound closure in the interest of prioritizing physiology.  Parallel damage control concepts have evolved in resuscitation of the critically ill trauma patient, and the management of shock in trauma we suggest aligns with these principles [14].

Summary (bullet points)

  • The injured patient presenting with shock is bleeding until proven otherwise and should be treated for hemorrhagic shock.
  • Treatment of hemorrhagic shock includes restoration of intravascular volume and rapid control of ongoing bleeding.
  • Blood products (either 1:1:1 balanced products or whole blood) are the resuscitation fluid of choice. Crystalloids should be used only when blood is not available, and a strategy of permissive hypotension can be used in patients without significant neurologic injury.
  • Principles of damage control surgery should be employed when the patient is in extremis, prioritizing physiology over definitive reconstruction.


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