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Approach to shock in the adult trauma patient

Approach to shock in the adult trauma patient
Literature review current through: May 2024.
This topic last updated: Feb 28, 2023.

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

In the setting of trauma, loss of circulating blood volume from hemorrhage is the most common cause of shock. Non-hemorrhagic causes include inadequate oxygenation, mechanical obstruction (eg, cardiac tamponade, tension pneumothorax), neurologic dysfunction (eg, high spinal cord injury), and cardiac dysfunction [1]. Shock is the leading cause of preventable death in injured patients and is second only to brain injury as the leading cause of overall death from trauma [2,3].

The recognition, causes, and principles of the initial management of shock in the adult trauma patient are reviewed here. The initial management of hemorrhagic and non-hemorrhagic shock in the adult trauma patient, general management of trauma in adults and children, and other aspects of shock (including the pathophysiology and differential diagnosis) are discussed separately.

Hemorrhage in adult trauma (see "Initial management of moderate to severe hemorrhage in the adult trauma patient")

General trauma management (see "Initial management of trauma in adults" and "Overview of inpatient management of the adult trauma patient" and "Trauma management: Approach to the unstable child")

Undifferentiated shock in adults (see "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock" and "Definition, classification, etiology, and pathophysiology of shock in adults")

PATHOPHYSIOLOGY — The pathophysiology of shock primarily relates to an imbalance in oxygen supply and demand. Patients in shock suffer from a critical reduction in oxygen available to the mitochondria. Adenosine triphosphate (ATP) can still be synthesized by anaerobic glycolysis but at only 5 to 10 percent of aerobic metabolism [4]. Anaerobic glycolysis results in hydrogen ion accumulation and generation of pyruvate, which is converted to lactate [5]. Any type of shock can occur in the injured patient (table 1), while hemorrhagic shock is by far the most common. The pathophysiology of shock is discussed in greater detail separately. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)

The compensatory physiologic responses to shock are an attempt to maintain adequate oxygen delivery to 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 metabolic acidosis along with hypoxemia ultimately causes the loss of peripheral vasoconstriction and cardiovascular collapse.

CLINICAL FEATURES OF SHOCK

Common clinical signs of shock — Obvious and immediately detectable manifestations of shock include:

Tachycardia (an exception is neurogenic shock, which may present with normal heart rate or bradycardia)

Hypotension

Cool extremities (an exception is neurogenic shock, which may present with warm extremities)

Weak peripheral pulses

Prolonged capillary refill (>2 seconds)

Narrowing of the pulse pressure (<25 mmHg)

Increased respiratory rate

Change in skin color (eg, pale, cyanotic)

Altered mental status not due to head injury (may range from mild agitation to coma)

Stages of hemorrhagic shock — The Advanced Trauma Life Support (ATLS) curriculum describes four classes of hemorrhage to emphasize the early signs of the shock state [3]. A significant blood pressure decrease is generally not seen until 30 percent of a patient's blood volume is lost (class III hemorrhage). These classes and the associated signs and symptoms exist along a clinical spectrum with variability among individuals.

Class I hemorrhage involves a blood volume loss of up to 15 percent. The heart rate is minimally elevated or 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 manifested clinically as tachycardia (heart rate of 100 to 120 beats per minute), tachypnea (respiratory rate of 20 to 24 breaths per minute), and a decreased pulse pressure, although systolic blood pressure changes minimally, if at all. The skin may be cool and clammy, and capillary refill may be delayed.

Class III hemorrhage involves a 30 to 40 percent blood volume loss, resulting in a drop in blood pressure and changes in mental status. Any hypotension (systolic blood pressure less than 90 mmHg) or drop in blood pressure greater than 20 to 30 percent of the measurement at presentation is cause for concern. Heart rate (≥120 beats per minutes and thready) and respiratory rate are markedly elevated, while urine output is diminished. Capillary refill is delayed.

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

Recognizing early and non-obvious signs — Early recognition, ideally before hypotension develops, is the first step in managing the injured patient with shock [6]. Recognizing shock in its early stages can be difficult but provides clinicians greater opportunity for reversal of end-organ hypoperfusion. The clinical presentation of traumatic shock depends on the rate, volume, and duration of bleeding, the patient's baseline physiology, and the presence of other acute pathologic processes (eg, tension pneumothorax, myocardial ischemia). In severe trauma, patients often sustain more than one injury that contributes to the shock state.

In patients with a significant traumatic mechanism, even if they initially appear "stable," serial examinations, vital signs, and bedside ultrasound studies can help identify occult and potentially life-threatening injuries [7]. Subtle changes in vital signs and physical exam findings are best detected by frequent reassessment, preferably by the same provider, and may offer the earliest clues to the presence of significant injury and/or early shock. Pallor or poor capillary refill may represent peripheral vasoconstriction. Diaphoresis can indicate physiologic stress and appear before vital sign abnormalities. Mild tachypnea may reflect compensation for metabolic acidosis. Increasing heart rate may reflect ongoing hemorrhage. Low urine output may indicate inadequate visceral perfusion. Patients who are unable to maintain a urine output greater than 0.5 mL/kg per hour may have underlying hypovolemia.

"Normal" vital signs — Shock may exist even in the setting of "normal" vital signs, particularly in older patients. Young patients without underlying comorbidities can maintain a blood pressure within the normal range despite substantial blood loss through compensatory vasoconstriction and increases in heart rate, which can be followed by an acute decompensation if the cause of the shock state is not addressed.

Bradycardia, which may be vagally mediated, can occur following intraperitoneal injury [8]. A paradoxical or relative bradycardia can also occur in hypoperfusing trauma patients. A retrospective review comparing initial heart rate with base deficits and lactate concentrations in more than 1700 trauma patients found that patients with hypoperfusion without tachycardia had a poor prognosis independent of injury severity, systolic blood pressure, and head injury [9].

Medications blunting tachycardia — Patients in shock who take cardioactive medications (eg, beta blockers) may not have typical vital sign responses, such as compensatory tachycardia.

Shock index – The shock index and modified shock index can help identify early shock. In a trauma patient, a shock index (the heart rate divided by the systolic blood pressure) greater than 0.9 is associated with increased likelihood of transfusion and increased mortality [10]. A normal shock index is 0.5 to 0.7. A modified shock index (the heart rate divide by the mean arterial pressure) greater than 1.3 or less than 0.7 is associated with increased mortality [11].

Older adults — Older patients are more likely to be taking anticoagulants or medications that affect the hemodynamic response to injury and are more likely to have baseline hypertension. Therefore, an older patient with a normal blood pressure may actually be hypotensive compared with their baseline if they have underlying hypertension [12]. Reviewing a patient's medication list and notes of previous medical encounters can often provide useful information such as their baseline blood pressure. (See "Geriatric trauma: Initial evaluation and management".)

Subtle alteration in mental status — Initial alterations in mental status caused by hypoperfusion may be subtle and are difficult to distinguish from drug or alcohol intoxication, head injury, or behavioral issues. In young, healthy patients, agitation, confusion, irritability, indifference to surroundings, or inattention to instructions may be the only early signs of shock. 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 cerebral hypoperfusion. Normal pulse oximetry and fingerstick glucose measurements in such patients further increase concern for cerebral hypoperfusion.

Pelvic injuries — Retroperitoneal hemorrhage from a pelvic fracture can be occult. As part of the examination, gentle compression of the pelvis should be done once only to test for pelvic instability, which is highly specific (albeit not sensitive) for pelvic fracture. Pressure should be directed posterior and medial in order to feel an unstable fracture "closing," and not to further displace ("open") an unstable injury. (See "Pelvic trauma: Initial evaluation and management".)

Superficial and extremity injuries — Scalp lacerations can bleed profusely, especially if the patient is taking an anticoagulant or antiplatelet medication. These wounds can be overlooked if there are distracting thoracic or abdominal injuries or if they bled significantly prior to arrival for medical care.

After a femur fracture, the thigh can hold up to one to two liters of blood. This may not be initially obvious and only become apparent after recognizing increasing thigh girth on re-evaluation.

CAUSES OF SHOCK IN THE TRAUMA PATIENT

Hemorrhagic sites — Hemorrhage is the most common cause of shock in the trauma patient and should be the presumed cause until proven otherwise (table 2). Massive hemorrhage can occur into the following possible locations:

External hemorrhage (eg, scalp laceration, open fracture site)

Thoracic cavity

Peritoneal cavity

Retroperitoneal space (often from pelvic fracture)

Muscle or subcutaneous tissue (often from a long-bone fracture)

Non-hemorrhagic — Other potential causes of shock in the injured patient include the following (table 1):

Cardiac tamponade (see "Cardiac tamponade")

Tension pneumothorax (see "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Pneumothorax')

Pulmonary dysfunction from pulmonary contusion or hemothorax (see "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Pulmonary contusion' and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Hemothorax')

Cardiac injury (eg, myocardial contusion, ventricular wall rupture, valve injury) (see "Initial evaluation and management of blunt cardiac injury")

Spinal cord injury (ie, neurogenic shock) (see "Acute traumatic spinal cord injury", section on 'Hemodynamic management')

Fat or air embolism (see "Fat embolism syndrome")

Septic shock can result from various injuries (for example, diaphragmatic rupture complicated by incarceration of abdominal organs and bowel perforation can lead to septic shock [typically occurs in penetrating trauma or high-velocity blunt trauma]) (see "Evaluation and management of suspected sepsis and septic shock in adults")

A nontraumatic cause of shock may have preceded or caused the injury, such as myocardial infarction (ie, cardiogenic shock) (see "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction")

Effects of pharmacologic or toxicologic agents (see "General approach to drug poisoning in adults" and "Initial management of the critically ill adult with an unknown overdose")

DIAGNOSIS AND MANAGEMENT

General principles — Diagnostic assessment and treatment are performed simultaneously in the seriously injured patient, especially when the cause of shock is not obvious (algorithm 1). The following immediate interventions are listed in order of priority:

Prevent or limit ongoing hemorrhage.

Ensure a patent airway while protecting the cervical spine. Definitive airway management may take priority in some situations, but it should be delayed, when possible, to assure optimal resuscitation and minimize the negative hemodynamic impact of induction and positive-pressure ventilation. When tension pneumothorax or cardiac tamponade are present, chest decompression or pericardiocentesis, respectively, should ideally be performed prior to initiating positive-pressure ventilation. Patients in shock have a sixfold increased risk of peri-intubation cardiac arrest following rapid sequence intubation [13]. (See "Approach to the difficult airway in adults for emergency medicine and critical care", section on 'High-risk physiology present'.)

Maximize oxygenation (ultimate goal is to maintain adequate oxygen delivery to vital organs).

Obtain intravenous (IV) access and initiate fluid resuscitation or blood transfusion as needed to restore intravascular volume. Initiating a massive transfusion protocol may be necessary.

Identify and address immediate threats to life (eg, tension pneumothorax, cardiac tamponade).

Obtain blood for laboratory and blood bank testing.

Notify trauma surgery consultant or transfer facility early in the patient's course.

Initial testing

Trauma ultrasound (ie, FAST) — Ultrasound evaluation performed as part of the initial examination and resuscitation of the trauma patient is known as the focused assessment with sonography for trauma (FAST) and can identify hemopericardium (image 1) and hemoperitoneum (image 2 and image 3). The extended FAST examination (E-FAST) adds pleural views to evaluate for pneumothorax (image 4) and hemothorax (image 5). Ultrasound cannot identify retroperitoneal bleeding. The E-FAST examination is now considered part of the trauma primary survey and is reviewed in detail separately. (see "Emergency ultrasound in adults with abdominal and thoracic trauma")

Limited role of diagnostic peritoneal lavage — When point-of-care ultrasound is unavailable, a hemodynamically unstable trauma patient who cannot be moved to radiology should have a diagnostic peritoneal lavage or aspiration (DPL/DPA) to identify life-threatening intraperitoneal bleeding. Routine use of DPL/DPA in unstable trauma patients has been supplanted by point-of-care ultrasound and rapid access to computed tomography (CT). (See "Diagnostic peritoneal lavage (DPL) or aspiration (DPA)".)

Diagnostic imaging — The standard initial trauma radiographs include the chest and pelvis. The portable chest radiograph (CXR) is most likely to reveal a life-threatening injury requiring immediate intervention. However, if hospital protocols offer immediate CT, the scanner is adjacent to the trauma bay, and the clinical scenario allows, CT can be obtained instead of plain radiographs. Plain lateral cervical spine radiographs, which were historically part of initial trauma imaging, have been supplanted by CT.

Laboratory evaluation — Standard laboratory tests are of limited use in the acute management of the trauma patient in shock. They are adjuncts and not substitutes for clinical assessment. (See "Initial management of trauma in adults", section on 'Laboratory tests' and "Blunt abdominal trauma in adults: Initial evaluation and management", section on 'Laboratory tests'.)

The following laboratory studies should be obtained in all patients with trauma-related shock:

Blood type and crossmatch – Any victim of significant trauma may require transfusion. In addition to obtaining a blood type and crossmatch sample, the blood bank should be notified directly of the need for uncrossmatched packed red blood cells and other blood products should a trauma victim present with potentially life-threatening hemorrhage.

Complete blood count – A hemoglobin or hematocrit serves as a baseline value but must be interpreted considering the extent of hemorrhage, time since the injury, pre-injury hematocrit when available, and the volume of IV fluid administered. An initially normal hematocrit does not rule out significant hemorrhage since equilibration of the hematocrit can be delayed by hours. The hematocrit is most helpful to assess ongoing hemorrhage when measured serially.

Coagulation studies – The prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT) are helpful to determine the need for blood factor or product replacement, especially in a patient taking anticoagulant medications. Where available, thromboelastography (TEG) and rotational thromboelastometry (ROTEM) provide faster and more accurate assessment of coagulopathy and can help guide ongoing clotting factor replacement while reducing unnecessary transfusion. (See "Etiology and diagnosis of coagulopathy in trauma patients", section on 'Viscoelastic hemostatic assays' and "Etiology and diagnosis of coagulopathy in trauma patients" and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient", section on 'VHA-based dosing'.)

Serum electrolytes and lactate – Shock creates a metabolic acidosis with a base deficit (ie, decreased serum bicarbonate) and increased serum lactate. While such findings suggest shock, clinicians must interpret them in the context of the patient's clinical appearance and presentation since they are not specific for any type of shock. Also, changes in laboratory values are typically delayed following clinical improvement after aggressive resuscitation.

Kidney function tests – The serum creatinine may be requested for patients receiving IV contrast for imaging studies, although abnormal kidney function should not deter necessary imaging.

Other tests – Additional laboratory testing may be needed depending on clinical circumstance. A pregnancy test should be performed for female patients of childbearing age. If pregnant, the patient's Rh status should be determined. Cardiac biomarkers or a serum concentration of an anticonvulsant should be obtained if an acute coronary syndrome or seizure, respectively, may have contributed to the trauma. A serum ethanol concentration is commonly obtained because of the high rate of ethanol intoxication in trauma patients.

Identifying and treating specific causes

Hemorrhagic shock — Management of moderate to severe hemorrhage and massive transfusion protocols are discussed in detail separately. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient" and "Massive blood transfusion", section on 'Trauma'.)

Permissive hypotension, also known as delayed fluid resuscitation with controlled hypotension, is discussed in detail separately. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Delayed fluid resuscitation/controlled hypotension'.)

Reversal of anticoagulant medication effects, if needed, is discussed in detail separately. (See "Management of warfarin-associated bleeding or supratherapeutic INR" and "Management of bleeding in patients receiving direct oral anticoagulants" and "Reversal of anticoagulation in intracranial hemorrhage".)

Use of tranexamic acid as an antifibrinolytic agent in trauma patients who present within three hours of injury is discussed in detail separately. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Patient within three hours of injury' and "Etiology and diagnosis of coagulopathy in trauma patients" and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient", section on 'Management of acute traumatic coagulopathy'.)

Topical hemostatic agents are presented in the table (table 3) and discussed separately. (See "Overview of topical hemostatic agents and tissue adhesives", section on 'Hemostatic agents'.)

Emergency thoracotomy and resuscitative endovascular balloon occlusion of the aorta (REBOA) procedures are salvage options for patients in extremis and discussed in detail separately. (See "Resuscitative thoracotomy in adults: Technique" and "Endovascular methods for aortic control in trauma".)

Diagnosis and management by specific site of hemorrhage is discussed in detail separately:

Scalp laceration (see "Assessment and management of scalp lacerations")

Thoracic (see "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Damage control sternotomy/thoracotomy' and "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation and management of penetrating thoracic trauma in adults" and "Overview of blunt and penetrating thoracic vascular injury in adults" and "Management of cardiac injury in severely injured patients")

Peritoneal (see "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Damage control laparotomy' and "Blunt abdominal trauma in adults: Initial evaluation and management" and "Initial evaluation and management of abdominal stab wounds in adults" and "Abdominal gunshot wounds in adults: Initial evaluation and management" and "Abdominal vascular injury" and "Management of splenic injury in the adult trauma patient" and "Management of hepatic trauma in adults")

Retroperitoneal – Pelvic instability identified on examinations should prompt "wrapping" with either a sheet or a commercial pelvic binder to reduce pelvic volume. "Wrapping" the pelvis reduces pelvic volume (creating a tamponade effect), stabilizes fracture fragments (reducing hemorrhage from the fracture sites), and improves patient comfort. Definitive management is discussed separately. (See "Overview of the diagnosis and initial management of traumatic retroperitoneal injury" and "Severe pelvic fracture in the adult trauma patient".)

Extremity – Hemorrhage should be controlled with direct pressure when feasible. Use of a tourniquet is acceptable when direct pressure does not adequately control bleeding in cases of amputation or severe extremity injury. Tourniquets should be released as soon as possible, and the time of application and duration of use should be clearly recorded. Definitive management may require interventional radiology or surgical control. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Pelvic/extremity stabilization' and "Severe lower extremity injury in the adult patient", section on 'Control of hemorrhage' and "Control of external hemorrhage in trauma patients".)

Non-hemorrhagic causes

Tension pneumothorax — A pneumothorax is a common injury in both blunt and penetrating trauma (image 6 and image 7 and image 8). Tension physiology occurs when the pneumothorax compresses the inferior vena cava, causing inadequate preload and obstructive shock. Signs and symptoms may include hypoxia, tachypnea, ipsilateral chest pain, unilateral diminished or absent breath sounds, subcutaneous air, deviation of the trachea away from the affected side, or unilateral hyperresonance to percussion, depending on underlying injuries and the extent of the pneumothorax. Tracheal deviation and hypotension occur late in the course, while hypoxemia occurs earlier than hypotension [14]. A small pneumothorax may develop tension physiology and shock if the patient is placed on positive-pressure ventilation. (See "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Pneumothorax'.)

A suspected pneumothorax in a stable patient is typically confirmed by CXR. Point-of-care ultrasound may be more sensitive compared with supine anteroposterior CXR in identifying small or moderate pneumothorax [15]. If the clinician suspects a tension pneumothorax and the patient is hypotensive or unstable, immediate chest decompression is necessary and must not be delayed for radiography. A chest tube can be placed rapidly, or a needle decompression or finger thoracostomy performed first followed by chest tube placement. These procedures are discussed in detail elsewhere. (See "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Role of needle/finger chest decompression' and "Thoracostomy tubes and catheters: Placement techniques and complications".)

Cardiac tamponade — Hemopericardium-producing cardiac tamponade can occur with penetrating or major blunt chest trauma. Tachycardia and hypotension are common, while distended neck veins and muffled heart sounds (part of Beck's triad) are not reliable signs. Immediate ultrasonography (ie, FAST exam) offers the best opportunity for rapid, early, and accurate diagnosis (image 1). Pericardiocentesis is performed if a pericardial effusion is found, cardiac tamponade is suspected, and the patient is hypotensive or clinically worsening despite aggressive resuscitation. If pericardiocentesis recovers blood and improves the patient's clinical status, surgical intervention (eg, thoracotomy, pericardial window, or median sternotomy) is indicated. Traumatic cardiac tamponade is discussed in detail separately. (See "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Cardiac injury'.)

Cardiac tamponade, bedside ultrasound diagnosis, the pericardiocentesis procedure, and emergency thoracotomy are discussed in detail separately. (See "Cardiac tamponade" and "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Pericardial and limited cardiac examination' and "Emergency pericardiocentesis" and "Resuscitative thoracotomy in adults: Technique" and "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Role of emergency department thoracotomy'.)

Cardiac injury — In addition to cardiac tamponade, other potential cardiac injuries that can cause shock include ventricular wall rupture, valve rupture, severe cardiac contusion, and acute dysrhythmia. Immediate assessment includes cardiac monitoring and echocardiography. (See "Initial evaluation and management of blunt cardiac injury".)

Neurogenic shock — A high spinal cord injury can interrupt autonomic pathways and result in loss of peripheral vascular resistance. Hypotension can be mild, while tachycardia can be absent because of decreased sympathetic tone. Hypotension, neurologic deficits distal to a spinal cord level (eg, loss of reflexes, motor function, and sensation), and the absence of peripheral vasoconstriction (eg, warm extremities and good urine output) is suggestive of neurogenic shock. However, hypotension should not be attributed solely to neurologic injury until hemorrhagic shock has been ruled out or managed appropriately. Also, neurologic deficits may not be apparent in the unresponsive patient.

Depending on the site of injury, immediate emergency interventions may not be needed for the patient with isolated neurogenic shock. Hypotension exacerbates secondary injury to the central nervous system, which should be addressed with vasopressor therapy (eg, norepinephrine infusion). The goal for the mean arterial pressure is 85 to 90 mmHg or higher. Volume status must be closely monitored because excess fluid administration may be harmful. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Spinal cord injury in the setting of hemorrhagic shock' and "Acute traumatic spinal cord injury".)

Pregnancy — The pregnant hypotensive trauma patient should be placed in the left lateral decubitus position in order to displace the gravid uterus off the inferior vena cava. This will improve venous return and may increase the blood pressure. (See "Initial evaluation and management of major trauma in pregnancy".)

Iatrogenic — Procedural complications may contribute to shock. As an example, a tension pneumothorax can develop from inadvertent puncture of a lung during central venous catheter placement. Endotracheal and thoracostomy tubes and central venous catheters can become dislodged or obstructed, particularly when a patient is moved. Initiation of positive-pressure ventilation can decrease venous return. A patient should be reassessed after significant moves and with any clinical change.

Delayed causes — Shock that develops 12 hours to three days after the initial trauma in a patient with a long bone fracture raises the possibility of fat embolism syndrome. (See "Fat embolism syndrome".)

Other delayed causes of shock that may develop during the hospitalization of an adult trauma patient include pulmonary embolism, loss of intravascular fluid into the extravascular space (ie, third-space), and sepsis, and are reviewed separately. (See "Overview of inpatient management of the adult trauma patient".)

DISPOSITION — Definitive management of the trauma patient with shock often requires emergency surgery. Ideally, a trauma surgeon should be involved as soon as possible in the care of any patient who has sustained significant trauma and may require operative or critical care interventions. If the patient must be transferred for definitive care, early communication with a trauma center and preparation for transfer should be performed concurrently with assessment and stabilization when possible. 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 a hypotensive patient with an identified injury (eg, high-grade splenic laceration), but with no trauma surgeon available, emergency consultation with a general surgeon may be necessary for stabilization laparotomy prior to a time-consuming transfer.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Use of point-of-care echocardiography and ultrasonography as a monitor for therapeutic intervention in critically ill patients" and "Society guideline links: General issues of trauma management in adults".)

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 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information 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 e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

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

SUMMARY AND RECOMMENDATIONS

Causes of traumatic shock – Loss of circulating blood volume from hemorrhage is the most common cause of shock in the adult trauma patient. Inadequate oxygenation, mechanical obstruction (eg, cardiac tamponade, tension pneumothorax), neurologic dysfunction (eg, high spinal cord injury), and cardiac dysfunction represent other potential causes or contributing factors. A list of potential causes of traumatic shock and classification of shock are provided in the tables (table 2 and table 1). (See 'Pathophysiology' above and 'Causes of shock in the trauma patient' above.)

Clinical features of traumatic shock – Obvious and immediately detectable manifestations of the shock state include altered mental status, tachycardia, hypotension, cool extremities, weak peripheral pulses, prolonged capillary refill (>2 seconds), and a narrowing of the pulse pressure (<25 mmHg). (See 'Common clinical signs of shock' above.)

A significant blood pressure decrease is generally not manifested until class III hemorrhage develops, and up to 30 percent of a patient's blood volume can be lost before this occurs. Slight alterations in mental status may be the earliest signs of shock. (See 'Stages of hemorrhagic shock' above.)

Recognizing shock early and with non-obvious signs – Early recognition, ideally before hypotension develops, is the first step in managing the injured patient with shock. Shock may exist even in the setting of "normal" vital signs. Subtle examination findings in early shock include pallor, poor capillary refill, diaphoresis, and tachypnea. Low urine output may indicate inadequate visceral perfusion.

Young, otherwise healthy patients can maintain a normal blood pressure despite substantial blood loss and present with subtle symptoms such as agitation as the only sign of early shock. Older adults are more likely to take medications (eg, beta blockers) that blunt the hemodynamic response to injury and are more likely to have baseline hypertension, thus confounding interpretation of a "normal" blood pressure. Bleeding from pelvic fractures, scalp lacerations, and thigh hematomas can occasionally be challenging to identify. (See 'Recognizing early and non-obvious signs' above.)

Initial testing – In addition to physical examination, bedside ultrasound (ie, extended focused assessment with sonography in trauma [E-FAST] examination) is an important tool for rapidly identifying hemopericardium, hemoperitoneum, pneumothorax, and hemothorax. (See 'Trauma ultrasound (ie, FAST)' above.)

The standard initial trauma radiographs are chest and pelvis, although depending upon hospital protocols and the clinical scenario, clinicians may forego pelvis radiographs in favor of computed tomography (CT). The portable chest radiograph (CXR) is the study most likely to reveal an injury requiring immediate intervention. (See 'Diagnostic imaging' above.)

Standard laboratory tests are of limited use in the acute management of the trauma patient in shock and should be used as adjuncts instead of substitutes for clinical assessment. Standard tests include blood type and crossmatch, complete blood count, coagulation studies (thromboelastography [TEG] if available), serum electrolytes and lactate, kidney function tests, pregnancy test in female patients of childbearing age, and serum ethanol concentration. (See 'Laboratory evaluation' above.)

General management principles – Initial management of traumatic shock is focused on the following (algorithm 1) (see 'General principles' above):

Prevent or limit ongoing hemorrhage

Ensure a patent airway while protecting the cervical spine

Maximize oxygenation

Obtain intravenous (IV) access and initiate fluid resuscitation or blood transfusion as needed

Identify and address immediate threats to life (eg, tension pneumothorax, cardiac tamponade)

Obtain blood for laboratory and blood bank testing

Notify trauma surgery consultant or transfer facility early in the patient's course

Identifying and treating specific causes

Sites of hemorrhage – Massive hemorrhage can occur into the chest, abdomen, retroperitoneum, external wounds (eg, scalp), and muscle or subcutaneous tissue (eg, thigh). (See 'Hemorrhagic sites' above and 'Hemorrhagic shock' above.)

Non-hemorrhagic causes – Other potential causes of shock in the injured patient include the following (table 1) (see 'Non-hemorrhagic causes' above):

-Tension pneumothorax (see 'Tension pneumothorax' above)

-Cardiac tamponade (see 'Cardiac tamponade' above)

-Other cardiac causes such as ventricular wall rupture, valve rupture, severe cardiac contusion, and acute dysrhythmia (see 'Cardiac injury' above)

-Neurogenic shock (see 'Neurogenic shock' above)

-Obstructive shock from inferior vena cava compression by gravid uterus (see 'Pregnancy' above)

-Procedural complications and tube and catheter dislodgement (see 'Iatrogenic' above)

-Delayed causes such as fat embolism syndrome, pulmonary embolism, and sepsis (see 'Delayed causes' above)

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Topic 127887 Version 4.0

References

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