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16/09/2018 Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock - UpToDate
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Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock
Author: Christopher Colwell, MD

Section Editor: Maria E Moreira, MD
Deputy 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: Aug 2018. | This topic last updated: Apr 19, 2018.
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. 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 [1]. Shock is a common and frequently treatable cause of death in injured patients and
is second only to brain injury as the leading cause of death from trauma [2,3].
This topic will review the evaluation of shock in the adult trauma patient, focusing on recognition of shock,
basic initial management, and acute interventions needed to treat non-hemorrhagic causes of shock. General
management of the adult trauma patient, management of hemorrhagic shock, and other aspects of shock,
including the pathophysiology and differential diagnosis, are discussed separately. (See "Initial management
of trauma in adults" and "Initial management of moderate to severe hemorrhage in the adult trauma patient"
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 the oxygen available to the mitochondria.
Adenosine triphosphate (ATP) can still be synthesized by anaerobic glycolysis but 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]. 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 acute hemorrhage 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 lactate production leads to worsening systemic metabolic acidosis, which along with hypoxemia
ultimately causes the loss of peripheral vasoconstriction and cardiovascular collapse.
The Advanced Trauma Life Support (ATLS) manual describes four classes of hemorrhage to emphasize the
early signs of the shock state [3]. Clinicians should note that significant drops in blood pressure are 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:
● 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.
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● 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), tachypnea (respiratory rate of 20 to 24), 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 significant 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 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). Urine output is minimal or absent. The skin is cold and pale, and capillary refill is delayed.
DIFFERENTIAL DIAGNOSIS — Hemorrhage is the most common cause of shock in the trauma patient.
Massive hemorrhage can occur in the chest, abdomen, pelvis, retroperitoneum, and from major external
wounds. The thigh can hold up to approximately 1 to 2 L of blood. Scalp lacerations can bleed profusely,
especially if the patient is on anticoagulants or antiplatelet medications. These wounds can be overlooked if
significant thoracic or abdominal injuries are present, or if the most significant blood loss occurred in the field.
The initial and subsequent management of the adult trauma patient with significant bleeding are reviewed
separately. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient" and
"Acute coagulopathy associated with trauma".)
A number of other potential causes of traumatic shock must also be considered, including (table 1 and table
2):
● Cardiac tamponade (see "Cardiac tamponade")
● Tension pneumothorax (see "Initial evaluation and management of blunt thoracic trauma in adults",
section on 'Pulmonary injury')
● Pulmonary contusion with resulting pulmonary dysfunction
● Hemothorax with resulting pulmonary dysfunction
● Myocardial infarction or contusion (ie, cardiogenic shock) (see "Clinical manifestations and diagnosis of
cardiogenic shock in acute myocardial infarction")
● Spinal cord injury (ie, neurogenic shock) (see "Acute traumatic spinal cord injury", section on
'Cardiovascular complications')
● Effects of pharmacologic or toxicologic agents
● Fat or air embolism (see "Fat embolism syndrome")
In penetrating trauma or high velocity blunt trauma, diaphragmatic rupture complicated by incarceration of
abdominal organs and bowel perforation can lead to septic shock. (See "Evaluation and management of
suspected sepsis and septic shock in adults".)
RECOGNITION OF SHOCK — Recognition is the first step in managing traumatic shock. Ideally, shock is
recognized before hypotension develops [6]. 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 development of shock.
Obvious and immediately detectable manifestations of the shock state include:
● Tachycardia (note that neurogenic shock may present with bradycardia)
● Hypotension
● Cool extremities (note that neurogenic shock 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 coma to agitation)
Hemorrhage is the most common cause of shock in the adult trauma patient. Large-scale bleeding can
occur at five 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)
When the cause of shock is not obvious, evaluation and treatment occur in tandem. A trauma ultrasound
examination, or extended Focused Assessment with Sonography for Trauma (eFAST), is performed early in
the assessment to look for hemopericardium, intraabdominal bleeding, and pneumothorax. Performance of
the eFAST examination is reviewed in detail separately. (See "Emergency ultrasound in adults with
abdominal and thoracic trauma".)
The three standard initial trauma radiographs include the chest, pelvis, and lateral cervical spine, although
depending upon the hospital and the clinical scenario clinicians may forego plain radiographs in favor of
computed tomography (CT), particularly if CT scanners are immediately available and adjacent to the trauma
bay. Of the standard plain radiographs, 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.
Shock may exist even in the setting of "normal" vital signs, making diagnosis potentially difficult. Patients on
cardioactive medications such as beta-blockers may typical vital sign responses in shock. In the setting of
significant trauma, remain skeptical of apparently normal vital signs. 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, only to decompensate acutely sometime later. A
bradycardic response to penetrating intraperitoneal injury, which may be vagally mediated, has been
described [7]. In addition, a paradoxical or relative bradycardia has been described in hypoperfusing trauma
patients [8]. A retrospective review of more than 1700 trauma patients that compared presenting heart rate
with base deficits and lactate concentrations reported that the absence of tachycardia in the presence of
hypoperfusion is associated with a poor prognosis independent 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 reversal
of end-organ hypoperfusion. Serial examinations and serial ultrasound studies can help to identify occult
injuries [9]. The importance of reassessing patients who appear "stable" initially following significant trauma
cannot be overstated. Subtle changes in vital signs and physical findings are best detected by serial
examinations and may offer the earliest clues to the presence of significant injury. While not all patients need
to be observed for extended periods, worsening vital signs (eg, increase in heart or respiratory rate),
concerning changes in the physical examination, or any sense that something just doesn't feel or look right
demands close attention and observation until the suspected injury becomes apparent or the source of
concern resolves.
Alterations in mental status caused by hypoperfusion may be subtle initially and can be difficult to distinguish
from drug or alcohol intoxication or associated 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 cerebral hypoperfusion. Normal pulse oximetry and fingerstick glucose measurements in
such patients further increase concern for cerebral hypoperfusion.
In young, otherwise healthy patients, subtle alterations, such as agitation, confusion, irritability, indifference to
surroundings, or inattention to instructions, may be the only sign of early shock. A patient who is
"aggravating" you or your staff may be showing early signs of shock, not the effects of intoxication. Be
extremely cautious before attributing abnormal vital signs or physical examination findings to nontraumatic or
behavioral causes.
Subtle examination findings may provide evidence of early shock. Pallor or poor capillary refill may represent
peripheral vasoconstriction. Diaphoresis may indicate physiologic stress and appear before vital sign
abnormalities. Mild tachypnea may reflect compensation for metabolic acidosis. 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 and have a high-urine specific gravity may be compensating for hypovolemia.
Elder adult patients are more likely to take medications (eg, beta blockers) that affect the hemodynamic
response to injury and are more likely to have baseline hypertension. It is important to interpret vital signs
with the patient's baseline in mind [10]. The emergency clinician may need to predict this physiologic baseline
based on age and other available information (eg, medication list). As an example, a systolic blood pressure
of 110 mmHg may be dangerously low in a patient with underlying hypertension. (See "Geriatric trauma:
Initial evaluation and management".)
Non-hemorrhagic causes of traumatic shock may demonstrate typical presentations, but often do not. As an
example, pericardial tamponade is classically described as exhibiting Beck's triad of hypotension, distended
neck veins, and muffled heart sounds, but these are late findings, when present at all. If significant, ongoing
hemorrhage exists or the pericardium periodically decompresses by emptying blood into the pleural space,
tamponade can occur without distended neck veins. Ultrasound examination (and possibly re-examination) is
critical. (See 'Immediate interventions to manage non-hemorrhagic shock' below and "Emergency ultrasound
in adults with abdominal and thoracic trauma", section on 'Pericardial and limited cardiac examination'.)
In addition to pericardial tamponade, other potential cardiac causes of trauma-related shock include
ventricular wall rupture, valve rupture, severe cardiac contusion, and acute dysrhythmia. Immediate
assessment includes cardiac monitoring and echocardiography. (See "Cardiac injury from blunt trauma".)
A large pneumothorax or hemothorax may be detected clinically by the appearance of respiratory distress,
unilateral diminished breath sounds, or air crepitus on palpation. Ultrasound is an important tool for
recognizing pneumothorax, particularly in the unstable or supine patient, as pneumothoraxes can be difficult
to detect on plain chest radiograph in such patients. (See "Emergency ultrasound in adults with abdominal
and thoracic trauma", section on 'Pleural examination' and "Imaging of pneumothorax".)
In the stable patient with suspected pneumothorax, confirmation by chest radiograph is prudent; in the
unstable patient, immediate treatment with needle 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 the trachea away from the affected side, and
hypotension from inadequate preload due to compression of the inferior vena cava. Tracheal deviation and
hypotension occur late. Animal studies suggest hypoxemia may be an earlier sign of tension pneumothorax
than hypotension [11]. Patients with small pneumothoraxes may develop tension physiology and shock if they
are intubated and placed on positive pressure ventilation. (See "Prehospital care of the adult trauma patient",
section on 'Needle chest decompression' and "Placement and management of thoracostomy tubes".)
Neurogenic shock may develop in the patient with a high-spinal cord injury. Neurologic deficits may not be
apparent in the unresponsive patient, but are usually obvious otherwise, as patients manifest some
combination of a loss of reflexes, motor function, and sensation distal to the level of the spinal cord injury.
Hypotension, which may be mild in these patients, results from the loss of peripheral vascular resistance.
Tachycardia is absent because of the loss of sympathetic tone. Hypotension associated with neurologic
deficits and the absence of peripheral vasoconstriction (these patients often have warm extremities and good
urine output) raises suspicion for neurogenic shock. Volume status must be closely monitored because
excess fluid administration may be harmful. Hypotension should not be attributed solely to neurologic injury
until hemorrhagic shock has been ruled out. (See "Acute traumatic spinal cord injury".)
Following any patient transfer to a new stretcher or any invasive procedure (eg, tracheal intubation and
mechanical ventilation, placement of central venous catheter), be aware that complications may contribute to
shock. As an example, inadvertent puncture of a lung during central line placement in an intubated patient
may produce a tension pneumothorax. Endotracheal and thoracostomy tubes can become dislodged or
obstructed when a patient is moved. It is prudent to reassess all patients after such a move, and certainly
with any change in their condition.
Shock that develops 12 hours to 3 days after the initial trauma raises the possibility of fat embolus syndrome,
likely from a long bone fracture. Other delayed causes of shock that may develop during the hospitalization of
an adult trauma patient are reviewed separately. (See "Fat embolism syndrome" and "Overview of inpatient
management in the adult trauma patient".)
PREHOSPITAL MANAGEMENT — The prehospital management of patients in traumatic shock is focused

on recognition, rapid transport, and stabilization of the airway, breathing, and circulation. Prehospital
clinicians must be diligent about looking for signs of hypoperfusion, ideally recognizing traumatic shock
before hypotension develops, and providing appropriate management according to their level of skill. Delayed
fluid resuscitation for penetrating trauma remains controversial. (See "Prehospital care of the adult trauma
patient" and "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on
'Delayed fluid resuscitation/controlled hypotension'.)
INITIAL HOSPITAL MANAGEMENT
Basic approach and initial interventions — Initial management of the adult trauma patient in shock is
focused on the following:
● Recognizing and reversing life-threatening injuries (eg, tension pneumothorax, cardiac tamponade)
immediately.
● Preventing or limiting ongoing blood loss.
● Restoring intravascular volume if necessary.
● Maintaining adequate oxygen delivery to vital organs.
Assessment and treatment are performed simultaneously in the seriously injured patient (algorithm 1). The
emergency clinician evaluates the airway and hemodynamic status and looks for hemorrhage while
performing the following immediate interventions listed in order of priority:
● Establish a patent and protected airway while protecting the cervical spine.
● Control hemorrhage.
● Maximize oxygenation.
● Gain intravenous (IV) access and initiate fluid resuscitation or blood transfusion as indicated.
● Identify and reverse immediate threats to life (eg, pericardial tamponade, tension pneumothorax).
● Obtain blood for laboratory and blood bank testing.
Direct pressure is the primary and preferred means for controlling external hemorrhage. While clamping
bleeding vessels under direct visualization is acceptable when necessary, blind clamping should NOT be
performed. Scalp lacerations can bleed profusely and are often overlooked if significant thoracic or abdominal
injuries are present. Scalp lacerations can be managed by injecting lidocaine with epinephrine directly into
the wound, by placing clips (eg, Raney clips (picture 1)), or by closing the wound with running (ie,
noninterrupted) or running locked stitches using heavy suture. Running or interrupted sutures may also be
used to control severe bleeding from extremity wounds when direct pressure is inadequate and the few
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 when
other 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 the
adult patient", section on 'Control of hemorrhage'.)
Vascular access is obtained as rapidly as possible. Two large-bore (16 gauge or larger) IV lines placed in the
antecubital region are ideal, but not always possible. Intraosseous devices can be placed rapidly and offer an
effective alternative when there is difficulty placing an IV catheter. (See "Peripheral venous access in adults"
and "Intraosseous infusion".)
Placement of a central venous catheter (size 8 French) can be performed when adequate peripheral access
cannot be obtained, and allows measurement of central venous pressure. Central line placement under
ultrasound guidance offers high success rates with fewer complications than procedures performed without
ultrasound [12,13]. Some experts advocate use of distal saphenous vein cutdowns due to ease of access
and consistency of anatomy [14]. (See "Principles of ultrasound-guided venous access" and "Overview of
central venous access".)
Traumatic shock occurs most often from hemorrhage, generally from an intraabdominal injury in blunt trauma.
Ultrasound is an integral part of the initial evaluation of the trauma patient, and reliably identifies free
intraabdominal fluid in the hands of proficient ultrasonographers [15]. During the initial resuscitation, the
extended Focused Assessment with Sonography for Trauma (eFAST) exam, is performed to assess first for
pericardial effusion and then for intraperitoneal bleeding and pneumothorax. (See "Emergency ultrasound in
adults with abdominal and thoracic trauma".)
Ultrasound has largely replaced diagnostic peritoneal lavage (DPL) in the initial assessment of the trauma
patient, although DPL retains an important role in specific circumstances. If ultrasound is unavailable or its
findings are equivocal or inconsistent with the clinical picture, a DPL or diagnostic peritoneal tap (DPT) can
provide important information. An example of such a scenario would be an unstable patient with major pelvic
trauma 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 peritoneal
lavage' and "Pelvic trauma: Initial evaluation and management", section on 'Diagnostic tests'.)
Unstable pelvic fractures and associated vascular injuries can cause hemorrhagic shock. Preliminary
stabilization of the pelvis by applying a circumferential pelvic binder or tying a sheet firmly around the pelvis
can reduce bleeding. Such interventions are most important with "open-book" pelvic fractures (in which the
symphysis pubis is disrupted (≥2.5 cm), the pelvis opened, and the retroperitoneal space enlarged) (image
1). In addition to immediate orthopedic consultation, interventional radiology and vascular surgery may be
needed to help control hemorrhage. (See "Pelvic trauma: Initial evaluation and management", section on
'Management'.)
Fluid resuscitation and blood transfusion — IV fluid resuscitation and transfusion of blood products are
critical elements of managing the adult trauma patient with hemorrhagic shock. The initial approach to such
resuscitation is discussed separately. (See "Initial management of moderate to severe hemorrhage in the
adult trauma patient".)
Interventions for non-hemorrhagic threats to life — As part of the primary (and secondary) survey, the
clinician must identify and reverse immediate threats to life. These include injuries that compromise
oxygenation and cardiac output, such as airway obstruction, tension pneumothorax, and pericardial
tamponade. Interventions such as tracheal intubation and tube or needle thoracostomy are performed as
soon as the need is recognized. (See "Initial management of trauma in adults", section on 'Primary evaluation
and management' and 'Immediate interventions to manage non-hemorrhagic shock' below.)
Reversal of anticoagulation — Some trauma patients, particularly elders with comorbidities, may be taking
anticoagulants. Provided below are several tables outlining methods for reversing particular anticoagulants in
cases of life-threatening bleeding, as well as links to more detailed discussions of how to manage bleeding
associated with these medications:
● Warfarin (see "Management of warfarin-associated bleeding or supratherapeutic INR", section on

'Serious/life-threatening bleeding'). Initial emergency treatment to reverse anticoagulation due to warfarin
in patients with severe hemorrhage is outlined in the following table (table 3).
● Direct thrombin inhibitors (eg, dabigatran) and factor Xa inhibitors (eg, rivaroxaban, apixaban, edoxaban)
(see "Management of bleeding in patients receiving direct oral anticoagulants"). Initial emergency
treatment to reverse anticoagulation due to direct oral anticoagulants in patients with severe hemorrhage
is outlined in the following table (table 4).
● 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').
Vasopressors — No human studies exist to support the use of vasopressors in the resuscitation of the adult
with multiple trauma [16]. Their use early in the management of hemorrhagic shock may be harmful [17].
Vasopressor therapy may be needed in the setting of neurogenic shock.
Laboratory evaluation — Hematology and chemistry laboratory tests are of limited use in the acute
management of the trauma patient in shock. Clinicians should consider them adjuncts to diagnosis and not
substitutes for clinical assessment. (See "Initial management of trauma in adults", section on 'Laboratory
tests' and "Initial evaluation and management of blunt abdominal trauma in adults", section on 'Laboratory
tests'.)
The following laboratory studies are obtained in all patients with trauma-related shock:
● Type and cross-match several units of packed red blood cells, plasma, and platelets
● Baseline hemoglobin or hematocrit
● Serum bicarbonate (base deficit) and serum lactate
The emergency clinician should order a blood type and cross-match for any victim of significant trauma in
anticipation of the need for transfusion. The blood bank should be notified directly (ie, by telephone or in
person) of the need for packed red blood cells, and other blood products, should a trauma victim present with
life-threatening 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 volume of exogenous
fluid administration. As an example, the clinician should not be reassured by a normal hematocrit in the acute
trauma victim with hypotension. The hematocrit is most helpful when measured serially to assess ongoing
hemorrhage.
Hemorrhagic shock may create a metabolic acidosis with a base deficit (ie, decreased serum bicarbonate) or
increased serum lactate. While such findings suggest shock, clinicians must interpret them in the context of
the patient's clinical appearance. Typically, laboratory values lag behind clinical improvement after aggressive
resuscitation.
Coagulation studies, a platelet count, and serum electrolytes are helpful to determine the need for blood
products and electrolyte replacement, if hemorrhage is ongoing. Where available, thromboelastography
(TEG) and rotational thromboelastometry (ROTEM) provide faster and more accurate assessment of
coagulopathy in the trauma patient and can help guide ongoing treatment with clotting factors as well as
reduce unnecessary transfusion. (See "Acute coagulopathy associated with trauma", section on
'Thromboelastography' and "Acute coagulopathy associated with trauma", section on 'Thromboelastography-
based transfusion'.)
Massive transfusion protocols for trauma are discussed separately. (See "Massive blood transfusion", section
on 'Trauma'.)
Additional laboratory testing may be needed depending on clinical circumstance. A pregnancy test (eg, urine
hCG) should be performed for women of child-bearing age. If pregnant, the patients Rh status should be
checked. Appropriate coagulation studies should be performed for patients taking anticoagulant medications.
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. Renal function tests may be needed
for patients receiving IV contrast for imaging studies.
IMMEDIATE INTERVENTIONS TO MANAGE NON-HEMORRHAGIC SHOCK
Pneumothorax — Pneumothorax occurs often in both blunt and penetrating trauma, and presenting
symptoms and signs may be delayed (image 2 and image 3). Patients may manifest tachypnea, chest pain,
hypoxia, unilateral diminished or absent breath sounds, subcutaneous air, or unilateral hyperresonance to
percussion, depending on underlying injuries and the extent of the pneumothorax.
Traumatic pneumothorax or hemothorax is typically managed by the placement of a large thoracostomy tube
(36 French or larger) in the lateral chest. A small or occult pneumothorax may be amenable to management
using a small catheter, aspiration, or close observation. (See "Placement and management of thoracostomy
tubes" and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Pulmonary
injury'.)
If the clinician suspects a tension pneumothorax and the patient is hypotensive, a needle thoracostomy can
be performed, as a temporizing measure, using a long, large (eg, 12 or 14 gauge) angiocatheter or needle
inserted above the rib at the second intercostal space in the mid-clavicular line, or at the fifth intercostal
space in the mid-axillary 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, but longer needles increase the risk of injuring the subclavian vessels or other structures [18,19].
However, depending on the patient's body habitus, needles as long as 8 cm may be required for effective
decompression. Should a 4.5 cm needle fail to decompress a tension pneumothorax and a tube
thoracostomy be delayed, clinicians should use a longer needle. (See "Prehospital care of the adult trauma
patient", section on 'Needle chest decompression'.)
Pericardial tamponade — Pericardial effusion producing cardiac tamponade can occur with penetrating or
major blunt chest trauma. The "classic" findings of Beck's triad (hypotension, distended neck veins, and
muffled heart sounds) are late findings, when present. Tachycardia and hypotension are common. (See
"Cardiac tamponade".)
Immediate ultrasonography (US) or echocardiography offers the best opportunity for rapid, early, and
accurate diagnosis (image 4). (See "Emergency ultrasound in adults with abdominal and thoracic trauma",
section on 'Pericardial and limited cardiac examination'.)
Pericardiocentesis is performed if pericardial tamponade is suspected and the patient is hypotensive and
worsening despite aggressive volume resuscitation. If pericardiocentesis recovers blood and improves the
patient's clinical status, emergency thoracotomy is indicated. If thoracotomy cannot be performed,
pericardiocentesis can be repeated as necessary or a J-shaped catheter can be inserted into the pericardial
space to allow continual drainage of the hemopericardium. (See "Emergency pericardiocentesis".)
Pericardiocentesis is "classically" performed using the subxiphoid approach [20]. However, some researchers
and a large observational study support the use of the para-apical or parasternal approach under ultrasound
guidance [21]. Use of the parasternal approach allows the needle entry site to be closer to the pericardium
and eliminates the risk of liver injury. No controlled trials have compared these approaches in trauma
patients.
During resuscitation, keep in mind that rapid sequence intubation followed by positive pressure ventilation
can compromise hemodynamic function and lead to cardiac arrest in patients with signs of cardiac
tamponade.
Emergency thoracotomy — In trauma patients who are profoundly hypotensive despite aggressive fluid
resuscitation, or have lost discernible blood pressure for only a few minutes, an emergency left lateral
thoracotomy to enable decompression of pericardial tamponade, vascular or pulmonary clamping, and direct
suture repair, may be life-saving. The indications, contraindications, and performance of emergency
thoracotomy are discussed in detail separately. (See "Initial evaluation and management of penetrating
thoracic trauma in adults", section on 'Emergency department thoracotomy (EDT)' and "Resuscitative
thoracotomy: Technique".)
Pregnancy — Hypotensive pregnant trauma patients are placed in the left lateral decubitus position or the
right side of their backboard is tilted up about 15 degrees in order to move the gravid uterus off of the inferior
vena cava. These maneuvers improve venous return and may increase the blood pressure. (See "Initial
evaluation and management of pregnant women with major trauma".)
Neurogenic shock — The diagnosis of neurogenic shock is made only after hemorrhagic shock has been
managed appropriately or ruled out. While immediate emergency interventions may not be needed for the
patient with isolated neurogenic shock, vasopressor therapy may be necessary to treat hypotension. (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".)
DISPOSITION — Definitive management of the patient with traumatic shock often requires emergency
surgery. Emergency clinicians should consult a trauma surgeon as soon as possible for all victims of
significant trauma who 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 is performed
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 a hypotensive patient with an identified injury (eg, high-grade splenic laceration), but no trauma
surgeon is available, emergency consultation with a general surgeon may be necessary for possible
laparotomy prior to a time-consuming transfer that would put the patient at risk.
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
echocardiography as a monitor for therapeutic intervention 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
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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
● 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 (table 2). (See 'Differential diagnosis' above.)
● Hemorrhagic shock is commonly divided into four classes based on clinical presentation (described in
detail above). Significant drops in blood pressure are 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. (See
'Pathophysiology' above.)
● Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from major external
wounds. The thigh can hold up to approximately 1 L of blood. Scalp lacerations can bleed profusely and
are often overlooked. Other potential causes of traumatic shock may include cardiac tamponade and
tension pneumothorax. Non-hemorrhagic causes of traumatic shock may have typical presentations, but
often do not. 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 pulse
pressure (<25 mmHg), and altered mental status. (See 'Recognition of shock' above.)
● Shock may exist even in the setting of "normal" vital signs. Young otherwise healthy patients can
maintain a blood pressure within the normal range despite substantial blood loss; subtle alterations, such
as agitation, confusion, irritability, or inattention, may be their only signs of early shock. Elder adults are
more likely to take medications (eg, beta blockers) that affect the hemodynamic response to injury, and
are more likely to have baseline hypertension. It is important to interpret vital signs in light of the patient's
known or likely baseline. (See 'Recognition of shock' above.)
● Altered mental status from inadequate cerebral perfusion can be difficult to distinguish from drug or
alcohol intoxication or associated 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 cerebral hypoperfusion. Other subtle presentations of traumatic shock are described in the
text. (See 'Recognition of shock' above.)
● Subtle examination findings may provide evidence of early shock. Pallor or poor capillary refill may
represent peripheral vasoconstriction. Diaphoresis may indicate physiologic stress and appear before
https://www.uptodate.com/contents/initial-evaluation-of-shock-in-the-adult-trauma-patient-and-management-of-non-hemorrhagic-shock/print?to… 10/24
vital sign abnormalities. Mild tachypnea may reflect compensation for metabolic acidosis. Low-urine
output may indicate inadequate visceral perfusion.
● Bedside ultrasound can be an important tool for rapidly identifying intraabdominal bleeding, pericardial
tamponade, and pneumothorax. (See "Emergency ultrasound in adults with abdominal and thoracic
trauma".)
● Initial management of the patient in traumatic shock is focused on the following:
• Recognizing and reversing life-threatening injuries (eg, tension pneumothorax, cardiac tamponade)
immediately.
• Preventing or limiting ongoing blood loss.
• Restoring intravascular volume as necessary – ideally with blood.
• Maintaining adequate oxygen delivery to vital organs.
Essential tasks include:
• Establishing a patent and protected airway (while protecting the cervical spine).
• Controlling hemorrhage.
• Maximizing oxygenation.
• Gaining intravenous access and initiating fluid resuscitation or blood transfusion as indicated.
• Obtaining blood for laboratory and blood bank testing (ie, blood typing and cross-matching).
Management is discussed in detail above and an algorithm is provided (algorithm 1). (See 'Initial hospital
management' above.)
● During resuscitation, do not allow an initial favorable response to volume replacement to distract from
possible severe, occult injury. Effective early resuscitation may mask ongoing significant hemorrhage.
Remember that the presence of one injury in no way excludes the possibility of other, more serious
injuries.
● The key to management of non-hemorrhagic causes of shock, primarily tension pneumothorax and
pericardial tamponade, is early recognition based on clinical, radiograph, and ultrasound findings.
Emergency thoracotomy may be indicated for pericardial tamponade, particularly in the setting of
penetrating thoracic trauma. (See 'Immediate interventions to manage non-hemorrhagic shock' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Britt LD, Weireter LJ Jr, Riblet JL, et al. Priorities in the management of profound shock. Surg Clin North
Am 1996; 76:645.
2. Siegel JH. The effect of associated injuries, blood loss, and oxygen debt on death and disability in blunt
traumatic brain injury: the need for early physiologic predictors of severity. J Neurotrauma 1995; 12:579.
3. American College of Surgeons. Advanced Trauma Life Support (Student Manual). American College of
Surgeons 1997.
4. Vukmir RB, Bircher N, Safar P. Sodium bicarbonate in cardiac arrest: a reappraisal. Am J Emerg Med
1996; 14:192.
5. Hindman BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic
considerations. Anesthesiology 1990; 72:1064.
6. Parks JK, Elliott AC, Gentilello LM, Shafi S. Systemic hypotension is a late marker of shock after
trauma: a validation study of Advanced Trauma Life Support principles in a large national sample. Am J
Surg 2006; 192:727.
7. Vayer JS, Henderson JV, Bellamy RF, Galper AR. Absence of a tachycardic response to shock in
penetrating intraperitoneal injury. Ann Emerg Med 1988; 17:227.
8. Mizushima Y, Ueno M, Watanabe H, et al. Discrepancy between heart rate and makers of
hypoperfusion is a predictor of mortality in trauma patients. J Trauma 2011; 71:789.
9. Biffl WL, Harrington DT, Cioffi WG. Implementation of a tertiary trauma survey decreases missed
injuries. J Trauma 2003; 54:38.
10. Oyetunji TA, Chang DC, Crompton JG, et al. Redefining hypotension in the elderly: normotension is not
reassuring. Arch Surg 2011; 146:865.
11. Barton ED, Rhee P, Hutton KC, Rosen P. The pathophysiology of tension pneumothorax in ventilated
swine. J Emerg Med 1997; 15:147.
12. Dunning J, Williamson J. Ultrasonic guidance and the complications of central line placement in the
emergency department. Emerg Med J 2003; 20:551.
13. Milling TJ Jr, Rose J, Briggs WM, et al. Randomized, controlled clinical trial of point-of-care limited
ultrasonography assistance of central venous cannulation: the Third Sonography Outcomes
Assessment Program (SOAP-3) Trial. Crit Care Med 2005; 33:1764.
14. Posner MC, Moore EE. Distal greater saphenous vein cutdown--technique of choice for rapid volume
resuscitation. J Emerg Med 1985; 3:395.
15. Ma OJ, Mateer JR, Ogata M, et al. Prospective analysis of a rapid trauma ultrasound examination
performed by emergency physicians. J Trauma 1995; 38:879.
16. Sperry JL, Minei JP, Frankel HL, et al. Early use of vasopressors after injury: caution before constriction.
J Trauma 2008; 64:9.
17. Plurad DS, Talving P, Lam L, et al. Early vasopressor use in critical injury is associated with mortality
independent from volume status. J Trauma 2011; 71:565.
18. Zengerink I, Brink PR, Laupland KB, et al. Needle thoracostomy in the treatment of a tension
pneumothorax in trauma patients: what size needle? J Trauma 2008; 64:111.
19. Wax DB, Leibowitz AB. Radiologic assessment of potential sites for needle decompression of a tension
pneumothorax. Anesth Analg 2007; 105:1385.
20. Vayre F, Lardoux H, Pezzano M, et al. Subxiphoid pericardiocentesis guided by contrast two-
dimensional echocardiography in cardiac tamponade: experience of 110 consecutive patients. Eur J
Echocardiogr 2000; 1:66.
21. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic echocardiographically
guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo
Clin Proc 2002; 77:429.
Topic 351 Version 45.0
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.
Graphic 63698 Version 3.0
Classification of shock
Septic Gram positive (Pneumococcus, Staphylococcus, Streptococcus,

Enterococcus, Legionella, Listeria)
Gram negative (Klebsiella, Pseudomonas, Escherichia,
Haemophilus, Neisseria, Moraxella, Rickettsia, Francisella
[tularemia])
Fungal (Candida, Aspergillus)
Viral (influenza, cytomegalovirus, Ebola, varicella)
Parasitic (Plasmodium, Ascaris, Babesia)
Mycobacterium (Mycobacterium tuberculosis, Mycobacterium
abscessus)
Non-septic Inflammatory shock (systemic inflammatory response syndrome)

Distributive – Burns, trauma, pancreatitis, postmyocardial infarction, post
coronary bypass, post cardiac arrest, viscus perforation, amniotic
fluid embolism, fat embolism, idiopathic systemic capillary leak
syndrome
Neurogenic shock – Traumatic brain injury, spinal cord injury
(quadriparesis with bradycardia or paraplegia with tachycardia),
neuraxial anesthesia
Anaphylactic shock – IgE-mediated (eg, foods, medications, insect
bites or stings), IgE-independent (eg, iron dextran),
nonimmumnologic (eg, exercise or heat-induced), idiopathic
Other – Liver failure, transfusion reactions, vasoplegia (eg,
vasodilatory agents, cardiopulmonary bypass), toxic shock
syndrome, toxicologic (eg, heavy metals), beriberi
Cardiomyopathic Myocardial infarction (involving >40% of the left ventricle or with

extensive ischemia)
Severe right ventricle infarction
Acute exacerbation of severe heart failure from dilated
cardiomyopathy
Stunned myocardium from prolonged ischemia (eg, cardiac arrest,
hypotension, cardiopulmonary bypass)
Advanced septic shock
Myocarditis
Myocardial contusion
Cardiogenic
Drug-induced (eg, beta blockers)
Arrhythmogenic Tachyarrhythmia – Atrial tachycardias (fibrillation, flutter, reentrant

tachycardia), ventricular tachycardia and fibrillation
Bradyarrhythmia – Complete heart block, Mobitz type II second
degree heart block
Mechanical Severe valvular insufficiency, acute valvular rupture (papillary or

chordae tendineae rupture, valvular abscess), critical valvular
stenosis, acute or severe ventricular septal wall defect, ruptured
ventricular wall aneurysm, atrial myxoma
Hypovolemic Hemorrhagic Trauma, gastrointestinal bleeding (eg, varices, peptic ulcer),

intraoperative and postoperative bleeding, retroperitoneal bleeding
(eg, ruptured aortic aneurysm), aortic-enteric fistula, hemorrhagic
pancreatitis, iatrogenic (eg, inadvertent biopsy of arteriovenous
malformation, or left ventricle), tumor or abscess erosion into
major vessels, ruptured ectopic pregnancy, postpartum
hemorrhage, uterine or vaginal hemorrhage (eg, infection, tumors,
lacerations), spontaneous peritoneal hemorrhage from bleeding
diathesis
Non- Gastrointestinal losses (eg, diarrhea, vomiting, external drainage);

hemorrhagic skin losses (eg, heat stroke, burns, dermatologic conditions); renal
losses (eg, excessive drug-induced or osmotic diuresis, salt-
wasting nephropathies, hypoaldosteronism); third space losses

into the extravascular space or body cavities (eg, postoperative
and trauma, intestinal obstruction, crush injury, pancreatitis,
cirrhosis)
Pulmonary Hemodynamically significant pulmonary embolus, severe

vascular pulmonary hypertension, severe or acute obstruction of the
pulmonic or tricuspid valve, venous air embolus
Mechanical Tension pneumothorax or hemothorax (eg, trauma, iatrogenic),

Obstructive pericardial tamponade, constrictive pericarditis, restrictive
cardiomyopathy, severe dynamic hyperinflation (eg, elevated
intrinsic PEEP), left or right ventricular outflow tract obstruction,
abdominal compartment syndrome, aorto-caval compression (eg,
positioning, surgical retraction)
Endocrine (eg, adrenal insufficiency, thyrotoxicosis, myxedema

coma)
Metabolic (eg, acidosis, hypothermia)
Mixed/unknown
Other – Polytrauma with more than one shock category, acute
shock etiology with pre-existing cardiac disease, late under-
resuscitated shock, miscellaneous poisonings
Aortic dissection causes shock when retrograde dissection results in cardiac tamponade, acute aortic insufficiency,
and myocardial infarction; please refer to the UpToDate topic text for details.
PEEP: positive end-expiratory pressure.
Traumatic shock: Initial management
IV: intravenous; IO: intraosseous; FAST: Focused Assessment with Sonography in

Trauma; CXR: chest x-ray; C-spine: cervical spine.
Raney clips
Scalp lacerations can sometimes bleed profusely. In such cases, scalp clips (like
the Raney Clips® pictured above) can tamponade bleeding.
Reproduced with permission from: Aesculap® Raney Clips. Copyright © 2010 B.

Braun Aesculap.
Open book fracture: Pubic symphysis diastasis
This anterior-posterior (AP) radiograph of the pelvis reveals significant diastasis at

the symphysis pubis of this trauma patient. Such fractures can cause significant
hemorrhage. Emergent treatment consists of closing the fracture and stabilizing the
pelvis by applying a pelvic binder or tying a sheet tightly around the lower pelvis.
Emergent reversal of anticoagulation from warfarin for life-threatening

hemorrhage in adults: Suggested approaches based upon available resources
A. If 4-factor 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 the infusion.
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. If 3-factor 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 the infusion.
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 if
volume overload is a concern.
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 administer loop
diuretic between FFP infusions if volume overload is a concern.
These products and doses are for use in life-threatening bleeding only. Evidence of life-threatening bleeding and
over-anticoagulation with a vitamin K antagonist (eg, warfarin) are required. Anaphylaxis and transfusion
reactions can occur.
It may be reasonable to thaw four units of FFP while awaiting the PT/INR. The transfusion service may substitute
other plasma products for FFP (eg, Plasma Frozen Within 24 Hours After Phlebotomy [PF24]); these products are
considered clinically interchangeable. PCC will reverse anticoagulation within minutes of administration; FFP
administration can take hours due to the volume required; vitamin K effect takes 12 to 24 hours, but
administration of vitamin K is needed to counteract the long half-life of warfarin. Subsequent monitoring of the
PT/INR is needed to guide further therapy. Refer to topics on warfarin reversal in individual situations for further
management.
PCC: unactivated prothrombin complex concentrate; 4F PCC: PCC containing coagulation factors II, VII, IX, X, protein S
and 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 and
single-factor 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 on
INR and patient weight if available. Refer to topic and Lexicomp drug reference included with UpToDate for INR-based
dosing.
Direct oral anticoagulant-associated bleeding reversal strategies
Type of bleeding Agent Possible interventions
Life-threatening or Dabigatran (Pradaxa) Idarucizumab

imminently fatal bleeding Activated PCC* (eg, FEIBA)
(eg, intracranial, Antifibrinolytic agent (eg, tranexamic acid, epsilon-
retroperitoneal, aminocaproic acid)
compartment syndrome,
Anticoagulant discontinuation
massive gastrointestinal)
Oral activated charcoal (if last dose within prior two
hours)
Hemodialysis
RBC transfusions if needed for anemia
Platelet transfusions if needed for thrombocytopenia
or impaired platelet function (eg, due to aspirin)
Surgical/endoscopic intervention if appropriate
Rivaroxaban (Xarelto), Andexanet alfa (AndexXa), if available

apixaban (Eliquis), 4-factor unactivated PCC* (eg, Kcentra)
edoxaban (Lixiana), Antifibrinolytic agent (eg, tranexamic acid, epsilon-
betrixaban (Bevyxxa) aminocaproic acid)
Anticoagulant discontinuation
Oral activated charcoal (if last dose recent enough)
RBC transfusions if needed for anemia
Platelet transfusions if needed for thrombocytopenia
or impaired platelet function (eg, due to aspirin)
Surgical/endoscopic intervention if appropriate
Minor bleeding (eg, Dabigatran (Pradaxa) Local hemostatic measures

epistaxis, uncomplicated Possible anticoagulant discontinuation
soft tissue bleeding, minor Half-life (normal renal function ¶): 12 to 17 hours
[slow] gastrointestinal
Possible antifibrinolytic agent (eg, tranexamic acid,
bleeding)
epsilon-aminocaproic acid)
Rivaroxaban (Xarelto), Local hemostatic measures

apixaban (Eliquis), Possible anticoagulant discontinuation
edoxaban (Lixiana), Half-lives (normal renal function ¶):
betrixaban (Bevyxxa)
Rivaroxaban 5 to 9 hours
Apixaban 8 to 15 hours
Edoxaban 6 to 11 hours
Possible antifibrinolytic agent (eg, tranexamic acid,
epsilon-aminocaproic acid)
The table describes measures that may be used to manage bleeding associated with DOACs. Clinical judgment is
essential in all cases of DOAC-associated bleeding in order to assess the risks of bleeding and weigh these against
the risks of thrombosis if anticoagulation is discontinued or reversed. Refer to UpToDate topics on the use of direct
thrombin inhibitors and direct factor Xa inhibitors and management of DOAC-associated bleeding for further
details and dosing. The onset of all of the agents discussed herein is approximately 2 to 4 hours.
PCC: prothrombin complex concentrate; FEIBA: factor eight inhibitor bypassing activity; RBC: red blood cell; DOAC: direct
oral anticoagulant.
* 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 half-life for rivaroxaban, apixaban, edoxaban, and betrixaban.
Pneumothorax
This posterior-anterior (PA) radiograph of the chest reveals a left pneumothorax.

The lateral border of the lung (arrows) no longer lies adjacent to the chest wall and
the 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 mainstem
bronchus. The border of the scapula (large arrowheads) is sometimes mistaken for
a pneumothorax.
Chest radiograph of a pneumothorax after stab wound
This plain chest radiograph shows a left apicolateral pneumothorax with typical
convex white visceral pleural line (yellow arrows).
Courtesy of Paul Stark, MD.
Normal chest radiograph
Posteroanterior view of a normal chest radiograph.
Courtesy of Carol M Black, MD.
FAST: Subxiphoid view with pericardial effusion
This ultrasound image reveals a large pericardial effusion (E) seen using a subxiphoid
view as part of the FAST examination.
FAST: Focused Assessment with Sonography for Trauma; LV: left ventricle.
Courtesy of Greg Snead, MD.
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 are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
Conflict of interest policy

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16/09/2018 Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock - UpToDate

Official reprint from UpToDate®

Author: Christopher Colwell, MD

PATHOPHYSIOLOGY — The pathophysiology of shock primarily relates to an imbalance in oxygen supply

● Cardiac tamponade (see "Cardiac tamponade")

● Pulmonary contusion with resulting pulmonary dysfunction

● Hemothorax with resulting pulmonary dysfunction

● Effects of pharmacologic or toxicologic agents

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

Obvious and immediately detectable manifestations of the shock state include:

● Tachycardia (note that neurogenic shock may present with bradycardia)

● 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)

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

● Retroperitoneal space (often from pelvic fracture)

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

PREHOSPITAL MANAGEMENT — The prehospital management of patients in traumatic shock is focused

INITIAL HOSPITAL MANAGEMENT

● Preventing or limiting ongoing blood loss.

● Restoring intravascular volume if necessary.

● Maintaining adequate oxygen delivery to vital organs.

● Obtain blood for laboratory and blood bank testing.

● Warfarin (see "Management of warfarin-associated bleeding or supratherapeutic INR", section on

● Baseline hemoglobin or hematocrit

● Serum bicarbonate (base deficit) and serum lactate

IMMEDIATE INTERVENTIONS TO MANAGE NON-HEMORRHAGIC SHOCK

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

SUMMARY AND RECOMMENDATIONS

● Initial management of the patient in traumatic shock is focused on the following:

• Preventing or limiting ongoing blood loss.

• Restoring intravascular volume as necessary – ideally with blood.

• Maintaining adequate oxygen delivery to vital organs.

Essential tasks include:

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 351 Version 45.0

Differential diagnosis of shock in trauma

2. Third spacing (eg, burns)

B. Neurogenic (high cervical cord injury)

II. High CVP

III. Other diagnoses to consider

B. Myocardial infarction (severe)

C. Diaphragmatic rupture with herniation

D. Fat or air embolism

CVP: central venous pressure.

Graphic 63698 Version 3.0

Septic Gram positive (Pneumococcus, Staphylococcus, Streptococcus,

Non-septic Inflammatory shock (systemic inflammatory response syndrome)

Cardiomyopathic Myocardial infarction (involving >40% of the left ventricle or with

Arrhythmogenic Tachyarrhythmia – Atrial tachycardias (fibrillation, flutter, reentrant

Mechanical Severe valvular insufficiency, acute valvular rupture (papillary or

Hypovolemic Hemorrhagic Trauma, gastrointestinal bleeding (eg, varices, peptic ulcer),

Non- Gastrointestinal losses (eg, diarrhea, vomiting, external drainage);

wasting nephropathies, hypoaldosteronism); third space losses

Pulmonary Hemodynamically significant pulmonary embolus, severe

Mechanical Tension pneumothorax or hemothorax (eg, trauma, iatrogenic),