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[English Forum] Management of shock in adult trauma

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发表于 2009-12-7 18:29:17 | 只看该作者 回帖奖励 |倒序浏览 |阅读模式
本帖最后由 shenxiu2 于 2009-12-7 18:51 编辑

这是篇很长的文章,但是内容很好,耐心读.:P

Management of shock in adult trauma

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 vascular obstruction, neurologic dysfunction, and cardiac dysfunction represent other potential causes or contributing factors . Shock is a common and frequently treatable cause of death in injured patients and is second only to traumatic brain injury as the leading cause of death from trauma .
This topic review will discuss the evaluation and initial management of shock in the trauma patient. A general overview of shock, including pathophysiology and differential diagnosis.

PATHOPHYSIOLOGY AND CLASSIFICATION — 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 . Anaerobic glycolysis results in the accumulation of pyruvate, which is converted to lactate .
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 hypoxia 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 . 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.

  • 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. While diminished anxiety or pain may contribute to such a drop, the clinician must assume it is due to hemorrhage until proven otherwise. 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 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, retroperitoneum, and from major external wounds. The thigh can hold up to approximately one liter of blood. Scalp lacerations can bleed profusely and are often overlooked if significant thoracic or abdominal injuries are present.
A number of other potential causes of traumatic shock must also be considered, including :
  • Cardiac tamponade
  • Tension pneumothorax
  • Pulmonary contusion or hemothorax with resulting dysfunction
  • Myocardial infarction or contusion (ie, cardiogenic shock)
  • Spinal cord injury (ie, neurogenic shock)
  • Effects of pharmacologic or toxicologic agents
  • Fat or air embolism
In penetrating trauma, diaphragmatic rupture complicated by incarceration of abdominal organs can lead to septic shock.

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.

EVALUATION AND MANAGEMENT

Recognition — Recognition is the first step in managing traumatic shock. Ideally, shock is recognized before hypotension develops . 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).
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)
  • Altered mental status
Large-scale bleeding occurs at five possible locations:
  • External hemorrhage
  • Thoracic cavity
  • Peritoneal cavity
  • Retroperitoneal space (often from a pelvic fracture)
  • Muscle or subcutaneous tissue (usually from a long-bone fracture).

When the cause of shock is not obvious, evaluation and treatment occur in tandem. A trauma ultrasound examination, or Focused Assessment with Sonography for Trauma (FAST), is performed to look for hemopericardium and intraabdominal bleeding. The three standard initial trauma x-rays (ie, chest, pelvis, and lateral cervical spine) are obtained. Of these, the portable chest x-ray 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. In some centers, clinicians may forego plain x-rays if CT scanners are immediately available and adjacent to the trauma bay.

Shock may exist even in the setting of "normal" vital signs, making diagnosis difficult. Young patients without underlying comorbidities can maintain a blood pressure within the normal range despite substantial blood loss by compensatory vasoconstriction and increases in heart rate. A bradycardic response to penetrating intraperitoneal injury, which may be vagally mediated, has been described . 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 .

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. 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 intoxication.

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/hour and have a high urine specific gravity may be compensating for hypovolemia.

Elderly 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. 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.
Nonhemorrhagic 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. If significant, on-going hemorrhage exists, tamponade can occur without distended neck veins. Ultrasound examination is critical.

A large pneumothorax or hemothorax may be detected clinically by the appearance of respiratory distress, unilateral diminished breath sounds, or air crepitus on palpation. In the stable patient with 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 .

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. 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 detrimental. Hypotension should not be attributed solely to neurologic injury until hemorrhagic shock has been ruled out.

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

  • Restoring intravascular volume
  • Maintaining adequate oxygen delivery
  • Limiting on-going blood loss

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:

  • Establishing a patent and protected airway while protecting the cervical spine
  • Maximizing oxygenation
  • Gaining intravenous access and initiating fluid resuscitation
  • Controlling hemorrhage
  • Obtaining blood for laboratory and blood bank testing

External hemorrhage is controlled by applying direct pressure. 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 treated with clips (eg, Raney&reg; clips) or by closing the wound with running (ie, noninterrupted) stitches using heavy suture.

Use of a tourniquet is acceptable to stop hemorrhage in cases of amputation when other measures have not successfully controlled bleeding. Tourniquets must be released periodically to avoid prolonged ischemia and possible tissue loss.

Vascular access is obtained as rapidly as possible. Two large-bore (16 gauge or larger) intravenous (IV) lines placed in the antecubital region is ideal, but not always possible. Placement of a central venous catheter (size 8 French) is performed when adequate peripheral access cannot be obtained, and allows measurement of central venous pressure. Central line placement under ultrasound (US) guidance offers high success rates with fewer complications than procedures performed without US . Some experts advocate use of distal saphenous vein cutdowns due to ease of access and consistency of anatomy .

Traumatic shock occurs most often from hemorrhage, generally from an intraabdominal injury in blunt trauma. Ultrasound (US) is an integral part of the initial evaluation of the trauma patient, and reliably identifies free intraabdominal fluid in the hands of proficient ultrasonographers . During the initial resuscitation, the Focused Assessment with Sonography for Trauma (FAST) exam, is performed to assess first for pericardial effusion and then for intraperitoneal bleeding.

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, DPL or diagnostic peritoneal tap (DPT) provides crucial information.

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, the pelvis opened, and the retroperitoneal space enlarged) .

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

Infusions of large volumes of NS can lead to the development of a nonanion gap hyperchloremic metabolic acidosis. This does not appear to have significant clinical consequences. On the other hand, large volume resuscitation using lactated ringers (LR) can cause a metabolic alkalosis, as lactate metabolism generates bicarbonate. This too does not appear to have significant clinical consequences. LR and blood must be infused through separate IV tubing because of the risk of clotting, which may be problematic in the setting of trauma.

Debate over the best approach to fluid resuscitation in traumatic shock is likely to continue. Some researchers claim LR is superior to NS in the resuscitation of uncontrolled hemorrhagic shock, stating that patients who receive large volumes of NS experience increased blood loss and greater hypercoagulability; other researchers argue just the opposite . We prefer NS for the initial resuscitation fluid, but feel it is reasonable to change to LR (L-isomer if available) after the initial resuscitation (ie, once 3 liters or 50 mL/kg of NS has been infused) in patients requiring additional IV fluid.

Clear end-points for fluid therapy remain undefined . Further resuscitation is based on the patient's response to initial IV fluids and overall condition. A mean arterial pressure (MAP) around 65 mmHg or a systolic blood pressure (SBP) around 90 mmHg is a reasonable goal in penetrating trauma. In blunt trauma patients, particularly those with possible traumatic brain injury (TBI), a mean arterial pressure above 105 mmHg or a systolic blood pressure above 120 mmHg is reasonable. These goals may need to be adjusted upward in patients with a known history of uncontrolled hypertension.

The ideal MAP or SBP for the multiple trauma patient remains unclear. Some authors advocate strictly limiting the amount of IV fluid used for trauma resuscitation in the absence of hypotension or obvious injury . Packed red blood cells are given if the goal blood pressure is not maintained following the initial IV fluid resuscitation.

Hypertonic saline has been evaluated extensively, and may provide benefit through osmotic movement of interstitial fluid into the vascular compartment and modulation of the inflammatory response to injury . While some clinical trials have shown a benefit , others have failed to do so, even in patients who would seem most likely to benefit (eg, patients with hypotension and severe TBI) . Further study is needed to clarify the role of hypertonic saline

The value of colloids (albumin, hetastarch, dextran) for resuscitation of traumatic shock is unproven. Colloids effectively increase intravascular volume and may maintain plasma oncotic pressure at more normal levels compared to crystalloids. However, a systematic review of 19 randomized controlled trials comparing resuscitation fluids found that use of colloids did not improve mortality or morbidity among trauma patients .

Research continues into oxygen-carrying resuscitation fluids that can serve as alternatives to PRBCs. The ideal replacement fluid would transport oxygen effectively, expand intravascular volume, exhibit few or no side effects, and demonstrate great durability. Potential replacement fluids are discussed elsewhere.

No human studies exist to support the use of vasopressors in the resuscitation of the adult with multiple trauma .

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

Controlled hypotension may be beneficial in patients with hemorrhagic shock due to torso injuries from gunshot or stab wounds. They may be detrimental to blunt trauma patients with brain injury, as hypotension reduces cerebral perfusion and increases mortality . The proposed mechanism for improved outcomes with delayed fluid resuscitation is that aggressive fluid administration might, via augmentation of blood pressure, dilution of clotting factors, and production of hypothermia, disrupt thrombus formation and enhance bleeding .

In one widely cited study of 598 patients with penetrating chest injuries treated at a major urban trauma center, delayed fluid resuscitation until operative intervention to control bleeding was associated with a statistically significant improvement in patient survival (70 versus 62 percent in those given immediate fluid repletion) . Other results favoring delayed fluid resuscitation or controlled hypotension have been reported in small clinical trials and a variety of animal models of hemorrhagic shock .

Adoption of the strategy of delayed fluid resuscitation or controlled hypotension into clinical practice must be undertaken cautiously . In the trial described above, stratification was not performed to identify which patients might benefit from delayed therapy . Furthermore, primarily young, healthy patients with penetrating trauma were involved, and the mean time from injury to operation was two hours, results that are not attainable in most circumstances.

We recommend that delayed fluid administration and controlled hypotension should NOT be implemented unless emergent surgical exploration can be performed . Further research is needed in this area .

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

In general, we suggest two units of packed red blood cells (PRBC) be transfused if hemodynamics fail to improve after the administration of 2 to 3 liters (or greater than 50 mL/kg) of crystalloid. Further transfusions are given based on the patient's injuries and response to the initial transfusion.

Typed and cross-matched PRBCs are best, but can require considerable time to prepare. If the patient's condition warrants, clinicians can transfuse immediately using type O Rh-positive for males and type O Rh-negative for girls and women of child-bearing age, until type-specific or typed and cross-matched blood is available.

In most instances, preparation of fully typed and cross-matched blood requires at least 20 minutes, and more likely 30 to 45 minutes. Type-specific blood can usually be obtained within 15 to 20 minutes. In general, type O blood is available immediately, depending on transport time from the blood bank to the emergency department (ED). Trauma centers often store type 0 blood in refrigerators in the ED.

The safety of the blood supply continues to improve, and although some risk of transmitting infectious agents persists, such events are rare (the risk for bacteremia is approximately 1 in 100,000 units of platelets and 1 in 500,000 units of PRBCs transfused; the risk of HIV transmission is estimated to be 1 in 500,000 units of PRBCs; the risk of hepatitis C transmission is approximately 1 in 100,000 units of PRBCs; the overall risk of any type of viral infection is 1 in 34,000 units of PRBCs) .

Research continues into oxygen-carrying resuscitation fluids that can serve as alternatives to PRBCs. The ideal replacement fluid would transport oxygen effectively, expand intravascular volume, exhibit few or no side effects, and demonstrate great durability. Potential replacement fluids are discussed elsewhere.

Transfusion of clotting factors and platelets — Treatment of hemorrhage with IV crystalloid and PRBCs increases the risk of coagulopathy from dilution of platelets and clotting factors, and possibly hypothermia . Prevention of coagulopathy with early transfusion of plasma and platelets is critical in the patient with severe hemorrhage .

There remain no clear answers to the questions when and how much to transfuse clotting factors in trauma patients requiring massive transfusion. If bleeding is severe, clinicians cannot wait for laboratory values to guide transfusion, and such measurements may be inaccurate in the setting of massive hemorrhage .

For patients with severe, on-going bleeding who have received four units of packed red blood cells (PRBC), we give one unit of fresh frozen plasma (FFP) for every unit of PRBCs. This calculation includes the initial four units of PRBCs transfused (ie, four units of FFP are given once four units of PRBCs are given). For patients with severe hemorrhage, we also give six units of platelets once six units of PRBCs have been transfused. Hypothermia must be controlled during transfusions.

Although no prospective, randomized outcome studies exist to determine the best approach to transfusion , a retrospective review has been published using data from a US combat support hospital during the second Iraq war . This review assessed the mortality of 246 severely wounded soldiers that required massive blood transfusion and found that patients given a higher ratio of plasma to red blood cells (RBC) had significantly higher survival rates. Patients were divided into three groups based on the plasma to RBC ratio: high ratio 1 to 1.14; medium ratio 1 to 2.5; and, low ratio 1 to 8. Injury severity scores were identical in all groups, although the low ratio group had more thoracic wounds and a lower average initial hemoglobin and blood pressure. Group survival was 65 percent, 34 percent, and 19 percent respectively. Logistic regression found that the plasma to RBC ratio was independently associated with survival (OR 8.6; 95% CI 2.1-35.2).

A subsequent retrospective study, also performed in combatants
during the second Iraq war, reported similar findings concerning the importance of using a higher platelet to RBC ratio . Improved survival with more aggressive plasma and platelet transfusion is consistent with other studies in both military and civilian populations . The determination of the optimal plasma to RBC transfusion ratio awaits further study .


In the civilian setting, individual trauma centers have developed effective transfusion protocols . Some advocate 2 units of FFP for every 6 units of PRBCs transfused. Other centers advocate more aggressive approaches . At one of the largest United States trauma centers, six units of FFP and one unit of platelets are given once six units of PRBCs are transfused . Another major urban trauma center transfuses one unit of FFP for each unit of PRBCs .

Some authors advocate using platelet counts and fibrinogen levels to determine when to transfuse platelets and cryoprecipitate . A platelet count of less than 100,000/microL is treated with ten units of platelets, and a fibrinogen level below 100 mg/dL is generally treated with ten units of cryoprecipitate (each unit of cryoprecipitate comes from one unit of whole blood, and raises the fibrinogen level by about 5 mg/dL). Provided massive, on-going hemorrhage is not present, using laboratory measurements to guide transfusion is a reasonable approach.

Laboratory tests — Hematology and chemistry laboratory tests are of limited use in the acute management of the trauma patient. Clinicians should consider them adjuncts to diagnosis and not substitutes for clinical assessment.
The following laboratory studies are obtained in all patients with traumatic shock:

  • Type and cross-match several units of packed red blood cells
  • 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 amount 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 on-going 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 on-going. Additional testing may be needed depending on clinical circumstance.

Management of nonhemorrhagic shock

  • Pneumothorax - Pneumothorax occurs often in both blunt and penetrating trauma, and may be delayed (picture 2 and picture 3). Traumatic pneumothorax or hemothorax is managed by the placement of a large thoracostomy tube (36 French or larger) in the lateral chest.

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 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 . Should a 4.5 cm needle fail to decompress a tension pneumothorax and a tube thoracostomy be delayed, clinicians should use a longer needle.


  • Pericardial tamponade - Pericardial tamponade can occur with penetrating or major blunt chest trauma. Immediate ultrasonography (US) or echocardiography offers the best opportunity for rapid, early, and accurate diagnosis. Pericardiocentesis is performed if pericardial tamponade is suspected and the patient is hypotensive and worsening despite volume resuscitation. If pericardiocentesis recovers blood and improves the patient's clinical status, emergent 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.

Pericardiocentesis is "classically" performed using the subxiphoid approach . However, some researchers and a large observational study support the use of the paraapical or parasternal approach under ultrasound guidance . 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.


  • 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. Victims of penetrating trauma, particularly stab wounds to the chest, have vastly better outcomes in response to emergency department thoracotomy than victims of blunt trauma .

Emergency thoracotomy is most likely to be beneficial in the following settings :
  • - Thoracic or trauma surgeon is available within 40 minutes, AND
  • - Patient has not been pulseless for longer than 20 minutes, AND
  • - Penetrating trauma is present

If a surgeon is available and the patient has sustained penetrating thoracic trauma leading to pericardial tamponade, an emergency thoracotomy is indicated. If pericardiocentesis is incapable of providing adequate drainage and maintaining blood pressure, emergency thoracotomy is indicated.
After thoracotomy, patients without cardiac activity or blood in the pericardium are pronounced dead. If present, pericardial tamponade is decompressed, and further treatment given based on the injuries identified. The descending aorta is cross-clamped if intraabdominal bleeding is suspected.
Emergency thoracotomy is futile in the following settings:
  • - No thoracic or trauma surgeon available within 40 minutes
  • - Blunt trauma without pulse or blood pressure in the field
  • - Prolonged pulselessness
  • 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.

Monitoring and endpoints for prolonged resuscitation — Clear end-points for initial fluid therapy remain undefined. A mean arterial pressure (MAP) around 65 mmHg or a systolic blood pressure around 90 mmHg is a reasonable goal in penetrating trauma. In blunt trauma patients, particularly those with possible traumatic brain injury (TBI), a mean arterial pressure above 105 mmHg or a systolic blood pressure above 120 mmHg is reasonable. Some authors advocate strictly limiting the amount of IV fluid used for trauma resuscitation in the absence of hypotension or obvious injury . Packed red blood cells are transfused, along with appropriate replacement of coagulation products, if the goal blood pressure is not maintained following the initial IV fluid resuscitation.

Some trauma patients, particularly in community hospitals, must be managed in the emergency department for prolonged periods when surgical resources or transport is unavailable. It remains unclear which endpoints are most useful for guiding such prolonged resuscitations. Those emergency clinicians without access to sophisticated noninvasive technologies rely on standard physiologic and laboratory measurements to determine whether resuscitation is adequate. An approach modeled on goal-directed therapy for septic shock, with the important caveat that greater emphasis be placed on blood transfusion and coagulation factor replacement, may be helpful .

The following parameters may be used to guide prolonged resuscitation of traumatic shock :

  • Blood pressure: maintain MAP above 65 mmHg for penetrating trauma, and above 105 mmHg for blunt trauma
  • Heart rate: maintain between 60 and 100 beats per minute
  • Oxygen saturation: maintain above 94 percent
  • Urine output: maintain above 0.5 mL/kg/hour
  • Central venous pressure: maintain between 8 and 12 mmHg
  • Lactate and base deficit: monitor serum lactate and serum bicarbonate every four hours to ensure end-organ perfusion is adequate or improving with resuscitation
  • Mixed central venous oxygen saturation: monitor every four hours to ensure end-organ perfusion is adequate or improving with resuscitation; goal is to maintain above 70 percent

Transfusion of blood products in patients without massive bleeding undergoing prolonged resuscitation of trauma-related shock may be performed using the following guidelines:
  • Hemoglobin: transfuse two units PRBCs if hemoglobin falls below 8 g/dL for patients without risk for acute coronary syndrome (ACS), or below 10 g/dL for patients at risk for ACS
  • Platelets: transfuse six units if level falls below 50,000/microL
  • International normalized ratio (INR): transfuse 2 units of FFP if INR rises above 2
  • Fibrinogen: transfuse 10 units of cryoglobulin if the fibrinogen level falls below 100 mg/dL

If bleeding is massive and ongoing, laboratory measurements can be inaccurate. Empiric guidelines for transfusion of blood products in this setting are provided above.

Some researchers advocate using the lactate concentration to assess the adequacy of resuscitation . Lactate levels may lag behind clinical improvement following aggressive resuscitation if rapid analyzers are unavailable. Other authors suggest that the magnitude of metabolic acidosis has prognostic value and that the admission base deficit (ie, serum bicarbonate) may be superior to plasma lactate in predicting injury severity and death . Both endpoints may provide useful feedback about tissue oxygen debt and the adequacy of resuscitation.

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

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.

DEVELOPING TREATMENTS
Hemostatic agents — In some circumstances, external hemorrhage cannot be controlled using direct pressure and standard dressings. A number of hemostatic products are being developed to control such bleeding, including chitosan dressing, QuickClot&reg; powder, and fibrin sealant dressing. Fibrin sealant dressing provided better hemorrhage control in a study using a swine model of severe extremity hemorrhage . Mineral based agents performed best in a subsequent animal study .Although some of these products have been used by military personnel in combat, controlled studies with human subjects are lacking and it remains unclear how these products can be used by civilian emergency clinicians.

Red blood cell substitutes — Red blood cell substitutes (eg, hemoglobin-based oxygen carriers, perfluorocarbons) continue to be studied in both animal and human trials. Preliminary research suggests these substitutes, capable of delivering oxygen, may be superior to conventional methods of resuscitation for hemorrhagic shock. This subject is discussed separately.

SUMMARY AND RECOMMENDATIONS

  • Hemorrhagic shock comprises the majority of cases of traumatic shock and 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.
  • Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from major external wounds. The thigh can hold up to approximately one liter of blood. Scalp lacerations can bleed profusely and are often overlooked. Other potential causes of traumatic shock may include cardiac tamponade and tension pneumothorax. A detailed list of potential causes of traumatic shock is provided .
  • 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.
  • 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. 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 above.
  • Initial management of the patient in traumatic shock is focused on restoring intravascular volume, maintaining adequate oxygen delivery, and limiting on-going blood loss. The essential tasks include establishing a patent and protected airway (while protecting the cervical spine), maximizing oxygenation, gaining intravenous access and initiating fluid resuscitation, controlling hemorrhage, and obtaining blood for laboratory and blood bank testing (ie, blood typing and cross-matching). Ultrasound (US) reliably identifies free intraabdominal fluid in the hands of proficient ultrasonographers. Management is discussed in detail above and an algorithm is provided (algorithm 1).
  • The best approach to fluid resuscitation remains controversial. We suggest that initial fluid resuscitation for trauma patients in hemorrhagic shock consist of two liters of normal saline (NS) (Grade 2C). The infusion is given as rapidly as possible through short, large gauge (16 or larger) peripheral IVs.
  • The best approach to blood transfusion in trauma is unknown. We suggest two units of packed red blood cells (PRBC) be transfused if hemodynamics fail to improve after the administration of 2 to 3 liters (or greater than 50 mL/kg) of crystalloid (Grade 2C). Further transfusions are given based upon the patient's injuries and response to the initial transfusion.
  • 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.
  • Treatment of hemorrhage with IV crystalloid and PRBCs increases the risk of coagulopathy from dilution of platelets and clotting factors, and possibly hypothermia. Prevention of coagulopathy is critical, but the best approach is unknown. If bleeding is severe, clinicians cannot wait for laboratory values to guide transfusion, and such measurements may be inaccurate. For patients with severe ongoing bleeding who have received four units of PRBCs, we give one unit of fresh frozen plasma (FFP) for every unit of PRBCs (ie, four units of FFP are given once four units of PRBCs are given). We also give six units of platelets once six units of PRBCs have been transfused.
  • The key to management of nonhemorrhagic causes of shock, primarily tension pneumothorax and pericardial tamponade, is early recognition based on clinical, x-ray, and US findings. Emergent thoracotomy may be indicated for pericardial tamponade, particularly in the setting of penetrating thoracic trauma.

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