Shock

Shock has been recognized as an important pathophysiologic event in surgery and trauma since the late 1800s. Pioneering studies by Wiggers and Blalock formed the foundation for current scientific studies in the field of shock research. Although the definition of shock may have changed greatly since these early investigations, the clinical syndrome and its profound impact on the care of injured patients remains essentially the same.

I. Definition and Classification

Although the clinical syndromes responsible for shock can originate from a variety of causes, the different forms of shock have a number of common features.

A. Definition

Shock occurs when tissue perfusion is inadequate to maintain normal cellular function and structure. It cannot be emphasized strongly enough that shock does not equal hypotension and, conversely, a “normal” blood pressure does not exclude the presence of hypoperfusion. Although direct cellular injury may become evident, its contribution to the sequelae of shock is unclear. Cellular dysfunction can become evident in a variety of ways.

B. Classification

• Hypovolemic shock is caused by decreased circulating volume from loss of red cell mass, plasma, and extracellular fluid, or a combination of these. This form of shock is the most common cause of shock in injured patients, and usually results from acute blood loss.
• Cardiogenic shock represents decreased tissue perfusion due to ineffective pump function. Cardiogenic shock can result from direct cardiac injury (myocardial contusion) or intrinsic cardiac disease (myocardial infarction, dysrhythmia).
• Vasogenic shock is caused by decreased vascular resistance so that the normal blood volume fails to maintain adequate circulatory perfusion.
  • Neurogenic shock is a form of vasogenic shock in which a high spinal cord injury (or spinal anesthesia) results in loss of sympathetic vascular tone, producing peripheral vasodilation. Bradycardia may also be present.
  • Septic shock is a form of vasogenic shock in which proinflammatory mediator release results in peripheral vasodilation, decreased peripheral arterial resistance, and increased peripheral venous capacitance. Tachycardia often accompanies it.
• Obstructive shock. Mechanical obstruction to cardiac function from either direct cardiac compression or obstruction of venous return (cardiac tamponade, tension pneumothorax) results in decreased peripheral perfusion.
• Traumatic shock includes elements of the above mentioned causes of shock that may not be sufficient to induce hypoperfusion in isolation, but markedly impair peripheral perfusion when combined. Generally includes the sequelae of hypovolemia from blood loss and activation of proinflammatory mediators elaborated as a result of long bone or soft tissue injury.

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II. Pathophysiology

A. Cardiovascular response

The body's normal response to hypovolemia is to adjust peripheral arterial resistance, cardiac output, and heart rate to maintain perfusion to essential organs such as the heart and brain.

• Peripheral arterial resistance increases in response to decreased circulatory volume or impaired pump function and decreases as a contributor to shock in septic states and with loss of sympathetic tone (neurogenic shock).
• Cardiac output will be intrinsically diminished because of pump failure in cardiogenic shock. May also be diminished by low circulatory volume (hypovolemia) or mechanical impediments (cardiac tamponade). Often increased in response to diminished peripheral arterial resistance in septic shock.
• Heart rate is increased in response to decreased circulatory volume, decreased peripheral arterial resistance, and mechanical impediments to cardiac function. Often unchanged in neurogenic shock because of loss of sympathetic cardiac input. The normal reflexive change to hypovolemia can be absent or impaired in elderly patients with significant intrinsic cardiac disease or those taking selected medications (β-blockers). If shock is sustained, tachycardia can evolve into bradycardia as a preterminal event.

B. Neuroendocrine response

The neuroendocrine response to shock, which is similar to that of injury, is covered in detail in Chapter 4.

C. Inflammatory mediators

Proinflammatory mediators, which can be produced in response to bacterial products, lead to decreased arterial resistance and impaired tissue perfusion (septic shock). In addition, other forms of shock can result in the production of a variety of systemic and local mediators such as cytokines, eicosanoids, and radical species (see Chapter 4).

D. Cellular response

To shock is a result of decreased oxygen delivery from hypoperfusion and direct changes in cell function caused by neural (adrenergic), humoral (corticotropin, vasopressin, glucagon), and proinflammatory (cytokine) mediators. Oxygen radicals, either intrinsically (i.e., xanthine oxidase) or extrinsically (i.e., neutrophil) derived, are produced in shock and can alter cell function. Alterations in the local microcirculatory environment, metabolic derangements, and hypoxia at the cellular level lead to cell membrane depolarization, increased intracellular water and cell swelling, dysfunction of the Na-K-adenosine triphosphatase (ATPase) pump, increased anaerobic metabolism, uncoupling of oxidative phosphorylation, and increased intracellular calcium changes in intracellular signaling pathways that regulate cell metabolism. Changes in cellular gene expression in response to shock and alterations in cellular protein production occur. The development of apop-tosis in animal models of shock has been described but its significance is unknown.

III. Diagnosis and Treatment

While the end-organ manifestations of shock may be the same regardless of the specific cause of shock, the treatment depends on the specific cause of the impaired perfusion.

A. Hypovolemic shock

Which represents the most common cause of shock in injured patients, is caused by acute blood loss. Severity of the shock insult depends on the depth and duration of shock. Mild shock of longstanding duration can be as lethal as acute, profound shock.

• Diagnosis. Signs of inadequate end-organ perfusion depend on the degree of volume loss. Hypotension can be a relatively late manifestation of decreased circulating volume if compensatory mechanisms are adequate. Tachycardia, diminished urine output, decreased pulse pressure, restlessness and anxiety, and cold, clammy extremities can be manifestations of reduced circulatory volume. Lethargy and stupor caused by hypovolemia represent profound volume loss and can signal impending cardiovascular collapse. Hypotension is a sign that the compensatory mechanisms have been exceeded. Patients in shock may not be hypotensive, but patients who are hypotensive should always be considered to be in shock.
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• Treatment. Treatment of hypovolemia focuses on simultaneous cessation of ongoing hemorrhage and restoration of circulating blood volume. Treatment for hypovolemia is usually instituted before a cause is identified.
  • ABCs. The airway should be secure and bilateral breath sounds present. Fluid resuscitation should be instituted with balanced crystalloid solution through two large-bore intravenous catheters. Patients who respond briefly or not at all to the above measures have a high likelihood of requiring operative intervention to control hemorrhage and early transfusion of blood should be considered.
  • Source. The source of blood loss in victims of penetrating injury depends on the nature, location, and path of the projectile. For blunt trauma victims, the potential sources of blood loss may be more difficult to localize. For both, the search for sites of hemorrhage is identical. Four main sites of large volume blood loss exist.
    • Chest. May be suspected in settings of penetrating chest wound or chest wall injury. May be identified by absent or reduced breath sounds, the presence of hemothorax on chest x-ray, or return of blood through a chest tube. Physical exam may be insensitive to exclude significant hemorrhage in the chest.
    • Abdomen. Physical examination is a relatively insensitive method for detecting significant hemoperitoneum. Hemoperitoneum may be identified in the resuscitation area by focused abdominal sonography for trauma (FAST) or diagnostic peritoneal lavage (DPL) or in the operating room by laparotomy.
    • Retroperitoneum or pelvis. Usually associated with pelvic fractures.
    • External. Visible on inspection, such as major vascular injuries from extremity wounds, large surface area wounds, or uncontrolled wounds in areas of increased vascularity (face, scalp).
    • Other sources of blood loss include long bone fractures and extensive soft tissue injury. Patients on anticoagulants can bleed extensively from relatively minor injuries. If no bleeding site is identified, consider alternative causes of shock (cardiac tamponade, neurogenic, cardio-genic). Also consider repeating the assessment of the chest, abdomen, and pelvis to ensure that no possible sources have been overlooked.

B. Cardiogenic Shock

In trauma patients, cardiogenic shock can be caused by either significant cardiac injury (myocardial contusion) or intrinsic cardiac disease (myocardial infarction, cardiac arrhythmia).

• Diagnosis. Suspicion of cardiogenic shock may be increased when hypov-olemic shock has been excluded or risk factors are identified (elderly patient, known preexisting cardiac disease, dysrhythmias present on electrocardiogram [ECG] or monitor, presence of sternal fracture). The diagnosis of cardiac pump failure as a source of ongoing shock in injured patients requires exclusion of other causes and demonstration of diminished cardiac function (decreased cardiac output, echocardiographic evidence of cardiac dysfunction).
• Treatment of cardiogenic shock in trauma patients involves restoration of cardiac function in conjunction with the treatment of acute traumatic injuries.
  • ABCs. The airway should be secure and bilateral equal breath sounds present. Fluid resuscitation should be instituted judiciously in patients with known cardiac dysfunction.
  • Invasive hemodynamic monitoring. An arterial line and pulmonary artery catheter may help guide therapy and assess the success of treatment.
  • Inotropic agents. Selective use can be guided by the results of invasive hemodynamic monitoring.
  • Circulatory support. Consider intraaortic balloon pump for refractory cardiac dysfunction.

C. Neurogenic shock

In trauma patients, is usually caused by injuries to the cervical or upper thoracic spinal column. Rarely, spinal cord injuries without bony abnormality (epidural hematoma of the cord) can result in neurogenic shock.

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• Diagnosis. The classic description of neurogenic shock includes hypotension and bradycardia, with warm, perfused extremities and presence of a sensory or motor deficit consistent with cord injury. Tachycardia can be present. Hypovolemia, in addition to the neurogenic component, can contribute to hypotension. The diagnosis is often made once hypovolemia has been excluded and a vertebral fracture in the appropriate area identified.
• Treatment
  • ABCs. The airway should be secure and equal bilateral breath sounds present. Fluid resuscitation should be instituted and restoration of intravascular volume may be sufficient to restore blood pressure and perfusion.
  • If the diagnosis of neurogenic shock is certain and hypotension persists, vasopressor support can be helpful. Phenylephrine or norepinephrine can be instituted as a continuous infusion. If vasopressor support is needed, its duration is typically brief (24–72 hours [h]). If vasopressor support is indicated, invasive hemodynamic monitoring (e.g., an arterial line, central venous pressure monitor, or pulmonary artery catheter) should be considered based on patient age, associated injuries, and preexisting medical condition.

D. Septic shock

In trauma patients, is an unlikely cause of shock in the emergency department or early in the hospital stay. Septic shock can develop later from infectious complications after injury.

• Diagnosis. A hyperdynamic hemodynamic profile is often present, with hypotension, tachycardia, and increased cardiac output. Fever, leukocytosis, and tachypnea are often present. Delirium or obtundation can also be present. Evidence of localized infection (pneumonia, urinary tract infection, intraabdominal abscess, empyema, soft tissue infection) should be sought. Bacteremia can be present and secondary infection of monitoring devices (continuous venous or arterial lines, intracranial pressure monitors) or prosthetic devices may need to be excluded.
• Treatment
  • ABCs. The airway should be secure and proper ventilatory mechanics established. Intravascular volume should be restored initially. If hypotension persists, pharmacologic support may be necessary. Invasive hemodynamic monitoring should be considered to guide therapy. A pulmonary artery catheter can assist in deciding if inotropic or vasopressor support should be instituted.
  • Treatment of the primary infection is essential. Systemic antibiotics should be instituted, purulent fluid collections should be drained (percutaneously or operatively), infected monitoring or prosthetic devices should be removed, and necrotic nonviable tissue should be debrided. Antibiotic therapy should be appropriate to cover the likely responsible organisms, based on the infectious cause, common organisms in the particular unit or institution, and the patient's previous history of infectious episodes. Antibiotics should be tailored to appropriate culture data when available and long-term empiric antibiotic usage should be discouraged to avoid the development of resistant organisms.
  • The use of most antiendotoxin strategies, cytokines, and anticytokine antagonists should be considered experimental. Their use has not proved to be effective in clinical trials. The use of activated protein C reduces mortality after sepsis but is an anticoagulant whose use in trauma patients that may have injuries that predispose to hemorrhage should be carefully evaluated.
  • Tight regulation of plasma glucose with exogenous insulin improves mortality in critically ill adults. The mechanism for this effect in unknown. Whether a similar benefit exists in injured patients has not yet been rigorously studied, but the preliminary evidence is encouraging.
  • Corticosteroids in large doses in septic patients may worsen infectious complications and outcome. Low-dose corticosteroid replacement in septic

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    patients who may have hypoadrenalism is suggested to be beneficial. The precise utility of corticosteroid treatment in sepsis requires further study.

E. Obstructive shock

Mechanical obstruction to perfusion is usually caused by the development of tension pneumothorax or cardiac tamponade. The diagnosis of these entities is covered in detail in Chapters 22 and 23. Correction of the primary cause should restore perfusion or additional causes should be sought.

F. Traumatic shock

Is usually caused by a combination of hypovolemic, cardiogenic, neurogenic, septic, and obstructive shock. Treatment of the contributing components can require rapid, coordinated medical decision making. After securing the airway, prompt control of hemorrhage is generally the major objective.

IV. Summary

The term shock represents a state of abnormal tissue and cellular perfusion. Reliance on predetermined blood pressure criteria can lead to substantially underestimation of shock states. In trauma patients, acute blood loss represents the most common form of shock but other causes should be kept in mind. Usually, treatment of shock is instituted before or in conjunction with steps to identify the underlying cause. Patients who are actively bleeding need prompt operative intervention and the need for operative treatment should be established early to avoid the potential end-organ dysfunction and death associated with continue tissue hypoperfusion.