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Hypovolemic shock occurs when rapid loss of fluids results in inadequate intravascular volume and subsequent inadequate perfusion. As previously noted, the most common cause of shock in the trauma patient is loss of circulating volume from hemorrhage. Acute blood loss causes decreased stimulation of baroreceptors (stretch receptors) in the large arteries resulting in decreased inhibition of vasoconstrictor centers in the brainstem, increased stimulation of chemoreceptors in vasomotor centers, and diminished output from atrial stretch receptors. These changes increase vasoconstriction and peripheral arterial resistance. Hypovolemia also induces sympathetic stimulation leading to the release of epinephrine and norepinephrine, activation of the renin–angiotensin cascade, and increased release of vasopressin. Peripheral and splanchnic vasoconstriction is prominent while lack of sympathetic effects on cerebral and coronary vessels and local autoregulation promote maintenance of blood flow to the heart and brain.19
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Shock in a trauma patient should be presumed to be due to hemorrhage until proven otherwise. Treatment is instituted as soon as shock is identified, typically before a source of hemorrhage is located.
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The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss.88 Loss of up to 15% of the circulating volume (700–750 mL for a 70-kg patient) may produce little in terms of obvious symptoms, while loss of up to 30% of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety. Hypotension, marked tachycardia (pulse >110–120 beats/min), and confusion may not be evident until more than 30% of the blood volume has been lost, while loss of 40% of circulating volume (2 L) is immediately life-threatening. Symptoms of the degrees of hypovolemic shock are summarized in Table 12-2. Thus, there is a fine line between the development of mild symptoms of shock and the presence of life threatening blood loss. Young, healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs. These patients may maintain a near-normal blood pressure until a precipitous cardiovascular collapse occurs. Elderly patients may be taking medications that either promote bleeding (warfarin, aspirin) or mask the compensatory response to hypovolemia (β-blockers). In addition, atherosclerotic vascular disease, diminished cardiac compliance with age, inability to elevate heart rate or cardiac contractility in response to hemorrhage, and overall decline in physiologic reserve decrease the ability of the elderly patient to tolerate hemorrhage.105,106
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Understanding the mechanism of injury of the patient in shock will help direct the evaluation and management. Identifying the source of blood loss in patients with penetrating wounds is relatively simple since potential bleeding sources will be located along the known or suspected path of the wounding agent. Patients with penetrating injuries who are in shock usually require operative intervention. Occasionally, patients in shock from penetrating injuries may have problems that are readily treated by simple maneuvers outside the operating room. Treatment of a tension pneumothorax (obstructive shock) with insertion of a thoracostomy tube in the emergency department (ED) is one example. Generally speaking, though, shock from penetrating wounds is typically due to ongoing hemorrhage that mandates operative control.
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Patients who suffer multisystem injuries from blunt trauma have multiple sources of potential hemorrhage. There are a limited number of sites, however, that can harbor sufficient extravascular blood volume to induce hypoperfusion or hypotension. Prehospital medical reports may confirm a significant blood loss at the scene of an accident, history of massive blood loss from wounds, visible brisk bleeding, or presence of an open wound in proximity to a major vessel. Injuries to major arteries or veins should be suspected when there is ongoing hemorrhage from an open pelvic fracture. While persistent bleeding from uncontrolled small vessels can, over time, precipitate shock if left untreated, attributing profound blood loss to these wounds (ie, scalp lacerations) should be done only after major intracavitary bleeding or other etiologies have been excluded. When major blood loss is not immediately visible, internal (intracavitary abdominal or thoracic) blood loss should be suspected. Intraperitoneal hemorrhage is probably the most common source of blood loss inducing shock. Its presence may be suspected based on physical examination (distended abdomen, abdominal tenderness, visible abdominal wounds), although the sensitivity of the physical examination for detecting substantial abdominal injuries after blunt trauma is notoriously unreliable. A large volume of intraperitoneal blood from abdominal injuries may be present before the physical examination is abnormal. Therefore, ultrasound Focused Assessment Sonography in Trauma (FAST) or diagnostic peritoneal aspiration is used frequently in the resuscitation area to rapidly identify potential intraperitoneal blood in the unstable patient. In selected patients, diagnostic laparotomy may be indicated. In addition, the chest can be a significant source of hemorrhage and each pleural cavity has the capacity to hold 2–3 L of blood. Diagnostic and therapeutic tube thoracostomy may be indicated in patients based on clinical findings, clinical suspicion, or evidence of a hemopneumothorax on a chest x-ray or pleural FAST. In addition, with the immediate removal of greater than 1000 mL of blood, a second CT should be considered to ensure patency and accurate monitoring of ongoing blood loss. Major retroperitoneal hemorrhage occurring in association with a pelvic fracture can be diagnosed by urgent pelvic radiography. The pattern of the pelvic fracture may provide clues as to the risk of massive blood loss, but none is adequately predictive in the individual patient to exclude further evaluation.107
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Control of ongoing hemorrhage is a central component of resuscitation of the patient in shock, and is part of the primary survey. Treatment of hemorrhagic shock is instituted concurrently with diagnostic evaluation to identify a source. As mentioned earlier, all trauma patients in shock should be presumed to have hemorrhage until proven otherwise. The method of treatment will depend on the patient’s response to resuscitation, the specific injury or injuries responsible for the blood loss, and consideration of factors such as mechanism of injury, age of the patient, associated injuries, and institutional resources. Patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing active hemorrhage from major vessels (external bleeding, pleural cavity, peritoneal cavity, retroperitoneum, or both thighs) and require prompt intervention. Identification of the body cavity harboring active hemorrhage will help focus operative efforts, but since time is of the essence, rapid treatment is essential and diagnostic laparotomy or thoracotomy may be indicated. Alternatively, dependent on most likely location of bleeding, endovascular control of difficult to achieve hemorrhage control can be attempted using emergent IR angiographic intervention with embolization or newly proposed retrograde endovascular balloon occlusion of the aorta (REBOA), where appropriate to rapidly control distal bleeding, with subsequent operative or angiographic control of bleeding source.108 The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage is achieved.
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Patients who respond to initial resuscitative efforts but then deteriorate hemodynamically frequently have injuries that require operative intervention. The duration of their response will dictate whether and which diagnostic maneuvers can be performed safely to identify the site of bleeding. Usually, however, hemodynamic deterioration denotes ongoing bleeding for which some form of intervention (operation or interventional radiology) is required. As noted earlier, with cessation of hemorrhage, even patients who have lost significant intravascular volume will often respond to resuscitative efforts if the depth and duration of shock have been limited.
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A subset of patients fails to respond to resuscitative efforts despite adequate control of ongoing hemorrhage. These patients present in the following manner: have ongoing fluid requirements despite adequate control of hemorrhage; have persistent hypotension despite restoration of intravascular volume; often require vasopressor support to maintain their systemic blood pressure; and may exhibit a futile cycle of uncorrectable hypothermia, hypoperfusion, acidosis, and coagulopathy that cannot be interrupted despite maximum therapy. These patients have classically been described to be in decompensated or irreversible shock,63 and mortality is inevitable once the patient manifests shock in its terminal stages; however, this is always a diagnosis made in retrospect. Hemodynamic decompensation or the paradoxical peripheral vasodilation that occurs with prolonged hemorrhage has been studied in animal models of shock,109 but the mechanisms responsible for its development and the clinical factors that predict its onset in humans with shock have not been elucidated. In patients with hemorrhagic shock, survival is improved if the time between injury and control of bleeding is reduced. Clarke et al demonstrated that trauma patients with major abdominal injuries requiring emergency laparotomy had an increased probability of death with increasing length of time in the ED.110 This probability increased approximately 1% for every 3 minutes in the ED up to 90 minutes.
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The priorities in patients with hemorrhagic shock are (a) secure the airway, (b) support breathing and ventilation, and (c) control the source of hemorrhage and volume resuscitation. In trauma, identifying the body cavity harboring active hemorrhage will help focus the operative effort. Because time is of the essence, simultaneous and rapid evaluation and treatment is essential. Diagnostic laparotomy or thoracotomy may be indicated. The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage has been achieved. There has been evolution in the management of these patients known as damage control resuscitation.111 This strategy begins in the ED, continues into the operating room, and into the intensive care unit. Initial resuscitation is limited to keep systolic blood pressure around 90 mm Hg. Overly aggressive resuscitation during this phase has been shown to increase bleeding from recently clotted injured vessels. Intravascular volume resuscitation is accomplished with blood products and limited crystalloids. Too little volume infusion with resultant persistent hypotension and hypoperfusion is dangerous, yet overly vigorous resuscitation may be just as deleterious, and results in dilutional coagulopathy (see Chapter 13), compartment syndromes, acute lung injury, cerebral edema, acid–base and electrolyte disorders, and immune dysfunction. Control of hemorrhage is achieved in the operating room or angiography suite, and efforts to prevent hypothermia and coagulopathy are employed in emergency department (ED), operating room, and intensive care unit.
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Cannon made the seminal observation that attempts to increase systolic blood pressure in soldiers with uncontrolled sources of hemorrhage are counterproductive, with increased bleeding and higher mortality.4 Several animal studies have confirmed the observation that attempts to restore normal blood pressure with fluids or vasopressors in the setting of active bleeding were rarely achievable and resulted in increased bleeding and higher mortality. A prospective, randomized clinical study compared delayed fluid resuscitation (on arrival in the operating room) with standard fluid resuscitation (with arrival of the paramedics) in hypotensive patients with penetrating torso trauma.15 The authors report that delayed fluid resuscitation resulted in a lower patient mortality. From these and other studies it is reasonable to conclude that in the setting of uncontrolled hemorrhage, any delay in surgical control of bleeding may increase mortality; with uncontrolled hemorrhage, attempting to achieve normal blood pressure may increase mortality, particularly with penetrating injuries and short transport times; a goal of systolic blood pressure of 80–90 mm Hg is adequate in the patient with penetrating injury; and profound hemodilution should be avoided by early transfusion of red blood cells. For the patient with blunt injury, where the major cause of death is traumatic brain injury, the increase of mortality with hypotension in the setting of brain injury must be avoided. In this setting, a systolic blood pressure of 110 mm Hg would seem to be more appropriate.
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Transfusion of packed red blood cells and other blood products is essential in the treatment of the patient in hemorrhagic shock (see Chapter 13). FFP should also be transfused in patients with massive bleeding due to the frequently associated coagulopathy.112,113 A number of retrospective studies in the military and civilian population support the concept of early transfusion of FFP, platelets, and packed red blood cells.113,114,115 A recent multicenter trial (PROPPR) comparing FFP, platelets and pRBC in a 1:1:1 ratio versus a 1:1:2 ratio indicted no overall improvement in survival at 24 hours or 30 days95, however, the interpretation of this study remains debated (see Chapter 13).
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Neurogenic shock refers to diminished mean arterial pressure (MAP) and tissue perfusion as a result of loss of vasomotor tone to peripheral vascular beds. Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is typically due to injuries to the spinal cord from fractures of the cervical or high thoracic vertebrae that disrupt sympathetic regulation of peripheral vascular tone (see Chapter 23). Occasionally, an injury such as an epidural hematoma impinging on the spinal cord can produce neurogenic shock without an associated vertebral fracture. Penetrating wounds to the spinal cord can produce neurogenic shock, as well. Sympathetic input to the heart that normally increases heart rate and cardiac contractility and input to the adrenal medulla that increases the release of catecholamines can be disrupted by a high injury to the spinal cord, preventing the typical reflex tachycardia that occurs with the relative hypovolemia from increased venous capacitance and loss of vasomotor tone. Acute spinal cord injury results in activation of multiple secondary injury mechanisms: (a) vascular compromise to the spinal cord with loss of autoregulation, vasospasm, and thrombosis, (b) loss of cellular membrane integrity and impaired energy metabolism, and (c) neurotransmitter accumulation and release of free radicals. Importantly, hypotension contributes to the worsening of acute spinal cord injury as a result of further reduction in blood flow to the injured spinal cord.
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The classic description of neurogenic shock consists of decreased blood pressure associated with bradycardia or normal heart rate indicating the absence of reflexive tachycardia due to disrupted sympathetic discharge, warm extremities due to loss of peripheral vasoconstriction, motor and sensory deficits indicative of an injury to the spinal cord, and radiographic evidence of a fracture in the vertebral column (see Chapter 23). Determining the presence of neurogenic shock may be difficult, however, since patients with multisystem trauma that includes an injury to the spinal cord often have a traumatic brain injury that may make identification of motor and sensory deficits difficult. Furthermore, associated injuries may cause hypovolemia and complicate the clinical presentation. In a subset of patients with injuries to the spinal cord from penetrating wounds, most patients with hypotension had blood loss as the etiology (74%) and not a neurogenic cause, and few (7%) had all the classic findings of neurogenic shock.116 Hypovolemia from hemorrhage should be sought and excluded before the diagnosis of neurogenic shock is made. To assume that the cause of hypotension in a multiply injured patient is due to neurogenic shock without first evaluating and treating potential hemorrhage is often a costly mistake. In patients who have neurogenic shock, the severity of the spinal cord injury seems to correlate with the magnitude of the cardiovascular dysfunction. Patients with complete motor deficits from spinal cord injury are over five times more likely to require vasopressors for neurogenic shock compared to those with incomplete lesions.117 Similarly, patients with high cervical spine injuries (C1–C5) were more likely to require cardiovascular intervention compared to those with lower C- or high T-spine injuries.118
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After the airway is secured and ventilation is adequate, fluid resuscitation and restoration of functional intravascular volume will often improve systemic blood pressure and perfusion in neurogenic shock. Most patients with neurogenic shock will respond to volume resuscitation alone, with adequate improvement in perfusion and resolution of hypotension. Administration of vasoconstrictors can improve peripheral vascular tone, decrease vascular capacitance, and increase venous return, but should only be considered once hypovolemia is excluded and the diagnosis of neurogenic shock established. If the patient’s blood pressure has not responded to appropriate volume resuscitation, continuous infusion of dopamine or a pure α-agonist such as phenylephrine may be used. Specific treatment for the shock state per se is often brief and the need to administer vasoconstrictors typically lasts only 24–48 hours. The duration of the need for vasopressor support for neurogenic shock may correlate with the overall prognosis for improvement in neurologic function.117 Appropriate rapid restoration of blood pressure and circulatory perfusion may also improve perfusion to the spinal cord, prevent progressive ischemia of the spinal cord, and minimize secondary injury to the spinal cord.119 Restoration of normal hemodynamics should precede any operative attempts to stabilize the vertebral fracture. Patients who are hypotensive from spinal cord injury are best monitored in intensive care unit, and carefully followed for evidence of cardiac or respiratory dysfunction.
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Cardiogenic shock refers to a failure of the circulatory pump leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock include sustained hypotension (ie, systolic blood pressure ≤90 mm Hg for at least 30 minutes), reduced cardiac index (<2.2 L/[min m2]), and elevated pulmonary artery occlusion pressure (>15 mm Hg).120 Acute myocardial infarction is the most common cause of cardiogenic shock. In this population, mortality for cardiogenic shock ranges between 50 and 80%. In the trauma patient, inadequate cardiac function after blunt thoracic trauma can be due to blunt myocardial injury, cardiac arrhythmia, myocardial infarction, or direct injury to a cardiac valve. As the average age of the population increases, the prevalence of comorbid medical conditions in trauma patients will also increase. Elderly patients with preexisting intrinsic cardiac disease will be more susceptible to suffering an acute myocardial infarction or significant arrhythmia associated with the stress of injury that can also induce cardiac failure and cardiogenic shock (see Chapter 56). Diminished cardiac output or contractility in the face of adequate intravascular volume (preload) may lead to under perfused vascular beds and reflexive sympathetic discharge. Increased sympathetic stimulation of the heart, either through direct neural input or from circulating catecholamines, increases heart rate, myocardial contraction, and myocardial oxygen consumption. Patients with fixed, flow-limiting stenoses of the coronary arteries may not be able to increase coronary perfusion to meet the increased myocardial oxygen demands and these lesions, therefore, further increase the risk for myocardial damage.19 Diminished cardiac output decreases coronary artery blood flow, resulting in a scenario of increased myocardial oxygen demand at a time when myocardial oxygen supply may be limited. Acute heart failure can also result in fluid accumulation in the pulmonary microcirculatory bed, impairing the diffusion of oxygen from the alveolar space, and decreasing myocardial oxygen delivery even further.
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Rapid identification of the patient with pump failure and institution of treatment are essential in preventing further decreases in cardiac output after such an injury. If increased myocardial oxygen needs cannot be met, there will be progressive and unremitting cardiac dysfunction. Blunt injury to the heart is rarely severe enough to induce pump failure,121 but manifestations of shock in the setting of a patient at risk should raise one’s index of suspicion (see Chapter 26). Elderly patients with known preexisting cardiac disease are at increased risk of suffering injury-related cardiac complications including cardiac failure. Furthermore, elderly patients with intrinsic cardiac disease are at risk to suffer a primary cardiac event that induces syncope, a fall, or loss of control of one’s vehicle that then leads to presentation to a trauma center.
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Making the diagnosis of cardiogenic shock involves the identification of cardiac dysfunction or acute heart failure in a susceptible patient. Since patients with blunt cardiac injury typically have multisystem trauma,122,123 hemorrhagic shock from intra-abdominal bleeding, intrathoracic bleeding, and bleeding from fractures must be excluded. In most instances of blunt cardiac injury the symptoms are self-limited with no long-term cardiac sequelae. Relatively few patients with blunt cardiac injury will develop dysfunction of the cardiac pump and those who do generally exhibit cardiogenic shock early in their evaluation.121 Therefore, establishing the diagnosis of blunt cardiac injury is secondary to excluding other etiologies for shock and establishing that significant cardiac dysfunction is present. Invasive cardiac hemodynamic monitoring, which generally is not necessary, may be useful in the complex patient with the combination of hemorrhagic shock and cardiogenic shock, when it is necessary to exclude right ventricular infarction or mechanical cardiac complications, or in the patient with known preexisting myocardial disease (see Chapter 55). This typically involves continuous monitoring of cardiac output and other hemodynamic variables using the pulmonary artery catheter (PAC).124,125,126,127 Transesophageal echocardiography (TEE) provides excellent views of the myocardium that are not hindered by subcutaneous air, bandages covering chest wounds, chest tubes, or unfavorable body habitus that may limit evaluation of cardiac function by transthoracic echocardiography. The rapid evaluation of cardiac function by TEE may be problematic, in the presence of severe maxillofacial trauma, or unstable injuries to the cervical spine that can interfere with placement of the probe. Trauma surgeons are becoming increasingly more experienced in the use of ultrasound as part of the initial resuscitation and to diagnose penetrating cardiac wounds.128,129 There is growing evidence that evaluation of cardiac function using bedside ultrasound by surgeons, emergency medicine, and intensivists demonstrates adequate accuracy to direct treatment.130,131
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Patients with blunt cardiac injury will often have associated injuries that produce hypovolemia, and expansion of intravascular volume as an initial maneuver can improve perfusion significantly. However, hypervolemia can magnify the physiologic derangements produced by cardiac dysfunction and should be avoided. In addition, under conditions of limited flow, anemia becomes a potential limiting factor and requires transfusion to higher levels as a buffer to help ensure adequate oxygen delivery. In the face of acute MI or acute myocardial ischemia, maintaining a hematocrit of 30 appears to be indicated.132 When profound cardiac dysfunction exists, ionotropic support may be indicated to improve cardiac contractility and cardiac performance.133 Several agents are available and selection is dependent on the overall cardiovascular pathophysiology (see Chapter 55).
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Patients whose cardiac dysfunction is refractory to cardiotonics may require mechanical circulatory support with an intra-aortic balloon pump.133 This can be inserted at the bedside in the intensive care unit via the femoral artery through either a cutdown or percutaneous approach. In addition, recent data support use of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for acute cardiac failure due to trauma.134 Aggressive circulatory support of patients with cardiac dysfunction from intrinsic cardiac disease has led to more widespread application of these devices and more familiarity with their operation by both physicians and critical care nurses (see Chapter 56). Patients who have suffered an acute myocardial infarction following injury should have preservation of existing myocardium and cardiac function as priorities of therapy. The use of anticoagulation or thrombolytic therapy for the management of acute coronary syndromes will depend on associated injuries and the risk of secondary bleeding. Patients in cardiac failure from an acute myocardial infarction may benefit from pharmacologic or mechanical circulatory support, similar to that of patients with cardiac failure related to blunt cardiac injury. Additional pharmacologic tools include the use of β-blockers to control heart rate and myocardial oxygen consumption, nitrates to promote coronary blood flow through vasodilation, and ACE inhibitors to reduce ACE-mediated vasoconstriction that increases myocardial workload and oxygen consumption.135 Selected patients who do not have significant associated injuries may be candidates for coronary angiography and subsequent procedures to improve coronary blood flow such as transluminal angioplasty, coronary artery stents, or urgent coronary artery bypass grafting.
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Septic Shock (Vasodilatory or Distributive Shock)
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The multidisciplinary consensus consortium, Surviving Sepsis Campaign, has established useful standardized definitions for the patient with an inflammatory response +/– sepsis.136 First, the systemic inflammatory response syndrome (SIRS) defines the clinical innate immune clinical manifestation that occurs in response to a wide variety of physiologic insults, and is defined as the presence of two or more of the following conditions: temperature greater than 38°C or, less than 36°C, pulse rate greater than 90 beats/min, respiratory rate greater than 20 breaths/min or PaCO2 less than 32 mm Hg, white blood cell count greater than 12,000/mm3 or less than 4000/mm3, or greater than 10% immature (band) forms. Sepsis is defined as the systemic inflammatory response in association with proven infection. Severe sepsis occurs when sepsis is associated with hypoperfusion and organ dysfunction. Perfusion abnormalities may be manifested by lactic acidosis, oliguria, or an acute alteration in mental status. Septic shock is a subset of severe sepsis and is defined as sepsis-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who require inotropic or vasopressor agents may no longer be hypotensive by the time they manifest hypoperfusion abnormalities or organ dysfunction, yet they would still be considered to have septic shock.137
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Septic shock is a clinical syndrome that occurs as part of the body’s immune and inflammatory response to invasive or severe localized infection, typically from bacterial or fungal pathogens. In its attempt to eradicate the pathogens, the innate immune system elaborates a wide array of proinflammatory mediators (cytokines and chemokines). These mediators enhance effector mechanisms for macrophage and neutrophil killing, increase procoagulant-induced microcirculatory thrombosis and fibroblast activity to localize the invaders, and increase surrounding microvascular blood flow to enhance delivery of bactericidal mediators to the area of invasion. When this response is overly exuberant or becomes systemic rather than localized, manifestations of sepsis become evident. These findings include peripheral vasodilation, fever, leukocytosis, and tachycardia.138,139 Sepsis is an uncommon etiology for shock in the acute presentation of a trauma patient unless there has been a substantial delay between injury and presentation to the ED. Typically, invasive infection in the injured patient occurs days to weeks after injury and is prevalent in the severely injured patient who develops a nosocomial infection in the intensive care unit.
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Attempts to standardize terminology have led to the establishment of criteria for the diagnosis of sepsis in the hospitalized adult. These criteria include manifestations of the host response to infection (fever, leukocytosis, mental contusion, tachypnea, tachycardia, hypotension, oliguria), as well as identification of an offending organism.136 Septic shock requires the presence of these conditions associated with hypotension resistant to volume resuscitation and evidence of organ dysfunction due to tissue hypoperfusion. Recognizing septic shock in the trauma patient begins with defining high-risk groups as follows: critically ill patients in the intensive care unit with organ dysfunction requiring invasive support and who are immunosuppressed from their injuries where nosocomial infection rates are high, patients who have suffered injuries associated with significant contamination (colorectal wounds with fecal spillage, soft tissue wounds embedded with soil or dirt), patients with injuries that may be associated with persistent devitalized tissue (crush injuries), patients whose wounds put them at risk for complications (anastomotic disruption, pancreatic leak), or patients with missed injuries. The clinical manifestations of septic shock should prompt the empiric initiation of treatment after obtaining appropriate cultures and before bacteriologic confirmation of an organism or source of active infection is identified. An aggressive search for the source of the infection includes a thorough physical examination, inspection of all wounds, evaluation of intravascular catheters or other foreign bodies, sampling of appropriate body fluids for culture, and adjunctive imaging studies as needed.
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The hemodynamic parameters characteristic of septic shock include peripheral vasodilatation with resultant decrease in systemic vascular resistance. Initially, there is a hyperdynamic cardiac state; and, after volume resuscitation, the cardiac output is significantly elevated. Changes in cardiac preload and filling pressures reflect the volume status of the patient. Diagnosis and treatment does not usually require placement of a pulmonary arterial catheter to guide therapy in patients with septic shock. Most of these patients can be resuscitated using central venous pressure, ScvO2, and serum lactate.
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Obtunded patients may require intubation to protect their airway while patients whose work of breathing is excessive may require intubation and mechanical ventilation to prevent respiratory collapse. Since vasodilation and a decrease in total peripheral resistance combine to produce hypotension, restoration of circulatory volume is essential. Empiric antibiotics that cover the most likely pathogens should be chosen while culture results are pending (see Chapter 18). Antibiotics should be tailored to cover the responsible organisms once culture data are available and, if appropriate, the spectrum of coverage narrowed. Long-term empiric use of broad-spectrum antibiotics should be minimized to reduce the development of resistant organisms and avoid the potential complications of fungal overgrowth and antibiotic-associated colitis from Clostridium difficile.140
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In the trauma patient, intravenous antibiotics alone will frequently be insufficient to adequately treat a severe surgical infection. Source control, that is, drainage of infected fluid collections, removal of infected foreign bodies, and debridement of devitalized tissue are essential to eradicate the infection. This process may require multiple operations. For patients who manifest symptoms of septic shock early in their hospitalization, consideration of the possibility of a missed injury to a hollow viscus should be entertained. Missed abdominal injuries represent a significant source of sepsis and the septic response leading to MODS/MOF.141,142 Vasopressor therapy may be required as a supportive measure when hypotension is refractory to volume infusion in patients in septic shock. α-Adrenergic agents promote peripheral vasoconstriction, improve systemic blood pressure, and can be titrated by continuous infusion to target an adequate mean arterial pressure to maintain core organ perfusion (see Chapter 55).
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In 2008 the multidisciplinary Surviving Sepsis Campaign published international guidelines for the management of severe sepsis and septic shock.137 These recommendations include the early goal-directed resuscitation of the septic patient during the first 6 hours after recognition, obtaining blood cultures before initiation of antibiotic therapy, prompt performance of imaging to identify the source of infection, the administration of broad-spectrum antibiotic therapy within 1 hour of diagnosis of septic shock, subsequent narrowing antibiotic coverage after microbiologic data are obtained, source control, and administration of crystalloid or colloids for fluid resuscitation.
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While prior clinical studies demonstrated improvements in outcome using these recommendations, recent clinical trials to evaluate the effect of these guidelines using protocol-based resuscitation for patients who present in septic shock have not demonstrated an improvement in outcomes compared to current standard therapy.143,144,145 The Surviving Sepsis Campaign last updated their guidelines in 2012, and the management in the first 6 hours after identification of septic shock continues to focus on goal-directed resuscitation.146
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Other issues to address in the care of the patient with sepsis include: 1. Stress-dose glucocorticoid therapy should be given primarily to patients with septic shock based on clinical parameters and only if hypotension is poorly responsive to fluid and vasopressor therapy, so-called “refractory shock.” 2. In the absence of active coronary artery disease with evidence of acute ischemia or acute ongoing hemorrhage, a target hemoglobin of 7 g/dL is appropriate to trigger transfusion. 3. All patients with acute lung injury or ARDS requiring mechanical ventilation should receive low pressure ventilation (LPV) support with low tidal volumes (6 mL/kg) and maintaining plateau airway pressures less than or equal to 30 cm H2O. 4. Controversy has existed regarding how tight glycemic control should be in the critically ill patient. Large randomized control trials suggest that complications of excessively tight glycemic control may outweigh the benefits,147,148,149 and therefore liberalizing maintaining blood glucose to 140–150 mg/dL appears to be a reasonable target.
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Multiple strategies for immune modulation have been developed and tested for the treatment of sepsis and septic shock. In the past, use of antiendotoxin antibodies, anticytokine antibodies, cytokine receptor antagonists, immune enhancers, antinitric oxide compounds, and oxygen radical scavengers have been tried.150,151,152,153,154,155,156 Each of these compounds is designed to alter a specific aspect of the host immune response to shock. However, to date each of these strategies has failed to demonstrate efficacy in improving patient outcome despite utility in well-controlled animal experiments. For example, previous trials demonstrated efficacy of activated protein C in improving mortality from sepsis,157 but subgroup analysis of patients with sepsis at low risk of death, documented an increased risk of bleeding complications associated with therapy without a substantial improvement in survival.158 It is unclear whether the failure of these interventions is due to poorly designed clinical trials, inadequate understanding of the interactions of the complex immune response to injury and infection, or use of animal models of shock that poorly represent human disease.159 Sepsis and nosocomial infections in critically ill patients continue to represent significant sources of morbidity and consume substantial health care resources. Despite advances in critical care, the mortality rate for severe sepsis and shock remains at 30–50%. In the United States, 750,000 cases of sepsis occur annually, one-third of which are fatal.160
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Hypoperfusion can be due to mechanical or anatomical obstruction impeding venous return to the heart or preventing cardiac filling. The end result of either of these two events is decreased cardiac output leading to decreased peripheral perfusion. Most commonly, obstruction is due to the presence of a tension pneumothorax, massive pulmonary embolism, or cardiac tamponade (see Chapter 26). Obstructive shock has also been described in adult patients with tense ascites and pediatric patients with extremely distended stomachs. With any of these conditions, there is decreased cardiac output associated with increased central venous pressure.
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Diagnosis and Treatment
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The manifestations of a tension pneumothorax are the presence of shock in the context of diminished breath sounds over one hemithorax, hyperresonance to percussion, jugular venous distension, and shift of mediastinal structures to the unaffected side. Unfortunately, not all of the clinical manifestations of tension pneumothorax may be evident on physical examination. Hyperresonance may be difficult to appreciate in a noisy resuscitation area. Jugular venous distension or tracheal deviation may be obscured by a cervical collar in the multiply injured patient and not seen unless specifically sought. Furthermore, hypovolemia from concurrent bleeding may diminish central venous pressure and prevent jugular venous distension even when increased pleural, pulmonary artery or pericardial pressure restricts outflow. For the multiply injured patient with life-threatening hypotension, the placement of bilateral chest tubes may be both diagnostic and therapeutic. In these circumstances, a chest x-ray is both unnecessary and potentially a dangerous waste of time. Due to the immediate threat to life, the diagnosis of tension pneumothorax should be a clinical one. If a chest x-ray is obtained, due to missing the diagnosis on clinical examination, the typical findings include deviation of mediastinal structures, depression of the hemidiaphragm (deep sulcus sign), and hypo-opacification with absent lung markings.
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Cardiac tamponade results from the accumulation of blood within the pericardial sac and most commonly occurs from penetrating trauma. While precordial wounds are most likely to injure the heart and produce tamponade, any projectile or wounding agent that passes in proximity to the mediastinum can potentially produce tamponade. Blunt rupture of the heart is fortunately rare, but the diagnosis is aided by the FAST examination that is performed immediately on all patients at risk. The manifestations of cardiac tamponade may be as catastrophic as total circulatory collapse and cardiac arrest or they may be extremely subtle. A high index of suspicion is warranted to make a rapid diagnosis. Patients who present with circulatory arrest due to cardiac tamponade from a precordial penetrating wound require emergency pericardial decompression through a left anterolateral thoracotomy, and the indications for this maneuver are reviewed in Chapter 14. Cardiac tamponade may also be associated with hypotension, muffled heart tones, jugular venous distension (Beck Triad), and elevated central venous pressure with tachycardia. Absence of these clinical findings, however, may not be sufficient to exclude cardiac injury and cardiac tamponade. Muffled heart tones may be difficult to appreciate in a busy trauma center, jugular venous distension and central venous pressure may be diminished by coexistent bleeding and hypovolemia. Therefore, patients at risk for cardiac tamponade whose hemodynamic status permits should undergo additional diagnostic tests.
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Invasive hemodynamic monitoring may support the diagnosis of cardiac tamponade if elevated central venous pressure, pulsus paradoxus (decreased systemic arterial pressure with inspiration), or elevated right atrial and right ventricular pressure by pulmonary artery catheter is present. These hemodynamic profiles suffer from lack of specificity, the time required to obtain them, and their inability to exclude cardiac injury in the absence of tamponade. Chest radiographs may provide information on the possible trajectory of a projectile, but are rarely diagnostic since the acutely filled pericardium distends poorly. Pericardial ultrasound as part of a surgeon-performed FAST examination, through either the subxiphoid or transthoracic approach, provides excellent results in detecting pericardial fluid.128,129 The yield in identifying pericardial fluid obviously depends on the skill and experience of the ultrasonographer, body habitus of the patient, and absence of wounds that preclude visualization of the pericardium. Standard two-dimensional transthoracic echocardiograpy (TTE) or transesophageal echocardiography (TEE) to evaluate the pericardium for fluid are typically performed by cardiologists or anesthesiologists skilled at evaluating ventricular function, valvular abnormalities, and integrity of the proximal thoracic aorta. These skilled examiners are not immediately available at all hours and waiting for this test may result in inappropriate delays. In addition, while both ultrasound techniques may demonstrate the presence of fluid or characteristic findings of tamponade (large volume of pericardial fluid, right atrial collapse, poor distensibility of the right ventricle), negative tests do not exclude cardiac injury per se.161,162 Pericardiocentesis to diagnose pericardial blood and potentially relieve tamponade has a long history in the evaluation of the trauma patient. Its inability to evacuate clotted blood and potential to produce cardiac injury make it a poor alternative. Diagnostic pericardial window represents the most direct method to determine the presence of blood within the pericardium (see Chapter 26). It can be performed through either the subxiphoid or transdiaphragmatic approach.163,164 Some authors report performing this technique using local infiltrative anesthesia. However, the ability to achieve satisfactory safety and visualization in the trauma victim who may be intoxicated, in pain, or anxious from hypoperfusion usually mandates the use of general anesthesia. Once the pericardium is opened and tamponade relieved, hemodynamics will usually improve dramatically and formal pericardial exploration can be performed. Exposure of the heart can be achieved by extending the incision to a formal sternotomy, performing a left anterolateral thoracotomy, or performing bilateral anterior thoracotomies (“clamshell”) as reviewed in Chapters 14 and 24.
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Some authors consider traumatic shock a separate clinical entity.63 Traumatic shock is used to define a combination of several insults after injury that, alone, may be insufficient to induce shock, but produce profound hypoperfusion when combined. Hypoperfusion from relatively modest loss of volume can be magnified by the proinflammatory activation that occurs following direct-injury or shock-induced tissue damage. The systemic response after trauma, combining the effects of soft tissue injury, long bone fractures, and blood loss, is clearly a different physiologic insult than simple hemorrhagic shock alone. In addition to ischemia or ischemia/reperfusion, simple hemorrhage alone can induce qualitatively proinflammatory activation and cause many of the cellular changes typically attributed previously only to septic shock.9,28,32 Examples of traumatic shock include small-volume hemorrhage accompanied by significant injury to tissue (femur fracture, crush injury) or combination of hypovolemic with neurogenic, cardiogenic, or obstructive shock that induces rapidly progressive activation of proinflammatory innate immunity and potential diffuse tissue and organ bystander injury. As a consequence, MODS/MOF, including ARDS, develops relatively often in the blunt trauma patient, but rarely after pure hemorrhagic shock alone. The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that occurs following the induction of shock and the release of “danger” stimuli following tissue damage.
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At a cellular level, the pathophysiology of traumatic shock may be attributable to the release of cellular products termed damage-associated molecular patterns (DAMPs, eg, mitochondrial DNA, ribonucleic acid, uric acid, and high mobility group box 1, HMGB1) that activate the same set of cell surface receptors as bacterial products, initiating similar cell signaling.8,9 The receptors are termed pattern recognition receptors (PRPs) and include the toll-like receptor (TLR) family of proteins. In laboratory models of traumatic shock, the addition of a soft tissue or long bone injury to the hemorrhage produces lethality with significantly less blood loss than when the animals are stressed by hemorrhage alone.
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Therapy for this form of shock is focused on correction of the individual elements to diminish the cascade of proinflammatory activation contributing to its progression. Therapeutic maneuvers include prompt control of hemorrhage, adequate volume resuscitation to correct oxygen debt, early debridement of nonviable tissue (including amputation as necessary), stabilization of bony injuries, and appropriate treatment of soft tissue wounds.