CHAPTER 74

Shock

Kelly D. Young, MD, MS, FAAP

Shock is defined as a state of circulatory dysfunction resulting in insufficient delivery of oxygen and other metabolic substrates to the tissues. Shock is not a disease but rather an abnormal physiologic state that may result from many disease processes. Early recognition and prompt management of shock are critical to avoid permanent end-organ damage or death.

Epidemiology

The most common type of shock in children worldwide is hypovolemic shock, and the most common causes are dehydration resulting from gastrointestinal infections that cause vomiting and diarrhea, and hemorrhage resulting from traumatic injury. Epidemiology may differ in tertiary care health care systems in developed countries, however. In a case series of 147 pediatric patients with shock (excluding trauma patients) from Children’s Hospital of Nevada at UMC, septic shock was the most common etiology, with 57% of patients presenting with that type. Of the remaining patients, 24% had hypovolemic shock, 14% had distributive shock, and 5% had cardiogenic shock. Shock may occur in any age group, but it is more difficult to recognize the early stages in young children because early clinical signs of shock in children are subjective and may be attributed to other causes. By the time young children have developed more typical signs, such as a thready pulse and hypotension, they are in the late stages of shock.

Clinical Presentation

Early signs of shock include tachycardia; cool, clammy, pale, or mottled skin; and delayed capillary refill time. The patient may have a history of decreased urine output. In this early compensated stage, perfusion to vital organs, such as the brain and heart, is maintained by compensatory physiologic processes. As the shock state progresses it becomes uncompensated, resulting in impairment of vital organ perfusion. Signs of uncompensated shock include hypotension; altered mental status (eg, irritability, lethargy, decreased interactivity); weak, thready, or absent pulses (although pulses may be bounding in “warm” septic shock); and severely mottled or cyanotic skin (Box 74.1). In the Nevada epidemiologic study, young children commonly presented with poor extremity perfusion and poor pulses, whereas adolescents presented with hypotension. Irreversible shock occurs when multiple organs fail and death occurs.

Pathophysiology

Shock occurs when oxygen delivery to tissues is impaired. Adequate oxygen delivery depends on sufficient blood oxygen content and adequate circulatory blood flow (Figure 74.1). The oxygen content in blood depends primarily on the concentration of hemoglobin and the amount of oxygen bound to hemoglobin. In children, oxygen consumption by end organs depends most on oxygen delivery, whereas in adults it depends on oxygen extraction by the tissues.

Blood flow, or cardiac output, is determined by heart rate and stroke volume. Stroke volume depends on preload, contractility, and afterload. Preload refers to the amount of blood entering the heart from the systemic vasculature. Increasing preload, for example, via administration of intravenous (IV) fluid boluses, will increase cardiac output until a point of optimal heart muscle fiber length is reached. The Starling curve demonstrates that increased stretching of a muscle fiber results in improved performance of that muscle fiber (ie, improved stroke volume and cardiac output); however, after the point of optimal stretching is reached, performance declines (Figure 74.2).

Contractility, or inotropy, is the intrinsic ability of the heart to contract and pump blood to the body. Afterload refers to the systemic vascular resistance impeding ejection of blood from the ventricles. Optimal cardiac output depends on sufficient preload, unimpaired cardiac contractility, and the ability of the heart to overcome any afterload. During states of decreased cardiac output resulting in decreased tissue perfusion, adults compensate primarily by decreasing systemic vascular resistance, increasing cardiac contractility, and increasing heart rate, whereas children compensate primarily by increasing their heart rate and by vasoconstriction (to preferentially redistribute blood to essential organs, such as the heart and brain). The vasoconstriction in children may make hypotension a late sign of shock. Irreversible septic shock in adults is often caused by vaso-motor collapse, whereas in children cardiac failure plays a larger role in this type of shock.

Figure 74.1. Pathophysiology of shock. Factors affecting oxygen delivery to tissue.

Figure 74.2. Starling curve of cardiac output. As muscle fiber length increases (A), performance increases. After muscle fiber reaches its optimal length (B), performance declines.

Differential Diagnosis

The several types of shock differ based on the underlying pathophysiology (Table 74.1). Hypovolemic shock is the most common type occurring in children and usually results from dehydration or traumatic hemorrhage. Hypovolemia results in inadequate preload, which leads to impaired cardiac output and impaired perfusion. Other causes of hypovolemic shock include dehydration caused by osmotic diuresis in diabetic ketoacidosis and third spacing of fluids (ie, shifting from intravascular to extravascular sites) from peritonitis and burns. Nontraumatic hemorrhage may occur from entities such as epistaxis, gastrointestinal bleeding, and vessel fistula formation.

Distributive shock is a relative hypovolemia; vasodilation results in inadequate circulating blood volume relative to the vasodilation (ie, the “tank” has been made larger by vasodilation, resulting in insufficient fluid to fill the tank). Causes include anaphylaxis and sepsis, which result in the release of vasoactive mediators that cause vasodilation. Spinal cord injury, which can result in neurogenic shock, may result in loss of sympathetic nerve-mediated vascular tone and subsequent vasodilation. Certain ingestions, such as iron, barbiturates, and tricyclic antidepressants, can cause vasodilation and distributive shock.

Cardiogenic shock is an uncommon but important cause of shock in children. Congestive heart failure caused by a congenital heart lesion, myocarditis, or cardiomyopathy results in impaired cardiac contractility and decreased cardiac output. Tachydysrhythmias, such as supraventricular tachycardia, may also result in cardiogenic shock because they do not allow sufficient time for the ventricles to fill with blood, resulting in decreased stroke volume.

Rare causes of shock in pediatric patients include obstructive and dissociative types. In obstructive shock, cardiac output to the systemic circulation is obstructed as the result of pulmonary embolus, cardiac tamponade, or tension pneumothorax. Closure of the ductus arteriosus in a neonate with a ductal-dependent congenital heart lesion is another cause of insufficient cardiac output and obstructive shock. In dissociative shock, abnormal hemoglobin (eg, methemoglobin), or carboxyhemoglobin caused by carbon monoxide poisoning results in decreased oxygen bound to hemoglobin and decreased oxygen delivered to tissues.

Septic shock combines elements of distributive, hypovolemic, and cardiogenic shock. Vasoactive mediators cause decreased systemic vascular resistance and relative hypovolemia. Third spacing of fluid results in a true intravascular hypovolemia as well. Additionally, mediators of sepsis cause impaired cardiac function.

Because shock is a physiologic state resulting from a variety of etiologies and because it is recognized through clinical findings, it is important to interpret individual findings in the context of the patient as a whole. Heart rate may be elevated for many reasons, including fear, anxiety, and fever. Capillary refill may appear delayed in the extremities of a child who is cold. Blood pressure may appear artificially low when too large a cuff is used to measure it. The health professional must consider whether the child’s history is consistent with risk for shock and whether the physical examination as a whole supports the diagnosis.

Evaluation

Early recognition and prompt treatment of shock is the goal. A rapid, focused history and physical examination should be performed to identify patients in shock, and early therapy should be instituted before taking the time to perform a more complete evaluation. Recognition of shock depends on history and physical examination alone; therapy should never be withheld while awaiting results of diagnostic tests.

History

A history of vomiting with or without diarrhea, decreased oral intake, and decreased urine output, especially in infants, should alert the physician to possible hypovolemic shock. Children presenting with major trauma should be evaluated for hemorrhagic shock. A history of fever, lethargy, or irritability, and sometimes a rash, may point toward septic shock. Patients with asplenia, sickle cell disease, or indwelling catheters and those who are immunocompromised (eg, young infants or children on chemotherapy) are at increased risk for sepsis. Children in cardiogenic shock may have a history of a murmur, poor feeding, sweating with feeds, cyanosis, tachypnea, or dyspnea, and the older child may have a history of palpitations.

Physical Examination

A brief physical examination to identify shock focuses on mental status, vital signs, pulses, and skin signs. Impaired level of consciousness, such as lethargy or lack of recognition of parents, occurs later in shock. Earlier in the process, children are anxious, fussy, or irritable. Tachycardia occurs early in shock but must be interpreted in the context of other signs of shock, because tachycardia also may result from fever, pain, or fear of the examination process. Bradycardia is a late, ominous sign in shock and often results from hypoxemia. Hypotension is also a late sign in pediatric shock. It is important to remember that normal values for heart rate and blood pressure vary by age. The lower limit of acceptable systolic blood pressure in a neonate from birth to 1 month is 60 mm Hg and in an infant from 1 month to 1 year is 70 mm Hg. For a child 1 year or older, the lower limit can be estimated using the formula 70 + (2 × age in years) mm Hg; the lower limit is 90 mm Hg for children 10 years or older. Systolic blood pressures lower than these guidelines represent hypotension and late uncompensated shock. Heart rate and blood pressure values requiring immediate attention are shown in Table 74.2.

Presence and quality of pulses should be checked. Weak, thready, or absent peripheral pulses are indicative of shock. However, in warm septic shock, pulses may be bounding. Skin color, moisture, and temperature give valuable clues to diagnosis. Children in shock may have pale, cyanotic, or mottled skin. Early in shock, however, skin color may be normal. Some infants may also have mottled skin normally. As with tachycardia, isolated signs must be correlated with the bigger clinical picture to diagnose shock. Decreased perfusion in shock results in cool and clammy skin. This is often best initially appreciated in the hands and feet.

Abbreviation: bpm, beats per minute.

Capillary refill is tested by compressing the capillary bed of a fingertip, palm, or dorsal foot with gentle pressure until it blanches. On release, color should return in 2 seconds or less; a capillary refill time of 3 seconds or more is abnormal and indicative of shock. Children in warm septic shock may display “flash” (ie, shortened) capillary refill time. Capillary refill should be tested with the extremity elevated above the heart so that arterial, not venous, perfusion is tested. Additionally, cool ambient temperatures can falsely delay capillary refill times.

In hypovolemic shock caused by dehydration, the patient should be assessed for signs of dehydration, such as dry mucous membranes, lack of tears, sunken eyes, sunken anterior fontanelle in infants, and poor skin turgor. Often, the degree of dehydration can be estimated clinically (see Chapter 80). Patients with hemorrhage, whether traumatic or nontraumatic, must be examined thoroughly to locate the source of hemorrhage.

Children with congestive heart failure and cardiogenic shock may demonstrate dyspnea on exertion, tachypnea, orthop-nea, rales, hepatomegaly, gallop rhythm, and a heart murmur; these physical examination signs may be difficult to appreciate in a tachycardic, fussy, ill child. Jugular venous distention and peripheral edema are appreciated less often in children compared with adults. Other signs may include hepatomegaly and/ or cardiomegaly on chest radiography as well as a differential in pulses, blood pressure, or pulse oximetry between upper and lower extremities.

Ductal-dependent cardiogenic shock should be suspected in the newborn who presents with shock and/or severe cyanosis unresponsive to oxygen therapy in the first few weeks after birth. Cardiac tamponade is suspected in the patient with muffled or decreased heart tones, paradoxical pulse (ie, decrease in systolic blood pressure >10 mm Hg during inspiration), and distended neck veins. Tension pneumothorax is suspected in patients with deviated trachea (ie, away from the affected side), decreased breath sounds and hyperresonance to percussion on the affected side, and distended neck veins. Pulmonary embolism is rare in pediatric patients, and the signs are subtle. It is mainly suspected in the presence of predisposing factors.

Approximately 20% of children with septic shock present with the classic adult form of warm shock, including increased cardiac output, hypotension, decreased systemic vascular resistance, warm non-mottled skin, bounding pulses, and flash capillary refill. Because children compensate for shock with vasoconstriction, they are more likely than adults to present with cold septic shock, including decreased cardiac output; increased systemic vascular resistance; normal blood pressure to hypotension; cool, clammy, or mottled skin; thready pulses; and delayed capillary refill. The remaining 20% of children with septic shock present with both decreased cardiac output and decreased systemic vascular resistance. Petechiae or purpura are suggestive of meningococcemia as the etiology of septic shock. A sunburn-like rash may occur in patients with toxic shock syndrome caused by streptococcus or staphylococcus.

Laboratory Tests

The suspected cause of shock dictates which laboratory tests are performed. In hypovolemic shock secondary to dehydration, a chemistry panel should be obtained for electrolyte abnormalities and acidosis. Serial hematocrit determinations and a type and crossmatch are important studies in traumatic and nontraumatic hemorrhage, whether known or suspected. In septic shock, a complete blood cell count and blood cultures should be obtained, as well as cultures of other potential sources of infection (eg, urine, cerebrospinal fluid, wound, indwelling venous access line). Results of coagulation studies, including panels to evaluate for disseminated intravascular coagulopathy, and results of electrolyte studies, including calcium and magnesium levels, are frequently abnormal in sepsis. Hypoglycemia is a common finding in any type of shock, and a rapid bedside glucose determination should be performed for all critically ill pediatric patients. Arterial blood gases can demonstrate adequacy of oxygenation and degree of acidosis and are necessary to diagnose elevated carboxyhemoglobin and methemoglobin levels. Initial lactate levels, particularly in patients with septic shock and in trauma patients, may be correlated with overall prognosis and can be followed serially to chart progress. Procalcitonin is another increasingly popular biomarker followed in suspected sepsis. Troponins may be useful in determining severity of disease and following patients with cardiogenic shock. D-dimer assay is useful in patients with suspected pulmonary embolism.

Other Studies

Chest radiography, electrocardiography, and echocardiography may be obtained for patients with cardiogenic or ductal-dependent obstructive shock to further elucidate the specific etiology. Workup of stabilized trauma patients may include bedside ultrasonography, radiography, or computed tomography. Imaging studies contribute to the diagnoses of cardiac tamponade, tension pneumothorax, and pulmonary embolism. Invasive monitoring with arterial lines for systemic arterial blood pressure and central venous lines for central venous pressure or pulmonary artery wedge pressure may be helpful in the ongoing management of shock, particularly fluid-resistant shock.

Management

The first management priority in the treatment of any critically ill child is attention to airway patency and ventilation. For the patient with significant respiratory compromise, bag-and-mask ventilation followed by endotracheal intubation is performed. Usually, however, patients in compensated shock do not require initial advanced airway management. Instead, the immediate priorities are administration of oxygen and initiation of cardiorespiratory monitoring. Oxygen by mask or nasal cannula, preferably heated and humidified, should be administered immediately. Elective rather than emergent endotracheal intubation should be considered to reduce metabolic demands caused by increased work of breathing. When intubating and sedating patients in shock, sedative agents with fewer hemodynamic effects, such as ketamine or fentanyl, are preferred over those that may contribute to hypotension, such as other opiates, benzodiazepines, and propofol. Etomidate, however, although its effects are hemodynamically neutral, is not recommended in septic shock because of its cortisol suppressive effect. Mechanical ventilation settings should emphasize a lung-protective approach.

Almost concurrently, the next priority is achieving intravascular access and, in most cases, administering fluids. Peripheral IV access should be attempted. If this is unsuccessful after 3 attempts or 90 seconds, an intraosseous line may be placed or IV access may be obtained by placement of a central venous catheter or by cut-down technique. Ultrasound-guided vascular access is another option. Intraosseous lines have been demonstrated to provide much more rapid vascular access compared with central line placement. Umbilical venous lines can sometimes be placed in neonates within the first 1 to 2 weeks after birth. More than 1 intravascular line is usually needed for managing patients in shock.

Decreased preload and hypovolemia (actual or relative) are present in the most common causes of pediatric shock. Cardiogenic shock is the only form of shock that may not benefit from increasing preload via a fluid bolus. For other forms of shock, an initial fluid bolus of 20 mL/kg isotonic crystalloid fluid (maximum 1 L), such as normal saline or lactated Ringer solution, should be rapidly infused over 5 to 10 minutes; this may require manually pushing the fluid using a large syringe or a pressure bag. Fluid boluses can be hand pushed into an intraosseous line. Colloid fluid (eg, albumin) theoretically has the advantage of remaining intravascular a longer period of time than normal saline, but this has not been proved to result in a measurable benefit. Crystalloid fluid is recommended for initial boluses because it is less expensive and more readily available than colloid fluid. If a patient with traumatic hemorrhage remains hemodynamically unstable after 2 crystalloid fluid boluses, packed red blood cells at 10 mL/kg may be required. The patient should be assessed for improvement in mentation, vital signs, peripheral pulses, and skin signs after each fluid bolus. Repeat fluid boluses of 20 mL/kg (1 L) to a total of 80 mL/kg (4 L) or more may be necessary to restore intravascular volume. Patients should be reassessed after each bolus before ordering another bolus. Development of hepatomegaly or rales may indicate fluid overload and the need to begin other therapies, such as vasoactive infusions. This is particularly true for cardiogenic and septic shock.

A well-designed and executed trial performed in Africa, the Fluid Expansion as Supportive Therapy (FEAST) trial, has called into question aggressive fluid resuscitation in patients with septic shock. Although patients randomized to rapid fluid therapy showed earlier improvement in circulatory parameters, their mortality was consistently higher. It has been suggested that the results of this trial may not be generalizable to patients in developed countries because of differences in malaria infection, nutritional status, and other factors. The authors suggest that aggressive fluid therapy is particularly associated with increased mortality in highly acidotic patients, especially in developing countries in which inotropic support and mechanical ventilation may not be available. Currently, expert guidelines still recommend early aggressive fluid therapy for septic shock in developed countries in which inotropes and mechanical ventilation are available.

The mnemonic SHOCKED (sound the alarm, help hypovolemia, optimize oxygenation, constrict and contract, keep in mind underlying causes, electrolytes and glucose normalized, decrease metabolic demand) may be used to recall overall management (Box 74.2). Further management in addition to fluids is dependent on the specific etiology. Patients in septic shock should receive empiric broad-spectrum antibiotic coverage within the first hour after presentation. Patients with toxic shock syndrome should receive antibiotics, including clindamycin. A surgeon must assist in identifying the source of hemorrhage and controlling the bleeding in patients with traumatic hemorrhage and may be required for management of nontraumatic hemorrhage as well depending on the specific etiology. Blood transfusions may be required. Spinal cord injury is treated with supportive care in consultation with a neurosurgeon. Anaphylactic shock is treated with IV epinephrine, IV diphenhydramine, antihistamine H₂ receptor blockers, glucocorticoids, and nebulized albuterol. Pericardial tamponade is relieved by pericardiocentesis, tension pneumothorax by needle or tube thora-costomy, and pulmonary embolus with supportive care and throm-bolytic agents. Carbon monoxide poisoning is managed with 100% oxygen and, if severe, hyperbaric oxygen therapy. Patients with methemoglobinemia appear cyanotic even while receiving 100% oxygen and may be treated with methylene blue. Supraventricular tachycardia should be managed with adenosine if the patient is hemodynamically stable and with synchronized cardioversion if the patient is unstable. Ductal-dependent obstructive shock should be treated with prostaglandin E₁ (PGE₁) infusion.

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