Sepsis is defined as the presence of the systemic inflammatory response syndrome (SIRS) caused by a presumed or confirmed infection (Box 2-1). Sepsis may occur because of bacterial, viral, fungal, or parasitic infections. Septic shock is defined as sepsis and cardiovascular dysfunction. Classifying septic shock may be difficult because of the developmental variability in physiologic response to sepsis. A clinical picture consistent with hypovolemic, distributive, or cardiogenic shock may be present in a child with sepsis. Additionally, studies have demonstrated that the cardiovascular pathophysiology of children with sepsis can evolve over time, and the adjustment of hemodynamic therapy is commonly necessary.

Box 2-1

Systemic Inflammatory Response Syndrome Criteria

Must have two of the following criteria, one of which must be abnormal temperature or leukocyte count:

Core temperature of >38.5°C or <36°C

Tachycardia (mean HR >2 standard deviations above normal for age) in absence of external stimuli, chronic drugs or pain, or otherwise unexplained persistent elevation over a 0.5- to 4-hour time period or bradycardia for children younger than 12 months of age (mean HR <10th percentile for age) in the absence of external vagal stimuli, β-adrenergic blocker drugs, congenital heart disease, or otherwise unexplained persistent depression over a 0.5-hour period

Mean respiratory rate >2 standard deviations above normal for age

Leukocyte count elevated or depressed for age or >10% immature neutrophils

HR, heart rate.

Adapted from American Academy of Pediatrics and American Heart Association. Pediatric Advanced Life Support. Dallas, 2006, AHA.

Clinical Manifestations and Evaluation

Shock remains a clinical diagnosis (Figure 2-1). Early recognition of the clinical signs of shock (including familiarity with normal ranges for vital signs by age; see Chapter 1) should lead to directed management. An accurate history should be obtained from the family and, if possible, the child, simultaneously with treatment initiation.

Figure 2-1 Clinical manifestations of shock.

A history of fluid loss, as with a gastrointestinal bleed, gastroenteritis, or diabetic ketoacidosis, is consistent with hypovolemic shock. A detailed trauma history is useful because an injured child may have hypovolemic shock from hemorrhage (i.e., with blunt abdominal trauma), neurogenic shock with spinal cord injury, or obstructive shock from tension pneumothorax. A child who has had fever or is immunocompromised may have features consistent with septic shock. Exposure to an allergen, such as a food or an insect bite, could suggest distributive shock caused by anaphylaxis. A history of ingestion or medications should always be included when speaking to the family because shock may be attributable to toxin exposure. Patients with underlying heart disease may present in cardiogenic shock. Patients with a history of adrenal insufficiency (i.e., chronic steroid therapy, congenital adrenal hyperplasia, or hypopituitarism) can present with adrenal crisis and shock.

A complete physical examination should be performed, including vital signs and pulse oximetry. When a child presents in shock, it is sometimes difficult to obtain an accurate weight, which can be essential for determining fluid requirements and medication doses. If the patient’s weight cannot be measured, one may be estimated using a length-based tape system (e.g., the Broselow tape) or the child’s age.

Children in shock tend to be tachypneic, as well as tachycardic. Blood pressure should be monitored closely. Remember, children with shock may have normal blood pressures. Narrow pulse pressure may occur as a result of a compensatory increase in SVR, as in hypovolemic or cardiogenic shock. Widening of the pulse pressure can be seen as the result of decreased SVR, as can occur with distributive shock. The child’s temperature should also be measured because fever—or in young infants, hypothermia—may suggest septic shock.

When first examining an ill child, one should do a rapid assessment of mental status. Change in the level of consciousness of a child may indicate decreased cerebral oxygenation or perfusion. Signs of diminished perfusion to the brain include confusion, irritability, lethargy, and agitation.

Examining the child’s skin is another way to assess perfusion and the degree of shock. A child with normal cardiorespiratory function should have warm and pink nailbeds, mucous membranes, palms, and soles. As shock progresses and poor perfusion develops, the skin may become cool, pale, or mottled. Capillary refill, although limited by clinician variability as well as ambient temperature and the child’s body temperature, can help to evaluate children in shock. Light pressure is applied to blanch the fingernail bed. The pressure is released, and the amount of time until color returns is measured. Normal is less than 2 seconds; volume depletion or poor perfusion can increase this time to greater than 3 seconds.

The evaluation of a child with poor perfusion and shock should always include an assessment of pulses. This includes the rate, strength, and regularity of the central and peripheral pulses. In healthy children, the carotid, brachial, radial, femoral, dorsalis pedis, and posterior tibial pulses are readily palpable. A rapid pulse is a nonspecific clinical sign of distress. An irregular pulse is a warning of cardiac dysrhythmia. A weak pulse raises the concern for shock and a severe hypovolemic state. An absence of central pulses indicates ineffective or absent cardiac contractions and signifies the need for immediate resuscitative action.

After the initial evaluation of airway, breathing, and circulation (the ABCs), a complete physical examination can help elucidate the type of shock. For example, central cyanosis, a gallop rhythm, crackles on lung examination, hepatomegaly, or heart murmur may indicate an underlying cardiac condition. Children with stridor, wheeze, urticaria, or edema may have anaphylactic shock. Purpura or petechiae can be seen in children with septic shock. Bruises and abrasions can be seen with traumatic injury and may give a clue to underlying hemorrhagic shock.

Management

General Principles

Early recognition of compensated shock is critical to ensuring appropriate and expedient therapy. Initial therapy of shock is universal, regardless of the cause of the shock state, with the goals of optimizing blood oxygen content, improving cardiac output, reducing oxygen demand, and correcting metabolic abnormalities (Figure 2-2). General principles of resuscitation should be applied immediately on presentation to medical care (see Chapter 1). Ultimately, after initial management has commenced, correction of the underlying cause is essential (e.g., stopping blood loss in hemorrhagic shock, antibiotics for shock caused by bacterial infection).

Figure 2-2 Algorithm for management of pediatric septic shock.

From Brierley J, Carcillo J, Choong K, et al: 2007 American College of Critical Care Medicine clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock. Crit Care Med 37(2):666-688, 2009.

Immediate attention to the ABCs is mandatory. Maintenance of a patent airway with positioning or endotracheal intubation should be performed immediately if airway compromise is present. Hypoxemia should be corrected without delay; all patients with compromised perfusion should receive supplemental oxygen at 100% FiO₂ (fraction of inspired oxygen). Insufficient respiratory effort should be addressed with positive-pressure ventilation.

Imminently life-threatening causes of shock should be identified and corrected. For example, a child with upper airway obstruction from anaphylaxis should receive epinephrine. If a child has severe respiratory distress, asymmetric breath sounds, and poor perfusion, a tension pneumothorax might need to be decompressed.

Vascular access is indicated in all cases. If possible, large-bore intravenous (IV) catheters should be inserted in peripheral veins. If an IV line is unable to be placed promptly, intraosseous (IO) cannulation should be performed. IV fluid boluses of 20 mL/kg of isotonic saline should be given rapidly and repeated as needed with reassessment occurring simultaneously. Rapid fluid administration should be actively performed using either a pressure bag or a push–pull system rather than using passive gravity flow for administration. IV fluids should be given with care in cardiogenic shock, so as to not worsen associated pulmonary edema.

Adequate hemoglobin is essential for optimal oxygen carrying capacity. Thus, in cases of hemorrhagic shock, O-negative packed red blood cells should be rapidly administered early in the resuscitation. Even in cases of nontraumatic shock, children who have cyanotic heart disease or neonates may require less fluid and higher hematocrit percentages to ensure adequate oxygen carrying capacity. Life-threatening metabolic abnormalities should be identified and corrected early. Hypoglycemia should be treated with 0.5 to 1 g/kg of IV dextrose. Hypocalcemia (especially decreased ionized calcium) is common in septic shock and can occur as acidosis resolves; it should be corrected with either calcium gluconate or calcium chloride.

Circulatory Support

Depending on the cause, patients in shock may require large volumes of fluid as well as vasoactive medications. Clinical studies of septic shock in children have demonstrated an association between higher volumes of fluid administration and survival. Current guidelines for septic shock recommend up to and over 60 mL/kg in the first 15 to 60 minutes. Every hour that goes by without implementation of this therapy is associated with a 1.5-fold increase in mortality. A retrospective chart review of 90 children with septic shock showed that those who received less than 20 mL/kg of fluid within the first hour had a mortality rate of 73%. Early fluid resuscitation was associated with a threefold reduction in the odds of death.

Vasoactive agents help improve cardiac output through their effects on myocardial contractility, heart rate, and vascular tone. These drugs target at least three types of receptors. The β₁-receptors mediate inotropic (contractility), chronotropic (rate), and dromotropic (increased conduction velocity) activity. The β₂-receptors mediate vasodilatation and smooth muscle relaxation in blood vessels and bronchial tree. The α-receptors mediate arteriole constriction systemically and bronchial muscle constriction. The dopaminergic receptors mediate smooth muscle relaxation and increase renal blood flow and sodium excretion.

Table 2-1 outlines commonly used vasoactive agents, their targeted receptors, and their hemodynamic effects. Data are varied on the choice of initial agent; current recommendations from the American College of Critical Care Medicine state that dopamine, epinephrine, or norepinephrine may be appropriate first-line therapy for septic shock, provided they are administered through a central venous catheter. Dopamine or low-dose epinephrine may be given via a peripheral vein while central venous access is obtained.

Table 2-1 Vasoactive Medications