We greatly appreciate the author of the fourth edition chapter Jonathan K. Marr, MD. This fifth edition chapter is an update of his previous chapter.

Shock is a manifestation of inadequate oxygen and substrate delivery to cells relative to metabolic demand. Oxygen delivery depends on multiple variables and includes heart rate, preload, contractility, afterload, hemoglobin content, oxygen saturation, and dissolved oxygen in the blood (Fig. 20-1). Disease processes create alterations in the above variables and the body has developed compensatory mechanisms to adjust. When the ability to adjust is exceeded, there is progression to impairment of organ function, irreversible organ failure, and death.

Children differ from adults with respect to their anatomy and physiology. In infants, cardiac output is dependent on heart rate since stroke volume is relatively fixed. In contrast, insufficient cardiac output is often due to low stroke volume. Maintaining oxygen delivery to tissues activates compensatory mechanisms. The first line of defense in maintaining cardiac output is tachycardia and this is often the first subtle sign of shock.¹ Common reasons for tachycardia in the emergency department other than shock include fever, pain, anxiety, hypoxia, and medications (e.g., albuterol).

The next compensatory mechanism is the redirection of blood from nonvital to vital organs through increasing systemic vascular resistance (SVR). Blood is shunted away from the skin, gut, kidneys, and muscle, and is clinically reflected by cool extremities, delayed capillary refill, and decreased urine output. Mechanisms such as increase in contractility and increasing smooth muscle tone to move blood from the venous system to the heart are other ways to augment increases in cardiac output.

Variation in these compensatory mechanisms is observed in the distinct presentations of shock when comparing adults and children. The majority of adults present in shock with evidence of low systemic vascular tone and normal or increased cardiac output with tachycardia, described as “warm shock”; whereas almost half of children presenting in shock have evidence of low cardiac output and elevated SVR with cool extremities, described as “cold shock.”²

The physiologic fight-or-flight response to stress involves central and sympathetic nervous system activation. Catecholamines increase cardiac output by increasing heart rate and stroke volume, and the result is an increase in blood pressure. Glucagon is also released to provide glucose via glycogenolysis and gluconeogenesis.

In contrast, the shock response results from decreased oxygen and substrate delivery. The levels of cortisol and catecholamines are 5 to 10 times higher in the shock state compared with the stress response.³ Intravascular volume is preserved and oliguria results. Supraphysiologic levels of cortisol and catecholamines with glucagon cause hyperglycemia. Ironically, hyperglycemia in sepsis is considered potentially harmful, as research suggests that it impairs neutrophil function,^4,5 acts as a procoagulant, induces cellular apoptosis, increases risk of infection, and impairs wound healing.

Shock can be subcategorized into compensated and hypotensive (decompensated) shock. Presence of inadequate perfusion with normal systolic blood pressure maintained by compensatory mechanisms delineates compensated shock. Signs of inadequate perfusion include tachycardia, delayed capillary refill, cool pale skin, and weak pulses. Once the body is unable to physiologically maintain normal systolic blood pressure, hypotension results and heralds impending cardiac arrest. The transition from compensated to hypotensive shock progresses along a physiologic continuum. Deterioration in mental status is a clinical observation that is indicative of compromised perfusion to the brain.

Shock can be subdivided into four general categories: hypovolemic, distributive, cardiogenic, and obstructive (Table 20-1). These categories of shock have pathophysiologic etiologies related to components of stroke volume (preload), contractility (cardiogenic), and afterload (obstructive). Preload is the volume of blood present in the ventricle before contraction and is estimated by the central venous pressure (CVP). Total blood volume in a newborn is estimated at 85 mL/kg, whereas in infants it is estimated to be 65 mL/kg.² Distribution of blood in the arteries, veins, and capillaries is estimated to be 8%, 70%, and 12%, respectively.³ Contractility is defined as the strength of the contraction. Afterload is the resistance through which the ventricle is pumping. Together, these components affect the stroke volume (the volume of blood ejected by the heart with each beat).

Hypovolemia is the most common cause of shock in children worldwide.¹ Fluid losses due to diarrhea and electrolyte abnormalities are a major cause of infant mortality in third world countries. Other causes of hypovolemic shock include acute hemorrhage following trauma, burns, and osmotic diuresis from diabetic ketoacidosis.

Volume depletion results in reduced preload and stroke volume with compensatory tachycardia. In acute hemorrhage from trauma, the reduction volume is compounded with the concomitant reduction in hemoglobin. Decreased cardiac output and oxygen content synergistically reduce oxygen delivery. Compensatory mechanisms such as catecholamines increase heart rate, contractility, and systemic vascular resistance, whereas the neuroendocrine system facilitates retention of sodium and water. Failure to correct volume depletion and oxygen-carrying capacity will progress to organ dysfunction, circulatory failure, and death.

Distributive shock is characterized by inappropriate distribution of blood volume causing inadequate organ and tissue perfusion. The three types of distributive shock include septic shock, anaphylactic shock, and neurogenic shock. All three have common features that include problems with vascular tone and integrity in the venous, capillary, or arterial vessels. The high cardiac output in distributive shock is unique, as the other forms of shock all have low cardiac outputs.¹

An international consensus definition of sepsis is “a life-threatening organ dysfunction caused by a dysregulated host response to infection.” Severe sepsis was previously used as a classification to define sepsis with sepsis-induced organ dysfunction or tissue hypoperfusion (i.e., hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia, or obtundation); however the new guidelines no longer use this term. Septic shock is defined as “a subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality,”⁶ with one study finding septic shock as the etiology for more than half of pediatric patients presenting in shock to a pediatric emergency department.⁷

Sepsis is the culmination of complex interactions between infection organisms and host immune, inflammatory, and coagulation responses. Existing research suggests that although early sepsis may be characterized by increases in proinflammatory mediators, as sepsis persists, there is a shift toward an anti-inflammatory immunosuppressive state.^4,8

Table 20-2 provides a summary of Pediatric Considerations in Sepsis.

Neurogenic shock is often due to acute spinal cord injury with resultant disruption of sympathetic control of blood vessels and the heart. Commonly caused by cervical trauma, injuries to the thoracic spine above T6 can result in failure of sympathetic tone and subsequent neurogenic shock leading to decreased peripheral resistance, hypotension, bradycardia, and decreased cardiac output.⁹

Anaphylaxis is a type I hypersensitivity reaction¹⁰ leading to the release of mediators that cause increased vascular permeability, bronchospasm, and vasodilation.¹ Most common causes of anaphylaxis in children are foods (peanuts, tree nuts, shellfish, fish, milk, and eggs),¹¹ medications, Hymenoptera (wasps, bees, and ants) envenomations, blood products, latex, vaccines, and radiographic contrast media.¹⁰ The diagnosis depends on involvement of two organ systems, but may present as an acute cardiac or respiratory event or with hypotension as the only manifestation. Target organs involved include skin (80%–90% of episodes), respiratory tract (70% of episodes), gastrointestinal tract (30%–45% of episodes), heart and vascular (10%–45% of episodes), and CNS (10%–15% of episodes).¹¹