Shock is a clinical condition that occurs when there is inadequate delivery of oxygen and other nutrients to meet the metabolic demands of the tissues. If left untreated, shock results in irreversible cell and organ damage and death. The clinician must be able to recognize shock early, initiate therapy rapidly, and arrange safe transport of the patient to an intensive care facility. These lifesaving tasks require that the clinician have a fundamental knowledge of the causes, presentations, therapies, and complications of shock.

Physiologically, shock can be classified as compensated, when the patient is able to maintain a normal blood pressure for age, or decompensated, when deterioration has led to hypotension. In general, compensated shock progresses to decompensated shock if left untreated, which emphasizes the importance of early recognition and intervention. Children can generally maintain a normal blood pressure until advanced stages of shock; therefore hypotension (see Table 36-1 for age-based definitions of hypotension) in a pediatric patient is an ominous sign of impending circulatory collapse. When measuring blood pressure with a sphygmomanometer, it is important to select the smallest cuff that covers two-thirds of the upper arm or leg.

Shock can also be classified by cause, with the main types being hypovolemic, cardiogenic, and distributive shock, which includes septic shock. The mechanisms may differ, but inadequate tissue perfusion is the common final pathway.

HYPOVOLEMIC SHOCK

Hypovolemic shock, by far the most common type of shock in children, occurs when a decrease in intravascular volume leads to decreased venous return and subsequently, decreased preload. Decreased preload results in decreased stroke volume. An increase in heart rate often maintains cardiac output initially, but when this compensatory response is inadequate, cardiac output diminishes. The formula that defines this relationship is as follows:

Decreased cardiac output results in decreased delivery of oxygen and other substrates to the tissues. The two main categories of hypovolemic shock are hemorrhagic and non-hemorrhagic; examples are provided in Table 36-2.

In the early stage of hypovolemic shock, autoregulatory mechanisms shunt blood flow preferentially to the brain, heart, and adrenal system thus preserving blood pressure. Because flow is diverted from less critical organs, patients may present initially with cool or mottled extremities and decreased urine output. Other signs may include dry mucous membranes, absence of tears, and abnormal skin turgor.

Hemorrhagic shock due to known trauma is typically diagnosed at the initial presentation; however, hemorrhagic shock can present during hospitalization, especially in postoperative patients. Victims of child abuse are also at risk for delayed diagnosis of hemorrhagic shock because the initial history may be incomplete, inaccurate, or misleading, and symptoms may progress over time. Nonhemorrhagic shock may present in patients with ongoing fluid losses (e.g. vomiting, diarrhea, gastric suctioning, burns), especially if there is inadequate replacement.

DISTRIBUTIVE SHOCK

Distributive shock is caused by a decrease in systemic vascular resistance. Abnormalities in vasomotor tone cause peripheral pooling of blood, which leads to a diminished effective preload, decreased cardiac output, and inadequate tissue perfusion. This process can occur without frank fluid loss. Causes of distributive shock are listed in Table 36-3.

Septic Shock

Sepsis is a clinical syndrome that results from overwhelming infection creating a cascade of endogenous inflammatory mediators resulting in widespread tissue injury. Shock occurring during sepsis begins with volume maldistribution due to leaky vessels, resulting in intravascular volume depletion, decreased flow to vital organs including the heart, and ultimately metabolic derangements at the cellular level. It is important to consider septic shock early, because a seemingly stable patient with minimal findings of infection can quickly progress to sepsis. In the early (compensated) phase, often designated as “warm shock,” septic shock may present with a hyperdynamic state including decreased vascular resistance, widened pulse pressure, increased cardiac output, tachycardia, tachypnea, warm extremities, and normal urine output. As it progresses to the decompensated phase, patients develop intravascular volume depletion, myocardial depression, cool extremities, thready pulses, central nervous system changes, respiratory distress, and decreased cardiac output, often denoted as “cold shock.”

Although anyone can develop septic shock, risk factors include young age, chronic medical condition, presence of central intravenous (IV) catheters, immunocompromise, burns, and malnutrition. Septic shock can result from bacterial, viral, or fungal infection. It is important to note that septic shock can occur when cultures or other diagnostic tests do not yield a definitive organism. Several studies have demonstrated that an organism is recovered only 50% of the time in the pediatric population. Shock can also develop from localized bacterial infections that produce toxins; this is referred to as toxic shock. This form of shock is most commonly associated with toxin-producing strains of group A Streptococci and Staphylococcus aureus.

Other Forms of Distributive Shock

Anaphylactic shock occurs when an exogenous stimulus causes an allergic systemic immunoglobulin E–mediated response that triggers the release of histamine and other vasoactive factors from mast cells, with resulting vasodilation (see Chapter 47). Neurogenic shock may occur with spinal cord transection above the first thoracic level, with severe injuries to the brainstem or with isolated intracranial injuries. An injury to the cervical cord may result in unopposed parasympathetic tone and subsequent vasodilation. Some drugs can cause severe vasodilation, resulting in shock; these drugs include those that cause anaphylaxis and those that cause severe hypotension (e.g. β-antagonists and calcium channel antagonists).

CARDIOGENIC SHOCK

Cardiogenic shock occurs when there is decreased cardiac output caused by pump failure. The main causes are listed in Table 36-4. Excluding patients with congenital heart disease, cardiogenic shock is much less common in children than in adults because of the relatively low incidence of coronary artery disease and congestive heart failure in the pediatric population. Cardiogenic shock should be strongly considered in the following clinical scenarios: no history of fluid losses, physical examination reveals hepatomegaly or rales, chest radiograph demonstrates cardiomegaly, and when there is no clinical improvement despite oxygenation and volume expansion. Worsening symptoms, including persistent tachycardia or shortness of breath, during volume resuscitation should also heighten one’s suspicion for cardiogenic shock.

Management of cardiogenic shock should focus on correcting arrhythmias if present, improving preload and cardiac contractility, and reducing afterload. The stress on the heart can be minimized by decreasing metabolic demand including achieving normothermia, correction of anemia if present, and sedation, intubation, and mechanical ventilation if necessary.