Version May 2024
INTRODUCTION — This topic will review the pathophysiologic determinants and classification of shock.
The initial evaluation and management of shock in children, in general, and hypovolemic and septic shock, specifically, are discussed separately. (See "Initial evaluation of shock in children" and "Shock in children in resource-abundant settings: Initial management" and "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management" and "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)
DEFINITION — Shock is a pathophysiologic state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery. Although the effects of inadequate tissue perfusion are initially reversible, prolonged oxygen deprivation leads to generalized cellular hypoxia and derangement of critical biochemical processes, including [1]:
●Cell membrane ion pump dysfunction
●Intracellular edema
●Leakage of intracellular contents into the extracellular space
●Inadequate regulation of intracellular pH
These abnormalities rapidly become irreversible and result sequentially in cell death, end-organ damage, failure of multiple organ systems, and death [1-3]. Mortality from shock is less among children than adults. Mortality in both children and adults has been decreasing, although incidence has been increasing. For children with severe sepsis, mortality is <10 percent [4-6]. Nevertheless, outcomes for children with shock (in terms of morbidity and cost) are significant. Furthermore, unique physiologic responses to poor perfusion among children make it a challenge for clinicians to recognize shock early (before hypotension develops), when responses to treatment are more favorable. (See "Initial evaluation of shock in children", section on 'Evaluation'.)
PHYSIOLOGY — Parameters that determine adequate oxygen delivery to tissues include blood flow to tissues (cardiac output), the regional balance between blood flow and metabolic demand, and the oxygen content of blood (hemoglobin concentration and percentage of hemoglobin saturated with oxygen) [3]. Physiologic variables that the body can manipulate to compensate for compromised perfusion include:
●Cardiac output (volume of blood flow per unit of time) is the product of stroke volume times heart rate. Hence, tachycardia is a common sign of decreased perfusion and early shock. Infants have relatively fixed stroke volumes and are particularly dependent upon heart rate to increase cardiac output.
●Stroke volume is determined by preload, cardiac contractility, and afterload. Compensatory mechanisms that improve stroke volume include increased venous smooth muscle tone (improves preload by shunting blood to the heart) and increased cardiac contractility (resulting in more complete emptying of the ventricles).
●Increased systemic vascular resistance (vasoconstriction) maintains perfusion pressure (measured as blood pressure) despite decreased cardiac output. In addition, blood is shunted away from peripheral structures (including skin, muscle, kidneys, and splanchnic organs) to the heart and central nervous system. As a result, children with compensated shock typically have normal blood pressures, despite signs of poor perfusion (such as decreased peripheral pulses and tachycardia). (See "Initial evaluation of shock in children", section on 'Evaluation'.)
While decreased perfusion directly reflects decreased cardiac output, the increased cardiac output observed in hyperdynamic shock states also is associated with decreased effective tissue perfusion [7]. This decreased effective perfusion derives from a complex interaction of numerous humoral and microcirculatory processes resulting in patchy, uneven local regional blood flow and a derangement of cellular metabolic processes [8].
STAGES OF SHOCK — The shock syndrome is characterized by a continuum of physiologic stages beginning with an initial inciting event that causes a systemic disturbance in tissue perfusion. Subsequently, shock may progress through three stages if not successfully treated, culminating in end-organ damage, irreversible shock, and death [2].
Compensated shock — During compensated shock, the body's homeostatic mechanisms rapidly compensate for diminished perfusion and systolic blood pressure is maintained within the normal range [3]. Heart rate is initially increased. Signs of peripheral vasoconstriction (such as cool skin, decreased peripheral pulses, and oliguria) can be noted as perfusion becomes further compromised.
Hypotensive shock — During this stage, compensatory mechanisms are overwhelmed. Signs and symptoms of organ dysfunction (such as altered mental status as the result of poor brain perfusion) appear. Systolic blood pressure falls, although children who have lost as much as 30 to 35 percent of circulating blood volume can typically maintain normal systolic blood pressures [3,9]. Once hypotension develops, the child's condition usually deteriorates rapidly to cardiovascular collapse and cardiac arrest.
Although hypotension is generally a late finding among children with shock, those with early distributive shock (as with sepsis) may have hypotension because of decreased systemic vascular resistance (SVR). Vital organ perfusion is initially maintained by increased cardiac output.
Irreversible shock — During this stage, progressive end-organ dysfunction leads to irreversible organ damage and death. At this stage in the outcomes are poor, despite resuscitative efforts.
CLASSIFICATION — Four broad mechanisms of shock are recognized: hypovolemic, distributive, cardiogenic, and obstructive. Each type is characterized by one primary physiologic derangement (table 1).
For any given condition that can cause shock, the classification may be mixed. Patients with distributive shock, in particular, often have multiple physiologic abnormalities. As an example, children with distributive shock from sepsis may also have volume loss (from vomiting, diarrhea, poor intake, or increased insensible fluid loss from tachypnea and fever) and myocardial depression from the effect of inflammatory mediators released in response to infection [3].
Hypovolemic shock — Hypovolemic shock is the most common type of shock encountered in children. It results from decreased preload from extravascular fluid loss (such as with diarrhea or osmotic diuresis) or intravascular fluid loss (as with capillary leak or hemorrhage). Because preload is one of the determinants of stroke volume, cardiac output falls when preload drops. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)
Distributive shock — Distributive or vasodilatory shock results from a decrease in systemic vascular resistance, with abnormal distribution of blood flow within the microcirculation and inadequate tissue perfusion. It can lead to functional hypovolemia with decreased preload [2,3,7]. Distributive shock generally is associated with a normal or increased cardiac output.
Causes of distributive shock include:
●Sepsis is the most common etiology of distributive shock among children. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)
●Anaphylaxis is an immediate, potentially life-threatening systemic reaction to an exogenous stimulus, typically an allergic, IgE-mediated immediate hypersensitivity reaction. Anaphylactoid responses are clinically indistinguishable reactions that occur by nonantigen/antibody-mediated mechanisms. (See "Anaphylaxis: Emergency treatment".)
●Neurogenic shock is a rare, usually transient disorder that follows acute injury to the spinal cord or central nervous system, resulting in loss of sympathetic venous tone.
Cardiogenic shock — Cardiogenic shock results from pump failure, manifested physiologically as decreased systolic function and depressed cardiac output [10,11]. Cardiogenic shock is uncommon among children (table 2), as compared with adults, among whom ischemic heart disease is the major cause.
Cardiac causes may result from inadequate contractility or excessively fast or slow rhythms:
●Cardiomyopathies – Primary myocardial injury is an uncommon cause of shock in children. Causes of myopathic pump failure include familial, infectious, infiltrative, and idiopathic cardiomyopathies. Prolonged ischemia, cardiopulmonary bypass, and the myocardial depression of late sepsis all can contribute to secondary myocardial dysfunction.
●Arrhythmias – Structural heart disease, drug intoxications, and hypothermia are leading causes of arrhythmia in children. Both atrial and ventricular arrhythmias can cause cardiogenic shock.
•Ventricular fibrillation and pulseless ventricular tachycardia abolish cardiac output, while diminished ventricular filling time during ventricular tachycardia decreases preload and stroke volume substantially. (See "Management and evaluation of wide QRS complex tachycardia in children".)
•Prolonged unrecognized supraventricular tachycardia (as can occur with the initial presentation for infants) can decrease cardiac output. (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children".)
•Bradyarrhythmias and complete heart block can result in shock caused by chronotropic (heart rate) insufficiency, independent of stroke volume. (See "Bradycardia in children".)
Obstructive shock — Obstructive shock and impaired cardiac output result when blood flow is physically obstructed. Acquired causes of obstructive shock include cardiac tamponade, tension pneumothorax and massive pulmonary embolism. Infants with ductal-dependent congenital heart lesions, such as coarctation of the aorta and hypoplastic left ventricle syndrome, may present in shock when the ductus arteriosus closes during the first few weeks of life [12]. (See "Approach to the ill-appearing infant (younger than 90 days of age)", section on 'Initial stabilization'.)
COMMON FEATURES — The clinical presentation of shock is variable, but several features are common. These include tachycardia and signs of compromised organ perfusion (skin, brain, and kidneys). Children often present before hypotension develops. (See "Initial evaluation of shock in children".)
●Tachycardia – Tachycardia is typical. Although tachycardia is an important early indicator of shock, it is a nonspecific finding. Many common conditions in children such as fever, pain, and anxiety can cause tachycardia without circulatory compromise. A normal heart rate with signs of compensated shock can occur with spinal cord injury and bradycardia can occur as the result of hypoxia, some ingestions (such as beta blockers and calcium channel blockers), or as an agonal event for patients with shock from any cause (table 3).
●Skin changes – In many shock states, regulatory processes compensate for decreased effective tissue perfusion. Potent vasoconstrictive mechanisms redirect blood from the peripheral, splanchnic, and renal vessels to maintain coronary and cerebral perfusion. As a result, the skin is typically cool, clammy, pale, or mottled.
Notable exceptions are the flushed, hyperemic skin of early distributive shock and the peripheral vasodilation of terminal shock states associated with failure of mechanisms that maintain increased peripheral vascular resistance (irreversible shock).
●Impaired mental status – Children with impaired cerebral perfusion may be initially listless or agitated and not interacting with caregivers. Mental status typically deteriorates to obtundation and coma as the shock state worsens.
●Oliguria – Oliguria with decreased glomerular filtration rate results from the shunting of renal blood flow to other vital organs and the fall in intraglomerular pressure, which normally drives glomerular filtration.
●Lactic acidosis – Progressive tissue hypoperfusion is associated with the development of lactic acidosis. Two factors contribute to this abnormality: increased lactic acid production caused by inadequate delivery of oxygen and decreased clearance of lactate by the liver, kidneys, and skeletal muscle [13]. (See "Causes of lactic acidosis".)
●Hypotension – Hypotension is typically a late finding among children in shock. Compensatory vasoconstriction is often so pronounced that systemic blood pressure can be maintained within the normal range, despite significant circulatory compromise. In this situation, the main clinical manifestations of shock are tachycardia and signs of organ hypoperfusion such as skin changes (prolonged capillary refill) and decreased urine output.
For children, hypotension is defined as a systolic blood pressure that is less than the fifth percentile of normal for age. Clinical guidelines propose several definitions for this threshold, and there is low to moderate agreement between these thresholds and population-based normative data [14]. We use the age-related criteria provided by the Pediatric Advanced Life Support Course [3]:
•Term neonates (0 to 28 days): <60 mmHg
•Infants (1 month to 12 months): <70 mmHg
•Children 1 to 10 years old: <(70 mmHg + [2 x age in years])
•Children ≥10 years old: <90 mmHg
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Shock in children".)
SUMMARY
●Definition – Shock is a physiologic state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery. Unique physiologic responses to poor perfusion among children make it a challenge for clinicians to recognize shock early (before hypotension develops), when responses to treatment are more favorable. (See 'Definition' above.)
●Physiology – Physiologic variables that the body can manipulate to compensate for compromised perfusion include cardiac output (stroke volume times heart rate), stroke volume (determined by preload, cardiac contractility, and afterload), and systemic vascular resistance (SVR). (See 'Physiology' above.)
●Stages of shock – During compensated shock, tachycardia (table 3) and peripheral vasoconstriction rapidly compensate for diminished perfusion; systolic blood pressure is maintained within the normal range. Once hypotension develops, the child's condition will deteriorate rapidly to cardiovascular collapse and cardiac arrest unless rapid resuscitation is instituted. Progressive end-organ dysfunction leads to irreversible organ damage and death. (See 'Stages of shock' above and 'Common features' above.)
●Classification – Types of shock and the corresponding primary pathophysiology include (table 1) (see 'Classification' above):
•Hypovolemic shock: Reduction in preload caused by fluid or blood loss
•Distributive shock: Decreased systemic vascular resistance with abnormal distribution of blood flow from sepsis, anaphylaxis, or nervous system injury
•Cardiogenic and obstructive shock: Pump failure as the result of cardiomyopathies, arrhythmias, blood flow obstruction or other causes (table 2) with clinical signs of increased preload or increased central venous pressure (if measured)
●Clinical findings of shock – Common features of compensated shock include tachycardia and signs of compromised organ perfusion (skin, brain, and kidneys). Children with shock often present before hypotension develops. (See 'Common features' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Mark Roback, MD, who contributed to earlier versions of this topic review.
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