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17
Shock
Introduction
Shock is a clinically diagnosed condition that results from many varied etiologies. It accounts for moremorbidity and mortality in children worldwide than any other diagnosis; dehydration and hypovolemicshock alone result in 6-20 million deaths annually in infants and children worldwide.Shock can damage any and all tissues and organ systems in the body. Delay in recognizing andquickly treating a state of shock results in a progression from compensated reversible shock towidespread multiple system organ failure to death. Morbidity may be widespread and can include renalfailure, brain damage, gut ischemia, hepatic failure, metabolic derangements, diffuse intravascularcoagulation (DIC), acute respiratory distress syndrome (ARDS), cardiac failure, and death.Pediatric practitioners treating acutely ill children from neonates to young adults are faced withdifferent degrees and causes of shock on a regular basis, making shock in infants and children one ofthe most common, and often life-threatening, conditions encountered.This article reviews the common physiologic foundations of shock that underpin all patients with thiscondition. The different pathophysiologic classifications of shock are defined along with their etiologies.The defining clinical findings of shock are described, and current diagnostic and therapeutic strategiesare presented to help guide the most effective and appropriate treatment for resuscitating the child inshock.For excellent patient education resources, visit eMedicine's Shock Center. Also, see eMedicine'spatient education article Shock.
Physiology
Shock is defined physiologically as inadequate delivery of substrates and oxygen to meet themetabolic needs of the tissues. As cells are starved of oxygen and substrate, they can no longersustain efficient aerobic oxygen production. Aerobic metabolism generates 36 ATP molecules perglucose molecule. As oxygen delivery (DO
2
) is impaired, the cell must switch to the much less efficientanaerobic metabolic pathway, which generates only 2 ATP molecules per molecule of glucose, withresulting production and accumulation of lactic acid.Eventually, cellular metabolism is no longer able to generate enough energy to power the componentsof cellular homeostasis, leading to the disruption of cell membrane ionic pumps, accumulation ofintracellular sodium with an efflux of potassium, and accumulation of cytosolic calcium. The cell swells,the cell membrane breaks down, and cell death ensues. Widespread cellular death results in multiplesystem organ failure and, if irreversible, death.This metabolic disruption may occur from either an absolute deficiency of DO
2
, defined as hypoxicshock, or a combination of hypoxia and deficient substrate delivery, predominantly of glucose, definedas ischemic shock. Most often they develop in combination, which results clinically in hypoxic-ischemic
 
18
injury. Because DO
2
is critical in either hypoxic or ischemic shock, considering DO
2
when definingshock physiologically is useful.DO
2
is defined as the amount of oxygen delivered to the tissues of the body per minute. DO
2
dependson the amount of blood pumped per minute, or cardiac output (CO), and the arterial oxygen content ofthat blood (CaO
2
). Thus, DO
2
may be defined by the following equation:DO
2
(mL O
2
 /min) = CaO
2
(mL O
2
 /L blood) X CO (L/min)The CaO
2
depends on how much oxygen-carrying capacity is available in terms of hemoglobin (Hb)content and depends on how much oxygen the patient's Hb contains, defined as the arterial oxygensaturation (SaO
2
). A small, but clinically irrelevant, amount of oxygen is directly dissolved in the bloodthat is not bound to Hb. Therefore, CaO
2
may be defined by the following formula:CaO
2
(mL/100 mL) = Hb (g/100 mL) X SaO
2
X 1.34 mL O
2
 /g + (0.003 X PaO
2
)A state of clinical shock may occur when CaO
2
is impaired either by hypoxia, which decreases SaO
2
,or by anemia, which reduces the amount of Hb and, hence, reduces the body's total oxygen-carryingcapacity.CO depends on the amount of blood pumped with each heartbeat, known as stroke volume (SV), andthe heart rate (HR). SV depends on the ventricular end-diastolic filling volume (commonly referred toas ventricular preload), the state of myocardial contractility, and the afterload on the heart. Each ofthese variables, which affect CO, can be impaired in clinical shock states. Thus, the followingrelationship is observed:CO = HR (beats/min) X SV (mL/beat)SV depends on (1) preload, (2) afterload, and (3) contractility.The recognition and treatment of pediatric shock depends on an understanding of these physiologicprinciples and definitions. Once understood, the different clinical presentations and causes of shock,as well as their most appropriate treatment strategies, are easily appreciated.
Etiology
Several etiologic classifications of shock are recognized. In each of these classifications, one or moreof the physiologic principles defined above are disturbed. The major categories are as follows:
•
 
Hypovolemic
•
 
Distributive
•
 
Cardiogenic
•
 
Septic
•
 
Obstructive
•
 
Miscellaneous
Hypovolemic Shock
Hypovolemic shock results from an absolute deficiency of intravascular blood volume. It is a leadingcause of pediatric mortality in the United States and worldwide, although the specific causative agents
 
19
may be different around the world. Gastroenteritis results in 6-20 million deaths in infants and childrenannually worldwide. Children with gastroenteritis may lose 10-20% of their circulating volume within 1-2 hours.
1
Rehydration is often impeded by concurrent vomiting, and deterioration may be rapid.Common infectious etiologies include bacterial causes of gastroenteritis, such as
Salmonella,Shigella,
and
Campylobacter
species and
Escherichia coli,
and viral causes, such as rotaviruses,adenoviruses, norovirus, and enteroviruses. Worldwide, infectious amebiasis and cholera are alsoimportant causes.Physiologically, rapid loss of intravascular volume reduces ventricular preload, resulting in decreasedstroke volume and CO and, thus, decreased DO
2
. In addition, a hemorrhagic component or dysenterymay reduce Hb content, resulting in decreased CaO
2
.In the United States, the leading cause of death in children older than 1 year is trauma. Trauma killsmore children than all other causes of death combined.
2
A major component of traumatic death ishemorrhage. Hemorrhagic shock reduces both CaO
2
and preload, resulting in decreased DO
2
to thetissues.Other causes of hypovolemia include capillary leak and tissue third spacing, which results in leakageof fluid out of the intravascular space into the interstitial tissues. Etiologies include burns, sepsis, andother systemic inflammatory diseases. Patients with such etiologies may appear "puffy" and total-bodyfluid overloaded; however, they are actually significantly intravascularly depleted, with inadequatepreload, and are in significant shock. By understanding the physiologic disturbance affectingintravascular volume and preload, such patients need even more fluid administration, despite theiroverall edematous appearance, in order to improve DO
2
and prevent or correct a state of shock.Therapy is discussed more in detail below (see Treatment of Shock and Pharmacologic Therapy).
Causes of hypovolemic shock
 
•
 
Intravascular volume loss
o
 
Gastroenteritis
o
 
Burns
o
 
Diabetes insipidus
o
 
Heat stroke
•
 
Hemorrhage
o
 
Trauma
o
 
Surgery
o
 
GI bleeding
•
 
Interstitial loss
o
 
Burns
o
 
Sepsis
o
 
Nephrotic syndrome
o
 
Intestinal obstruction
o
 
Ascites
Distributive Shock
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