In the ED, the specific etiology is less important than recognizing and responding to shock. Remember, it is the inability to provide substrate at the cellular level that unifies all types of shock, and a child’s response may be subtle at first. In early or compensated shock, tachycardia, mild tachypnea, slightly delayed capillary refill (greater than 2-3 seconds), and mild irritability may be seen. (See Table 3.) Unfortunately, each of these can also be seen in a relatively well child presenting to a loud and busy ED, and the symptoms may easily be discounted or overlooked. Yet these early responses are evidence of the body’s compensatory mechanisms at work to increase cardiac output and preserve blood flow to vital organs, such as the brain, heart, and kidneys.



In children, tachycardia must be recognized as an early sign of the relative inability to meet metabolic demands. Because immature myocardium has a decreased proportion of contractile elements relative to structural elements, the primary mechanism of increasing cardiac output is increasing heart rate. Delay in capillary refill is the result of increased sympathetic tone in response to decreased baroreceptor stimulation. As a continuum, this may progress to cool and clammy extremities. This vasoconstrictive response has been termed “cold shock.” In some instances, rather than vasoconstriction and delayed capillary refill, there is actually increased capillary blood flow. This vasodilatory response is caused by pathogenic bacteria and results in “warm shock.” In this situation, cardiac output is actually increased, and systemic vascular resistance is low. Clinically, the skin is warm, and pulses are bounding with a widened pulse pressure. (See Table 1.)

If shock continues, early compensatory mechanisms become inadequate to meet the substrate demands of organs and tissues, and a state of uncompensated shock ensues. Cellular ischemia and the release of vasoactive metabolites and inflammatory mediators start to affect the microcirculation, and evidence of brain, heart, and kidney hypoperfusion is evident. There is further perturbation of vital signs, with increasing elevation of heart rate and respiratory rate. Skin changes seen in compensated shock are worsened, and the skin becomes mottled or extremely cool with decreased pulses. When hypotension is evident, decreased perfusion to the kidneys results in oliguria. The mental status is more severely altered; irritability may become agitation or confusion, and may progress to unconsciousness and coma if not treated. Increased oxygen demand and acidosis caused by anaerobic metabolism result in increased respiratory drive. This rapid presentation of respiratory distress, tachypnea, and hypoxia are the hallmarks of acute respiratory distress syndrome (ARDS). As many as 32% of children with septic shock have been shown to develop ARDS.¹³

Eventually, all organs can be affected if shock is not reversed. Once MOSF develops, heroic efforts are often required to reverse this level of shock. Altered mental status, respiratory failure, cardiac failure, hepatic failure, and renal failure are all witnessed at the end of uncompensated shock, as damage becomes irreversible and refractory shock is recognized.

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