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While the incidence of shock varies by country, in developed countries such as the United States, pediatric patients in shock account for approximately 37% of transfers from community hospitals to tertiary medical centers.¹  Pediatric patients in shock have over three times the mortality rate compared with pediatric patients not in shock (11.4% vs 2.6%, respectively) regardless of whether their shock was caused by trauma or another etiology, such as diarrhea or vomiting.¹

Hypovolemic shock, i.e. shock resulting from excessive intravascular fluid loss or hemorrhage, is the most common type of shock in pediatric patients.  The most common cause of hypovolemic shock worldwide is diarrhea and/or vomiting secondary to gastrointestinal (GI) illness.²  Due to physiological differences, children can lose a significant percentage of their circulating volume within a few hours yet remain in a “compensated” phase of shock as evidenced by normal blood pressures.  While children are still in the compensated stage of shock, they typically exhibit tachycardia as a result of their body’s attempt to increase cardiac output to compensate for the lower circulating fluid volume.  These children may also exhibit mild tachypnea and delayed capillary refill along with a temporary slight rise in diastolic blood pressure as a result of systematic vasoconstriction.³  While delayed capillary refill is not present in every child who is in compensated shock, when it is present, it can be a red flag that aggressive fluid resuscitation must be initiated.  A systematic review and meta-analysis by Fleming et al.⁴ found that a child with prolonged capillary refill time has a 4-fold greater risk of dying compared to a child with normal capillary refill time.

This blog is the first in a series of two on pediatric hypovolemic shock.  The patient below initially presented to an Emergency Department (ED) in compensated hypovolemic shock that appeared to be gastrointestinal in nature, but he eventually became hypotensive, had delayed capillary refill, and required rapid fluid resuscitation.

8-month-old male

An 8-month-old, 6 kg male with a history of premature birth presented to the ED with a two-week history of diarrhea and decreased oral intake. He had recently completed a course of antibiotics for otitis media.  He had been to another local ED 3 days prior where his bloodwork was reassuring, with no indication of infection, but his mother had refused a catheterized urinalysis during that visit, so his urine was not tested.  The infant had also been to his pediatrician within the last two weeks for the diarrhea.  His pediatrician suspected that a milk protein allergy was causing his GI symptoms and had recently changed the infant’s formula.

On the current presentation to the ED, this infant had a fever of 102.5 rectal, heart rate of 183, respiratory rate of 48, and O2 saturation of 98%.  His skin was pink and his capillary refill was brisk.  No blood pressure could be obtained in triage due to the infant’s crying.  His mother reported that over the last 24 hours he had been sleepier and fussier than usual and had fewer wet diapers than usual.  His mother agreed to a catheterized urinalysis this time, which came back positive for a UTI.  The infant received antipyretics, a total of 20 mls/kg normal saline bolus IV, and a dose of IV antibiotics in the ED, then was admitted to the pediatric floor for observation.

Soon after his transfer to the pediatric floor, the infant’s nurse noted that the infant had dusky hands and feet, was mottled from head to toe, had delayed capillary refill, and had rigors.   At that point, the infant’s temperature was 101.3 rectal, his heart rate was in the 220s, and his respiratory rate was in the 70s.  The infant was becoming irritable and difficult to console. His nurse was unable to obtain a blood pressure, likely due to poor perfusion and irritability.  It was not clear whether the deterioration was related to sepsis or hypovolemia, but the infant was clearly deteriorating into decompensated shock; a PICU transfer was anticipated.  In contrast to his ED presentation a few hours earlier, this time the infant was mottled and had delayed capillary refill.

The infant immediately received antipyretics and a total of two, 20 ml/kg rapid normal saline boluses within 5 minutes via the LifeFlow rapid infuser, including set-up time, with immediate improvement in his perfusion, his tachycardia and his tachypnea.  In contrast, the same volume administered at the highest speed by an IV pump would have taken almost 20 minutes including set-up time.   Immediately after the 40 ml/kg boluses, the infant had a temperature of 102 rectal, heart rate of 184, respiratory rate of 58, blood pressure of 99/59, and pulse ox of 99% on room air.  Within minutes, the infant calmed and then tolerated oral fluids for the first time in several hours.  He was able to avoid a PICU admission and remain on the pediatric unit until he was discharged home the next day. His blood culture was negative, and he went home on oral antibiotics for the UTI.

Conclusion

Children are known for their strong compensatory mechanisms that include a unique ability to remain in compensated shock longer than adults.^3,4  Decompensated shock occurs after approximately 30% loss of volume.³  It can be easy to forget that in an infant who weighs 6kg, this is only about 180 mls. It is critical that infants and children in hypovolemic shock be identified and fluid resuscitated in the compensated phase, before hypotension develops, to prevent decompensated shock that can quickly lead to tissue ischemia, organ failure and death. Careful but aggressive fluid resuscitation for children in compensated hypovolemic shock is key to helping prevent decompensated shock and minimizing the complications associated with it.    Infusing intravenous fluids via LifeFlow allows the user to provide the hypovolemic child needed fluids over a much shorter timeframe than an IV pump, delivering the fluid in 10 ml increments that allow for closer, ultimately safer, administration and monitoring.

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