”Children are not Small Adults!“

Abstract

The recognition, diagnosis, and management of sepsis remain among the greatest challenges in pediatric critical care medicine. Sepsis remains among the leading causes of death in both developed and underdeveloped countries and has an incidence that is predicted to increase each year. Unfortunately, promising therapies derived from preclinical models have universally failed to significantly reduce the substantial mortality and morbidity associated with sepsis. There are several key developmental differences in the host response to infection and therapy that clearly delineate pediatric sepsis as a separate, albeit related, entity from adult sepsis. Thus, there remains a critical need for well-designed epidemiologic and mechanistic studies of pediatric sepsis in order to gain a better understanding of these unique developmental differences so that we may provide the appropriate treatment. Herein, we will review the important differences in the pediatric host response to sepsis, highlighting key differences at the whole-organism level, organ system level, and cellular and molecular level.

Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock

“…Infants and children differ developmentally from adults in ways that explain the differences in the hemodynamic response to sepsis, as well as the response to therapeutic agents (26). Some of these differences include preexisting elevated HR, a relatively decreased left ventricular mass in comparison to the adult myocardium (27), an increased ratio of type I collagen (decreased elasticity) to type III collagen (increased elasticity) (28), increased connective tissue content in the infant heart, and diminished actin and myosin content (29).…”

Shared and Distinct Aspects of the Sepsis Transcriptomic Response to Fecal Peritonitis and Pneumonia

“…This predictive gene set includes genes involved in cell growth (DYRK2), cell cycle (CCNB1IP1), stem cell maintenance (TDRD9), and DNA damage (ADGRE3), consistent with the observed pathway enrichment (cell death, apoptosis, necrosis) and with immune response through lymphocyte activation (ZAP70), major histocompatibility complex class II export (ARL14EP), and myeloid cell interactions in immunity (MDC1). The lack of overlap with pediatric sepsis endotypes that we observed requires further validation and may reflect developmental differences impacting pathophysiology and host immune dysfunction (39,40).…”

Comparison of the New Adult Ventilator-Associated Event Criteria to the Centers for Disease Control and Prevention Pediatric Ventilator-Associated Pneumonia Definition (PNU2) in a Population of Pediatric Traumatic Brain Injury Patients*

“…Consequently, the proposed changes in PEEP and FiO 2 may not be sensitive or specific when surveying a pediatric cohort for respiratory complications. (23) Using the current CDC ventilator-associated pneumonia definition that requires a positive microbiologic specimen (PNU2)(12) as the gold standard, we calculated and compared test characteristics of both the original and our modified pediatric criteria.…”