Although thoracic injuries occur less frequently in children than adults, they remain a source of substantial morbidity and mortality. Disparate problems such as rib fractures, lung injury, hemothorax, pneumothorax, mediastinal injuries, and others may present in isolation or in combination with one another. Knowledge of the manner in which pediatric anatomy, physiology, and injury patterns change with age may expedite the evaluation of the pediatric chest after trauma. Differences in pulmonary functional residual capacity, blood volume, chest wall and spinal soft-tissue mobility, and cardiac function may translate into problems or benefits of important consequence. For example, although more predisposed to hypoxemia, young children may remain well compensated hemodynamically, despite significant blood loss. Rare injuries in children, such as cardiac and great vessel trauma, may remain undiagnosed precisely because of their scarcity and protean symptoms.

Chronic inflammatory diseases are often associated with decreased red blood cell (RBC) mass. The cytokines cachectin/tumor necrosis factor-alpha (TNF) and interleukin 1 (IL 1) are produced by monocytes/macrophages in response to many inflammatory stimuli and have been implicated in the anemia of chronic disease. This study was undertaken to evaluate the mechanisms by which cachectin/TNF, IL 1, or endotoxin induce anemia. Hematologic parameters and RBC kinetics were quantitated in rats given chronic sublethal quantities of either recombinant human cachectin/TNF, recombinant human IL 1 alpha, or Salmonella endotoxin for 7 days. Cachectin/TNF or endotoxin treatment resulted in a 25 or 31% decrease, respectively, in total RBC mass, whereas RBC mass was unchanged by IL 1 administration. Anemia associated with either chronic cachectin or endotoxin administration was characterized by normal mean corpuscular volume, mean corpuscular hemoglobin content, and reticulocyte numbers. [59Fe]RBC survival was significantly shortened in animals given cachectin, IL 1 or endotoxin, but the magnitude of the response was greatest in cachectin/TNF-or endotoxin-treated rats. Although cachectin/TNF-IL 1-, or endotoxin treatment resulted in similar hypoferremia and shortened plasma iron half-life, endotoxin or cachectin/TNF treatment (but not IL 1) significantly reduced the incorporation of plasma 59Fe into newly synthesized RBCs. We conclude that chronic cachectin/TNF administration produces anemia by decreasing RBC synthesis and reducing the life span of circulating RBCs. An endogenous cachectin/TNF response during inflammatory disease may contribute to an associated anemic state, whereas the modestly reduced red cell life span induced by IL 1 does not lead to a net reduction in RBC mass, presumably owing to a preserved RBC synthetic rate.

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Younger children with appendicitis have reduced hospital days and charges when they are treated by PSs.