Blood volume was studied in 160 infants and children aged from one hour to 14 years. From these data linear and logarithmic regression equations relating blood volume to weight, height and surface area were calculated. Equations utilizing combined weight and logarithmic weight values were found to be the most accurate for predicting blood volume. Therefore, nomograms were constructed for reading blood volume directly from height and weight.
An inflammatory response and a capillary leak syndrome frequently develop during the treatment of neonatal respiratory failure by extracorporeal membrane oxygenation (ECMO). The present study was performed to investigate leukocyte activation and endothelial cell dysfunction that are associated with prolonged contact of blood components with synthetic surfaces. Laboratory ECMO was performed with fresh human blood at 37°C for 8 h (n ϭ 6). Leukocyte activation was measured by L-selectin (CD62L) and CD18 integrin surface expression and by neutrophil-derived elastase release. To monitor endothelial activation, endothelial cell ICAM-1 (CD54) expression was measured in cultured endothelial cells from human umbilical veins (HUVEC) after incubation with plasma from the ECMO experiments. CD18 integrin expression was found significantly upregulated on polymorphonuclear neutrophils and monocytes after 2-4 h of laboratory ECMO. L-selectin was reduced on both cell types during the total duration of the experiments. Soluble L-selectin (sCD62L) and total and differential leukocyte counts remained unchanged during the experiment. Neutrophil-derived elastase content was maximal after 8 h of ECMO. Plasma from the ECMO experiments did not induce ICAM-1 expression of cultured HUVEC. We conclude that prolonged contact with synthetic surfaces during ECMO activates phagocytes, which may contribute to the inflammatory response seen in ECMOtreated patients. Activated phagocytes do not accumulate in the extracorporeal system nor release humoral factors inducing ICAM-1 expression on endothelial cells. ECMO is the standard treatment for newborn infants with respiratory failure unresponsive to conventional pulmonary support (1). During ECMO treatment, an inflammatory reaction with neutropenia (2), activation of PMN (3), and a capillary leak syndrome with systemic and pulmonary edema (4, 5) have been described. However, it is not clear, to what extent this changes result from the patient's disease (6) or from the effects of extracorporeal circulation of the blood. We therefore performed laboratory ECMO without connecting the system to a patient, to study the isolated effects of prolonged extracorporeal circulation of blood on leukocyte number, expression of leukocyte adhesion molecules, and the release of mediators that might activate endothelial cells.During hemodialysis or cardiopulmonary bypass (CPB), leukocytes are activated (2, 7, 8) and humoral mediators are generated, which impairs endothelial cell integrity (9 -11). The induction of an inflammatory response and the loss of endothelial integrity represent a hallmark of the capillary leakage commonly observed in CPB (7) and neonatal ECMO (4, 5), with systemic and pulmonary edema often prolonging the duration of ECMO. In spite of evidence for activation of PMN in neonatal ECMO (3), it is unclear to what extent this activation is due to the underlying disease or the leukocyte-synthetic surface interaction and whether this activation is linked to the clinically observed changes in endothel...
Our body weight curves are more adequate to evaluate growth of preterm infants than older published reference values because they are based on infants treated according to current nutritional standards.
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