Very few data exist on phosphate metabolism in critically ill neonates. The
refore we studied the incidence of hypophosphataemia, the intracellular met
abolism of phosphate by measuring adenosine 5'-triphosphate (ATP) and 2,3-d
iphosphoglycerate (2,3-DPG) in rod blood cells, and excretion of phosphate
in urine. The aims of the study were early detection of changes in phosphat
e metabolism as possible diagnostic markers of sepsis and defining the caus
e of hypophosphataemia.
Neonates, treated in multidisciplinary paediatric intensive care unit (PICU
), included in the study, were less than three days of age. Eighteen of the
m had respiratory distress syndrome (RDS) and 16 had microbiologically conf
irmed or clinical sepsis. The overall incidence of hypophosphataemia in cri
tically ill neonates was over 80%, and was more common (88%) and more profo
und in those with sepsis than in those with RDS (79%). Therefore the septic
neonates needed significantly larger amounts of phosphate to maintain norm
ophosphataemia. In septic neonates ATP concentration in red blood cells was
significantly lower than in neonates with RDS and controls, while the 2,3-
DPG concentration was increased as a result of compensation. In septic neon
ates urinary losses of inorganic phosphate (Pi) were significantly higher t
han in neonates with RDS. Hypophosphataemia in critically ill neonates is a
t least partly due to higher urinary losses of phosphate.