Lactic acidosis and oxygen debt in african children with severe anaemia.
A syndrome of severe anaemia (Hb ¾5 g/dl), particularly severe malarial anaemia (SMA), remains a major cause of childhood mortality in sub-Saharan Africa.
We hypothesized that the lactic acidosis which identifies those at the greatest risk of death often represents an oxygen debt incurred as a result of inadequate tissue perfusion.
To examine this hypothesis, we measured oxygen consumption (VO2) using a portable metabolic monitor.
Blood lactate and acid-base status were also determined.
Pre-transfusion data on 44 children (28 with mild symptoms, 7 with respiratory distress and 9 controls) demonstrated very close dependence of VO2 on body surface area (BSA, R2=0.86, p<0.001).
After correcting for BSA, no significant differences were observed in mean VO2 values of the three clinical groups, indicating that a critical reduction in oxygen delivery is not the sole explanation for the development of a lactic acidosis and severe symptoms.
Nine children (including five of the original 44) were monitored during transfusion.
In four of the five with SMA, severe symptoms and severe lactic acidosis, transfusion produced a marked, transient increase in VO2 (maximum 30-41%), with a marked fall in blood lactate and clinical improvement.
These data suggest that some children with SMA and respiratory distress accumulate an oxygen debt when a relatively high oxygen demand outstrips supply, this debt being repaid when supply is increased during transfusion. (...)
Mots-clés Pascal : Anémie, Paludisme, Protozoose, Parasitose, Infection, Etude comparative, Lactique acide, Oxygène, Dette, Hypothèse, Facteur risque, Tissu, Perfusion, Evaluation, Enfant, Homme, Afrique, Mortalité, Hémopathie, Activité biologique
Mots-clés Pascal anglais : Anemia, Malaria, Protozoal disease, Parasitosis, Infection, Comparative study, Lactic acid, Oxygen, Debt, Hypothesis, Risk factor, Tissue, Perfusion, Evaluation, Child, Human, Africa, Mortality, Hemopathy, Biological activity
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0461368
Code Inist : 002B19A01. Création : 03/02/1998.