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Lactic acidosis and oxygen debt in African children with severe anaemia
M English1, B Muambi, S Mithwani
1Clinical Research Centre, KEMRI Kilifi Unit, Kenya.
Insights
Severe anaemia in children, particularly severe malarial anaemia (SMA), causes mortality. Lactic acidosis may indicate oxygen debt, but studies show oxygen consumption is linked to body surface area, not solely oxygen delivery issues.
Area of Science:
- Pediatrics
- Hematology
- Critical Care Medicine
Background:
- Severe anaemia, especially severe malarial anaemia (SMA), is a leading cause of childhood mortality in sub-Saharan Africa.
- Lactic acidosis in these children often signifies a high risk of death, potentially due to inadequate tissue perfusion and oxygen debt.
Purpose of the Study:
- To investigate the relationship between oxygen consumption, lactic acidosis, and clinical outcomes in children with severe anaemia.
- To test the hypothesis that lactic acidosis in severe anaemia results from oxygen debt due to poor tissue perfusion.
Main Methods:
- Measured oxygen consumption (VO2) using a metabolic monitor in 44 children with varying anaemia severity.
- Assessed blood lactate and acid-base status.
- Monitored nine children during blood transfusion to observe immediate physiological responses.
Main Results:
- Oxygen consumption (VO2) strongly correlated with body surface area (BSA) in all children.
- After adjusting for BSA, no significant differences in VO2 were found between clinical groups, suggesting reduced oxygen delivery isn't the sole cause of lactic acidosis.
- Blood transfusion in four children with SMA and lactic acidosis led to increased VO2, decreased lactate, and clinical improvement, indicating oxygen debt repayment.
- One child showed increased VO2 with rising lactate and deterioration, suggesting complex pathophysiological mechanisms.
Conclusions:
- In some children with severe malarial anaemia and respiratory distress, lactic acidosis may stem from an oxygen debt incurred when high oxygen demand exceeds supply.
- Blood transfusion can alleviate this oxygen debt, increasing oxygen supply and improving clinical status.
- Complex pathophysiological mechanisms, beyond simple oxygen debt, may contribute to severe lactic acidosis and poor outcomes in a subset of these children.
Abstract:
A syndrome of severe anaemia (Hb < or = 5 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. However, in the remaining one of these five children, an increase in VO2 (maximum 20%), was accompanied by a rise in blood lactate and clinical deterioration, suggesting that more pathophysiologically complex mechanisms, which may predominate in some children.