Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1093/qjmed/90.9.563

Type

Journal article

Journal

QJM

Publication Date

09/1997

Volume

90

Pages

563 - 569

Keywords

Africa, Africa South Of The Sahara, Age Factors, Anemia, Biology, Blood Transfusion, Child, Comparative Studies, Demographic Factors, Developing Countries, Diseases, Eastern Africa, English Speaking Africa, Examinations And Diagnoses, Hematological Effects, Hemic System, Kenya, Laboratory Examinations And Diagnoses, Metabolic Effects, Physiology, Population, Population Characteristics, Research Methodology, Research Report, Studies, Treatment, Youth, Acidosis, Lactic, Anemia, Blood Transfusion, Child, Child, Preschool, Female, Humans, Infant, Kenya, Lactic Acid, Malaria, Male, Oxygen Consumption