English M, Muambi B, Mithwani S, Marsh K
Clinical Research Centre, KEMRI Kilifi Unit, Kenya.
QJM. 1997 Sep;90(9):563-9. doi: 10.1093/qjmed/90.9.563.
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.
严重贫血综合征（血红蛋白≤5g/dl），尤其是严重疟疾性贫血（SMA），仍然是撒哈拉以南非洲儿童死亡的主要原因。我们推测，识别出死亡风险最高者的乳酸酸中毒通常代表因组织灌注不足而产生的氧债。为检验这一假设，我们使用便携式代谢监测仪测量了氧耗量（VO2）。还测定了血乳酸和酸碱状态。44名儿童（28名有轻度症状、7名有呼吸窘迫和9名对照）输血前的数据显示，VO2与体表面积（BSA，R2 = 0.86，p < 0.001）密切相关。校正BSA后，三个临床组的平均VO2值未观察到显著差异，这表明氧输送的严重降低并非乳酸酸中毒和严重症状发生的唯一解释。9名儿童（包括最初44名中的5名）在输血期间接受了监测。在5名患有SMA、严重症状和严重乳酸酸中毒的儿童中，有4名输血后VO2出现明显的短暂升高（最高30 - 41%），血乳酸显著下降且临床症状改善。这些数据表明，一些患有SMA和呼吸窘迫的儿童在相对较高的氧需求超过供应时会积累氧债，输血期间供应增加时该氧债得以偿还。然而，在这5名儿童中的另外1名中，VO2升高（最高20%）伴随着血乳酸升高和临床症状恶化，这表明存在更多病理生理上更为复杂的机制，在某些儿童中可能占主导地位。
