Lactic acidosis and oxygen debt in African children with severe anaemia
Lactic acidosis and oxygen debt in African children with severe anaemia
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DOI：
10.1093/qjmed/90.9.563
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发表时间：
1997-09-01
期刊：
影响因子：
--
通讯作者：
Marsh, K
中科院分区：
文献类型：
--
作者：
English, M;Muambi, B;Marsh, K
严重贫血综合症（血红蛋白低于或等于5克/分升），特别是严重疟疾性贫血，仍然是撒哈拉以南非洲儿童死亡的主要原因。我们假设，乳酸酸中毒，确定那些在最大的死亡风险往往代表了一个氧债所产生的组织灌注不足的结果。为了验证这一假设，我们使用便携式代谢监测仪测量了耗氧量（VO 2）。还测定了血乳酸和酸碱状态。44例患儿（28例轻度症状，7例呼吸窘迫，9例对照）输血前数据显示VO 2与体表面积有非常密切的依赖关系（BSA，R-2 = 0.86，P < 0.001）。校正BSA后，三个临床组的平均VO 2值无显著差异，表明氧输送严重减少不是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）接受了监测。在5例SMA、重度症状和重度乳酸酸中毒患者中，4例患者输血后VO 2显著一过性增加（最大30- 41%），血乳酸显著下降，临床改善。这些数据表明，当相对较高的氧气需求超过供应时，一些患有SMA和呼吸窘迫的儿童积累了氧债，当输血期间供应增加时，这种债务得到偿还。然而，在这5名儿童中的其余1名儿童中，VO 2增加（最大20%），伴随着血乳酸升高和临床恶化，这表明在某些儿童中可能占主导地位的病理生理学机制更为复杂。
A syndrome of severe anaemia (Hb less than or equal to 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. Pretransfusion 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, R-2 = 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 duping 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.