HYPOGLYCEMIA ON AND AFTER ADMISSION IN KENYAN CHILDREN WITH SEVERE MALARIA

We investigated the pathophysiology of hypoglycaemia in severe malaria in African children, especially the potential importance of glycerol as a substrate for gluconeogenesis, and whether substrate limitation c ontributes to hypoglycaemia in severe disease. Of 171 children with mo derate or severe malaria, 16% were hypoglycaemic on admission, while a t least 9% of children with severe malaria treated with quinine and a concurrent 4% dextrose infusion had a definite episode of hypoglycaemi a after admission. Blood levels of gluconeogenic precursors are as hig h (alanine and lactate) or higher (glycerol) in those with either hypo glycaemia on ol after admission as they are in children never having a n episode of hypoglycaemia. Among children with severe malaria, howeve r, those having a definite episode of hypoglycaemia at some stage are more acidotic and have greater evidence of renal impairment than those who are never hypoglycaemic (mean base excess -14.4 vs. -7.2, p<0.001 , mean creatinine 97 vs. 64, p < 0.001 and mean urea 8.1 vs. 5.8, p = 0.03, respectively). These data do not support a role for reduced gluc oneogenic substrate supply in the pathogenesis of hypopglycaemia in se vere childhood malaria, but do support the hypothesis that gluconeogen esis is impaired. Commonly-used bedside blood glucose monitoring devic es may overestimate blood glucose measurements in the normal range, an d paradoxically may also seriously overestimate the frequency of hypog lycaemia.