A disordered sensorium, a cardinal sign of lactic acidosis, is commonly attributed to the acidosis resulting from increased production and decreased utilization of lactate. We report hyperlactataemia in 22 children with encephalopathy following viral, rickettsial and bacterial infections. On admission there was normoglycaemia together with anion gap acidosis (p less than 0.02), hyperlactataemia (p less than 0.003), fatty acidaemia (p less than 0.004) and increased serum creatinine (p less than 0.0004) when compared to the results in convalescence. Management with two types of hyperglycaemia-producing infusions, one of them containing lactate, resulted in hyperglycaemia (p less than 0.002) from the 2nd to 4th days of admission. This was associated with a decrease in lactate, creatinine and acidosis and with clinical recovery. Infusions of either glucose or lactate would normally result in hyperlactataemia, more so if there was difficulty with lactate utilization. The fall in lactate supports the hypothesis that the hyperlactataemia is probably due to an adaptive increase in lactate production as an alternative cerebral fuel which is consequent on poor glucose utilization by brain, the cause of the encephalopathy. Additionally it leads to increased Cori cycle activity. Hence the clinical and metabolic recovery with such management.