Two hypotheses have recently been raised to explain the metabolic acidosis (increased blood acidity) of severe malaria, and both are relevant to treatment. The first suggests that a decreased blood volume (hypovolaemia) has an important role in severe malaria; following this, treatment should be based on the current standard paediatric management of acidosis in children with features of cardiovascular compromise. The second hypothesis contends that acidosis in malaria has a metabolic cause and proposes treatment with dichloroacetate. Both hypotheses are plausible and are not mutually exclusive. In truth, the risks and benefits of either treatment are uncertain, and will remain so until large multicentre, randomised controlled trials provide appropriate supportive evidence. As both views involve complex physiological rationales, beyond the usual scope of this journal, I attempt here to present the largely academic aspects of these hypotheses within the practical and contextual aspects of childhood severe malaria.