Does reduced oxygen delivery cause lactic acidosis in falciparum malaria? An observational study

Abstract

Background

Lactic acidosis with an elevated lactate–pyruvate ratio suggesting anoxia is a common feature of severe falciparum malaria. High lactate levels are associated with parasitized erythrocyte sequestration in the microcirculation. To assess if there is an additional contribution to hyperlactataemia from relatively inadequate total oxygen delivery, oxygen consumption and delivery were investigated in patients with malaria.

Methods

Adult Bangladeshi and Indian patients with uncomplicated (N = 50) or severe (N = 46) falciparum malaria or suspected bacterial sepsis (N = 27) and healthy participants as controls (N = 26) were recruited at Chittagong Medical College Hospital, Chittagong, Bangladesh and Ispat General Hospital, Rourkela, India. Oxygen delivery (DO₂I) was estimated from pulse oximetry, echocardiographic estimates of cardiac index and haematocrit. Oxygen consumption (VO₂I) was estimated by expired gas collection.

Results

VO₂I was elevated in uncomplicated median (IQR) 185.1 ml/min/m² (135–215.9) and severe malaria 192 ml/min/m² (140.7–227.9) relative to healthy persons 107.9 ml/min/m² (69.9–138.1) (both p < 0.001). Median DO₂I was similar in uncomplicated 515 ml/min/m² (432–612) and severe 487 ml/min/m² (382–601) malaria and healthy persons 503 ml/min/m² (447–517) (p = 0.27 and 0.89, respectively). The VO₂/DO₂ ratio was, therefore, increased by similar amounts in both uncomplicated 0.35 (0.28–0.44) and severe malaria 0.38 (0.29–0.48) relative to healthy participants 0.23 (0.17–0.28) (both p < 0.001). VO₂I, DO₂I and VO₂/DO₂ did not correlate with plasma lactate concentrations in severe malaria.

Conclusions

Reduced total oxygen delivery is not a major contributor to lactic acidosis in severe falciparum malaria.