Malarial pneumonopathy in Malawian children with cerebral malaria.

backgroundRespiratory distress is a well-recognized clinical presentation in pediatric malaria and is associated with increased mortality. Traditionally described as "acidotic breathing," this phenomenon has been attributed to compensatory hyperventilation secondary to metabolic acidosis. However, this explanation may not adequately capture causative mechanisms. We sought to quantify the prevalence of respiratory distress in children with cerebral malaria (CM) and to evaluate underlying pathophysiologic contributors.

methodsIn this prospective, observational study, 97 Malawian children aged 6 months to 12 years meeting the World Health Organization (WHO) criteria for CM were enrolled. Vitals were recorded, including oxygen saturation and oxygen supplementation when present. Clinical signs of respiratory distress were documented on admission using WHO definitions. Admission lactate levels and blood gas analyses were obtained to characterize acid-base status. A standardized 12-zone point-of-care lung ultrasound was performed to assess pulmonary aeration patterns.

resultsTwenty-seven participants (28%) met WHO-defined criteria for respiratory distress. Despite elevated lactate levels (median 7.0 mmol/L [4.2, 13.3]), median pH remained 7.41. Metabolic acidosis was the sole disturbance in only 12 children (12%). A primary respiratory alkalosis was observed in 33% of the cohort, and lung ultrasound revealed subcentimeter consolidations in 88% of all participants. Larger consolidations (≥ 1 cm) consistent with pneumonia were less common. Absence of diffuse edema on lung ultrasound made cardiac or renal failure an unlikely primary cause of respiratory distress. No child met criteria for pediatric acute respiratory distress syndrome. Respiratory distress was not associated with increased mortality in this cohort.

conclusionsOur findings challenge the longstanding attribution of respiratory distress in CM to metabolic acidosis alone. The frequent occurrence of a primary respiratory alkalosis, together with the near-universal presence of subpleural consolidations on lung ultrasound, suggests that alternative mechanisms-including pulmonary microvascular obstruction, interstitial inflammation, and dysregulation of the central respiratory drive-are likely contributing to the observed respiratory patterns. We propose the terminology malarial pneumonopathy to describe this broader spectrum of lung involvement. Reframing the traditional concept of "acidotic breathing" as malarial pneumonopathy may better reflect the spectrum of respiratory dysfunction in CM, improve diagnostic accuracy, and guide future research, clinical guidelines, and interventions.