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Acidosis in severe childhood malaria
M English1, R Sauerwein, C Waruiru
1CRC KEMRI Kilifi Unit, Kenya.
Insights
Severe malaria in Kenyan children often causes high-anion-gap metabolic acidosis. Coma and respiratory distress indicate greater renal dysfunction, lower pH, and higher mortality, suggesting distinct pathophysiological mechanisms.
Area of Science:
- Pediatrics
- Infectious Diseases
- Critical Care Medicine
Background:
- Severe malaria is a significant cause of mortality in children.
- Metabolic acidosis is a common complication of severe malaria.
- Understanding the pathophysiology of severe malaria complications is crucial for improving outcomes.
Purpose of the Study:
- To investigate the clinical and biochemical characteristics of severe malaria in Kenyan children.
- To identify factors associated with metabolic acidosis and mortality in severe malaria.
- To explore the pathophysiological mechanisms underlying coma and respiratory distress in severe malaria.
Main Methods:
- Prospective data collection on 306 Kenyan children with severe malaria.
- Analysis of blood gases, renal function markers (urea, creatinine), plasma osmolality, lactate, and hemoglobin levels.
- Comparison of clinical and biochemical parameters between children with different clinical presentations (coma, respiratory distress, or both).
Main Results:
- Severe malaria caused high-anion-gap metabolic acidosis in at least 43% of children.
- Children with both coma and respiratory distress (CM + RD) exhibited greater renal dysfunction, lower pH, higher plasma osmolality, and higher blood lactate compared to isolated findings.
- Children with CM + RD had lower hemoglobin, were younger, and accounted for 63% of all deaths.
Conclusions:
- Hypovolemia and renal impairment are implicated in the pathogenesis of metabolic acidosis in severe childhood malaria.
- Anemia is associated with lactic acidosis in acidotic children, potentially contributing to its pathogenesis.
- Coma in acidotic children (CM + RD) and isolated encephalopathy (CM) may arise from different pathophysiological mechanisms.
Abstract:
Data were prospectively collected on 306 Kenyan children, including blood gases in 258 (75%). Severe malaria caused a predominantly high-anion-gap metabolic acidosis in at least 43% of children. Children with coma and respiratory distress (CM + RD) had greater evidence of renal dysfunction, lower mean pH and higher mean plasma osmolality than those with respiratory distress (RD) or coma (CM) as isolated findings (mean urea 10.7 vs. 6.0 vs. 4.3 mmol/l; mean creatinine 97 vs. 74 vs. 58 mumol/l; mean osmolality 301 vs. 288 vs. 283 mosmol/l; and mean pH 7.16 vs. 7.29 vs. 7.39, respectively, p < 0.001 for each comparison of CM + RD vs. RD or CM). In addition, children with CM + RD had a higher mean blood lactate (6.7 vs. 3.3 mmol/l, p < 0.001), a lower mean haemoglobin (5.5 vs. 7.0 g/dl, p = 0.002) and a lower mean age (26.4 vs. 41.9 months, p < 0.001) than children with CM and accounted for 15/24 (63%) of all deaths. These and previous data implicate hypovolaemia and renal impairment in the pathogenesis of metabolic acidosis in severe childhood malaria. In children who are acidotic, anaemia is strongly associated with lactic acidaemia and may therefore contribute to its pathogenesis. These data also imply that coma in acidotic children (CM + RD) and those with an isolated encephalopathy (CM) may result from quite different pathophysiological mechanisms.