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Acidosis in severe childhood malaria
M English1, R Sauerwein, C Waruiru
1CRC KEMRI Kilifi Unit, Kenya.
QJM : Monthly Journal of the Association of Physicians
|April 1, 1997
Summary
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.