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Mortality from severe malaria remains unacceptably high in sub-Saharan Africa. Several markers of cardiovascular compromise and metabolic acidosis correlate with mortality. The role of cardiac dysfunction in the pathogenesis of severe childhood malaria remains unknown.We examined 30 children admitted with severe malaria by using portable echocardiography to assess their cardiac function and hemodynamic status on admission (day 0), day 1, and discharge. We compared hemodynamic parameters in two study groups: children presenting with metabolic acidosis (base deficit >8) and children without acidosis.High-dependency unit, Kilifi District Hospital, Kenya.Acidotic patients received fluid resuscitation with either dextran 70 or starch at admission.Several markers of hemodynamic compromise were noted on admission, including severe tachycardia, low stroke volume index, and high inferior vena cava collapsibility index, which improved with subsequent readings. Overall, cardiac function assessed by ejection fraction (63.1% ± 5.2% vs. 71.9% ± 2.8%; p < .001) and left myocardial performance index (0.32 ± 0.16 vs. 0.25 ± 0.08; p = .03) was mildly abnormal on admission compared with discharge. Acidotic patients had worse hemodynamic indicators, with a significantly higher inferior vena cava collapsibility index on day 0 than nonacidotic patients (52.1 ± 21 .9 vs. 37.7 ± 15.4; p = .03), plus lower stroke volume index and worse cardiac function with higher left myocardial performance index (0.38 ± 0.18 vs. 0.26 ± 0.11; p = .05). Stroke volume index increased after first fluid bolus in 80% of children.Children with severe malaria and metabolic acidosis have evidence of hypovolemia and evidence of cardiac dysfunction.