title: Cardiac function and hemodynamics in Kenyan children with severe malaria.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  High-dependency unit, Kilifi District Hospital, Kenya.
  
  
  METHODS
  Acidotic patients received fluid resuscitation with either dextran 70 or starch at admission.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Children with severe malaria and metabolic acidosis have evidence of hypovolemia and evidence of cardiac dysfunction.
authors.affiliation: Department of Infectious Diseases and Immunity, Hammersmith Campus, Imperial College, London, UK.
authors.forename: Sophie
authors.initials: S
authors.lastname: Yacoub
authors.forename: Hans-Joerg
authors.initials: HJ
authors.lastname: Lang
authors.forename: Mohammed
authors.initials: M
authors.lastname: Shebbe
authors.forename: Molline
authors.initials: M
authors.lastname: Timbwa
authors.forename: Eric
authors.initials: E
authors.lastname: Ohuma
authors.forename: Robert
authors.initials: R
authors.lastname: Tulloh
authors.forename: Kathryn
authors.initials: K
authors.lastname: Maitland
mesh_terms: D000138:Acidosis / Q000503:physiopathology; D000962:Antimalarials / Q000627:therapeutic use; D037621:Artemisinins / Q000627:therapeutic use; D000077332:Artesunate; D002648:Child; D002675:Child, Preschool; D017322:Clinical Trials, Phase II as Topic; D003906:Developing Countries; D003911:Dextrans / Q000008:administration & dosage; D004452:Echocardiography / Q000187:drug effects; D005260:Female; D005440:Fluid Therapy / Q000379:methods; D006333:Heart Failure / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006895:Hydroxyethyl Starch Derivatives / Q000008:administration & dosage; D007223:Infant; D015278:Intensive Care Units, Pediatric; D007630:Kenya; D016778:Malaria, Falciparum / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D011803:Quinine / Q000627:therapeutic use
chemical_list: D000962:Antimalarials; D037621:Artemisinins; D003911:Dextrans; D006895:Hydroxyethyl Starch Derivatives; D000077332:Artesunate; D011803:Quinine