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Cardiac failure in children with pneumonia in Papua New Guinea
F Shann1, D MacGregor, J Richens
1Royal Children's Hospital, Melbourne, Australia.
Insights
Right ventricular failure is common in children with severe pneumonia, likely due to pulmonary hypertension. Clinical signs of heart failure in these cases are often unreliable, and digoxin showed no effectiveness.
Area of Science:
- Pediatric critical care medicine
- Cardiology
- Infectious diseases
Background:
- Cardiac failure is a suspected, yet undefined, contributor to pneumonia mortality in children in developing nations.
- Pneumonia is a leading cause of child mortality globally, particularly in resource-limited settings.
Purpose of the Study:
- To investigate the role of cardiac failure in pediatric pneumonia mortality.
- To determine the prevalence and causes of cardiac dysfunction in children with severe pneumonia.
Main Methods:
- Prospective study of 47 children with severe pneumonia admitted to Goroka Hospital, Papua New Guinea.
- Utilized echocardiography, chest radiography, and cardiac enzyme assays (creatine kinase, lactate dehydrogenase).
- Assessed for myocardial injury, right ventricular dilatation, and hepatic vein changes.
Main Results:
- 15% of children died; 72% had severe or very severe pneumonia.
- No evidence of myocardial injury from sepsis was found.
- 26% of children exhibited signs of right ventricular failure (dilated right ventricle/hepatic veins), with a 33% mortality rate in this subgroup. Right ventricular failure was associated with hepatomegaly but not tachycardia.
Conclusions:
- Right ventricular failure, likely secondary to pulmonary hypertension, is common in severe pediatric pneumonia.
- Clinical signs of heart failure are unreliable indicators in this population.
- Digoxin demonstrated no efficacy in treating right ventricular failure associated with pulmonary hypertension in severe pneumonia.
Background:
Cardiac failure is suspected of contributing to mortality from pneumonia in children in developing countries, but its role has not been clearly defined.
Methods:
A convenience sample of 47 children admitted to Goroka Hospital in Papua New Guinea was studied prospectively with ultrasound, chest radiographs and assays of creatine kinase and lactate dehydrogenase. Results. Seven (15%) of the 47 children died. Of the 43 children who had a chest radiograph, 31 (72%) had severe or very severe pneumonia. No child had poor contractility of the heart on ultrasound examination or unequivocally raised cardiac isoenzymes; therefore no evidence of myocardial injury from sepsis was found. However, ultrasound examination showed dilatation of the right ventricle or hepatic veins in 12 (26%) of the children (both were dilated in 7 children) and 4 (33%) of these children died; this suggests that right ventricular cardiac failure secondary to pulmonary hypertension was present in 26% (95% confidence interval, 14 to 40%) of these children with severe pneumonia. Tachycardia was not associated with right ventricular dilatation on ultrasound, but 3 of the 4 children with more than 3 cm of liver palpable in the abdomen had right ventricular dilatation. Only 4 of the 12 children with right heart failure had hepatomegaly, tachycardia, raised jugular venous pressure or peripheral edema.
Conclusions:
Right ventricular failure is common in children with severe pneumonia, and it is probably caused by pulmonary hypertension rather than septic toxemia. The clinical signs of heart failure are unreliable. There is no evidence that digoxin is effective treatment for right ventricular failure secondary to pulmonary hypertension.
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