Background
Case fatality in African children with severe acute malnutrition (SAM) remains high despite implementation of WHO management guidelines. Many deaths occur suddenly and unexpectedly leading to
speculation about sudden cardiac death. Fluid therapy remains controversial since SAM children are thought to be at high risk of cardiac failure. The evidence base for these recommendations is limited. We conducted a systematic review of the literature on cardiac function in severe malnutrition, and a comprehensive prospective observational study of Cardiac Physiology in Malnutrition (The CAPMAL Study).

Methods
Eighty-eight hospitalised Kenyan children with SAM were prospectively recruited and a detailed cardiovascular profiling including clinical, biochemical, echocardiographic and
electrocardiographic assessment at admission, during nutritional rehabilitation, and at 28-day follow-up was undertaken. The findings were compared with a group of non- malnourished hospital controls (n=22), frequency matched by age, gender and presenting clinical syndrome.
Results
Little evidence was found of clinically significant cardiac failure among children with SAM, including those who received intravenous fluids. Echocardiography indicated that cardiac dysfunction was common but typically associated with underlying comorbidities such as sepsis and HIV. We also found increased SVRI, which was negatively correlated with the severity of malnutrition. We did not find strong evidence that children with SAM were more likely to have cardiac dysfunction or arrhythmias than matched controls, or that the cardiovascular profile of marasmus differed from kwashiorkor.
Conclusions Clinical cardiac failure and sudden death from arrhythmias were not common among children in our study. The appropriate physiological response observed to IV fluids suggests they may be better tolerated than current guidelines suggest. Further studies are urgently needed to define optimal IV fluid regimens for children with SAM and shock and to investigate the role of increased systemic vascular resistance on gut perfusion and myocardial wall stress.