Growth is considered to be the best global indicator of children's well-being, and growth impairment has both short- and long-term consequences.26–39
Progressive decline in nutritional status is linked with active and poorly controlled disease, and deteriorating cardiac function, morbidity and mortality.4–6
The present study reports a very high prevalence of malnutrition, in particular, severe forms of wasting and stunting, which were well above the WHO national estimates for growth deficiency in sub-Saharan Africa.28
Overall, the prevalence of CHD-related malnutrition was 90.4%, with 61.2% of cases having severe malnutrition. Among cases, the relative proportions of wasting, stunting and underweight were 41.1%, 28.8% and 20.5%, respectively. Contrary to the usual distribution of growth deficiency in the general paediatric population according to WHO reports, wasting was the most prevalent type of malnutrition in our study, rather than underweight and stunting.28 29
In the present study, the prevalence of wasting in children with CHD is five times higher than the WHO national estimate for wasting in Nigeria.
Wasting was associated with acyanotic CHD, while stunting was linked to cyanotic CHD.
As in the present study, previous reports showed that CHD-related malnutrition is especially common in developing countries, but prevalence varies widely from 27% up to 90.4% in the present study.19 20 22–24
Mehrizi and Drash23
reported a lower overall malnutrition prevalence of 27% among Turkish children based on percentiles. In South India, Vaidyanathan and colleagues reported a higher prevalence of underweight (59.0%) and wasting (55.9%) in children with CHD compared with the present findings, with wasting being more prevalent than stunting in children with CHD, as also in our study.19 20
Plausible explanations for the magnitude, severity and distribution of CHD-related malnutrition in the present study include the study setting, the distribution of cardiac lesions in the study cohort, the presence of severe complications of CHD such as CHF, and poor standard of care. This study was conducted in a tertiary teaching hospital to which cases with severe disease and CHD complications are likely to be referred for evaluation. Also, left to right shunt lesions in association with predominantly moderate to severe CHF were the most common cardiac lesions in the present study. Wasting, also called acute malnutrition, is attributable to acute events, while stunting (chronic malnutrition) is usually associated with prolonged suboptimal dietary intake. The present study did not investigate the role of acute infections, such as recurrent chest infections, diarrhoeal disease and other acute childhood illnesses, that may have contributed to the high prevalence of wasting. The prolonged duration of unoperated CHD suggested by the broad age range of the children in our study, in association with chronic hypoxaemia and/or chronic heart failure, and protracted suboptimal dietary intake, predispose to stunting in these patients.
In the present study, children with acyanotic CHD were more likely to be wasted, while those with cyanotic CHD were more likely to be stunted. Previous reports on the patterns of malnutrition in acyanotic and cyanotic CHD vary widely.24 30 34
Linde and colleagues34
reported that both wasting and stunting were more common in cyanotic CHD than in acyanotic CHD. Varan and colleagues24
noted that most infants (88%) with cyanotic CHD without pulmonary hypertension had mild malnutrition and that stunting was more common than wasting in these patients. This finding is somewhat similar to that of the present study even though we did not investigate the role of pulmonary hypertension. According to Varan and colleagues, cyanosis and pulmonary hypertension were important predictors of nutrition and growth in cyanotic CHD. Salzer and coworkers30
observed a preponderance of wasting in acyanotic CHD in association with left to right shunts and heart failure, compared with cyanotic CHD, which is similar to our findings. Notwithstanding the wide variation in the patterns and distribution of malnutrition in CHD, overall our findings are consistent with some previous reports, while some differences have been observed and highlighted.24 30 34
The heterogeneous nature of study methodologies across previous reports on somatic growth in CHD limits comparison of their findings. Studies differed in their design, eligibility criteria, study settings and sample size, as well as in the clinical characteristics of their study populations (symptomatic and asymptomatic), classification of malnutrition and reference growth standards used for interpretation of anthropometric indicators. Also, regional variations in the prevalence and distribution of undernutrition may also contribute to differences.28
The predictors of malnutrition in the present study included CHF, type of CHD, duration of symptoms, age under 5 years and poor dietary fat intake. These predictors are similar to those in previous reports and are generally modifiable by early corrective interventions, growth monitoring and nutrition supplementation. Previous studies that compared growth impairment in CHD before and after corrective interventions including surgery have demonstrated satisfactory recovery in somatic growth, although most such studies focused on infants.15–18
However, Vaidyanathan and colleagues20
in South India recently reported that severe malnutrition is not always reversed by corrective intervention. They found that persistent malnutrition after corrective intervention is predicted by nutritional status at presentation, birth weight and parental anthropometry. Prolonged unoperated symptomatic CHD suggested by the wide age range of children in the present study leads to long-term severe growth impairment. The high proportion (64.3%) of young children aged 0–59 months in this study and its predictive effect of CHD on severe malnutrition may be related to the natural history of CHD in addition to the role of inadequate and poor breastfeeding, weaning, and complementary and supplementary feeds in this age group. Under fives are the most vulnerable age group affected by malnutrition (undernutrition) in the general population.28 29
The predictive effect of pulmonary hypertension, birth weight, parental anthropometry, recent hospitalisation and recurrent respiratory infections on malnutrition in CHD, which have been previously reported,19 20
were not investigated in the present study.
It is noteworthy that notwithstanding the lower cut-off used (ie, a smaller p value to determine predictors of malnutrition in multiple regression analysis), a number of plausible predictors of malnutrition, some possibly related to one another (eg, low haemoglobin and low arterial oxygen saturation), were still highly and independently linked to the outcome. We postulate that this finding could reflect the strength of the impact of these factors on the development of malnutrition in this cohort of children. However, because our study had some limitations, especially possible selection bias due to the tertiary healthcare setting and aspects of our eligibility criteria, we cannot make any definite conclusions. Our study setting may have led to over-representation of children with severe and protracted disease, thereby increasing the number of factors significantly predicting malnutrition in these children. On the other hand, our eligibility criteria may have excluded some children with milder forms of malnutrition. Therefore, our finding cannot be extrapolated to the general population of children with CHD but will no doubt benefit from further investigations by other researchers in a more representative and heterogeneous population of children with symptomatic CHD.
The increased prevalence of anaemia as a complicating problem in children with symptomatic CHD is a new finding in our study. Also, the additive and predictive effect of anaemia and moderate to severe CHF in CHD-related growth deficiency is unique to the present study and deserves special comment. Anaemia with features suggestive of iron deficiency was highly prevalent in cases with CHD. Up to 66% of children with symptomatic CHD had anaemia, defined in this study as haemoglobin levels of ≤10.0 and ≤15 g/dl in acyanotic and cyanotic CHD, respectively. Anaemia was more common in acyanotic CHD (54.6%) than in cyanotic CHD (11.4%), and was associated with microcytic and hypochromic red blood cells in over half of the cases, suggesting that it may be caused by iron deficiency. Iron deficiency anaemia is linked with linear growth retardation in young children.40
However, we are not completely sure that iron deficiency anaemia was present as we did not estimate serum levels of iron and other indicators of iron deficiency. Based on multivariate logistic analysis, children with CHD who had low haemoglobin levels were six times more likely to be malnourished, and so the high prevalence of anaemia may be a consequence of the moderate to severe malnutrition. However, in children with cyanotic CHD, the anaemia may have been relative rather than absolute due to their higher haemoglobin levels and, in some cases, polycythaemia. Future studies may explore in greater detail the incidence, distribution and determinants of anaemia in CHD.
Notwithstanding the limitations regarding the definition of anaemia in CHD in our study, a high prevalence of anaemia in CHD can exacerbate the symptoms and complications of CHD, such as exercise intolerance and heart failure, as well as contribute to growth deficiency.40
The present study investigated the relationship between CHD-related malnutrition and categories of heart failure severity based on a validated scoring system.33
Although the predictive effect and mechanisms of heart failure in CHD-related malnutrition are widely reported,7–20
previous studies on malnutrition in CHD did not relate their findings to the severity of heart failure. In the present study, moderate to severe heart failure (Ross score of 7–15) was highly prevalent and predictive of malnutrition, which was predominantly moderate to severe. Children with CHD complicated by heart failure were four times more likely to be malnourished. We recommend future research explores further the association between heart failure and malnutrition in CHD, and a possible reciprocal relationship.
The strengths of the present study include its case–control design that allows temporal relationships and associations between CHD and malnutrition to be examined. Also, anthropometric measurements and categorisation of malnutrition are based on standard reference growth standards and the study population is well characterised. Furthermore, the broad age range of these children with unoperated CHD allows long-term growth impairment (wasting and stunting) to be evaluated.
There are few limitations to the present study, which include exclusion of children with palliated or corrected CHD, those with confirmed or suspected genetic syndromes, hospitalised children with CHD, and children with asymptomatic CHD. Our exclusion criteria may have caused selection bias, leading to underestimation of the true prevalence of malnutrition as some excluded cases may have had more severe malnutrition. The tertiary hospital setting may have led to over-representation of more severely affected children with CHD and, therefore, severe malnutrition. Also, our definition of anaemia in cyanotic CHD may have overestimated the proportion of anaemia in this subgroup of patients.
The present study describes growth abnormalities in children with CHD in a situation where their course is much closer to the natural history of these cardiac anomalies than in developed countries where early intervention is the rule. Among children with CHD in a developing country in sub-Saharan Africa, severe malnutrition in association with anaemia and moderate to severe heart failure, is highly prevalent preoperatively. The predictors and risk factors of severe malnutrition are modifiable through growth monitoring, nutrition counselling, nutrition supplementation, adequate control of CHD symptoms, use of booster blood transfusions and early corrective interventions. Although the effects of severe and chronic malnutrition on surgical morbidity and mortality are not explored in the present study, they are likely to be significant.19 20
Our study suggests that early weaning in acyanotic CHD may be a marker of fatigability associated with heart failure, which could help early recognition of CHD.
Findings in the present study could have significant implications for future research and for physicians caring for children with CHD as well as for policymakers in Nigeria and other developing countries. We recommend aggressive nutritional supplementation for the study population, while efforts at early definitive corrective interventions including surgery should be intensified.
Future research should explore the areas mentioned above as well as the short- and long-term impacts of nutrition supplementation on morbidity and mortality before and after corrective interventions for CHD. Also, micronutrient deficiencies in CHD should be examined so that this population of children can be given comprehensive nutrition supplementation.