DEVELOPMENTAL AND SOCIAL QUOTIENT AMONG 0-15 YEARS OLD CHILDREN WITH
CONGENITAL HEART DISEASE
Dissertation
Submitted to
THE TAMILNADU Dr. M.G.R MEDICAL UNIVERSITY In partial fulfilment of the requirements for
the award of the degree of M.D. PEDIATRICS
B
RANCHVII
MAY 2020
CERTIFICATE - I
This is to certify that this dissertation entitled “Developmental and Social Quotient Among 0-15 Years Old Children with Congenital Heart Disease” is a bonafide record of the work done by Dr. D.Shivaashankari., under guidance and supervision of Dr. Elizabeth K.E. in the Department of Pediatrics during the period of her postgraduate study for M.D. Paediatrics [Branch-VII ] from 2018-2020.
Dr. Rema V. Nair, M.D., D.G.O.,
Director
Sree Mookambika Institute of Medical Sciences [SMIMS]
Kulasekharam, K.K District, Tamil Nadu - 629161
Dr. Elizabeth K.E., MD
[Guide]
Professor and HOD Department of Paediatrics, Sree Mookambika Institute of Medical Sciences [SMIMS]
Kulasekharam, K.K District, Tamil Nadu - 629161
Dr. Padmakumar, MS., Mch
Principal
Sree Mookambika Institute of Medical Sciences [SMIMS]
Kulasekharam, K.K District, Tamil Nadu -629161
CERTIFICATE - II
This is to certify that this dissertation work titled “Developmental and Social Quotient Among 0-15 Years Old Children with Congenital Heart Disease” of the candidate Dr. D. Shivaashankari., with registration Number 201817702 for the award of MD in the branch of Pediatrics [Branch-VII]. I personally verified the urkund.com website for the purpose of plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 6 percentage of plagiarism in the dissertation.
Guide & Supervisor sign with Seal
DECLARATION
In the following pages is presented a consolidated report of the study
“Developmental and Social Quotient Among 0-15 Years Old Children with Congenital Heart Disease” on cases studied and followed up by me at Sree Mookambika Institute of Medical Sciences, Kulasekharam from 2018-2020.
This thesis is submitted to the Dr. M.G.R. Medical University, Chennai in partial fulfilment of the rules and regulations for the award of MD Degree examination in Pediatrics.
Dr. D. Shivaashankari Junior Resident
Department of Pediatrics, Sree Mookambika Institute of Medical Sciences,
Kulasekharam, K.K District, Tamil Nadu- 629161.
Dr. Elizabeth K.E., MD
[Guide]
Professor and HOD Department of Paediatrics, Sree Mookambika Institute of Medical Sciences [SMIMS]
Kulasekharam, K.K District, Tamil Nadu - 629161
ACKNOWLEDGEMENT
It's time to look back and express my gratitude to all those wonderful people without whom my journey as a postgraduate wouldn't have been a smooth sailing.
Hence at the outset let me thank the almighty for giving me all I have and making all this possible.
My deepest gratitude and respect to my beloved Chairman Dr. C.K. Velayuthan Nair and Director Dr. Rema V. Nair for providing facilities to accomplish my dissertation work.
I also extend my sincere thanks to Principal Dr. Padmakumar for the great support.
I would like to express my sincere thanks to Vice Principal Dr. R.V. Mookambika for her immense help.
It is my distinct privilege and honour to have worked under the guidance and supervision of Dr. Elizabeth K.E, Professor and HOD of Paediatrics, Sree Mookambika Institute of Medical Sciences, Kulasekharam. I express my feeling of gratitude and sincere appreciation for her guidance, constant support and encouragement in making the study possible. Her constant help, patience and guidance helped me at every stage from conception to completion of this dissertation.
I am blessed and privileged to be taught by such an eminent teacher.
I express my gratitude and sincere thanks to the Dr. Rugmini K, Professor, for her immense help, unconditional support and constant encouragement in preparing this dissertation.
I express my gratitude to the Dr. Nedunchezhiyan, Associate Professor, for his invaluable help in preparing this dissertation.
I also express my gratitude and sincere thanks to Dr. Sanjay Masaraddi, Associate Professor, for his immense help, valuable suggestion and encouragement in completing this study.
I express sincere gratitude to my co postgraduates to Dr. Divya, Dr. Newsha, Dr. Naveen, Dr. Anjana for helping and supporting me in preparing this thesis.
I am thankful to all other non-teaching staff members for their support and co- operation in completing this work.
Lastly, I am forever indebted to my parents, Mr.Dharmalingam, Mrs R. Vijayalakshmi, my younger brother Mr. D. Maheshwar and other family
members for their support, and understanding throughout my study period.
I would like to thank Mr.Randeep, clinical pediatric psychologist for immense help in completing this dissertation.
I would like to thank Leos Data Makers for their immense help in completing this dissertation.
I am grateful to all the parents of children of the study for their kindly cooperation.
Finally, I pay my prayers to the Almighty God for his blessings without which I could not have completed my dissertation.
Dr. D. Shivaashankari
ABBREVIATION
CHD - Congenital Heart Disease
DQ - Developmental quotient
SQ - Social Quotient
PDA - Patent Ductus Arteriosus TGA - Transposition of great arteries DORV - Double outlet right ventricle VSD - Ventricular Septal Defect ASD - Atrial Septal Defect TOF - Tetrology of Fallot
RBSK - Rashtriya Bal Swasthya Karyakram
WFA - Weight for age
HFA - Height for age
WFH - weight for height
BMI - Body Mass Index
WHO - World Health Organization IAP - Indian Academy of Pediatrics DST - Developmental screening Test VSMS - Vineland Social Maturity scale AGA - Appropriate for Gestational age LBW - Low Birth Weight
LIST OF CONTENTS
Sl. No Contents Page No
1 Introduction 1
2 Aims and Objectives 3
3 Hypothesis & Scientific Justification 4
4 Review of Literature 5
5 Materials and Methods 40
6 Results 44
7 Discussion 67
8 Summary 77
9 Conclusion 79
10 Limitation & Recommendation 82
9 Bibliography i - xiv
10 Appendix
LIST OF TABLES
Sl. No Tables Page no.
1 Age distribution 44
2 Gender distribution 45
3 Distribution according to age and gender 46
4 Distribution according to socio economic status (Modified
Kuppuswamy socio economic scale-2019) 47
5 Distribution according to type of CHD 48
6 Distribution according to family members with CHD 49 7 Distribution according to gestational age 50
8 Distribution according to birth weight 51
9 Distribution according to weight for age (IAP
Classification) 52
10 Comparison of underweight according to type of CHD 53 11 Distribution according to HFA (Stunting)- Waterlow’s
Classification 54
12 Comparison of stunting according to type of CHD 55 13 Distribution according to WFH (Wasting) -Waterlow’s
Classification 56
14 Comparison of wasting with type of CHD 57
15 Distribution according to BMI (WHO BMI chart 0-5 years.
& WHO BMI chart 5-18years) 58
16 Comparison of BMI according to type of CHD 59 17 Distribution of developmental delay according to Bharat
Raj Developmental screening test 60
18 Distribution of DQ score according to Bharat raj
Developmental screening test 61
19 Comparison of DQ in ACHD and CCHD 62 20 Distribution of Social quotient according to Vineland
Social Maturity Scale - Indian adaptation by Malin 63
21 Comparison of SQ In ACHD and CCHD 64
22 Comparison of SQ with developmental delay 65 23 Comparison of mean DQ and SQ in ACHD and CCHD 66
LIST OF FIGURES
Sl. No. Figures Page no.
1 Bar chart of age distribution 44
2 Pie chart of gender distribution 45
3 Clustered bar chart of distribution according to age and
gender 46
4 Pie chart of socioeconomic status distribution (Modified
Kuppuswamy socio-economic scale-2019) 47
5 Pie chart of distribution according to type of CHD 48 6 Bar chart of distribution according to family members
with CHD 49
7 Pie chart of distribution according to gestational age 50 8 Pie chart of distribution according to birth weight 51 9 Pie chart of distribution according to WFA
(Underweight)-IAP Classification 52
10 Clustered bar chart of comparison of underweight
according to type of CHD 53
11 Pie chart of distribution according to HFA (Stunting)
Waterlow’s Classification 54
12 Stacked bar chart of comparison of stunting according to
type of CHD 55
13 Pie chart of Distribution according to WFH (Wasting) -
Waterlow’s Classification 56
14 Stacked bar chart of comparison of wasting with type of
CHD 57
15
Clustered bar chart of comparison distribution according to BMI (WHO BMI chart 0-5 years &WHO BMI chart 5- 18years)
58
16 Stacked bar chart of comparison of BMI according to type
of CHD 59
17 Pie chart of distribution of developmental delay
according to Bharat raj Developmental screening test 60 18 Pie chart of distribution of DQ according to Bharat Raj
Developmental screening test 61
19 Clustered bar chart of comparison of DQ in ACHD and
CCHD 62
20
Pie chart of distribution of social quotient according to Vineland Social Maturity Scale - Indian adaptation by Malin
63
21 Stacked bar chart of comparison of SQ In ACHD and
CCHD 64
22 Stacked bar chart of comparison of SQ with
developmental delay 65
23 Line chart of comparison of mean DQ in ACHD and
CCHD 66
ABSTRACT
ABSTRACT
Background
Children with CHD are at higher risk for malnutrition, developmental delay and impaired social maturity. Recently there is a shift in focus from heart related morbidity to concern for developmental outcome and social maturity related assessment and rehabilitation.
Objectives
To assess the nutritional status, developmental and social quotient of children aged 0-15 years with CHD and to find out the relation of nutritional status, developmental and social quotient with type of CHD.
Methodology
The present study included 60 children with CHD attending Department of Pediatrics, Sree Mookambika Institute of Medical science, Kulasekharam during the period from January 2019 to August 2019. Detailed history including socio economic status and physical examination findings were recorded using structured questionnaire, Anthropometric measurements were undertaken to assess nutritional status, Developmental quotient were assessed using developmental screening test by Bharat Raj and the Social quotient was assessed using Vineland social maturity scale- Indian adaptation by Dr.Malin respectively.
Results
In the present study out of 60 children aged 0-15 years with CHD, 28(46.7%) belonged to 0-5 years age group and 32(53.3%) belonged to 5-15 yrs age group. The
Male to female ratio was 1:1.4. 52(86.6%) had ACHD and 8(13.4%) had CCHD. The most common was VSD 19(31.6%) followed by ASD 18(30%). 37(61.7%) were underweight, 31(59.6%) in ACHD group and 6(75%) in CCHD group. 29(48.3%) had stunting, 23(44.2%) in ACHD group and 6(75%) in CCHD group indicating chronic malnutrition. Stunting was significantly more in CCHD group 6(75%) compared to ACHD group 23(44.2%). 40(66.7%) had wasting, 33(63.5%) in ACHD group and 7(87.5%) in CCHD group indicating acute malnutrition.
As per BMI, 8(28%) thinness in 0-5 years group compared to 21(65.6%) in 5- 15 years group. This difference was statistically significant (P value-0.006).
24(46.2%) in ACHD group and 5(62.5%) in CCHD group. 39(63.3%) had developmental delay, 31(59.6%) in ACHD group compared to 7(87.5%) in CCHD group. This difference was statistically significant (P value 0.001). 52 children (86.7%) had impaired social maturity (SQ<85), 44(84.6%) in ACHD group, 8(100%) in CCHD group. The mean DQ in children with CHD was 74.2(+/-17.9). DQ was significantly more in ACHD group 77.23(+/-17.2) compared to 57.87(+/-16) in CCHD group. The mean SQ in children with CHD was 63.18(+/-17.5). SQ was significantly more in ACHD group 65.21(+/-17.2) compared to 50(+/-12.8) in CCHD group.
Conclusion
More number of female children were enrolled for intervention under RBSK scheme in this study. Malnutrition especially stunting, developmental delay and impaired social maturity were more in children with CHD. Stunting, developmental delay were significantly more in CCHD than ACHD. This necessitates early screening for nutritional status, developmental delay and social maturity.
Early identification and appropriate nutritional and developmental interventions are recommended in children with CHD under RBSK Scheme and Chief Minister’s Comprehensive Health Insurance Scheme.
Keywords:
Congenital heart disease, Developmental delay, Development quotient, Social maturity, Social quotient.
INTRODUCTION
Page 1
INTRODUCTION
Congenital heart disease (CHD) is the most common group of congenital anomalies.1,5 The prevalenceof CHD has been reported as 8-12/1000 live births in India and globalprevalence is 9per 1000 live birth.Survival rates inchildren with CHDhasbeenincreasingwithadvancesinbetterdiagnosticmodalitiesandsurgical, nonsurgical interventions. Children with CHD are considered to be at high-risk for neurodevelopment delay.6 Currently there is a shift in focus from heart-related morbidity to concern for nutritional, developmental and neurological outcomes in the view of risk formalnutrition, lower developmental quotient (DQ)and impaired socialquotient(SQ)duetovariousmedicalandsocioeconomicreasons.7
In children with CHD, both in utero and after birth there may be an impact on brain development due to altered cerebral blood flow with impaired cerebral oxygen delivery. Thebrain is lessmature and morevulnerable atbirth. Thecritical time for brain growth and maturation, myelination, and development of neural networksarethefoetalandneonatalperiods.Anyalteredbrainmaturityandcerebral blood flow duringthese sensitive developmentalperiods maylead to increasedrisk ofdevelopmentaldelay.8
The children with CHD are with adverse neurodevelopmental outcomes,
malnutrition in large proportion and experience varying degrees of developmental delaysinseveral domainsthatcanpersist throughoutchildhoodandadult life.They are often restricted from interactive play and social gatherings and have less social interaction due to cardiac debilitation, exercise intolerance, prematurity, low birth weight issues which impact their social quotients adversely.9 Those with CHD are
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not regularly being provided proper screening for malnutrition, developmental and social maturity. Parental anxiety and overprotectiveness of children with CHD may reduce child’s exposure to peers which might influence the child’s social competence.10
A number of studies have been undertaken on children with CHD and its effect on nutritional and developmental status. Indian data on impact of CHD on developmental and social quotient in the children with CHD is scanty. The present study focuses on association between nutritional status, DQ and SQ among children with congenital Heart disease.
Periodic anthropometric, developmental, and social maturity assessment and early identification and intervention at appropriate age can alter the long-term nutritional status, neurodevelopmental outcomes and social maturity in the children with CHD. Hence this study was planned to evaluate nutritional status, DQ and SQ in children aged 0-15 years with CHD. This is expected to create opportunities and support to enhance later academic, behavioral, psychosocial and adaptive function.
AIMS & OBJECTIVES
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AIM AND OBJECTIVES
Primary objective: To assess the nutritional status by anthropometric measurements, Developmental quotient using Developmental screening testand Social Quotient using The Vineland Social Maturity Scale- Malin’s Indian Adaptation in children aged 0-15 years with CHD
Secondary objective: To find out the relation of nutritional status, developmental quotient and social quotient with type of CHD.
HYPOTHESIS &
SCIENTIFIC JUSTIFICATION
Page 4
HYPOTHESIS & SCIENTIFIC JUSTIFICATION
Scientific Justification:
In children with CHD, altered cerebral blood flow with impaired cerebral oxygen delivery, both in utero and after birth may impact brain development. In utero brain development is delayed in children with some types of complex CHD, the brain is less mature and more vulnerable at birth. The foetal and neonatal periods are a critical time for brain growth and maturation, myelination, and development of neural networks. Altered cerebral blood flow and brain immaturity during these sensitive developmental periods may lead to increased risk of Developmental Delay.
Parental anxiety and overprotectiveness of CHD children may reduce child’s exposure to peers which might influence the child’s social competence and affects the social quotient. Children with CHD are more prone for acute and chronic malnutrition due to chronicity of cardiac morbidity, hypoxia, recurrent infections, frequent hospitalisation, and poor absorption of nutrients in the gastrointestinal tract due to congestive heart failure.
Alternate Hypothesis:
There is a relation between nutritional status, DQ and SQ with type of CHD
REVIEW OF LITERATURE
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REVIEW OF LITERATURE
Historical Review
In 1673 the first description of congenital heart defect was given by Danish anatomist Nicolas Steno which was named by Fallot of Marseilles as Tetralogy of Fallot in 1888. The monumental work of Maude Abbott’s atlas of congenital cardiac disease in 1936 made a remarkable advance and became a milestone in understanding the pathophysiology and anatomy of diverse CHD.5 The team approach between clinicians, physiologists interested in cardiopulmonary hemodynamics and electrophysiology, radiologists and daring surgeons including those involved in animal experimental surgery been highlighted as second era of progress.
The third era begins in the mid 1970 with cardiac repair surgeries with concurrent understanding of cardiovascular anatomy. The mysteries of genetic, molecular, and teratological basis of fetal cardiac malformations been unravelled in early 1990’s. This helped in working out possible preventive strategies in occurrence of CHD.5 The rapid embryonic growth and the consequent nutrient requirements necessitates early development of a functional heart and vascular system. This facilitates the early operational cardiovascular circulation in foetus to supply nutrients, growth factors and cellular signaling molecules to various developing tissue and organ systems by day 21.
Problem statement
The prevalence of CHD has been reported as 8-12/1000 live births in India and global prevalence is 9 per 1000 live birth.6 CHD is the most common congenital anomaly contributing to almost one third of all birth defects. The increased survival
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of children with CHD is achieved through massive breakthrough in cardiovascular diagnostics and surgery. Its etiology is mostly unknown, some are chromosomal abnormalities, prenatal exposure of certain therapeutic drugs, maternal illnesses, combinations of environmental teratogens and genetic and chromosomal conditions.
Congenital heart disease is a gross structural abnormality of the heart or intrathoracic great vessels that is actually or potentially of functional significance.9
There will be obvious differences between the serious lesions like TOF and large ventricular septal defect (VSD) with Atrial septal defect (ASD). It is useful to grade CHD into three groups based on their severity.9
1) Severe CHD9
It indicates the category of the children who present in the newborn period or early infancy and severely ill.
A) All those with cyanotic heart disease
Tetralogy of Fallot, including pulmonary atresia and absent pulmonary valve.
D-transposition of the great arteries.
Hypoplastic right heart
Tricuspid atresia
Pulmonary atresia with an intact ventricular septum
Ebstein anomaly
Hypoplastic left heart
Aortic atresia
Mitral atresia
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Single ventricle
Double outlet right ventricle (DORV)
Truncus arteriosus
Total anomalous pulmonary venous connection (TAPVC)
Critical Pulmonary Stenosis (PS)
Miscellaneous uncommon lesions like double outlet left ventricle, certain unusual malposition and some form of L- transposition of the great arteries.
B) Acyanotic lesions
AVSD
Large VSD
Large PDA
Critical or severe AS
Severe PS
Critical Coarctation of aorta
2) Moderate CHD
These require less intensive than those listed above but expert care. Most of these are detected in a clinical study. They include
Mild or moderate AS or Aortic incompetence
Moderate PS or incompetence
Non critical coarctation of aorta
Large ASD
Complex forms of VSD
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3.Mild CHD
This is the most numerous groups. They are asymptomatic often undergo early spontaneous resolution of the heart lesions, this group greatly influences the incidence of CHD.
Small VSD
SmallPatent ductus arteriosus (PDA)
Mild PS
Bicuspid aortic valve (BAV) without Aortic stenosis (AS) or aortic incompetence, they may move to moderate or severe categories if they deteriorate with age.
Small or spontaneously closed ASD Epidemiologyof CHD
The prevalence of severe CHD been reported as 8-12/1000 live births in India. Echocardiography usage is associated with increased birth prevalence of CHD. The children with CHD seeking health care facility is determined by the individual conditions and natural history.6
Current status of CHD
The important concern pertaining to care of the children with CHD is the gross disparity between high income and low, middle income countries. In Asia one cardiac centre serves16 million population whereas 1,20,000 in North America. The number of cardiac surgeons serving are more in Europe and North America are 1 cardiac surgeon per 3-5 million population whereas in India one cardiac surgeon per 25 million population. A large pool of older infants and children without intervention whomay have survived adding to burden of CHD.5
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Regional variations
In various part of India, there are marked regional variations in the population and crude birth rate. The total birth is higher in Northern and eastern parts so the total children with CHD is higher in these states with increased birth rate. Jharkhand, Uttar Pradesh, Madhya Pradesh have much higher CHD burden.
The children born with CHD in southern India have a 70% chance of getting cardiac care than other parts of India.
Obstacles to pediatric care in India 6
1) Lack of awareness and delay in diagnosis.
Substantial home deliveries may prevent the early diagnosis of infant with ductus dependent CHD and also due to early discharge from hospital may escape early diagnosis.
Pre discharge screening with pulse oximetry often not practiced mainly in rural and urban centers. Since primary caregivers and frontline health workers are not sensitized to the problem of CHD, leads to delay in referral results in poor outcomes as complications and co morbidities like under nutrition would have started occurring.6 2) Maldistribution of resources.
There are maldistribution and inadequate availability of resources. Poverty remains the greatest barrier to treatment of CHD. Another neglected issue in India is transport of newborn and infants with CHD.
3) Financial constraints.
Most of cardiac Centre are in private sector which are not affordable and half of families borrowing money and losing their wages during care of their sick
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children. 20% of cardiac surgeries are funded by charitable organization. Only few are providing completely free of cost. Availability of medical insurance not equally existent in India except for Tamilnadu and few states.
4) Health seeking behaviour of the community.
Due to illiteracy, there is delay in seeking medical care. Girls may be put at a disadvantage compared to boys due to gender bias.
5) Lack of follow up care.
Large number of children from middle or low socioeconomic strata are lost to follow up for long term care and good outcome.
Risk factors in CHD
Children with CHD are at risk of preterm birth and low birth weight due to hemodynamic disturbance, chronic hypoxia and associated anomalies, among them important cause of low birth weight is the spontaneous preterm delivery. The recurrence risk of CHD is higher when their parents or siblings affected with CHD denoting multifactorial inheritance and its genetic basis. Other important factors which increases the risk of CHD along with genetic causes are the socioeconomic status and maternal education which determines the incidence of CHD and its prevention by antenatal checkups, avoiding teratogenic drugs, and screening for maternal illnesses like Gestational diabetes and preeclampsia.8
Øyen et al in 2009 conducted a national cohort study on 18708 CHD patients found that in the first-degree relatives, the recurrence risk ratio was 79.1, Atrioventricular septal defect was 24.3, isolated ASD was 7.1, isolated VSD -3.4.
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Overall recurrence risk ratio for the same defect was 8.15. Strong familial clustering in first degree relatives ranging from 3 fold to 80 fold showed by specific CHD.10
Peyvandi et al in 2014 at the children hospital of Philadelphia in their cross- sectional study in relatives of probands with conotruncal defects to examine the risk of CHD reported that the risk of CHD was higher in siblings (44%) than in parents.
Probands with tetralogy of fallot had the highest risk, and lowest in D-TGA. They concluded that the recurrence risk varies by lesion and relationship based on cardiac lesion and complexity particularly among siblings.11
Ellesøe GS et al in 2016 at university of Copenhagen, Denmark in their observational study found the familial co- occurrence of lesions follows specific patterns. District groups of cardiac malformation co-occur in families, and also suggest the influence from underlying developmental mechanisms.12
Steurer AM et al, in 2012 at university of California in their cohort study they quantified gestational age specific mortality and neonatal morbidity in infants with CCHD was lowest at 39 to 42 weeks (0.2%) and highest at 29 to 31 weeks’
gestation (0.9%). The morbidity remains increased across all gestational group comparison with infants born at 39 to 42 weeks.13
Lass E et al, in 2012 in their population based study reported that there was 2 fold increase in preterm birth in infant with CHD than the general population and there was increased risk of spontaneous preterm birth than medically induced preterm delivery. Risk of preterm delivery is higher for left ventricular outflow tract anomalies than isolated ventricular septal defect and the risk existed even after excluding other congenital anomalies. They concluded that the higher risk of preterm birth in CHD was due to spontaneous preterm delivery.14
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Levy et al, from Children’s hospital, Boston in their study reported that there was increased association of major CHD in children with lower mean birth weight.
Atrial septal defect and Patent ductus arteriosus had lower mean birth weight, and pulmonic stenosis, hypoplastic left heart, D-transposition had greater mean birth weight.15
Yu D et al, in 2014 from department of cardiothoracic surgery, Nanjing University, China in their meta analysis reported that there was an association between low socioeconomic status and increased risk of CHD including maternal education, family income, maternal occupational prestige and concluded that the maternal education is the main factor in preventing development of CHD. They suggested to find the at risk population based on socioeconomic status to device government policies in order to prevent CHD.16
Nutritional status in children with congenital heart disease
Children with CHD are more prone for acute and chronic malnutrition due to chronicity of cardiac morbidity, hypoxia, recurrent infections, frequent hospitalisation, and poor absorption of nutrients in the gastrointestinal tract due to congestive heart failure. In India majority of the children who live below the poverty line in an environment of multi deprivation and starvation have physical and developmental retardation. Severe forms of malnutrition like marasmus and kwashiorkor represent only tip of the iceberg. Many more suffer from moderate, mild or invisible malnutrition.17,18
Malnutrition is generally classified according to weight for age. Chronic malnutrition is classified according to height for age and acute malnutrition according to weight for height.
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B) Classification according to weight for age: WFA is the most commonly used parameter to classify nutritional status / underweight.4
a) Gomez Classification: Gomez and his associates gives first classification of malnutrition which came in 1956. It has three degrees. All cases of oedema are included in third degree malnutrition irrespective of weight for age.4
Nutritional status Underweight WFA (% of expected)
Normal >90
First degree 75-90
Second degree 60-75
Third degree* <60
*—-> All cases with edema to be included in third degree irrespective of weight for age.
b) Jelliffe’s classification: It has four degrees of malnutrition and it was proposed in 1965.
Nutritional status -Underweight WFA -% of expected
Normal >90
First degree 80-90
Second degree 70-80
Third degree 60-70
Fourth degree <60
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c) Wellcome trust or International Classification:
It is a clinical classification suggested by the Wellcome trust in 1970. It is based on weight for age and the presence or absence of edema.
WFA (% of expected) Oedema Clinical type of malnutrition
60-80 + Kwashiorkor
60-80 — Underweight
<60 — Marasmus
<60 + Marasmus kwashiorkar
d) Indian Academy of Pediatrics Classification:
It is the most popular classification in India proposed by IAP in 1972. It has four grades. Weight for age <60% is further classified to grade III, IV to highlight that very severe malnutrition exists. If the patient has oedema of nutritional origin the letter ‘K’ is placed along with grade of malnutrition to denote kwashiorkor.
Nutritional status - Underweight WFA % of expected
Normal >80
Grade I 71-80
Grade II 61-70
Grade III 51-60
Grade IV <50
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B) Classification according to height for age:
The calculation based on weight for age does not help to find malnutrition is of recent or past onset. Waterlow from London and McLaren from Beirut, independently came out with HFA and WFH concept to indicate stunting and wasting respectively in 1972.4
HFA is used to grade stunting. It indicates past or chronic malnutrition.
Classification according to HFA4 Waterlow’s classification
Stunting HFA % of expected
Normal >95
First degree stunting 90-95
Second degree stunting 85-90
Third degree stunting <85
Mclaren’s classification
Stunting HFA % of expected
Normal >93
Short 80-93
Dwarf <80
Visweshwara rao classification
Stunting HFA% of expected
Normal >90
First degree stunting 80-90
Second degree stunting <80
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C) Classification according to weight for height (WFH)
It is used to grade wasting. Wasting indicates recent or acute malnutrition.
Waterlow’s Classification
Wasting WFH ( % of expected weight for that height)
Normal >90
First degree wasting 80-90
Second degree wasting 70-80
Third degree wasting <70
Mclaren’s classification
Wasting WFH ( % of expected weight for that height)
Normal >90
Mild wasting 85-90
Moderate wasting 75-85
Severe wasting <75
Body mass index (BMI)
This is expressed as weight in kg / height2 expressed in meter square. It is very good index of body’s reserve or loss of fat. The extent of wasting, and tendency for obesity can be obtained. It is assessed using reference curves. In adult 18.5-25 is considered normal. <-3 SD in the WHO BMI chart denotes severe Thinness and <-2 SD denotes thinness in growing children. BMI > 25 indicates overweight and > 30 indicates obesity.4,5
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Prevalence, Predictors and Pathophysiology of Malnutrition in CHD Hassan et al, in 2015 in their study on children with congenital heart diseases found that the prevalence of wasting and stunting were significantly higher in children with CHD. Malnutrition correlated significantly with low arterial oxygen saturation, heart failure, pulmonary hypertension, and poor dietary history.19
Vaidyanathan et al, in 2008 in their study on Malnutrition in congenital Heart disease reported that the malnutrition was very common in children with CHD and is predicted by presence of congestive heart failure, older age at correction and lower growth potential. Corrective intervention significantly improved nutritional status on short- term follow-up.20
Forchielli ML et al, in 1994 opined in their study that the type of cardiac lesion in CHD decides the mechanism of malnutrition. Low energy intake due to loss of appetite and anorexia, acidosis, malabsorption, increased requirements, hyper metabolism raised out of multiple infective episodes, increased oxygen consumption, increased basal body temperature, low body fat stores, age at time of surgery, prenatal factors such as parental height, genetic factors, intrauterine feta, birth weight are the other deciding factors of malnutrition.21
Jackson M et al, in 2007 at Liverpool in their study on failure to thrive infant with congenital heart disease found that the main contributing factors are lower energy intake, high energy expenditure. They found that the mean weight gain is increased after increasing energy intake.22
Hubschman L et al, in 2013 at Newyork opined in their study that the increased metabolic demands, inadequate nutrient intake due to delayed feeding
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milestones and volume overload on the right ventricle, and decreased splanchnic perfusion leading to insufficient nutrient absorption contributes to the main pathophysiology of malnutrition.23
Varan B et al, in 1998 at Turkey in their study found that the severe malnutrition were more in acyanotic CHD with pulmonary hypertension and mild or borderline malnutrition found in cyanotic group with pulmonary hypertension.24
Elizabeth KE et al, in 2015 in their study on Clinical profile and referral pattern among children with CHD before and after introduction of the RBSK scheme, reported that the proportion of underweight children with CHD was 81.4%, wasting was 58.6% and stunting was 61.4%.25
Swagata M et al, in July 2016 at Karnataka in their case control study assessed the effect of congenital heart disease on growth and affected areas on anthropometry. She concluded 82% were underweight and 86% were stunted.26
Rubia et al, in 2018 in Department of Pediatrics, Jawaharlal Nehru Medical College, 2018, India in her case control study on anthropometric assessment on children with CHD found that 58.72% of children were underweight compared to 41.6% of controls and 82.53% were wasted when compared to 24.6% of controls.
They reported that there was statistically significant correlation between malnutrition with congestive heart failure and pulmonary hypertension.27
Balogun MF et al, Department of Pediatrics, University College Hospital, Nigeria in 2018 in their case control study reported that the socioeconomic status, cyanotic congenital heart disease and delayed surgical intervention highly correlated with malnutrition in children with CHD.28
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NEURODEVELOPMENT IN CHD
In children with CHD, altered cerebral blood flow with impaired cerebral oxygen delivery, both in utero and after birth may impact brain development. The foetal and neonatal periods are a critical time for brain growth and maturation, myelination, and development of neural networks. Altered cerebral blood flow and brain immaturity during these sensitive developmental periods may lead to increased risk of Developmental Delay.29,30
Neurodevelopment refers to a process of functional maturation and acquisition of new skills related to maturation of neural structures. It is the biological, psychological, and emotional changes that occur in humans in the period between birth and the end of adolescence as the individual progresses from dependency to increasing autonomy.2,5
Growth implies increase in size of organs and body whereas development implies differentiation and maturation of function.
Growth —> Quantitative growth Development —> Qualitative growth
Development is influenced by the physical, emotional and social environment. Cognitive growth and development are difficult to differentiate from behavioral and neurological maturation in early childhood. In later childhood cognitive abilities and communicative skills can be measured. It is a continuous process with a predictable sequence and yet it has a unique course for every child.
Social, moral and language development occurs simultaneously in the course of development. It also refers to the qualitative changes occurring in a progressive, orderly and coherent manner that enable the child for higher level of function.
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Progressive —> changes are unidirectional (forward)
Orderly and coherent —> Significant attainment of a particular skill build on achievement of earlier skills and skills are not skipped.
During development of the brain, the most important phase of neuronal proliferation and migration occurs in the intrauterine period, hence antenatal care and health of the child who is prospective mother is of utmost importance. After birth, first 2 years of life include a period of rapid brain growth and myelination. By 2 years of age brain attains 80% of growth and myelination becomes complete, hence any insults or deprivation in blood supply or nutrition will grossly affects the brain growth.5
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Laws of Development
1) It is continuous process from conception to maturity and is related to maturation and myelination of nervous system.
2) It occurs in an orderly and predictable sequence which is intrinsically determined.
3) Attainment of new skills builds on achievement of earlier skills.
4) Proceeds in cephalocaudal direction i.e. from head to toe.
5) It follows proximodistal principle i.e. from the centre of the body outwards 6) It proceeds at different rates influenced continuously by intrinsic factors
that produce individual variation and make each child’s development unique.
7) There occurs developmental dissociation i.e. development in one field may not necessarily parallel development in other fields.
8) It proceeds from general to specific i.e response to generalized reflexes to discrete voluntary actions.
9) Cognitive development proceeds from simple to complete tasks.
10) Before achieving voluntary functions, certain primitive reflexes have to be lost. Persistence of primitive reflexes beyond the age at which they should disappear denotes abnormal development.
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Factors affecting development
Intrinsic ( biological factors ) Extrinsic ( environmental factors )
Temperament Parental health status
Brain dysfunction Parenting style
Genetic and chromosomal disorders Family environment Defects of vision Social cultural environment
Hearing loss Environmental toxin exposure
Gestational age Stress
Nutrition Chronic illnesses
Developmental delay
Developmental delay is a term used for condition in which the child not developing or achieving age appropriate skills. It refers to a childhood mental or physical impairment or both which results in substantial functional limitations in major life activities. It is critical to identify it early for the wellbeing of children and their families.
Milestone checklists or informed questions to parents give a snapshot of dynamic process and helps in the detection of developmental disabilities. It is absolute mandatory to screen every high-risk infant for developmental delay.
Children with developmental delay should be given stimulation and educational services either in regular classes with extra resources i.e. mainstreaming them or in special classes. Early identification is important for implementing educational and rehabilitative services for children to improve outcome.
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Developmental assessment
Developmental assessment is an integral component of comprehensive child evaluation. It needs a thorough understanding of normal and typical sequence of development to assess the child’s true developmental status.
Acceptable variations and knowledge of normal development along with the clinical examination findings with accuracy is essential to recognize pathological early patterns to indicate developmental disability. This is very essential for follow up of high-risk babies. Referral and early intervention of these developmental disabilities necessitates early recognition of developmental delay. This enables the child to attain the maximum development potential as brain plasticity permits reorganization of neural networks and there are critical windows of opportunity for learning different types of skills. Normal findings during developmental assessment can be reassuring to parents. 26 Knowledge of normal development has important role in behavioral assessment. It can be interpreted as child’s level of developmental function. Child can be significantly advanced in one domain but lacks in other domain needs environmental and educational placement adjustments to attain their full potential.
Developmental screening test
It is a brief standardized test which helps in identifying children at risk of a developmental disorder. Screening tools like ages and stages questionnaire can be completed by moderately educated parents and the answers can be scored even by a non- physician. Final interpretation must be done by the paediatrician. It is not diagnostic but identifies the areas where the child is lagging. Developmental screening test should be administered periodically.
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Referral to rehabilitation services
When a child is identified to have developmental delay, they should be referred to a center which has specialized services. The pediatrician should be aware of the centers in the local areas where psychologists, occupational therapists, audiologists and other such facilities are available.30,31
Development Assessment scales
b) Denver developmental screening test (DDST): It was originally designed as a screening test. It is now increasingly used as a tool for routine developmental
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assessment. It is suitable for the guided assessment of all the four areas of development in children up to 6 years of age. This will take 10-25 minutes only.
c) GESELL development schedule: It measures the four functional areas of development in children up to 5 years of age. It will take 30-40 minutes. It is concerned with the diagnosis and evaluation of abnormalities than the attainment of various milestones.
d) Bailey scale of infant development (BSID): This scale provides the motor scale, mental scale and the infant behavior record in children up to 30 months of age. The combined scores on the motor and mental scales provide overall developmental index. It takes approximately 30-60 minutes.
e) Baroda development screening test: This is screening test based on BSID, Baroda norms. The Baroda norms were standardized on Indian children. It evaluates motor, mental development and infant behavior. To follow up of high- risk neonates an abbreviated BSID is available.
f) Trivandrum developmental screening chart (TDSC): On the basis of 17 selected items from BSID Baroda norms, the test was designed in the child developmental center, SAT hospital, Trivandrum, for children up to 24 months of age. This simple tool can be administered and interpreted by any person with minimal training. It takes 5-7 minutes to apply.
g) Developmental screening test (DST): This is a simple scale that can be administered up to age of 15 yrs. It was standardized on Indian children.
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h) Brazelton neonatal behavioral assessment scale: This scale is based on the observation of the baby and the response to 20 primitive reflexes.
i) Developmental observation card (DOC): This was designed in the child developmental Centre of SAT hospital, Trivandrum based on the observation that the large majority of developmental delays can be identified using four key milestones social smile, head holding, sitting alone and standing alone, taking few steps with or without support that appear not later than 2, 4, 8 and 12 months respectively.
j) Seguin form board test: The Seguin Form Board Test (SFBT) has been developed by Edward Seguin and it is the most commonly used performance test for measuring psychomotor and visuo-perceptual abilities for children between four to twenty years age group. It is also used as a quick measure of general intelligence in children between 3 to 11 years age and for mentally retarded adults.
Screening tests when culturally appropriate measure major cognitive and mental abilities. Test suitable for Indian children like Indian modification of Wechsler intelligence scale for children (WISC), Stanford Binet test, Draw a man test, Bharat raj DDST, Vineland Social Maturity Scale - Indian adaptation by Malin can be administered.
Developmental tools have very low predictive value regarding future IQ and have limitations. The cross-cultural use of these scales is not ideal for Indian children who have motor skills ahead of others, but the language and personal social skills are often behind.
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The assessment by these tools furnishes information on these stages of development and gives the parents a chance to realize what stage of development their child is and degree of retardation. Through these assessments we can detect the developmental age of the children by which DQ can be calculated
DQ is computed with the following formula
DQ = Developmental age / Chronological age x 100 Bharat Raj Developmental screening test (DST)
DST is a simple quick intelligence test for children from birth to 15 years of age and provides a brief and fairly dependable assessment without requiring the use of performance test. There are 88 items distributed according to the age scales 3 months,6 months, 9 months, 1 year, one and half years, 2 to 13 years and finally at 15 years.36
Simplicity, precision, objectivity, validity, economy, and reliability are the cardinal features of a good assessment test. The DST sets these criteria satisfactorily.
This test is designed for the purpose of measuring development of children from birth to 15 years of age. Large number of items at early age levels permits assessment of very young children. This test provides for a brief and fairly dependable assessment without requiring the use of performance test. 60% of items can be evaluated on the spot and 40% by information given by parents.
The test can be done in a semi structured interview with the child and a parent or a person well acquainted with the child. At early age levels considerable number of motor milestones appear as it has many neurological and integrative developmental implications and constitute the natural starting point for
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development itself. There are items of milestones which represent sensorimotor adjustment to objects, persons, and situations. Language development items find a place which are inclusive of all visible and audible forms of communication like vocalization, words etc. Personal social developmental items also find a place as they comprise of a child’s responsiveness to the social culture of which he is a member e.g. play cooperativeness.
Each item is discrete and self-explanatory and can be assessed objectively by a parent, clinician or a teacher. This test has a few culturally laden items. In this test the point under consideration is whether the concerned milestone has emerged in the child or not i.e. whether the child is capable of doing it or not. The items in the test stand for discrete behavioral characteristics representation of the respective age levels.
At each age levels, items are drawn from behavioral fields like motor development, speech language development and personal social development.
Nearly 25% of the items are on speech development. 60% of items stands for behavioral characteristics enabling the clinician on the spot evaluation of the item.
The items in the test are chosen to lessen the bias from the informant. The DST items are not to be scored quantitatively. It is more a clinical instrument intended for use in estimating the developmental status of a child. The DQ calculator incorporated in the plastic test folder helps in ready computation of DQ from developmental age and chronological age.
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Grading of development as per score obtained from Bharat Raj’s Developmental Screening test.
DQ Score GRADING
Above 160 Highly gifted
146-160 Very superior
131-145 Superior
116-130 Above average
85-115 Normal
68-84 Borderline retardation
52-67 Mild retardation
36-51 Moderate retardation
20-35 Severe retardation
Less than 20 Profound retardation
Verma et al in 1979 in their study on cross validation of Developmental Screening Test which was administered to 170 children aged 1-15 yr old children, along with this Gesell drawing test, Senguin form board were also administered by dividing the study population into 3 groups 1-5, 6-10, 11-15 yrs. DST showed very high positive correlations with other intelligence or developmental tests. The result showed that it is a valid test for all 3 age groups. Interscorer reliability and test retest reliability are found to be high than other tests.37
Mallhi et al in 1999 reported that the entire process of developmental screening rests on the premise that early identification of children with developmental delay can help in starting early treatment and intervention, before it effects the functioning of the child and the family. To successfully identify children, who require interventions, it is
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important that the practitioners be skilled in the use of some screening tests.
Combination of relying on clinical judgement based on history, physical examination and office observation, addressing parental concerns and performing a formal screening test will help in identifying most children with delayed development.38
Dhanesh et al in 2012 in their study, they used DST Developmental Screening Test developed by Bharath Raj as a screening tool and mentioned that this tool was designed for the purpose of measuring the developmental sequences of children from birth to 15 years of age. They also reported that the DST showed very high positive correlations +.7215 to +.9968 with other intelligence tests. Inter scorer reliability (+.928) and test reliability (.98) were also found to be high and satisfactory.39
Prevalence and pathophysiology of neurodevelopmental delay in CHD
Wernovsky et al in 2005 in their study on central nervous system outcomes in children with complex congenital heart diseases reported that the children with CHD have had lower scale IQ, more motor, speech and language impairment, and more behavioural problem and their brain growth have similar pattern to that of the premature child. Almost 25% of neonates with complex CHD noted to have periventricular leukomalacia.46
Miller et al in 2007 in their studies on newborns with TGAand SV using Magnetic Resonance Imaging (MRI), Magnetic Resonance spectroscopy and diffuse tensor imaging found abnormal brain microstructure and metabolism in utero due to impaired cerebral oxygen. 55% of newborns with hypoplastic left heart syndrome are microcephalic and 21% have an immature cortical mantle.47
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Licht et al in 2009 in their study on children with left hypoplastic heart disease, and transposition of great arteries (TGA) by assessing brain maturation, myelination, cortical infoldings, involution of glial cell migration bands, and presence of germinal matrix tissue through MRI found that maturation was lower than normal children with similar gestational age. They found that the head circumference was smaller than the expected for their gestational age. The high prevalence of Periventricular leukomalacia among term infants with CHD in the preoperative, intraoperative, and postoperative periods suggested an enhanced susceptibility to white matter injury from brain immaturity, possibly related to the CHD.48
Sakazaki et al in 2015in their simulation study on the circulation in fetuses with hypoplastic left heart syndrome, tricuspid atresia and d-transposition of the great arteries with mathematical modeling found that the cerebral oxygen saturation is dramatically reduced in the heart lesions. The fetal cerebral blood oxygen saturation in hypoplastic left heart syndrome and tricuspid atresia is estimated to be about 50%
compared to the normal foetal Saturation (75%). The estimated cerebral blood oxygen saturation in d-transposition of the great arteries is lowest at 43%. 49
Von Rhein et al in 2015study shows that infants with severe CHD without overt brain lesions have smaller global brain volumes on preoperative MRI compared with control. These findings confirmed the previous reports of brain abnormalities in neonates with CHD before surgery, indicating fetal developmental and maturation abnormalities in the brain of infants with CHD. They found that the effects on brain development in CHD are not focal but involve all regions of the brain.50
Knutson et al in 2016 in their study on implementation of Developmental screening guidelines for children with congenital heart diseases opined that the
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children with CHD showed altered cerebral blood flow and oxygen with reduced brain volume with delayed brain maturation. Hypoxia, decreased cardiac output, altered circulation pattern, polycythemia, prolonged hospitalization, and risk for stroke contributed to their neurodevelopmental morbidity.51
Nattel et al in 2017 in their study on CHD and Neurodevelopment opined that the children with cyanotic heart disease have low average IQ than acyanotic heart disease. This long-term outcome in cognition is due to hypoxia and hypoperfusion.52
Solomon et al in 2018 in their study on early neurodevelopmental outcomes in children with CHD opines Postnatal studies in term neonates with complex CHD have shown smaller head circumference compared with normal neonates due to cerebral hypo-oxygenation. Neurodevelopmental evaluation should be included for all children with CHD whenever deficit is detected. Neurodevelopmental clinics need to function in collaboration with a multidisciplinary team comprising of developmental pediatrician, neurologists, Paediatric cardiologist and occupational therapist.53
Mussatto et al in 2014 in their study on 99 children with CHD reported that the presence of feeding difficulty, poor growth, medical comorbidities and more complex treatment, increased the risk for developmental delay. They concluded that the surveillance throughout the childhood into adulthood is necessary, because exposure to risk and prevalence of developmental delay will be changed over time.54
Lata et al in 2015 in their study on neurodevelopmental status of the children aged 6-30 months with congenital heart disease found that the children with CHD are at
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an increased risk of developmental delay. They suggested that the periodic surveillance, screening and evaluation should be instituted in them for early identification and appropriate interventions to enhance later academic, behavioural, psychosocial and adaptive function.7
Mari et al in 2015 in their observational study on CHD and impacts on child development reported that the children with CHD showed psychomotor development changes due to contributing pathological factors such as low birth weight, cyanosis, numerous hospitalisation, repeated examinations, physical constraints and school withdrawal.55
Li, Yin et al in 2015 found in their meta-analysis found that the neurodevelopmental delay with critical congenital heart disease was mainly from prenatal injury and not due to infant cardiac surgery. Cardiac surgery and cardiopulmonary bypass caused a certain amount of injury to the brain and disturbed its metabolism, but only for a short time. Neurodevelopmental delay was a result of abnormal fetal hemodynamics, suggesting that the origin of such injury was mainly preoperative. They concluded that the impaired brain metabolism and microstructures could progress to neurodevelopmental delay after birth.56
Birna BW et al in 2008 in their case control study on 194 subjects with CHD compared with healthy peers as control group found that 58.7% of children with CHD had moderate to severe deficit in gross motor skills and 31.9% had severe motor deficit. There were significant deficit in fine motor development also. They opined in their study, that the parental anxiety and over protection may reduce the child exposure to peers leading to decreased physical activity which may influence the motor development, social competence and caused decrease in the
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developmental and social quotient. They concluded that it is necessary to focus and pay attention to the gross motor and fine motor development of children with CHD and on the deficits in the development in order to implement therapeutic measures as early as possible. They did suggest in their study that the physical ctivity should be improved to minimise the negative consequences in perceptual and motor experience and children with CHD should be allowed to participate in indoor and outdoor activities as far as possible without restriction to improve the developmental and social competence.57
Stieh et al in 1999 at department of pediatric cardiology from Germany in their case control study on children aged 5-14 years with CHD compared with 30 healthy controls reported that the gross motor development were lower in children with uncorrected cyanotic CHD. Mean motor quotient (MQ) was 74.8 +/- 11.7 after corrective surgery mean motor quotient was 81.2 +/-16.6, controls had mean motor quotient 102.8 +/-11.8. Follow up after 2 years in the CHD children mean MQ reaches nearly normal values 97.1+/-17.0. They concluded that the longstanding hypoxemia in infancy may be an important cause for the motor disturbances and also it is necessary to have early neurological evaluation of these children with CHD and a specialized motor physiotherapy.58
Brandlisteun et al in 2010 in their case control study on 236 CHD concluded that there was more than 5 times probability of gross motor development, more than 2 times probability of fine motor impairment and more than 3 times probability of social development impairment in children with CHD.59
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Impact of CHD on Social maturity
Children with CHD are often restricted from interactive play and social gatherings and have less social interaction due to cardiac debilitation, exercise intolerance, prematurity, low birth weight issues which impact their social quotients adversely . Those with CHD are not regularly being provided proper screening for social maturity at appropriate age. Parental anxiety and overprotectiveness of CHD children may reduce the child’s exposure to peers which might influence the child’s social competence.59,60
Social maturity or social competence defined as the performance of the daily activities that required for social and personal sufficiency. Social maturity increases with age and in response to instruction in the absence of interfering circumstances. It is related to how well people understand the nature of the social world they live with. It has been described and defined at different age levels of children. It is also culturally bound as they are identified by the standards of other in the society. In every culture there is a process of socialization through which the children move from uncultured and unskilled stage to a condition of interpersonal affiliation and harmony as a member of this society. Therefore, social maturity degree of a child can be defined as the level of significant social behavior aimed at a given age.60
Social maturity assessment focusses on assessing ability, social skills, and communications skills. Education does not mean studying academic subjects alone but also means learning self-care activities and social skills. Nutritional status, socio economic factors and maternal IQ etc. may influence growth, development and social maturity. Maternal and other retarding environment variables also influence the school performances, cognitive development, and social maturity adversely.
