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1 Respiratory morbidity in children with Esophageal atresia/Tracheo Esophageal fistulae who underwent primary repair in a Tertiary care centre in South India A DISSERTATION SUBMITTED IN PARTIAL FULFILLMENT OF THE REGULATION FOR THE AWARD OF THE DEGREE OF MD PAEDIATRICS (BRANCH VII) THE TAMIL NADU DR. MGR MEDICAL UNIVERSITY CHENNAI, TAMIL NADU MAY -2018

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Respiratory morbidity in children with

Esophageal atresia/Tracheo Esophageal fistulae

who underwent primary repair in a Tertiary care

centre in South India

A DISSERTATION SUBMITTED IN PARTIAL FULFILLMENT OF THE

REGULATION FOR THE AWARD OF THE DEGREE OF MD PAEDIATRICS

(BRANCH VII)

THE TAMIL NADU DR. MGR MEDICAL UNIVERSITY

CHENNAI, TAMIL NADU

MAY -2018

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CERTIFICATION

This is to certify that the dissertation titled “Respiratory morbidity in

Children with Esophageal atresia/Tracheo Esophageal fistulae who

Underwent primary repair in a tertiary care centre in South India” is the

bonafide original work done by Dr. P. Madhan Kumar under my guidance

during his academic term April 2016 to March 2018, in the Department of

Child Health at Christian Medical College, Vellore, in partial fulfillment of

the requirement for M.D in Child Health examination of the Tamil Nadu Dr.

M.G.R. Medical University, Chennai to be conducted in May 2018.

Dr. Sneha Deena Varkki

Professor

Department of Child Health - Unit 3

Christian Medical College

Vellore - 632 004

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CERTIFICATION

This is to certify that the dissertation titled “Respiratory morbidity in

Children with Esophageal atresia/Tracheo Esophageal fistulae who

Underwent primary repair in a tertiary care centre in South India” is the

bonafide original work done by Dr. P. Madhan Kumar under my guidance

during his academic term April 2016 to March 2018, in the Department of

Child Health at Christian Medical College, Vellore, in partial fulfillment of

the requirement for M.D in Child Health examination of the Tamil Nadu Dr.

M.G.R. Medical University, Chennai to be conducted in May 2018.

Dr. Indira Agarwal

Professor and Head

Department of Child Health

Christian Medical College

Vellore - 632 004

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CERTIFICATION

This is to certify that the dissertation titled “Respiratory morbidity in

Children with Esophageal atresia/Tracheo Esophageal fistulae who

Underwent primary repair in a tertiary care centre in South India” is the

bonafide original work done by Dr. P. Madhan Kumar under my guidance

during his academic term April 2016 to March 2018, in the Department of

Child Health at Christian Medical College, Vellore, in partial fulfillment of

the requirement for M.D in Child Health examination of the Tamil Nadu Dr.

M.G.R. Medical University, Chennai to be conducted in May 2018.

Dr. Anna B pulimood

Principal

Christian Medical College

Vellore - 632 004

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CERTIFICATE -II

This is to certify that this dissertation work titled “Respiratory morbidity in

Children with Esophageal atresia/Tracheo Esophageal fistulae who

Underwent primary repair in a tertiary care centre in South India” the

candidate Dr. P. Madhan Kumar with registration Number 201617452 for the award

of Degree of MD Paediatrics 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 ZERO percentage of plagiarism in the

dissertation.

Guide & Supervisor sign with Seal.

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ACKNOWLEDGEMENT

My heartful and sincere thanks to Dr. Sneha Deena Varkki my guide for her

immense patience, valuable guidance, encouraging words and support which was offered

to me throughout the study. A special thanks to Dr. Kala Ebenezer who was my DCH

guide who thought me the basis of thesis.

I would like to express my sincere and humble thanks to my co-investigators,

Child health departments, Paediatric surgery, Paediatric ENT, Child health unit 3 office

staffs especially Mrs. Padmini and Radiologist for their help and the guidance which was

offered to me till the end of this study. Special thanks to Mrs. Gowri for all the statistical

work and enlightening sessions on statistical analysis also Mr. Madhan who helped in

making the data sheet.

I am always grateful to Dr. Jolly chandran and Dr. Pragathesh who encouraged

and supported me not only in this study but throughout my carrier as a pediatrician.

I would like to acknowledge my family especially my wife Kavitha and daughter

shamitha who bearded all my absence and difficulties during the study period. A special

thanks my brother Dr. Gopinath and my father Mr. Palani who helped me in recruiting

children.

And finally without the help of the Almighty and my parents Mr. Palani and Mrs.

Indira nothing would have been possible in my life.

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TABLE OF CONTENTS

Contents

INTRODUCTION……………………………………. 09

AIMS AND OBJECTIVES…………………………... 12

REVIEW OF LITERATURE………………………… 15

MATERIALS AND METHODS…………………….. 46

RESULTS AND ANALYSIS………………………… 52

DISCUSSION………………………………………… 91

CONCLUSION AND RECOMMENDATION ……... 96

BIBLIOGRAPHY……………………………….……. 98

APPENDIX…………………………………………… 105

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Introduction

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Introduction:

Esophageal atresia and Tracheo esophageal fistula are a group of developmental

defects involving the trachea and esophagus. The former has a blind end on the

esophagus without fistulae to the trachea and the later has a fistula to the trachea(1).

Among the congenital anomalies of foregut, esophageal atresia/Tracheo esophageal

fistula is one among the most common defects that involves esophagus and trachea. The

incidence of this condition is almost similar throughout the world ranging from 1 in 2500

- 4500(2–4). A population based study showed that the prevalence of EA/TEF was 2.82

per 10,000 births with no secular variations(5). Worldwide, the incidence of this

condition has been on a decreasing trend without a clear reason. In various studies the

relative risk of this condition is reported to be 2.56 in twin pregnancy when compared to

singleton pregnancy. Even though there is a higher male predominance the reasons are

largely unclear.

In 1697, Thomas Gibson gave the first description of esophageal atresia associated

with Tracheo esophageal fistula after a postmortem examination of an infant. Although

Charles steel began to operate the neonates with esophageal atresia as early as 1888(6), it

was not until 1941 Cameron Haight(7–9) performed the first successful surgical repair of

this condition(6–8). Following this 1st successful surgery, the technique for operating

esophageal atresia/ Tracheo esophageal fistula has improved resulting in a better

outcome.

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With advancements in the fields of anesthesia, surgical techniques, materials used

during surgeries, post operative intensive care, good nutritional support and antibiotics,

the survival rate following the repair has reached more than 90%(12) over recent years.

When there are no major anomalies and risk factors, the survival rate is nearly 98%(13).

Improvement in survival rate has brought attention to the importance of preventing

morbidity in these children post repair of esophageal atresia.

Respiratory complications and morbidity, following esophageal

atresia/Tracheo esophageal fistula is relatively high when compared to the

general population. In developing countries like India, where post surgery

follow up is not optimum, children tend to present to the clinician after

irreversible damage has occurred to the respiratory and other systems. Most

of the follow up studies have been done in developed countries evaluating

the morbidity in adulthood. There are no clear guidelines or consensus as to

the frequency or components of the follow up care of these children.

Present study was planned to address the lacunae in the follow up care of

operated TEF patients, to collect information on antenatal, Perinatal and

peri-operative period and assess the respiratory morbidity in the survivors.

It is hoped that the information obtained will help us to anticipate

complications and sequelae at various time points so that preventive steps

can be taken to decrease morbidity and prevent or limit lung damage.

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Aims and objectives

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Aim and objectives:

Aim:

To study the respiratory morbidity in children who had oesophageal

atresia/Tracheo esophageal fistulae primary repair in the neonatal period in a tertiary care

centre in south India.

Objective:

Primary:

1. To estimate the prevalence of respiratory morbidity in infancy in

children who underwent corrective surgery for OA/TEF by clinical

history and information from hospital records.

2. To assess the prevalence and extent of current respiratory morbidity

by history, clinical examination and Objective assessment of

pulmonary status using appropriate radiological imaging (CXR +/_

HRCT chest).

Secondary:

1. To assess the prevalence of oro-digestive co-morbidities which can

impact respiratory health by clinical assessment and radiological

imaging (barium swallow).

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2. To correlate peri-operative and patient characteristics with selected

respiratory outcomes in these children.

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Review of literature

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Review of literature:

Esophageal atresia and Tracheo oesophageal fistula are a group of developmental

defects involving the trachea and esophagus. The former has a blind end on the

esophagus without fistulae to the trachea and the later involves a fistula to the trachea(1).

Among the congenital anomalies of foregut esophageal atresia/Tracheo esophageal

fistulae is one among the most common defects of esophagus and trachea.

Embryology:

Knowledge of embryology of foregut development is important to understand the

pathogenesis of OA +/- TEF.

After formation of three germ layers in early embryo, a series of morphogenetic

folding occurs in the flat endoderm which leads to the formation of primitive foregut,

which gives rise to trachea and esophagus. This usually occurs during the second stage of

lung formation (Pseudo glandular stage). During this process a ventral diverticulum is

formed from the caudal part of foregut, following which Tracheo esophageal fold fuses

longitudinally to form the septum which divides esophagus and trachea(14–17).

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Figure.1: A. Laryngo tracheal diverticulum forms as a ventral out pouching from

the caudal part of the primitive pharynx. B. Longitudinal Tracheo esophageal folds

begin to fuse towards the mid-line and eventually form the Tracheo esophageal

septum. C. Tracheo esophageal septum has fully formed. D. If the Tracheo

esophageal septum deviates to the posterior side, esophageal atresia with a Tracheo

esophageal fistula develops.

The exact process by which the trachea is defined and separates from the original

foregut tube is still controversial. However, there are three theories which try to explain

this condition.

1. According to this theory Tracheo oesophageal malformations results from the

growth failure of trachea(14).

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2. The formation of ascending mesenchymal septum in the coronal plane separating

the foregut tube into trachea ventrally and esophagus dorsally which is from the

distal ends to the proximal ends of foregut. Any disruption in this process can lead

to Tracheo oesophageal anomalies(15).

3. This theory combines the above mentioned theories. It states that Tracheo

oesophageal division is due to the result of development of foregut folds. Any

disruption of the part of a previously formed tube owing to the regression towards

the main part of the embryo can lead to Tracheo oesophageal anomalies.

The history of oesophageal atresia treatment:

Dr. William Durston of England in 1670 published an article “A narrative of a

monstrous birth at Plymouth” (18) describing a baby girl which was one of the twins of a

thoracophagus conjoined twin who had a blind-ending upper esophagus.

However it was in 1697, Dr. Thomas Gibson's described the typical form of

esophageal atresia with Tracheo esophageal fistulae (EA-TEF) in a neonate who had

“difficulty in feeding, choked whatever was fed and brought out everything through the

mouth nose‟ in the 5th edition of the book named “The Anatomy of Human Bodies

Epitomized”(19).Post mortem findings confirmed this anomaly in this case. After another

124 years, in 1921, Dr. Martin reported a female child with blind upper end of esophagus

and lower end was connected to the trachea which is now described as Type C

fistula(20).

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The first association of EA/TEF with other congenital anomalies was published by

Dr. Thomas Hill(21) in a neonate who also had rectal agenesis. By 1922 10 cases were

reported in the literature(22).

Dr. Timothy Holmes who first explained the feasibility of surgical option

regarding esophageal anastomosis for isolated esophageal atresia in 1869(23). He stated

that if the parents are willing for the surgery then it should be done (24).In 1873 the first

description regarding “H” type fistula was made by Dr. Lamb(25).

Dr. Morell Mackenzie published his famous article in 1880 named “Malformation

of the esophagus” in which he extensively described about 57 cases of congenital

esophageal anomalies among which 37 had tracheal or bronchial esophageal fistula(26).

He described elaborately associations with other congenital anomalies such as anal

agenesis, vertebral malformation, renal anomalies, etc.,

In 1888 Dr. Charles Steele from London became the first surgeon to perform the

correction of esophageal atresia without Tracheo esophageal fistula on a 2 day old

neonate(6). Even though the neonate died in the next 24 hours of surgery, it was

considered a revolution in the field of surgery. The first gastrostomy was performed by

Dr. Hoffman in 1898 on a neonate with esophageal atresia(27).

In the 19th century different attempts were made to correct the defect. Dr. H. M.

Richter in 1913 proposed a plan for anastomosis of the two ends of the esophagus(28).

Dr. Smith tried ligation at the cardia of the esophagus in 1923 and in 1936 Dr. Gage and

Dr. Oschner did a cervical oesophagostomy with gastrostomy.

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Dr. Thomas Lenman from Boston in 1936-37 and Dr. Robert Shaw from Texas in

1938 were the first to attempt fistula ligation along with primary anastomosis(29,30).

However none of these surgeries were successful in improving outcome of children with

these defects.

It was in 1939 Dr. William Ladd achieved a successful repair by a staged

approach(31). Almost during the same time Dr. Leven from Minnesota used a similar

surgical approach on a boy baby(32) whom he subsequently adopted.

Dr. Cameron Haight and Dr. Harry Towsley performed the first successful

primary repair of esophageal atresia with Tracheo esophageal fistula during 1941 from

Michigan(33).This technique has been adopted by many centers worldwide. Minimally

invasive thoracoscopic repair with favorable outcome was devised by Dr. Thom Lobe

and Dr. Steve Rothenberg from America(34), Dr Bax and Dr. Van in the Netherland(35).

The first thoracoscopic repair of the TEF was done in 1999 by Dr. Thom Lobe et al(36).

Epidemiology:

Throughout the world the incidence of esophageal atresia/Tracheo esophageal

fistula is almost similar ranging from 1 in 2500 - 4500(2–4) .The etiology is not clear, it

is considered to be denovo occurrence or multifactorial or sporadic in nature; Animal

studies have shown that defects in „sonic hedgehog gene‟ expression may be a

contributing factor for this condition. The incidence is 2 to 3 times more common in

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twins thereby demonstrating a genetic predisposition(37) .Recurrence risk in siblings is

estimated to be 1%(37), Worldwide the incidence of this condition has a decreasing trend

without a clear reason. Even though there is a higher male predominance the reasons are

largely unclear. Majority of cases are sporadic and less than 1% represents

familial/syndromic causes(38).

Associated anomalies:

There are multiple congenital anomalies that can occur along with esophageal

atresia/Tracheo esophageal fistulae. It has been reported that approximately 50% of

children with esophageal atresia have another associated congenital anomaly. Half of

these associations are syndromic in nature and the remaining are non syndromic(39–41).

The usual syndromic associations are VACTERL (vertebral, ano-rectal, cardiac, Tracheo

esophageal, renal and limb abnormalities), CHARGE (coloboma, heart defects, atresia

choanae, retardation of mental, genital hypoplasia and ear deformities), Goldenhar, Opitz

G syndrome, Fanconi anemia and other non classified chromosomal syndromes(42).

Of the known syndromic association VACTERL is found in 50% of the cases with

vertebral/ribs and the cardiovascular system being their commonest associations. This

association was first described by Dr. Quan and smith in 1973(43). Elisabeth M et all in

2008 published the data which described that other than VACTERL defects, genital

defects (23.3%), single umbilical artery (20%) and respiratory tract anomalies (13.3%)

are associated in VACTERL syndrome.

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Table 1: Shows the common anomalies that are associated with EA/TEF(44)

Systems Involved Associated anomalies

Cardiac (25%) Ventricular septal defect, Atrial septal

defect, Tetralogy of fallot, Right-sided

aortic arch, Patent ductus arteriosus.

Gastrointestinal (20%) Duodenal atresia, Mal-rotation,

Imperforate anus, Meckel's diverticulum,

Annular pancreas Intestinal malformations

Musculoskeletal (15%) Rib malformations, Hemi-vertebrae,

Syndactyly, Polydactyl, Scoliosis, Lower

limb defects, Radial dysplasia or Amelia.

Genitourinary (20%) Renal agenesis or dysplasia, Polycystic

kidney, Horse shoe kidney, Hypo-spadias,

Urethral and Ureteral malformations.

The study done by Sharma et al.(45) from India showed low associated anomalies

with EA/TEF with Ano-rectal (15%) being the most common followed by cardiac (7%),

however a earlier study done in our institution showed very high association with cardiac

anomalies (45%) with a low Ano-rectal malformation (2.8%)

Classification:

Esophageal atresia/ Tracheo esophageal atresia can be classified based on their

1. Anatomical variation

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2. Prognostic factor for surgical outcome.

Anatomical classification:

This classification of esophageal atresia anomalies is based on the location of the

atresia with or without a fistula to the trachea. The first anatomical classification was

done by Dr. E.C. Vogt in 1929(46); however in 1953 Dr. Gross modified the original

classification made by E.C Vogt(47).

Table 2: Showing the Gross classification for esophageal atresia/Tracheo esophageal

fistula

Gross Vogt Description

- Type 1 Esophageal agenesis

Type A Type 2 Proximal and distal esophageal bud – Normal esophagus

with a missing mid segment

Type B Type 3A Proximal esophageal termination on the lower trachea

with distal esophageal bud.

Type C Type 3B Proximal esophageal atresia (esophagus continuous with

the mouth ending in a blind loop superior to the sternal

angle) with a distal esophagus arising from the lower

trachea or carina. (Most common, up to 87% of cases.)

Type D Type 3C Proximal esophageal termination on the lower trachea or

carina with distal esophagus arising from the carina.

Type E

(H Type)

- A variant of type D: If the two segments of esophagus

communicate, this is sometimes termed an H-type fistula

this is TEF without EA.

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Figure 2: Diagrammatic representation of the gross classification for EA/TEF.

Below is the summary of Studies including the study that was done in Christian

medical college, Vellore with the frequency of various types of esophageal atresia with or

without Tracheo esophageal fistula(48)

Table no. 3: Summary of Studies including the study that was done in Christian

medical college, Vellore with the frequency of various types of esophageal atresia

with or without Tracheo esophageal fistula.

Studies Number of

patients

Type A Type B Type C Type D Type E

German, et

al.

(1964–1974)

102 6 2 83 9 2

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Sillen, et al.

(1967–1984)

110 7 1 100 1 1

Poenaru, et

al.

(1969–1989)

95 8 0 80 1 6

Engum, et

al. (1971–

1993)

227 29 2 178 5 13

Holder, et

al.

(1973–1986)

100 2 1 85 6 6

Spitz, et al.

(1988–1994)

410

27

4

353

9

17

Harsh, et

al.(48)*

(2000-2011)

79 12 1 64 0 2

Total 1,123 91

(8.1%)

11

(0.97%)

943

(83.9%)

31

(2.7%)

47

(4.1%)

Classification by prognostic factors:

Although the survival rate following the primary repair was persistently increasing

between 1940‟s to 1960‟s there was no risk stratification till 1962. It was in 1962 when

Waterston proposed the first preoperative risk factors for this condition(49). This

classification included birth weight, associated congenital anomalies and presence or

absence of pneumonia.

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Waterston classification of esophageal atresia according to predictors of survival,

surgical timing and the rate of survival:

Table 4: Waterston classification of esophageal atresia

Category Weight/Co-morbidities Surgical timing Survival (%)

A >2,500 gm Can undergo surgery 100

B 1,800 – 2,500 gm or

pneumonia or congenital

anomaly

Short-term delay,

needs stabilizing

treatment before

surgery

85

C <1,800 gm or severe

pneumonia or congenital

anomaly

Requires staged repair 65

Even though Waterston classification was popular with a good prognostic

stratification a new classification was brought by Spitz in 1994(50). According to his

classification birth weight and major cardiac anomalies are the two important predictors.

Spitz classification - According to predictors of survival and their survival rate is

shown in table 5.

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Table 5: Spitz classification

Group Features Survival (%)

I Birth weight >1,500 gm and no cardiac

anomaly

98.5

II Birth weight <1,500 gm or major cardiac

anomaly**

82

III Birth weight <1,500 gm and major cardiac

anomaly**

50

**Major cardiac anomaly - Cyanotic congenital heart disease that requires a corrective

surgery or required palliative condition or non-cyanotic heart disease that requires

medical or surgical treatment for congestive cardiac failure.

Since the discrimination ability of Spitz classification was unclear, a more

accurate prognostic classification was developed by Tatsuya Okamoto in 2009(51). He

also considered birth weight and major cardiac anomalies as the parameters;

Okamoto classification - According to predictors of survival and their survival rate

is shown in table 6.

Table 6: Okamoto classification

Class Features Risk Survival (%)

I Birth weight ≥ 2000 gm and

no major cardiac anomaly

Low 100

II Birth weight < 2000 gm and

no major cardiac anomaly

Moderate 81

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III Birth weight ≥ 2000 gm and

major cardiac anomaly

Relatively high 72

IV Birth weight < 2000 gm and

major cardiac anomaly

High 27

Diagnosis:

Esophageal atresia and Tracheo oesophageal fistula can be diagnosed as early as

second trimester of gestational period usually in the 18th week of gestation(38). Prenatal

diagnosis is usually made by the ultrasound findings which shows a small or absent fetal

stomach associated with maternal polyhydramnios(52). Even though the predictive value

for the diagnosis with the above mentioned features is only 44% and 56% in two

series(53), this is considered to be one of the most important modality. Fetal Magnetic

resonance imaging is an upcoming diagnostic modality for this condition.

The diagnosis of esophageal atresia is often made in the post natal wards when a

neonate develops regurgitation followed by choking and coughing episodes after the first

feed which ultimately leads to cyanosis and severe respiratory distress. The chest and

abdomen roentgenogram after inserting a Naso-gastric tube will demonstrate coiled tube

in the upper esophagus with absent air bubble in stomach. Presence of air bubble in the

stomach represents that a connection between the trachea and the esophagus proximally

or distally. If the diagnosis is unclear a bronchoscopy can be done.

In rare occasions the catheter can go in to the lungs through the opening in case of

“H” type fistula. Usually “H” type fistula is recognized late when children present with

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recurrent choking episodes following feeds, recurrent lower respiratory tract infection

and failure to thrive. In order to confirm the “H” type fistula, bronchoscopy and dynamic

prone contrast esophagoscopy are being done. Multi-detector row Computerized

Tomography esophagography can give information if scopy and contrast studies are

negative(54). Karnak I et al. presented a series of children with “H” type fistula in which

the diagnostic time ranged between 26 days to 4 years of life(55).

Once diagnosis is confirmed, infants should be thoroughly examined for other

visible anomalies and specifically to look for single umbilical artery. It is mandatory to

do the following investigations to identify associated anomalies

Table no.7: Investigation modalities to identify the associated anomalies that can

occur with OA±TEF.

Investigation modalities To look for

Roentgenogram of chest

and abdomen

Vertebrae/Skeletal anomalies, Congenital scoliosis,

Cardiomegaly, Diaphragmatic hernia and Intestinal atresia

Ultrasonography of brain

and kidneys

Renal agenesis or Hypoplasia, Reflux disease, E.tc.

Echo cardiograph Congenital cardiac disease – Ventricular septal defect,

Atrial septal defect, Right side aortic arch, Complex heart

disease, E.tc.

Pre-operative care:

Pre op management will include, maintaining supine position with head end

elevated, applying low pressure suction through a No. 10 size Replogle placed in the

esophagus in order to minimize the risk for aspiration pneumonia and pneumonitis.

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Nutritional support, strict asepsis and maintaining electrolyte balance is important.

Ventilation strategy is important with endotracheal tube fixed distal to the fistula and a

low pressure mode is preferred

Timing of surgery:

The correction of EA/TEF usually is not a surgical emergency except in case of

preterm neonate with severe respiratory distress requiring ventilator support. Corrective

surgery is to be done as an emergency in preterm, because of the gastric distention

secondary to gases that escape through the distal fistula which can lead to rupture of

stomach causing pneumoperitoneum.

The condition where the neonates should be considered for non-surgical

management is as tabulated below because these children will have a mortality of more

than 90% before their first birthday(1).

Table no.8: Condition where the neonates should be considered for non-surgical

management with OA±TEF.

Trisomy 18

Potter's syndrome

Grade IV Intraventricular hemorrhage

Uncorrectable major cardiac defects

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The surgery option depends whether it is long or short gap. In case of long gap

cervical oesophagostomy with gastrostomy is done and for short gap end to end

anastomosis is done.

A minimal invasive thoracoscopic procedure for esophageal atresia is now being

widely used with a good outcome in the recent years(56).

Post operative care:

Post-operative care of these neonates is very important. In NICU close monitoring

with ventilator support, positioning to avoid undue stress of the operated site, avoidance

of oral feeds for 48 hours followed by gradual feeding and special care not to disturb the

trans-anastamotic tube are important .Proper sedation, Intravenous fluid therapy and

adequate antibiotic cover should be instituted.

Post operative complication:

The post operative complications can be classified as

1. Early complications

2. Late complications

Early complication:

Esophageal stricture following the surgery is the most common complication and

recurrent intervention. The incidence, presentation and treatment of the various

complications(57,58) are tabulated below and elaborated.

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Table no.9: Early complication following surgical management with OA±TEF.

Anastamotic leaks

Pneumonia

Esophageal strictures

Anastamotic leak:

The incidence of anastamotic leak follows the repair ranges from 7% to 21% and

the most common reason being loose sutures or increased tension in the sutures(59–62).

In majority of the cases supportive therapy is usually given which includes appropriate

antibiotics, adequate drainage, and good nutritional support. Studies have shown that

95% usually resolves spontaneously or with minimal intervention such as pleural

drainage. In situation where the leak is massive may require re-exploration for drainage

of the leak and to patch the leak with pleural or pericardial. Almost half of the patient

with anastamotic leak develop esophageal stricture later in their life.

Esophageal stricture:

A stricture of esophagus is the common complication and the most common cause

for recurrent interventions in children following the surgery. Increased tension in the

anastamotic site, gastro esophageal reflex and anastamotic leak are the major risk factors

for stricture in the post operative period(58,63). The various symptoms following the

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strictures are recurrent respiratory tract infection secondary to aspiration, dysphagia and

foreign body obstruction. These symptoms occur due to narrowing of the esophagus there

by causing the symptoms of obstruction which can be appreciated in endoscopy or

contrast esophagogram. Endoscopic dilatation is done in most of the children with

esophageal atresia(41,63). Gastro esophageal reflux disease (GERD) management should

be done aggressively in order to prevent the recurrent stricture formation. Children who

don‟t respond to endoscopic dilatation with persistent complaints may require resection

of stricture with re-anastomosis or esophageal replacement.

Late complications:

Table no.10: Late complication following surgical management with OA±TEF.

Gastro-oesophageal reflux disease Dysphagia

Oesophageal dysmotility Tracheomalacia

Oesophageal epithelial changes Respiratory disorders

Chest wall deformities Recurrent TEF

Esophageal strictures

A systematic review of long-term outcomes in adulthood after EA repair during

infancy reported the following pooled estimated prevalence(64):

- Dysphagia – 50.3 percent

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- Gastro esophageal reflux disease (GERD) with esophagitis – 40.2 percent

- GERD without esophagitis – 56.5 percent

- Respiratory tract infections – 24.1 percent

- Asthma ( Physician diagnosed ) – 22.3 percent

- Wheeze – 34.7 percent

- Persistent cough – 14.6 percent

- Barrett esophagus – 6.4 percent

- Esophageal cancer ( Squamous cell carcinoma) – 1.4 percent

Dysphagia:

Dysphagia is defined as difficulty during swallowing which can be to solids,

liquids or mixed. Following the surgery abnormal peristalsis is noted in 75% to 100% of

children(65).

Recurrent Tracheo esophageal fistula:

Recurrence of TEF following the primary repair can vary between 3% and

14%(58,59,66,67). These children usually present in the later infancy or childhood with

history suggestive of H – Type fistula such as recurrent lower respiratory tract infection,

coughing, choking and cyanosis during and after feed. The diagnosis is usually confirmed

by bronchoscopy, cookie swallow or prone position video fluoroscopy but in difficult

scenario computerized tomography of the chest is done. Re-exploration with ligation of

the fistula should be done.

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Gastro esophageal reflux disease (GERD):

Gastro esophageal reflux disease is one of the common complications among

children following the primary repair with an incidence of 40% to 70%(68–70). The

presence of gastro esophageal reflux doesn‟t warrant intervention unless it is

pathological. The major predisposing factors for this condition are alteration in the gastro

esophageal junction anatomy following the primary repair, tension anastomosis

and intrinsic esophageal motor dysfunction(41,71). To know the incidence and etiology

of GERD Koch A et al studied these patient with radiographic, manometric and

endoscopic examinations. He suggested that decreased esophageal clearance, Superior

displacement of esophagastric junction and delayed gastric emptying were the main

reason for the cause of GERD.

Multiple studies have shown that as the age increases the incidence of GERD

decreases significantly (R - Long term analysis). The presentations of these are

regurgitation following feeds, vomiting, acute or chronic respiratory illness, failure to

thrive and growth failure. In long standing cases of GERD esophagitis, Stricture, Barrett

esophagus, hiatus hernia and epithelial metaplasia can occur(58). The diagnosis is

confirmed by contrast swallow, esophagoscopy and 24 hour pH probe.

In children with gastro esophageal reflux disease (GERD) the treatment options

can be medical or surgical which is determined by the severity of the reflux and

associated complications. In milder cases medical treatment such as upright positioning

following feeds, thickening of feeds, and use of Proton pump inhibitors, histamine-2

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blockers and pro kinetic agents. In children with severe GERD symptoms or children

who doesn‟t respond to medical therapy Nissen fundoplication and its modifications can

be offered to the children(41).

Esophageal dysmotility:

Following surgery abnormal peristalsis of esophagus is noted in 75% to 100% of

children. The esophageal dysmotility can be primary or secondary. The primary cause is

due to the inherent congenital abnormal neural development in the esophagus or

secondary to the primary repair. These children will have symptoms of dysphagia, food

bolus impaction and aspiration which may lead to aspiration pneumonia(62,66).

Respiratory complications:

Respiratory complication following the primary repair is one of the common

causes for hospital admission in children who had repaired EA/TEF. The respiratory

complaints can vary from recurrent lower respiratory tract to bronchiectasis depending

upon the treatment given during the respiratory complaints. Inadequate treatment, poor

follow up, non compliance to medications is some of the major contributory factor for the

respiratory morbidity. In the modern surgical era the mortality of the TEF/EA decreased

consistently(72) and most of the times survival nearing about 90%(12). However

following the repair, children are not routinely followed up for their long term

complications which are mainly of respiratory/esophageal origin. An article from the

Arch Disease Child 1976 highlighted the respiratory complications in long-term

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survivors and found that 78% of the total patients had frequent respiratory symptoms and

almost 48% needed admission for the respiratory tract infection(73). Recurrent

respiratory infection is usually due to esophageal motility disorders leading to micro-

aspirations into the respiratory tract.

Detailed literature review on respiratory morbidity of survivors of

OA±TEF repair:

There were multiple studies showing the importance of regular follow up after a

primary repair of EA. Many Western studies have looked at pulmonary morbidity of

these children in childhood and adulthood. Most of these patients had a stormy infancy.

S.Beardsmore et al from the University of Leicester followed up 16 patients who

underwent EA/TEF repair and reviewed them within 3 months of surgery (during

infancy). These patients underwent the measurement of Maximum velocity (Vmax),

Functional residual capacity (FRC), Thoracic gas volume (TGV) and Airway resistance

(Raw) to assess the respiratory status. 7 of these infants remained well whereas 9 had

abnormal initial respiratory function. The functional abnormalities detected by these tests

corresponded to the clinical severity of the symptoms(74). The European study findings

were similar to the above study, where lung function test was done within 3 months after

the primary repair. The investigators concluded that lung function tests help in providing

a guide for clinical prognosis(75).

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Data from the French registry where patients from 38 centers across France are

registered was analyzed for the morbidity and mortality following post-op EA/TEF

repair. A total of 307 patients were registered. 59% required admission within a year of

surgery with a mean hospital admission of 2.5 per person. 48% of this were for

respiratory problems(76). The common abnormalities encountered in this study were

upper airway disorders, bronchiolitis, respiratory infection and Tracheomalacia.

The Philadelphia study was one of the largest studies with 3,479 patients of

EA/TEF managed in 43 children‟s hospitals. In-hospital mortality was 5.4% and the

Independent predictors of mortality included congenital heart disease, lower birth weight,

other congenital anomalies and preoperative morbidities(77).54.7% of patients were

readmitted within 2 years and 11.7% needed fundoplication.

In 1979, study from Toronto looked at the PFT in 7-18 year old children who had

EA/TEF repair .Out of 159 survivors 24 were included in this study only 1 child had

normal lung functions, while 13 children had obstructive airway disease, five had a

restrictive defect and 15 had a positive methacholine challenge. Continuing micro-

aspiration into the lung was postulated to be the cause of these abnormalities(78).

The following is a table which lists the causes of acute and chronic respiratory

symptoms in infants and children following EA/TEF repair.

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Table no. 11: The causes of acute and chronic respiratory symptoms in infants and

children following EA/TEF repair.

Vocal cord paresis/paralysis Aspiration of upper airway

secretions

Dysphagia/aspiration Tracheomalacia and/or

bronchomalacia

Aberrant airway anatomy Atelectasis related to poor

mucociliary clearance/impaired

cough

Lower airway flow obstruction with Or without

bronchodilator response

Atelectasis related to impaired

cough

Restrictive lung disease Diverticulum of posterior trachea

at the site of TEF repair

Aspiration pneumonia Laryngeal cleft

Recurrent oesophageal stricture Eosinophilic esophagitis

Recurrent TEF Esophageal foreign body

impaction

Recurrent lower respiratory tract infection:

Multiple studies have shown that the cause of recurrent lower respiratory tract

infection is due probably due to aspiration(79). The aspiration may be the result of

disordered peristalsis or may be due to the poor tone in lower esophageal sphincter. It

has been very clearly shown that the cause of respiratory morbidity in patient is those

who had recurrent respiratory tract infection in infancy period. These children with

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recurrent infection have an increased lower esophageal sphincter tone and disordered

peristalsis which increases the risk for aspiration pneumonia. Tracheomalacia, gastro

esophageal reflux disease, recurrence of Tracheo esophageal fistula, aspiration and

stricture are the major etiological factors responsible for the respiratory illness in

children. The pattern of lung disease varies thorough out the world. In Canada the study

done in McGill university have shown that 52% of patients have abnormal pulmonary

function out of which 69% had an restrictive lung pattern, 23% had obstructive lung

disease and 8% have both patterns. It is hypothesized that the cause of decreased

pulmonary function is due to the bronchial inflammation followed by remodeling which

causes irreversible damage to the lungs.

Increased bronchial responsiveness:

Increased bronchial responsiveness occurs mainly due to the chronic subclinical

aspiration and not due to the atopy. The incidence of this condition ranges from 22% to

65% among various studies(80).

Tracheomalacia:

Tracheomalacia is the most common cause for Stridor during infancy and

childhood and is present in 10 – 20% of children following the surgery(12). The cause of

stridor is due to partial or complete collapse of tracheal wall during expiration thereby

leading to obstruction of lumen. The diagnosis is usually made by bronchoscopy which

show slit like lumen of trachea. If the collapse is <50% it is categorized as mild, 50% to

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75% is moderate and more than 75% is severe form (R-longitudinal). Although majority

of children with EA/TEF repair have tracheomalacia only 10 – 20 % of them have

significant problem which needs medical assistance and approximately 50% of these

children will require surgical correction. Life threatening episodes and recurrent lower

respiratory tract infection due to severe tracheomalaciawill need aortopexy and if fails

tracheostomy can be done. Children who have mild to moderate symptoms are managed

conservatively and usually they improve with time.

Thoracic wall deformity

During the early surgical period thoracic wall deformity is the one of the common

post operative complication following the repair owing to the thoractomy procedure

during those periods. This not only causes thoracic wall deformities but also spinal

deformities. The other major reason for this complication is syndromic manifestation

which is associated with vertebral or skeletal anomalies. However after the extrapleural

approach as decreased significantly in the current scenario. The common deformities that

are mentioned in various series are as follows(81,82).

Table no. 12: The common deformities in children following EA/TEF repair.

Anterior chest wall deformities

Scoliosis

Winged scapula

Rib fusion

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Female breast deformities

Shoulder asymmetry

In conclusion, it is clear that with improvement in operative management,

prognosis for children born with OA +/-TEF has improved. While survival rate is close to

98%, there is significant morbidity related to the aero digestive tract especially in

infancy. If left untreated they can lead to irreversible damage of lung. Some of these

complications can be prevented with good follow up care, anticipatory guidance, and

timely interventions as problems arise. It is important to know the prevalence of the

morbidity among children operated in a developing country as there may be multiple

environmental and socioeconomic factors which contribute to morbidity. This follow up

study is intended to collect the data on morbidity of these children .It is our hope that

information from this study will help us to propose a follow up strategy which is feasible

in a developing country like ours with limited resources.

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STATISTICAL METHODS

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Statistical methods:

Sample size calculation:

The study done by Banjar et al showed that pulmonary morbidity was present in

more than 70% of the children in the post-op Period(83). Hence we have taken average

morbidity as 80% and the sample size was calculated using the following formulae

n = 4pq/d2

= 4x80x20/225

= 28

Where,

p = Prevalence of respiratory morbidity i.e. 80%

q = 1-p i.e. 20%

d = Precision i.e. 15%

A sample size of 28 patients is needed to detect 80% prevalence rate with a

precision of 15% with 95% confidence interval. As per our hospital records

approximately 8 neonates with OA/TEF are operated per year. Hence we decided to

include patients operated over 8 year period which will give approximately 64 patients.

Accounting for mortality and inability to come for the follow up (not contactable,

unwilling to come), we estimated that we will be able to recruit around 50% of these

children (32 -35 children).

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Consent and Approval:

The data collection from the Inpatient and outpatient records was done after

obtaining approval from the Unit Heads of Department of Paediatric Surgery and Medical

Records Department, Christian Medical College and Hospital, Vellore. Aim and purpose

of the study were informed to the parents and children and their informed consent and

assent were obtained. Participants‟ identity and all the data were kept confidential.

The study was presented in the Institutional Review Board and was accepted.

(Ref: IRB Min. No. 10351 dated 03.11.2016)

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MATERIALS AND METHODS

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Methods and Methodology:

All children operated for EA/TEF by Paediatric surgery in Christian medical

college during the period January 2008- December 2015 were identified from the

database .There were 3 parts to the study.

Part 1: A retrospective data collection was done from medical records of

all the patients operated.

Part 2: Study of the early life respiratory morbidity of the operated

children.

Part 3: The cross sectional observational study on current respiratory

morbidity.

The duration of this study was from December 2016 to June 2017. The inclusion

and the exclusion criteria of our study is as follows

Inclusion criteria:

- Any child who was diagnosed with EA/TEF who underwent primary

repair in the neonatal period between January 2008- December 2015

(for all 3 parts)

- Children who were survivors beyond 6 months of age (for part 2 &

3)

- Those who were consenting for clinical examination and diagnostic

evaluation.(part 3)

-

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Exclusion criteria:

- Cases operated here beyond neonatal period.

- Children who died within the post operative period (for part 2&3).

Information regarding all these patients was collected from the medical

records. Using a structured proforma available data on the antenatal and perioperative

period was collected. Contact information of all these patients excluding those who died

in the neonatal period and discharged at request from NICU, was obtained from the

records. Principal Investigator contacted all those who could be contacted by phone. If

phone numbers were not available, using the postal address attempt was made to trace

the remaining children by home visits.

As per the inclusion criteria, those patients who lived beyond 6 months of

age were eligible to be recruited to the observational study. If information was available

in the medical records about first year followup,it was collected for part 2 of the study.

Consent was obtained from 27 families after briefing about the study and

providing written information about the study. One family expressed inability to come to

the hospital for the evaluation. The information such as demographic factors, antenatal,

peri-natal period were collected from the database and confirmed with the parents during

the interview. Information about morbidity in infancy and current symptoms were

collected from them by phone. All these data was entered on the structured proforma.

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Other 26 patients were given an appointment to come to CMC hospital and

meet the primary investigator. The primary investigator again explained the study

purpose and obtained written consent (annexure 2) and assent from the children (more

than 8 years) recruited to the study. Detailed history regarding demographics, respiratory

symptoms frequency, hospitalization, treatment details, any (other) surgeries, symptoms

related to swallowing was collected. Details were verified with patient‟s own medical

records whenever available. Information on other risk factors of respiratory morbidity

like exposure to cigarette smoke, overcrowding, relevant family history and

immunization history also collected. Detailed clinical examination including growth

assessment, upper/lower respiratory tract examination and systemic examination were

done.

After the initial examination, all children underwent Chest X-ray and barium

swallow. HRCT was done if subject had recurrent respiratory infections or clinical

features of bronchiectasis &/ parenchymal changes on CXR.

In the barium swallow abnormal swallow phase, oesophageal motility, any

laryngeal penetration or gastro esophageal reflux was specifically looked for. A senior

radiologist evaluated the CXR and HRCT using a structured format.

ENT evaluation with NPL – Scopy by a single ENT surgeon was done on those

who gave consent for procedure.

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All in formation were entered on structured proforma. Following flow chart

outlines the recruitment of patients and study procedures.

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Data entry and analysis:

Data entry was done using Epidata and converted to Microsoft excel. Data

analysis was done using Statistical Package for Social Sciences (SPSS) version 16.

Association between the categorical variable(Y/N, MMS) and presence of respiratory

morbidity will be analyzed using chi-square statistics. The continuous variable

(Gestational age, birth weight) will be compared using independent + - test. Logistic

regression will be used to analyze the unadjusted and adjusted effect of predictors over

respiratory morbidity. The risk will be give as odds ratio (95% CI).

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RESULTS

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Results:

From January 2008 to December 2015 fifty patients were operated in the

neonatal period for esophageal atresia with or without tracheoesophageal fistula.

Among them 24 were inborn babies and 26 were referred from elsewhere between

the age of 2 hrs to 8 days after birth. Excluding 11 infants (8 infants who died

before 6 months of age and 3 who were discharged at request in the immediate post

op period) 39 infants qualified the inclusion criteria of this follow up study. Only

30 families could be contacted using the available contact details and all consented

for their information to be used in the study. Three of these babies had died before

the first birthday.Remaining 26 families brought their infants for this follow up

study and the other 1 gave information by a phone interview.

Results of this study are presented in 3 parts:

Part 1 – Pre-op and peri operative characteristics of 50 infants

Part 2 – Pulmonary morbidity in early life (first year) in 34 infants

Part 3- Cross sectional Observational study on 26 infants (Whose

Parental consent was obtained) for current respiratory

Morbidity assessment.

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30 Families were contacted

3 Children Died

Active participation with written consent = 26

Phone interview and verbral consent = 1

History and Clinical Examination = 26

Chest X - Ray = 26

Barium swallow = 26

HRCT = 21

(Planned for 21 since CXR and Examination

was normal for 5 children)

NPL - Scopy = 24

(2 Parents denied)

39 children eligible for recruitment

First year of life data available from medical records and direct history taking - 34 children

From database 50 infants were identified who were diagnosed to have OA/TEF underwent surgery in CMC, Vellore between January

2008 - December 2015.

Total number of children operated - 50

Died in NICU - 8

DAMA - 3

Data available:

• Pre - Operative data: 50

• Intra - Operative data: 49

• Post - Operative data: 48

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Characteristics of infants operated for TE Fistula (n = 50):

The outcome characteristics:

The outcome characteristics of the operated children are tabulated below

(Figure 3).

Figure 3: Demonstrating the characteristics of the children.

Sex ratio:

Out of the 50 operated patients 24 were males and 26 females with M: F

ratio 0.92:1 which is represented below in a diagrammatic representation.

35

8

43

Outcome characteristics

Alive beyond 6 months age

Died in the Neonatal period

Died after 6 months of age

DAMA in the Neontal period

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Figure 4: Demonstrating the sex differentiation of the children.

Types of esophageal atresia +/- fistulae:

There are five types of esophageal atresia +/-fistulae described in literature.

In our study majority (90%) were type C followed by type B and type A, 4% and

6% respectively by Gross classification.

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Male Female

2426

Sex

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Figure 5: Types of OA±TEF with the percentage.

Birth weight:

The mean birth weight of this cohort was 2289.5 grams. The minimum birth

weight was 1220 grams and maximum was 3600 gm. 56% were low birth weight

(defined as birth weight < 2500gm).

Table no 13: Frequency of birth weight (n=50).

Birth weight Frequency (n = 50) Percentage (%)

1000 – 1500 Grams 4 8%

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1500 – 2500 Grams 24 48%

>2500 Grams 32 64%

Total 50 100%

Gestational age:

Mean gestational age was 37.74 weeks. Fifteen out of the 50 babies were

born premature (30%). The maximum gestational age was 41 weeks and minimum

was 31 weeks.

Table no 14: Frequency of gestational age (n=50).

Gestational age Frequency (n = 50) Percentage (%)

<32 Weeks 1 2%

32 – 35 Weeks 6 12%

35 – 37 Weeks 8 16%

>37 Weeks 35 70%

Total 50 100%

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Figure 6: Distribution of the gestational age (n=50).

Antenatal period:

In the antenatal period TEF was suspected and documented in 6 patients

(12%). Clinical polyhydramnios was noted and documented in the medical records

of 23 mothers (46%). Abnormal antenatal ultrasound was documented in 44%

mothers and the most common finding was polyhydramnios.

Other antenatal complications included maternal urinary tract infection,

fever, pregnancy induced hypertension, Gestational diabetes mellitus, and Etc.

1

6

8

35

Gestational age

Less than 32 Weeks

32 - 35 Weeks

35 - 37 Weeks

More than 37 weeks

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Peri natal period:

Out of the 50 children 22 were delivered by LSCS (44%) which is higher than

average LSCS rate of 25-30% in our hospital and all were singleton pregnancies.

Figure 7: Distribution of the type of delivery (n=50).

Presenting symptom:

Five patients were referred to our hospital with a diagnosis of oesophageal atresia.

Review of the records showed that respiratory distress was the commonest symptom in

80% of total patients. The 2nd

commonest symptom was drooling of saliva (78%)

followed by vomiting (28%), choking of feeds and cyanosis in 18%.

22

22

6

Type of Delivery

LSCS

NVD

Assisted

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It is interesting to note that 18 infants ( 13 inborn and 5 out born) were admitted to

NICU with a diagnosis of prematurity for care and during routine NG tube insertion, TEF

was suspected due to inability to successfully insert tube into the stomach. Abdominal

distention was a notable feature in 4 term infants, three of whom had perforation of the

stomach likely due to aerophagia resulting in gastric distention. The other infant had

associated imperforate anus.

Diagnosis:

Coiling of Naso-gastric tube in the esophagus on plain X-ray was documented in

all babies. In 3 children barium swallow was done to confirm the diagnosis and one

patient underwent Computerized Tomography of the chest for confirmation of diagnosis.

Pre – Operative period:

All the 50 babies were admitted in neonatal intensive care unit in the pre –

operative period. Pre – operative ventilator support was required for 9 babies (18%) and

supplemental oxygen was given to 96% of patients. For more than 24 hours continuous

oesophageal suction was given for 31 patients.

During the preoperative period, lower respiratory tract infection was diagnosed in

18 babies. Cause of the LRTI in all the children was due to the aspiration of the feeds or

foregut contents.

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Cardiac anomalies were the most common associated anomaly in these patients

(74%). The incidence of various cardiac disease is tabulated and represented in the

diagram below

Figure 8: Distribution of the type of congenital cardiac anomalies (n=37).

1: PDA – patent ductus arteriosus, 2: ASD – Atrial septal defect, 3: VSD – ventricular

septal defect.

Associated anomalies:

Apart from the cardiac anomalies there were multiple other anomalies noted. The

most common vertebral anomaly was hemi-vertebrae.

26

23

7

5

4 1

Types of congenital cardiac anomalies

PDA

ASD

Right sided aortic arch

VSD

Other's

Complex Heart disease

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Table no 15: Associated anomalies with Oesophageal atresia.

Anomaly Number Percentage (%)

Vertebral Anomaly 8 16%

Single umbilical artery 6 12%

Imperforate Anus 4 8%

Renal anomaly 5 10%

Cloacal Anomaly 3 6%

VACTERL 7 14%

Day of surgery:

Majority of patients underwent corrective surgery on day 2 of life.

Figure 9: The day of surgery after the birth (n=50)

6

24

17

1 1 1

Day of surgery

Day 1 Day 2

Day 3 Day 4

Day 6 Day 9

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Intra – Operative period (N=49):

The most common surgical procedure was end to end anastomosis. This

procedure was done for 43 patients and remaining 7 patients underwent cervical

oesophagostomy.

Operative notes were not available for 1 patient. Feeding gastrostomy was

placed in 12 patients out of the 49 patient. 4 children were diagnosed with Ano-Rectal

malformation and these children underwent colostomy and later corrective surgery.

Post – operative period and complications (N=48):

Details of postoperative period were available for all except 2 patients. During the

post – operative period, leakage from the anastomosis site was noted in 15 (31.25%)

patients. This was managed conservatively in all but one child. Ventilation for more than

7 days was required for 16 (33.33%) of the 48 patients. The commonest reason for

prolonged ventilation was Hospital acquired infection and Pneumonia.

Ventilation associated complications such as Ventilator associated pneumonia

or failed extubation or post extubation stridor were noted in 20 (41.67%) of children.

A total of 27 patients (56.25%) had consolidation of the lung parenchyma

during the post – operative period, whereas collapse of the lung and Pneumothorax was

found in 8 (16.67%). In 2 patients lung collapse persisted long term. Pleural effusion and

chylo-thorax was noted in 4.17% and 6.25% respectively.

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Hospital acquired infection is a major risk in any hospitalized child. The risk

increases in post – operative patients since they may develop wound infection which can

eventually lead to blood stream infection. Hospital acquired infections include blood

stream infection; Ventilator associated pneumonia and urinary tract infection. In our

study we found that 16 patients (33.33%) had positive blood culture and 7 more children

with probable sepsis (Positive clinical feature, increased serological marker for sepsis

with Negative blood culture).

Figure 10: The incidence of hospital acquired infection in the post operative period

(n=48)

16

12

7 7

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Blood stream infection Ventilator associated pneumonia

Surgical site infection Probable sepsis

Hospital acquired infection

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Feeding intolerance was another important complication that occurred in the

post – operative period. Data was available only for 38 children out of which 11

(28.95%) patients had feed intolerance. Bilateral abductor palsy and hiatus hernia was

present in 2.08% of the children and noted during the post – operative period.

Part 2:

Data available for respiratory morbidity in the first year of

life on children who lived beyond 6 months of age (n=34):

Twenty six patients completed the cross sectional study of evaluation of past

respiratory morbidity and assessment of their current respiratory system health. In

addition, information on 1 child (collected by phone interview), data collected from

medical records for 7 infants who were on follow up in our hospital beyond 6 months of

life (3 of whom died subsequently and 4 were lost to follow up) is presented in the

following section.

Environmental history:

The environmental history was collected for 30 children (27 live children and 3

children who died after 6 months of life). These include type of house they live and

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smoke exposure history was collected. Around 53.33% of the children lived in Pucca

house and the remainder either lived in Semi – Pucca or a Kutcha house

Figure 11: Type of house that the children live currently (n=34).

Table no 16: Active smokers in home that the children live currently (n=34).

Smokers living in the

same house

Number Percentage (%)

Yes 10 29.41%

No 20 58.82%

Data not available 4 11.76%

Total 34 100%

47%

35%

6%

12%

Type of house

Pucca

Semi - Pucca

Kutcha

No data

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Table no 17: Mode of cooking that the children live currently (n=34).

Mode of cooking Number Percentage (%)

Cooking with

wood

9 26.47%

Cooking with

gas

21 61.76%

Data not available 4 11.76%

Total 34 100%

Respiratory morbidity (n=34):

In two third of patients hospital admission was indicated for respiratory morbidity

in the first year of life. Lower respiratory tract infection (defined as cough and fever with

chest retraction or physician diagnosis of pneumonia) was the most common problem in

the 1st year of life. Persistent cough (which is defined as cough which persists for more

than four weeks) was reported in 91.18% of the patients and in most of them it persisted

throughout and beyond infancy. Though 82.35% reported wheeze, only 55.88% had

evaluation for recurrent wheeze out of that only 12 (35.29%) patients were prescribed use

of inhaled steroids/bronchodilators via metered dose inhalers.

Other than cough and wheeze, stridor/Abnormal sound was an important

complaint in the 1st year of life 17 (50%). However except one baby, none were

evaluated for the same. The child who underwent scopy had laryngomalacia.

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Table no 18: Respiratory morbidity in the first year of life.

Respiratory morbidity Frequency (n = 34) Percentage (%)

History of Recurrent LRI 27 79.41%

Diagnosed LRI at least once 33 97.06%

Prolonged Cough history 31 91.18%

Wheeze history 28 82.35%

Evaluated for recurrent

Wheeze

19 55.88%

Stridor/Noisy breathing history 17 50%

Hospital admission for

respiratory symptoms

23 67.65%

Figure no 12: Showing the bar diagram of the respiratory morbidity in the first year of

life

0102030405060708090

100

History of recurrent LRI

Diagnosed LRTI atleast once

Prolonged cough history

Wheeze history Hospital admission for

respiratory

symptoms

27

33 3128

23

Respiratory morbidity in the first year

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Respiratory morbidity beyond the first year of life:

We had data on only 27 children about their respiratory morbidity beyond

first year of life. Hence comparison of respiratory morbidity of first year and later years

of these 27 children is shown below as table.

Table no 19: Comparison of the respiratory morbidity during the first year with

consecutive years.

Variables During the 1st year

(n = 27)

During the

subsequent years

(n = 27)

History of Recurrent LRI 20(74.07%) 21(77.78%)

Diagnosed with at least one

episode of LRI

26(96.29%) 21(77.78%)

Prolonged cough history 23(85.18%) 23(85.18%)

Wheeze history 22(81.48%) 18(66.67%)

Stridor/ Noisy breathing 13(48.14%) 11(40.74%)

Hospital admission for

respiratory symptoms

17(62.96%) 14(51.85%)

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Figure no 13: Showing the bar diagram of the comparison of the respiratory morbidity

with the first year and consecutive year of life.

There was a substantial reduction in the frequency of lower respiratory

infection, wheeze episodes and the need for hospital admission in the 27 children

studied.

History of recurrent LRI

Diagnosed LRI >/= 1

Prolonged cough history

Wheeze history

Hospital admission for

respiratory

symptoms

First Year 74.07 96.29 85.18 81.48 62.96

Consecutive years 77.78 77.78 85.18 66.67 51.85

Per

cen

tage

Comparison between the first and consecutive years

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Gastro – Oesophageal morbidity:

Gastro – Oesophageal symptoms in the first year of life:

Gastro – oesophageal symptoms were common among the children operated for

oesophageal atresia ± TEF. Gastrointestinal manifestation varied from simple

regurgitation to food bolus impaction. Vomiting/Regurgitation of the feeds were seen in

22 of the 34 children which is more than 64%. Significant Gastro – esophageal reflux

disease (demonstrated by barium swallow) was present in 50% of the children and

required Anti – reflux medications during the 1st year of life.

A total of 10 children (29.41%) underwent fundoplication in the 1st 2 years for the

severe GER disease. Among those patients who had a diagnosis of GERD, 60%

underwent fundoplication indication being Severe GERD, Failure to thrive or recurrent

respiratory tract infection. Others were managed with medications. Out of the 39 children

8 (20.51%) had feeding gastrostomy. Indication for this procedure was to provide enteral

feeding when cervical oesophagostomy was done and 2 children underwent this

procedure after 6 months of age for severe failure to thrive.

The other commonly noted gastro – oesophageal problem was dysphagia

secondary to oesophageal stricture. A total of 17 patients (50%) had dysphagia. Food

bolus impaction was documented in 12 (35.29%) of these children and required

oesophageal dilatation at least once.

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Table no 20: Gastro – Oesophageal morbidity in the first year of life.

Variables Frequency

(n=34)

Percentage (%)

Dysphagia 17 50%

Regurgitation/Vomiting 22 64.71%

Food bolus impaction 12 35.29%

GERD 17 50%

Oesophageal stricture 12 35.29%

Gastro – Oesophageal symptoms beyond first year of life (N=27):

Table no 21: Comparison of the Gastro-Oesophageal morbidity during the first year with

consecutive years.

Variables During the 1st Year

(n=27)

During Consecutive

Year (n=27)

Dysphagia 13(48.14%) 16 (59.25%)

Regurgitation/Vomiting 17(62.96%) 10(37.03%)

Food bolus impaction 8(29.62%) 10(37.03%)

GERD 12(44.44%) 11(40.74%)

Oesophageal stricture 9(33.33%) 10(37.03%)

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Below flowchart shows the comparison of the Gastro- Oesophageal complaints

Figure no 14: Showing the bar diagram of the comparison of the Gastro - Oesophageal

morbidity with the first year and consecutive year of life.

There was significant improvement in symptoms of vomiting and regurgitation of

first year of life. Reported dysphagia symptoms and incidence of food bolus impaction

worsened after first year of life likely due to introduction of solid food.

Regurgitation/Vomiting

Dysphagia GERD Oesophageal stricture

Food bolus impaction

First Year 62.96 48.14 44.44 33.33 29.62

Consecutive years 37.03 59.25 40.74 37.03 37.03

Per

cen

tage

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Figure no 15: Showing the bar diagram of the Gastro - Oesophageal procedure that have

been done so far.

Cardio vascular problems:

Cardiac conditions contributed to significant morbidity. As we have earlier seen

that 37 of the 50 children had cardiac disease ranging from atrial septal defect to complex

heart disease. Of the 34 children anti – failure medication was started for 8 patients

(23.53%) who had cardiac failure and 6 (75%) of these children underwent cardiac

surgery for the refractory failure.

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Oesophageal dilatation Fundoplication Feeding gastrostomy

1210

2

Gastro - Oesophageal procedures done so far

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Table no 23: Current cardiac morbidity of the 34 children.

Cardiac problem Frequency (n=34) Percentage (%)

Cardiac failure 8 23.52%

Anti – failure medication 8 23.52%

Cardiac surgery 6 17.64%

Part 3

Evaluation of current respiratory and related GI morbidity

in 26 patients:

26 children completed cross sectional follow up study. These children were

examined in child health outpatient department in Christian medical college, Vellore by

the primary investigator.

Age and sex distribution:

The age and sex of the 26 children are discussed below. The mean age of the

group were 64 months with minimum age of 13 months, maximum of 103 months and a

median of 67.5 months. The age group of these children was tabulated below. Of the 26

children 12 were boys and 14 were girls.

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Table no 24: Age group distribution of the 26 children.

Age group Frequency (n=26) with percentage

1 – <2 Years 1(3.84%)

2 –< 5 Years 9(34.62%)

5 – <9 Years 16(61.54%)

Total 26(100%)

Figure 16: Showing the sex distribution in the 26 children

General examination:

General examination showed clinical pallor in 23 children (88.46%). Nine children

had clubbing (34.62%). Facial dysmorphism was observed in 5 patients.

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Male Female

12 14

Sex

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Nutritional evaluation:

The weight and height were documented for the 26 children and were plotted in

the IAP growth chart. Body mass index was calculated and plotted on the chart. Each

color represents each child in the weight and height percentile. The same color has also

been used for the BMI chart.

Figure 17: Height and weight chart of the 26 children according the IAP – Growth chart.

Each color represents one child.

Body Mass Index percentile:

The body mass index was calculated for 25 of the total children since one child

was 13 months. 60% of these children have current BMI less than 5th centile

(underweight by CDC classification) and 72% below 10th

centile.

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Figure 18: Body mass index of the 25 children according the CDC guidelines.

Figure 19: Body mass index chart of the 25 children according the CDC growth chart.

Each color represents one child.

153

2

3

1 1

BMI Percentile

Less than 5

5 to 10

10 to 25

25 to 50

50 to 75

75 to 85

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Deformity:

Chest deformity was apparent in 69.23% of the children followed by spinal

deformity with frequency of 12 (46.15%).

Facial dysmorphisms is seen in 4 of the 26 patients. The dysmorphisms that were

noted are Dolicocephaly, Hypertelorism, synorphs, etc.

Respiratory system examination:

The respiratory system examination was done 26 children. Findings such as

tachypnoea, chest retraction, localized decreased breath sounds, crepitations and wheeze

are tabulated below

Table no 25: Current respiratory findings of the 26 children.

Respiratory findings Frequency (n=26) with Percentage

Tachypnoea 10 (38.46%)

Chest retraction 10 (38.46%)

Localized decreased breath sounds 7 (26.92%)

Crepitations 16 (61.54%)

Wheeze 9 (34.62%)

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Radiological investigation:

Chest X – Ray:

All the 26 children underwent chest X – ray which was reported by the same

radiologist. The parameters such as scaring, volume loss, hypoplasia, bronchial wall

thickening and bronchial dilatation were assessed and reported by a single radiology

consultant.

Table no 25: Chest X – ray finding of the 26 children (n=26)

Chest X – ray finding Frequency (n=26) Percentage (%)

Scarring 3 11.54%

Volume loss/collapse 8 30.77%

Bronchial wall thickening 11 41.67%

Bronchial dilatation 3 11.54%

Normal 8 30.77%

Barium swallows:

Barium swallow was done for all the 26 children who were recruited in the study

and was abnormal in 18 (69.23%). In this procedure swallowing phase abnormality, in

co-ordination, reflux disease, stricture and diverticulum were looked for. The most

common finding was gastro esophageal reflux which was present in 11 patients (42.31%).

8 had reflux up to clavicles and the remaining till mid thoracic region. Ten out of these

eleven children were asymptomatic.

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The next common finding that was observed in barium swallow was oesophageal

stricture. This was present in 10 children (38.46%) though none reported symptoms.

Swallowing phase was normal in 17 children out of the 26 children.

Of the 9 children who had fundoplication in the past either for failure to thrive or

severe GER disease, 4 had persisting GER and 1 had delayed transit in the esophagus

demonstrated by barium swallow.

Out of the 9 children except 2 children all others had abnormal Barium swallow

with 4 children having Reflux disease, 2 children with delayed transit, 5 children with

stricture and 1 child with Para-esophageal hernia.

Figure 20: Barium swallow finding (n=26).

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Abnormal swallowing

Reflux disease Stricture Diverticulum Normal

9

11 10

3

8

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High Resolution Computerized Tomography – Chest (HRCT –

Chest):

HRCT of the chest was done for 21 children. The parameters that was looked for

were Esophagus – Dilatation, Narrowing and diverticulum , Trachea – Narrowing,

Widening and Diverticulum, Bronchi – Bronchiectasis, Bronchial wall thickening, Lung

parenchyma – scarring, collapse, hyperinflation and consolidation.

Esophagus:

Dilatation of the esophagus was noted in more than 52.38% of the 19 patients. The

dilatation was present in the proximal region of the site of anastomosis. Narrowing and

diverticulum was present in 2 patient.

Trachea:

The most common finding in the trachea was diverticulum which was present in

15 of the 21 children whom underwent HRCT. Narrowing of the trachea was noted in 4

patients.

Bronchi:

Bronchiectasis was present in 34.61% of the children evaluated either by HRCT

/clinical examination/CXR. HRCT was done only if clinically indicated and hence only

21 children had the study done. The other 5 had no clinical or CXR features to suggest

bronchiectasis. Bronchial wall thickening was noted in 6 HRCT studies.

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Lung parenchyma:

Lung parenchymal changes included scarring, collapse, hyperinflation and

consolidation. Collapse was seen in 2 children; these 2 children had collapse in the post

operative period and persisted to have collapse of the lung. Both these children are under

regular follow – up. Hyperinflation of the lung was seen in only one patient who has a

diagnosis of asthma and is on treatment.

Table 26: Showing the HRCT – Chest findings (n=21)

HRCT – chest finding Frequency (n=21) Percentage (%)

Tracheal narrowing 2 7.69%

Tracheal diverticulum 15 57.69%

Bronchiectasis 9 34.61%

Bronchial wall thickening 6 23.07%

Scaring 8 30.76%

Collapse 2 7.69%

Hyperinflation 1 3.85%

Oesophageal narrowing 2 7.69%

Oesophageal diverticulum 2 7.69%

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Figure 21: HRCT – Chest finding (n=21).

NPL – Scopy:

NPL – Scopy was done for 24 patients since parents of 2 patients did not consent

for the procedure. The parameters which were looked for in the scopy were vocal cord

mobility, vocal cord nodule, reflux laryngitis and adenoid hyperplasia. Vocal cord nodule

was the commonest finding with a frequency of (37.5%).The next common finding was

reflux laryngitis and adenoid hyperplasia 33.33%. Unilateral vocal cord palsy was seen in

3 patients who were not diagnosed previously. Except one child the remaining two

children were currently asymptomatic. However 2 of the 3 children had stridor during the

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

2

15

9

68

21

2 2

HRCT – Chest

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initial period of life. The remaining one child was complaining of hoarseness of voice

during evaluation.

Figure 22: Finding of the NPL – Scopy (n=24).

Correlation between the patient characteristics and outcome

– mortality:

The characteristics of infants who survived the post operative period were

compared to those who died. Though this study was not designed to assess the risk

factors for poor outcome, certain observations were made.

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

vocal cord nodule

Reflux laryngitis Adenoid hyperplasia

Normal Vocal cord palsy

98

7 7

3

NPL - Scopy

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Pre operatively low gestational age and birth weight less than 2.5 kg was showed

positive correlation with mortality. There was a higher rate of mortality in those infants

who had single umbilical artery and who required preoperative ventilation.

Post operative ventilation, ventilator associated pneumonia, post operative

consolidation or collapse lung and blood culture positivity, cardiac disease, imperforate

anus, vertebral anomaly, renal anomaly and cloacae anomaly did not show positive

correlation with mortality.

Table 27: Correlation between the patient characteristics and outcome – mortality

Variables

Alive

Death

“ p “

value

Gestational age < 37 wks 11 6 0.04

≥37 wks 24 2

Birth weight <2.5 kg 18 8 0.15

≥2.5 kg 17 0

Single umbilical cord Yes 3(8.57%) 3(37.5%) 0.07

No 32(91.43%) 5(62.5%)

Pre – Operative

ventilation

Yes 3 (8.57%) 4(50%) 0.02

No 32 (91.43%) 4(50%)

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Type of surgery End to end

anastomosis

34(97.14%) 6 (75%) 0.08

Cervical

oesophagosto

my

1 (2.86%) 2(25%)

Post – operative

leakage

Yes 8(22.86%) 4(66.67%) 0.05

No 27(77.14%) 2(33.33%)

Post – operative

ventilation for >7 days

Yes 7(20%) 4(66.67%) 0.04

No 28(80%) 2(33.33%)

Re – do surgery Yes 1 (2.86%) 3(33.33%) 0.01

No 34(97.14%) 4(66.67%)

LRI/Consolidation in

the post operative

period

Yes 14(40%) 6(100%) 0.01

No 21(60%) 0

Collapse in the post

operative period

Yes 11(31.43%) 5(83.33%) 0.03

No 24(68.57%) 1(16.67%)

Positive blood culture Yes 8(22.86%) 5(83.33%) 0.01

No 27(77.14%) 1(16.67%)

Ventilator associated

pneumonia

Yes 4(11.43%) 5(83.33%) 0.001

No 31(88.57%) 1(16.67%)

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Correlation between patient characteristics and outcome –

Bronchiectasis:

History of regurgitation and vomiting in the first year showed statistically

significant correlation to development of bronchiectasis. Two factors namely recurrent

LRTI in the first year and presence of tracheal diverticulum in the HRCT showed a trend

towards development of bronchiectasis.

Post – operative leakage, Feed intolerance, chronic cough, wheeze, stridor,

dysphagia, food bolus impaction, hospital admission for the respiratory problem, Etc., did

not have show statistically significant correlation. However due to small numbers no

meaningful conclusion can be drawn from this.

Table 28: Correlation between patient characteristics and outcome – Bronchiectasis

Variables Bronchiectactic Non -

Bronchiectactic

Fisher’s

exact

Post – operative leakage Yes 1(11.11%) 6(35.29%) 0.35

No 8(88.89%) 11(64.71%)

Positive blood culture Yes 0 6(35.29%) 0.06

No 9 (100%) 11(64.71%)

Feed intolerance Yes 2(22.22%) 8(50%) 0.2

No 7(77.78%) 8(50%)

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Recurrent LRI with wheeze in

1st year

Yes 9 (100%) 10(58.82%) 0.05

No 0 7(41.18%)

Regurgitation and vomiting

after 1st year

Yes 6(66.67%) 4(23.53%) 0.04

No 3(33.33%) 13(76.47%)

Hospital admission after 1st

year

Yes 7(77.78%) 7(41.18%)

0.1 No 2(22.22%) 10(58.82%)

Right sided aortic arch

Yes 3(42.86%) 0

0.03 No 4(57.14%) 12(100%)

Tracheal diverticulum in

HRCT

Yes 9(100%) 6(50%) 0.02

No 0 6(50%)

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DISCUSSION

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Discussion:

This observational study on a retrospective cohort of children operated in

neonatal period threw light on many important aspects on the care of these

children.

Comparison of antenatal and peri-natal characteristics as shown in table 29

below highlights some features. Antenatal diagnosis rate, prematurity, associated

anomalies etc are comparable with literature from the rest of the world.

A higher occurrence of surgery related morbidity could be due to late

referrals from other hospitals and inadequate preoperative care.

Main post surgical complications are related to infections including blood

stream infections. It mirrors the high rates of hospital acquired infections (in India)

prevalent in babies with complex neonatal issues.

Table 29: Showing comparison of data on 50 operated infants with the data from

the rest of the world during the Peri-natal and post operative period.

Current

study

Previous studies Ref

Antenatal

diagnosis

12% 9.2% and 24% Sparey et al and De Vigan et al

Average birth wt. 2289.5

grams

(Mean)

2.5 +/- 0.7 Kg Seo et al(84)

Prematurity 30% 31.95% Korean study (84)

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Cardiac anomaly 74% 30 – 60 % Bishop PJ et al

Type of fistulae 90% -

Type C

81.01% - Type C Bal et al(48)

Surgical site

anastamotic leak

31.3% 15 – 20% Chetcuti et al(85)

Early life morbidity is staggering as revealed in the study.96% of those we

followed up (N 26) had significant respiratory illness. Recurrent LRTI requiring

hospital admissions is much higher than reported from other countries as shown in

table 30. In a study by Nicholas E. Dudley et al t 58 of the 78 children were

admitted at least once for respiratory complaints within 8 years(86). Though

medical personnel caring for neonates in NICU and pediatric surgery ward counsel

the parents about anticipated GI complications, very little information is given to

them about respiratory morbidity, early identification and prevention.

Table 30: Showing comparison of persisting respiratory morbidity data of 26

children with literature data.

Current

study (n-

=26)

Previous

studies

Number

of

children

Ref with

country

Oesophageal

stricture

38.46% 52% 144 Konkin et al,

Columbia

(87)

GERD 42.31%

(Current)

48% 69 Little et al,

Indiana (88)

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Respiratory

morbidity

96.15% 78% 105 Porcaro et al,

Italy (89)

Hospital

admission for

LRTI

61.54% (First

year)

44% 334 Chetcuti and

Phelan et al,

Australia(85)

Diagnosed LRTI 96.15% 56% 169 Sistonen et al,

Finland (90)

Bronchiectasis 34.61%

(n=26)

17% 41 Banjar and

Al-Nassar et

al, Saudi (83)

Vocal cord palsy 12.5% (n=24) 7.69% 21 Robertson et

al ,

Columbus,

Ohio (91)

In the Korean study(84) dysphagia with esophageal stricture was present in 65%

(Out of 72 children) and our study showed 50% had dysphagia and stricture in 35.29%.

Banjar and Al-Nassar et al(83) showed GERD in 95% of the children out of which 59%

underwent Nissen fundoplication and Mortell AE et al(92) showed GERD present in 40

a- 65% of the patients. However in our study we found significant GERD in 50%

requiring anti – reflux medication and 26.47% underwent fundoplication. Irregular follow

up may be the reason for low pick up rate.

Kristina et al studied 31 children survivors of TEF surgery with a mean age of

13.7 yrs in whom prevalence of respiratory and esophageal problems were 41% and 44%.

They showed that pulmonary complication occurred in >70% with bronchiectasis

occurring in 17%. Bronchiectasis rate was much higher in our study the reason for which

is multi-factorial.

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The study done by Kristina et al showed that doctor diagnosed Asthma was

present in 22% with a weekly episode of wheezing in approximately 33%.We did not

seek to find the prevalence of asthma as diagnostic tests are not possible in the age group

we studied.

Cudmore RE et al showed that 16% of children had isolated chest wall deformity

and 42% had chest wall deformity compared to 69.23% in our study.

This study highlights the need for focus on preventable risk factors for poor

respiratory outcome like malnutrition, exposure to environmental smoke etc.

Association of certain variables in the peri-natal period with mortality and

subsequent years with development of bronchiectasis has been discussed in the

results section. Of note is presence of tracheal diverticulum at surgical site. This

may be contributing to poor drainage of airway secretions and thereby

bronchiectasis. We could not find reference this risk factor in the published

literature. We have not assessed prevalence of tracheo-bronchomalacia in this

study as it will involve invasive bronchoscopy. Airway-malacia may be

contributing to morbidity either independently or in association with other factors.

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CONCLUSION

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Conclusion:

In survivors of neonatal TEF surgery,

• There is a high prevalence of respiratory morbidity in terms of significant

symptoms pertaining to respiratory system and GI system in the first year of life.

• While respiratory symptoms show a trend toward improvement after the first year

of life, GI symptoms persist more often.

• One third of children studied had developed bronchiectasis.

• There is significant malnutrition in the survivors of TEF surgery.

• ENT evaluation revealed significant findings.

• Only 8 were on regular follow up in CMC. Most of them had no follow up at all.

(Many were unaware of the lung damage the child has already suffered.)

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Pediatr Gastroenterol Nutr. 2011 May;52 Suppl 1:S35-36.

65. Kovesi T, Rubin S. Long-term Complications of Congenital Esophageal Atresia and/or

Tracheoesophageal Fistula. Chest. 2004 Sep;126(3):915–25.

66. Spitz L. Esophageal atresia: Lessons I have learned in a 40-year experience. Journal of

pediatric surgery. 2006 10//;41(10):1635-40.

67. Ein SH, Stringer DA, Stephens CA, Shandling B, Simpson J, Filler RM. Recurrent

tracheoesophageal fistulas seventeen-year review. Journal of pediatric surgery. 1983

8//;18(4):436-41.

68. Spitz L. Esophageal atresia: past, present, and future. J Pediatr Surg. 1996;31(1):19–25.

69. Parker AF, Christie DL, Cahill JL. Incidence and significance of gastroesophageal reflux

following repair of esophageal atresia and tracheoesophageal fistula and the need for anti-

reflux procedures. J Pediatr Surg. 1979 Feb;14(1):5–8.

70. Filston HC, Rankin JS, Kirks DR. The diagnosis of primary and recurrent

tracheoesophageal fistulas: value of selective catheterization. J Pediatr Surg. 1982

Apr;17(2):144–8.

71. Rintala RJ, Sistonen S, Pakarinen MP. Outcome of esophageal atresia beyond childhood.

Seminars in pediatric surgery. 2009 Feb;18(1):50-6. PubMed PMID: 19103423. Epub

2008/12/24. eng.

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72. Allin B, Knight M, Johnson P, Burge D, BAPS-CASS. Outcomes at one-year post

anastomosis from a national cohort of infants with oesophageal atresia. PloS One.

2014;9(8):e106149.

73. Dudley NE, Phelan PD. Respiratory complications in long-term survivors of oesophageal

atresia. Arch Dis Child. 1976 Apr;51(4):279–82.

74. Beardsmore CS, MacFadyen UM, Johnstone MS, Williams A, Simpson H. Clinical findings

and respiratory function in infants following repair of oesophageal atresia and tracheo-

oesophageal fistula. Eur Respir J. 1994 Jun 1;7(6):1039–47.

75. Kovesi T, Rubin S. Long-term Complications of Congenital Esophageal Atresia and/or

Tracheoesophageal Fistula. Chest. 2004 Sep;126(3):915–25.

76. Schneider A, Blanc S, Bonnard A, Khen-Dunlop N, Auber F, Breton A, et al. Results from

the French National Esophageal Atresia register: one-year outcome. Orphanet J Rare Dis.

2014 Dec 11;9:206.

77. Sulkowski JP, Cooper JN, Lopez JJ, Jadcherla Y, Cuenot A, Mattei P, et al. Morbidity and

Mortality in Patients with Esophageal Atresia. Surgery. 2014 Aug;156(2):483–91.

78. Milligan DW, Levison H. Lung function in children following repair of tracheoesophageal

fistula. J Pediatr. 1979 Jul;95(1):24–7.

79. LeSouëf PN, Myers NA, Landau LI. Etiologic factors in long-term respiratory

functionabnormalities following esophageal atresia repair. J Pediatr Surg. 1987 Oct

1;22(10):918–22.

80. Malmström K, Lohi J, Lindahl H, Pelkonen A, Kajosaari M, Sarna S, et al. Longitudinal

Follow-up of Bronchial Inflammation, Respiratory Symptoms, and Pulmonary Function in

Adolescents after Repair of Esophageal Atresia with Tracheoesophageal Fistula. J Pediatr.

2008 Sep;153(3):396–401.e1.

81. Chetcuti P, Myers NA, Phelan PD, Beasley SW, Dickens DR. Chest wall deformity in

patients with repaired esophageal atresia. Journal of pediatric surgery. 1989;24(3):244-7.

82. Westfelt JN, Nordwall A. Thoracotomy and scoliosis. Spine. 1991 Sep;16(9):1124-5.

PubMed PMID: 1948403. Epub 1991/09/01. eng.

83. Banjar HH, Al-Nassar SI. Gastroesophageal reflux following repair of esophageal atresia

and tracheoesophageal fistula. Saudi Med J. 2005 May;26(5):781–5.

84. Seo J, Kim DY, Kim AR, Kim DY, Kim SC, Kim IK, et al. An 18-year experience of

tracheoesophageal fistula and esophageal atresia. Korean J Pediatr. 2010 Jun;53(6):705–10.

85. Chetcuti P, Phelan PD. Respiratory morbidity after repair of oesophageal atresia and

tracheo-oesophageal fistula. Arch Dis Child. 1993 Feb;68(2):167–70.

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86. Dudley NE, Phelan PD. Respiratory complications in long-term survivors of oesophageal

atresia. Arch Dis Child. 1976 Apr;51(4):279–82.

87. Konkin DE, O‟Hali WA, Webber EM, Blair GK. Outcomes in esophageal atresia and

tracheoesophageal fistula. J Pediatr Surg. 2003 Dec;38(12):1726–9.

88. Little DC, Rescorla FJ, Grosfeld JL, West KW, Scherer LR, Engum SA. Long-term

analysis of children with esophageal atresia and tracheoesophageal fistula. J Pediatr Surg.

2003 Jun;38(6):852–6.

89. Porcaro F, Valfré L, Aufiero LR, Dall‟Oglio L, De Angelis P, Villani A, et al. Respiratory

problems in children with esophageal atresia and tracheoesophageal fistula. Ital J Pediatr

[Internet]. 2017 Sep 5 [cited 2017 Sep 9];43. Available from:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5584000/

90. Sistonen SJ, Pakarinen MP, Rintala RJ. Long-term results of esophageal atresia: Helsinki

experience and review of literature. Pediatr Surg Int. 2011 Sep 30;27(11):1141.

91. Robertson JR, Birck HG. Laryngeal problems following infant esophageal surgery. The

Laryngoscope. 1976 Jul 1;86(7):965–70.

92. Orringer MB, Kirsh MM, Sloan H. Long-term esophageal function following repair of

esophageal atresia. Ann Surg. 1977 Oct;186(4):436–43.

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ANNEXURES

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Annexure: 1

Serial Number:

Proforma for Respiratory morbidity in children with

Esophageal atresia/Tracheo Esophageal fistulae who

underwent primary repair in a Tertiary care centre in South

India

1. Demographic Details:

a. Name: b. Hospital number:

c. Date of birth: d. Age:

e. Sex: f. Religion:

g. Address: h. Phone number: I

II

2. Antenatal period:

Variables Yes No Comments

Poly-hydramnios

Fever with rash

Abnormal USG

Any other

complications

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3. Perinatal period:

Variables Comments

Gestational Age

Birth weight

Mode of delivery

APGAR

Meconium stained liquor

4. Presenting complaints before surgery:

Variables Yes No Comments/Time

in hrs after birth

Drooling

Choking of feeds

Cyanosis

Vomiting

Respiratory distress

Antenatal diagnosis

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5. Diagnosis made by:

Variables Yes No Comments/Time

in hrs after birth

Not able to pass

NGT and coiling in

CXR

Barium study

Other modalities

6. Pre Operative:

Variables Yes/No Duration Comments/Time

in hrs after birth

Admitted in NICU

Ventilated

Oxygen

Continuous suction

LRI

Cardiac disease

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7. OA/TEF defect:

Type I/II/III/IV/V

Gap

Other association

8. Intra operative complication/ Other findings:

Variables Yes No Comments

Cardiac arrest

Hemorrhage

Pneumothorax

Ends not

approximated

Hypotension

requiring

Inotrophes

9. Post operative period:

Variables Yes/No Duration Comments

Leakage

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Prolonged

ventilation (>7

days)

Ventilated

complication

Failed surgery

Redo surgery

Radiological

abnormalities:

Collapse

Pneumothorax

Positive Blood C/S

VAP

Time of start of

feeds

Feed Intolerance

Full feeds on

10. Environmental and family History:

a. Smoker in the house: Yes/No

b. Type of house: Pucca/SemiPucca/ Kutcha

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c. Mode of cooking: Gas/Wood

d. Overcrowding: Yes/No

e. Any pets in home: Yes/No

If yes, what pet:

f. Family history of asthma/Lung problem/Similar problems:

11. First year Post Operative:

Variables

Yes/No

Frequency and

duration

Comments

Cough

Breathing difficulty

Wheeze

Stridor

Dysphagia

Regurgitation

Heart burn

Food bolus

impaction

Doctor Diagnosed

LRI

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Hospital Admission

Height percentile

Weight percentile

12. Subsequent year Post Operative:

Variables Yes/No Frequency and

duration

Comments

Cough

Breathing difficulty

Wheeze

Stridor

Dysphagia

Regurgitation

Heart burn

Food bolus

impaction

Doctor Diagnosed

LRI

Hospital Admission

Height percentile

Weight percentile

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Grade of PEM (1-5

yrs)

13. Immunization history:

14. Current symptoms and medications:

15. Personal history:

a. History of allergy:

b. Missed school: Y/N

1. If yes, how many days per year:

16. Investigation done:

Investigation

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

CXR

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Barium

swallow

HRCT

Others

17. Current medication:

Since when

Stopped when

Currently

Anti-Reflux

MDI

Cardiac failure

Others

18. Surgery:

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Procedure

Date

Date

Date

Date

Date

date

Fundoplication

Gastrostomy

Foreign body

Dilatation

Cardiac

Others

19. Examinations:

a. General Examination:

Variables Yes No Comments

Pallor

Cyanosis

Clubbing

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Any dysmorphic

features:

Facial

Skeletal

Chest

deformity

Rib

Abnormality

Shoulder

function

b. Vital signs:

Variables

Heart rate

Resp. rate

Saturation

c. Anthropometry:

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Variables Comments

Height with percentile

Weight with percentile

MUAC (<5 yrs of age)

PEM grade(1-5 Years)

d. Ear, Nose and Throat:

Larynx:

Upper airway:

Palate:

e. Systemic examination:

Resp. system:

Chest deformity:

Breath sounds:

Crepitations/wheeze:

Other adventitious sounds

Others:

Cardiovascular system:

Abdomen:

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Central nervous system:

20. Current Investigation:

a. Chest X-Ray:

b. HRCT:

Bronchiectasis:

Interstitial:

Infection:

Others:

c. Barium swallow:

Swallowing:

Co-ordination:

Reflux:

d. Laryngeal anatomy:

21. Others:

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22. Investigation done:

Investigation

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

Date

with

finding

CXR

Barium swallow

HRCT

Others

23. Current medication:

Since when

Stopped when

Currently

Anti-

Reflux

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MDI

Cardiac

failure

Others

24. Surgery:

Date

Date

Date

Date

Date

date

Fundoplication

Gastrostomy

Foreign body

Dilatation

Cardiac

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Annexure: 2

INFORMED CONSENT

Department of Child health

Christian Medical College, Vellore

Respiratory morbidity in children with Esophageal atresia/Tracheo Esophageal fistulae

who underwent primary repair in a Tertiary care centre in South India

Information sheet

Introduction:

Esophageal atresia/Tracheo Esophageal fistula, a communication between food

pipe and breathing pipe is the most common abnormality of the food pipe a baby can

have at birth. It affects less than 2 babies out of 10,000 babies born. Surgery for this

problem is usually done soon after birth as in your child‟s case. It has been observed that

after the surgery though the main defect is corrected, many children continue to get

breathing/lung symptoms and sometimes problems with feeding and swallowing. If these

problems are not detected, it can progress and can cause permanent damage. World over

a lot of attention is paid to the follow up of children operated with EA/TEF. However in

India many children do not come back to the doctor regularly for check up after the

surgery and lung damage is recognized very late.

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122

Hence we are planning this study to understand what is the current lung status

of the children who we have operated in our institution and take corrective actions if

needed.

What is the benefit from the study?

Your child will get a thorough clinical examination for the problem mentioned

above. Tests like Chest X Ray, Barium swallow will be done. CT Scan may be advised if

needed. This will help us identify and take steps to prevent further damage.

In addition results obtained from this study will give us valuable information about

the respiratory health of the affected children which in turn will help in planning better

care in the future.

If you take part what will you have to do?

If you agree to participate in this, you will need to give consent for us to obtain details of

your child‟s condition. You will be enquired about the past and present medical history of your

child. All the children recruited in our study will undergo chest x ray and upper respiratory

evaluation. If needed CT- Thorax and barium swallow will be advised for your child.

Can you withdraw from this study after it starts?

You are free to withdraw from the study at any time .Your child‟s treatment in this

hospital will not be in any way affected by that decision.

What will happen if child develops any study related injury?

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123

Child is not expected to develop any adverse reaction due to the study. All

investigations planned are routinely used in the hospital for management of such patients.

CT scan and barium swallow involves exposure to radiation. Only children who need the

test based on clinical assessment will be subjected to it and the benefit far outweighs the

risk.

What happens after the study is over?

Results of the study will be analyzed and the information will be made available

for future management of children with TEF/OA. If your child is detected to have lung or

swallowing defect, appropriate treatment will be advised.

Will your personal details be kept confidential?

The results of this study will be published in a medical journal but your child will

not be identified by name in any publication or presentation of results. However, your

child‟s medical notes may be reviewed by people associated with the study, without your

additional permission.

For details please contact:

Dr. P. Madhan Kumar (Post graduate registrar)

Child health office – 3

Christian medical college

Vellore -632004

Phone number – 9600441010

E- Mail: [email protected]

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124

CONSENT FORM FOR THE STUDY

CONSENT TO TAKE PART IN A CLINICAL TRIAL: Respiratory morbidity in children

With Esophageal atresia/Tracheo Esophageal fistulae who underwent primary repair in a

Tertiary care centre in South India.

Study Title: Respiratory morbidity in children with Esophageal atresia/Tracheo esophageal

fistulae who underwent primary repair in a Tertiary care centre in South India.

Serial Number:

Participant’s name: Date of Birth / Age (in months):

I_____________________________________________________________

___________, Mother/Father of ___________________________________

Declare that I have read the information sheet provided to me regarding this study and

have clarified any doubts that I had. I also understand that my participation in this study

is entirely voluntary and that I am free to withdraw permission to continue to participate

at any time without affecting my usual treatment or my legal rights.

I understand that I will not receive any other financial compensation

I understand that my identity will not be revealed in any information released to third

parties

I voluntarily agree to take part in this study.

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125

Name:

Relation to child:

Date:

Thumb Impression/Signature

Name of witness:

Relation to participant:

Date:

Thumb Impression/Signature

Name: Dr. P. Madhan Kumar

Principal investigator

Signature:

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126

INFORMED ASSENT

Department of Child health

Christian Medical College, Vellore

Respiratory morbidity in children with Esophageal atresia/Tracheo Esophageal fistulae

who underwent primary repair in a Tertiary care centre in South India

Information sheet

Introduction:

Esophageal atresia/Tracheo Esophageal fistula, a communication between food

pipe and breathing pipe is the most common abnormality of the food pipe a baby can

have at birth. It affects less than 2 babies out of 10,000 babies born. Surgery for this

problem is usually done soon after birth as in your case. It has been observed that after

the surgery though the main defect is corrected, many children continue to get

breathing/lung symptoms and sometimes problems with feeding and swallowing. If these

problems are not detected, it can progress and can cause permanent damage.

World over a lot of attention is paid to the follow up of children operated with

OA/TEF. However in India many children do not come back to the doctor regularly for

check up after the surgery and lung damage is recognized very late.

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127

Hence we are planning this study to understand what the current lung is status

of the children who we have operated in our institution and take corrective actions if

needed.

What is the benefit from the study?

You will get a thorough clinical examination for the problem mentioned above.

Tests like Chest X Ray, Barium swallow will be done. CT Scan may be advised if

needed. This will help us identify and take steps to prevent further damage.

In addition results obtained from this study will give us valuable information about

the respiratory health of the affected children which in turn will help in planning better

care in the future.

If you take part what will you have to do?

If you agree to participate in this, you will need to give assent for us to obtain

details of you and consent will be obtained from your parents. You and your parents will be

enquired about the past and present medical history. All the children recruited in our study will

undergo chest x ray and upper respiratory evaluation. If needed CT- Thorax and barium swallow

will be advised.

Can you withdraw from this study after it starts?

You are free to withdraw from the study at any time .Your treatment in this

hospital will not be in any way affected by that decision.

What will happen if child develops any study related injury?

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128

You are not expected to develop any adverse reaction due to the study. All

investigations planned are routinely used in the hospital for management of such patients.

CT scan and barium swallow involves exposure to radiation. Only children who need the

test based on clinical assessment will be subjected to it and the benefit far outweighs the

risk.

What happens after the study is over?

Results of the study will be analyzed and the information will be made available

for future management of children with TEF/OA. If you are detected to have lung or

swallowing defect, appropriate treatment will be advised.

Will your personal details be kept confidential?

The results of this study will be published in a medical journal but you will not be

identified by name in any publication or presentation of results. However, your medical

notes may be reviewed by people associated with the study, without your additional

permission.

For details please contact:

Dr. P. Madhan Kumar (Post graduate registrar)

Child health office – 3

Christian medical college

Vellore -632004

Phone number – 9600441010

E- Mail: [email protected]

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129

ASSENT FORM FOR THE STUDY

ASSENT TO TAKE PART IN A CLINICAL TRIAL:

Respiratory morbidity in children with Esophageal atresia/Tracheo Esophageal

fistulae who underwent primary repair in a Tertiary care centre in South India

Study Title: Respiratory morbidity in children with Esophageal atresia/Tracheo Esophageal

fistulae who underwent primary repair in a Tertiary care centre in South India

Study Number:

Participant’s name:

Date of Birth / Age (in years):

I_____________________________________________________________

___________, S/o or D/o ___________________________________

Declare that I have read the information sheet provided to me regarding this study and

have clarified any doubts that I had. I also understand that my participation in this study

is entirely voluntary and that I am free to withdraw permission to continue to participate

at any time without affecting my usual treatment or my legal rights.

I understand that I will not receive any other financial compensation

I understand that my identity will not be revealed in any information released to third

parties I voluntarily agree to take part in this study.

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130

Name:

Signature:

Date:

Thumb Impression

Name of witness:

Relation to participant:

Date:

Thumb Impression

Name: Dr. P. Madhan Kumar

Principal investigator

Signature:

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131

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Rthrf; Foha;f;Fk; ,ilapy; FWfpa ,izg;G cs;sJk;jhd; czT Fohapd; kpf nghJthdjhf fhzg;gLfpwJ. ,J gj;jhapuj;jpy; 2 Foe;ijfSf;F gpwg;gpNyNa ,Uf;Fk;. cq;fs; Foe;ijf;F ele;j mWit rpfpr;ir Nghd;W ,JNghd;W FohAld; gpwf;Fk; Foe;ijfSf;F mWit rpfpr;ir Nkw;nfhs;s Ntz;Lk;. ,g;NghJs;s Ma;twpf;iffs; $WtJ vd;dntd;why; mWit rpfpr;irf;F gpd; gy Foe;ijfs; EiuaPuy; kw;Wk; ,e;j gpur;rpidfshy; ghjpf;f gLfpwhh;fs; vd;W njhpate;Js;sJ. mij gw;wpa tpopg;Gzh;T kf;fsplk; ,y;iy.

cyfk; KOtJk; ,g;nghOJ mWit rpfpr;irf;F gpd;

,f;Foe;ijfs; tiu gpd;gw;wgLfpwhh;fs;. Mdhy; ekJ ehl;by; mWit rpfpr;irf;Fgpd; ,f;Foe;ijfs; rhptu tiu gpd;gw;w tUtjpy;iy.

,jdhy; ehq;fs; jq;fspd; Foe;ijapd; EiuaPuy;; NehAs;s

jd;ikapd; msit ghpNrhjpf;Fk; Ma;twpf;if ,J.

1) jq;fspd; Foe;ij milaf;$ba gyd; vd;d?

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,e;j Ma;tpypUe;J ve;j NeuKk; jhq;fs; tpyfpf;nfhs;syhk;

,e;epiyapy; cq;fs; Foe;ijapd; tptuq;fs; ePf;fg;gLk;. jhq;fs; ,e;j Ma;tpy; gq;Nfw;fhtpl;lhYk; ,jdhy; tof;fkhd rpfpr;ir ngWjy; ve;j tifapYk; ghjpf;fg;glhJ.

2) ,e;j Ma;twpf;ifapy; gq;F ngw ePq;fs; vd;d nra;aNtz;Lk;?

,e;j Ma;twpf;ifapy; gq;F ngw tpUk;gpdhy; cq;fs; Foe;ijia

gw;wpa tptuq;fis vq;fSf;F ju rk;kjpf;fNtz;Lk;. cq;fs; Foe;ijAila fle;j kw;Wk; epfo;fhy kUj;Jt tptuq;fs; Nfl;fg;gLk;. ,e;j Ma;tpy; gq;F ngWk; midj;J Foe;ijfSk; khh;G vf;];Nu kw;Wk; Rthrk; gw;wpa tptuq;fs; Nfl;L mwpag;gLk;. Njitg;gl;lhy; cq;fs;

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Foe;ijf;F rpb njhuhf;]; kw;Wk; Nghpak; ];thNyh vf;];Nu vLf;fg;gLk;.

3) ,e;j Ma;tpy; gq;Nfw;w gpd;G tpLglKbAkh?

,e;j Ma;tpy; cq;fs; gq;F Kw;wpYk; jd;dpr;irahdJ. ePq;fs; tpUg;gg;gl;lhy; ,jpypUe;J vg;NghJ Ntz;LkhdhYk; tpyfpf;nfhs;syhk;. ,jdhy; ,e;j kUj;Jtkidapy; cq;fs; tof;fkhd rpfpr;ir ve;jtpjj;jpYk; ghjpf;fhJ.

4) ,e;j Ma;tpy; gq;Nfw;gjhy; vd;Dila Foe;ijf;F gpur;rpid Vw;gLkh?

,e;j Ma;tpy; gq;Nfw;gjhy; cq;fSila Foe;ijf;F gpur;rpid

Vw;glhJ. kUj;Jtkidapy; nra;ag;gLk; tof;fkhd ghpNrhjidfSld; Nkw;nfhs;sg;gLtjhy;; ve;jtpj gpur;rpidAk; Vw;gl tha;g;gpy;iy. rpb ];Nfd; kw;Wk; Nghpak; ];thNyh fjphpaf;fj;jhy; Nkw;nfhs;sg;gLk; ghpNrhjidfs;.ntF rpy Foe;ijfSf;F kl;LNk ,e;j ghpNrhjidfSf;F cl;gLj;jg;gLth;.

5) ,e;j Ma;T Kbe;jgpd; vd;dhFk;?

Ma;T KbTfs; ghprPypf;fg;gl;L Foe;ijfspd; gpw;fhy rpfpr;irf;fhf

fye;jhuhag;gl;L jfty;fs; mspf;fg;gLk;. cq;fs; Foe;ijf;F EiuaPuy; gpur;id ,Ug;gJ fz;lwpag;gl;lhy; jFe;j rpfpr;ir ngw mwpTj;jg;gLk;.

6) cq;fSila jfty;fs; ghJfhf;fg;gLkh?

,e;j Ma;tpd; KbT kUj;Jt ehNsl;by; gpuRupf;fg;gLk; Mdhy;

cq;fs; Foe;ijapd; ngaiuf; nfhz;L Foe;ijia gw;wp KbTfis ,e;j Ma;tpy; fz;lwpa KbahJ. MapDk; cq;fs; Foe;ijapd; kUj;Jt gjpNtLfs; Ma;T FOtpy; cs;sth;fs; kl;LNk cq;fSila $Ljy; mDkjpAld; ghh;f;fg;gLk;.

சந்தேகம் இருக்கும் நிலையில் தேொடர்பு தகொள்ள தவண்டிய

முகவரி: டொக்டர். மேன் குமொர் முேன்லம ஆய்வொளர் குழந்லே நை பிரிவு - 3

கிருத்துவ மருத்துவ கல்லூரி தவலூர் - 632004 தேொலைதபசி எண்: 9600441010

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fpwpj;Jt kUj;Jt fy;Y}hp> NtY}h;

Foe;ijeyg;gphpT

gq;F ngWgthpd; xg;Gjy; gbtk;

Ma;tpd; jiyg;G: czT Fohapy; Jthuk; ,y;yhky; gpwe;j

Foe;ijfSila mWit rpfpr;irf;F gpd; mth;fspd; EiuaPuypd;

NehAs;s jd;ikapd; msit Fwpj;j Ma;T.

Ma;T vz;: gq;F ngWgthpd; je;ij: gq;F ngWgthpd; ngah;: gpwe;j Njjp/taJ (khjq;fspy;):

- ehd; ,e;j Ma;it gw;wpa jfty;fis Fwpj;J KOikahf thrpj;J

vd;Dila vy;yh re;Njfq;fisAk; njspTgLj;jpf; nfhz;Nld;.

- ,e;j Ma;tpy; vd;Dila gq;Nfw;G jd;dpr;irahdJ vd;Wk; ve;j

Neuj;jpYk; ,jpypUe;J tpyfpf; nfhs;syhk; vd;gijAk;> ,jdhy;

tof;fkhd rpfpr;ir ngWjypd; rl;lG+h;tkhd chpik ve;j tifapYk;

ghjpf;fg;glhJ vd;gijAk; Ghpe;Jnfhz;Nld;.

,e;j Ma;T FOtpid rhh;e;j gzpahsh;fNsh kw;Wk; kUj;Jt FO

cWg;gpdh;fNsh jw;Nghija Ma;tpw;Fk; ,J njhlh;ghd ,d;Dk; gpw

Ma;tpw;fhf vd;Dila kUj;Jt gbtq;fis ghh;itapl vd;Dila

mDkjp ngw Njitapy;iy vd;gij Ghpe;Jnfhz;Nld;. ,jw;F ehd;

rk;kjpf;fpNwd;. vd;id gw;wpa tptuq;fis ntsp egh;fsplk; njhptpg;gNjh

my;yJ ntspaplNth khl;lhh;fs; vd;gij Ghpe;J nfhz;Nld;.

- ,e;j Ma;tpd; Kbtpy; fpilf;Fk; jftiy kUj;Jt Ma;tpw;fhf kl;Lk;

gad;gLj;Jtij jil nra;akhl;Nld;;> mjw;F rk;kjpf;fpNwd;.

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- ,e;j Ma;tpy; vd;Dila Foe;ij gq;F nfhs;s ehd; KOkdNjhL

rk;kjpf;fpNwd;.

gq;Nfw;gthpd; ghJfhtyh;/ngw;Nwhhpd; ifnahg;gk;:

ghJfhtyh;/ngw;Nwhhpd; iftpuy; Nuif gjpT:

Njjp:

rhl;rpapd; ifnahg;gk; / iftpuy; Nuif gjpT: rhl;rpapd; cwTKiw :

Njjp:

ifnahg;gk;

lhf;lh;. kjd; Fkhh;

Kjd;ik Ma;thsh;.

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slno outcome ifdied age sex religion polyhydra feverrash abusg ultrapoly antenoth ga gaperiod bw delimode apgar drooling choking cyanosis vomiting respirat antenat precare poorfeed abdomdist vertebal ngtcxr barium admitnicu surgeryday ventilated oxygen suction lri cardiac

1 1 74 1 1 2 2 2 2 Nil 40 1 2200 3 1 2 2 2 2 1 2 1 2 2 2 1 2 1 2 2 1 2 2 1

2 1 98 2 1 2 2 2 2 HBsAg 40 1 3600 1 1 1 1 1 1 1 2 2 2 2 2 1 2 1 2 1 1 1 1 1

3 1 75 2 1 2 2 2 2 Nil 40 1 3155 1 1 1 1 2 1 1 2 2 2 2 2 1 1 1 6 2 1 2 1 2

4 1 67 1 1 2 2 2 2 Nil 39 1 3000 3 1 1 1 2 2 1 2 2 1 2 2 1 2 1 2 2 1 2 1 2

5 1 65 2 1 2 2 2 2 PPROM 32 4 1500 1 1 1 2 2 2 1 2 1 2 2 2 1 2 1 2 2 1 2 2 1

6 1 43 1 1 2 1 2 2 Nil 40 1 2200 1 1 1 2 2 1 1 2 2 2 2 1 1 2 1 3 2 1 1 2 2

7 1 81 1 1 2 2 2 2 PIH 40 1 2580 1 2 2 2 2 2 1 2 2 2 2 2 1 2 1 2 1 1 2 2 1

8 1 53 1 1 1 2 1 1 Nil 38 1 2600 3 1 1 2 1 2 1 1 2 2 2 2 1 2 1 2 2 1 2 1 1

9 1 103 1 1 1 1 1 1 Nil 37 1 2440 3 1 1 2 2 2 1 2 2 2 2 2 1 2 1 1 2 1 2 1 1

10 1 91 1 1 1 2 1 1 PIH. IUGR. PPROM. Cord prolapse 32 4 1290 3 1 1 2 2 2 1 1 1 2 2 2 1 2 1 3 2 1 1 2 1

11 1 89 1 1 2 2 2 2 Nil 40 1 2300 2 1 1 2 2 2 1 2 1 2 2 2 1 2 1 2 2 1 1 2 1

12 1 76 1 1 1 2 1 1 Nil 40 1 1830 3 2 1 1 1 2 1 2 1 2 2 2 1 2 1 2 2 1 2 2 1

13 1 50 2 1 2 2 2 2 Nil 40 1 2900 1 1 2 2 2 2 1 2 2 2 1 2 1 2 1 2 2 1 1 2 1

14 1 81 2 1 2 2 2 2 Spontaneous preterm 33 3 1560 1 1 2 2 2 2 1 2 1 2 2 2 1 2 1 2 2 1 1 1 1

15 1 24 2 1 2 2 2 2 Nil 40 1 2690 1 1 1 2 1 2 1 2 2 2 2 2 1 2 1 2 2 1 1 2 2

16 1 90 2 1 1 2 2 2 Nil 40 1 2900 1 1 1 2 2 2 1 2 2 2 2 2 1 1 1 3 2 1 1 2 1

17 1 70 2 1 2 2 2 2 PIH 39 1 2600 3 1 1 2 2 2 2 2 2 2 2 2 1 2 1 3 2 1 1 2 1

18 1 13 1 1 1 2 1 1 Nil 37 1 2960 3 1 1 2 2 1 2 2 2 2 2 1 1 2 1 2 2 2 1 2 1

19 1 68 2 1 1 2 1 1 PIH. Anemia 41 1 2500 3 1 1 2 2 2 2 2 2 2 2 2 1 2 1 2 2 1 1 2 1

20 1 55 1 1 2 2 2 2 Nil 40 1 2610 1 1 1 2 2 1 1 2 2 2 2 2 1 2 1 3 2 1 2 1 2

21 1 85 2 1 2 2 1 2 PIH 31 4 1220 3 1 1 2 2 2 1 2 1 2 2 2 1 2 1 3 1 1 1 1 1

22 1 30 2 1 2 2 2 2 Nil 37 1 2300 3 1 1 2 2 2 1 2 2 2 2 2 1 2 1 3 2 1 1 2 2

23 1 61 2 1 2 2 2 2 Fever 33 3 2040 3 1 2 2 2 2 2 2 1 2 2 2 1 2 1 2 2 1 2 2 2

24 1 37 2 1 1 2 2 2 PIH 36 2 1300 3 1 1 2 2 2 1 2 2 2 2 2 1 2 1 1 2 1 1 2 1

25 1 30 1 1 2 2 2 2 Maternal UTI 40 1 2680 2 1 1 2 2 1 1 2 2 2 2 2 1 2 1 1 2 1 1 2 1

26 1 40 2 3 1 2 1 1 PIH. Abruption 39 1 2180 3 1 1 2 2 2 1 2 2 2 2 2 1 2 1 2 2 1 1 2 2

27 1 54 2 3 1 2 1 1 Diabetes 38 1 2600 1 1 1 2 2 1 1 2 2 1 2 2 1 2 1 1 2 1 1 1 2

28 1 84 1 1 2 2 2 2 Nil 38 1 3000 1 1 1 2 1 2 1 2 2 2 2 2 1 2 1 3 2 1 1 1 1

29 1 77 2 1 2 2 2 2 Nil 38 1 2700 3 1 2 2 2 2 1 2 2 1 1 2 1 2 1 3 2 1 2 1 2

30 1 77 2 1 1 2 1 1 Nil 36 2 1860 1 2 2 2 2 2 2 2 1 2 2 2 1 2 1 1 2 1 2 2 2

31 1 58 1 1 1 2 1 1 Nil 39 1 2500 1 1 1 1 2 1 1 2 2 2 2 2 1 2 1 2 2 1 2 1 2

32 1 92 1 1 2 2 2 2 Nil 40 1 2800 2 1 1 2 2 1 1 2 2 2 2 2 1 2 1 3 2 1 2 1 1

33 1 90 1 1 2 2 2 2 Nil 40 1 2700 3 1 1 2 2 2 2 2 2 2 1 2 1 2 1 2 2 1 1 2 1

34 1 53 1 1 2 2 2 2 PIH 40 1 2495 1 1 1 2 2 1 1 2 2 2 2 2 1 2 1 2 2 1 2 2 1

35 3 2 1 1 2 1 1 Abnormal end diastolic 37 1 1960 3 2 1 1 2 2 1 2 1 2 2 2 1 1 1 3 2 1 1 2 1

36 3 1 1 1 2 1 1 Nil 40 1 1800 1 1 1 1 2 2 1 2 2 2 2 2 1 2 1 3 2 2 2 2 1

37 3 2 1 1 2 1 1 Nil 40 1 2750 3 1 1 2 2 1 1 2 2 2 2 2 1 2 1 2 2 1 1 2 1

38 2 2 1 1 1 2 1 1 PIH 36 2 1620 1 1 2 2 2 2 2 2 1 2 2 2 1 2 1 3 2 1 1 2 1

39 2 2 1 1 2 2 2 2 Nil 40 1 2200 3 1 1 2 1 2 1 2 2 1 2 2 1 2 1 3 2 1 1 1 2

40 2 2 2 1 1 2 1 1 Single umblica artery 40 1 2460 1 1 1 2 2 2 1 2 2 2 2 2 1 2 1 1 2 1 1 2 1

41 2 2 2 1 1 2 1 1 Nil 35 2 2060 1 2 2 2 2 2 2 1 1 2 2 2 1 2 1 3 2 1 1 2 1

42 2 2 1 1 1 2 1 1 PIH.PPROM 35 2 1680 2 1 1 2 2 2 1 1 1 2 2 2 1 2 1 4 1 1 2 1 1

43 2 2 2 1 2 2 2 2 Nil 34 3 1750 2 1 1 2 2 2 1 2 1 2 2 2 1 2 1 2 1 1 1 2 1

44 2 2 1 1 1 2 1 1 Nil 35 2 1785 1 1 1 2 1 2 1 2 1 2 2 2 1 2 1 2 1 1 2 2 1

45 2 2 1 3 2 2 2 2 APH 37 1 2500 3 1 1 1 1 1 1 2 2 2 2 2 1 2 1 9 1 1 1 1 1

46 2 1 1 1 2 2 2 2 Nil 40 1 2900 1 1 1 1 2 1 1 2 2 2 1 2 1 2 1 3 1 1 2 2 1

47 2 1 2 1 1 2 1 1 PIH 35 2 1540 3 1 2 2 2 2 2 1 1 2 2 2 1 2 1 2 2 1 1 1 1

48 2 1 2 1 2 2 2 2 Nil 40 1 1800 3 1 1 2 2 1 1 2 1 2 2 2 1 2 1 3 2 1 1 1 1

49 2 1 2 1 1 2 1 1 PROM 36 2 2090 2 1 1 2 1 2 1 1 2 2 2 2 1 2 1 2 1 1 1 2 1

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pda asd vsd tga aortic cardioth gastric umblical imperanus vertebral renal vacterl type gap umblical1 imperanus1 laryng vertebral1 renal1 cloacal vacterl1 surgertype feedgastro colostomy cardiarres hemorrhage pneumoth leakage prolong venticomp surgerfail redosurger gastrosto collapse lriconso pneumotho pleural suspected posblood vao ionotrop chyloth

2 2 2 2 1 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2

1 2 2 2 1 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 1 2 2 1 2 2 2 2

2 1 1 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 2 2 1 2 1 3 1 2 2 2 1 2 2 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2

1 1 2 2 2 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2

2 1 2 2 2 2 2 1 1 1 2 1 3 1 1 1 2 1 2 2 1 1 2 1 2 2 2 1 2 1 2 2 2 2 2 2 2 2 2 2 1 2

1 1 2 2 1 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 1 2 2 2 1 2 2 2 2 2 2 1 2

1 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 1 2 2 2 1 1 2 2 2 2 2 2 2

1 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

1 1 2 2 2 2 2 2 1 1 2 1 2 1 2 1 1 1 2 1 1 1 1 1 2 2 2 2 2 2 2 2 1 2 2 2 2 2 1 2 1 2

1 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 1

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2

1 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 1 2 2 2 1 1 1 1 1 2 1 1 1 1 2 2 1 1 1 2

1 1 2 2 2 2 2 2 1 1 1 1 3 2 1 1 2 1 1 1 1 1 2 1 2 2 2 2 1 2 2 2 1 1 2 2 2 2 2 2 1 2

1 2 2 2 2 2 2 2 1 1 2 1 3 1 2 1 2 1 2 1 1 1 1 1 2 2 2 1 1 1 2 2 1 2 2 2 2 2 1 1 1 2

1 2 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 1 2 2 1 2 2 2 2

2 2 2 2 1 2 3 1 2 2 2 2 1 2 2 1 2 2 2 2 2 1 2 2 2 2 2 2 1 2 2 1 2 2 1 2

1 1 2 2 2 2 1 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 1 2 2 2 1 1 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 1 2 2 1 1 1 2 2 2 2 1 1 1 2 1 1 1 1

1 2 2 2 2 2 2 1 2 1 1 1 3 1 1 2 2 1 1 2 1 1 2 2 2 2 2 1 1 1 2 2 2 2 1 1 2 2 1 1 1 2

1 1 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 2 2 1 2 2 2 1 2 2 2 1 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2

2 1 1 2 2 1 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 1 2 2 2 2 2 1 2 2 2 1 2 1 2

1 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 1 2

2 2 2 2 2 2 1 2 2 2 1 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2

2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

1 1 2 2 2 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2

2 2 2 2 1 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 1 2 2 2 1 2 2 2 1 2 2 2 2 1 2 2 2 1 2 1 2

2 1 1 2 1 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

1 2 1 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 1 1 1 2 2 2 1 1 1 2 2 1 1 1 2

1 1 2 2 2 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 1 1 1 2 1 1 1 1 2 1 2 2 1 2

1 2 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 1 2 2 2 2 1 1 1 2 2 1 2 1 1 2 2 1 1 1 2

2 2 2 2 1 2 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 1 2 2 2 2 2 1 1 1 1 1 1 1 1 2 2 2 1 1 1 2

2 2 2 2 2 2 3 1 2 2 1 2 2 2 2 1 2 2 2 2 2 1 1 1 1 1 2 1 1 1 2 2 1 1 1 2

1 2 2 2 1 2 2 1 2 2 2 2 3 1 1 2 2 2 2 2 2 1 2 2 2 1 2 1 1 1 2 2 2 1 1 2 2 2 1 1 1 2

2 2 2 1 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1

2 1 2 2 2 1 2 1 2 2 2 2 3 2 1 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 1 2 2 1 1 2 2 2 1 2 2 2

1 2 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 1 2 2 1 1 2 2 2 1 1 2 2 1 2 1 1 2

1 1 2 2 2 2 2 1 2 1 1 1 3 1 1 2 2 1 1 2 1 1 2 2 2 2 2 1 2 1 2 2 2 2 1 2 2 2 1 1 1 2

2 1 2 2 2 1 2 2 2 2 2 2 3 2 2 2 2 2 2 2 2 2 1 2 1 1 2

1 1 2 2 2 2 1 2 2 2 2 2 3 2 2 2 2 2 2 2 2 2 1 2 2 2 2 1 1 1 2 2 1 1 1 2 2 2 1 1 1 2

1 1 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 1 1 1 2 2 2 2 2 2 2

1 2 2 2 2 2 2 2 2 2 2 2 3 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 1 1 2 2 2 1 1 2 2 2 2 2 1 2

1 1 1 2 2 1 2 1 2 2 2 2 3 2 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 1 2 1 1 1 1 2 2 2 2 2 1

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feedstart feedintol feedfull bilateral pusculture hiatus smoker housetype cookmode overcrowd pets asthma lung similar cough breath breathyes wheeze wheezeyes stridor dyspag vomit heartburn foodbolus doctorlri lriyes hosadmit hosadyes lriwheeze wheezeasth mdi gerd antireflux fundogerd feedgastr1 esopbody esopdilat cardfail antifail cardsurger

5 2 10 2 2 2 1 2 2 2 0 2 2 2 1 1 6 1 10 2 2 2 2 2 1 6 1 6 1 1 2 1 1 2 2 2 2 2 2 2

6 2 12 2 1 2 2 2 1 2 1 2 2 2 1 1 10 1 10 1 1 1 2 1 1 12 1 12 1 2 2 2 2 2 2 1 1 2 2 2

4 2 10 2 2 2 2 2 1 2 0 2 2 2 1 1 5 1 5 1 1 1 2 1 1 3 2 1 1 1 1 1 2 2 1 1 2 2 2

2 2 2 1 1 1 2 4 1 1 2 1 1 6 1 12 2 2 1 2 2 1 2 2 1 2 2 2 2 2 2 2 2 2 2 2

6 1 21 2 2 2 1 2 1 2 1 2 2 2 1 1 5 1 8 2 2 2 2 2 1 3 1 3 1 1 1 2 2 2 2 2 2 1 1 1

5 2 10 2 2 2 2 1 1 2 0 2 2 2 2 2 2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 1 1 2 2 2

4 2 9 2 2 2 2 1 1 2 1 2 2 2 1 1 6 1 10 1 1 2 2 1 1 5 1 5 1 1 1 1 1 2 2 1 1 2 2 2

7 1 22 2 2 2 2 1 1 2 0 2 2 2 1 1 6 1 8 2 1 1 2 1 1 1 1 1 2 2 2 1 1 1 1 1 1 2 2 2

9 2 17 2 2 2 1 3 2 1 0 2 2 2 1 1 8 1 8 1 1 1 2 2 1 3 1 1 1 1 1 1 1 1 1 2 2 2 2 2

5 1 31 2 2 2 2 1 1 2 0 2 2 2 1 1 2 1 2 2 2 1 2 2 1 3 1 2 1 2 2 2 2 2 2 2 2 2 2 2

9 2 13 2 2 2 2 2 2 1 4 1 2 2 1 1 8 1 10 2 2 1 2 2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2

5 2 13 2 2 2 1 1 1 2 1 1 1 2 1 1 1 2 2 1 1 2 2 1 2 2 1 2 2 2 2 2 2 2 2 1 1 1

4 2 8 2 2 2 2 2 2 1 1 2 2 2 1 1 8 1 6 1 1 2 2 1 1 5 2 1 1 1 1 1 1 1 1 1 1 1 2

15 2 18 2 2 2 2 3 1 2 0 2 2 2 1 1 2 2 2 1 1 2 2 1 4 1 1 1 2 2 2 2 2 2 1 1 2 2 2

3 2 10 2 2 2 2 1 1 2 0 2 2 2 2 2 2 1 2 2 2 2 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2

10 1 42 2 2 2 2 2 2 1 4 2 2 2 1 1 6 1 6 1 2 2 2 2 1 2 2 1 1 2 2 2 2 2 2 2 2 2 2

10 1 18 2 2 2 1 2 2 2 0 2 2 2 1 1 6 1 8 2 1 1 2 2 1 3 1 1 1 1 2 1 1 1 2 1 1 2 2 2

24 1 40 2 1 2 2 1 1 2 0 2 2 2 2 2 1 1 1 2 2 2 2 1 1 2 2 2 2 1 1 2 2 2 2 1 1 1

5 2 11 2 2 2 2 1 1 2 0 2 2 2 1 1 6 1 8 1 1 2 2 1 1 1 2 2 2 2 1 1 2 2 2 2 2 2 2

14 1 24 2 1 2 1 2 2 2 0 2 2 2 1 1 4 1 6 2 1 1 2 2 1 2 1 1 1 1 2 2 2 2 2 1 1 2 2 2

7 2 17 2 2 1 2 1 1 2 0 2 2 2 1 1 4 1 8 2 2 1 2 1 1 5 1 1 1 1 1 2 2 2 2 2 2 2 2 2

5 2 10 2 2 2 2 1 1 2 0 2 2 2 1 1 2 1 2 1 1 1 2 2 1 2 1 1 1 1 1 1 1 1 2 2 2 2 2 2

14 1 25 2 2 2 2 1 1 1 0 2 2 2 1 1 8 1 10 1 2 1 2 2 1 2 1 2 1 1 1 1 1 1 2 2 2 2 2 2

34 1 89 2 1 2 2 1 1 2 0 1 2 2 1 1 8 1 10 2 2 1 2 1 1 3 1 1 1 1 2 1 1 1 2 2 2 1 1 1

4 2 10 2 2 2 2 1 1 2 0 2 2 2 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 2 2 2 1 1 1

6 2 9 2 2 2 1 2 1 2 0 2 2 2 1 1 1 1 1 1 2 2 2 2 1 3 1 1 1 2 2 2 2 2 2 2 2 2 2 2

6 2 11 2 2 2 1 1 2 1 2 2 1 1 2 2 1 4 1 1 1 1 2 1 1 1 1 2 2 2 2 2

5 2 9 2 2 2 1 1 2 2 2 1 2 1 1 2 1 2 1 1 2 2 2 2 1 2 2 1 1 1

2 2 2

14 2 16 2 2 2

3 2 7 2 2 2

4 2 11 2 2 2

3 2 10 1 2 2 1 1 2 2 1 1 2 1 1 3 1 2 1 2 2 2 2 2 2 1 1 2 2 2

6 2 11 2 2 2 1 1 1 1 1 1 1 1 2 1 1 2 1 1 1 2 2 1 1 2 2 1 1 1 1 1

2 2 2 2

2 2 2

2 1 2

2 1 2

2 1 2

2 2 2

2 2 2

2 2 2

5 1 8 2 2 2

2 2 2 1 2 2 2 0 2 2 2 1 1 2 1 2 1 2 2 2 2 1 6 2 1 1 1 2 2 2 1 2 2 2 2 2

4 2 8 2 2 2

5 2 10 2 2 2 1 2 2 2 0 2 2 2 1 1 1 2 2 1 1 2 1 1 5 1 5 1 1 1 1 1 1 1 1 1 2 2 2

7 2 10 2 2 2 2 1 1 2 1 2 2 2 1 1 2 1 2 2 2 2 2 2 1 3 1 3 1 1 1 1 1 2 1 2 2 1 1 2

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cough1 breath1 breathyes1 wheeze1 wheezeyes1 stridor1 dyspag1 vomit1 heartburn1 foodbolus1 doctorlri1 lriyes1 hosadmit1 hosadyes1 lriwheeze1 wheezeast1 mdi1 gerd1 antireflu1 fundogerd1 feedgastr2 esopbody1 esopdilat1 cardfail1 antifail1 cardsurge1 immunicomp currsymp antireflu2 mdisalbut antifail2 othsurger gerd2 laryngo esopstri esopdysm hisaller misschool gastros pallor

1 1 10 1 12 2 2 2 2 2 1 10 1 5 1 1 2 2 2 2 2 2 2 2 2 2 2 LRI 2 2 2 2 2 2 2 2 2 1 2 1

1 1 10 1 8 1 1 1 1 1 1 10 1 3 1 1 2 2 2 2 2 1 1 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 1

1 1 1 2 1 1 1 1 1 2 2 2 2 2 1 1 2 2 1 1 2 2 2 2 Nil 2 2 2 2 2 2 2 2 2 2 2 1

1 1 6 1 10 2 1 1 1 2 1 6 1 1 1 1 1 1 1 1 2 2 2 2 2 2 1 RAD on MDI 1 1 2 2 1 2 2 2 1 2 2 1

1 1 6 1 6 2 2 2 2 2 1 4 1 2 1 1 1 2 2 2 2 2 2 1 1 1 1 Nil 2 2 2 2 2 2 2 2 2 2 2 1

2 2 1 2 2 1 2 2 1 2 2 2 2 2 2 2 2 2 1 1 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 1

1 1 4 1 4 1 1 2 2 1 1 2 2 1 1 1 1 1 2 2 2 2 2 2 2 1 MDI and Lanzole 1 1 2 2 2 2 2 2 2 2 2 1

1 1 2 1 10 2 1 1 2 1 1 2 1 1 1 1 1 1 1 1 1 1 1 2 2 2 1 Recurrent Wheeze on MDI 2 1 2 1 1 2 2 2 2 2 2 1

1 1 4 1 6 1 1 2 2 1 1 14 1 2 1 1 1 1 1 1 1 1 1 2 2 2 2 Whistling sound. Dysphonic speech. Recurrent cough. 2 2 2 1 1 1 2 2 1 1 2 1

1 1 1 2 2 2 2 2 2 1 2 2 1 2 2 2 2 2 2 2 2 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 2

1 1 5 1 5 2 1 1 2 2 1 3 1 1 1 1 2 2 2 2 2 2 2 2 2 2 1 Recurrent LRI. Dysphagia 2 2 2 2 2 2 2 2 2 1 2 1

1 1 2 2 1 1 2 2 1 3 2 1 2 2 2 2 2 2 2 2 1 1 1 1 Dysphagia. Cough. Vomiting 2 2 2 2 2 2 2 2 2 2 2 1

1 1 10 1 10 1 2 2 2 2 1 3 1 1 1 1 1 1 1 1 1 1 1 1 1 2 1 LRI. Wheeze 1 1 1 1 1 2 2 2 2 2 2 1

1 1 2 2 2 1 1 2 1 1 4 2 1 2 2 2 2 2 2 1 1 2 2 2 2 Nil 2 2 2 2 2 2 1 2 2 2 2 1

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 1

1 2 2 2 2 2 2 2 1 3 2 1 1 2 2 2 2 2 2 2 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 2

1 1 6 1 10 1 1 1 1 1 1 1 1 1 1 1 2 1 1 1 2 1 1 2 2 2 1 Nil 2 2 2 1 2 2 2 2 2 2 2 1

2 2 2 1 1 2 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 1 1 Nil 1 2 2 1 1 2 2 2 1 2 2 1

1 1 2 2 1 1 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 Continous cough. 2 2 2 2 1 2 2 2 2 1 2 1

1 1 2 1 4 2 1 2 2 1 1 1 2 1 1 2 2 2 2 2 1 1 2 2 2 1 Cough. Not on any medication 2 2 2 2 2 2 2 2 2 2 2 1

1 1 6 1 8 2 1 1 1 2 1 6 1 1 1 1 1 2 2 2 2 2 2 2 2 2 1 Nil 2 2 2 2 2 2 2 2 2 2 2 1

1 1 4 1 6 1 2 1 2 2 1 4 1 1 1 1 1 1 1 1 2 2 2 2 2 2 1 MDI. Asthalin PRN 2 1 2 2 2 2 2 2 2 2 2 1

1 1 6 1 10 1 1 2 2 2 1 7 1 4 1 1 1 1 1 1 2 1 1 2 2 2 1 Cough. Developmental delay. LRI 1 1 2 2 1 2 2 2 2 2 2 1

1 1 3 1 4 2 2 2 2 2 1 4 1 1 1 1 2 1 1 1 2 2 2 1 1 1 1 LRI. Regurgitation. 1 2 2 1 1 2 2 2 2 1 2 1

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 1 1 1 Nil 2 2 2 2 2 2 2 2 2 2

1 1 1 1 2 2 2 2 1 1 2 1 2 2 2 2 2 2 2 2 2 2 2 2 Nil 2 2 2 2 2 2 2 2 2 2

1 1 1 2 2 2 2 2 2 1 2 2 1 1 1 1 1 1 1 1 2 2 2 2

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cyanosis1 clubbing facial facialyes skelet skeletyes chest chest1 rib ribyes shoulder shouldyes heartrate resprate saturation htpercent wtpercent chestdefor chestyes breatsound breathabn crepit creptiyes wheeze2 wheezeyes2 advensound othsound cardiovas abdomen cns cnsabn scaring volumeloss hypoplas broncial bronchus narrowing widening divert bronectis bronalwal scaring1 consald collapse1 hyperinfl dilated narrowing1 widening1 divert1 othanomal

2 1 1 Small mandible. Large ears 1 Scoliosis 1 Asymetry 2 2 114 24 99 50 75 1 Asymetry 2 1 1 2 1 1 1 2 1 2 2 1 2 2 1 1 1 2 2 2 2 2 1 2

2 2 2 2 1 Asymetry 2 2 81 20 100 50 97 1 Asymetry 1 1 2 2 1 1 1 2 2 2 2 2 2 2 1 1 2 2 2 2 2 2 2 2

2 2 2 1 Scoliosis. Torticolis 1 Asymetry. Precardial buldge 2 1 Dysfunction 80 20 100 5 10 1 Asymetry. Precardial buldge 1 2 2 2 1 1 1 2 1 2 2 1 2 2 1 1 2 1 2 2 2 2 2 2

2 1 2 2 1 Asymetry 2 2 117 20 98 97 97 1 Asymetry 1 2 2 2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2

2 1 2 1 Scoliosis 1 Asymetry, Shrugging of shoulder 1 1 90 24 100 10 75 1 Scoliosis, Asymetry, Harison sulcus 1 2 2 2 1 1 2 Scoliosis 2 2 2 1 2

2 2 2 1 Scoliosis. Butterfly verterbrae 1 Asymetry 2 2 134 22 100 5 75 1 Scoliosis 1 2 2 2 1 1 1 1 2 2 2 2 1 2 1 2 2 1 2 2 2 1 2 2 Double SVC

2 1 2 2 1 Asymetry 2 2 84 24 94 50 75 1 Asymetry 2 No airentry on left side 1 2 2 1 1 1 2 1 2 2 2 2 2 1 2 2 2 2 1 2 2 2 2

2 1 2 2 1 Asymetry 1 1 84 24 100 75 97 1 Asymetry 2 1 1 1 1 2 1 2 1 2 2 2

2 2 1 Prognathia. large nose and ear. Open mouth. Dysphonic speech 1 1 2 2 101 30 100 50 50 1 Asymetry. Scoliosis 2 Bronchial. Decreased on right side 1 1 2 1 1 1 1 1 2 1 1 2 2 1 1 1 1 2 1 2 1 2 1

2 2 1 Hypertelorism 2 1 Asymetry 2 2 90 20 100 5 75 1 Asymetry 1 1 2 2 1 1 1 2 1 2 2 2 2 2 1 2 2 2 2 2 2 1 2 2

2 2 2 1 Scoliosis. Asymetry. Harison sulcus 1 Left side scoliosis 2 2 90 24 100 75 75 1 Asymetry. Scoliosis. 1 1 2 2 1 1 1 2 2 2 1 2 2 2 2 2 2 2 2 2 2 1 2 2

2 2 2 1 Lumbar lordosis. Scoliosis 1 Asymetry 2 2 108 20 100 25 75 1 Asymetry 1 1 2 2 1 1 1 2 2 2 1 2 2 2 1 1 2 2 2 2 2 1 2 2 ASD closure

2 2 2 2 2 2 2 90 26 88 5 5 2 1 2 2 2 1 1 1 2 2 2 1 2 1 2 2 2 1 2 2 2 2 1 2 2 Hiatus hernia

2 2 2 2 2 2 2 77 20 100 97 50 2 1 2 2 2 1 1 1 2 2 2 1 2 2 2 1 2 1 2 2 2 2 2 2 2

2 2 2 2 2 2 2 126 28 100 10 50 2 1 2 2 2 1 1 1 2 2 2 2 2

2 2 2 1 Asymetry of the chest. Left side hallowing. Sub clavicular hallowing 1 1 1 Decreased 98 20 97 50 75 1 Asymetry. Sub clavicular hallowing 1 1 2 2 1 1 1 2 1 2 1 2 2 2 1 2 1 1 2 2 2 1 2 2 2

2 1 2 1 Asymetry. Scoliosis. Right hallowing 1 Asymetry. Scoliosis. Right hallowing 2 2 124 20 100 10 25 1 Asymetry. Scoliosis. Right hallowing 1 1 1 2 1 1 1 2 2 2 1 2 2 2 1 1 2 2 2 2 2 2 2 2 Verterbral segmentation anomalous

2 2 2 2 1 Pectus carnitum 2 2 96 30 94 50 75 1 Pectus carnitum 2 1 1 1 1 1 1 2 2 2 1 2

2 2 2 2 2 2 2 113 20 100 10 97 2 1 1 2 2 1 1 1 2 2 2 2 2 2 2 1 2 2 2 2 2 2 1 2 2

2 1 2 2 2 2 2 107 18 100 50 75 1 Asymetry 1 2 2 2 1 1 1 1 1 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2

2 2 2 2 2 2 2 124 24 100 50 75 2 1 2 2 2 1 1 1 2 2 2 1 2 2 2 1 1 2 2 2 2 2 2 2 2

2 2 2 2 2 2 2 132 30 100 10 50 2 1 1 1 2 1 1 1 2 2 2 2 2 2 2 1 1 2 1 2 2 2 2 2 2

2 2 1 Synorphs. Upslanting 1 Scoliosis 1 Assymetry 2 2 100 22 94 25 97 1 Asymetry 1 1 1 2 1 1 2 Developmental delay 2 2 2 2 2

2 1 1 Dolicocephaly 1 Scoliosis 1 Asymetry 2 2 98 30 98 5 10 1 Asymetry 2 1 1 2 1 1 1 2 2 2 2 2 2 2 2 2 2 1 2 2 1 1 2 2 Thin rib on left side. Post op

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prebarium prereflux prerefluxy prestrict prediverti barium1 swallow coordi reflux refluxyes strict diverti laryngmal vocalmob vocalpalsy vocalnodul refluxlary adenoid

2 1 2 1 2 1 1 1 2 2 2 2 1 2 2 2 2

2 2 1 2 2 1 1 1 2 2 2 2 1 2 2 2 2

2 1 2 1 2 2 1 1 1 2 1 2 2 1 2 1 2 2

2 2 1 2 2 2 2 2 1 2 2 1 2 1 1 2

2 2 2 1 2 2 1 1 1 2 1 2 1 2 2 2 1

1 2 2 2 2 1 1 2 1 2 1 1 2 1 2 2

2 1 2 1 2 2 1 1 2 2 2 2 1 2 2 2 2

2 1 2 1 2 2 1 1 1 2 1 2 2 1 2 2 2 1

2 1 2 1 2 2 1 2 1 1 1 2 2 2 1 2 1 1

1 2 2 2 2 2 1 2 2 2 2 1 2 2 1 1

1 2 2 2 2 1 1 1 1 2 2 2 1 2 1 2 1

2 2 1 2 2 2 2 2 1 1 2 1 2 2 2 2

2 1 1 1 2 2 1 1 2 1 1 2 1 2 1 1 1

2 2 1 2 2 2 1 2 1 2 2 1 2 1 2 1

2 1 1 2 2 2 1 1 1 2 2 2 2 1 2 2 1 2

1 2 2 2 1 2 2 2 2 2 2 2 1 2 2 2

2 1 1 1 2 2 1 1 1 2 1 2 2 1 2 2 2 2

2 1 2 1 2 2 2 1 1 2 1 2

2 1 1 2 2 1 1 1 2 2 2 2 1 2 1 2 2

2 1 1 2 2 1 1 1 2 2 2 2 1 2 1 2 2

1 2 2 2 1 1 1 2 2 2 2 1 2 2 2 2

2 1 2 2 2 1 1 1 2 2 2 2 1 2 1 1 2

2 1 2 1 2 2 1 1 1 2 2 2

2 1 2 2 2 2 1 1 1 2 2 2 2 2 1 2 1 2