This document discusses esophageal atresia, a birth defect where the esophagus fails to develop properly, resulting in an abnormal connection or closure. It defines the condition, describes its epidemiology and embryology, classifications, associated anomalies, pathophysiology, diagnosis, and treatment. Esophageal atresia occurs in about 1 in 3000-4500 births and is diagnosed prenatally by ultrasound or after birth based on symptoms like choking during feeding. Treatment involves surgical repair of the esophagus.

1. Kingdom of Saudi Arabia
Ministry of Higher Education
King Faisal University
College of Medicine
By Fahad H. Al Hulaibi
208004222

2.  Definition.
 Epidemiology.
 Embryology of esophagus & Trachea.
 Types & classifications.
 Associated anomalies.
 Pathophysiology.
 Diagnosis & Treatment.

3. is a disorder of the digestive system in which
the esophagus does not develop properly.

4.  Atrasia:
Congenital absence or closure of a normal
body opening.
Normal Atrasia

5.  Fisula:
Is a permanent abnormal passageway between
two organs in the body or between an organ
and the exterior of the body.
Normal Fistual

6. 1 case in 3000-4500 births.
 thehighest incidence of this disorder is in
Finland, where it is 1 case in 2500 births.

7.  2% risk of recurrence is present when a
sibling is affected.
 Increase in advanced maternal age.

9.  Atweek 4 , the
Tracheabroncheal
diverticulum developed to
Tracheabroncheal sputum.
There is a failure to
separation in the sputum
leading to fistula.
 During week 8, the primitive
gut failure to recanalization.
That lead to atrasia.

11.  Type A - Esophageal atresia without fistula or so-
called pure esophageal atresia (10%)
 Type B - Esophageal atresia with proximal TEF (<
1%)
 Type C - Esophageal atresia with distal TEF (85%)
 Type D - Esophageal atresia with proximal and
distal TEFs (< 1%)
 Type E - TEF without esophageal atresia or so-
called H-type fistula (4%)
 Type F - Congenital esophageal stenosis (< 1%)
(This is not discussed in this article)

12.  Currently,most authorities believe that the
development of esophageal atresia has a
nongenetic basis.
 Ina 1987 Kluth eschews has the concept that
esophageal vascular events, ischemic
events, or both may be causes in cases of
esophageal atresia without fistula.
 In 2003, Spilde et al reported esophageal
atresia-TEF formations Adriamycin induced
teratogenesis.

13. (VACTERL)
 Vertebral defects.
 Anorectal malformations.
 Cardiovascular defects.
 TrachoEsophageal deffect.
 Renal anomalies.
 Limb deformities.
25% of all patients with esophageal atresia

14. CHARGE
 Coloboma.
 Heart defects.
 Atresia choanae.
 Developmental retardation.
 Genital hypoplasia.
 Ear deformities .

15.  Neurologic defects -Neural tube
defects, hydrocephalus, tethered
cord, holoprosencephaly
 GI defects -Duodenal atresia, ileal
atresia, hypertrophic pyloric
stenosis, omphalocele, malrotation, Meckel
diverticulum
 Pulmonary defects - Unilateral pulmonary
agenesis, diaphragmatic hernia
 Genitalia defects - Undescended
testicles, ambiguous genitalia, hypospadias

17. A fetus with EA cannot effectively
swallow amniotic fluid.
A fetus with esophageal atresia and a
distal TEF, amniotic fluid presumably
flows through the trachea and down
the fistula to the gut 
Polyhydramnios  premature labor

18.  The neonate with EA cannot swallow and
there is copious amounts of saliva.
 Aspiration of saliva or milk, if the baby is
allowed to suckle, can lead to an aspiration
pneumonitis.

19.  In a baby with esophageal
atresia and a distal TEF, the
lungs may be exposed to
gastric secretions.
 Also, air from the trachea can
pass down the distal fistula
when the baby
cries, strains, or receives
ventilation. This condition can
lead to an acute gastric
perforation, which is often
lethal.

20.  Prenatal:
1. polyhydramnios

21. 2. Prenatal
Ultrasonography
sensitivity 40%
Abscenc of stomach
bubbles, with fliud
filled loops of bowels

22.  Post-natal:
1. White, frothy bubbles of mucus in the
mouth and, sometimes, the nose.
2. Episodes of coughing, choking and cyanosis.
3. These episodes may be exaggerated during
feeding.

23.  Laboratory Studies:
CBC count
Electrolyte levels
Venous gas concentrations
BUN and serum creatinine levels
Blood glucose level
Serum calcium level
ABG concentrations, as necessary

24.  Genetic testing:
chromosome analysis
microarray genomic hybridization (array GH)

25. Chest radiography
NG tube arrested
Air in stomach
AP view
Lateral view

26. CT scan

27. Renal UltraSonography
is used to evaluate associated kidney
anomalies, ureteral anomalies, or both.

28. Echocardiography.
who have clinical signs of cardiovascular disease.

29. Limb radiography
if the limbs appear abnormal.

30.  Preoperative management:
1. The oral pharynx should be cleared.
2. The infant's head should be elevated.
3. IV fluids (10% dextrose in water).
4. Oxygen therapy is used.
5. In infants with respiratory failure,
endotracheal intubation should be
performed.
6. broad-spectrum antibiotics(such as
ampicillin plus gentamicin)

31.  Surgical
techniques vary according to
surgeons' preferences and variations in
pathologic anatomy.
 Thebest esophagus is the patient's
esophagus.

32.  Infantsborn with esophageal atresia without
fistula  early gastrostomy

33. Kimura, Livaditis, Scharli, or Foker procedures

34.  Infantsborn with esophageal atresia with
fistula  early gastrostomy

36.  Roberta A Pagon, Editor-in-chief, Thomas D Bird, Cynthia R Dolan, Karen
Stephens, and Margaret P Adam, GeneReviews™, Seattle (WA): University
of Washington, Seattle; 1993.
 Amulya K Saxena, Esophageal Atresia With or Without Tracheoesophageal
Fistula, Medscape. eMedicine, Updated: Apr 25, 2012, link:
(http://emedicine.medscape.com/article/935858-overview#showall )
 DWAYNE C. CLARK, Esophageal Atresia and Tracheoesophageal Fistula,
1999 Feb 15;59(4):910-916.
 Kronemer KA, Snyder-Warwick A. Esophageal
atresia/tracheoesophageal fistula. 2008. Available online
at eMedicine. Accessed 4-1-11.