ATRESIA

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 DEFINITION
• Congenital obstruction
• Caused by complete occlusion of the intestinal
lumen

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DUODENAL ATRESIA

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 HISTORY
• Calder of Glasgow-1773
• First successfully treated case Vidal from
France in 1905 ( gastrojejunostomy)

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 EMBRYOLOGY
• Second month of intra uterine life,exuberant
growth of epithelial lining
• Vacuolization of the solid core of cells
• Lumen is recanalised by the end of 8th to 10th
week
• Failure of coalescent vacoulization
-obstruction

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 EMBRYLOGY
• Associated with other malformations specially
Down’s Syndrome, incomplete rotation of gut,
congenital heart disease, anorectal
malformations
• Error occurs most commonly at the site of
Papilla of Vater

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 PATHOLOGY
• Frequently associated with annular pancreas
• Anomalies of intestinal rotation & fixation also
noted
• Persistence of a primitive vitelline vein may
result in anterior portal vein which may lead
to intrinsic compression of the 2nd part of
duodenum
• May be partial or complete

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 ANNULAR PANCREAS
• Most common form of external compression
• Thin flat segments of pancreatic tissue either
partially or completely surround the
duodenum
• In some cases it is found as an incidental
finding

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ANNULAR PANCREAS

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Treatment
• Duodeno-duodenostomy—ideal
• Duodeno-jejunostomy
• Do not resect the ring
• G-J not done

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 ATRESIA
3 types of atresia:-
• Type 1 : Intact diaphragm or membrane
formed of mucosa & submucosa.[A]
1.Muscularis intact
2.Wind sock anomaly[E]
• Type 2 :Blind ends of duodenum are
connected by a short fibrous cord along the
edge of intact mesentry[B]
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 ATRESIA
• Type 3 :No fibrous cords between the blind
ends
1.Separated by a distance
2.Mesentry absent
3.Annular pancreas may be associated[F]
4.V shaped defect[C]

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Various types of anomalies of duodenal
atresia

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 INCIDENCE
• Limited to the first & second parts of
duodenum
• 85% of the cases of duodenal obstruction are
distal to the ampulla
• 1 in 10,000 live births

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 SYMPTOMS & SIGNS
• Vomiting -- bile stained
• Continuous vomiting may lead to blood
stained vomitus
• Fullness in the epigastrium
• Abdominal distension

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 SYMPTOMS & SIGNS
• Diagnosis is not always made during neonatal
period.
• Some cases are not even diagnosed until adult
life
• Depending on degree of obstruction, it may
mimic a feeding problem

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 DIAGNOSIS
• Plain abdominal supine radiograph
• Large air distended stomach with a fluid level
• Markedly distended first part of duodenum
with a fluid level
• No evidence of air in remaining gut
• Double- bubble sign
• Contrast barium swallow

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Abdomen in supine position showing gastric
& proximal duodenal distention

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DOUBLE BUBBLE SIGN

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 DIAGNOSIS
• Ultrasonography – annular pancreas
• Whirlpool sign
• Upper gastro intestinal contrast study
• Fibre optic upper G.I. endoscopy in older
children

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USG showing Double bubble sign

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 DIFFERENTIAL DIAGNOSIS
• Annular pancreas
• Wilkie’s syndrome (Superior mesentric artery
syndrome)

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 MANAGEMENT
• Pre operatively
• Correction of anomaly not a surgical
emergency
• Volvulus to be excluded
• Orogastric tube is passed into the stomach &
catheter taped in place
• Stomach aspirated & wash given
• Vit K 1mg I.M.
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 MANAGEMENT
• Operation
• Transverse right upper quadrant supra
umbilical incision
• Duodenoduodenostomy (side to side)
• Diamond shaped duodenoduodenostomy
• Simple duodenal web or diaphragm excised &
to be opened from the lateral side
• Kimura’s anastomosis
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INTRA OPERATIVE FINDING

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 MANAGEMENT
• Post operative care
• Nil by mouth till stomach aspirate becomes
clear & volume less than 1 ml/kg/hour
• 5 – 12 days post operatively
• Parental nutrition
• Oral feeding resumed with liquids - 2 to 5 ml is
given every 3 hourly
• Breast milk & formula feed resumed
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CONGENITAL HYPERTROPHIC
PYLORIC STENOSIS

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• Hypertrophy of musculature of pyloric antrum
• Especially circular muscle fibres
• Primary failure of pylorus to relax
• Duodenum is normal

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 CLINICAL FEATURES
• Common in first born males (4:1)
• Incidence is 4 in 1000 births
• Familial
• Seen between 3rd & 6th week of age
 Time taken by the hypertrophied muscle to
cause complete obstruction

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 CLINICAL FEATURES
• Vomiting—forcible, projectile, non bilious
• Visible gastric peristalsis (VGP)
• Palpable lump of hypertrophied pylorus,
better felt from left side
• Mobile, smooth, firm mass, with all borders
well made out, moves with respiration
• Impaired resonance on percussion

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VISIBLE GASTRIC PERISTALSIS

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 CLINICAL FEATURES
• Constipation
• Dehydration
• Loss of weight
• Electrolyte imbalance—hypokalemic
metabolic alkalosis

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 CLINICAL FEATURES
In premature infants
• VGP & mass is better seen & felt
• Vomiting is regurgitant
• Anorexia is common

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 DIAGNOSIS
• Clinical examination
• Ultrasound of abdomen
 Doughnut sign
 Pyloric muscle—4mm or more in thickness
 Length of pyloric canal >1.8 cm
• Barium meal shows obstruction

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DOUGHNUT SIGN

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 DIFFERENTIAL DIAGNOSIS
• Duodenal atresia (bilious vomiting)

• High intestinal obstruction

• Intracranial hemmorhage

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 TREATMENT
1. Correction of dehydration & electrolyte
imbalance
2. Surgery—Ramstedt’s operation
• Laparotomy
• Hypertrophied muscle cut along the whole
length until mucosa bulges out
• Pyloromyotomy

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RAMSTEDT’S OPERATION

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RAMSTEDT’S OPERATION

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RAMSTEDT’S OPERATION

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RAMSTEDT’S OPERATION

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 TREATMENT
3. Medical management
• Not advisable
• Atropine methyl nitrate orally
• To relax the pylorus muscle

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 COMPLICATIONS
• Postoperative pyrexia

• Gastroenteritis

• Electrolyte imbalance

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