Amol -Congenital anamolies of GIT

EMBRYOGENESIS OF GASTROINTESTINAL TRACT
As a result of cephalocaudal and lateral folding of
Embryo , endoderm lined yolk sac is incorporated into
The embryo to form primitive gut.
Primitive gut is blind ended however midgut is connected
To yolk sac by means of vitelline duct / yolk stalk.
Pharyngeal gut : buccopharngeal membrane to tracheo
Bronchial diverticulum.
Foregut : caudal to pharyngeal tube extends upto
Liver outgrowth.
Midgut :caudal to liver upto right 2/3rd to left 1/3rd of
Transverse colon.
Hindgut :left 1/3rd of transverse colon to cloacal
Membrane

Endoderm forms lining of git , perenchyma of glands ;
Liver and pancreas
Splanchnic mesoderm forms muscle , connective tissue
& peritoneal components.
Mesoderm dictates type of struture i.E. Lung in thorax
Via hox code.
Mesentry is double layers of peritoneum that enclose
An organ and connect it to body wall (intraperitoneal)
At 5 wks gut is suspended by dorsal mesentry which
Extends from lower esophagus to cloaca.
Ventral mesentry is derived from septum transversum

Imaging
Barium is contraindicated in the immediate postoperative period,
following
recent rectal biopsy, or any other circumstance in which an
intraperitoneal or mediastinal leak could occur.
It should also be avoided in patients at high risk of aspiration
In neonates ,it is advisable to use water soluble
contrast agents rather than barium for both upper and lower
gastrointestinal studies.

Low osmolar water-soluble contrast agents include
iohexol
(Omnipaque 240, 300) and iopamidol (Niopam 200,
300).
They have little adverse effect if extravasated into the
peritoneum or
mediastinum, or aspirated into the respiratory tract.

generally used undiluted or mildly diluted for a contrast meal
and diluted approximately
1 in 2 for an enema.
Earlier hyperosmolar water-soluble
agents such as meglumine/sodium (Gastrografin) and
iothalamate meglumine (Conray) were associated with
considerable fluid shifts,
drawing water into the bowel lumen with the risk of severe
dehydration
and haemodynamic compromise in infants.

If aspirated,they may result in severe pulmonary
oedema.
The only remaining indication for Gastrograffin, used in
dilution, is in the enema treatment
of meconium ileus, when hyperosmolarity is beneficial.
For a contrast meal examination, barium or water-
soluble contrast can be administered via a cup-and-
straw, feeding bottle, or cautiously syringed directly
into the mouth if necessary.

Contrast should be introduced just over the
base of the tongue so that the infant still will have to swallow.
Contrast should not be delivered with the patient in the supine
position.
The infant should be in the lateral or right anterior-oblique
position, because this guards against aspiration.

With contrast enema examinations in newborn and young
infants, the most important practical point is to have
adequate
occlusion of the anus.
A Foley catheter is preferred and should be inserted
before
taping of the buttocks.

When one is looking for low rectal
pathology, such as Hirschsprung's disease, it is best not to
blow up
the balloon.
In many
cases, extensive preparation of the colon is not required and,
in
Hirschsprung's disease, is contraindicated.

Omit the feeding before the examination.
Overnight fasting is not required and is detrimental.
In the neonate and young infant, fluid and electrolyte
balance is delicate, and it is most
important that these infants not be dehydrated for
prolonged
periods

FOREGUT
ESOPHAGUS
AT 4th WK RESPIRATORY DIVERTICULUM APPEARS AT VENTRAL
WALL OF FOREGUT.
ESOPHAGOTRACHEAL SEPTUM
RESPIRATORY PRIMORDIUM
(VENTRAL)
ESOPHAGUS
(DORSAL)
MUSCULAR COAT IS FORMAD BY SPLANCHNIC MESENCHYME
STRIATED IN UPPER 2/3rd (VAGUS)
SMOOTH IN LOWER 1/3rd (SPLANCHNIC PLEXUS)

In neonatal esophagus mucosal
folds are not as prominent as in
adults, but indentations by the
aortic arch, left main stem
bronchus, and normal left atrium
are frequently noted, even in the
neonate
Normal peristaltic activity usually
is evident at
birth but may not be as
pronounced as in later life.
Normal esophagus. Latera view
showing normal indentations
produced by aortic arch (A) and left
main bronchus (B).

In the recumbent position,
emptying of the esophagus
may be somewhat prolonged.
In the neonate, the esophagus
is flexible and can assume
peculiar configurations during
various phases of the
respiratory cycle.
The resulting bizarre, tortuous
configuration of the
esophagus at any level may at
first appear startling, but repeat
study
usually demonstrates a normal
esophagus
Tortuous esophagus. A. Bizarre,
tortuous-appearing esophagus in
young infant. B.
Moments later, the esophagus
appears normal.

Air in the Esophagus (Pneumoesophagus)
Many infants demonstrate small amounts of air in the
esophagus on
regular chest films, and the finding is entirely normal.
some infants demonstrate massive collections of air in the
esophagus, or so-called mega-aeroesophagus .
Such air collections are readily visible on
plain chest films and can be startling
In most of these cases, the underlying problem usually is
gastroesophageal reflux , but excessive air in the
esophagus also can be a sign of
the presence of a tracheoesophageal fistula.

Massive pneumoesophagus (i.e .. mega-aero esophagus). A. Note the marked
distention of the air-filled esophagus (arrows). This air is much more
voluminous than that seen
under normal circumstances. Most often, such massive distention of the
esophagus is the result of
gastroesophageal reflux. B. Premature infant. Supine position with air reflux
from the stomach
into the esophagus (arrows).

Transient Esophageal Hypotonia of the Neonate
In some newborn infants, the esophagus appears
almost totally
inactive, and even with prolonged examination,
little peristaltic activity is noted
These infants frequently have difficulty
with swallowing, and regurgitation is common.

This is why they are referred to the radiologist for
examination.
No obstructing lesions are found, and the
phenomenon is transient.
Within a week or less, normal peristaltic activity
prevails, feeding difficulties disappear, and the
infant has no further problems.
This lack of normal motility is
simply a reflection of normal, but transient,
neuromuscular immaturity.

Transient esophageal hypotonia
of the neonate. On these
four spot films, taken in rapid
sequence, note that there is no
suggestion of
peristaltic activity of the
esophagus. Anyone of the spot
films could be
interpreted as normal, but when
it is noted that on none is there
evidence of
peristalsis of the esophagus,
transient hypotonia should be
suspected.

Most Common Causes of GI Tract Obstruction by
Age
Age Cause of Obstruction
0â€“1 month Congenital anomalies
Atresia/stenosis
Malrotation/volvulus
Hirschsprung disease
Meconium plug/small left colon
syndrome
Meconium ileus
1â€“5 months Hernias
5 monthsâ€“3 Intussusception
years
3 years and older Perforated appendicitis
Adhesions
Regional enteritis

Causes of Esophageal Obstruction
Congenital atresia/stenosis
Web/diverticulum
Foreign body
Stricture (peptic, caustic)
Extrinsic compression (cysts, neoplasms,
vascular)
Achalasia

The trachea and oesophagus arise from the common
foregut.
Anomalies in the separation of these two structures by
the oesophagotracheal septum result in oesophageal
atresia, with or without an associated tracheo-
oesophageal fistula, with an incidence of 1 in 2-4000
live births.
Diagnosis may be suspected on antenatal ultrasound
if the
gastric bubble is small or not visualised, or if a
distended proximal
oesophageal pouch is seen.
ESOPHAGEAL ATRESIA & TRACHEOESOPHAGEAL FISTULA :

Polyhydramnios is commonly associ-ated.
Postnatally, infants present with drooling,
choking, coughing
and episodes of cyanosis on feeding.
When attempts to pass a naso-gastric tube
are made, resistance is met and a chest
radiograph will show
the tube coiled in a dilated air-filled proximal
oesophageal
pouch

Since air usually
is seen in the stomach within 1 5 minutes afrer birth, an airless
abdomen in the neonate should suggest the strong possibility
of esophageal atresia with no tracheoesophageal fistula.

ESOPHAGEAL ANOMALIES
ESOPHAGEAL ATRESIA & TRACHEOESOPHAGEAL FISTULA :
Atretic segment usually at the junction of proximal
& middle 1/3rd.
If TOF is present , found proximal to carina.
Mortality with esophageal atresia is due to congenital
Anomalies.
TYPES:
•O.A. With trachea and distal esophageal fistula (85%)
•O.A. Without fistula (10%)
•Isolated tracheoesophageal fistula,h-type (5%)
•O.A. With proximal fistula (rare)
•O.A. With proximal & distal fistula (rare)

ANTENATAL DIAGNOSIS
•Polyhydroamnios
•Absent fundic bubble
NEONATAL DIAGNOSIS
•Excessive salivation , coughing and choking
•Orogastric tube curls in proximal esophageal pouch
Plain radiography
•Air filled proximal esophageal pouch
•Gasless abdomen in isolated O.A. Or O.A. With proximal
fistula.
•Gas in abdomen means distal fistula
•Aspiration pneumonia
•Vertebral anomalies (vater)
Contrast study for proximal fistulas
1 ml OF LOCM TO BE USED IN LATERAL POSITION .
H - TYPE FISTULA DEMONSTATED IN PRONE POSITION

Figure 2: (a) Contrast swallow showing an oesophageal
atresia, overflow of contrast into the bronchial tree and a distal
tracheooesophageal fistula with contrast in the stomach
Figure 2: (b) Lateral chest X-ray demonstrating a contrast-fi
lled blind ending proximal oesophagus and trachea outlined by
aspirated contrast

Oesophageal atresia with tracheo-
oesophageal fistula. A coiled
tube is seen in the dilated proximal
oesophageal pouch (top
arrow). The presence of distal air-filled
bowel implies an associated
tracheooesophageal fistula. Thirteen
pairs of ribs are noted, compatible with
VATER
syndrome (lower arrow

H-type fistulas generally present later in infancy or childhood
with episodes of choking or apnoeas during feeding or recurrent
lower respiratory tract infections.
If suspected clinically, a 'tube
oesophagram' should be performed.
A nasogastric tube is passed and
water-soluble contrast instilled while the tube is slowly withdrawn the
oesophagus.
Most fistulas involve the proximal third of the
oesophagus and care should he taken to distend this segment well in
order to maximise visualisation of a fistula which passes anteriorly
and superiorly between the oesophagus and the trachea, in more of
an `N' than an `H' configuration

Contrast oesophagram demonstrating oblique track (arrows) of a
tracheo-oesophageal fistula with contrast filling the tracheobronchial tree.

It is important for the
surgeon to know whether the aortic arch is right or left sided to
facilitate surgical repair. This can be difficult to demonstrate in
neonates, and magnification, high-kilovoltage techniques, and
CTand MR examinations have been used to meet this end.
Ultrasonography also can identify the aortic arch and
determine
whether it is left or right sided, but the study is not always easy
to
accomplish.

Congenital esophageal stenosis is a far less common
cause of
congenital esophageal obstruction.
As in esophageal atresia,
esophageal stenosis arises from faulty tracheal and esophageal
separation, where tracheobronchial cartilage remnants remain in the
wall of the esophagus.
On barium swallow, small diverticula (mucous
glands) can be seen in the areas of stenosis
ESOPHAGEAL STENOSIS

Congenital esophageal stenosis without O.A. Is associated:
•Tracheobronchial remnants
•Intraluminal membranes
TRACHEOBRONCHIAL REMNANTS represent abnormal rests of
Respiratory tissue in esophageal wall.
Localized narrowing of distal esophagus with proximal
Dilatation.
Multiple small diverticulum like structures
(Tracheobronchial glands) perpendicular to esophagus
INTRALUMINAL MEMBRANE
Thin radioluscent defect that traverses esophageal
Lumen at rt. Angle.
Degree of obstruction depends upon size of aperture.

ESOPHAGEAL BRONCHUS
Abnormal origin of bronchus from esophagus
Cause:incomplete cleavage b/w trachea and esophagus
In utero.
Recurrent , persistent infection in the area supplied by
Abnormal esophagus

FOREGUT CYSTS
•BRONCHOGENIC
•GASTROENTERIC
•NEURENTERIC
CLASSIFIED AS :
BRONCHOGENIC CYSTS :
Cause :
Abnormal ventral branching of tracheobronchial tree
Lined by respiratory epithelium
Symptomatic due to compression of trachea or incidental
Plain radiography
Oval or round mediastinal mass in subcarinal or right
Paratracheal region.
Foregut cysts push the carina forward and esophagus
Backward; thyroidal masses and aberrant left pulmonary
Artery behave similarly

ON BARIUM EXTRINSIC COMPRESSION OF ESOPHAGUS BY MASS
CT : THIN WALLED WATER DENSITY MASSES OR
SOFT TISSUE MASSES (CONFUSED WITH TUMOUR)

GASTROENTERIC CYST
Known as esophageal duplication cyst
Cause : arise from diverticulum of primitive foregut or
Abnormal recanalization of gut.
Clinically silent or may cause dysphagia , pain
Imaging similar to bronchogenic cyst except
•Posterior mediastinum
•Thick wall
•On barium extrinsic or intramural compression
Variety of enteric cysts communicate with esophagus.
Tc 99m identifies enteric duplication cysts if they
contain gastric mucosa.

Extrinsic mass causes displacement of
esophagus towards the right and mass
effect on the esophagus.
Cyst behind the carina deviating the
esophagus to the right side.

NEURENTERIC CYST
Incomplete seperation of foregut from notochord
Cyst wall contains
gastrointestinal
Neural elements
Round or oval lobulated mass in posterior mediastinum b/w
Esophagus and spine.
Associated with congenital anomalies of spine i.e.
Hemivertebra, spina bifida.
MRI to delineate intraspinal anomalies.

VASCULAR ANOMALIES
•Double aortic arch
•Right aortic arch with aberrant left subclavian a.
•Aberrant left pulmonary artery
Clinical presentation
•Dysphagia
•Recurrent respiratory infection
•Dyspnea
Suspicion (aortic)
•Trachea deviated to left side
•Tracheal indentation on right or posteriorly
•Absent aortic arch on left
Barium swallow
•Posterior indentation of esophagus(lateral view)
•Unilateral/ bilateral indentation (frontal view)
Preoperative ct/ mri/ dsa for vascular anatomy

ABERRANT ORIGIN OF LEFT PULMONARY ARTERY
Known as pulmonary sling
Left pulmonary arise from right pulmonary artery
Diagnosis
Plain radiograph
Normal
Obstructive emphysema rt. Lung
Barium swallow
Indentation on anterior wall of esophagus at the level
Of carina

ABERRANT SUBCLAVIAN A. ABERRANT PULMONARY A.

STOMACH
FUSIFORM DILATION OF FOREGUT IN 4th
wk.
Longitudinal axis rotation
Rotates 90 degree clockwise
Left side face anteriorly(left vagus)
Right side face posteriorly(rt. Vagus)
Posterior wall grows faster (greater curvature)
Dorsal mesogastrium pulled towards rt. Side forming
Lesser peritoneal sac or omental bursa
Anteroposterior axis rotation
Pyloric part moves to right& upwards
Cardiac portion to left & downwards

CONGENITAL ANOMALIES
Situs solitus : stomach bubbble on left side
Situs invesus : stomach bubble on rt. Side
Situs ambigus :associated with polysplenia/ asplenia
Duplication of stomach
Bowel has additional loop or cystic component
Antrum esp. Along greater curvature
F>m
Infant with vomiting , fever , pain
Diagnosis :
Usg:echogenic bowel wall surrounded by hypoechoic
muscle with cyst full of echofree fluid
Tc99m: TUBULAR OR COMMUNICATING CYSTS

MICROGASTRIA & AGASTRIA
ABSENT STOMACH (AGASTRIA)
SMALL UNDERDEVELOPED STOMACH
(MICROGASTRIA)ASSOCIATED WITH:
•MALROTATION
•CHD
•AGANGLIONOSIS
•ASPLENIA

GASTRIC ATRESIA / WEB
•FAILURE OF LUMEN TO DEVELOP IN STOMACH
•PARTIAL / COMPLETE
•SECONDARY TO ISCHAEMIA
DIAGNOSIS
PLAIN RADIOGRAPHY:
COMPLETE: DISTENDED STOMACH WITH NO SMALL BOWEL GAS
BARIUM STUDY RARELY INDICATED
PARTIAL : BARIUM STUDY WITH TANGENTIAL PROJECTION

Gastric diaphragm. A, Note the thin membrane
(arrows) crossing the fluid-filled gastric antrum. B,
The same
diaphragm seen during a contrast upper GI series (arrows).

ECTOPIC PANCREAS
Small areas of ectopic pancreas may be found
anywhere in GIT
Gastric antrum with rudimentary duct(commonest)
Diagnosis
•Asymptomatic
•Smooth , sessile polyp- type mass projecting into
Gastric antrum below pylorus on greater curvature
•Duct system on barium study seen as central niche
Mimics ulcer
•USG : FOCAL ANTRAL THICKNING UPTO 5 mm(unreliable)

HYPERTROPHIC PYLORIC STENOSIS
•Pyloric muscle hypertrophy
•Unknown etiology
•First born male
•PRESENTS SOON AFTER BIRTH UPTO 10 wks
Clinical features:
•Projectile vomiting
•Palpable lump

Diagnosis:
Palpation of olive shaped tumour,rarely radiology
Required for diagnosis
Usg :
•Fill stomach with dextrose
•Failure of passage of gastric contents
•Marked gastric peristalsis
•Shouldering & beaking
•Single / double curved echogenic structures on
Long. Section(central mucosa)
•LENGTH >15mm ABNORMAL
•12 – 15 mm BORDERLINE

BARIUM MEAL
•USG CAN MISS 8 % OF CASES
•LONG, CURVING SINGLE OR DOUBLE PYLORIC CANAL
(STRING SIGN)
•SHOULDERING TO ANTRUM
•MUSHROOM SHAPED APPEARANCE OF DUODENUM
•DELAY UPTO 20min. CAN BE NORMAL
The classic appearance of pyloric stenosis on ultrasound is that of
(a)elongation of the pyloric canal;
(b) persistent spasm of the pyloric canal with little, if any, fluid
passing into the duodenum;
(c) persistent thickening of the circular muscle in the elongated
canal; and
(d) a sonolucent donut (thickened muscle) on cross section

The thickness at which
the muscle is considered hypertrophied is 3 mm or
greater.
Pyloric canal length of 1.5 cm is considered diagnostic
of pyloric stenosis when seen in conjunction
with thickened pyloric muscle.
In practice, however,normal canal length is much shorter than
this and is often impossible to measure.
Measurement of canal
length is more problematic than measurement of muscle
thickness and therefore a less reliable criterion.

Pylorospasm and Minimal Muscular Hypertrophy
In some vomiting infants, sonography shows a persistently
contracted and elongated canal, but the degree of
muscular thickening is less than the criterion of 3 mm for
surgically correctible HPS.
With extended observation, eventually the canal opens and
fluid is seen to pass
into the duodenum,but the periods of spasm predominate
In the vast majority of cases,
there is no thickening of the pyloric muscle or mucosa,
and the problem is primarily nonspecific pylorospasm
(antral dyskinesia)

This condition can accompany milk allergy or other forms
of gastritis.
In some cases the pyloric muscle is mildly thickened,
measuring 2 to 3 mm.
Such patients should be distinguished
from those with normal muscle thickness(<2 mm)
because some patients with minimal muscle
hypertrophy can eventually progress to classic pyloric
Stenosis
Many of these infants will
respond to medical therapy and require no surgery

Normal stomach. Normal antrum of
stomach (S), pyloric canal (P), and proximal
duodenum (D). Four
gastric wall layers are visible (from inside out):
echogenic mucosa,
hypoechoic muscularis mucosae, echogenic
submucosa,
Pyloric stenosis. AXR showing distended
gastric air bubble.
hypoechoic outer circular muscle.

Pyloric muscle tangential imaging artifacts. A, When imaging the antrum
in cross section, the muscle
will appear thickened if obtained through plane 1, but will show normal thickness if

HPS
A, Longitudinal scan shows markedly thickened, hypoechoic
gastric antral muscle (arrows). Elongated canal is
nearly 2 cm in length.
B, Transverse scan shows typical,
hypoechoic “doughnut” (arrows). Central echogenic
mucosa with anechoic fluid-filled crevices.

Pylorospasm. A, The pylorus remained
contracted early in the examination of this
infant, but the muscle is normal
in thickness (arrows). B, After slightly extended
period of viewing, the pylorus relaxed and
appeared normal (arrows)

Pyloric stenosis. Barium meal showing an
elongated pyloric canal
and shouldering of the antrum due to the
hypertrophied pyloric muscle.

Empty stomach artifact. A, Before fluid is administered, the antrum is
contracted and the pyloric muscle appears
thickened (arrows). B, When fluid distends the antrum, the true normal
thickness of the muscle is seen (arrows).

MIDGUT
5 wks embryo suspend by short dorsal mesentry
Rapid elongation of gut &mesentry form primary
Intestinal loop.
Cephalic limb:
•Distal part of duodenum
•Jejunum
•Part of ileum
Caudal limb :
•Lower portion of ileum
•Caecum , appendix
•Asc. COLON & PROX 2/3 rd OF TR. Colon

Malrotation and midgut volvulus is one of the major paediatric
surgical emergencies and the role of radiology in its diagnosis critical.
Delay in diagnosis can result in infarctive necrosis of the entire
small bowel and is potentially fatal.
At approximately week 6 of gestation the duodenojejunal
and ileocolic segments of the primitive gut herniate into
the extraembryonic coelom in the umbilical cord.
Both loops elongate
and rotate 270° anticlockwise around the axis of the superior
mesenteric artery.

By the end of the third month of gestation the
bowel loops are returned to their final positions in the abdominal
cavity, with their mesenteries becoming fixed to the parietal peritoneum
at several sites.
The duodenal loop is fixed with the duodenojejunal
junction (DJJ) in the left upper quadrant at the ligament
of Treitz and the ileocaecal junction fixed in the right lower quadrant.
The normal DJ flexure lies to the left of the
midline (at least over the vertebral pedicle) at the level of the
pylorus. In malrotation, it is displaced medialy, inferiorly or both
The normal small bowel mesentery therefore has a broad
diagonal base across the abdomen.

Physiological hernia :
During 6 th wk.
Rapid elongation of cephalic limb
Rapid growth of liver
Abdominal cavity is small so contents herniate
into extraembronic cavity
Rotation of midgut
Around SMA axis 270 degree counterclockwise
Rotation viewed from front
•Rotation during herniation (90 deg.)
•Return of intestinal loops(rem. Of 180 deg.)
•Caecum forms during herniation
Elongation of intestinal loops continue

Retraction of herniated loops
At 10 wks
•Regression of mesonephric kidney
•Reduced growth of liver
•Expansion of abdominal cavity
Proximal jejunum first part to enter (lies on left)
Caecal bud last part to enter back(below rt. Lobe of
Liver)
Appendix develops during descent of caecum,
Frequently retrocaecal/ retrocolic

MALROTATION
Any child with bilious vomiting considered to have
Malrotation unless proved otherwise
Malrotation is associated with malfixation so
GI study to locate DJ junction
Normally to the Lt. of left vertebral pedicle at the
Level of duodenal cap
DJ junction is mobile in children less than 4 months
SMV is ventral or to the Lt. of artery in malrotation
SMV spirals around SMA , artery shows hyperdynamic
Circulation
Band of ladd’s gives z-configuration of DJ junction

TYPE I MALROTATION (NONROTATION)
STOP ROTATING AFTER 90 DEG. COUTERCLOCKWISE
DJ JUNCTION LIES ON RT. SIDE
CAECUM LIES ON LT. SIDE
CLINICALLY INSIGNIFICANT BECAUSE OF GOOD FIXATION

TYPE II MALROTATION (REVERSED MALROTATION)
B/W 6WKS– 10WKS
AFFECTS DUODENUM ONLY
DUODENUM ENDS UP IN FRONT OF SMA OR OBSTRUCTED BY
LADD’S BAND
MIMICKS DUODENAL ATRESIA
DJ JUNCTION ON RT. & CAECUM ON RT. SIDE

TYPE III MALROTATION
ERROR IN ROTATION AFTER 10 WKS
DJ JUNCTION & CAECUM USUALLY MIDLINE
MOST DANGEROUS FORM OF MALROTATION
VOLVULUS , GANGRENE & DEATH COMMON.
VOLULUS GIVES BEAKED APPERENCE(COMPLETE OBST.)
CORKSCREW (INCOMPLETE OBST.)
LATE PRESENTATION

Midgut volvulus presenting as a classic
'corkscrew' appearance of the duodenum
and proximal jejunum on lateral view

on ultrasound in a patient with volvulus, vigorous peristalsis of
the obstructed duodenal C-loop is seen with characteristic
tapering of the distal, twisted end
When color Doppler ultrasound
is used, the twisted mesenteric vessels are seen
swirling in a clockwise direction (whirlpool sign), and
this finding is highly suggestive of midgut volvulus

Midgut volvulus. Vigorous peristaltic
activity fails to empty the duodenum, and
the third portion of the
duodenum has beak deformity (arrow);
S, stomach

Midgut volvulus: altered relationship
of mesenteric vessels. A, Normal
superior mesenteric vein (V) lies to the
right of the superior mesenteric
artery (A). B, Intestinal malrotation
and midgut volvulus; the
vein (V) lies to the left of the artery (A). C,
Color Doppler shows a clockwise
whirlpool of vessels (arrows) around
a volvulus.
(

DUODENAL ATRESIA & STENOSIS
•1 IN 6000 LIVE BIRTHS
•ATRESIA MORE COMMON THAN STENOSIS
•ASOCIATED WITH
DOWN’S SYNDROME, ESOPHAGEAL ATRESIA ,ARM, LADD’S
BAND, RENAL ANOMALIES,BILIARY ATRESIA
TYPES :
TYPE I WEB (DIAPHRAGM OCCLUDING LUMEN)
TYPE II BLIND END CONNECTED BY FIBROUS CORD
TYPE III (MOST COMMON) NO CONNECTING CORD WITH
DEFICIT OF MESENTERY
TYPE IV MULTIPLE ATRESIAS

ANTENATAL DIAGNOSIS
•DOUBLE BUBBLE
•POLYHYDROAMNIOS
CLINICAL FEATURES
BILIOUS VOMITING(DAY 1)
PLAIN RADIOGRAPHY
•DOUBLE BUBBLE APPERENCE
•GAS DISTAL S/O INCOMPLETE ATRESIA
Because an abdominal fluid collection can have other
etiologies, it is important to demonstrate a continuum between
the stomach and the cystic mass on ANC scan.
A prominent incisura angularis of the stomach may be
mistaken for a “double bubble” if these are in different planes,
but a careful real-time longitudinal
examination of the stomach can eliminate this possibility.

Duodenal atresia in a fetus with trisomy
21. A, Transverse fetal pelvis at 18
weeks with echogenic bowel (arrow E).
B, Same fetus at 21 weeks. Transverse
view of abdomen with stomach (arrow S) on left
and fluid-filled duodenum (arrow D).
C, Same fetus at 25
weeks. There is a “double bubble.” The stomach
is
visible inferiorly (S), with the dilated proximal
duodenum
(D) visible crossing the midline.

DOUBLE BUBBLE APPEARENCE DUODENAL WEB
DUODENAL ATRESIA

most common congenital anomaly of the pancreas.
Pancreatic tissue encircles the descending duodenum and
narrows its lumen.
the bilobed ventral component of the pancreas fuses with the
dorsal pancreas on both sides of the duodenum.
often presents in childhood, especially in children with Down
syndrome, about half of cases do not present until adulthood.
Symptoms in adults -
nausea, vomiting, abdominal pain, and occasionally jaundice.
ANNULAR PANCREAS

PREOPERATIVE DIFFERENTIATION FROM DUODENAL ATRESIA
IS DIFFICULT
DIAGNOSIS
The UGI series typically demonstrates eccentric or concentric narrowing
of the descending duodenum
CT pancreatic tissue seen surrounding 2nd
part of
Duodenum
ERCP a segment of pancreatic duct encircling the
Duodenum

Annular
Pancreas. Upper
GI series
demonstrates a 3-cm
long circumferentially
narrowed segment
(arrows) of the
descending
duodenum. No
ulceration was
evident. CT
confirmed an annular
pancreas. Db,
duodenal bulb.

Annular pancreas. A, Axial T1-weighted fat-suppressed MR image
demonstrates pancreatic tissue completely
circumscribing the descending portion of the duodenum B, Corresponding MRCP
shows the extrinsic compression around the second
portion of the duodenum

PREDUODENAL PORTAL VEIN
PRESENTS AS DUODENAL ATRESIA/ STENOSIS
PORTAL VEIN LIES ANTERIOR DUODENUM
ASSOCIATED WITH
•SPLENIC ANOMALIES
•MALROTATION
USG CAN DEMONSTRATE VEIN ANT. TO DUODENUM

Pre-duodenal portal vein seen anterior to duodenum, and posterior to intra-
peritoneal pancreas (arrow)

Jejunal /ileal atresia
Commonest bowel atresia
Etiology
Intrauterine ischaemic insult
Primary
Secondary : due to antenatal volvulus
Severity of ischaemia determines extent of atresia
Proximal jejunum & distal ileum are common sites
Clinical features
•Bilious vomiting
•Abdominal distention
•Meconium passage depends upon time of insult &
Site of obstruction

BARIUM ENEMA
Preoperative enema is required to exclude
Distal atresias
Locm is preferred
Microcolon is normal finding except
High obstruction
Low obstruction with late intrauterine insult
Diagnosis
•Dilated bowel loops to the level of atresia
•Meconium peritonitis with calcification present if
Intrauterine perforation has occured

Apple peel syndrome
Intrauterine occlusion of distal sma
•Proximal jejunal atresia
•Agenesis of mesentery
•Absence of mid small bowel
Distal ileum spirals around it’s narrow vas. Pedicle
Malrotated microcolon usually present
•multiple sites of severe stenosis and a spiral configuration of the
atretic segment. This condition tends to be familial

TRIPLE BUBBLE APPEARENCE
JEJUNAL ATRESIA
Jejunal Atresia. Plain film shows distention of
the stomach (S), duodenum (D), and loops of the upper intestine
(arrows). No air is present distal to the proximal jejunum

DILATED BOWEL LOOPS MICROCOLON WITH REFLUX INTO
TERMINAL ILEUM
ILEAL ATRESIA

MECONIUM ILEUS
High protein content of meconium cause distal bowel
Obstruction
90%have cystic fibrosis
Clinical features
•Bilious vomiting
•Abdominal distention
•Failure of passage of meconium
Antenatal diagnosis
Multiple echogenic foci
Meconium cysts
Plain radiography
Bubbly pattern of bowel gas in rt. Iliac fossa
Dilatation of small bowel

Barium enema
To determine true nature of obstruction
In uncomplicated therapeutic as well as diagnostic
Isoosmolar contrast medium
Gastrograffin diluted half strenght with saline or water
Barium sulphate inspissates & risk of perforation
1/3rd pt. Too sick--require surgery
1/3rd pt. Enema unsuccessful
1/3rd pt. One or more enema req. To remove sticky meconium
Usg : dilated loops with echogenic material

Complicated meconium ileus
Intraabdominal calcification
Bowel wall calcification
Soft tissue mass
In utero perforation causes chemical peritonitis
(Snow storm appearance) on usg
Meconium pseudocyst is due to vascular compromise

MECONIUM ILEUS
BUBBLY APPEArance

Meconium Ileus. A. Plain film shows the
soap-bubble effect of air mixed with meconium in the
numerous distended loops of intestine. B. Contrast enema
demonstrates a typical microcolon with reflux into the terminal
ileum, which is filled with pellets of meconium (arrows).

misleading name for a condition caused by functional immaturity
and abnormal peristalsis of the distal colon.
Also known as small left colon syndrome, this condition
should not be confused with meconium ileus.
a normal to dilated proximal colon filled with meconium
and an empty distal descending colonic segment are characteristic
The meconium in infants with this condition is normal
and is not the cause of obstruction.
Meconium plug syndrome

more common in
normal large infants and infants of diabetic mothers.
functional obstruction is transient and can often be
treated by rectal stimulation or saline enemas
Normal ganglion cells are present in these infants, and
once the meconium has passed, the patient will defecate
Normally.

Meconium Plug Syndrome (Small Left Colon
Syndrome). A. Numerous loops of intestine are distended
with
air. Also, note air in the relatively narrow rectosigmoid colon
(arrow). B. Contrast enema demonstrates a small left colon
with
the characteristic transition zone (arrow). These findings mimic

VITELLINE DUCT ANOMALIES
Meckel's diverticulum
•2--4 % population vitelline duct persist
•40--60 cm FROM IC JUNCTION
CLINICAL FEATURES
•BRIGHT RED PAINLESS RECTAL BLEEDING
•Obstruction secondary to intussusception
Vitelline cyst / enterocystoma cause strangulation
or volvulus
Vitelline fistula : duct patent entire length
(fecal discharge)
Tc pertechnate scan dignostic for heterotrophic
pancreatic tissue ,gastric mucosa

Meckel Diverticulum. A scan performed with
technetium-99m-pertechnate shows an abnormal collection of
tracer in the right lower quadrant (arrow), whose intensity
parallels that of the stomach (S). Gastric mucosa within the
Meckel diverticulum is responsible for the tracer localization. B,
bladder.

HINDGUT
HINDGUT GIVE RISE TO DISTAL 1/3rd OF TR. Colon,descending colon
Sigmoid , rectum & upper part of rectal canal
Terminal portion of hindgut enters posterior reg. Of cloaca
(Primitive anorectal canal )
Allantois enters anterior portion ,primitive urogenital sinus
Urorectal septum forms perineum
Ectodermal proliferation closes distal most part of anal canal
which is recanalized
Junction b/w ectoderm & endoderm , pectinate line

Normal appearance in neonate
Haustral patterns are hardly developed
Large bowel is redundant, sigmoid reaching upto hepatic
Flexures
Caecum can appear higher
Lymphoid follicles , tiny nodular filling defect,upto 2mm
Upto 5 yrs is s/o good coating
Lymphoid hyperplasia >3 mm ,found in
• dysgammaglobulinemia
• Ibd
• Lymphoma

Large bowel atresia
Rarer than small bowel atresia
Clinical features
•Failure to pass meconium
•Abd. Distention
•Vomiting
Types :type I -- web
Type II -- gap bridged by atretic cord
Type III -- complete seperation (most com.)
Right colon is mostly involved
Diaphragm prolapse in retrograde fashion into dilated prox.
Segment, windsock appearence

Functional motility disorder
Hischprung's disease
1 in 5,000 live births, m>f
Absence of myenteric ganglion in distal large bowel
Hypertonic aganglionic segment
Zone of transition gradual change from ganglionosis to
aganglionosis
Rectosigmoid region is most common (70%),
 25% extend to the splenic flexure or transverse colon (long segment)
and 5% involve the entire colon (total colonic Hirschsprung's disease).

Cause : due to arrest in the normal cranial-to caudal
neural cell migration, resulting in absence of ganglion
cells within the myenteric plexus of the bowel wall
Clinical features
failure to pass meconium within the first 48 h of life.
A smaller number present with intractable
constipation later in childhood and occasionally into
adulthood.
Enterocolitis occurs in 15% of patients and can be
the initial presentation, with fever and diarrhoea.
Diagnosis
Biopsy is definitive
Radiology and manometery helpful

Plain radiography
OBSTRUCTION ( >3 cms)
Cross table lateral with pt . prone for zone of transition
Contrast enema
No bowel prepration
Water soluble contrast media preferred
Lateral position to recognize zone of transition
Absence of tr. Zone does not exclude disease
Delayed film showing retention is also s/o disease
Reversal of rectosigmoid ratio
Irregular saw tooth contractions in aganglionic seg.

The normal neonatal rectum is of greater calibre than the sigmoid colon.
Inversion of the rectosigmoid
index, often in association with irregular contractions of the
aganglionic rectum and difficulty in obtaining good rectal distension,
is indicative of Hirschsprung's disease

Hirschsprung's disease. An abrupt
transition zone is seen at
the rectosigmoid junction on this lateral
rectal view from a contrast enema
performed on a 2-day-old boy with
failure to pass meconium. The rectum
was difficult to distend well and
showed irregular contractions.

Enteric duplication cyst
Additional portion of gut develops
Non communicating with bowel except tubular type
Mesenteric side of iileum , common site
Muscle layer continuous with bowelwall
Clinical features
•Vomiting due to obstruction
•Abdominal pain
•Palpable abdominal mass
Usg :
•Unilocular anechoic cystic mass
•Double layered
•Tc 99m req. In tubular & communicating cyst

Mesenteric cyst / lymphangioma
Sequestration of lymphatic vessels
Omental cysts ( in omentum)
Intermitent symptoms
Soft & mobile , difficult to palpate
Usg :
•Uniloculated / multiloculated
•Thin or thick septations
Anechoic or echogenic debris

Anorectal malformation
Absence of normal anus,
First day presentation with obstruction
1 in 5,000 live births
Male > female
Cause : abnormality in formation of cloaca
Posterior portion of cloaca is small so hindgut opening
Shifts anterioly
Classification :
On basis of rectum above or below puborectalis sling
•High
•Intermediate
•Low

Low variety
No communication with gu tract
Visible perineal opening anterior (ectopic anus)
High variety
No visible perineal opening
Comm. With gu tract present
Imperforate anus
No anal opening , lack of recanalization of lower
Portion of anal canal.
Associations:
Oeis (5%) omphalocele-exstrophy-imperforate anus-spinal defects)
Vacterl (45%)
Down syndrome (2-8%)
Currarino's triad;anorectal stenosis
Scimitar sacrum
Presacral mass lesions

Plain radiograph
Distal bowel obstruction
Invertogram no more used , cross table lateral taken.
Intravesicle air s/o high variety
Calcified intraluminal meconium (high variety)
Vertebral anomalies (vater)
Usg :
Renal tract anomalies( ectopic, horseshoe)
Spinal usg to rule out cord tethering
Transperineal for distance b/w anal dimple & distal large bowel
Loopogram :
Size of bowel distal to colostomy
Any fistula
To look for leaks or obstruction after pull through surgery or
Before colostomy closure
Ct/ mri ;
Indicated if incontinence or constipation after operation

BODY WALL DEFECTS
Omphalocele
Herniation of abdominal viscera covered by amnion
through enlarged umblical ring
Cause : failure of bowel to return to body cavity from
physiological herniation
2.5/ 10,000 live births
Mortality 25%
Cardiac anomalies 50%
Antenatal presence of sac with umblical insertion

Gastroschisis
1/ 10,000 live birts
Increased incidence with cocaine use
Herniation of bowel contents directly into amniotic cavity
Right lateral to umblicus (regression of rt. Umblical vein)
Not covered by amnion or peritonium
No chromosomal anomalies
Bowel are short, edematous & coated with fibrocollagenous
Coating
Excellent survival

Gastroschisis.
Several air-filled
extra-abdominal
loops of bowel
are seen in this infant
of 26 weeks
gestation. A small left
congenital
diaphragmatic hernia
was also present.

Amol -Congenital anamolies of GIT

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