DUODENAL OBSTRUCTION

IRFANSYAH
ANATOMY
 Functional divisions of primitive GI system
PARASYMPAT
DIVISION ARTERY VEIN LYMPHATICS SYMPATHETIC
HETIC

FOREGUT:
Oesophagus
Stomach PORTAL VEIN
CELIAC
Proximal half of duodenum (up to Spleenic vein CELIAC NODES CELIAC GANGLIA VAGUS
ARETERY
common bile duct (CBD)) Gastric vein
Liver
Pancreas

MIDGUT:
Distal half of duodenum (from
CBD)
Jejunum SUPERIOR SUPERIOR SUPERIOR SUPERIOR
Ileum MESENTERIC MESENTERIC MESENTERIC MESENTERIC VAGUS
Appendix ARTERY VEIN NODES GANGLIA
Cecum
Ascending colon
Right 3/4 of transverse colon

HINDGUT:
GANGLIA
Left 1/4 of transverse colon INFERIOR INFERIOR INFERIOR PELVIC
 
Descending colon MESENTERIC MESENTERIC MESENTERIC SPLANCHNIC
HYPOGASTRIC
All of rectum down to ano-rectal ARTERY VEIN NODES NERVES
PLEXUS
line
 25 days 32 days

Langman’s Medical Embryology, 9th ed. 2004.

Celiac artery supplies the foregut

Superior mesenteric artery supplies the midgut
Inferior mesenteric artery supplies the hindgut
Duodenum was divided into four parts:
1)Pars Superior
2)Pars Descending
3)Pars Horizontal
4)Pars Ascenden
 Artery, Vein, Nerve
• 1/2 sup → a.pancreaticoduodenalis
superior, cabang a.gastroduodenalis
superior
• 1/2 inf → a.pancreaticoduodenalis
inferior, cabang a.mesenterica superior
 Cont. AVN
• v.pancreaticoduodenale sup. → v.porta
• v.pancreaticoduodenale inf. → v.mesenterica
superior → v.porta

Innervated by N. Vagus simpatis and

parasimpatis from plexus mesentericus
superior and plexus coeliacus
 Duodenal Obstruction (DO)
• Congenital duodenal obstruction (DO) is a
frequent cause of congenital intestinal
obstruction in the newborn
• Occur in 1 per 5,000–10,000 live births, and
affecting Boys > girls
• DO  intrinsic or extrinsic
• Intrinsic DO  duodenal atresia, stenosis
diaphragm, perforated diaphragm, or a ‘wind-
sock’web  duodenal membrane that
balloons distally as a result of peristalsis from
above.
• Extrinsic  annular pancreas, malrotation, or
preduodenal portal vein
Causative theories of congenital duodenal
obstruction include
•abnormalities of pancreatic development
•vascular disruption,
•failure of recanalization of the duodenal lumen
from its solid cord stage.
• More than 50% of patients with duodenal atresia or duodenal
stenosis have associated congenital anomalies: Down
syndrome  30% of patients
The mortality rate is higher in neonates born with three or
more anomalies of the VACTERL association with an overall
survival rate of 40–70%
•V, vertebral or vascular defects;
•A, anal malformation;
•C, cardiac anomaly;
•TE, tracheoesophageal fistula with esophageal atresia;
•R, renal anomalies; and
•L, radial limb anomalies
 Prenatal Diagnosis
• Duodenal obstruction is being increasingly
diagnosed prenatally.
• The prenatal sonographic diagnosis of DO
relies on the demonstration of the “double
• bubble” sign, which is due to the simultaneous
distension of the stomach and the first portion
of the duodenum
 Diagnosis
The diagnosis of DO
• prenatal ultrasonography,
• early clinical symptoms,
• physical examination,
• and plain radiographic abdominal films.
 Clinical features
• Vomiting and intolerance of attempted feedings are the
most common symptoms on the first day of life
• 80% of obstructions located in the postampullary region
of the duodenum, vomitus  bile-stained. In supra-
ampullary atresia, it is nonbilious.
• Abdominal distention (-) high level of obstruction
 Clinical features
• Infants may pass some meconium in the first 24 h of
life and thereafter constipation may develop
• Dehydration with weight loss and electrolyte
imbalance
• Incomplete duodenal obstruction (e.g., duodenal
membrane with a central aperture) usually leads to
thedelayed onset of symptoms, which may appear a
few months or years after birth.
 Radiological Diagnosis
• The diagnosis of the duodenal atresia is confi
rmed on X-ray examination
• An abdominal radiograph a dilated stomach
and duodenum a “double bubble sign”
 Radiological Diagnosis
• In partial duodenal obstruction  a “double bubble” appearance
some air in the distal intestine

• Radiographic findings in the annular pancreas are usually

indistinguishable from duodenal atresia and stenosis.

• Partial duodenal obstruction plain films may be normal  the upper

gastrointestinal tract contrast radiography is indicated

• Occasionally, a duodenal diaphragm may be stretched and

ballooned distally giving the wind-sockappearance on contrast study
 Differential Diagnosis
• All the various conditions of upper
gastrointestinal obstruction should be
included in the differential diagnosis of DO
• The most important ones for the pediatric
surgeon are DO  malrotation  Ladd’s
bands across the duodenum and volvulus of
the midgut loop
Differential Diagnosis
 Malrotation
• The incidence of malrotation has been estimated at 1
in 6000 live births
• An increased incidence of 0.2% has been found in
barium swallow studies, whereas autopsy studies 
1% of the total population
• Up to 75% of patients the first month of life.
Another 15%  within the first year
• Classic malrotation with midgut volvulus is often
discovered in a previously healthy term neonate
 Malrotation
• Volvulus, intestinal gangrene, and mortality have
been noted regardless of the patient’s age or
chronicity of symptoms
• Bilious vomiting the cardinal sign of neonatal
intestinal obstruction, and malrotation must be the
presumed diagnosis until proven
• Other signs in the neonate include abdominal
pain and distention, metabolic acidosis quickly
advances to hypovolemic shock
 Malrotation
• Late signs  abdominal wall erythema and
hematemesis or melena from progressive
mucosal ischemia
• Mesenteric vascular compromise rapidly leads
to peritonitis, sepsis, shock, and death
• Laboratory investigation leukocytosis or
leukopenia, hyperkalemia, and
thrombocytopenia
 Duodenal atresia and stenosis
• The obstruction at the level of the duodenum :
complete or incomplete
• Duodenal atresia cause complete bowel obstruction 
into three types:
Type I : the most common (65%) is represented
by a mucosal web with normal muscular wall
Type II : by a short fibrous cord connecting the two
atretic ends of the duodenum (18%)
Type III : by a complete separation of the atretic ends
with a mesenteric defect (18%)
 Duodenal atresia and stenosis
• Congenital duodenal atresia and stenosis is a 
occurring in 1 per 5000 to 10,000 live births and
affecting boys > girls
• More than 50% of affected patients  congenital
anomalies, with trisomy 21  approximately 30% of
patients
• At present, either laparoscopic or open
duodenoduodenostomy, with or without tapering
duodenoplasty, has become standard with early
postoperative survival rates of greater than 90%
Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
 Duodenal atresia and stenosis
• The most common cause of duodenal obstruction is atresia.
• This intrinsic lesion caused by a failure of recanalization of
the fetal duodenum complete obstruction
• Early in the 4th week of gestation, the duodenum begins
to develop from the distal foregut and the proximal midgut
during the 5th and 6th weeks of gestation,
• The duodenal lumen temporarily obliterates owing to
proliferation of its epithelial cells.

Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
 Duodenal atresia and stenosis
• Vacuolation due to degeneration of the epithelial cells during
the 11th week of gestation then leads to recanalization of the
duodenum
• An embryologic insult during this period can lead to an
intrinsic web, atresia, or stenosis.
• The extrinsic form of duodenal obstruction is due to defects
in the development of neighboring structures such as the
pancreas, a preduodenal portal vein, or secondary
to malrotation and Ladd’s bands.34,35

Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
 Annular Pancreas
• Annular pancreas is an uncommon etiology for duodenal
obstruction
• It forms of obstruction is likely due to failure of duodenal
development rather than a true constricting lesion
• Thus, the presence of an annular pancreas is simply a visible
indicator for an underlying stenosis or atresia
• Between the fourth and eighth weeks of gestation, the
pancreatic buds merge

Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
 Annular Pancreas
• In annular pancreas, the tip of the ventral pancreas
becomes fixed to the duodenal wall forming a
nondistensible, ring-like or annular portion of
pancreatic tissue surrounding the descending part of
the duodenum.
• In annular pancreas associated with duodenal
obstruction, the distal biliary tree is often abnormal
and may open proximal or distal to the atresia or
stenosis

Ashcraft’s pediatric surgery / [edited by] George Whitfield Holcomb III, J. Patrick Murphy ;
associate editor, Daniel J. Ostlie. — 5th ed.
 Preoperative management
• X-ray
• Cardiac and renal ultrasound should be carried out
routinely in all these babies
• A micturating cystourethrogram abnormal
urogenital ultrasound or an associated anorectal
anomaly.
• Once the diagnosis is established early surgical
exploration
• Nasogastric decompression and fluid and electrolyte
replacement
• Preserve body heat and avoid hypoglycemia
 Management
• Duodenal atresia, stenosis, and annular pancreas  the
recommended surgical procedure  bypass the obstruction
by duodenoduodenostomy.
• Duodenoduodenostomy  either side-to-side fashion or
proximal transverse to distal longitudinal (diamond shape)
anastomosis
• In both surgical techniques, the downstream
duodenum patency  passing a catheter or infusing saline to
examine the distal bowel for other associated atresia or
luminal
 COMPLICATIONS
• Dalla Vecchia et al  138 patients reported
Low early complication rate:
 anastomotic obstruction in 3%
 congestive heart failure in 9%
 prolonged adynamic ileus in 4%
 pneumonia in 5%
 and wound infection in 3%
 COMPLICATIONS
• Late complications include
– adhesive bowel obstruction in 9%
– megaduodenum with duodenal dysmotility that
required tapering duodenoplasty in 4%
– duodenogastro esophageal refl ux (GERD)
requiring surgery in 5% of cases.