Introduction and Learning Points
Although most newborns have some grade of spitting up, forceful and
repeated vomiting should be taken seriously and practitioners should
suspect a surgical condition like bowel obstruction. is case report
describes a newborn with vomiting, its diagnostic approach and initial
e patient was a female baby born by c-section due to fetal
decelerations at 35 4/7 weeks gestation to a 24 year-old female G1P1.
e pregnancy was uneventful, and her mother received usual prenatal
care. Her mother experienced reduction in fetal movements few days
before delivery; prenatal ultrasound showed polyhydramnios. During
delivery, APGAR scores were 4 at 1 minute and 6 at 5 minutes. She
required bag mask support and recovered to APGAR of 9 at 10
minutes. She was taken to the nursery for standard care. Her initial
physical examination was within normal limits. Her weight was
1633 gr (<3%), her head circumference was 30 cm (3-10%) and her
length was 43 cm (3-10%). Shortly after initiation of feedings, she
had repeated postprandial vomiting. An abdominal ﬁlm suggests the
diagnosis. See ﬁgure 1.
Patient’s abdominal ﬁlm showed a “double bubble” sign with absence
of gas in the remaining small and large bowel. ese results, and the
baby’s history of repeated postprandial vomiting, were consistent with
the diagnosis of duodenal atresia (DA). Echocardiogram was normal.
Patient was promptly taken to the OR for surgical repair after initial
DA occurs in 1 per 5,000 to 10,000 live births. It is an isolated ﬁnding
in 30 to 50% of cases, however, it is often associated with other
malformations, including gastrointestinal (biliary atresia, agenesis of
the gall bladder), cardiac (20%), renal, and vertebral anomalies (1). In
25-40% of cases, the anomaly is found in Down syndrome (2).
Prenatally, DA increases the risk of prenatal asphyxia and death caused
by bradycardia/asystole following vagal overactivity due to distension
of the UGI tract (3). Polyhydramnios occurs in 33% to 50% of
patients with duodenal atresia (3) (4).
Most babies are born at term or near term and tend to be small
for gestational age (5). While bilious vomiting is a typical clinical
presentation, it may be nonbilious due to defects proximal to the
ampulla of Vater (3). Babies may have distention or normal abdominal
examination. Complications of poor feeding and vomiting, including
volume depletion, electrolyte imbalance, and aspiration pneumonia
may occur (1).
The Baby Is Vomiting
Janeth Ceballos Osorio, MD
University of Kentucky • Department of Pediatrics
e ﬁrst study imaging should be a plain abdominal radiograph; a characteristic
ﬁnding is a double-bubble image of an air-ﬁlled stomach proximal to an air-ﬁlled
ﬁrst portion of the duodenum (6). Diﬀerential diagnosis of UGI obstruction
should be in mind. See table 1. (1)
Treatment of DA includes initial medical preoperative management and surgical
correction. Adequate IV hydration, TPN, and gastric decompression are essential
until the neonate has been stabilized for surgical repair (1). e surgical correction
is a duodenoduodenostomy (“diamond shaped”) (7) (4). See Figure 2. (8)
Early mortality rate is 5%. Most deaths are associated with multiple anomalies
(usually complex cardiac defects). Late complications may occur in 12% to 15% of
patients, among them are delayed gastric emptying, severe gastroesophageal reﬂux,
bleeding peptic ulcer, megaduodenum, duodenogastric reﬂux, gastritis, blind-loop
syndrome, and intestinal obstruction related to adhesions. Long-term survival is
excellent at rates reported between 86% and 90% (4).
1. Bilious vomiting in the newborn: rapid diagnosis of intestinal obstruction. Kimura,
K. and Loening-Baucke, V. 2000, Am Fam Physician, Vol. 61, pp. 2791-2798.
2. Congenital gastrointestinal defects in Down syndrome: a report from the Atlanta and
National Down Syndrome Projects. Freeman, S. B., et al. 2009, Clin Genet, Vol.
75, pp. 180-184.
3. Fetal duodenal obstructions: increased risk of prenatal sudden death. Brantberg, A.,
et al. 2002, Ultrasound Obstet Gynecol, Vol. 20, pp. 439-446.
4. Duodenal atresia and stenosis: long-term follow-up over 30 years. Escobar, Mauricio
A, et al. 2004, J Pediatr Surg, Vol. 39, pp. 867--71; discussion 867-71.
5. Intrauterine growth rate in relation to anorectal and oesophageal anomalies. Cozzi, F.
and Wilkinson, A. W. 1969, Arch Dis Child, Vol. 44, pp. 59-62.
6. e double bubble sign. Traubici, J. 2001, Radiology, Vol. 220, pp. 463-464.
7. Diamond-shaped anastomosis for congenital duodenal obstruction. Kimura, K., et al.
1977, Arch Surg, Vol. 112, pp. 1262-1263.
8. Karrer, Frederick Merrill. Duodenal Atresia: Multimedia. Emedicine. [Online]
Medscape, March 3, 2009. [Cited: April 09, 2009.] http://emedicine.medscape.
Figure 1 Table 1: Diﬀerential Diagnosis of Upper GI
Obstruction in Newborns
Figure 2: Diamond Shape
Type of obstruction Cause and
in 1 per 5,000 live
births; 25% have Down
Few hours after birth;
billious vomiting, no
Abdominal ﬁlm, “double-
rotation occurring during
7th to 12th weeks of
At 3 to 7 days; bilious
Upper GI spiral sign on
location of the superior
accident during fetal life
in 1 per 3,000 live births
Within 24 hours of birth;
Air-ﬂuid levels on
Necrotizing ileus Cause unknown in 2.4
per 1,000 live births
10 to 12 days after birth;
air in the aortal vein
Genetic, occurs in 15%
of newborns with cystic
ﬁbrosis, and in 1 per
5,000 to 10,000 live
Immediately after birth;
levels, sweat test,