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Congenital duodenal obstruction: Timing of diagnosis during the newborn

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Article  in  Journal of Perinatology · October 2009

DOI: 10.1038/jp.2009.143 · Source: PubMed

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 Journal of Perinatology (2010) 30, 197–200
r 2010 Nature Publishing Group All rights reserved. 0743-8346/10 $32
www.nature.com/jp
ORIGINAL ARTICLE
Congenital duodenal obstruction: timing of diagnosis during
the newborn period
H Kilbride1, C Castor1 and W Andrews2
1
Department of Pediatrics, Children’s Mercy Hospitals & Clinics, University of Missouri-Kansas City School of Medicine,
Kansas City, MO, USA; 2Department of Surgery, Children’s Mercy Hospitals & Clinics, University of Missouri-Kansas City
School of Medicine, Kansas City, MO, USA
Objective: To determine age at diagnosis for congenital duodenal
obstruction in the neonatal period and the relationship to clinical outcomes.
Study Design: A children’s hospital database reflecting a 7 ½-year
period was reviewed to identify infants with the diagnosis of duodenal
obstruction in the neonatal period. Infants were grouped according to
time of diagnosis: antepartum, postpartum in-hospital or after hospital
discharge. Clinical descriptors and outcome variables were assessed
between infants in these three groups.
Result: In total, 27/51 (53%) infants were diagnosed antenatally. Infants
with prenatal diagnosis were less mature, more likely to have Down
syndrome or other birth defects and the pregnancy was more likely to be
complicated by polyhydramnios. Of the 24 infants diagnosed postnatally,
8 (33%) were diagnosed after hospital discharge. These infants tended to
be breast fed and discharged before 48 h of age. They had greater weight
loss and more metabolic disturbances at readmission for surgery. One
infant in the late diagnosis group died.
Conclusion: Infants with congenital duodenal obstruction, particularly
if breast fed, may not present with classical findings of upper
gastrointestinal obstruction in the first days of life. Careful in-hospital
evaluation of infants with persistent regurgitation, even low volume, is
recommended to avoid missing this diagnosis.
Journal of Perinatology (2010) 30, 197–200; doi:10.1038/jp.2009.143;
published online 1 October 2009
Keywords: duodenal obstruction; early newborn discharge;
polyhydramnios
Introduction
Congenital obstruction of the duodenum accounts for nearly
one-half of all intestinal obstructions seen in the newborn1 and
is reported to occur once in 2500 to 10 000 deliveries.2,3
Correspondence: Dr H Kilbride, Department of Pediatrics, University of Missouri–Kansas City
School of Medicine, Children’s Mercy Hospitals and Clinics, 2401 Gillham Road, Kansas City,
MO 64108, USA. E-mail: HKilbride@cmh.edu
Received 27 April 2009; revised 12 August 2009; accepted 23 August 2009; published online 1
October 2009
The classic description in surgical and medical textbooks
includes early and frequent vomiting, often bilious, which would
suggest that these lesions should be easily identified before
discharge from the hospital.2–4 However, the clinical presentation
of congenital duodenal obstruction is related to the type of
anatomic defect that may be complete or partial, including
duodenal atresia, duodenal stenosis, duodenal web or extrinsic
compression from an annular pancreas.3,5 Two-thirds of infants
with complete atresia will present with bilious emesis, but they can
present with clear emesis if the obstruction is proximal to the
insertion of the common bile duct. It is known that infants with a
perforated web or stenosis may not present in the newborn period,
because formula or breast milk are often able to pass through the
partial obstruction. However, delayed diagnosis of a complete
proximal intestinal obstruction would seem unlikely. We cared for
an infant with a complete duodenal atresia, which was not
diagnosed until several days after discharge from the birth hospital.
The poor outcome for that infant prompted this review of infants
referred to a tertiary children’s hospital for care of congenital
duodenal obstruction to determine the age at diagnosis and
associated outcomes for this disorder.
Methods
Study approval was granted by the Institutional Review Board with
exempt status. Children’s Mercy Hospital’s Intensive Care Nursery
database was accessed to identify all infants cared for between 1
January 1999 and 31 July 2006, and discharged with a diagnosis
indicating duodenal obstruction in the neonatal period (<28 days
of age). Children’s Mercy Hospital is the regional referral center for
newborn surgical cases in the Kansas City metropolitan area.
Medical record review was undertaken to determine whether the
diagnosis of duodenal obstruction had been known antenatally or
determined during the postpartum course, and whether the infant
was discharged from the initial newborn hospitalization without
diagnosis of bowel obstruction. Other data assessed included
pregnancy complications, feeding difficulty during the initial
nursery course, age and condition at discharge, the presence
 Congenital duodenal obstruction
H Kilbride et al
198

of other birth defects, clinical complications leading to the Table 1 Newborn with duodenal obstruction pre- versus postnatal diagnosis
rehospitalization, condition at admission and outcome. Clinical Prenatal Postnatal P-values
and outcome variables were compared between infants referred (N ¼ 27) (N ¼ 24)
after antenatal diagnosis and those diagnosed postnatally. Infants
diagnosed during the postnatal period were grouped to compare Maternal age (years) 30.5±7.7a 25.7±5.8 0.019
those recognized during the newborn hospitalization and those Primips 9 (33%) 9 (38%) 0.76
diagnosed only after hospital discharge to assess factors that Prenatal care 27 (100%) 20/23 (87%) 0.09
may have been associated with delayed diagnosis. Statistical Polyhydramnios 25 (93%) 4/22 (18%) <0.001
Cesarean section delivery 11 (41%) 10 (42%) 0.95
analysis was performed using the Statistical Package for Social
Birth weight (kg) 2.38±.82 2.75±0.78 0.11
Sciences (SPSS, Version 15.0, Chicago, IL, USA), using t-tests
Gestational age (weeks) 35.0±2.7 37.0±2.5 0.011
and w2-tests, as appropriate; P<0.05 was used to determine Gestational age <36 weeks 15 (56%) 5 (21%) 0.02
statistical significance. Associated syndrome 17 (63%) 8 (33%) 0.035
Age at referral (DOL) 0.6±.6 3.8±3.4 <0.001
Surgery (DOL) 2.5±1.6 5.5±4.0 <0.001
Results Length of stay (days) 31±14 26±11 0.13
During the 7 ½-year study period, 51 infants aged <28 days Abbreviation: DOL, day of life.
were referred with duodenal obstruction to the Children’s Mercy a
Mean±1 standard deviation.
Hospital. A total of 27 (53%) were diagnosed prenatally. Infants
with prenatal diagnosis were less mature and tended to be lighter Table 2 Newborn with duodenal obstruction diagnosed postnatally
than those diagnosed postnatally (Table 1). Polyhydramnios was Diagnosed during Delayed P-values
significantly more likely for those with prenatal diagnosis; however, birth hospitalization diagnosisa
this complication had also been noted in nearly 20% of cases not (N ¼ 16) (N ¼ 8)
diagnosed until after birth. Other birth defects, particularly Down’s
syndrome, were significantly more likely for those diagnosed Birth weight (kg) 2.70±0.90 2.84±0.48 0.685
prenatally. As expected, infants with prenatal diagnosis were Gestational age (weeks) 36.6±2.7 37.8±2.1 0.24
significantly younger at age of referral and at time of surgery Small for gestational age 4 (25%) 1 (13%) 0.63
Female gender 13 (81%) 7 (88%) 1.0
compared with those diagnosed after birth.
Prenatal care 14/15 (93%) 6 (75%) 0.27
Of the 24 infants diagnosed postnatally, 8 (33%) were identified
History of polyhydramnios 4/15 (27%) 0/7 0.26
only after discharge from the birth hospital (‘delayed diagnosis’). All Maternal age (year) 27.6±5.9 21.9±3.3 0.019
eight infants with delayed diagnosis had been delivered vaginally, Cesarean section delivery 10 (63%) 0 0.003
significantly different than those diagnosed during the birth Breast feeding 6 (58%) 7 (88%) 0.03
hospitalization, of which 63% were delivered by cesarean section History of emesis 14 (88%) 7 (88%) 1.0
(Table 2). Mothers of infants with delayed diagnosis were significantly Bilious emesis 6 (38%) 3 (38%) 1.0
younger and were more likely to be breast feeding. There were no
differences in other demographic variables or in clinical signs, Anatomical findings
including emesis, which was frequent in both groups (88%). About Duodenal atresia 13b (81%) 5 (63%) 0.31
40% of the infants in both groups had some bilious emesis by history. Annular pancreas 0 1 (13%)
The mean age at hospital discharge for the delayed diagnosis group Duodenal web 3 (19%) 2 (25%)
a
was 37 h (range: 24 to 48 h of age). In total, 57% percent were Infants diagnosed after birth hospital discharge (includes one home birth).
b
discharged at <36 h of age. On average, they were readmitted for Four also with annular pancreas.
evaluation of possible bowel obstruction at 5 days of age (range: 2.5 to
8 days of age). In comparison, 13 of the 16 infants (81%) diagnosed hospital, and were more likely to have hypochloremia, metabolic
with duodenal obstruction during the birth hospitalization had alkalosis and findings of prerenal azotemia (Table 3). One infant
evaluation for intestinal obstruction initiated within 24 h of birth and who was initially discharged without diagnosis of duodenal
all 16 infants were evaluated by 72 h of life. There were no significant obstruction was readmitted on day 4 of life after aspiration and
group differences in anatomical findings at surgery. All eight infants respiratory arrest, which led to the infant’s death.
with delayed diagnosis had complete obstructions, six with atresias
and two with duodenal webs.
Compared with infants identified with bowel obstruction during Discussion
birth hospitalization, infants with delayed diagnosis had With congenital duodenal obstruction, the stomach and pro-
significantly greater weight loss at referral to the children’s ximal duodenum are markedly dilated, which account for the

Journal of Perinatology

Table 3 Condition at referral for surgery
Referral from Admissions P-values
birth hospital from home
(N ¼ 16) (N ¼ 8)
Admission weight (kg) 2.52±.83 2.39±.47
Weight loss (%) 6.9±7.1 15.7±6.4
Admitting laboratory studies
Serum Na (mmol l1) 138±3.5 141±6.5
Serum K 4.4±.79 4.8±.93
Serum CO2 25±3 30±8
Serum Cl 102±4.6 91±13.5
BUN (mg per 100 ml) 15±8 42±27
Creatinine (mg per 100 ml) 1.1±.73 2.5±1.6
Total serum bilirubin (mg per 100 ml) 9.5±4.2 12.2±5.6
Abbreviation: BUN, blood urea nitrogen.
‘double bubble’ identified on roentgenogram after birth and which
may be identified antenatally by ultrasound.1 However, this finding
may not be evident if the prenatal ultrasound studies are per-
formed for pregnancy dating and screening before 20 weeks of
gestation, as the anatomical findings of duodenal atresia may not
be apparent that early in gestation.6 Another prenatal marker is
polyhydramnios, which occurs in approximately half of the cases
due to inability of the fetus to absorb the swallowed amniotic
fluid.1 In addition, in B50% of cases, there may be associated
anomalies, including trisomy 21 in 40%,7 and less frequently,
intestinal malrotation, congenital heart disease and tracheal
esophageal fistula.8 Growth retardation or prematurity may occur
in one-third or more of the patients without chromosomal
disorders. In the absence of antenatal detection, aspiration of
>20 ml of gastric fluid volume at birth should suggest a proximal
intestinal obstruction.9
Although fetal identification of congenital duodenal obstruction
may occur when there are associated findings, our study
found that nearly 50% of cases were not diagnosed until after
birth and as many as a third of those were missed during the initial
newborn hospitalization. These findings are consistent
with two other series documenting postnatal diagnosis in 56%
of cases of congenital duodenal obstruction.10,11 Although these
reports did not provide details of neonatal condition, one indicated
that diagnosis occurred at a mean of 5.7 days of life; later diagnosis
was associated with delayed surgery and longer hospital stay.11
In our report, infants whose defect was diagnosed prenatally
had earlier surgery than those diagnosed postnatally; however, there
was no difference in length of hospitalization, probably because those
diagnosed antenatally were less mature and more likely to have other
birth defects compared with the postnatal diagnosis group.
In our review, infants with a delayed diagnosis of duodenal
obstruction generally were breast fed. Although most infants with
Congenital duodenal obstruction
H Kilbride et al
199
obstruction had spitting, many did not have large emesis during
the nursery stay, presumably because initial feedings were low
volume, particularly when breast fed. In these cases, clinicians
seemed to focus on the disturbed feeding as related to ‘breast-
feeding failure’ rather than on need for evaluation of anatomical
0.706 causes of emesis. It is of interest that none of the infants with
0.007 delayed diagnosis had history of polyhydramnios as a complication
of the pregnancy, which may suggest that the dilated proximal
stomach and intestine in these cases were able to sequester
0.19
unusually large volumes of fluid. It should also be noted that none
0.27
0.036
of the delayed diagnosis group were delivered by cesarean section,
0.006 which would have provided an additional day in the hospital for
0.001 identification of the lesion.
0.006 Failure to recognize duodenal obstruction in the immediate
0.24 newborn period may result in clinically important metabolic
disturbances. The loss of gastric secretions with recurrent emesis
led to dehydration and hypochloremic metabolic alkalosis for
infants with delayed diagnosis in this study (Table 3). Although
such metabolic consequences have been described with duodenal
atresia, the clinical significance has not been noted. Previously
reported case series of duodenal atresia have focused on operative
complications and associated mortality.1,12,13 None of the reports
have discussed delayed diagnosis as a contributor to increased
morbidity or mortality. One of eight (12.5%) infants with delayed
diagnosis in our report died as a result of the metabolic and
pulmonary disturbances related to the proximal bowel obstruction.
The impact of the dehydration and alkalosis for the other infants is
unknown, although these disturbances required intravenous fluid
correction before surgery.
Newborns may routinely have small volume regurgitations up to
a few milliliters, especially when burping.14 However, clinicians
need to be vigilant when regurgitations persist or are associated
with other markers of possible gastrointestinal obstruction. In this
review, all infants with duodenal obstruction born by cesarean
section remained hospitalized long enough for the diagnosis to be
recognized and evaluated. Strict adherence to AAP (American
Academy of Pediatrics) and ACOG (American College of Obstetrics
and Gynecology) guidelines,15 which outline requirements for
hospital discharge before 48 h of life, including uncomplicated
pregnancy and successful feedings, may have facilitated earlier
consideration of anatomical obstruction for some of the other
infants. This report serves to remind the clinician that persistent
emesis in the newborn, even if low volume, should prompt further
evaluation before the discharge of the newborn, including careful
examination, assessment for excessive weight loss and selective use
of radiographic studies.
Conflict of interest
The authors declare no conflict of interest
Journal of Perinatology
 Congenital duodenal obstruction
H Kilbride et al
200
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