Duodenal Atresia and Stenosis

31
Emily Partridge and Holly L. Hedrick

Abstract
Congenital duodenal atresia and stenosis is a common cause of intestinal
obstruction in the neonate, with an incidence of 1 in 5000 to 10,000 live births
and an increased prevalence in males. More than 50% of affected patients have
associated congenital anomalies, including annular pancreas, intestinal malro-
tation, esophageal atresia, Meckel’s diverticulum, imperforate anus, renal
anomalies, lesions of the central nervous system, and biliary tract malforma-
tions. The most common anomalies associated with duodenal atresia include
Trisomy 21, diagnosed in one third of patients, and isolated cardiac defects,
which occur in approximately 30%. The presence of trisomy carries an
increased risk for congenital heart defects requiring operative repair.
Approximately 45% of patients are born prematurely, with one-third exhibit-
ing failure to thrive and persistent growth retardation. Presently, laparoscopic
or open duodenoduodenostomy has become the standard of care, with survival
rates of greater than 95% and mortality primarily attributed to associated
anomalies of other organ systems.

Keywords
Congenital duodenal obstruction • Prenatal diagnosis • Associated anoma-
lies • Embryology • Surgery • Outcomes

H.L. Hedrick, MD (*)

E. Partridge, MD, PhD
Center for Fetal Research, Children’s Hospital of
Philadelphia, Philadelphia, PA, USA
Department of Pediatric General, Thoracic, and Fetal
Surgery, Children’s Hospital of Philadelphia,
34th Street and Civic Center Boulevard, Wood, 5117
Philadelphia, PA, USA
Perelman School of Medicine at the University of
Pennsylvania, Philadelphia, PA, USA
Department of Pediatric General, Thoracic, and Fetal
Surgery, Children’s Hospital of Philadelphia,
34th Street and Civic Center Boulevard, Wood, 5117
Philadelphia, PA, USA
e-mail: Hedrick@email.chop.edu

© Springer-Verlag London Ltd., part of Springer Nature 2018 675

P.D. Losty et al. (eds.), Rickham’s Neonatal Surgery, https://doi.org/10.1007/978-1-4471-4721-3_31
676
31.1 Duodenal Atresia
and Stenosis
Congenital duodenal atresia and stenosis is a com-
mon cause of intestinal obstruction in the neonate,
with an incidence of 1 in 5000 to 10,000 live births
and an increased prevalence in males [1]. More
than 50% of affected patients have associated con-
genital anomalies, including annular pancreas,
intestinal malrotation, esophageal atresia, Meckel’s
diverticulum, imperforate anus, renal anomalies,
lesions of the central nervous system, and biliary
tract malformations [2]. The most common anom-
alies associated with duodenal atresia include
Trisomy 21, diagnosed in one third of patients [3],
and isolated cardiac defects, which occur in
approximately 30% [4]. The presence of trisomy
carries an increased risk for congenital heart
defects requiring operative repair [5].
Approximately 45% of patients are born prema-
turely, with one-third exhibiting failure to thrive
and persistent growth retardation [6]. Presently,
laparoscopic or open duodenoduodenostomy has
become the standard of care, with survival rates of
greater than 95% and mortality primarily attributed
to associated anomalies of other organ systems [7].
31.2 Etiology
Duodenal atresia occurs due to a failure of recana-
lization of the fetal duodenum, resulting in com-
plete obstruction. Early in the fourth week of
gestation, the duodenum develops from the distal
foregut and proximal midgut. During the fifth and
sixth weeks of gestation, the duodenal lumen is
temporarily obliterated due to proliferation of the
epithelium. Subsequently, degeneration of the epi-
thelial cells leads to recanalization of the duode-
num by the eleventh week of gestation. Embryonic
insult during this developmental window may
result in an intrinsic web, atresia or stenosis.
Unlike atresias distal to the Ligament of Treitz,
vascular insult is not thought to play a role in the
etiology of duodenal stenosis. Although no spe-
cific genetic mutation has been shown to correlate
with duodenal atresia, the coincidence of the con-
dition within sibling cohorts supports the likeli-
hood of an underlying genetic predisposition [8].
E. Partridge and H.L. Hedrick
31.3 Classification
Anatomically, congenital duodenal obstruction is
classified as either an atresia or stenosis. Incomp­
lete obstruction due to a fenestrated web or dia-
phragm is considered a stenosis, while atresias, or
complete obstructions, are classified into three
morphologic types [9]. Type I atresias account for
more than 90% of all congenital duodenal obstruc-
tions, and contain a luminal diaphragm including
mucosal and submucosal layers with an intact mes-
entery. A variant of type I duodenal atresia, the
‘windsock’ deformity, presents with distal dilation
of the luminal diaphragm, and may pose particular
challenges to surgical repair as a segment of dilated
duodenum may persist distally to the point of true
obstruction. Type II atresias account for less than
1% of all cases and are characterized by a segment
of proximal dilation and distal decompression con-
nected by a fibrous cord with an intact mesentery.
Type III atresias account for approximately 7% of
all cases, and are distinguished by a V-shaped mes-
enteric defect. There is no connection between the
blind proximal and distal duodenal segments.
31.4 Postnatal Presentation
The postnatal presentation of congenital duodenal
obstruction depends greatly on the grade of obstruc-
tion and its location in relation to the ampulla of Vater.
Neonates classically present with bilious vomiting in
the first hours of life, although in approximately 15%
of cases the obst­ruction occurs proximal to the ampulla,
resulting in non-bilious emesis [10]. The abdomen is
generally scaphoid, and abdominal distension is rarely
apparent [11]. Patients with incomplete obstruction, or
stenosis, may have a delayed presentation dependent
on the initiation of enteral feeds. Delayed diagnosis
can result in aspiration, dehydration and the develop-
ment of acid-base disorders.
Suspected cases of duodenal obstruction may
be confirmed by a plain upright X-ray of the
abdomen, with the classical finding of the “dou-
ble bubble” sign generated by the proximal left-­
sided air- and fluid-filled stomach tapering at the
pylorus and the distal dilated proximal duode-
num to the right of the midline (Fig. 31.1).
Generally the distal bowel is gasless, however in
31  Duodenal Atresia and Stenosis 677

cases of anomalous bifurcated bile duct with ter-
mination of one duct distal to the point of obstruc-
tion, distal gas may be visualized [12]. In the
setting of neonates who have undergone place-
ment of a nasogastric tube, 30–60 mLs of instilled
air may reproduce the “double bubble” sign, or a
limited upper gastrointestinal contrast study may
be performed to confirm the diagnosis and
exclude malrotation or volvulus.
Fig. 31.1  Duodenal atresia showing classic ‘double bub-
ble ‘sign features indicating proximal foregut obstruction
31.5 Prenatal Diagnosis
Advances in prenatal imaging have led to
increased diagnosis of a number of anomalies
of the gastrointestinal tract, including stenosis
and atresias of the small and large bowel [13].
Prenatal diagnosis may be made in as many as
50% of cases of congenital duodenal obstruc-
tion [14]. Prenatal diagnosis is more common
in the presence of other congenital anomalies,
and is therefore associated with higher overall
mortality rates [15]. Polyhydramnios is a fre-
quent complication in the setting of congenital
duodenal obstruction [16], and may prompt
increased imaging surveillance leading to
definitive diagnosis. Prenatal ultrasonography
may detect two fluid-filled structures consistent
with a double bubble sign (Fig. 31.2a). With the
advent of fetal MRI, detailed delineation of soft
tissue anomalies has become possible across a
wide range of gestational ages, and may be use-
ful in confirming the diagnosis and ruling out
other anomalies (Fig. 31.2b). Low fetal and
birth weight is also commonly observed, and
may be attributed in part to reduced swallowing
and transit of amniotic fluid through the fetal
bowel [17].
Duodenal atresia is most commonly prena-
tally diagnosed in the second half of pregnancy
[18], although cases of accurate diagnosis in the
first of early second trimester have been reported
[19, 20]. It has been hypothesized that the rela-
tively late appearance of significant duodenal dis-
tension may be attributed to immature fetal
swallowing and gastric emptying. Peristaltic
movement of the small intestine may be appreci-

a b

Fig. 31.2 Prenatal
radiographic imaging of
duodenal stenosis. (a)
Duodenal stenosis
imaged by
ultrasonography of the
fetus, with a “double-­
bubble” sign. (b)
Appearance of duodenal
stenosis by fetal
magnetic resonance
imaging
678 E. Partridge and H.L. Hedrick

ated by ultrasonography as early as 6–7 weeks tomotic complications in their cohort of 14

gestational age and may transiently mimic the patients [26]. The approach was widely adopted,
appearance of dilated intestinal segments, l­ eading although continued reports of complications
to the possibility of a false diagnosis [19]. including blind loop syndrome and duodenal dila-
Importantly, in cases of true obstruction the dila- tion requiring tapering [27] or duodenoplasty [28]
tion of the affected segment is observed con- prompted continued technical modifications. In
stantly, therefore scans of several minutes 1977, Kimura and colleagues reported an anasto-
duration are required to minimize the likelihood motic technique with a side-to-side duodenoduo-
of false positive diagnoses. denostomy closed in two layers with the bowel
incisions arranged to form a diamond-shaped
anastomosis to achieve a larger stoma [29]. The
31.6 Postnatal Management technique was widely adopted with a favorable
functional profile, and was further refined by
In suspected cases of duodenal stenosis or atresia, Kimura to incorporate a transverse incision on the
placement of a nasogastric tube is an appropriate distal end of the proximal duodenum and a longi-
initial maneuver to achieve gastric decompres- tudinal incision in the distal duodenum (Figs. 31.3
sion and reduce the risk of aspiration. After con- and 31.4). By this technique, bowel function is
firmation of the diagnosis by plain radiograph recovered in a significantly shorter time period
with or without contrast, a complete metabolic with a low incidence of complications and good
profile is obtained including complete blood cell long-term results [30]. The procedure of choice
count, electrolyte panel, blood gas, and coagula- for duodenal atresia, irregardless of type, is pres-
tion studies. Appropriate resuscitation is required ently duodenoduodenostomy with a proximal
to correct any underlying fluid imbalance or elec-
trolyte disorder. Due to the high risk of congeni-
tal heart disease in this patient population, cardiac
investigations including an electrocardiogram
and echocardiogram should be performed prior to
surgical intervention. Generally it is only in the
setting of an inability to exclude the possibility of
malrotation or volvulus that emergent surgical
intervention is undertaken.
Prior to the mid-1970s, duodenojejunostomy
was the preferred approach for correction of duo-
denal atresia [21]. Rarely, gastrojejunostomy was
performed as an alternative to duodenojejunos-
tomy [22], but was found to result in a high inci-
dence of marginal ulceration and bleeding [23].
Duodenojejunostomy was found to result in
delayed anastomotic function often requiring use
of parenteral nutrition or trans-anastomotic feed-
ing tubes [24]. Blind-loop syndrome and mega-
duodenum also appear to result more commonly
in patients treated with duodenojejunostomy, and
may require reoperation and conversion to a duo-
denoduodenostomy to achieve satisfactory func- Fig. 31.3  Kimura technique operative duodenal atresia
repair. A transverse incision is made in the distal portion
tional outcomes [25]. Weitzman and Brennan first
of the proximal obstructed duodenum segment. A longitu-
reported the results of a direct side-to-side duode- dinal incision is then created in the nearby portion of duo-
noduodenostomy approach in 1974, with no anas- denum distal to the site of the atretic obstruction
31  Duodenal Atresia and Stenosis
Fig. 31.4  A wide diamond shaped anastomosis is formed
by joining the two duodenal segments
transverse to distal longitudinal, or diamond-
shaped, anastomosis.
In the open approach, a right upper quadrant
supraumbilical incision is made, and the ascend-
ing and transverse colon is mobilized medially to
expose the duodenum. The position of the bowel
should be assessed at this time, as malrotation
may occur in up to 30% of cases of congenital
duodenal obstruction [31]. Eviscerating and posi-
tioning the small bowel and colon cephalad and
to the left of the incision achieves ideal exposure
of the third and fourth duodenum. The decom-
pressed duodenum is mobilized distal to the point
of obstruction to permit a tension-free anastomo-
sis. With the aid of tacking sutures, a transverse
duodenotomy is made in the anterior wall of the
distal portion of the distended proximal duode-
num, and a vertical duodenotomy is made on the
anti-mesenteric border of the distal duodenum.
To rule out an additional web or windsock defor-
mity, a catheter should be passed proximally into
the stomach and distally into the jejunum and
pulled back. The ends of the distal vertical duo-
denotomy incision are then approximated to the
679
mid-portion of the proximal transverse duode-
notomy incision with stay-sutures, and the poste-
rior wall of the anastomosis is constructed by
placing interrupted sutures using a repeating
bisecting technique. The anterior row of the anas-
tomosis is then completed in a similar fashion
(Figs. 31.3 and 31.4). In the setting of gross dila-
tion of the proximal segment, an anti-mesenteric
tapering duodenoplasty may be performed as to
expedite postoperative recovery of bowel func-
tion [32]. This may be performed by resection
using a gastrointestinal anastomosis (GIA) sta-
pler over a large red rubber catheter. Tapering is
performed on the anterior or anterolateral portion
of the proximal duodenum to avoid damage to the
common bile duct and ampulla of Vater. Finally,
the anastomosis is examined for patency, and the
intestine is returned to the abdomen. In cases of
malrotation, a formal Ladd’s procedure is per-
formed. Prior to closure of the abdomen, proper
positioning of the nasogastric tube is confirmed.
Placement of a transanastomotic feeding tube
may hasten the time to tolerance of full oral
­feeding [33], although the literature on this
approach is limited.
The laparoscopic approach to repair of con-
genital duodenal obstruction was first reported by
Rothenberg in [34], with no complications and
rapid initiation of oral feeds in the three patients
described. The laparoscopic approach begins
with insufflation of the abdomen through an
umbilical port, with two additional ports placed
in the right lower quadrant and the left mid-­
quadrant. A liver retractor may be placed via a
fourth port in the right or left upper quadrant as
indicated, or the liver may be retracted by place-
ment of a stay-suture around the falciform liga-
ment secured to the abdominal wall. The
duodenum is exposed and mobilized, and rota-
tional position of the bowel inspected. The proxi-
mal and distal duodenotomies are performed in a
manner similar to that utilized in the open
approach, with either running or single inter-
rupted sutures used to anastomose the anterior
and posterior walls. Alternatively, U-clips may
be used to perform the anastomosis, with favor-
able outcomes reported in one series to date [35].
Results of an additional series of seventeen neo-
680
nates undergoing laparoscopic repair following
Rothenberg’s initial report noted no intraopera-
tive complications, no conversions to open proce-
dures, and no anastomotic leaks [36]. Due to the
relatively recent advent of laparoscopic repair of
duodenal stenosis, long-term outcomes are not
yet reported in the literature. Reports of long-­
term complications and functional outcomes will
facilitate a critical comparison of open versus
laparoscopic repair of congenital duodenal
obst­ructions.
Postoperatively, total parenteral nutrition is
continued with monitoring of nasogastric tube
outputs, and feedings are initiated when the vol-
ume of nasogastric output is diminished and
non-bilious.
31.7 Outcomes
Early postoperative mortality for duodenal atre-
sia is low. The most common complication
encountered in the postoperative course is pro-
longed feeding intolerance. Prokinetic agents
may have some benefit in this population, with
one randomized controlled trial reporting shorter
duration of TPN requirements, earlier achieve-
ment of full enteral feeding, and reduced length
of hospitalization in a cohort of 30 neonates
undergoing primary anastomosis for congenital
small bowel atresias [37]. While some variability
in return of bowel function is expected, feeding
intolerance beyond the second week postopera-
tively should prompt concern for residual
obstruction, anastomotic stricture, or a compli-
cating motility disorder. An upper gastrointesti-
nal series is helpful to rule out anastomotic
stricture, although it should be noted that residual
dilation of the proximal duodenum may be appar-
ent for several months in the setting of a fully
functional anastomosis.
Long-term complications reported after
repair of duodenal obstruction include chronic
severe gastrointestinal reflux, bleeding peptic
ulcer, megaduodenum, gastritis, blind-loop syn-
drome, and adhesive bowel obstructions [38].
Patients with additional foregut anomalies,
including esophageal atresia and gastroduode-
nal motility disorders, are the most likely to
E. Partridge and H.L. Hedrick
have gastroesophageal reflux disease [39].
Dysmotility in duodenal atresia may be attrib-
uted to smooth muscle cell injury secondary to
ischemia or hypoplasia of the enteric nerves
[40], while the dilated proximal segment may be
associated with impaired transit and low con-
traction amplitude [41]. Megaduodenum may be
diagnosed up to eighteen years postoperatively,
and is associated with poor weight gain, fre-
quent emesis, abdominal pain, and blind-loop
syndrome [38]. An anti-­ mesenteric tapering
duodenoplasty may be performed to manage
cases of megaduodenum manifesting in the
postoperative period [42]. Overall survival rates
have improved over the past half-century from
45 to 95%, with the majority of deaths attributed
to complications arising from associated con-
genital anomalies [43]. Long-term follow-up is
essential for infants treated for congenital duo-
denal obstruction, with early diagnosis and
management of late complications to achieve
optimal outcomes.
References
1. Fonkalsrud EW, DeLorimier AA, Hays DM. Congenital
atresia and stenosis of the duodenum: a review com-
piled from members of the Surgical Section of the
American Academy of Pediatrics. Pediatrics. 1969;43:
79–83.
2. Litwin A, Avidor I, Schujman E, et al. Neonatal
intestina perforation caused by congenital defects
of the intestinal musculature. Am J Clin Pathol.
1984;81:77–80.
3. Stauffer UG, Irving I. Duodenal atresia and stenosis—
long-term results. Prog Pediatr Surg. 1977;10:49–60.
4. Buchin PJ, Levy JS, Schullinger JN. Down’s syndrome
and the gastrointestinal tract. J Clin Gastroenterol.
1986;8(2):111–4.
5. Keckler SJ, St Peter SD, Spilde TL, Ostlie DJ, Snyder
CL. The influence of trisomy 21 on the incidence and
severity of congenital heart defects in patients with
duodenal atresia. Pediatr Surg Int. 2008;24(8):921–3.
6. Grosfeld JL, Rescorla FJ. Duodenal atresia and ste-
nosis: reassessment of treatment and outcome based
on antenatal diagnosis, pathologic variance, and long-­
term follow-up. World J Surg. 1993;17:301–9.
7. Murshed R, Nicholls G, Spitz L. Intestinal duode-
nal obstruction: trends in management and outcome
over 45 years (1951–1995) with relevance to prenatal
counseling. Br J Obstet Gynecol. 1999;106:1197–9.
8. Gahukamble DB, Khamage AS, Shaheen AQ. Duodenal
atresia: its occurrence in siblings. J Pediatr Surg.
1994;29(12):1599–600.
31  Duodenal Atresia and Stenosis
9. Gray SW, Skandalakis JE. Embryology for surgeons.
Philadelphia, PA: Saunders Elsevier; 1975. p. 147–8.
10. Aguayo P, Ostlie DJ. Duodenal and intestinal atre-
sia and stenosis. In: Holcomb GW, Murphy JP, edi-
tors. Ashcraft’s pediatric surgery. Philadelphia, PA:
Saunders Elsevier; 2005. p. 400–5.
11. Kullendorff CM. Atresia of the small bowel. Annales
Chirurgiae et Gyneacologiae. 1983;72(4):192–5.
12. Komuro H, Ono K, Hoshino N, Urita Y, Gotoh C,
Fujishiro J, Shinkai T, Ikebukuro K. Bile duct duplica-
tion as a cause of distal bowel gas in neonatal duode-
nal obstruction. J Pediatr Surg. 2011;46(12):2301–4.
13. Benacerraf BB. The Sherlock Holmes approach
to diagnosing fetal syndromes by ultrasound. Clin
Obstet Gynecol. 2012;55(1):226–48.
14. Hemming V, Rankin J. Small intestinal atresia in a
defined population: occurrence, prenatal diagnosis
and survival. Prenat Diagn. 2007;27:1205–11.
15. Choudry MS, Rahman N, Boyd P, Lakhoo K. Duodenal
atresia: associated anomalies, prenatal diagnosis and
outcome. Pediatr Surg Int. 2009;25:727–30.
16. Dalla Vecchia LK, Grosfeld JL, West KW, Rescorla
FJ, Scherer LR, Engum SA. Intestinal atresia and
stenosis: a 25-year experience with 277 cases. Arch
Surg. 1998;133(5):490–6.
17. Francannet C, Robert E. Epidemiological study of
intestinal atresias: central-eastern France Registry
1976–1992. Journal de Gynecologie, Obstetrique et
Biologie de la Reproduction. 1996;25(5):485–94.
18. Hertzbery BS. Sonography of the fetal gastrointes-
tinal tract: anatomic variants, diagnostic pitfalls and
abnormalities. Am J Roentgenol. 1994;162:1175–82.
19. Zimmer EZ, Bronshtein M. Early diagnosis of duo-
denal atresia and possible sonographic pitfalls. Prenat
Diagn. 1996;16:564–6.
20. Tsukerman GL, Krapiva GA, Kirillova IA. First tri-
mester diagnosis of duodenal stenosis associated with
oesophageal atresia. Prenat Diagn. 1993;13:371–6.
21. Weber TR, Lewis JE, Mooney D, Connors R. Duodenal
atresia: a comparison of techniques of repair. J Pediatr
Surg. 1986;21:1133–6.
22. Puri P, Sweed Y. Duodenal obstructions. In: Puri
P, editor. Newborn surgery. Oxford: Botterworth-­
Heinemann; 1996. p. 290–7.
23. Buck P, Sacrez R, Juif JG, Beauvais P. Long delayed
compliations of gastrojejunostomy for duodenal steno-
sis in the newborn. Ann Chir Infant. 1962;3:130–5.
24. Becker JM, Schneider KM. Tube jejunostomy in the
treatment of upper intestinal obstruction in the neo-
nate. Surg Gynecol Obstet. 1963;116:123–5.
25. Rescorla FJ, Grosfeld JL. Duodenal atresia in infancy
and childhood: improved surgical survival and long-­
term follow-up. Contemp Surg. 1988;33:22–7.
26. Weitzman JJ, Brennan LP. An improved technique for
the correction of congenital duodenal obstruction in
the neonate. J Pediatr Surg. 1974;9(3):385–8.
27. Weisgerber G, Boureau M. Resultats immediats et
secondaires des duodeno-duodenostomies avec mod-
elage dans le traitement des obstructions duodenales
congenitales complete du nouveau-ne. Chirurgie
Pediatrique. 1982;23(6):369–72.
681
28. Dewan PA, Guiney EJ. Duodenoplasty in the manage-
ment of duodenal atresia. Pediatr Surg Int. 1990;5(4):
253–4.
29. Kimura K, Tsugawa C, Oqawa K, Matsumoto Y,
Yamamoto T, Asada S. Diamond-shaped anastomo-
sis for congenital duodenal obstruction. Arch Surg.
1977;112(10):1262–3.
30. Kimura K, Mukohara N, Nishijima E, Muraji T,
Tsugawa C, Matsumoto Y. Diamond-shaped anastomo-
sis for duodenal atresia: an experience with 44 patients
over 15 years. J Pediatr Surg. 1990;25(9):977–9.
31. Bailey PV, Tracy TF Jr, Connors RH, Mooney DP,
Lewis JE, Weber TR. Congenital duodenal obstruction:
a 32-year review. J Pediatr Surg. 1993;28(1):92–5.
32. Adzick NS, Harrison MR, de Lorimier AA. Tapering
duodenoplasty for megaduodenum associated with
duodenal atresia. J Pediatr Surg. 1989;21(4):311–2.
33. Arnbjörnsson E, Larsson M, Finkel Y, Karpe
B. Transanastomotic feeding tube after an operation
for duodenal atresia. Eur J Pediatr Surg. 2002;12(3):
159–62.
34. Rothenberg SS. Laparoscopic duodenoduodenostomy
for duodenal obstruction in infants and children. J
Pediatr Surg. 2002;37(7):1088–9.
35. Spilde TL, St Peter SD, Keckler SJ, Holcomb GW,
Snyder CL, Ostlie DJ. Open vs laparoscopic repair of
congenital duodenal obstructions: a concurrent series.
J Pediatr Surg. 2008;43(6):1002–5.
36. Kay S, Yoder S, Rothenberg S. Laparoscopic duo-
denoduodenostomy in the neonate. J Pediatr Surg.
2009;44(5):906–8.
37. Razzaq A, Safdar CA, Ali S. Erythromycin establishes
early oral feeding in neonates operated for congeni-
tal intestinal atresias. Pediatr Surg Int. 2009;25(4):
361–4.
38. Spigland N, Yazbeck S. Complications associ-
ated with surgical treatment of congenital intrin-
sic duodenal obstruction. J Pediatr Surg. 1990;25:
1127–30.
39. Hassall E. Wrap session: Is the Nissen slipping?
Can medical treatment replace surgery for severe
gastroesophageal reflux disease in children? Am J
Gastroenterol. 1995;90:1212–20.
40. Molenaar JC, Tibboel D, van der Kamp AW, Meijers
JH. Diagnosis of innervation-related motility disorders
of the gut and basic aspects of enteric nervous system
development. Prog Pediatr Surg. 1989;24:173–85.
41. Takahashi A, Tomomasa T, Suzuki N, Kuroiwa M,
Ikeda H, Morikawa A, Matsuyama S, Tsuchida Y. The
relationship between disturbed transit and dilated
bowel, and manometric findings of dilated bowel in
patients with duodenal atresia and stenosis. J Pediatr
Surg. 1997;32(8):1157–60.
42. Ein SH, Shandling B. The late nonfunctioning duo-
denal atresia repair. J Pediatr Surg. 1986;21(9):
798–801.
43. Escobar MA, Ladd AP, Grosfeld JL, West KW,
Rescorla FJ, Scherer LR, Engum SA, Rouse TM,
Billmire DF. Duodenal atresia and stenosis: long-­term
follow-up over 30 years. J Pediatr Surg. 2004;39(6):
867–71.