eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Duodenal Atresia

Frederick Merrill Karrer, MD, The David R and Kiku Akers Chair in Pediatric Surgery, The Children's Hospital; Head, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, University of Colorado School of Medicine
D Dean Potter, MD, Fellow in Pediatric Surgery, The Children's Hospital; Casey M Calkins, MD, Assistant Professor of Surgery, Division of Pediatric Surgery, Department of Pediatric Surgery, Medical College of Wisconsin; Consulting Staff, Children's Hospital of Wisconsin

Updated: Mar 3, 2009

Introduction

Relatively speaking, congenital duodenal atresia is one of the more common intestinal anomalies treated by pediatric surgeons, occurring 1 in 2500-5000 live births. In 25-40% of cases, the anomaly is encountered in an infant with trisomy 21 (Down syndrome).¹ The definitive intervention to correct the anomaly is surgical and consists of duodenoduodenostomy in the newborn period.

History of the Procedure

Calder published the first report of duodenal obstruction in 1733 when he described 2 children with "preternatural confirmation of the guts." Both infants died, as did subsequently reported infants with this defect. Scattered reports of duodenal obstruction appeared in the European literature over ensuing years. In 1916, the first survivor was reported, yet survival in the early 20th century remained rare. Morbidity and mortality significantly improved only over the last 50 years.² Because of progress in pediatric anesthesia, neonatology, and surgical techniques, survival is about 90% in infants who present with this anomaly. The standard operative procedure today consists of duodenoduodenostomy via a right upper quadrant incision, although recent advancements have enabled some surgeons to repair the defect by minimally invasive means.^3,4

Problem

Differential diagnosis of neonatal upper GI obstruction includes the following:

• Esophageal atresia
• Malrotation with midgut volvulus
• Pyloric stenosis
• Duodenal atresia and stenosis
• Annular pancreas
• Preduodenal portal vein
• Any intestinal atresia
• Duodenal duplication
• Foreign body obstruction
• Hirschsprung disease
• Gastroesophageal reflux

Duodenal obstruction may be complete or incomplete.

Complete duodenal obstruction.

Incomplete duodenal obstruction (duodenal stenosis).

Duodenal atresia can take many forms, but proximal and distal intestinal segments always end blindly. The intestine on either side of the defect may be in apposition (type 1), separated by a fibrous cord (type 2), or gap (type 3). Regardless of atresia severity, the proximal intestinal segment is typically dilated and the distal segment empty; these are hallmarks of duodenal atresia. Although obstruction may occur anywhere within the duodenum, it is most common in the vicinity of the ampulla of Vater.

Stenosis may manifest as a stricture or a perforated intraluminal diaphragm. The perforation within the diaphragm is usually singular and centrally located within the lumen of the duodenum, although variations have been reported. A windsock abnormality is a thin diaphragm that has ballooned distally as a result of peristalsis. Together, both duodenal atresia and stenosis comprise a frequent cause of intestinal obstruction in the newborn.³

Frequency

Reported incidence rates range from 1:2,500 to 1:40,000 live births; published rates in the United States and internationally do not appear to differ. Duodenal atresia is not usually regarded as a familial condition, despite isolated reports of this condition in multiple siblings.

Etiology

Although the underlying cause of duodenal atresia remains unknown, its pathophysiology has been well described. Frequent association of duodenal atresia or stenosis with other neonatal malformations suggests both anomalies are due to a development error in the early period of gestation. Duodenal atresia differs from other atresias of the small and large bowel, which are isolated anomalies caused by mesenteric vascular accidents during later stages of development. No predisposing maternal risk factors are known. Although up to one third of patients with duodenal atresia have Down syndrome (trisomy 21), it is not an independent risk factor for developing duodenal atresia.³

Pathophysiology

Duodenal maldevelopment occurs secondary to either inadequate endodermal proliferation (gut elongation outpaces proliferation) or failure of the epithelial solid cord to recanalize (failure of vacuolization).

Multiple investigators have demonstrated that the epithelium of the duodenum proliferates during 30-60 days' gestation, completely plugging the duodenal lumen. A subsequent process termed vacuolation occurs whereby the solid duodenum is recanalized. Vacuolation is believed to occur by way of apoptosis, or programmed cell death, which occurs during normal development within the lumen of the duodenum. Occasionally, duodenal atresia is associated with annular pancreas—pancreatic tissue that surrounds the entire circumference of the duodenum. This is likely due to failure of duodenal development rather than robust and/or abnormal growth of the pancreatic buds.

At the cellular level, the GI tract develops from the embryonic gut, which is composed of an epithelium derived from endoderm, surrounded by cells of mesodermal origin. Cell signaling between these two embryonic layers appears to play a critical role in coordinating patterning and organogenesis of the duodenum. Sonic hedgehog genes encode members of the Hedgehog family of cell signals. Both are expressed in gut endoderm, whereas target genes are expressed in discrete layers in the mesoderm. Mice with genetically altered sonic hedgehog signaling display duodenal stenosis, which suggests that genetic defects in the sonic hedgehog family of genes may influence the development of duodenal abnormalities.

Presentation

Duodenal atresia is a disease of newborn infants. Cases of duodenal stenosis or perforated duodenal web (diaphragm) rarely remain undiagnosed until childhood or adulthood; these cases represent the exception rather than the rule. Duodenal atresia appears to be equally distributed between infants of both sexes, with no reported predilection for one race.

The use of modern ultrasonography has allowed many infants with duodenal obstruction to be identified prenatally. In a large cohort study of 18 different congenital malformation registries from 11 European countries, 52% of infants with duodenal obstruction were identified in utero.⁵ Duodenal obstruction is characterized by a double-bubble sign on prenatal ultrasonography. The first bubble corresponds to the stomach and the second to the postpyloric and prestenotic dilated duodenal loop. Prenatal diagnosis allows the mother the opportunity to receive prenatal counseling and to consider delivery at or near a tertiary care facility that is able to care for infants with GI anomalies.^5,6

Presenting symptoms and signs are the result of high intestinal obstruction. Duodenal atresia is typically characterized by onset of vomiting within hours of birth. While vomitus is most often bilious, it may be nonbilious because 15% of defects occur proximal to the ampulla of Vater. Occasionally, infants with duodenal stenosis escape detection of an abnormality and proceed into childhood or, rarely, into adulthood before a partial obstruction is noted. Nevertheless, one should assume any child with bilious vomiting has a proximal GI obstruction until proven otherwise, and further workup should be begun expeditiously.

Once delivered, an infant with duodenal atresia typically has a scaphoid abdomen. One may occasionally note epigastric fullness from dilation of the stomach and proximal duodenum. Passing meconium within the first 24 hours of life is not usually altered. Dehydration, weight loss, and electrolyte imbalance soon follow unless fluid and electrolyte losses are adequately replaced. If intravenous (IV) hydration is not begun, a hypokalemic/hypochloremic metabolic alkalosis with paradoxical aciduria develops, as with other high GI obstruction. An orogastric (OG) tube in an infant with suspected duodenal obstruction typically yields a significant amount of bile-stained fluid.

Indications

Although duodenal atresia is a surgically treated disease, operating on an infant with duodenal obstruction in the middle of the night is unnecessary. Only 2 limitations apply to timing the repair: stabilization of the fluid and electrolyte balance and exclusion of overwhelming congenital defects that would preclude use of a general anesthetic (ie, complex congenital heart disease). Correction can begin any time after these issues are addressed and optimized.

Relevant Anatomy

Relevant anatomy of duodenal atresia is addressed in Problem.

Contraindications

Contraindications to immediate repair include electrolyte or fluid balance disturbances; severe cardiac defects, which should be repaired prior to addressing the duodenal abnormality; and severe respiratory insufficiency that would preclude a safe operation. Infants can be maintained on orogastric OG suction and intravenous nutrition with aggressive repletion of fluid and electrolyte losses while these life-threatening issues are addressed.

Workup

Laboratory Studies

The following studies are indicated in duodenal atresia:

• Serum electrolytes
  • Once delivered, neonates must be resuscitated well and electrolyte disturbances must be corrected prior to repair of duodenal atresia.
  • If duodenal atresia is diagnosed early, electrolyte and fluid balance should be normal. If the diagnosis is delayed at all, laboratory assessment of electrolyte and fluid status is imperative for an infant with duodenal atresia. As noted above, prolonged vomiting can result in a hypokalemic/hypochloremic metabolic alkalosis with paradoxical aciduria.
  • Obtain blood to measure serum electrolytes in order to confirm electrolyte status to prepare for adequate resuscitation.
• Urinalysis
  • Urine specific gravity can serve as a reliable indicator of fluid status.
  • Fluid status can also be adequately assessed by urine output, capillary refill, mucous membrane examination, and fontanelle character.
• Chromosome analysis: When trisomy 21 is suspected, a full genetic analysis should be performed; however, but this is not necessary to obtain prior to operative repair of the duodenal anomaly.

Imaging Studies

• Prenatal ultrasonography
  • Perform prenatal ultrasonography during any pregnancy with associated polyhydramnios. Examination of a fetus with duodenal atresia may reveal a dilated fluid-filled stomach and duodenum in addition to other (eg, cardiac) abnormalities. However, absence of these findings does not rule out duodenal obstruction.
  • Fetal vomiting may be associated with normal ultrasonographic findings in the presence of a duodenal atresia. Mothers with amniotic fluid abnormalities should be monitored with repeat scans.
  • Prenatal ultrasonography does not detect duodenal stenosis. Diagnosis prior to birth enables prenatal consultation with a pediatric surgeon and provides parents an opportunity to discuss plans for postnatal care and management.
• Erect and recumbent plain radiography of the abdomen
  • When duodenal atresia is suspected, erect and recumbent plain radiography of the abdomen should be the first imaging study obtained.
  • A characteristic finding of duodenal obstruction is the double-bubble image of an air-filled stomach proximal to an air-filled first portion of the duodenum. Absence of gas in the remaining small and large bowel suggests atresia, whereas scattered amounts of gas distal to the obstruction suggests stenosis or malrotation/volvulus.
• Cardiac and/or renal ultrasonography: Ultrasonography of the heart and kidneys may be warranted to identify potentially life-threatening abnormalities prior to definitive repair of the duodenal obstruction.
• Upper GI contrast evaluation
  • Upper GI contrast evaluation in the infant with duodenal atresias is unnecessary unless correction is going to be delayed.
  • An upper GI contrast study may be useful if surgery is delayed to detect the presence of malrotation with midgut volvulus or to confirm the presence of an intrinsic duodenal obstruction.

Histologic Findings

• Histologic examination is rarely performed or necessary because repair does not involve removal of the obstruction.

Treatment

Medical Therapy

No medical therapies are available for the definitive treatment of duodenal atresia or stenosis; all treatment is surgical. Adequate intravenous (IV) hydration, total parenteral nutrition, and gastric decompression are essential until the neonate has been stabilized for surgical repair.

Surgical Therapy

Duodenal atresia and stenosis are treated surgically. In patients with duodenal obstruction, a duodenoduodenostomy is the most commonly performed procedure. A duodenojejunostomy is now uncommonly performed due to its higher risk of long-term complications. Duodenal repair may be performed via a right upper quadrant incision, an umbilical incision, or laparoscopically, depending on surgeon preference.

Preoperative Details

Little preoperative preparation is necessary if the diagnosis is secured within the first 24 hours. Placement of an orogastric (OG) tube and maintenance of intravenous (IV) hydration is mandatory in all infants with duodenal obstruction. If prolonged OG suction is necessary, IV fluid replacement of the gastric aspirate with one half normal saline with added potassium should be administered. Prior to proceeding with operative repair, the surgeon should ensure that both fluid and electrolyte derangements are adequately corrected. The surgeon should also perform a thorough examination of the infant, with special attention to cardiac and pulmonary function before undertaking duodenal repair.

Intraoperative Details

As with all neonatal surgery, pay attention to preserving body temperature. Coordination with an anesthesiologist with specialized training in neonatal surgery is advantageous when possible because advances in pediatric anesthesia have contributed to improved overall survival of these infants. When ready to proceed, the abdomen is entered through a transverse skin incision begun 2 cm above the umbilicus from the midline and extending approximately 5 cm into the right upper quadrant (see Media file 3).

Incision for duodenal exposure.

Thoroughly explore the abdomen for evidence of other abnormalities. Then mobilize the duodenum using the Kocher maneuver and use an OG tube to determine the location of the obstruction without opening the stomach. The stomach and proximal duodenum are often thickened and dilated. When a significant gap is present between the proximal and distal ends, the distal duodenum must be adequately mobilized.

The authors prefer a duodenoduodenostomy for repair, when possible. This may be performed in either a side-to-side or a diamond-shaped fashion (authors' preference). For the side-to-side technique (see Media file 4), make parallel incisions in both the proximal and distal segments.

Side-to-side duodenoduodenostomy.

Diamond-shaped duodenoduodenostomy.

In patients with a duodenal web, the surgeon can identify the site of the web's origin by passing the OG tube through the pylorus into the duodenum and noting the indentation of the duodenal wall caused by tenting of the web. A duodenotomy can be performed along the site of this indentation. Again, prior to repair, examine the distal duodenum for a second defect. Thereafter, the surgeon must identify the ampulla and note its relationship to the web because the medial portion of most of these defects is located close to the ampulla. Accordingly, excision of the web should proceed from the lateral duodenal wall, leaving the medial third of the web alone to avoid damaging the sphincter of Oddi or ampulla. Oversew the resection line with 4.0 Dexon and close the duodenotomy either longitudinally or transversely in one layer as described above.

In patients with an annular pancreas, pancreatic tissue should not be divided for fear of pancreatic fistula. Instead, a diamond-type or side-to-side duodenoduodenostomy is recommended. Patients who present with associated malrotation should undergo a Ladd procedure at the time of duodenal repair. Although gastrostomy tubes were often used in the past, complications associated with their placement and long-term problems with gastroesophageal reflux (following gastrostomy) have prompted the authors to avoid these adjuncts, except in cases where gastrostomy is likely to be needed in the future (ie, an infant with trisomy 21 and complex congenital heart disease).⁷

If possible, the authors prefer placement a small, transanastomotic feeding tube (5F silastic nasojejunal feeding tube) across the anastomosis to facilitate postoperative enteral feeding. The authors also always leave an OG tube in place for gastric decompression. One should consider placing a peripheral intravenous central catheter (PICC) or central intravenous catheter at the time of operation because of the expected prolonged ileus and the need for parenteral nutrition.

Many patients have a very dilated proximal duodenum at the time of initial repair.  In patients with an extensively floppy and distended duodenum (megaduodenum) with persistent symptoms of obstruction, an antimesenteric tapering duodenoplasty can be used to address duodenal dysmotility. An autostapling device is the most common method to resect excess duodenal tissue. Alternatively, resection with a 2-layer closure or plication with interrupted sutures over a dilator can be used. In most cases, the proximal dilatation of the duodenum resolves with time after a successful duodenoduodenostomy. A small number of infants develop megaduodenum later in life. However, the authors do not recommend duodenoplasty at the initial operation.^8,9

Close the abdominal wound in layers. Close the peritoneum and posterior fascia separately from the anterior fascia, using 4.0 PDS or Vicryl suture. Close the skin with a running subcuticular suture of 5.0 Vicryl.

An umbilical approach for the treatment of pyloric stenosis was described in 1986; recently, this incision has been applied to other intra-abdominal anomalies such as duodenal atresia and stenosis. A semicircular umbilical incision is made in a skin fold and the peritoneum is entered in the midline. The pliability of the neonatal abdominal wall allows retraction to expose the right upper quadrant. Repair of the duodenal anomaly proceeds in a similar fashion as described above.¹⁰

For the laparoscopic approach, neonatal laparoscopic instruments (3 mm) and trocars are used. The patient is placed supine at the end of the operating table. The operating surgeon stands at the patient's feet. The abdomen is insufflated through a 5-mm umbilical port. Two other ports, one 3 mm and one 5 mm are placed in the right lower quadrant and left mid quadrant, respectively. The left mid-quadrant port is placed for the introduction of suture. At times, a fourth port is placed in the right upper quadrant to retract the liver. After the duodenum is Kocherized, the site of the obstruction typically becomes easily visible. A standard diamond anastomosis is then performed using interrupted sutures or u-clips (see Media file 6).¹¹
 

Upper GI contrast study following laparoscopic duodenal atresia repair. No leak is present, and an open anastomosis is shown. The white arrow highlights the anastomosis, which was performed using u-clips.

As with the open repair, stay sutures are placed at each corner to facilitate the anastomosis. The distal bowel is then examined to identify another distal atretic segment or suggestion of a web. Once completed, the ports are removed and the sites are closed with absorbable suture.

One retrospective case series compared the right upper quadrant incision to a laparoscopic repair for duodenal atresia or stenosis.¹²  Fourteen patients were in the open group, and 15 patients were in the laparoscopic cohort. No anastomotic leaks were reported in either group. Patients that underwent a laparoscopic repair were advanced to full feeding quicker (9 d vs 17 d) and were discharged from the hospital sooner (13 d vs 20 d) compared with patients who underwent open repair.

Postoperative Details

Nutrition should be provided by intravenous alimentation or via a transanastomotic feeding tube. Maintain low intermittent suction on an OG tube until stool is passed and drainage from the OG is less than 1 mL/kg/h and is clear. Feeding can then be advanced slowly by mouth.

Follow-up

See infants 2 weeks following discharge from the neonatal intensive care unit to assess wound healing and ensure adequacy of nutrition and gastrointestinal function. Thereafter, see infants on a yearly basis to assess for the long-term complications of duodenal repair and to ensure that current practices are not contributing to long-term morbidity.

Complications

Despite improvements in early mortality rates, as many as 22% of children may incur late complications. Late complications include blind-loop syndrome, megaduodenum with altered duodenal motility, gastritis with duodenal-gastric reflux, peptic ulcer, esophagitis and gastroesophageal reflux, pancreatitis, and cholecystitis. Blind-loop syndrome can be corrected by conversion to a duodenoduodenostomy. Megaduodenum with abnormal duodenal motility can be addressed by performing a tapering duodenoplasty. Today, these issues may be addressed at the time of initial operation by performing the duodenoduodenostomy along with duodenoplasty when necessary.^13,14,15

Outcome and Prognosis

The overall mortality rate for infants with duodenal atresia was 33% in a large series published in 1967. Today, the early mortality rate associated with this condition has declined to approximately 3% in most series. Most deaths occurring in association with duodenal atresia are attributed to the presence of multiple associated anomalies (usually complex cardiac defects). Improvement in survival rates is most likely a result of advances in neonatal care such as high-frequency ventilation, surfactant supplementation, nutritional support, pediatric anesthesia, and sophisticated cardiac surgery. Long-term survival is excellent at rates reported between 86% and 90%.

Future and Controversies

Endoscopic excision of a duodenal web is possible but is not widely practiced and is of questionable efficacy because of the precision required to avoid damaging the ampulla when excising the membrane. Laparoscopic duodenoduodenostomy is a reasonable undertaking when the surgeon is comfortable with advanced minimally invasive techniques in infants. The ideal candidate for a laparoscopic intervention is an infant of reasonable size (>2.5 kg) without significant congenital cardiac disease. The latter may preclude maintenance of a pneumoperitoneum, which is necessary to complete the procedure safely.

Timing for the initiation of oral feeds has been traditionally based on return of bowel function (ie, passage of stool, decreased orogastric [OG] tube aspirate volume and change from bilious to clear gastric fluid). However, routine postoperative fluoroscopic evaluation for duodenal leak after laparoscopic repair has contributed to earlier initiation of oral feeds and quicker discharge from the hospital. Routine use of fluoroscopic evaluation, regardless of the technique of duodenal repair, may reduce the need for parenteral nutrition and decrease the length of hospital stays.¹²

The value of gastrostomy at the time of duodenal repair remains controversial. In 1969, some 80% of pediatric surgeons surveyed routinely used gastrostomy. Some purport large-caliber gastrostomy offers better gastric drainage when compared to an OG tube, but the authors have had little difficulty in achieving adequate gastric decompression with OG tubes. The authors believe that a gastrostomy tube adds no advantage in postoperative management, and it may contribute to late development of gastroesophageal reflux.

The authors use a transanastomotic feeding tube when it can be easily accomplished at the time of surgery. If the tube does not easily pass into the upper jejunum, attempts to place it are abandoned. A transanastomotic tube protects the anastomosis in the early postoperative period when reinstituting feeding and has low risk of causing postoperative complications. Previous worries of anastomotic complications following transanastomotic tube placement are no longer justified. The slender silicone character of newer tubes remains supple in the lumen of the bowel unlike earlier polythene and plastic tubes, which hardened in situ. Nevertheless, pediatric surgeons remain divided in their use of transanastomotic tubes.

Multimedia

Media file 1: Complete duodenal obstruction.

Media file 2: Incomplete duodenal obstruction (duodenal stenosis).

Media file 3: Incision for duodenal exposure.

Media file 4: Side-to-side duodenoduodenostomy.

Media file 5: Diamond-shaped duodenoduodenostomy.

Media file 6: Upper GI contrast study following laparoscopic duodenal atresia repair. No leak is present, and an open anastomosis is shown. The white arrow highlights the anastomosis, which was performed using u-clips.

References

1. Freeman SB, Torfs CP, Romitti PA, et al. Congenital gastrointestinal defects in Down syndrome: a report from the Atlanta and National Down Syndrome Projects. Clin Genet. Feb 2009;75(2):180-4. [Medline].

2. Piper HG, Alesbury J, Waterford SD, Zurakowski D, Jaksic T. Intestinal atresias: factors affecting clinical outcomes. J Pediatr Surg. Jul 2008;43(7):1244-8. [Medline].

3. AppleBaum H, Lee SL, Puapong DP. Duodenal atresia and stenosis – annular pancreas. In: Grosfeld, O'Neill, Fonkalsrud, and Coran. Pediatric Surgery. Philadelphia, PA: Mosby Elsevier; 2006:1260-1268.

4. Aubrespy P, Derlon S, Seriat-Gautier B. Congenital duodenal obstruction: a review of 82 cases. Prog Pediatr Surg. 1978;11:109-24. [Medline].

5. Haeusler MC, Berghold A, Stoll C, et al. Prenatal ultrasonographic detection of gastrointestinal obstruction: results from 18 European congenital anomaly registries. Prenat Diagn. Jul 2002;22(7):616-23. [Medline].

6. Hancock BJ, Wiseman NE. Congenital duodenal obstruction: the impact of an antenatal diagnosis. J Pediatr Surg. Oct 1989;24(10):1027-31. [Medline].

7. Fonkalsrud EW, DeLorimier AA, Hays DM. Congenital atresia and stenosis of the duodenum. A review compiled from the members of the Surgical Section of the American Academy of Pediatrics. Pediatrics. Jan 1969;43(1):79-83. [Medline].

8. Adzick NS, Harrison MR, deLorimier AA. Tapering duodenoplasty for megaduodenum associated with duodenal atresia. J Pediatr Surg. Apr 1986;21(4):311-2. [Medline].

9. Ein SH, Shandling B. The late nonfunctioning duodenal atresia repair. J Pediatr Surg. Sep 1986;21(9):798-801. [Medline].

10. Soutter AD, Askew AA. Transumbilical laparotomy in infants: a novel approach for a wide variety of surgical disease. J Pediatr Surg. Jun 2003;38(6):950-2. [Medline].

11. Rothenberg SS. Laparoscopic duodenoduodenostomy for duodenal obstruction in infants and children. J Pediatr Surg. Jul 2002;37(7):1088-9. [Medline].

12. Spilde TL, St Peter SD, Keckler SJ, Holcomb GW 3rd, Snyder CL, Ostlie DJ. Open vs laparoscopic repair of congenital duodenal obstructions: a concurrent series. J Pediatr Surg. Jun 2008;43(6):1002-5. [Medline].

13. Escobar MA, Ladd AP, Grosfeld JL, et al. Duodenal atresia and stenosis: long-term follow-up over 30 years. J Pediatr Surg. Jun 2004;39(6):867-71; discussion 867-71. [Medline].

14. Grosfeld JL, Rescorla FJ. Duodenal atresia and stenosis: reassessment of treatment and outcome based on antenatal diagnosis, pathologic variance, and long-term follow-up. World J Surg. May-Jun 1993;17(3):301-9. [Medline].

15. Spigland N, Yazbeck S. Complications associated with surgical treatment of congenital intrinsic duodenal obstruction. J Pediatr Surg. Nov 1990;25(11):1127-30. [Medline].

Keywords

duodenal atresia, duodenal obstruction, duodenal abnormalities, intrinsic duodenal obstruction, duodenal stenosis, Down syndrome, trisomy 21, duodenoduodenostomy, upper GI obstruction, esophageal atresia, malrotation with midgut volvulus, pyloric stenosis, annular pancreas, preduodenal portal vein, atresia, foreign body obstruction, Hirschsprung disease, gastroesophageal reflux, atresias of the small and large bowel, duodenal maldevelopment, vomiting, hypokalemic/hypochloremic metabolic alkalosis, complex congenital heart disease, polyhydramnios

Contributor Information and Disclosures

Author

Frederick Merrill Karrer, MD, The David R and Kiku Akers Chair in Pediatric Surgery, The Children's Hospital; Head, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, University of Colorado School of Medicine
Frederick Merrill Karrer, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society of Transplant Surgeons, and Western Surgical Association
Disclosure: Nothing to disclose.

Coauthor(s)

D Dean Potter, MD, Fellow in Pediatric Surgery, The Children's Hospital
D Dean Potter, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, International Pediatric Endosurgery Group, and Minnesota Medical Association
Disclosure: Nothing to disclose.

Casey M Calkins, MD, Assistant Professor of Surgery, Division of Pediatric Surgery, Department of Pediatric Surgery, Medical College of Wisconsin; Consulting Staff, Children's Hospital of Wisconsin
Casey M Calkins, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, and American Pediatric Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

Jayant Deodhar, MD, Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

David A Piccoli, MD, Chief, Division of Gastroenterology and Nutrition, Department of Pediatrics, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine
David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, State University of New York, Downstate Medical Center College of Medicine; Distinguished Lecturer, New York Medical College, School of Public Health
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

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