Gastrointestinal (GI) duplications are rare congenital malformations that may vary greatly in presentation, size, location, and symptoms. 
In 1733, Calder published the first report of an intestinal duplication. In 1937, Ladd introduced the term duplication of the alimentary tract. This condition consists of a group of congenital anomalies with the following three characteristics:
A well-developed coat of smooth muscle is present
The epithelial lining represents some portion of the alimentary tract
Duplications are frequently intimately attached to some portion of the GI tract
Alimentary tract duplications are uncommon and may present as solid or cystic tumors, intussusception, perforation, or GI bleeding. A high index of suspicion is required in such cases. Appropriate investigations, including imaging techniques, should be directed toward adequate and planned surgery. GI duplications have an extremely variable presentation, and surgical management depends on the location, size, and shape of the duplication. Controversies and future management strategies are related to management of duplications, as well as the associated anomalies.
GI duplications may be divided into the following types:
Thoracic and thoracoabdominal duplications
Other small-intestine duplications
Cervical duplications are generally duplications of the esophagus.
In as many as one third of thoracic and thoracoabdominal duplications, there is a second or third duplication cyst below the diaphragm; therefore, computed tomography (CT) should include the abdomen. Almost all patients with thoracic or thoracoabdominal duplications have vertebral anomalies, and the central nervous system (CNS) may be involved. The histological similarity and anatomic proximity of bronchogenic cysts and intramural esophageal duplications supports their common origin. 
Gastric duplications are generally cystic. They are generally located on the greater curvature and have no communication to the stomach.
Duodenal duplications generally do not communicate with the intestinal lumen. They can arise from the bile ducts or the pancreas.
Most small-intestine duplications are located in the ileum. Duplications may be cystic or tubular and are located on the mesenteric border, often sharing a common muscular wall and blood supply with the native intestine. Multiple small-intestine duplications may be present. 
Cystic colonic duplications may be isolated or may have an external fistula to the skin, urinary tract, or normal colon. Tubular colonic duplications can also occur with duplication or triplication of the colon. Tubular duplication of the colon is often associated with duplication of the anus, vagina, and penis. Multiple short-segment duplications of the colon may also be present. 
Rectal duplications occur in the retrorectal space.
Associated anomalies are common with certain duplications, and screening for these anomalies should be performed in appropriate patients. The following are examples:
Thoracoabdominal duplications - Vertebral anomalies (approximately 75%)
Enteric cystic duplications - Intestinal atresias
Tubular hindgut duplications - Genitourinary malformations
GI duplications are most frequently single, tubular, or cystic and are most often located on the mesenteric side of the native alimentary tract structure. Symptoms are often related to the location of the duplication; oral and esophageal lesions can create respiratory difficulties, whereas lower GI lesions may cause nausea, vomiting,  bleeding, perforation, or obstruction. 
Patients with cervical esophageal duplications or thoracic/thoracoabdominal duplications may present with respiratory distress that is caused by compression of the airway; this can be life-threatening.
The presence of heterotopic mucosa (eg, gastric mucosa) in a duplication can lead to peptic ulcerations, bleeding, and perforation with peritonitis.
Neoplastic changes have been reported in GI duplications.
The true etiology of GI tract duplications is not known.  Several theories have been postulated.
The idea that the initial developmental abnormality occurs in the gastrulation stage and results in a split notochord has been proposed. During early embryogenesis, the notochord is open, and the endoderm of the yolk sac and the ectoderm of the notochord are fused; a tube called the neuroenteric canal connects the yolk sac and the amnion.
As part of the development of the split notochord, an endodermal-ectodermal adhesion between the cord has been proposed to result in the persistence of an endomesenchymal tract between the yolk sac and the amnion. The endomesenchymal tract formed is responsible for the anomalies of the entire GI system. However, not all duplications are compatible with this theory, and other etiologies have been proposed.
Some duplications of the foregut and hindgut may result from "partial twinning." These duplications may be associated with other paired structures, such as those found in the genital and urinary tract. Other duplications, especially those of the ileum, may occur as a result of persistent embryologic diverticula. Some portions of the intestinal tract have a solid stage during development; therefore, duplications of these structures may result from "aberrant luminal recanalization." Finally, intrauterine environmental factors, such as trauma or hypoxia during a vascular accident, may cause duplications at any level of the GI tract.
GI duplications are observed in 1 of every 4500 autopsies, predominantly in white males. Synchronous GI duplications occur in as many as 15% of patients. Relative frequencies of the various types are as follows:
Cervical duplications - Cervical esophageal duplication cysts are the most unusual GI duplication, with fewer than 10 cases reported
Thoracic and thoracoabdominal duplications - These make up 4% of all GI duplications
Gastric duplications - These account for 7% of all GI duplications
Pyloric duplications - These are extremely rare; however, they are reported in the literature 
Duodenal duplications - These account for 5% of all GI duplications
Small-intestine duplications - The small intestine is the most frequent site of GI duplications, accounting for 44% of cases 
Colonic duplications - These may be cystic or tubular; they represent 15% percent of duplications
Rectal duplications - These represent up to 5% of GI duplications 
The outcome of surgical (or medical) management of GI duplications is favorable. Metaplastic changes that have been reported in untreated GI duplications can be prevented, depending on the location of the duplication, by appropriate surgical intervention.
The severity and types of malformations associated with GI duplications play a significant role in determining morbidity and mortality.