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INTRODUCTION

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Enteric (or alimentary tract) duplications are typically benign congenital lesions that can occur anywhere from the mouth to the anus. They are frequently recognized in the first 2 years of life. Enteric duplications often are asymptomatic and discovered incidentally, or can present with symptoms of bleeding or obstruction. They typically are lined by intestinal epithelium and may communicate with the normal intestinal lumen. Mesenteric and omental cysts are benign congenital abdominal cysts that are found in the mesentery, retroperitoneum, or omentum. They are rarer than enteric duplications and are of lymphatic, not gastrointestinal, origin. Surgical evaluation and management of these lesions is indicated in all cases to treat or prevent possible complications.

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PATHOGENESIS AND EPIDEMIOLOGY

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Enteric duplications can be either tubular or cystic in form (Fig. 396-1). Communication with the normal intestinal lumen is more common with tubular duplications than with cystic ones. Most commonly, the duplication will be lined by the mucosa of the adjacent gastrointestinal structure. However, it may instead have ectopic mucosa, such as gastric or pancreatic, in up to 30% of cases. No genetic predisposition is known. While congenital in origin, the underlying pathogenesis of enteric duplications is unspecified. Multiple theories exist to explain the variants seen clinically. Because of the association with the spinal canal, the theory of split notochord syndrome has been proposed to explain the occurrence of neurenteric cysts (Fig. 396-2). Others have proposed that enteric duplications arise as a consequence of failed regression of embryonic intestinal diverticulum or aberrant recanalization of the embryologic intestinal lumen. Another postulate is that duplications arise as a result of environmental stressors such as trauma, hypoxia, and vascular insufficiency, similar to that of intestinal atresia. Lastly, duplications may arise as a function of partial or abortive twinning. This best explains those with doubling of the colon or genitourinary structures. There is unlikely to be 1 unifying etiology for this anomaly since there are so many variations of intestinal duplications.

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Figure 396-1

Panels A, B, and C show various configurations of the openings of tubular duplications, and panel D shows a cystic duplication of the small bowel. (Adapted with permission from Oldham KT, Colombani PM, Foglia, RP, et al: Principles and Practice of Pediatric Surgery. Philadelphia: Lippincott Williams & Wilkins; 2005.)

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Figure 396-2

Split notochord theory for the embryogenesis of enteric duplications. (Adapted with permission from Oldham KT, Colombani PM, Foglia, RP, et al: Principles and Practice of Pediatric Surgery. Philadelphia: Lippincott Williams & Wilkins; 2005.)

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Mesenteric and omental cysts are thin walled and contain nonmucinous fluid. The embryologic mechanism leading to the formation of mesenteric and omental cysts is unknown. The most commonly accepted theory is benign proliferation of lymphatics within the mesentery ...

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