Abstract
Segmental intestinal dilatation (SID) is a rare developmental anomaly of the midgut, characterized by sharply demarcated dilatation of a gastrointestinal segment with clinical findings of intestinal obstruction. Although morphologic criteria for SID are clearly delineated, etiological origin of dilated intestine is unknown. Histology of the resected segment is usually reported to have normal presence of ganglion cells in the myenteric and submucosal plexuses. Intestinal muscle is hypertrophied, and heterotopic gastric mucosa may also be encountered. A 3-day-old male infant presenting with clinical findings of intestinal obstruction was diagnosed to have SID and had supernumerary intestinal muscle coat (SIMC) in the dilated segment, without any evidence of neurological abnormality. Histopathological findings of the resected ileal segment are reported to discuss the role of architectural malformation of muscularis propria as a cause of SID.
Highlights
Segmental intestinal dilatation (SID) is a rare gastrointestinal anomaly introduced by Rossi and Giocomoni [1]
Anemia is the first sign of SID in patients with heterotopic gastric mucosa
SID is a congenital anomaly of gastrointestinal tract with clinical findings of intestinal obstruction
Summary
Segmental intestinal dilatation (SID) is a rare gastrointestinal anomaly introduced by Rossi and Giocomoni [1]. According to the criteria proposed by Swenson and Rathauser, SID is defined as limited bowel dilatation with three- to fourfold increased size, with an abrupt transition between dilated and normal bowel, without any intrinsic and extrinsic barrier distal to the dilatation or abnormal neurological innervation [2]. Half of the SID cases are seen in the first days of life, and clinical findings of intestinal obstruction are the most common presentation [3]. Diagnostic criteria of SID are well established, the etiology of the disease is unclear. Histology of the involved bowel usually shows normal neurological innervation with a hypertrophied or thin muscle layer [4]. None of the histopathological findings are able to explain the etiology of SID
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