Intestinal duplications are rare anomalies usually appearing during the first year of life (1–4). Although ultrasonography, computed tomographic (CT) scans, and scintigraphy may be helpful in diagnosis, intestinal duplications are often unexpectedly found during laparotomy (1–4). The blood supply and the muscular coat of the intestinal duplication are commonly shared by the adjacent bowel, which usually precludes selective surgical excision (2–5).
A case of a new clinical presentation of intestinal duplication is described.
An 11-year-old boy was brought for treatment of a 2-day course of mild abdominal pain and vomiting. There was no history of trauma. He was pale, with tachycardia and an axial temperature of 37.6°C. Abdominal examination revealed painful lower quadrants, without distension or tenderness. Ultrasonography demonstrated a moderate amount of free intraperitoneal fluid.
A laparotomy was performed with the presumptive diagnosis of peritonitis secondary to acute appendicitis. However, a mild hemoperitoneum was found, and exploration revealed a cystic mass located at the mesenteric border of the ileum. The adjacent mesentery and bowel were inflamed, with a considerable amount of fibrin between the cyst and the intestinal wall. Careful dissection of the common muscular coat up to the communication, followed by a transverse enteroplasty, was performed.
Histologic examination showed an intestinal duplication lined with an acid-secreting type of gastric mucosa. There was a perforated ulcer near the communication with the adjacent ileum (Fig. 1).
The postoperative course was uneventful, and the child was asymptomatic at 6 months of follow-up.
Duplications of the alimentary tract are rare congenital anomalies that often mimic other surgical diseases. Thus, they are commonly diagnosed at laparotomy without preoperative suspicion (1–5).
In approximately 60% of the cases, the condition appears during the first year of life as a palpable abdominal mass or as complications such as intestinal obstruction due to extrinsic compression, volvulus, or intussusception. Gastrointestinal bleeding from ulceration, either within the duplication itself or in the adjacent intestine is well known and occurs in approximately 25% of patients. Peritonitis due to perforation has been reported rarely and may result from gangrene of a fully filled, secretory, noncommunicating duplication or from peptic ulceration (4–6).
To our knowledge, hemoperitoneum secondary to a complicated intestinal duplication has not been reported before. It was probably caused by erosion of a blood vessel adjacent to the perforation that had been sealed off at laparotomy. It is also possible that some free abdominal blood resulted from intestinal or cystic mucosal bleeding through the perforation into the peritoneal cavity.
Enteric duplication warrants excision. Even asymptomatic patients should undergo surgery because of the risk of perforation, bleeding, and development of carcinoma (1,5–9).
The surgical excision is usually undertaken by enterectomy of adjacent bowel. However, complete excision of the cyst without adjacent bowel resection, as performed in our case, is the procedure of choice, because it promotes a lower risk of anastomosis failure and avoids intestinal resections. This technique is feasible, because the blood supply of the small bowel is doubled with collateral anastomosis between anterior and posterior branches (7–8).
In conclusion, we present a new and potentially severe complication of intestinal duplication. Therefore, in the presence of spontaneous hemoperitoneum, intestinal duplication should be considered in addition to entities such as epiploic torsion and tubular pregnancy in females.
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