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March 16, 2009

Image of the Month—Diagnosis

Arch Surg. 2009;144(3):287-288. doi:10.1001/archsurg.2008.551-b

Answer: Left Paraduodenal Hernia

This patient had a left paraduodenal hernia. Approximately 90 cm of proximal jejunum was herniated through the left paraduodenal fossa of Landzert (Figure 2). The bowel contained in the hernia sac was injected and fluid filled but was otherwise viable. The hernial defect was repaired primarily by approximating the surrounding loose areolar tissue with 3 interrupted 3-0 nonabsorbable sutures, taking care not to injure the duodenojejunal flexure medially and the inferior mesenteric vein laterally. The procedure was completed laparoscopically using 4 ports and was well tolerated.

Figure 2. 
Intraoperative view of the internal hernia orifice lateral to the duodenojejunal flexure after reduction of 90 cm of viable herniated jejunum.

Intraoperative view of the internal hernia orifice lateral to the duodenojejunal flexure after reduction of 90 cm of viable herniated jejunum.

Paraduodenal (also termed congenital mesocolicor mesentericoparietal) hernias represent less than 1% of all intestinal obstruction cases but account for approximately half of all internal hernias. They occur 3 times more commonly on the left side. By 1981, 477 cases had been reported, but some of these were probably duplicates.1

A classic left paraduodenal hernia is defined by the following anatomic relationships. The midgut rotation around the superior mesenteric artery is normal, with the cecum situated in the right lower quadrant; the inferior mesenteric vein lies in the anterolateral border of the sac; and the left colic artery lies in the left or right wall of the sac.2

Most evidence suggests that paraduodenal hernias are produced by abnormalities of intestinal rotation.2Left paraduodenal hernias are believed to result from invagination of the jejunum and ileum through the left paraduodenal fossa into an unsupported area of the descending mesocolon during the tenth week of embryologic development, as the midgut returns to the celomic cavity. The autopsy finding of 4 layers of peritoneum in the anterior wall of a left paraduodenal hernia sac confirms this embryologic origin.

Gradual enlargement of the sac with time may account for the peak incidence of symptomatic paraduodenal hernias in adults. Nearly half of all patients with paraduodenal hernias develop intestinal obstruction.1Some patients have a history of chronic intermittent obstructive symptoms or signs of inferior mesenteric vein thrombosis, such as hemorrhoids.2

Upper gastrointestinal contrast studies and computed tomography may aid in diagnosis, especially during symptomatic periods. The herniated bowel will appear clustered in the left upper quadrant, and encapsulated in a hernia sac, often causing posterior mass effect in the stomach. Stasis of oral contrast in the hernia contents with proximal dilatation will invariably be present.3

The basic principles of internal hernia surgery are reduction of contents and repair of the defect by means of either closure or wide opening of the hernia orifice. Right paraduodenal hernias are often associated with malrotation of the midgut and are sometimes complicated by strangulation. Therefore, division of the lateral attachments of the right colon is needed to allow reduction of the bowel by retraction to the left.1,2Left paraduodenal hernias can usually be reduced manually without difficulty, as in the present patient, and simple closure of the hernia orifice is sufficient, taking care to avoid vascular injury. If incarceration is encountered, the hernia ring can be divided, sacrificing the inferior mesenteric vein, although a more effective method of incising the hernia sac parallel to the course of the inferior mesenteric vein has been described.1,2

Four cases of laparoscopic repair of left paraduodenal hernia without bowel compromise have been reported since 1998.4-7These cases, collectively with the present case, illustrate the feasibility of laparoscopic diagnosis and management of this disease process.

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Correspondence:George A. Poultsides, MD, Department of Surgery, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-3955 (

Accepted for Publication:April 4, 2007.

Author Contributions:Study concept and design: Poultsides, Zani, Bloom, and Tishler. Acquisition of data: Poultsides and Tishler. Analysis and interpretation of data: Poultsides, Bloom, and Tishler. Drafting of the manuscript: Poultsides and Zani. Critical revision of the manuscript for important intellectual content: Bloom and Tishler. Administrative, technical, and material support: Poultsides, Bloom, and Tishler. Study supervision: Bloom and Tishler.

Financial Disclosure:None reported.

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