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    Prof. of Hepatology & Gastroenterology, Cairo University.

    Consultant of Hepatology,Gastroenterology and Endoscopy

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    Chief of Hepatology unit El Manial University Hospital (1994-1998).

    • Chief of Gastroentero ICU in Cairo university hospital (1997-2000)

    • President of the board of AlfaScope GI Specialized center (2004-2014).

    • Head of Endoscopy Unit in Cairo University Hospitals (2005-2010).       


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Superior mesenteric artery syndrome

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Superior mesenteric artery syndrome


Superior mesenteric artery syndrome is an unusual cause of proximal intestinal obstruction. The syndrome is characterized by compression of the third portion of the duodenum due to narrowing of the space between the superior mesenteric artery and aorta and is primarily attributed to loss of the intervening mesenteric fat pad.

the normal angle between the superior mesenteric artery and the aorta is between 38 and 65º due, in part, to the mesenteric fat pad. This angle correlates with body mass index.

In superior mesenteric artery syndrome, the angle

 can be narrowed to as low as 6º which minimizes the space between the superior mesenteric artery and aorta leading to duodenal compression.

Susceptible patients:

Several factors can decrease the acuity of the angle between the aorta and superior mesenteric artery.

1. The most common is significant weight loss leading to loss of the mesenteric fat pad as a consequence of medical disorders (as malignancy & malabsorption), psychological disorders ( as anorexia nervosa & depression) or surgery.

2. Anatomic abnormalities, congenital, or acquired (as corrective spinal surgery for scoliosis & esophagectomy) can also contribute.

Clinical presentation:

Patients may present acutely or gradually by symptoms of proximal small intestinal obstruction.

Patients with mild obstruction may have only postprandial epigastric pain & early satiety.

Those with more advanced obstruction may have severe nausea, bilious vomiting & weight loss. Patients may also have symptoms of reflux.

Symptoms may be relieved when patient is lying prone, in the left lateral decubitus, or in a knee-chest position. These positions remove tension from the mesentery and superior mesenteric artery, opening the space between the superior mesenteric artery & aorta.

Physical examination is normal, but abdominal distension & succussion splash may be present.

Electrolyte disturbances may be present with severe vomiting.

Complications may occur as:

  • Fatalities due to electrolyte disturbances.
  • Fatalities due to gastric perforation.
  • Gastric pneumatosis and portal venous gas.

Diagnostic investigations:

1. Plain abdominal erect:

May reveal findings suggestive of proximal small intestinal obstruction, such as gastric distension, dilation of the proximal duodenum, and, occasionally, an abrupt vertical cutoff of air in the third portion of the duodenum.

2. Gastrografin (or barium) follow-through:

Usually demonstrate marked delay in passage of the contrast from the duodenum into the more distal small bowel. Passage of contrast typically halts abruptly at the third portion of the duodenum. The proximal duodenum and stomach are dilated and show prolonged retention of the contrast.

3. CT with oral & intravenous contrast:

  • Dilated proximal duodenum & stomach.
  • Duodenal obstruction with an abrupt cutoff in the third portion.
  • An aorto-mesenteric artery angle of ≤25° is the most sensitive measure of diagnosis.

4.  Ultrasonography:

Trans-abdominal and endoscopic ultrasonography can identify and measure the aorto-mesenteric angle.

5. Arteriography:

Conventional, CT, and MR arteriography demonstrate the superior mesenteric artery superimposed upon the barium-filled duodenum. And demonstrate the narrowing of the aorto-mesenteric angle


I. Conservative treatment:

1. Inserting a Nasogastric tube:

Nasogastric tube decompresses the dilated stomach and proximal duodenum and improves patient discomfort.  

2. Correction of electrolyte disturbances:

Vomiting can lead to hypovolemia, hypokalemia, and metabolic alkalosis. Fluid and electrolyte correction should be done.

3. Nutritional support: (the major component of therapy).

Psychiatric evaluation, to manage eating disorders.

Enteral or parenteral  nutrition is usually required, at least in the initial stages until patients are able to increase oral intake. Once significant weight gain is noted, the diet is advanced slowly.

II. Surgical treatment:

Surgery is the option if conservative nutritional therapy fails to resolve the condition.

  • Strong’s procedure – Strong’s procedure mobilizes the duodenum by dividing the ligament of Treitz.
  • Gastrojejunostomy by open or laparoscopic surgery.
  • Duodenojejunostomy.   

Outcomes of surgery:

In a study included 16 patients who were followed seven years after surgery, weight loss had been corrected & vomiting, was significantly decreased. In another study of eight patients, symptoms were improved; however, significant weight gain was not seen.

Last Updated on Thursday, 18 May 2017 11:13


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