Superior Mesenteric Artery Syndrome
The superior mesenteric artery is a large artery in the abdominal cavity that provides blood to the
small intestine, cecum, and colon. Superior mesenteric artery (SMA) syndrome is characterized
by the compression of the third portion of the duodenum between the aorta and the superior
mesenteric artery. It is attributed to loss of the mesenteric fat pad.
Roughly 400 cases are described in English language literature, but many have doubted its
existence. However, it is a well-recognized complication of scoliosis surgery (usually presenting
6 to 12 days following surgery), anorexia, and trauma. No racial differences are seen, but more
females are affected than males. SMA syndrome most often occurs in patients who are 10 to 30
years of age.
Etiological factors
Etiological factors that appear to increase the risk of developing SMA syndrome include:
 Thin body build; rapid linear growth without corresponding weight gain
 Exaggerated lumbar lordosis; spinal disease, deformity, or trauma
 Visceroptosis and abdominal wall laxity
 Malabsorption
 Described in conjunction with many disorders that lead to extreme weight loss, including
acquired immunodeficiency syndrome, burns, trauma, bariatric surgery, cancer, cardiac
cachexia, spinal cord injury, paraplegia, drug abuse, anorexia nervosa, psychiatric conditions,
and prolonged bed rest
 Other surgeries that distort normal anatomy, such as esophagectomy (may lead to
development)
 Anatomic abnormalities (rare)
 Unusual causes:
– Traumatic aneurysm of the superior mesenteric artery post-stab wound
– Abdominal aortic aneurysms
– Mycotic aortic aneurysms
– Familial SMA syndrome
– Recurrent SMA syndrome
Symptoms of SMA syndrome
Symptoms of SMA syndrome include:
 Epigastric pain and postprandial discomfort
 Nausea
 Belching
 Voluminous vomiting
 Early satiety
 Subacute small bowel obstruction
 Symptoms of reflux
 Abdominal distension
Patients often report relief of these symptoms when in the left lateral decubitus, prone, or knee-to
chest position. Worsening of the symptoms may occur when the patient is in the supine position.
This relates to the small bowel mesenteric tension at the aortomesenteric angle. Peptic ulcer
disease is noted in 25% to 45% of the patients, and hyperchlorhydria is noted in 50% of patients.
Diagnosis and treatment
If diagnosis and treatment of SMA syndrome are delayed, the following can result:
 Malnutrition
 Dehydration
 Electrolyte abnormalities
 Gastric pneumatosis and portal venous gas
 Formation of an obstructing duodenal bezoar
 Hypovolemia secondary to massive gastrointestinal (GI) hemorrhage
 Death from gastric perforation
The differential diagnosis of SMA syndrome includes:
 Other causes of bowel obstruction
 Diseases associated with duodenal dysmotility, including diabetes mellitus, collagen vascular
diseases, scleroderma, and chronic idiopathic intestinal obstruction
 Chronic mesenteric ischemia (especially common in smokers or individuals with other risk
factors for atherosclerosis who present with food intolerance and weight loss)
 Other causes of reflux
Diagnosis of SMA syndrome often is based on exclusion of other possible diagnoses. It is
suspected that 0.013% to 0.78% of findings from upper GI tract barium studies support a
diagnosis of SMA syndrome. Plain radiograph demonstrates a dilated, fluid- and gas-filled
stomach, and barium radiography shows dilatation of the first and second part of the duodenum,
extrinsic compression of the third part, and a collapsed small bowel distal to the crossing of the
superior mesenteric artery.
Diagnostic imaging criteria for diagnosis includes:
 Duodenal obstruction and active peristalsis
 An aortomesenteric artery angle of ≤25°
 High fixation of the duodenum by the ligament of Treitz, abnormally low origin of the superior
mesenteric artery, or anomalies of the superior mesenteric artery
Treatment of SMA syndrome is often conservative initially and includes nutrient provision,
nasogastric decompression, correction of electrolyte abnormalities, and proper positioning of the
patient postprandially. Patients may develop refeeding syndrome following relief of duodenal
obstruction. Enteral feeding via a double-lumen nasojejunal tube passed distal to the obstruction
is effective for patients with rapid, severe weight loss. Some patients will require a combination
of enteral and parenteral nutrition. If a patient is completely obstructed or unable to tolerate
liquids, total parenteral nutrition becomes necessary.
It is crucial to monitor body weight and record it daily, using the same scale and with the patient
wearing the same clothing. The goal is to increase the mesenteric fat pad, so patients will require
up to two times their estimated caloric needs. It is necessary to advance the patients’ diet slowly,
first to clear liquids and then to full liquids and finally to small frequent meals of soft foods.
Some patients benefit from initiation of metoclopramide treatment. Some patients who have a
history of an eating disorder will need psychiatric evaluation.
However, some patients may continue to lose weight or will present with pronounced duodenal
dilation with stasis or complicating peptic ulcer disease. If 4 to 6 weeks of conservative treatment
is not successful, these patients will require surgical intervention. If surgery has altered the
anatomy, it is not likely that conservative treatment will succeed.
Surgical options
Duodenojejunostomy: The obstruction is bypassed. The compressed portion of the duodenum is
released, and an anastamosis between the duodenum and jejunum anterior to the superior
mesenteric artery is created. Complications include risk of bleeding, leakage, or stricture. This is
the preferred route for surgical intervention and is usually successful. Laparoscopic
duodenojejunum is a less invasive alternative and often especially beneficial for debilitated
patients.
Gastrojejunostomy: To bypass the obstruction, a loop of jejunum is brought up to the stomach
and a side-by-side anastomosis is performed. This is usually reserved for those patients who are
unable to undergo a duodenojejunostomy.
Duodenal derotation procedure (Valdoni-Strong’s procedure): This alters the
aortomesenteric angle and places the third and fourth positions of the duodenum to the right of
the superior mesenteric artery (often most appropriate for pediatric patients with possible
congenital anatomic conditions). A laparotomy is performed, and the duodenum is mobilized
after division of the ligament of Treitz. The jejunum is then passed behind the superior
mesenteric artery. It is positioned so that it does not lie in the acute angle between the aorta and
the superior mesenteric artery.
References and recommended readings
Karrer FM. Superior mesenteric artery syndrome. Medscape Reference Web site.
http://emedicine.medscape.com/article/932220-overview. Accessed August 7, 2013.
National Center for Advancing Translational Sciences, Office of Rare Disease Research, Genetic
and Rare Diseases Information Center (GARD). Superior mesenteric artery syndrome. National
Institutes of Health Web site.
http://rarediseases.info.nih.gov/GARD/Condition/7712/Superior_mesenteric_artery_syndrome.as
px. Updated July 26, 2012. Accessed August 7, 2013.
Roy A, Gisel JJ, Roy V, Bouras EP. Superior mesenteric artery (Wilkie’s) syndrome as a result
of cardiac cachexia. J Gen Intern Med. 2005;20(10):C3-C4. doi:10.1111/j.15251497.2005.0201.x.
Superior mesenteric artery syndrome. UpToDate® Web site.
http://www.uptodate.com/contents/superior-mesenteric-artery-syndrome. Updated September 19,
2012. Accessed August 7, 2013.
Contributed by Elaine Koontz, RD, LD/N
Review Date 8/13
G-1898