Superior Mesenteric Artery (SMA) Syndrome is a rare gastrointestinal disorder that can cause significant digestive distress. This condition involves the third, or transverse, portion of the duodenum, the first segment of the small intestine. It results in a partial or complete obstruction of this segment as it is squeezed by major abdominal blood vessels.
Underlying Anatomical Mechanism
The core issue in SMA Syndrome stems from the anatomical relationship between the duodenum, the abdominal aorta, and the superior mesenteric artery (SMA). The aorta is the body’s largest artery, and the SMA branches off it to supply blood to the mid-gut. The third part of the duodenum passes through a narrow space positioned between these two large vessels.
In a healthy individual, a protective cushion of retroperitoneal fat surrounds the SMA, maintaining a wide angle between the two arteries. This fat cushion holds the SMA forward and away from the aorta, allowing the duodenum to pass without being squeezed.
SMA Syndrome develops when this protective fat pad is significantly reduced or lost, causing the SMA to drop closer to the aorta. The resulting acute narrowing of the space reduces the aortomesenteric angle and the distance between the vessels. This pinched position traps the duodenum, causing the physical compression that obstructs the passage of food.
Common Causes and Risk Factors
The primary factor leading to the loss of the protective fat pad is rapid, significant weight loss. This weight loss can stem from severe illness, cancer-related cachexia, or eating disorders like anorexia nervosa. Patients who have undergone bariatric surgery are also at an elevated risk due to the dramatic reduction in body mass.
Other conditions that cause extreme body wasting or change abdominal anatomy can also precipitate the syndrome. These include severe trauma or burns, chronic malabsorptive diseases, and prolonged immobilization, such as extended bed rest. These factors contribute to the loss of fat tissue and abdominal wall laxity.
In some cases, the syndrome is triggered by spinal corrective surgery for conditions like scoliosis, especially in thin patients. The sudden lengthening of the spine can acutely stretch the superior mesenteric artery, reducing the angle with the aorta. This change in internal architecture effectively compresses the duodenum, even without a major loss of mesenteric fat.
Recognizing the Signs and Symptoms
The compression of the duodenum leads to gastrointestinal symptoms often experienced after eating. Patients commonly report severe, cramping abdominal pain, typically located in the upper abdomen. This discomfort is often accompanied by early satiety, the feeling of being full despite eating only a small amount of food.
Nausea and vomiting are prominent features, often occurring shortly after a meal. The vomiting can be projectile and frequently contains bile, indicating the obstruction is located beyond the stomach’s outlet. This cycle leads to an intense fear of eating, known as sitophobia, which results in significant weight loss.
A distinctive clue is the postural relief of symptoms, sometimes called the Hayes maneuver. Patients often find that lying on their left side or adopting a prone position with their knees drawn to their chest can temporarily alleviate the pain. These specific positions help shift the abdominal organs, slightly widening the aortomesenteric angle and relieving pressure on the duodenum.
Diagnostic Procedures and Management Strategies
Diagnosis relies on clinical suspicion and objective evidence from imaging. Computed tomography (CT) scans, often performed with intravenous contrast, are the preferred diagnostic tool. CT scans allow physicians to directly measure the aortomesenteric angle and the distance between the vessels, confirming anatomical compression. An upper gastrointestinal endoscopy may also be performed to rule out other potential causes of duodenal obstruction, such as ulcers or tumors. Imaging findings that indicate the syndrome include a dramatically reduced aortomesenteric angle, a diminished distance between the vessels, and a visibly distended stomach and duodenum proximal to the compressed segment.
Initial management focuses on conservative treatment, aiming to reverse the underlying cause by restoring the protective fat pad. This involves intensive nutritional support, including a regimen of small, frequent, high-calorie meals. If oral feeding is not tolerated due to severe vomiting, nutritional support is escalated. This may involve tube feeding or total parenteral nutrition (TPN) to bypass the digestive tract entirely.
If conservative measures fail to resolve the obstruction or if the patient’s condition is severe, surgical intervention becomes necessary. The most common procedure is a duodenojejunostomy, often performed laparoscopically. This operation creates a connection between the duodenum and the jejunum, the next segment of the small intestine, effectively bypassing the compressed third portion of the duodenum and relieving the obstruction.