Superior Mesenteric Artery (SMA) Syndrome is an uncommon digestive condition resulting from a structural issue in the abdomen. This disorder involves the mechanical compression of the third part of the duodenum (the first section of the small intestine). The compression occurs as the duodenum is squeezed between two major blood vessels: the abdominal aorta and the superior mesenteric artery. This anatomical pinching leads to a partial obstruction, hindering the passage of food into the rest of the small intestine.
Understanding the Causes and Mechanism of SMA Syndrome
The direct cause of SMA Syndrome is a significant reduction in the angle and distance between the aorta and the superior mesenteric artery. Normally, the superior mesenteric artery branches off the aorta at an angle ranging from 38 to 56 degrees, maintaining a distance of 10 to 20 millimeters. In SMA Syndrome, this aortomesenteric angle narrows sharply, often falling to 6 to 25 degrees, with the distance shrinking significantly.
This narrowing is usually triggered by a loss of the protective cushion of retroperitoneal fat tissue that normally separates the two arteries. Factors that cause rapid or severe weight loss are the primary risk factors, as they deplete this fat pad. Conditions such as anorexia nervosa, severe burns, malignancy, highly restrictive diets, or major trauma can precipitate the syndrome.
The syndrome can also be triggered by events that change the anatomical relationship regardless of fat loss. These factors include prolonged bed rest, which allows the abdominal organs to shift, or spinal surgery like scoliosis correction, which can cause hyperextension of the spine. Constitutional factors, such as a naturally thin body build or an exaggerated lumbar lordosis (inward curve of the lower back), can also predispose an individual to the condition.
Initial Management: Nutritional and Conservative Therapies
The initial approach to managing SMA Syndrome is conservative, focusing on nutritional rehabilitation to reverse the underlying anatomical mechanism. The primary goal is to restore the retroperitoneal fat pad, which acts as the cushion separating the aorta and the superior mesenteric artery. This restoration should widen the aortomesenteric angle, relieving the compression on the duodenum.
A structured nutritional plan involves a gradual increase in caloric intake, often delivered through small, frequent, energy-dense meals. If symptoms like vomiting and nausea make oral intake difficult, nutritional support may be provided through a feeding tube. Enteral feeding, such as a nasojejunal tube, can be placed beyond the point of duodenal compression to ensure nutrients are absorbed and weight gain is achieved.
For patients who cannot tolerate enteral feeding, total parenteral nutrition (TPN) may be necessary, delivering fluids and nutrients directly into a vein. Alongside nutritional support, specific body positions can be used immediately after eating to temporarily alleviate the obstruction. Lying in the left lateral decubitus position (on the left side) or the prone position (on the stomach) can shift the abdominal contents and pull the superior mesenteric artery away from the duodenum.
This non-invasive strategy is successful in most patients, with reported success rates for conservative management ranging between 70 and 80 percent, particularly when the syndrome developed acutely following a weight-loss event. Clinicians recommend a trial of conservative therapy lasting at least four to six weeks before considering more invasive options. Monitoring weight gain and the resolution of obstructive symptoms are the main indicators of success during this period.
When Surgery Becomes Necessary
When a patient’s symptoms persist, or if they continue to experience severe weight loss despite a dedicated course of nutritional and positional management, surgical intervention is considered. Surgery is reserved for cases that are medically refractory, meaning conservative measures have failed to provide lasting relief or restore adequate nutrition. The goal of any surgical procedure is to permanently bypass or eliminate the duodenal compression.
The most common surgical solution is a duodenojejunostomy. This procedure involves dividing the compressed third portion of the duodenum and creating a new connection, or anastomosis, between the duodenum and the jejunum (the next section of the small intestine). This effectively reroutes the flow of food around the compressed area, bypassing the obstruction entirely.
Duodenojejunostomy is often performed using minimally invasive laparoscopic techniques, resulting in a shorter hospital stay and faster recovery time compared to traditional open surgery. This bypass procedure boasts a high success rate, with long-term symptom resolution reported to be around 90 percent or higher.
A less frequently performed surgical option is the Strong’s procedure, also known as duodenal derotation. This technique involves dividing the Ligament of Treitz, which anchors the end of the duodenum, allowing the surgeon to mobilize and reposition the duodenum to the right side of the superior mesenteric artery. The repositioning aims to increase the aortomesenteric angle and distance directly. While it avoids creating an intestinal anastomosis, the Strong’s procedure is less favored than the duodenojejunostomy due to a higher potential for failure or recurrence.
Prognosis and the Definition of a “Cure”
The question of whether SMA Syndrome can be cured is best answered by considering the definition of a cure in this context. For SMA Syndrome, a cure means the complete and sustained resolution of obstructive symptoms alongside the restoration of normal body weight and eating patterns. Both conservative and surgical treatments offer a positive prognosis for achieving this outcome.
With successful nutritional therapy, the restoration of the retroperitoneal fat pad eliminates the vascular compression, leading to a functional cure. Similarly, successful surgery permanently resolves the mechanical obstruction, allowing the patient to eat and maintain weight without restriction. Success rates for both approaches are high, suggesting that the condition is often fully reversible.
Long-term monitoring is important, as the potential for recurrence exists if the underlying cause returns. For instance, a patient cured through weight restoration could experience the syndrome again if a future illness leads to another rapid loss of body fat. While the anatomical compression and associated symptoms can be fully resolved, maintaining a healthy weight remains a factor in preventing the condition’s return.