Secondary Logo

Journal Logo


Diagnosis and treatment of superior mesenteric artery compression syndrome complicated with gastroesophageal reflux disease

Zhang, Rui1; Li, Zhi-Tong2; Han, Xin-Wei2; Liang, Li-Dan3; Wang, Zhong-Gao2; Ji, Feng2

Editor(s): Ji, Yuan-Yuan

Author Information
doi: 10.1097/CM9.0000000000001430

To the Editor: Superior mesenteric artery compression syndrome (SMAS) is a relatively rare disease caused by the narrowing of the angle between the abdominal aorta and the superior mesenteric artery, thus compressing the third segment of the duodenum.[1] SMAS is mainly characterized by post-prandial epigastric pain, abdominal distension, nausea, vomiting, anorexia, and weight loss. Conservative approaches, including nutritional support, are effective, although approximately 75% of patients still require surgical treatment.[2]

Gastroesophageal reflux disease (GERD) is a chronic gastrointestinal disease, which involves the excessive stomach and duodenal contents being expressed into the esophagus, causing a series of esophageal and extraesophageal symptoms, as well as other complications, including reflux esophagitis, Barrett esophagus, and reflux cough.[3] SMAS is closely related to GERD. Our previous studies have shown that in some cases, SMAS causes cardia relaxation and even leads to GERD. To investigate the clinical features and surgical effect of SMAS complicated with GERD, a retrospective study was conducted in patients with SMAS and GERD in the Interventional Department of the First Affiliated Hospital of Zhengzhou University between January 2013 and June 2018. The study was approved by the Ethics Committee of the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. All patients gave informed consent.

The recruitment process is outlined in Supplementary Figure 1, The clinical characteristics of the patients diagnosed with SMAS and GERD are shown in Supplementary Table 1, The data were shown as mean ± standard deviation, or median (minimum, maximum). There were 30 cases (eight males and 22 females) with a male to female ratio of 4:11, and the average age was 41.3 ± 16.4 years. The body mass index (BMI) was 18.7 kg/m2 (15.6, 23.3 kg/m2), and the course of the disease was 4.0 years (2.1, 30.5 years). The main symptoms were anorexia in 18 cases, heartburn in 17 cases, and acid regurgitation in 14 cases. A total of 27 patients underwent 24-h pH-impedance monitoring, and the DeMeester score was 15.4 (0.9, 125.2). Thirteen patients did not exhibit pathological acid reflux, and 14 patients showed weak acid reflux [Supplementary Table 2,]. High-resolution esophageal manometry showed a minimum lower esophageal sphincter (LES) resting pressure of −1.3 mmHg (−17.0, 12.8 mmHg) and an average LES resting pressure of 4.7 mmHg (−11.2, 17.3 mmHg). Gastroscopy revealed reflux esophagitis in 16 cases and bile reflux gastritis in 11 cases, of which seven cases were complicated with reflux esophagitis. Among the 30 cases that underwent an X-ray barium meal examination of the digestive tract, all cases exhibited a “pencil-shaped” indentation of the horizontal segment of the duodenum in the supine position, delayed passage of barium through the duodenum, dilation of the proximal intestinal tube, and “pendulum” peristalsis [Figure 1A]. Eighteen cases also exhibited gastroptosis. Abdominal computed tomography-enhanced scanning showed that the angle between the abdominal aorta and the superior mesenteric artery was between 10° and 22° [Supplementary Figure 2,].

Figure 1
Figure 1:
X-ray barium meal examination revealed a “pencil-shaped” indentation of the horizontal segment of the duodenum in the supine position (arrow), obstruction of barium through the duodenum, and dilation of the proximal intestinal tube before surgery (A). Barium was able to pass through the duodenum after surgery (B).

Twelve patients who received only drug treatment (gastrointestinal motility drugs, gastric mucosal protectants) and nutritional support demonstrated relief from their symptoms. Laparoscopic Toupet fundoplication combined with the ligament of Treitz release (LOTR) was performed in the remaining 18 patients [Supplementary Figure 3,]. The surgery duration was 65.0 min (45.0, 100.0 min), and the intra-operative blood loss was 38.0 mL (26.0, 40.0 mL). No complications occurred during the surgeries, such as subphrenic abscess, shock, or death. The post-operative hospital stay was 7.0 days (5.0, 19.0 days). After 2 years of follow-up, the patients’ BMIs were significantly increased to an average of 20.8 kg/m2 (18.0, 24.7 kg/m2). Following surgery, the X-ray barium meal examination of the digestive tract revealed normal passage of barium through the duodenum [Figure 1B]. The scores for anorexia, heartburn, acid regurgitation, abdominal distension, nausea, vomiting, and belching were significantly lower than the scores taken before surgery (P < 0.05, respectively; Supplementary Table 3, According to the curative effect evaluation criteria,[4] the total effective rate was 100%, with 17 cases (57%) that were cured and 13 cases (43%) determined to be effective.

The possible mechanisms of GERD caused by SMAS are as follows: First, duodenal obstruction caused by SMAS results in food retention and frequent reverse peristalsis in the proximal intestine. Consequently, there is a gradual increase in the pressure inside the duodenum, stomach, and esophagus, followed by reflux of the gastrointestinal contents into the esophagus, which results in GERD. Second, gastroesophageal reflux is caused by relaxation of the LES and weakening of the anti-reflux effect. In addition to acid reflux, the duodenogastric reflux contents are mixed with basic reflux contents, both of which damage the digestive tract mucosa. Third, a majority of patients who have SMAS are thin and exhibit complications of gastroptosis. This, in turn, causes delayed gastric emptying and insufficient gastrointestinal motility resulting in increased intragastric pressure and gastric distension, which promote reflux. Most of the 30 cases of SMAS with GERD were emaciated females with a high proportion exhibiting gastroptosis. Reflux esophagitis and/or bile reflux gastritis was detected by gastroscopy, identifying weak acid reflux as the main clinical manifestation with a decrease in LES pressure. Our results confirmed that SMAS might cause GERD, because bile could reflux into the stomach, neutralizing gastric acid, and promoting weak acid reflux.

The suggested treatment strategies for SMAS combined with GERD are as follows: Drug therapy and other non-invasive approaches are the first choices, especially for patients with mild symptoms. The treatment methods include diet adjustment, posture changes, the use of proton pump inhibitors, and the use of gastric mucosal protectants along with nutritional support. When such conservative treatments prove ineffective, surgical options are warranted, based on the individual patient's clinical situation. The commonly used surgical methods that achieve favorable therapeutic outcomes include open or laparoscopic gastrojejunostomy, duodenojejunostomy, duodenojejunostomy combined with LOTR, LOTR, and duodenal vascular anterior transposition. However, gastrojejunostomy, duodenojejunostomy, and duodenal vascular anterior transposition can cause significant trauma, which results in further complications.[5] On the other hand, LOTR can relieve duodenal compression without changing the digestive tract structure, which is relatively safe and has fewer complications.[6] Therefore, LOTR was selected for use in this study. However, for patients with SMAS complicated with GERD and who exhibit obviously decreased LES, LOTR alone might not be enough for therapeutic effect. Since Toupet 270 degrees fundoplication is commonly recommended for patients with GERD, LOTR combined with fundoplication could simultaneously resolve SMAS and GERD. The efficacy of the combined surgery was verified in this study where clinical symptoms were significantly relieved or disappeared after surgery, and patient's weights were significantly increased.

In summary, SMAS combined with GERD seriously affects an individual's quality of life. Thus, appropriate treatments should be selected based on each patient's clinical characteristics. Favorable results obtained after laparoscopic Toupet fundoplication combined with LOTR has confirmed this to be an appropriate and effective surgical method for SMAS combined with GERD.


This study was supported by the Medical Science and Technology Research Program of Henan Province (No. 2018020042).

Conflicts of interest



1. Merrett ND, Wilson RB, Cosman P, Biankin AV. Superior mesenteric artery syndrome: diagnosis and treatment strategies. J Gastrointest Surg 2009; 13:287–292. doi: 10.1007/s11605-008-0695-4.
2. Mandarry MT, Zhao L, Zhang C, Wei ZQ. A comprehensive review of superior mesenteric artery syndrome. Eur Surg 2010; 42:229–236. doi: 10.1007/s10353-010-0561-y.
3. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol 2013; 108:308–328. doi: 10.1038/ajg.2012.444.
4. Shaw MJ, Talley NJ, Beebe TJ, Rockwood T, Carlsson R, Adlis S, et al. Initial validation of a diagnostic questionnaire for gastroesophageal reflux disease. Am J Gastroenterol 2001; 96:52–57. doi: 10.1016/S0002-9270(00)02244-9.
5. Yang WL, Zhang XC, Zhang WF, Yan CQ, Wang FJ, Ma YL. Selection and evaluation of surgical treatment for superior mesenteric artery syndrome. Chin J Gastrointest Surg 2007; 10:288–290. doi: 10.3760/cma.j.issn.1671-0274.2007.03.030.
6. Dekonenko C, Hill JA, Sobrino JA, Snyder CL, Oyetunji TA. Ligament of Treitz release with duodenal lowering for pediatric superior mesenteric artery syndrome. J Surg Res 2020; 254:91–95. doi: 10.1016/j.jss.2020.04.006.

Supplemental Digital Content

Copyright © 2021 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.