SMAS was first described in 1861 by Rokitansky [7]. In patients with SMAS, the third portion of the duodenum is compressed between the SMA and aorta. The symptoms of SMAS are nonspecific and identical to those of ileus. SMAS is diagnosed by contrast-enhanced CT. The angle between the SMA and aorta (aortomesenteric angle) is normally 45° to 60° [8], and the distance between the SMA and aorta (aortomesenteric distance) usually ranges from 10 to 34 mm [9]. In the present case, the aortomesenteric angle was 36° and the aortomesenteric distance was reduced from 12 mm on preoperative CT to only 2 mm on postoperative CT (Figure 4A, B). An upper gastrointestinal series revealed an obstruction in the third portion of the duodenum (Figure 2A), and a CT scan demonstrated gastric and duodenal distension with a transition point in the third portion of the duodenum near the origin of the SMA (Figure 3). We confirmed that the cause of the duodenal obstruction was SMAS.
One cause of SMAS is believed to be loss of the intraabdominal fat that separates the SMA from the aorta. Other reported causes of SMAS include traction of the SMA and changes in spine extension [1]. There are three populations of patients with SMAS: those who have undergone surgery, those who have experienced severe weight loss, and those with hyperextension of the spine. Among those who have undergone surgery, although few, the most common surgical operations are those performed for treatment of colorectal cancer. In the most recent few decades, IPAA has been the gold standard construction technique following the performance of total proctocolectomy. IPAA is performed for sphincter preservation after total proctocolectomy in patients with UC. Because the SMA is the main vascular pedicle for the constructed ileal pouch during the performance of IPAA, and because the SMA is stretched to some extent, it seems that many cases of SMAS after IPAA should have been reported to date. However, to the best of our knowledge, only five cases of SMAS after IPAA have been reported [2-6]. We suppose that the PF might have affected the development of SMAS in this case. The PF might have developed after SMAS because the drainage volume was small and we were able to remove the drainage tube early after the operation. Furthermore, the fluid collection near the PF was slightly displaced from the obstruction in the duodenum when we performed the drainage. We speculated that the high intraduodenal pressure secondary to SMAS could have created the high pressure at the main pancreatic duct, resulting in prolongation of the PF (Figure 6). Conservative treatment for SMAS reportedly involves an increase in both weight and the mesenteric fat pad [10]; therefore, we initially treated our patient conservatively. However, the patient’s postsurgical weight loss was >10 kg at 3 months postoperatively. The primary cause of SMAS in this case might have been the stretching and traction of the SMA due to the IPAA, which was localized deep in the pelvic cavity. Goes et al. [5] reported that some technical details may make it difficult for the pouch to reach the anal canal. Therefore, undesirable tension could be transmitted to the root of the mesentery, narrowing the aortomesenteric angle and increasing the risk of duodenal compression. In addition to the stretching of and traction on the SMA, the presence of a PF might affect the reduction of the fat pad between the SMA and aorta because pancreatic lipase digests fat. Appropriate nutritional management normally increases the fat pad between the SMA and aorta, but the vicious circle between the PF and SMAS might interfere with this process. Truong et al. [2] recently reported a case of SMAS after IPAA; conservative treatment was effective, and the symptoms disappeared 4 weeks later.
Surgical treatments that may be considered for SMAS include laparoscopic, robotic, or open duodenojejunostomy [10-13]. In the present case, we chose open duodenojejunostomy because of the history of open total colectomy and drainage of the PF. The patient’s symptoms improved, and gastroduodenal endoscopy showed no GERD or food residue after this operation. The fluid collection at the pancreatic stump disappeared soon after the duodenojejunostomy (Figure 5), indicating that the cause of the PF was SMAS.
In summary, we experienced a very rare case of SMAS after construction of an IPAA. The SMAS was induced by stretching of and traction on the SMA associated with IPAA. The SMAS caused high pressure to develop in the duodenum and main pancreatic duct, resulting in PF formation. This PF might have reduced the fat pad between the SMA and aorta, resulting in prolonged SMAS. Surgical treatment was finally required (Figure 6). Management of SMAS is normally conservative. However, inappropriate nutritional management and other complications might affect the treatment of SMAS. We should keep in mind that SMAS can occur after IPAA.