Open repair and subsequent stenting to treat median arcuate ligament syndrome secondary to Roux-en-Y gastric bypass

Abstract

Median arcuate ligament syndrome (MALS) is characterized by external compression of the celiac artery (CA) by the median arcuate ligament. There have been three reports of MALS following gastric bypass surgery, but this pathophysiology remains incompletely understood. We report a patient with MALS and a surgical history including Roux-en-Y gastric bypass. After workup, she was treated with open release of the median arcuate ligament and CA patch angioplasty, with subsequent CA artery stenting for recurrent stenosis. We will discuss potential mechanisms by which Roux-en-Y gastric bypass can lead to MALS and management strategies for it.

A 32-year-old female with a past medical history of irritable bowel syndrome, small intestinal bacterial overgrowth, and duodenal ulcers presented to the vascular surgery clinic with a 2-year history of severe, postprandial epigastric pain. She endorsed an unintentional 10-pound weight loss over 4 weeks secondary to her pain, and she also reported associated headache, nausea, bilious vomiting, and shortness of breath. Past surgical history was significant for Roux-en-Y gastric bypass (RYGB) 4 years ago with an associated 125-lb weight loss, cholecystectomy, and hysterectomy. Her weight and body mass index on presentation were 193 lbs and 30.7 kg/m², respectively.

Physical examination showed a mildly tender, soft abdomen with no bruits. A previous computed tomography (CT) scan showed severe short segment celiac artery (CA) stenosis and an absent left gastric artery. Previous esophagogastroduodenoscopy was unremarkable. Duplex ultrasound (DUS) of her CA was performed at force expiration and inspiration. The CA origin showed elevated peak systolic velocity (PSV) of 372 cm/s and end diastolic velocity (EDV) of 136 cm/s, and the common hepatic artery had a PSV of 226 cm/s. The PSV and EDV were highest at the proximal CA, measuring 473 cm/s and 180 cm/s, respectively, suggestive of greater than 70% stenosis. Repeat abdominal CT scan (Fig 1, A) confirmed severe CA stenosis with compression by the median arcuate ligament (MAL). She was offered laparoscopic and open release and elected to have an open MAL release with CA patch angioplasty.

Fig 1.

Sagittal computed tomography (CT) scans of the abdominal aorta, celiac artery (CA; yellow arrow), and superior mesenteric artery. (A) Preoperative CT scan showing characteristic CA “hook sign,” representative of CA compression and stenosis. (B) Post-median arcuate ligament (MAL) release CT scan showing patent CA and superior mesenteric artery.

Initial exploration identified the Roux-en-Y limb at the appropriate location of the gastric pouch and no signs of internal hernia. The gastrohepatic ligament was incised around the lateral segment of the liver, and the aorta was exposed inferiorly. After excision of the MAL and surrounding neuronal fibers extending to the hepatic and splenic segments, there was still significant narrowing of the CA; thus, vessel reconstruction was necessary. The aorta was dissected inferiorly to the superior mesenteric artery, and a Satinsky clamp was placed across the aorta once the patient was systemically heparinized. An arteriotomy was performed from the origin of the aorta through the stenotic segment of the CA, ending distally at the proximal common hepatic artery. A patch angioplasty was then performed. Subsequent DUS signals were within normal limits. The patient had an uncomplicated recovery and was discharged 4 days later after postoperative CT showed reduced stenosis (Fig 1, B).

At 1-month follow-up, the patient’s symptoms had initially improved, but she has since returned to her preoperative baseline. PSV was still elevated in the CA origin (352 cm/s) and proximal CA (250 cm/s). Additionally, the PSV in the superior mesenteric artery and inferior mesenteric artery increased postoperatively from 146 cm/s to 279.5 cm/s, and 70.4 cm/s to 113 cm/s, respectively. An aortogram with selective celiac angiogram showed CA mid-segment stenosis of 70% and no sign of aortoiliac disease or renal artery stenosis. Thus, a 7 × 19 mm balloon-expandable covered stent was placed endovascularly in the CA at the level of the reconstruction and angioplastied to nominal diameter. Follow-up angiography showed sufficient flow through the CA and hepatic and splenic arteries without residual stenosis (Fig 2).

Fig 2.

Post-stent celiac artery (CA) angiogram showing patent CA with sufficient flow.

Two days after her discharge, she reported to the gastroenterology clinic. She endorsed symptom improvement following the stent but continued to have abdominal pain, steatorrhea, and vomitus. At her 1-month vascular follow-up, CA patency was confirmed via mesenteric DUS with no stenosis (PSV, 132 cm/s).

Further exploration of gastroenterological etiologies was deemed necessary, and she was instructed to return to the vascular clinic in 6 months for a follow-up mesenteric DUS.

The patient has consented to the publication of this manuscript.

Discussion

Median arcuate ligament syndrome (MALS) is characterized by external compression of the CA by the MAL.¹ The MAL is a fibrous band extending anteriorly across the aorta, superior to the origin of the CA, that connects the diaphragmatic crura.² Epidemiologically, two cases per 100,000 persons of MALS are observed annually, commonly affecting females and those aged 30 to 50 years.³ MALS can manifest as postprandial or exercise-induced abdominal pain, nausea, vomiting, and unintentional weight loss.

MALS is a rare complication following upper abdominal surgery, with few documented cases following bariatric surgery.[4], 5, [6] This patient’s history of obesity and absence of significant weight loss or postprandial pain prior to her RYGB suggest that her MALS likely developed postoperatively, related to anatomical and physiological changes induced by the surgery.

This case highlights three unexplored mechanisms linking RYGB to MALS development: (1) loss of intraabdominal fat pad resulting in change in angulation of the CA (Fig 3, A); (2) crural hypertrophy causing mechanical compression (Fig 3, B); and (3) gradual caudad displacement of the diaphragm following reduced intra-abdominal pressure (Fig 3, C). We postulate that crural hypertrophy following bariatric surgery and surgical division of the left crus may alter the diaphragmatic aortic angle, increasing mechanical compression of the CA and plexus.^7,8 Resulting neurogenic irritation may contribute to pain and ischemia, supported by temporary symptom relief following diagnostic celiac ganglion block.^9,10 Although not performed, a celiac ganglion block could have served useful in pain characterization and treatment planning.

Fig 3.

Possible mechanisms by which Roux-en-Y bypass (RYGB) may contribute to development of median arcuate ligament syndrome (MALS). (A) Loss of intra-abdominal fat pad alters angulation of the celiac artery (CA). (B) Postoperative crural hypertrophy may compress the celiac trunk and associated nerve plexus. (C) Reduction in intra-abdominal volume leads to gradual caudal displacement of the diaphragm.

Rapid post-bariatric weight loss may alter the diaphragmatic aortic angle, allowing caudal shift of the MAL and increased celiac trunk compression, particularly during expiration.^3,5,11 The patient lost 125 lbs over 4 years and developed symptoms 2 years post-RYGB, suggesting that gradual anatomical changes contributed to delayed onset of MALS symptoms.

Imaging techniques like CT angiography, magnetic resonance angiography, and respiratory-phase DUS are frequently employed to identify dynamic vascular compression.¹² CA PSV thresholds of 240 cm/s and 320 cm/s were identified as most accurate for detecting 50% to 70% stenosis on DUS.¹³

There remains a notable discrepancy between radiological findings and clinical symptoms. Studies indicate that between 13% and 50% of asymptomatic individuals can show radiologic evidence of CA compression.³ The patient’s abdominal CT demonstrated clear narrowing at the origin of the CA with DUS confirming elevated CA velocities during expiration. Considering her young age, characteristic MALS symptoms, and radiologic evidence, she was diagnosed with MALS.

Mainstay treatment is open or laparoscopic decompression of the MAL and often celiac ganglionectomy.^3,4 A review of 400 surgically treated patients with MALS reported that 85% of patients observed immediate postoperative symptom relief.² Of these patients, 78% received open surgery, whereas 96% received laparoscopic surgery. Laparoscopic release is associated with symptom improvement (71%-93%), shorter hospitalization, and fewer complications, whereas an open approach can help navigate aberrant anatomy.14, 15, 16 In patients with MALS following bariatric surgery, laparoscopic MALS division was reported in two of three cases,^4,5 with no reported recurrence of symptoms. Refractory cases may require advanced revascularization, with endovascular stenting needed in 30% to 40% of patients following MAL release.^17,18 CA patch angioplasty resulted in decreased DUS expiratory PSV as well as resolution of abdominal pain in 60% of these patients.^3,14,15 Larger studies are needed to define the role of endovascular treatment in MALS.

Conclusions

Given the rise in bariatric surgeries and the potential anatomical consequences of rapid weight loss, recognition of MALS as a rare post-bariatric complication is of increasing clinical relevance. Prospective studies with long-term follow-up are needed to clarify patient selection criteria, optimal management strategies, and predictors of symptom resolution or recurrence.

Funding

None.

Disclosures

None.