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JAMA Surgery Clinical Challenge
March 2016

Postprandial Abdominal Pain

Author Affiliations
  • 1Division of Vascular Surgery, Northwestern University, Feinberg School of Medicine, Chicago, Illinois
  • 2Interventional Radiology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois
  • 3Jesse Brown, Veterans Affairs Medical Center, Chicago, Illinois
  • 4Editor, JAMA Surgery
JAMA Surg. 2016;151(3):287-288. doi:10.1001/jamasurg.2015.4715

An active man in his early 80s presented to the hospital with a 6-month history of cramping epigastric abdominal pain that occurred 30 minutes after eating solid food and was associated with nausea and vomiting. His medical history was significant for atrial fibrillation and a history of an open abdominal aortic aneurysm repair. Review of systems revealed a 9-kg weight loss. A recent esophagogastroduodenoscopy was unremarkable, but prior colonoscopy showed focal colitis that was treated with antibiotics. Physical examination revealed he was in sinus rhythm. He had no abdominal tenderness but had an abdominal bruit. Laboratory examination results were unremarkable. Mesenteric duplex ultrasonography showed the following: celiac artery velocity of 394 cm/s on inspiration (Figure, A) and 608 cm/s on expiration (Figure, B), superior mesenteric artery (SMA) velocity of 380 cm/s, and an occluded inferior mesenteric artery. Subsequent angiography corroborated findings.

Mesenteric duplex ultrasonography showing celiac artery velocities with inspiration (A) and expiration (B).

Mesenteric duplex ultrasonography showing celiac artery velocities with inspiration (A) and expiration (B).

Box Section Ref ID

What Is Your Diagnosis?

  1. Gastroparesis

  2. SMA syndrome

  3. Acute mesenteric ischemia

  4. Median arcuate ligament syndrome

Read the Discussion.


D. Median arcuate ligament syndrome

The patient was an elderly, but independent man who had postprandial abdominal pain leading to weight loss. He had a history of an open abdominal aortic aneurysm repair and was dependent on his celiac artery and SMA for mesenteric perfusion. Imaging revealed atherosclerotic disease of the SMA with near occlusion of the celiac artery on full expiration. These findings are suggestive of median arcuate ligament (MAL) syndrome.

Median arcuate ligament syndrome, also known as celiac artery compression syndrome or Dunbar syndrome, is a clinical entity caused by extrinsic compression of the celiac axis by the fibers of the diaphragmatic crura, leading to postprandial abdominal pain, nausea and/or vomiting, and weight loss.1 It has a female-to-male ratio of approximately 4:1,2 and its diagnosis is often one of exclusion and controversy.

The anatomic pathogenesis is thought to arise from an abnormally low insertion of the diaphragm and/or high origin of the celiac axis.1,3 Although the degree of compression varies by individual, inspiration causes inferior displacement of the aorta and anterior displacement of the MAL, causing release of the celiac axis and thereby perfusion into the celiac artery.4 Histologically, repetitive compression of the celiac artery by the MAL causes fibrotic changes of all layers of the vessel wall leading to neointimal hyperplasia and medial and adventitial hyperplastic fibrosis.5

The diagnosis of MAL syndrome is often one of exclusion, although the relief of symptoms after treatment has been argued to validate its true entity. When MAL syndrome is suspected, mesenteric duplex with measurements on inspiration and expiration is the preferred initial imaging modality. Findings typically include elevated velocities of the celiac artery on expiration, which normalize on inspiration. Other findings include abnormal origins of the celiac artery, reversal of flow of the hepatic artery, and normalization of the celiac artery when standing erect.6 Findings are often confirmed with computed tomography angiography/magnetic resonance angiography and/or digital subtraction angiography, which can show dynamic variability of celiac artery flow according to breathing cycle.

The treatment for MAL syndrome is ligament release through either a laparoscopic or open approach. A minority of patients require celiac ganglionectomy and/or concomitant celiac artery revascularization, but overall 85% of patients report immediate postoperative relief.7 Some reports demonstrate that patients who undergo ligament release with concomitant revascularization have lower rates of recurrence than with decompression alone.8 In general, endovascular interventions alone have not demonstrated long-term efficacy.9,10

Because of the concomitant atherosclerotic nature of the SMA, the patient underwent an angioplasty with improvement in his postprandial abdominal pain. His age, comorbidities, and previous abdominal surgery made him a poor candidate for laparoscopic MAL release. The patient chose to have close follow-up and modify his diet to multiple small meals per day instead of open surgery.

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Article Information

Corresponding Author: Melina R. Kibbe, MD, Division of Vascular Surgery, 676 N St Clair, Ste 650, Chicago, IL 60611 (mkibbe@nm.org).

Published Online: January 20, 2016. doi:10.1001/jamasurg.2015.4715.

Conflict of Interest Disclosures: None reported.

Disclaimer: Dr Kibbe is the Editor of JAMA Surgery but was not involved in the editorial review or the decision to accept the manuscript for publication.

Section Editor: Pamela A. Lipsett, MD, MHPE.
Duffy  AJ, Panait  L, Eisenberg  D, Bell  RL, Roberts  KE, Sumpio  B.  Management of median arcuate ligament syndrome: a new paradigm. Ann Vasc Surg. 2009;23(6):778-784.
Trinidad-Hernandez  M, Keith  P, Habib  I, White  JV.  Reversible gastroparesis: functional documentation of celiac axis compression syndrome and postoperative improvement. Am Surg. 2006;72(4):339-344.
Lipshutz  B.  A composite study of the coeliac axis artery. Ann Surg. 1917;65(2):159-169.
Reuter  SR, Bernstein  EF.  The anatomic basis for respiratory variation in median arcuate ligament compression of the celiac artery. Surgery. 1973;73(3):381-385.
Bech  FR.  Celiac artery compression syndromes. Surg Clin North Am. 1997;77(2):409-424.
Scholbach  T.  Celiac artery compression syndrome in children, adolescents, and young adults: clinical and color duplex sonographic features in a series of 59 cases. J Ultrasound Med. 2006;25(3):299-305.
Jimenez  JC, Harlander-Locke  M, Dutson  EP.  Open and laparoscopic treatment of median arcuate ligament syndrome. J Vasc Surg. 2012;56(3):869-873.
Reilly  LM, Ammar  AD, Stoney  RJ, Ehrenfeld  WK.  Late results following operative repair for celiac artery compression syndrome. J Vasc Surg. 1985;2(1):79-91.
Wang  X, Impeduglia  T, Dubin  Z, Dardik  H.  Celiac revascularization as a requisite for treating the median arcuate ligament syndrome. Ann Vasc Surg. 2008;22(4):571-574.
Matsumoto  AH, Angle  JF, Spinosa  DJ,  et al.  Percutaneous transluminal angioplasty and stenting in the treatment of chronic mesenteric ischemia: results and longterm followup. J Am Coll Surg. 2002;194(1)(suppl):S22-S31.