Clinical anatomy of celiac artery compression syndrome: A review

Abstract

Anatomic variations are often responsible for a variety of clinical conditions. In this review we investigate compression of the celiac artery and the superior mesenteric artery by the median arcuate ligament (MAL), diaphragmatic crura, or the celiac nerve plexus. This clinical condition known as celiac artery compression syndrome (CACS) has proven controversial in definition and relevance. This condition was first described as chronic abdominal pain because of the mesenteric ischemia caused by extrinsic compression of the celiac artery. Dunbar and others presented surgical approaches to decompress the celiac artery by releasing the MAL. Definitive answers have been sought to classify and relieve the clinical symptoms patients experience postprandially. Persistent symptoms following surgical treatment for CACS have led investigators to question the existence of this disease. Advances in technology such as angiographic MRI and color duplex ultrasonography have refreshed the importance of considering compression of the celiac artery during differential diagnoses. Because of the varying anatomic etiologies of disease, it is not possible to pinpoint a single cause for CACS. Potential etiologies for compression of the celiac artery include a "high take off" origin of the celiac artery compressed by normal diaphragmatic crura and MAL, a normal origin of the celiac artery with long diaphragmatic crura and MAL, large bilaterally fused celiac ganglia (with or without the involvement of the superior mesenteric ganglia) compressing the celiac trunk, celiacomesenteric trunk compression by diaphragmatic crura and MAL, or combinations of the above mentioned entities. In this review we describe potential sources of compression of the celiac artery by regional structures and treatments of CACS in an effort to justify the relevance of CACS in modern medicine.

Pancreatic Arcade Artery Aneurysm—A Rare Complication after Replacement of Thoracoabdominal Aortic Aneurysm

“…1,2) In some cases, compression by the median arcuate ligament can explain the mechanism of CA stenosis. 3,4) Once the CA becomes stenotic or occluded, retrograde blood supply from the SMA into the pancreatic arcade is increased. This hemodynamic alteration might evoke dilatation or aneurysmal change in the pancreaticoduodenal artery.…”

“…Generally, etiology of the disease includes celiac artery (CA) stenosis or occlusion, atherosclerosis, infection, and trauma. 1,2) In some cases, compression by the median arcuate ligament can explain the mechanism of CA stenosis 3,4) and subsequent aneurysmal formation. 5) Regarding the formation, that mechanism has been speculated that once the CA becomes stenotic or occluded, a flow and pressure within the pancreatic arcade relatively increase, resulting in subsequent development of the aneurysm.…”

Dunbar’s syndrome: A rare and unclear entity

“…Dunbar's syndrome, median arcuate ligament syndrome (MALS) or celiac artery compression syndrome (CACS) is caused by external compression of the celiac trunk by the MAL, and is characterized by postprandial abdominal pain, nausea, vomiting, and weight loss (1). MALS is a rare entity, which is diagnosed in only 2 of 100,000 patients with ambiguous upper abdominal pain (2).…”

Median Arcuate Ligament Syndrome: An Unusual Cause of Chronic Abdominal Pain

“…One hypothesis is that the median arcuate ligament has a compressive effect on the celiac trunk causing pain and ischemia [7]. Another proposed mechanism for the pain in MALS is direct irritation of the celiac plexus, which lies in close proximity to the celiac artery [8]. Stimulation of the bundle of nerves that comprise the celiac plexus may either prompt inappropriate stimulation of pain fibers resulting in abdominal discomfort [9] or induce fibrotic changes such as celiac plexus neuromas that subsequently constrict the celiac trunk [10].…”