In Reply to: Case 997_05 -- Median arcuate ligament syndrome posted by Editor on September 16, 1997 at 10:57:08:
The median arcuate ligament syndrome has been one of the controversial topics in vascular surgery primarily in the mid 80's although it does flare up occasionally. I took the liberty and copied the abstract of a landmark paper from San Francisco.
Reilly LM; Ammar AD; Stoney RJ; Ehrenfeld WK. Late results following operative repair for celiac artery compression syndrome. Journal of Vascular Surgery, 1985 Jan, 2(1):79-91.
Abstract: The clinical significance of celiac artery compression by the median arcuate ligament of the diaphragm remains unsettled. The controversy stems from an undefined pathophysiologic mechanism and the existence of celiac compression in asymptomatic patients. This study was therefore conducted to evaluate the late results of operative therapy among our patients and possibly to identify parameters that might correlate with sustained symptom relief. Among 51 patients (12 men and 39 women) (mean age 47 years) who underwent operative treatment for symptomatic celiac artery compression, 44 (86%) were available for late follow-up. Their clinical status was determined between 1 and 18 years postoperatively (mean 9.0 years) by patient interview (36) or chart review (7). Operative treatment consisted of celiac axis decompression only (16 patients), celiac decompression and dilatation (17 patients), or celiac decompression and reconstruction by primary reanastomosis or interposition grafting (18 patients). Sustained symptom relief occurred more often with a postprandial pain pattern (81% cure), age between 40 and 60 years (77%), and weight loss of 20 pounds or more (67%). A negative correlation with clinical improvement was demonstrated for an atypical pain pattern with periods of remission (43% cure), a history of psychiatric disorder or alcohol abuse (40%), age greater than 60 years (40%), and weight loss of less than 20 pounds (53%). Eight of 15 patients (53%) treated by celiac decompression alone remained asymptomatic at late follow-up in contrast to 22 of 29 patients (76%) treated by celiac decompression plus some form of celiac revascularization.Late follow-up arteriograms (18 studies) showed a widely patent celiac artery in 70% of asymptomatic patients but a stenosed or occluded celiac
axis in 75% of symptomatic patients. These findings suggest that persistent clinical improvement in patients with symptomatic celiac axis compression can be achieved by an operative technique that ensures celiac axis patency.
Although some clinical features are identified that correlate with
long-term benefit, reliable diagnosis of the symptomatic patient awaits definition of the pathophysiologic mechanisms involved in this syndrome.
Does the proposed pathophysiology of mesenteric ischemia make sense. Probably not. Yet it is an entity that the surgeons claim they can sometimes fix. Are they fixing mesenteric ischemia or perhaps something else. Another theory claims that what is really entraped and causes symptoms is the celiac ganglion. This makes a lot more sense to me. Attempting to treat a celiac lesion as seen in this well illustrated case percutaneously, in my opinion, would not be a good idea.