RESUMO
Median arcuate ligament syndrome (MALS) is caused by constriction of the celiac artery (CA) by the median arcuate ligament of the diaphragm. Ligament release improves perfusion of the CA, resulting in resolution of abdominal symptoms. A 51-year-old female had postprandial abdominal pain for 10 years and underwent computed tomography (CT) scan showing severe stenosis of the CA with pancreatoduodenal arcade aneurysm formation. MALS was diagnosed, and open median arcuate ligament incision was performed to decompress the CA. Intraoperative ultrasonography showed bidirectional turbulent flow in the common hepatic artery (CHA). The median arcuate ligament was uneventfully incised, and compression of the CA released. The perfusion in the CHA was changed to an antegrade direction, and the flow increased. Seven days after the laparotomy, the patient was discharged uneventfully. Follow-up CT scan 20 days after operation showed a diminished pancreatoduodenal arcade aneurysm and inferior pancreatoduodenal artery. Epigastric pain and postprandial distress symptoms were improved. In conclusion, perfusion of the CHA became normalized after median arcuate ligament release. Surgical intervention for MALS not only improved blood flow in the tributaries but also diminished the pancreatoduodenal arcade aneurysm.
RESUMO
BACKGROUND AND AIM: Pancreaticoduodenal arcade aneurysms (PDAAs) are uncommon lesions associated with a significant risk of rupture and mortality. This study describes the etiology, clinical presentation, and endovascular management strategies of PDAAs across a spectrum of indications. METHODS: The clinical records of patients with PDAAs referred for endovascular management from January 2018 till November 2019 were retrospectively reviewed. Data on presenting symptoms, associated etiologies, and outcomes after endovascular treatment were collected and studied. RESULTS: We found 15 patients with false and 1 patient with true aneurysm of pancreatoduodenal arcade (PDA). The associated conditions were coeliac artery stenosis, severe necrotizing pancreatitis, and chronic pancreatitis or iatrogenic (postendoscopic papillotomy and percutaneous metallic biliary stenting). The main presenting feature was gastrointestinal bleed, while 2 patients had abdominal pain and 1 had gastric outlet obstruction. A multiphase computed tomography scan demonstrated the ruptured aneurysm in all patients. Site of origin of PDAA influenced the choice of transarterial endovascular strategy (coiling for aneurysms of main trunk of arteries and glue injection for those arising from small arterial branches). This was carried out in an emergency setting for 12 patients and as an elective procedure in 4 patients. Technical success was demonstrated in all patients and clinical success in 14. The two patients who had rebleed were salvaged by repeat endovascular procedure. Postembolization syndrome was seen in three patients. CONCLUSIONS: With advancing technology, endovascular strategies continue to evolve. Careful attention to ensure hemodynamic resuscitation and stability, correction of pre-existing coagulopathy and attention to technique can lead to the possibility of endovascular approaches as a dependable option in the management of ruptured PDAAs.