PurposeThe pipeline embolization device (PED) is a flow diverter that has shown promise in the treatment of intracranial aneurysms. Close to one-fifth of aneurysms, however, fail to occlude after PED placement. This study aims to identify anatomical features and clinicopathologic factors that may predispose failed aneurysm occlusion with the PED.Materials and MethodsWe retrospectively reviewed all anterior circulation unruptured saccular aneurysms treated with the PED in a single-center. The primary outcome measure was angiographic occlusion. Anatomical features and potential predictors, including gender, aneurysm location, size, height, aspect ratio, neck width, prior treatment and the number of PED, were studied using binary logistic regression.Results29 anterior circulation unruptured saccular aneurysms with a mean size of 6.99 mm treated with the PED in a single center were retrospectively studied. The overall occlusion rate was 79.3% after a mean follow-up of 9.2 months. Four aneurysms were related to the fetal-type posterior communicating artery (PComA), and all were refractory to flow diverter treatment. Female gender was significantly associated with a higher occlusion rate. We present the anatomical features and propose possible pathophysiological mechanisms of these PComA aneurysms that failed flow diverter treatment.ConclusionA PComA aneurysm with persistent fetal-type circulation appears to be particularly refractory to flow diverter treatment, especially when the aneurysm incorporates a significant portion of the PComA. Our experience suggested that flow diverting stents alone may not be the ideal treatment for this subgroup of aneurysms, and alternative modalities should be considered. Female patients were found to have a significantly higher rate of treatment success.
A 72-year-old woman had a history of carcinoma of the hypopharynx treated by total laryngectomy, circumferential pharyngectomy and free jejunal graft. Endoscopic dilation of the pharyngojejunal anastomotic stricture resulted in synchronous perforations of the oesophagus and stomach. We postulate that the perforations were caused by high intraoesophageal and intragastric pressure resulted from air insufflation during the procedure; in a situation simulating closed-loop obstruction, because of proximal obstruction by the endoscope at the stricture site and distal obstruction by pylorospasm. The sites of perforations were inherent points of weakness at the left side of the distal oesophagus and at the high lesser curve of stomach. Satisfactory outcome of our patient was attributed to prompt diagnosis and surgical repair. Endoscopists should be aware of this possibility during oesophagogastroduodenoscopy and dilation. Rapid and over insufflation of air should be avoided.
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