PURPOSE: To assess the frequency of diaphragmatic weakness and its determinant factors after transcatheter arterial chemoembolization of the right inferior phrenic artery (IPA) in patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: From June 2006 to October 2006, 60 patients (48 men, 12 women; mean age, 59 years) who had undergone chemoembolization of the right IPA underwent follow-up angiography of the right IPA and fluoroscopic diaphragmatic movement assessment. Diaphragmatic weakness was determined by the presence of paradoxical or decreased movement at fluoroscopy. As determinant factors, the extent of embolization (selective chemoembolization of the anterior or posterior branch vs nonselective chemoembolization), the use of gelatin sponge pledgets, additional cisplatin infusion, the size of a tumor supplied by the right IPA (>or=48 mm vs <48 mm), multiplicity of right IPA chemoembolization, and the extent of occlusive changes (single vs both branches) at follow-up right IPA angiography were assessed. The chi(2) and logistic regression tests were used to identify determinant factors of diaphragmatic weakness. RESULTS: Diaphragmatic weakness occurred in 11 of the 60 patients (18%). All 11 patients complained of shoulder pain during chemoembolization, but persistent dyspnea did not develop. Nonselective embolization (P = .005) and occlusive changes of both right IPA branches at follow-up angiography (P = .002) were significant determinant factors, as determined with univariate analysis. As determined with multivariate analysis, an occlusive change of both right IPA branches was the only significant determinant factor (P = .009; odds ratio, 17.2). Diaphragmatic weakness developed in 10 of the 28 patients (36%) with occlusive changes of both right IPA branches and only one (3.1%) of the remaining 32 patients. CONCLUSIONS: When chemoembolization of the right IPA is nonselectively performed and with permanent occlusive changes of the right IPA, diaphragmatic weakness can develop in one-third of patients as an ischemic complication.
PURPOSE: To assess the frequency of diaphragmatic weakness and its determinant factors after transcatheter arterial chemoembolization of the right inferior phrenic artery (IPA) in patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: From June 2006 to October 2006, 60 patients (48 men, 12 women; mean age, 59 years) who had undergone chemoembolization of the right IPA underwent follow-up angiography of the right IPA and fluoroscopic diaphragmatic movement assessment. Diaphragmatic weakness was determined by the presence of paradoxical or decreased movement at fluoroscopy. As determinant factors, the extent of embolization (selective chemoembolization of the anterior or posterior branch vs nonselective chemoembolization), the use of gelatin sponge pledgets, additional cisplatin infusion, the size of a tumor supplied by the right IPA (>or=48 mm vs <48 mm), multiplicity of right IPA chemoembolization, and the extent of occlusive changes (single vs both branches) at follow-up right IPA angiography were assessed. The chi(2) and logistic regression tests were used to identify determinant factors of diaphragmatic weakness. RESULTS:Diaphragmatic weakness occurred in 11 of the 60 patients (18%). All 11 patients complained of shoulder pain during chemoembolization, but persistent dyspnea did not develop. Nonselective embolization (P = .005) and occlusive changes of both right IPA branches at follow-up angiography (P = .002) were significant determinant factors, as determined with univariate analysis. As determined with multivariate analysis, an occlusive change of both right IPA branches was the only significant determinant factor (P = .009; odds ratio, 17.2). Diaphragmatic weakness developed in 10 of the 28 patients (36%) with occlusive changes of both right IPA branches and only one (3.1%) of the remaining 32 patients. CONCLUSIONS: When chemoembolization of the right IPA is nonselectively performed and with permanent occlusive changes of the right IPA, diaphragmatic weakness can develop in one-third of patients as an ischemic complication.