Changing Ischemic Lesion Patterns and Hemodynamics of the Posterior Cerebral Artery in Moyamoya Disease.

OBJECTIVE: The aim of this study was to determine how hemodynamics of the posterior cerebral artery (PCA) are associated with cerebral ischemic lesions in moyamoya disease (MMD). METHODS: Thirty-six patients with ischemic MMD (Suzuki grade IV-V) were retrospectively analyzed. Hemodynamic parameters of the PCA were measured by transcranial color-coded sonography. We classified the range of ischemic lesions into 3 grades and perfusion levels into 3 grades according to computed tomography (CT) results. PCA steno-occlusion and leptomeningeal collaterals were confirmed by digital subtraction angiography. Ultrasonographic parameters in the PCA were compared with these radiographic findings. RESULTS: The velocity in the involved PCA (mean flow velocity [MFV] median, 42.00 [range, 34.50-58.00] cm/s) was significantly lower than that in the normal PCA (MFV median, 95.00 [range, 76.50-119.50] cm/s) (P < .001). The velocity in the PCA increased significantly as the leptomeningeal collateral stage advanced (MFV stage 1: median, 38.50 [range, 29.75-63.50] cm/s; stage 2: median, 55.00 [range, 44.00-96.00] cm/s; stage 3: median, 94.00 [range, 54.00-118.25] cm/s; stage 4: median, 85.50 [range, 70.50-117.75] cm/s, respectively) (P < .05). Decreased PCA velocities were associated with a larger ischemic area on CT (P ≤ .001). PCA velocity had no correlation with CT perfusion level of the temporal and frontal lobes. PCA velocity had significant correlations with perfusion level in the occipital (P < .001) and parietal lobes (P < .05). CONCLUSIONS: Our results suggest ischemic lesion patterns (as demonstrated on CT imaging) are associated with PCA velocity measurements in the advanced stage of MMD. Thus, monitoring PCA velocity in patients with advanced MMD may provide additional information to assist in managing these patients.

Etiology and surgical treatment of hilar bile duct stricture.

OBJECTIVE: To improve the surgical effects of hilar duct stricture. METHODS: The clinical data of 76 patients with hilar bile duct stricture treated at our hospital from 1990 to 2000 were analyzed. The diagnosis was determined by triad signs of cholangitis, increase of ALP and gamma-GGT levels, dilation of intrahepatic and extrahepatic bile ducts confirmed by ultrasonography (US), computed tomography (CT), percutaneous transhepatic cholangiography (PTC) or endoscopic retrograde cholangiopancreatography (ERCP). The location of stricture was divided according to the Bismuth classification standard. RESULTS: Among the 76 patients, 46 (60.5%) suffered from injurious stricture, including 13% of Bismuth type I, 39% of type II, 19.4% of type III, and 28.2% of type IV. Inflammatory stricture was found in 28 patients, locating in the left hepatic duct (LHD) 46.4% (13/28), the right hepatic duct (RHD) 35.7% (10/28), and the common hepatic duct (CHD) 17.9% (5/28), respectively. The percentages of patients with stricture due to Mirizzi's syndrome, bile duct cyst, and sclerosing cholangitis were 9.2%, 3.9% and 2.6%, respectively. Bile duct repair procedures included biliary reconstruction with pedicled umbilical vein graft for 9.2% of the patients, and proximal cholangiojejunostomy combined with LHD and RHD plasticity for 92.2%. Seventy of the 76 patients were followed up for 2-10 years, and the excellent outcome rate was 94.7%. CONCLUSIONS: Injurious stricture is the major type of hilar bile duct stricture. Inflammatory stricture is mainly composed of RHD. Hilar bile duct stricture should be treated surgically according to various etiological features and technical principles of biliary repair.