Abstract: Objective:To summarize the clinicopathological characteristic, diagnosis and treatment of iatrogenic biliary tree destruction.
Methods:The retrospective crosssectional study was conducted. The clinical data of 11 patients with iatrogenic biliary tree destruction who were admitted to the Chinese PLA General Hospital (9 patients) between January 1990 and December 2013 and Beijing Tsinghua Changgung Hospital (2 patients) between December 2014 and May 2017 were collected. Observation indicators: (1) causes and parts of destruction; (2) clinical manifestation; (3) imaging performance; (4) treatment; (5) followup. Followup using outpatient examination and telephone interview was performed to detect longterm prognosis of patients up to April 2018. Measurement data with skewed distribution were described as M (range).
Results:(1) Causes and parts of iatrogenic biliary tree destruction: causes of iatrogenic biliary tree destruction in 11 patients: transcatheter arterial embolization for hepatic hemangioma was performed in 7 patients, high intensity focused ultrasound for hepatic hemangioma in 1 patient, arterial embolization for false aneurysm in 1 patient, sclerosant injection for hepatic echinococcosis in 1 patient, and cyberknife radiotherapy for hepatocellular carcinoma in 1 patient. Parts of biliary tree destruction of 11 patients: 5, 3, 2 and 1 respectively involved bilateral biliary tree, right biliary tree, bilateral main biliary ducts in hepatic port and left biliary tree. (2) Clinical manifestation: 11 patients had symptoms of recurrent chills and fever, and combined with different degrees of jaundice. The initial symptom occurred in 2 weeks to 3 months after iatrogenic biliary tree destruction. Of 11 patients, 7 were complicated by different degrees of hepatic abscess, and abscess involving left and right half liver were detected in 4 patients, aggregating in right half liver in 2 patients and aggregating in left half liver in 1 patient. Eight patients had secondary biliary cirrhosis, portal hypertension, splenomegaly and hypersplenism during the late course of disease. (3) Imaging performance: magnetic resonanced cholangiopancreatography (MRCP) and cholangiography examinations showed missing bile duct in necrosis area, beadinglike stricture and dilation of damaged biliary tree, reducing proximal bile duct branches and associated gallbladder necrosis. CT and MRI examinations showed that structure of distribution area of damaged biliary tree disappeared or bile duct wall was thickened, and hepatic abscesses of patients were scattered and multiple. Five patients had significantly secondary liver atrophyhypertrophic syndrome, showing atrophy of right liver and hyperplasia of left liver. Radiotherapyinduced biliary tree destruction showed a characteristic of continued progress, localized abnormality in the early stage and typical imaging changes after the damage stability in the late stage. (4) Treatment: of 11 patients, 4 didn′t undergo surgery, and 7 underwent 18 intentional and conclusive surgeries (1-4 times / per case). (5) Followup: 11 patients were followed up for 2-132 months, with a median time of 73 months. During the followup, 2, 1 and 8 patients had respectively excellent, good and poor prognoses. Among 11 patients, 4 died (2 died of severe infection and 2 died of biliary cirrhosis), and 7 survived.
Conclusions:Iatrogenic biliary tree destruction is easy to cause hepatic abscess, liver atrophyhypertrophic syndrome or biliary cirrhosis, and it can be diagnosed by imaging examination. The definitive treatment should be followed by liver resection or liver transplantation of involving area according to the extent of damage.