2021年 · 第59卷第04期

Biliary casting is composed of sediment-like stones accumulated in the bile duct, filling the intrahepatic and extrahepatic bile ducts, and running in line with the bile duct^［1］The appearance is mostly gray-black, dead branch-like, and the texture is tough. Biliary casting filling into the biliary tree can cause varying degrees of biliary stenosis, biliary dilatation, cholangitis, and/or liver microabscess. Once the biliary casting is formed, it is extremely difficult to treat, and it is mostly a serious complication after liver transplantation, with an incidence rate of over 7%^［2］。 Biliary casting after non-transplantation has been reported occasionally at home and abroad. Because of its rare incidence and no specific clinical signs, it is easy to cause misdiagnosis and misdiagnosis. The clinical data, auxiliary examinations and treatment methods of 2 patients with non-transplanted biliary cast syndrome (BCS) admitted to our hospital are analyzed in order to improve the understanding of this disease.

The patient, a 58-year-old male, was admitted to the hospital on 25-Nov-2019 due to "1 d of upper abdominal pain after eating". The patient had no obvious trigger to develop upper abdominal pain after eating, accompanied by fever, yellowing of the skin and mucosa of the whole body, chills, general fatigue, no diarrhea, no pain in urination, frequent urination, no cough, expectoration, and no sore throat. The emergency department was admitted to the hospital with "acute cholangitis". The previous patient underwent orthotopic liver transplantation in our hospital on August 14, 2001 due to "post-hepatitis B cirrhosis and liver failure". He recovered well after the operation and regularly took immunosuppressant anti-rejection treatment. In 2007, he voluntarily stopped taking all anti-rejection drugs. He has a history of diabetes for more than 20 years. Oral Baitangping and metformin are used to control blood sugar, but blood sugar control is not good. Physical examination after admission: body temperature 39.3 ℃, heart rate 110 beats/min, breathing 22 beats/min, blood pressure 90/60 mmHg (1 mmHg =0.133 kPa); Soft abdomen, tenderness in the upper abdomen, no rebound pain, muscle tension and other peritonitis manifestations. Emergency blood test showed white blood cell count 13.0×10⁹/L, neutrophil percentage 93%; Liver function tests showed total bilirubin 207.2 μ mol/L, direct bilirubin 160.8 μ mol/L, albumin 26.4 g/L and blood glucose 10.90 mmol/L; Magnetic resonance cholangiopancreatography showed calculi of the common bile duct and common hepatic duct, partial dilatation of the intrahepatic bile duct, and multiple wall thickening of the intrahepatic bile duct and common bile duct (FIG. 1A）。 Diagnosis considers cholangitis, common bile duct and common hepatic duct stones are more likely. After consultation with the gastroenterology department on November 30, 2019, nasobiliary drainage was performed. Intraoperative angiography showed that the intrahepatic bile duct was slender, the bile duct near the hilar anastomosis was disordered and slightly narrowed, and multiple filling defects of 0.2~0.4 cm were seen in the common bile duct and the bile duct above the anastomosis. On December 6, 2019, endoscopic retrograde cholangiopancreatography cholangiolithotomy was performed. Two black stones were removed from a net basket, the largest of which had a maximum diameter of 1.2 cm, and placed into nasobiliary duct for drainage. The patient's body temperature and bilirubin level gradually decreased after operation, and the nasobiliary duct was removed and discharged from hospital on December 11th.

The patient, a 79-year-old male, was admitted to the hospital on March 24, 2019 mainly due to "loss of appetite with acid reflux and heartburn for more than 10 days". More than 10 days ago, the patient developed loss of appetite without obvious trigger, self-complaining of bitter mouth, accompanied by acid reflux and heartburn, which occurred at night, accompanied by abdominal distension, which was persistent and had nothing to do with eating. There was no abdominal pain, diarrhea, hematemesis, melena, fever, palpitations and hand tremor. The outpatient clinic was admitted to the hospital with "reflux esophagitis". Parenteral nutritional support was given after admission with a tumor marker of 151.04 U/ml for CA19-9 and 47.83 U/ml for CA50. Abdominal CT examination showed localized thickening of the wall of the ascending colon and narrowing of the lumen, which was considered malignant. Gastroscopy: duodenal bulb mucosal lesions, duodenal bulb stenosis; The results of biopsy showed chronic inflammation of intestinal mucosa with eosinophil infiltration and some glandular epithelial hyperplasia. Colonoscopy: Colon Cancer? Biopsy results showed colonic tubular adenoma, villous adenoma, moderate dysplasia of the glandular epithelium, and some severe dysplasia. Enhanced CT scan of the abdomen: localized thickening of the wall of the ascending colon and narrowing of the lumen, considering the possibility of malignancy, poor duodenal filling and obvious thickening of the wall (Figure 1）。 PET-CT showed: soft tissue thickening of ascending colon with abnormal hypermetabolism, which was considered malignant, and peripheral infiltration was not excluded; Duodenal localized abnormal hypermetabolism (Figure 2), CT images showed faint thickening, not excluding malignancy. Preoperative diagnosis: duodenal occupation, ascending colon occupation.

A 55-year-old male was admitted to the hospital on June 19, 2019 due to "recurrent middle and upper abdominal pain for 2 years, aggravated with skin and sclera yellowing for 3 days". In 2009, the patient underwent right posterior lobectomy in a foreign hospital due to primary liver cancer. In 2015, he underwent exploratory laparotomy, radiofrequency ablation of liver tumor and gastrojejunostomy due to recurrence of liver cancer. After operation, he underwent three hepatic artery chemoembolization treatment due to tumor recurrence. At present, he has been taking sorafenib orally for more than half a year. Two years ago, the patient began to experience pain and discomfort in the middle and upper abdomen, accompanied by radiating pain in the lower back, occasionally accompanied by nausea and vomiting. The patient developed chills and fever 3 days ago, and the maximum body temperature reached 39.5 ℃. Physical examination: Moderate yellowing of the skin and sclera throughout the body, tenderness in the right upper abdomen, no rebound pain and muscle tension. After admission, he was given hepatoprotective, antispasmodic and anti-infective treatment. The results of CT examination of the upper abdomen showed: (1) Space-occupying lesions of the gallbladder, considering the possibility of new biology, thickening of the wall of the lower common bile duct, considering the possibility of cholangitis, not excluding the possibility of new biology; (2) Liver cirrhosis, low density shadow near the second hepatic hilum, considering the possibility of inflammatory lesions (Figure 1）。 Liver function tests: albumin 37.1 g/L, total bilirubin 125.7 μ mol/L, direct bilirubin 72.9 μ mol/L, AST 111.5 U/L, ALT 355.8 U/L, glutamyl transpeptidase 289.1 U/L. Tumor marker: alpha-fetoprotein 401.23 μ g/L. Blood routine: white blood cell count 16.47×10⁹/L, the percentage of neutrophils was 94.9%. Four items of coagulation: the international normalized ratio of prothrombin time was 1.64, and prothrombin time was 13.8 s. Blood inflammatory markers: procalcitonin 4.77 μ g/L, IL-6 201.5 ng/L, hepatitis B surface antigen negative. Preoperative diagnosis: (1) acute cholangitis; (2) The gallbladder occupies space, and gallbladder cancer is possible.

The physician can do all he has to do with speed and precision, but he must never appear to be in a hurry, and never absent-minded.