Case 1: A female, 63 years old, was admitted to our hospital with jaundice caused by gallbladder cancer infiltrating the bile ducts, two years after interventional internal stenting, and recurrent fever. The current situation is that stent placement after bile duct blockage can contact jaundice, especially the large bile duct branches, but the intrahepatic bile ducts are called bile duct trees and there are many, many small branches, which are infiltrated by the tumor, causing cholangitis, recurrent fever, and extremely poor quality of life. Because of the progression of the tumor, it is no longer possible to remove it surgically. Because of the poor prognosis of cholangiocarcinoma and gallbladder cancer, many patients or family members would choose the less invasive interventional treatment and refuse surgery, in fact, surgery is the only way to have long-term health survival, interventional is only a palliative treatment that cannot be operated. This patient is a typical surgical jaundice, who should have been operated on. The fact that he survived two years after the intervention indicates that the tumor is not highly malignant and not prone to metastasis and recurrence. Survival would be longer and the quality of life would be better if the surgery was successfully removed. Jianfeng Xue, Department of Hepatobiliary-Pancreatic and Liver Transplantation, First Affiliated Hospital of Zhengzhou University
Case 2: This patient was treated a few years ago and was more impressed because of the twists and turns of his treatment.
Male, 28 years old, a patient with hereditary spherocytosis, working in Guangdong, he was seen locally for jaundice and fever, his condition was mild and severe, and because of inconvenience, he had been seen in local sub-county hospitals and never diagnosed correctly. After returning home for vacation in the Spring Festival, he was diagnosed in the Department of Hematology of our hospital and was cured after being transferred to the Department of Hepatobiliary Surgery for surgical removal of the spleen.
Both patients were relatively simple patients. The first one was diagnosed correctly and the treatment choice was less appropriate. The second one had a long diagnostic process, simple treatment and a good prognosis. So to give you some ideas about the diagnosis of the cause of jaundice.
1 First determine the presence or absence of jaundice: identification of jaundice should be done in full natural light. True jaundice is caused by elevated serum bilirubin. Pseudo-jaundice is pigment-induced tissue yellowing, commonly caused by carotene, pumpkin, citrus large amounts of ingestion can cause yellowing of the whole body, but the palms of the hands, feet and plantar yellowing is significant, the sclera is generally not yellowing; yellowing caused by adipine to the corner of the eye sclera exposed parts of the most obvious, the closer the conjunctival fornix the lighter the yellow, sand exposure or the elderly two internal adjacent can occur yellow spots, should also be distinguished from jaundice. At this time, go to the hospital for laboratory tests: serum bilirubin measurement, urine bilirubin measurement, urinary urobilinogen.
2 Next, determine the type of jaundice: and according to the test results, whether the direct bilirubin is high or the indirect bilirubin is high; sometimes both can be elevated at the same time. Then, depending on the bilirubin elevation, you can roughly determine what kind of jaundice it is, and then go to the appropriate specialist.
3 If elevated indirect bilirubin (non-conjugated bilirubin) is predominant, hemolytic jaundice is more likely.
Features of hemolytic jaundice.
① mild jaundice of the sclera mostly in a light lemon color, with fever and back pain in acute attacks (hemolytic crisis), and often marked pallor of the skin mucosa.
(ii) The skin is not pruritic.
(iii) There is splenomegaly.
④ there are signs of vigorous bone marrow proliferation, such as an increase in peripheral blood reticulocytes, the presence of nucleated red blood cells, and active proliferation of the bone marrow red blood cell system.
⑤ an increase in total serum bilirubin, usually not exceeding 85umlol/L, mainly for unconjugated bilirubin.
⑥increased urinary urobilinogen without bilirubin, hemoglobinuria with a soy sauce color in acute attacks, increased urinary iron-containing heme in chronic hemolysis, and increased urinary bilirubin excretion in the feces over 24 hours.
(vii) In hereditary spherocytosis, there is an increase in erythrocyte fragility, and in thalassemia, fragility is reduced.
Most often, the patient is first seen in internal medicine, and if treatment is ineffective or medication is not tolerated, surgery may be performed.
4 Direct bilirubinemia (conjugated bilirubin), should be distinguished as hepatocellular jaundice or cholestatic jaundice
4.1 Features of hepatocellular jaundice
① light yellow to dark golden yellow skin and sclera, with sometimes pruritic skin.
(ii) Elevated unconjugated and conjugated bilirubin in the blood.
③positive bilirubin in the urine and increased urobilinogen, but at the peak of the disease, urobilinogen is reduced or absent due to intrahepatic biliary sludge, and similarly the urobilinogen content in the feces can be normal, reduced or absent.
④ Serum transaminases are markedly increased, often exceeding the upper limit of normal by a factor of 10, and often below 8 times normal in the presence of biliary sludge. Alkaline phosphatase activity tends to be greater than 2.5 times the upper limit of normal in cholestasis. If transaminases are greater than 10 times normal and alkaline phosphatase is less than 2.5 times normal, 90% are liver parenchymal disorders (e.g., hepatitis) and conversely, 90% are cholestasis.
(v) Blood markers for hepatitis virus are often positive.
(6) Liver biopsy is important for the diagnosis of diffuse liver disease.
It is mostly seen in: viral hepatitis, alcoholic liver, autoimmune hepatitis, drug-related liver injury, etc.
Most of them need medical treatment. For some patients with splenomegaly, hypersplenism, upper gastrointestinal bleeding, etc., surgical adjuvant treatment is available.
4.2 Characteristics of cholestatic jaundice
① dark yellow, yellow-green or greenish-brown complexion.
② significant skin pruritus, which often occurs before the appearance of jaundice.
③ Increased bilirubin in the blood, mainly conjugated bilirubin, with a direct response to qualitative bilirubin test.
④positive urinary bilirubin, but reduced or absent urobilinogen.
(5) Decreased or absent urobilinogen in the feces, with light gray or clay-colored feces.
(6) Increased serum total cholesterol, alkaline phosphatase, gamma glutamyl transpeptidase, and positive lipoproteins.
Differentiation of intrahepatic or extrahepatic type
According to the etiology and mechanism of occurrence, extrahepatic obstruction, intrahepatic obstruction and intrahepatic cholestatic jaundice can be classified according to the anatomical site causing the biliary sludge.
1) Extrahepatic obstructive cholestasis: cholelithiasis, biliary ascariasis, cholangitis, cancer infiltration, post-surgical bile duct stenosis; extrahepatic obstruction includes bile duct compression caused by periampullary cancer, pancreatic head cancer, hepatocellular carcinoma, metastasis of lymph nodes around the hilar or common bile duct, etc.
(2) Intrahepatic obstructive cholestasis includes intrahepatic sediment-like stones, primary liver cancer invading intrahepatic bile ducts or forming cancer emboli, and schistosomiasis of T. huaji.
(3) Intrahepatic cholestasis is seen in viral hepatitis, drug-related jaundice (such as those caused by chlorpromazine and methyltestosterone), primary biliary cirrhosis and recurrent jaundice during pregnancy.
Identify the cause of extrahepatic cholestasis and treat it surgically.
The etiology of intrahepatic cholestasis is identified and treated medically.
There are also some congenital non-hemolytic jaundice