Jaundice

Introduction to Huang Wei Jaundice is a clinical manifestation of hyperbilirubinemia, in which blood bilirubin increases and yellow stains the sclera, skin, mucous membranes, and other tissues and body fluids. The bilirubin in normal blood is only 17mol/L (1.0mg/dl). If the bilirubin exceeds the normal value and the jaundice is still invisible to the naked eye, it may be called recessive or subclinical jaundice. Astragalus is not an independent disease, but a symptom and sign of many diseases, especially in liver, biliary and pancreatic diseases. Astragalus is an important pathological change of liver dysfunction, but not all jaundice is caused by liver dysfunction, such as erythrocyte destruction caused by hemolytic jaundice, obstructive jaundice caused by extrahepatic bile duct obstruction. basic knowledge The proportion of sickness: 0.01% Susceptible people: more in children Mode of infection: non-infectious Complications: acute yellow accumulation

Cause of jaundice

Hemolytic jaundice (20%):

Any disease that causes hemolysis due to massive destruction of red blood cells can cause hemolytic jaundice. The common diseases are as follows.

(1) Congenital hemolytic anemia: such as thalassemia (hemoglobinopathy), hereditary spherocytosis.

(2) Acquired acquired hemolytic anemia: such as autoimmune hemolytic anemia, hereditary glucose-6-phosphate dehydrogenase deficiency (folly bean disease), hemolysis after heterotypic transfusion, neonatal hemolysis, falciparum malaria, primaquine Lin and other drugs, snake venom, poisonous cockroach poisoning, paroxysmal nocturnal hemoglobinuria.

Hepatocyte jaundice (20%):

Various liver diseases, such as viral hepatitis, toxic hepatitis, drug-induced liver disease, various types of cirrhosis, primary and secondary liver cancer, sepsis and leptospirosis, can cause jaundice due to diffuse damage of liver cells. .

Obstructive jaundice (cholestasis jaundice) (15%):

According to the site of obstruction, it can be divided into two types: extrahepatic bile duct and intrahepatic bile duct obstruction.

(1) common diseases causing obstruction of extrahepatic bile duct, including common bile duct stones, stenosis, inflammatory edema, aphids, tumors and congenital biliary atresia; common diseases or causes of bile duct obstruction leading to obstruction of common bile duct, pancreatic Head cancer, chronic pancreatitis with enlarged pancreatic head, ampullary carcinoma, common bile duct cancer, liver cancer, and lymph nodes (cancer metastasis) around the hilar or common bile duct.

(2) intrahepatic bile duct obstruction can be divided into intrahepatic obstructive cholestasis and intrahepatic cholestasis. The former is common in intrahepatic bile duct-like stones, cancerous thrombosis (mostly liver cancer), clonorchiasis, etc.; Common in capillary bile duct viral hepatitis, drug-induced cholestasis (such as chlorpromazine, methyltestosterone, oral contraceptives, etc.), bacterial sepsis, recurrent jaundice during pregnancy, primary biliary cirrhosis And a few heart or abdominal surgery and so on.

Congenital non-hemolytic jaundice (10%):

It refers to the congenital defects of bilirubin metabolism. The incidence is more common in infants, young children and young people. It often has a family history. If you can survive without death in infants and young children, the jaundice can recur, often in a cold or exercise. Infection, induced after fatigue, but the general health of the patients is good, such jaundice is less common in clinical, sometimes misdiagnosed as hepatobiliary diseases, the common diseases of this type of jaundice are the following.

(1) Gilbert syndrome: The mechanism of jaundice is the uptake of unconjugated bilirubin by hepatocytes (light, the most common type of familial jaundice in the clinic) and the lack of glucuronyltransferase in hepatocyte microsomes (heavy Due to poor prognosis, the disease is characterized by other normal liver function tests, increased serum unconjugated bilirubin concentration, and increased erythrocyte fragility; after oral administration of gallbladder contrast agent, gallbladder development is good, liver biopsy is not abnormal.

(2) Dabin-Johnson syndrome: The cause of jaundice is that the unconjugated bilirubin is converted into conjugated bilirubin in hepatocytes, and the bilirubin transport and biliary excretion function are impaired. Serum binding to bilirubin increased; gallbladder was not developed after oral gallbladder contrast agent; liver appearance was greenish black (observed under laparoscopy), liver biopsy showed diffuse brown pigment particles in liver cells, and the prognosis of this disease was good.

(3) Rotor syndrome: The cause of jaundice is caused by the uptake of unconjugated bilirubin by hepatocytes and the partial discharge of bilirubin into the capillary bile duct. The disease is characterized by both serum non-binding and bilirubin binding. Increased; indocyanine green (ICG) excretion test disorder (reduced); most of the gallbladder angiography is well developed, only a few are not developed; no pigmentation in the liver, liver biopsy is normal, the prognosis of this disease is generally good.

(4) Crigler-Najjar syndrome: The cause of jaundice is the lack of glucuronyltransferase in hepatocyte microsomes, which makes unconjugated bilirubin unable to convert into bilirubin. The syndrome can be divided into heavy or light, the former Because the concentration of unconjugated bilirubin in the blood is very high, and has a strong affinity with adipose tissue in brain tissue, it is prone to bilirubin encephalopathy (nuclear jaundice), which is more common in newborns, and its prognosis is very poor, mostly after birth. One year died; the latter is a part of hepatocyte microsomes lacking glucuronyltransferase, so the symptoms are milder and the prognosis is slightly better.

Pathogenesis

Normal bilirubin metabolism

(1) Source and formation of bilirubin: 80% to 85% of bilirubin is derived from hemoglobin of mature red blood cells. The average life span of normal red blood cells is 120 days, and hemoglobin released from aging and damaged red blood cells is mononuclear- The macrophage system (spleen, liver, bone marrow) swallows, destroys and decomposes, becomes heme, iron and globin under the action of cathepsin (iron is reused by the body, globin enters the protein metabolism pool), hemoglobin is red The action of sputum oxygenase is converted to biliverdin, and biliverdin is reduced to bilirubin by biliverdin reductase. The hemoglobin produced by normal humans is destroyed by red blood cells by about 60-80g/L, and the bilirubin is produced. The total amount is about 340-510 mol/L, with an average of 425 mol/L; in addition, 15% to 20% of bilirubin is derived from hemoglobin (ineffective hematopoiesis) of immature red blood cells in the bone marrow, and hemoglobin free in the liver. Heme-containing proteins (including myoglobin, catalase, peroxidase, cytochrome P450, etc.), which produce bilirubin called bypass bilirubin; bile decomposed from hemoglobin Red pigment (also including bypass) Bilirubin) is called unconjugated bilirubin; unconjugated bilirubin rapidly binds to serum albumin to form unconjugated bilirubin albumin complex, which is transported to the liver via blood circulation. The erythromycin is insoluble in water and cannot be filtered out from the glomerulus. Therefore, the urine does not contain unconjugated bilirubin, but the unconjugated bilirubin is fat-soluble and has a good affinity with adipose tissue.

(2) Liver's intake, binding and excretion functions for unconjugated bilirubin:

1 The uptake of unconjugated bilirubin by the liver: The liver is an important site for bilirubin metabolism. When the unconjugated bilirubin albumin complex is transported to the liver cells by blood, according to the ultrastructural observation, unconjugated bilirubin and After albumin separation, the hepatic sinusoidal Disse's gap is taken up by the microprojections of hepatocytes, and after entering the hepatocytes, the unbound bilirubin is carried by the special proteins y and Z in the hepatocyte cytoplasm (y and Z proteins are used as The carrier is transported to the microsomes of the smooth endoplasmic reticulum of hepatocytes.

2 unbound bilirubin binding (ie, binding to bilirubin formation): glucuronyltransferase in the microsomes of the smooth endoplasmic reticulum, unbound bilirubin combined with glucuronic acid under the action of the enzyme Formation of glucuronic acid ester, or Conjugated bilirubin, combined with one molecule of glucuronic acid, bound bilirubin called bilirubin I (monoester), combined with two molecules of glucuronic acid Combined with bilirubin called bilirubin II (diester), most of the bound bilirubin excreted from bile is diester bilirubin, which is water-soluble due to bilirubin binding and can be filtered by glomerulus. Excreted from the urine, the urine bilirubin qualitative test was positive.

3 combined with the excretion of bilirubin: how to remove from the liver cells after the formation of bilirubin, the exact mechanism has not been fully elucidated, it is considered to be completed by the energy-consuming process of active excretion, combined with bilirubin transported to the capillary by the Golgi apparatus Biliary microtubules, microbiliary duct, thin bile duct, small bile duct, common hepatic duct, common bile duct, discharged into the duodenum through the duodenal papilla.

4 Intestinal hepatic circulation of bilirubin: combined with bilirubin discharged into the intestine through the biliary tract can not be absorbed by the intestinal mucosa, but reduced to urobilinogen at the end of the ileum and the colon by anaerobic reductase (daily intestine) The total amount of urobilinogen formed by the tract is about 68-473 mol). Most of the urinary biliary oxidization is excreted from faeces by excretion of urinary bilirubin, also known as feline (or fecal biliary tract); 10% to 20%) is absorbed by the ileum and colonic mucosa, and returns to the liver through the portal vein bloodstream. Most of the urobilinogens that return to the liver are converted to bilirubin by the action of hepatocytes. It is also discharged into the intestine with bile. This process is called "intestinal hepatic circulation of bilirubin". A small part fails to transform into bilirubin, but is a systemic circulation (ie, a small part of urinary biliary hepatic vein Inferior vena cava heart systemic circulation), excreted by the kidneys, the urine urinary tract excreted by urine in normal people every day generally does not exceed 6.8 mol, and the urine urinary biliary original test is weakly positive or positive.

2. Hemolytic jaundice

After massive destruction of red blood cells (hemolysis), the formation of unbound bilirubin increases, and a large amount of unconjugated bilirubin is transported to the liver, which inevitably increases the burden on the liver (hepatocytes), and exceeds the uptake of unconjugated bilirubin by the liver. When combined, it causes an increase in the concentration of unconjugated bilirubin in the blood. In addition, anemia caused by a large amount of hemolysis makes the hepatocytes in the state of hypoxia and ischemia, and their ability to bind unconjugated bilirubin is inevitable. It will be further reduced, resulting in a higher concentration of unconjugated bilirubin in the blood and jaundice.

3. Hepatocyte jaundice

Due to extensive damage (denaturation, necrosis) of hepatocytes, the uptake of unconjugated bilirubin by hepatocytes and the occurrence of binding disorders, the concentration of unconjugated bilirubin in serum is increased, and some unimpaired hepatocytes are still Can continue to ingest, combined with unconjugated bilirubin, to convert it into bilirubin, but part of it combined with bilirubin failed to excrete in the capillary bile duct, but through the necrotic hepatocyte gap back into the liver lymph In the blood, or due to hepatocyte degeneration, swelling, inflammatory lesions in the portal area, and formation of capillary bile ducts, bile duct bile plugs, so that the excretion of bound bilirubin is blocked, resulting in the binding of bilirubin through the small bile duct overflow (small bile duct When the pressure is increased and the rupture occurs, the blood flow to the liver and the blood flow eventually leads to an increase in the concentration of bound bilirubin in the serum and jaundice.

4. Obstructive jaundice (cholestasis jaundice)

Whether it is capillary bile duct in the liver, microbiliary duct, small bile duct, or extrahepatic bile duct, total hepatic duct, common bile duct and ampulla of the ampulla, etc., obstruction or cholestasis, obstruction or stagnation of the upper bile duct The internal pressure is constantly increasing, and the bile duct is continuously expanding, which will inevitably lead to the intrahepatic small bile duct or microbiliary tube. The capillary bile duct will rupture, causing the combined bilirubin to overflow from the ruptured bile duct, and will flow into the blood and cause jaundice. In addition, some intrahepatic Cholestatic stagnation is not caused by mechanical factors such as bile duct rupture (such as drug-induced cholestasis), but also due to reduced bile secretion (secretory dysfunction), increased permeability of capillary bile ducts, bile concentration, stasis and flow Reduced, eventually leading to the formation of bile duct salts and the formation of bile.

Astragalus prevention

Have a diet, do not drink alcohol, do not eat unclean food and eat spicy hot fat, jaundice patients should pay attention to rest, keep a good mood, diet should be light, once the disease is discovered, immediately isolate treatment, and The utensils and utensils are cleaned, and the excrement is buried deeply or disinfected with bleaching powder.

Jaundice complications Complications

The outcome of this disease is related to the nature of jaundice, physical strength, treatment and other factors. Yanghuang, Yinhuang and Jihuang are different in nature, different in weight, but can be transformed under certain conditions. Poor, sick and evil, jaundice is deepening, and the symptoms of hot poisonous flaming can be turned into acute yellow; Yanghuang can also be changed from spleen yang to wetness, and from wet to hot yellow; Can be issued as a yellow; acute yellow if the heat is flaming, invagination, or a large amount of bleeding, liver and kidney yang failure can occur; yin and yellow treatment for a long time, can be turned into accumulation, bulging.

In general, the positive prognosis of Yanghuang is good, only the Huangxie people's heart camp, blood and blood, the prognosis is too bad, as for the yin and yellow, if the yang is gradually recovered, the jaundice gradually recedes, the prognosis is better; if the yin and yellow are cured for a long time, Heat injury and yin and blood, jaundice deepened, into a bulging severe disease, the prognosis is poor; acute yellow disease mortality rate, if there is liver and kidney yang failure, the prognosis is very poor.

In addition, it can also cause bilirubin encephalopathy.

Symptoms of jaundice Common symptoms Liver palm indigestion Spider sputum skin is light yellow or deep golden yellow palm yellow skin yellow green or green brown nausea skin itching appetite loss abdominal pain

Because the primary disease of jaundice varies, the clinical manifestations are diverse, both caused by the primary disease and by the jaundice itself. In addition, only the common performance of patients with jaundice is briefly described.

(1) Yellow staining of tissues such as skin and sclera

Bilirubin has a greater affinity for tissues containing elastin, so the sclera, skin and mucosa containing the tissue are most prone to jaundice. When the jaundice is deepened, urine, sputum, tears and sweat are also yellowed, and saliva generally does not change color. The color of the yellow dye is different, which is related to the primary disease causing jaundice and the duration of jaundice.

(2) Color change of urine and feces

Hepatic and obstructive jaundice is darker, even dark brown, and the degree of dark urine is related to urinary bilirubin content. Some patients first noticed darker urine, while others first noticed yellow staining of the sclera, skin and mucous membranes. Although hemolytic jaundice has yellow staining on the sclera skin, the urine color is not deep. In acute acute hemolysis, hemoglobinuria appears in the urine and the urine is soy sauce color. When obstructive jaundice, the color of the feces becomes lighter and even completely gray.

(three) digestive tract symptoms

Cases of jaundice often have symptoms such as abdominal distension, abdominal pain, loss of appetite, nausea, vomiting, diarrhea or constipation, which are often slightly different due to different primary diseases.

(four) the performance of bile saltemia

Extrahepatic obstructive jaundice and intrahepatic cholestasis can be retained in the blood due to obstruction of bile salt excretion, which is called bile saltemia. Its main manifestations are: 1 skin itching, but the degree of itching and jaundice can be consistent; 2 bradycardia is seen in deep jaundice, which is related to bile salt stimulation of vagus nerve and inhibition of cardiac conduction; 3 intestinal tract due to lack of bile salts, affecting fat digestion and Absorption of fat-soluble vitamins, resulting in abdominal distension, bleeding tendency, steatorrhea and night blindness; 4 fatigue, listlessness and headache, seems to be related to the toxic effects of bile salts on the central nervous system.

Astragalus inspection

There are many laboratory tests for jaundice, which is helpful for the differential diagnosis of the cause and should be reasonably selected.

(1) Liver function test

1. Determination of serum bilirubin: serum bilirubin is divided into two minutes: bilirubin and total bilirubin. The former is equivalent to binding bilirubin (CB), and the normal does not exceed 3.4 mol/L (0.2 mg/dl), and the fluctuation range is .85 to 3.4 mol/L (0.05 to 0.2 mg/dl). Total bilirubin (TB) is a combination of unbound and bilirubin, mainly unconjugated bilirubin, and does not exceed 17 mol/L (1.0 mg/dl).

2. Urine bilirubin: hemolytic jaundice urine does not contain bilirubin, hepatic and obstructive jaundice are positive.

3. Urinary urinary urinary tract: In the case of acute massive hemolysis, the urinary biliary tract in the urine is significantly increased. When the chronic small amount of hemolysis occurs, the urinary biliary content does not change much. In the case of hepatic jaundice, urine urinary biliary tract can be increased; intrahepatic cholestasis can be reduced or even disappeared. In the extrahepatic obstruction, there is no urinary biliary in the urine, especially cancerous jaundice.

4. Urine biliary tract in feces: Obstructive jaundice can be seen to decline, calculus obstruction is often incomplete, and cancerous obstruction can be complete.

5. Protein metabolism test: serum protein quantification and protein electrophoresis analysis have little significance for the identification of astragalus. Decreased plasma albumin is seen in severe hepatic parenchymal damage such as chronic hepatitis, decompensated cirrhosis, and advanced liver cancer. The increase in plasma globulin and the ratio of albumin and globulin inversion are found in active chronic liver disease and connective tissue disease. Changes in total plasma protein were more pronounced in hepatic jaundice. Long-term extrahepatic obstruction and biliary cirrhosis, plasma 2 and globulin were significantly increased.

6. Blood cholesterol, cholesterol ester and protein X (LP-X) assays reflect the lipid metabolism function of hepatocytes and the excretory function of biliary lines.

7. Determination of serum bile acid: bile acid is synthesized and secreted in the liver, and the serum content of normal humans does not exceed 10 mol/L. In hepatobiliary diseases, bile acid metabolism is disordered. Hepatocytes have different mechanisms of bile acid and bilirubin uptake and excretion. In the case of unconjugated hyperbilirubinemia such as Gilbert's disease and hemolytic jaundice, there is no bile acid retention, which contributes to the identification of jaundice.

8. Serum enzymology: blood sputum enzyme activity (referred to as blood enzyme) determination can be helpful for the diagnosis of jaundice. There are two major types of blood enzymes commonly used in clinical practice: 1 enzymes that reflect hepatocyte damage, mainly alanine aminotransferase (ALT), and aspartate near acid aminotransferase (AST), other aspartic acid Succinic acid lyase (ASAL), aldolase (ALD), spermatoxin (ARG) and ornithine aminomethyltransferase (ChE), in hepatitis, blood content decreased, 2 reflects biliary tract disease Enzymes such as alkaline phosphatase (ALP) and -glutamyltranspeptidase (GGT), leucine peptidase (LAP) and 5' nucleotidase (5'-NT). The enzymogram of citrate is a micro-assay for a series of enzymes that contribute to the differential diagnosis of jaundice. For example, ALT, AST, OCT, ALP, GGT and 5'NT6 enzymes are measured at one time. If the first three enzymes rise, it is hepatic jaundice, and the latter three increase is obstructive jaundice. However, blood enzyme tests do not help to identify intrahepatic biliary fistula and extrahepatic obstructive jaundice (see "viral hepatitis").

9. Determination of plasma prothrombin time: Vitamin K can promote the formation of prothrombin in liver cells. In hepatic jaundice, the formation of prothrombin is reduced and the prothrombin time is prolonged. Vitamin K is fat-soluble and is absorbed into water by the action of bile salts in the intestine. Therefore, prothrombin time can be prolonged when obstructive jaundice.

10. Dye excretion function test: Indocyanine green (ICG) excretion test ICG is rapidly in contact with albumin and is taken up by liver cells after being infused into the bloodstream. It is directly discharged from the biliary tract into the intestine after being metabolized in the liver, so it can correctly reflect liver cells. Excretion function. Normal people were given an IVG dose of 0.5 mg/kg body weight, and the intravenous retention after 0 minutes was 0-10%.

(two) immunological examination

1. Immunoglobulin: IgG is significantly increased in chronic active hepatitis, and IgM is significantly increased in primary biliary cirrhosis. In the case of extrahepatic obstruction, the immunoglobulin is normal.

2. Alpha-fetoprotein (AFP): AFP content in normal adult blood is extremely small (<20ng/ml).

3. Autoantibody assay: The immunofluorescence assay determines the positive rate of mitochondrial antibodies in jaundice cases, the primary biliary cirrhosis is about 95%, the chronic active hepatitis is 30%, and the long-term extrahepatic obstruction is even positive.

4. Viral hepatitis-specific markers: such as anti-HAV-IgM positive, suggesting hepatitis A virus infection; HBsAg and anti-HBc-IgM positive, helpful for the diagnosis of hepatitis B; ALT abnormality with anti-HCV positive, should Consider hepatitis C; anti-HEV-IgM positive, suggesting hepatitis E virus infection.

(three) hematology examination

Hemolytic jaundice, in addition to anemia, increased reticulocytes in the surrounding blood (usually 5% to 50%, even more than 90%), and multiple erythrocytes appear. Bone marrow examination also showed compensatory changes such as nuclear red blood cell hyperplasia.

(4) X-ray examination

1. X-ray film in the liver area helps to understand the size and shape of the liver. In combination with fluoroscopy, it can also determine the position of the diaphragm, whether the face is smooth, and whether the diaphragm activity is limited.

2. Upper gastrointestinal barium meal imaging may find esophageal varices. Duodenal hypotonography or a diagnosis of extrahepatic obstruction.

3. Conventional oral and intravenous cholangiography often cannot be developed due to the deep jaundice. For example, when some contrast agents (such as 40% cholovue) are used, the total bilirubin is greater than 102-119 mol/L (6-7 mg/dl). Still angiographic.

4. Duodenoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC) can show the location and extent of biliary obstruction, which is helpful for the identification of intrahepatic and extrahepatic obstructive jaundice. In order to avoid complications of hepatic cholangiopancreatography such as hemorrhage and biliary peritonitis, jugular vein catheterization has been advocated, from the jugular vein to the hepatic vein, and then the blood vessel is inserted into the bile duct for angiography.

5. Selective celiac angiography has little significance in the differential diagnosis of jaundice. From the changes in the displayed blood vessels, it is possible to speculate on the location and extent of the lesion, which may be helpful for pancreatic diseases.

6. Splenic portal vein and umbilical vein angiography can show the vascular morphology of the portal system, which is helpful for the diagnosis of portal hypertension, liver occupying lesions and preoperative estimation of the portal shunt. This type of examination is less common in jaundice.

7. Computerized stratified photographic examination (CT) Abdominal CT may show a tomographic image of the abdominal organs such as hepatobiliary and pancreatic, which has a great reference value for the presence or absence of space-occupying lesions in the liver and pancreas and whether the bile duct and gallbladder are dilated. Helps to diagnose the cause of obstructive jaundice.

(5) Ultrasound examination

Abdominal B-mode ultrasound is helpful for the identification of medical jaundice and surgical jaundice. The latter common bile duct inner diameter is often dilated (>6mm), the intrahepatic bile duct dilatation is branched and there is no echogenic dark band or small aura, the gallbladder coefficient is enlarged, and the endometrium is often not smooth; the liver echo is mostly similar to normal.

(6) Radionuclide inspection

(7) Duodenal drainage

This method does not have the special significance of differential diagnosis of jaundice, but it has value in determining extrahepatic obstruction.

(8) Liver biopsy

The diagnosis of diffuse liver disease, such as chronic hepatitis, early cirrhosis and drug jaundice and other marginal diseases, such as the differentiation of chronic hepatitis staging; drug-induced intrahepatic cholestasis and the identification of extrahepatic obstruction are helpful.

(9) Laparoscopy

Laparoscopy is not the main method for differential diagnosis of jaundice. However, some parts of the liver, the sacral ligament, the gallbladder and the diaphragm can be directly seen in the external appearance and intra-abdominal conditions. According to the size, shape, color, surface condition of the liver, varicose veins of the falciform ligament and the nature of ascites, it is helpful for the diagnosis of some jaundice, especially diffuse liver lesions.

(10) Adrenal cortex hormone treatment test

Application of prednisone or other experimental treatment, such as 10 to 15 mg of prednisone, 3 to 4 times a day, serum bilirubin concentration can be reduced by 40% to 50% before taking the drug, which is beneficial to hepatic jaundice and liver. Internal sputum (clinically resembles extrahepatic obstruction), and there is no significant change in extrahepatic obstructive jaundice.

Diarrhea diagnosis

diagnosis

(1) medical history

Should be detailed: 1. Age, 2. Gender, 3. Occupation and Birthplace, 4. Diet and Nutrition, 5. Family History, 6. History of Hepatic Exposure, 7. Blood Transfusion, Injection, History of Surgery, and History of Medicine, 9. Ben. Secondary jaundice sweeping and development, 10. abdominal pain, 11. other gastrointestinal symptoms, 12. fever and chills, 13. other data, analysis of its possible relationship with jaundice.

(2) Physical examination

A comprehensive system of physical examination is very important. The first step is to determine if there is any jaundice that should be examined under natural light.

Focus on the following information:

1. Skin color: Hepatic jaundice varies in severity, and the color of acute jaundice is mostly golden yellow; the skin color of chronic intrahepatic cholestasis is deeper. The skin color of obstructive jaundice is the deepest, and the skin color is related to the degree of obstruction. It is golden yellow at the beginning, and then turns from dark yellow to green, and later dark or even dark brown. This is related to the oxidation of bilirubin to biliverdin and even to bilirubin. Choletyanin) related.

2. Other skin manifestations: Pigmentation is seen in chronic liver disease and long-term biliary obstruction, which is systemic, but the face is especially around the eyelids. Yellow tumors or jaundice are associated with lipid retention in the blood (both are not identical). Yellow tumors can also shrink or disappear when blood lipids are reduced or severe liver failure occurs. Hepatocyte jaundice is more common in the skin and mucous membranes, and there are bleeding in the nasal mucosa, gums and oral mucosa. In the case of fulminant hepatic failure, hemorrhagic foci such as subcutaneous large ecchymosis occur, and clotting factor deficiency, thrombocytopenia or DIC related. The bleeding of obstructive jaundice is generally mild.

3. Shallow lymph node enlargement: Acute jaundice with swollen body swelling, should be suspected of infectious mononucleosis. There is no shallow lymph node enlargement in acute viral hepatitis. Progressive jaundice with shallow lymph nodes on the collarbone and other areas should also consider whether it is cancerous jaundice. Lymphoma, malignant histiocytosis, miliary structure, and pulmonary invasive disease can present both jaundice and superficial lymphadenopathy.

4. Abdominal signs:

(1) Abdominal shape: Liver occupying lesions, giant spleen, retroperitoneal tumors and pelvic tumors have local bulging of corresponding parts. When a large amount of ascites is frog-shaped, the umbilicus is prominent, and abdominal wall spasm and umbilical hernia can also occur. Abdominal wall varices are seen in portal hypertension, portal or inferior vena cava obstruction. Abdominal surgical scars sometimes also contribute to the etiology of jaundice, such as cholelithiasis and cholecystitis.

(2) Liver condition: In acute viral hepatitis, jaundice and hepatomegaly coexist, and the liver is soft, tenderness and sputum pain are more obvious. In acute and subacute hepatic necrosis, jaundice is rapidly deepened, but hepatomegaly is not enlarged or reversed. In chronic hepatitis and cirrhosis, hepatomegaly is not as obvious as acute hepatitis, and the texture is increased, and there is no tenderness; It can also be found with uneven edges and large and small nodules. Hepatocarcinoma is more common in liver cancer, but it can lose normal shape, firmness, and can cause large tumors or small nodules. The tenderness can be insignificant, but the liver surface is smooth and can not line up deep cancer or subclinical "small liver cancer". When the liver abscess approaches the surface of the liver, the local skin may have signs of inflammation such as redness and tenderness. In the case of giant liver abscess, hepatic hydatidosis, polycystic liver and hepatic cavernous hemangioma, the liver area may have a cystic or fluctuating sensation.

(3) splenomegaly: jaundice with splenomegaly, more common in the decompensation of various types of cirrhosis, chronic hepatitis, acute hepatitis, hemolytic jaundice, systemic infectious diseases and invasive diseases. When the cancer invades the portal vein and the splenic vein, it also causes splenomegaly. The rare splenic infarction and spleen abscess also have similar splenomegaly and tender signs.

5. Other conditions: whether there is liver odor, flapping tremor, hepatic encephalopathy and other neuropsychiatric abnormalities, rare hair, testicular atrophy, clubbing, hyperkeratosis, key nails, multiple venous thrombosis (discovered in pancreatic cancer) ) and bradycardia. Patients with advanced cancerous jaundice can still show signs of cancer metastasis. Liver failure can present with encephalopathy and intracranial hemorrhage. Bloody abdomen, biliary peritonitis, biliary nephropathy and shock can also be seen in cancerous jaundice.

A diagnosis can be made in conjunction with laboratory tests.

Differential diagnosis

(a) hemolytic jaundice

1. There may be a history of hemolysis, such as blood transfusion, medication, infection, family history (genetic factors) and so on.

2. Acute onset of hemolysis or hemolytic crisis, rapid onset of hemolysis, such as chills, high fever, vomiting, abdominal pain, headache and general malaise, fatigue, and even shock, coma, severe anemia and jaundice and acute renal failure Wait.

3. Chronic small amount of hemolysis, the symptoms are very mild, may have pale, fatigue and other anemia symptoms, jaundice is less obvious. The spleen is swollen to varying degrees, and hepatomegaly is not uncommon.

4. Choline pigment examination In addition to hemolytic crisis, there may be deep jaundice, serum total bilirubin is often less than 85mol / L (5mg / dl), of which unconjugated bilirubin accounted for more than 80%. Urinary urinary biliary weak positive, bilirubin negative; 24-hour urinary biliary tract is significantly increased, a large number of hemolysis can reach more than 1,000mg. The urinary biliary tract in the feces also increased, and the 24-hour excretion was greater than 300 mg, and there were also more than 1,00 mg.

5. Hematological examination In addition to anemia, reticulocytes in the surrounding blood increase (usually 5% to 20%, even more than 90%), and multiple erythrocytes appear. Bone marrow examination also showed compensatory changes such as nuclear red blood cell hyperplasia.

6. Other tests for autoimmune hemolysis were positive for the anti-human globulin (Coombs) test. In the case of paroxysmal nocturnal hemoglobinuria, the acid hemolysis (Ham) test was positive. Hemoglobin may be secreted in acute massive hemolysis; hemosiderin urine is more common in chronic hemoglobinuria, especially paroxysmal nocturnal hemoglobinuria.

(two) hepatic jaundice

1. If caused by acute hepatitis, the patient has symptoms such as fever, fatigue, loss of appetite, pain in the liver area, liver enlargement, and obvious tenderness. The liver texture of chronic hepatitis increases, and there is a lot of tenderness. Patients with cirrhosis are mostly thin, dark skin, may have spider mites, abdominal wall or varicose veins, liver can be small, hard and often no tenderness, spleen can be swollen; late ascites, bleeding tendency, renal function Damage, and even hepatic encephalopathy.

2. Blood bilirubin examination: serum total bilirubin generally does not exceed 170 mol / L (10 mg / dl), which combined with bilirubin often increased, accounting for more than 30%.

3. Urinary bile test: urinary bilirubin positive, due to liver and intestinal dysfunction, urinary bile from the intestine can not be oxidized in the liver and then discharged to the intestine, can be discharged by the blood through the blood circulation, so urine in the urine The biliary is positive. In the early stage of acute hepatitis (such as the pre-jaundice), the intrahepatic capillary tube is compressed by swollen hepatocytes, which affects the discharge of bilirubin into the intestine. The urine urinary bilirubin and urobilin may be temporarily negative, usually about one week. In intrahepatic cholestasis, the ability of hepatocytes to excrete bilirubin is reduced, and urinary urinary bile is often reduced or absent.

4. Fecal examination: When intrahepatic cholestasis or obstruction, the urinary biliary tract is reduced in the feces, and the faeces are lighter and even terracotta faeces can appear.

5. Other liver function tests: In the case of hepatic jaundice, the following tests are abnormal: 1 serum transaminase is elevated; 2 plasma prothrombin time is prolonged, which is related to the production of vitamin K-related clotting factor in liver cells, vitamins K often can not be corrected; 3 severe liver damage, plasma cholesterol, cholesterol esters and serum cholinesterase can be reduced; 4 serum alkaline phosphatase activity is mostly normal, intrahepatic cholestasis time increased; 5 blood stasis anterior white Protein (prealbumin) and albumin decreased, serum globulin increased, white and spherical ratio was imbalanced; in biliary cirrhosis, and and globulin often increased significantly

6. Immunological examination: Immunofluorescence assay for mitochondrial antibodies contributes to the diagnosis of primary biliary cirrhosis. Detection of serological markers of various hepatitis viruses contributes to the diagnosis of viral hepatitis (see "Viral Hepatitis"). Serum alpha-fetoprotein (AFP) is also useful for the diagnosis of primary liver cancer.

7. Liver biopsy: The significance of the diagnosis of jaundice caused by wet liver disease, such as viral hepatitis, cirrhosis, fatty liver and intrahepatic cholestasis. In addition to optical microscopy, electron microscopy, fluorescence immunoassay, immunohistochemistry, and ultra-micro assays for liver tissue enzymes are available.

8. Liver radionuclide scanning, B-ultrasound and CT imaging techniques are helpful for the diagnosis of intrahepatic space-occupying lesions.

(three) obstructive jaundice

1. Clinical manifestations: acute cholecystitis, gallstone disease sudden onset, more with epigastric cramps, but also fever, vomiting and gallbladder area tenderness and muscle health and other manifestations, jaundice comes quickly; stones caused by repeated recurrence. Early symptoms of pancreatic head cancer can be concealed, jaundice is progressive deepening; late abdominal pain, loss of appetite and weight loss, fatigue symptoms. Obstructive jaundice, due to the retention of bile salts in the blood to stimulate the nerve endings of the skin and more itching; and due to the lack of bile in the intestine, affecting the absorption of fat-dense vitamin K, can cause bleeding tendency, injection of vitamin K can be corrected.

2. Astragalus condition: mainly depends on the location, extent and duration of biliary obstruction. The jaundice is shallower in the early stage of incomplete obstruction; if the bile duct obstruction is gradually aggravated, the jaundice can also be deepened, yellow, brown, or even black (called black sputum). In the case of complete biliary obstruction, the blood bilirubin can reach 510mol/L (30mg/dl) or more, and the combined bilirubin accounts for more than 35% (up to about 60%). Calculous jaundice is often fluctuating, and cancerous obstruction is progressive jaundice, but ampullary carcinoma can cause a brief reduction in jaundice due to cancer ulcers.

3. Urinary bile test: urinary bilirubin positive, but urinary bile reduced or disappeared. In patients with obstructive jaundice, if the urinary bile is persistently negative for more than one week, the possibility of obstruction caused by cancer should be highly suspected. Complete biliary obstruction is easy to cause secondary infection, and urinary urinary biliary tract can also be positive.

4. Characteristics of fecal color: The more complete the obstruction, the lighter the color of the feces, the color of the terracotta color, and the quantitative reduction of urinary biliary tract in the feces in 24 hours is completely reduced or completely absent. There may be black feces or fecal occult blood positive in ampullary carcinoma with ulcer or obstructive jaundice with biliary mucosal inflammation or ulceration.

5. Liver function test: blood ALP activity and cholesterol content can be significantly increased. Long-term biliary obstruction often leads to secondary hepatic parenchymal damage, and serum transaminase rises. Plasma albumin also decreased.

6. Other examinations: abdominal (hepatobiliary and pancreatic) plain film, gallbladder and biliary angiography, abdominal B-ultrasound and abdominal CT examination, endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiopancreatography (PTC), Both contribute to the diagnosis of obstructive jaundice, biochemical and immunological cancer markers, such as carcinoembryonic antigen (CEA), CA19-9, ferritin, 1-antitrypsin, such as assisted diagnosis of cancerous obstruction, But they are all non-specific.

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