What Is Cholestatic Jaundice?

Cholestatic jaundice means that bile acids and bilirubin in the blood are higher than normal due to cholestasis. The so-called cholestasis is due to various harmful factors that cause liver cells to excrete bile dysfunction, inhibition of bile secretion, or obstruction of bile ducts inside or outside the liver, resulting in slow or stagnant bile flow. Cholestatic jaundice is dominated by combined direct bilirubin elevation.

Basic Information

English name

cholestatic jaundice

Visiting department

Internal medicine

Common locations

bile duct

Common causes

Tumors, stones, inflammation, followed by benign stenosis or obstruction and parasites

Common symptoms

Biliary colic, fever, vomiting, chills, high fever, abdominal pain, rapid shock, etc.

Causes of cholestatic jaundice

The most common causes are tumors, stones, inflammation, followed by benign stenosis or obstruction and parasites.

According to the anatomical site that causes cholestasis, it can be divided into three types: extrahepatic obstruction, intrahepatic obstruction and intrahepatic cholestasis.

The pathogenesis of cholestatic jaundice

In bile duct obstruction, bile is stagnated in the bile duct, and the pressure in the bile duct increases. After reaching a certain level, the Hering ampulla, which connects the capillary and bile ducts, ruptures, bile enters the lymph, and then enters the blood circulation, causing jaundice.

Intrahepatic cholestasis may occur alone or coexist with parenchymal liver damage. The mechanism is not completely clear at present, and many factors are often involved. It is generally considered to be associated with changes in the structure and function of liver cell membranes, microfilament and microtubule dysfunction, capillary bile duct membrane and Increased tight junction permeability and abnormal bile acid metabolism.

Clinical manifestations of cholestatic jaundice

Varies with the cause, site and nature of the obstruction.

Manifestation of primary disease

Cholecystitis and cholelithiasis are often accompanied by biliary colic, fever, vomiting and other symptoms. Jaundice comes and goes quickly; purulent cholangitis starts quickly, and chills, high fever, abdominal pain, and rapid shock occur; malignant diseases often have epigastric pain, progressive Wasting, hepatomegaly, and jaundice; painless jaundice is often manifested by pancreatic head cancer.

2. The manifestation of obstructive jaundice

Skin tone appears dark yellow, yellow-green or green-brown, and even black. The patient's skin is markedly itchy and often appears before jaundice. Intermittent jaundice is a manifestation of gallstone disease; persistent jaundice, which gradually gets worse and deeper, is usually caused by malignant tumors. And the periampullary cancer jaundice appeared earlier and showed progressive aggravation, but a small number of patients may temporarily disappear or reduce due to tumor necrosis, recanalization of the bile duct, but later deepen again, showing fluctuating jaundice; due to bile salt entering the intestine Intestinal deficiency is often caused by bile acid, which can lead to bloating, fatty diarrhea, and fat-soluble vitamins (A, D, E, and K). When vitamin K is lacking, bleeding tends to occur because the liver cannot synthesize coagulation factors , , , and X. ; Due to partial or complete obstruction of the biliary tract, lack of bilirubin or urobilinogen in the feces, the feces cannot be yellowed, so the feces are gray-white (white clay color). Both intrahepatic and extrahepatic obstructions are accompanied by cholestatic liver enlargement. When the obstruction is located below the gallbladder duct, it is often accompanied by gallbladder enlargement without tenderness.

Cholestatic jaundice examination

1. Bile pigment test items

(1) Serum bilirubin In cholestatic jaundice, because direct bilirubin (DBIL) cannot be excreted from liver cells and capillary bile ducts, serum bilirubin is significantly increased, and total bilirubin (TBIL) can reach 510 mol / L. Above, DBIL is the main factor, and the ratio of DBIL and TBIL is usually above 60%, and the highest can reach 90%. Calculus jaundice is often fluctuating, and cancerous obstruction is progressive jaundice, but ampullary cancer can temporarily reduce jaundice due to cancerous ulcers.

(2) Urinary bilirubin Cholestasis during cholestatic jaundice increases the internal pressure of the liver and bile ducts, leading to rupture of the capillary bile ducts. DBIL cannot be discharged into the intestine and the inflow of blood is discharged from the urine. Therefore, the urine bilirubin test is positive.

(3) Urinary bile cholestatic jaundice due to intrahepatic and extrahepatic cholestasis, bile is blocked from entering the intestinal tract, the amount of choline progenitor in the intestine is reduced, and the amount of choline progenitor leaked from the intestine by the enterohepatic circulation is also reduced. The original discharge is reduced.

(4) Fecal cholestasis In cholestatic jaundice, due to the reduction of bile excreted to the intestine, fecal cholestasis is significantly reduced or completely absent, causing faecal choline to stay in the intestine for further oxidation. White clay, this is a characteristic of extrahepatic cholestasis.

2. Other liver function tests

(1) Serum alkaline phosphatase (ALP) serum ALP activity is often significantly increased in early stage during jaundiced jaundice, even reaching 10 to 15 times the upper limit of the reference value.

(2) When serum -glutamyltransferase (GGT) is a biliary disease such as cholelithiasis, biliary inflammation, and extrahepatic obstruction, GGT not only has a high positive rate, but also increases significantly, which can reach 5 to 30 times the upper limit of the reference value. It is helpful for the differential diagnosis of hepatocellular jaundice and cholestatic jaundice.

(3) Serum total bile acid (TBA) Serum TBA measurement has a high sensitivity for the diagnosis of extrahepatic bile duct obstruction and intrahepatic cholestasis, including bile duct obstruction, bile cirrhosis, neonatal cholestasis, and pregnancy-induced cholestasis. TBA was significantly increased in serum.

(4) Serum 5'-nucleotide (5'-NT) The increase of 5'-NT is mainly found in hepatobiliary diseases, but the activity of 5'-NT is significantly increased during cholestatic jaundice, which is generally 2 to 3 times that of normal people. This is helpful for the differential diagnosis of hepatocellular jaundice and cholestatic jaundice. In extrahepatic biliary obstruction, 5'-NT activity is generally parallel to ALP, but 5'-NT activity does not generally increase during short-term obstruction. When longer-term obstruction is lifted, 5'-NT activity decreases faster than ALP .

Cholestasis jaundice diagnosis

Cholestasis jaundice has the following clinical features:

1. Have the above clinical manifestations.

2. The bilirubin concentration gradually increases, generally around 171 / mol / L (10mg / dl), not more than 256.5mol / L (15mg / dl), and it can exceed 513mol / L (30mg / dl). Among them, conjugated bilirubin increased, accounting for> 60% of total serum bilirubin.

3. Urinary bilirubin is positive, urobilinogen is reduced or disappeared.

4. Decreased or absent urobilinogen in feces. If the obstruction is caused by cancer around the ampulla, the feces may be black or occult blood positive due to bleeding.

5. Liver function test: The most obvious are elevated alkaline phosphatase and -glutamyltransferase. Serum total cholesterol can be increased, and lipoprotein-X can be positive. Long-term obstruction can increase serum transaminase and decrease albumin. For example, vitamin K deficiency can prolong prothrombin time. At this time, vitamin K injection can increase prothrombin time. correct.

6. Other tests: B-ultrasound tests are helpful in the diagnosis of cholestasis jaundice.

Differential diagnosis of cholestatic jaundice

Hemolytic jaundice

Due to the massive destruction of red blood cells in a short period of time, the release of bilirubin greatly exceeds the processing capacity of liver cells and jaundice occurs. The increase of bilirubin in serum is mainly indirect bilirubin. Such as neonatal jaundice, malaria, or jaundice caused by improper blood transfusion, all fall into this category. The latter may have symptoms such as chills, fever, headache, muscle soreness, nausea, and vomiting. The urine is soy sauce-colored and has hemoglobinuria, but there is no bilirubin in the urine.

2. Hepatocellular jaundice

Due to extensive damage to liver cells, the ability to process bilirubin decreases, resulting in the accumulation of unbound (indirect) bilirubin in the blood; at the same time, due to the obstruction of bile excretion, direct bilirubin in the blood stream also increases. Due to the increase in indirect and direct bilirubin in the blood, urinary bilirubin and urobilinogen also increased. Hepatitis and jaundice caused by cirrhosis fall into this category.

3. Obstructive jaundice

Obstruction of bile excretion (can be caused by intrahepatic or extrahepatic lesions, usually bile duct obstruction), direct bilirubin in the bile flows back into the blood and jaundice occurs. It can be detected clinically that the serum bilirubin content increases directly, urine bilirubin is positive, and urobilinogen decreases or disappears. Because bilirubin and other bile substances are retained in the body, it can cause itchy skin and bradycardia. Jaundice caused by biliary tract compression such as cholelithiasis and tumors belongs to this category.

Cholestatic jaundice treatment

1. Septic jaundice caused by infection

Anti-infection treatment, removal of germs, and elimination of endotoxemia are the most important measures. You can also consider using glucocorticoids carefully on the basis of anti-infection. In addition, ursodeoxycholic acid and S-adenosylmethionine can also be used.

2. Drug-induced silting jaundice

The first is immediate withdrawal. Jaundice usually resolves within a few weeks after the withdrawal, but a few chronic cases require months or more than one year to resolve the jaundice without special treatment.

3. Alcohol-induced stasis jaundice

Need to quit drinking and general liver protection treatment.

4. Benign recurrent intrahepatic cholestasis

Generally, antihistamine drugs can be used for treatment, and bile acid binding resin and cholestyramine can also be used. The effects of glucocorticoids and phenobarbital are difficult to be sure.

5. Cholestasis due to autoimmune bile duct disease

Autoimmune bile duct diseases mainly include three diseases: primary biliary cirrhosis (PBC), autoimmune cholangio disease (AIC) and primary sclerosing cholangitis (PSC), which should be treated separately.

(1) PBC and AIC generally control pruritus and fatty diarrhea. Those with cholestasis supplement with vitamin A, vitamin D, vitamin K and calcium. The main use of glucocorticoids is better. ALT, AKP) role.

(2) PSC treatment The effects of glucocorticoids and penicillinamine are not obvious. If necessary, surgery and artificial stent liver transplantation can be considered.

6. Cholestasis due to pregnancy

Yin Zhi Huang, Qiang Li Ning, Gan Lixin and Simetai are mostly used in China, but the curative effect is not ideal.