Viral hepatitis (including type A, type B, type C, type D and type E) is a statutory category B infectious diseases, with a strong contagious, complex transmission channels, widespread prevalence, high incidence; some patients with hepatitis B, C and D can become chronic, and can develop into cirrhosis and primary hepatocellular carcinoma, the health of the people is very dangerous.
Prevention and treatment of viral hepatitis to implement the prevention-oriented approach, strengthen leadership, in-depth publicity, mobilize the masses, improve patriotic health campaigns, and take comprehensive preventive and curative measures. For hepatitis A and E to cut off the fecal-oral route; for hepatitis B and D to vaccination for hepatitis B; hepatitis C to control the extra-intestinal (such as through the blood) transmission route is the main. We should strive for early detection, early diagnosis, early isolation, early reporting, early treatment, and early treatment of epidemics to prevent epidemics and improve the effectiveness of treatment. It is important to protect susceptible populations and reduce morbidity.
Diagnostic criteria of viral hepatitis
The clinical manifestations of viral hepatitis are complex, so it is important not to make a diagnosis subjectively and unilaterally by relying only on one or one abnormal examination, but to make a comprehensive analysis based on the epidemiological history, clinical symptoms and signs, laboratory and imaging findings, and to make a good differentiation by combining the patient’s specific situation and dynamic changes. Then the pathogenic diagnosis should be made according to the results of hepatitis virology test, and the final diagnosis should be confirmed.
I. Clinical diagnosis
(A) Clinical typing
1. Acute hepatitis.
(1)Acute jaundice free type
(2) Acute jaundice type.
2. Chronic hepatitis.
(1)Mild ;
(2)Moderate;
(3) severe.
3, Heavy hepatitis.
(1) Acute heavy hepatitis;
(2)Sub-acute heavy hepatitis;
(3) chronic heavy hepatitis.
4, biliary hepatitis.
5, hepatitis cirrhosis.
(B) the clinical diagnosis of each type of hepatitis based on
1, acute hepatitis.
(1) Acute hepatitis without jaundice: should be based on epidemiological history, clinical symptoms, signs, laboratory and pathogenic test results, and exclude other diseases.
(1) Epidemiological history Such as history of close contact and history of injection. Close contact history refers to those who ate, lived, or lived with patients with confirmed viral hepatitis (especially in the acute stage) or had frequent contact with hepatitis virus contaminants (such as blood and feces) or had sexual contact without taking protective measures. Injection history Refers to having received blood transfusions, blood products and injection of drugs with instruments not strictly sterilized, immunizations and needle stick treatments within six months.
②Symptoms Refers to symptoms that appeared recently and lasted for more than a few days but can be explained by no other causes, such as weakness, loss of appetite, nausea, etc.
③Signs Refer to hepatomegaly with pressure pain and percussion pain in the liver area, and some patients may have mild splenomegaly.
④Laboratory tests Mainly refers to elevated serum ALT.
⑤ Positive pathogenetic test.
Any positive laboratory test with two positive tests in the epidemiological history, symptoms and signs, or significant positive tests and signs (or tests and symptoms), and excluding other diseases can be diagnosed as acute non-jaundice hepatitis. Any single elevated serum ALT, or only symptoms, signs, or epidemiological history and ②, ③, ④ one of the three positive cases, are suspected cases. Suspected cases should be dynamically observed or combined with other tests (including liver histopathology) to make a diagnosis. If the pathogenic diagnosis of the suspected case is positive, and except for other diseases, the diagnosis can be confirmed.
(2) Acute jaundiced hepatitis Where the diagnostic conditions of acute hepatitis are met, serum bilirubin >17.1μmol/L, or positive urinary bilirubin, and other causes of jaundice are excluded, acute jaundiced hepatitis can be diagnosed.
2.Chronic hepatitis.
Acute hepatitis of more than six months duration, or the original history of hepatitis B, C, D or HBsAg carriage, and this time again due to the same pathogen hepatitis symptoms, signs and liver function abnormalities can be diagnosed as chronic hepatitis. If the date of onset is unknown or there is no history of hepatitis, but the histopathological examination of the liver is consistent with chronic hepatitis, or if the diagnosis is based on a comprehensive analysis of symptoms, signs, laboratory tests and ultrasound examination, the corresponding diagnosis can also be made. To reflect the degree of liver function damage, chronic hepatitis can be clinically classified as.
(1) Mild: clinical symptoms and signs are mild or absent, and only one or two liver function indicators are mildly abnormal;
(2) Moderate: symptoms, signs and laboratory tests are between mild and severe;
(3) Severe: with obvious or persistent hepatitis symptoms, such as weakness, poor appetite, abdominal distension, yellow urine, loose stools, etc., accompanied by liver disease face, liver palms, spider nevus, splenomegaly and exclude other causes, and without signs of portal hypertension. Laboratory tests with recurrent or persistent elevation of serum ALT and/or AST, reduced albumin or abnormal A/G ratio, and significantly elevated gammaglobulin. In addition to the aforementioned conditions, those with albumin ≤ 32 g/L, bilirubin > 5 times the upper limit of normal value, prothrombin activity 60%-40%, cholinesterase < 2500 U/L, and one of the four tests reaching the above degree can be diagnosed as severe chronic hepatitis, and the reference indexes of the abnormal degree of laboratory tests for chronic hepatitis are shown in Table 1. ultrasound findings can be used as a reference for the diagnosis of chronic hepatitis.
(1) Mild: no obvious abnormal changes in liver and spleen on ultrasound examination.
(2) Moderate: ultrasound shows thickened echogenicity in the liver, mild enlargement of the liver and/or spleen, and the intrahepatic ducts (mainly the hepatic veins) are mostly clear, without widening of the internal diameter of the portal and splenic veins.
(3) Severe: ultrasound examination shows that the echogenicity of the liver is significantly thickened and unevenly distributed; the surface of the liver is not smooth, the edges are blunt, the course of the intrahepatic ducts is not clear or mildly narrowed and distorted; the internal diameter of the portal vein and splenic vein is widened; the spleen is enlarged; the gallbladder is sometimes seen as a “double layer sign”.
Table 1 Reference indicators of the abnormal degree of laboratory tests for chronic hepatitis
Item
Mild
Moderate
Severe
ALT and/or AST(IU/L)
≤3 times normal
>3 times normal
>3 times normal
Bilirubin Bil(μmol/L)
≤2 times normal
>2 times normal to 5 times normal
>5 times normal
Albumin(A)(g/L)
≥35
<35～>32
≤32
A/G
≥1.4
<1.4～>1.0
<1.0
Electrophoresis γ globulin(γEP)(%)
≤21
>21～<26
≥26
Prothrombin activity(PTA)(%)
>70
70～60
<60～>40
Cholinesterase(CHE)(U/L)
>5400
≤5400～>4500
≤4500
3.Heavy hepatitis.
(1) Acute heavy hepatitis.
Starting with acute jaundice type hepatitis, within 2 weeks there is extreme weakness, gastrointestinal symptoms are obvious, rapid emergence of more than II degree (according to IV degree) hepatic encephalopathy, prothrombin activity less than 40% and exclude other causes, progressive narrowing of the hepatic turbid circles, jaundice sharply deepened; or jaundice is very shallow, or even has not yet appeared jaundice, but the above-mentioned manifestations should be considered this disease.
(2) Subacute severe hepatitis.
With acute jaundice type of hepatitis, 15 days to 24 weeks of extreme weakness, gastrointestinal symptoms are obvious, while prothrombin time is significantly prolonged, prothrombin activity is less than 40% and exclude other causes, jaundice rapidly deepens, rising ≥ 17.1μmol/L per day or total serum bilirubin is greater than 10 times normal, first appear more than II degree of hepatic encephalopathy, called encephalopathy type (including cerebral edema, brain The first to appear ascites and its related symptoms (including pleural fluid, etc.), known as ascites type.
(3) Chronic severe hepatitis.
The pathogenesis is based on the following
(1) A history of chronic hepatitis or cirrhosis;
② history of chronic hepatitis B virus carriage;
(3) No history of liver disease and no history of HBsAg carriage, but there are signs of chronic liver disease (such as liver palms, spider nevus, etc.), imaging changes (such as spleen thickening, etc.) and biochemical test changes (such as elevated gammaglobulin, decreased or inverted albumin/globulin ratio);
④Liver puncture tests supporting chronic hepatitis;
⑤ Chronic hepatitis B or C, or chronic HBsAg carriers with overlapping hepatitis A, E or other hepatitis virus infection should be analyzed specifically, except for acute or subacute severe hepatitis caused by hepatitis A, E and other hepatitis viruses. The clinical manifestations of chronic severe hepatitis are the same as those of subacute severe hepatitis at the onset, and worsen as the disease progresses, reaching the diagnostic criteria of severe hepatitis (prothrombin activity less than 40%, total serum bilirubin greater than 10 times normal).
For the purpose of determining the efficacy and estimating the prognosis, subacute heavy and chronic heavy hepatitis can be divided into early, intermediate and late stages according to their clinical manifestations.
(1) Early stage Meet the basic conditions of heavy hepatitis, such as severe malaise and gastrointestinal symptoms, rapid deepening of jaundice, serum bilirubin greater than 10 times normal, prothrombin activity ≤40% to >30%, or confirmed by pathology. However, no obvious encephalopathy occurred, and no ascites appeared.
(2) Middle stage With grade II hepatic encephalopathy or obvious ascites, bleeding tendency (bleeding spots or petechiae), prothrombin activity ≤30% to >20%.
(3) Late stage With refractory complications such as hepatorenal syndrome, gastrointestinal hemorrhage, severe bleeding tendency (petechiae at the injection site, etc.), severe infection, electrolyte disorders that are difficult to correct or hepatic encephalopathy of grade II or higher, cerebral edema, and prothrombinogen activity ≤20%.
4, bilious hepatitis: the onset is similar to acute jaundice, but the conscious symptoms are often mild, skin itching, gray stools, often with obvious liver enlargement, liver function tests, serum bilirubin is significantly elevated, mainly direct bilirubin, prothrombin activity > 60% or a week after the application of vitamin K injection can rise to 60% or more, serum bile acid, γ glutamyl transpeptidase, alkaline phosphatase, cholesterol levels can If the jaundice persists for more than 3 weeks, excluding other causes of intra- and extra-hepatic obstructive jaundice, the diagnosis of acute biliary hepatitis can be made. If the above clinical manifestations occur on the basis of chronic hepatitis, it can be diagnosed as chronic biliary hepatitis.
4.Hepatitis cirrhosis.
(1) Hepatitis liver fibrosis
The diagnosis is mainly based on histopathological examination results, and ultrasound examination results are available for reference. ultrasound examination shows echogenic enhancement and thickening of liver parenchyma, the surface of liver is not smooth, the edges become blunt, liver and spleen may be enlarged, but the surface of liver is not yet granular, and liver parenchyma is not yet nodule-like changes. Serological indicators of liver fibrosis such as four indicators of hyaluronic acid (HA), type III procollagen (PC-III), type IV collagen (IV-C), and laminin (LN) have some correlation with liver fiber stage, but they cannot represent the amount of fiber deposited in liver tissue.
(2) Hepatitis cirrhosis: it is the result of the development of chronic hepatitis, and early hepatic sclerosis is difficult to be diagnosed by clinical data alone but must rely on pathological diagnosis. Diagnosis by imaging ( B-type ultrasound, CT) and laparoscopy has a reference value. In patients with chronic hepatitis, there is definite evidence of portal hypertension, such as abdominal wall, esophageal varices, ascites. Diagnostic imaging: liver shrinkage, spleen enlargement, widening of portal vein and splenic vein. And except for other causes that can cause portal hypertension, all of them can be diagnosed as clinical liver stiffness.
①Compensated cirrhosis.
Refers to early cirrhosis, usually of Child-Pugh grade A. Although there may be mild weakness, reduced appetite or abdominal distension symptoms, there is no obvious manifestation of liver failure yet. Serum albumin is reduced, but still ≥35g/L, bilirubin <35μmol/L, and prothrombin activity is more than 60%. Serum ALT and AST are mildly elevated, AST may be higher than ALT, and γ-glutamyl transpeptidase may be mildly elevated. There may be portal hypertension, such as mild esophageal varices, but no ascites, hepatic encephalopathy or upper gastrointestinal bleeding.
②Decompensated cirrhosis Refers to intermediate to advanced cirrhosis, usually in Child-Pugh B or C grade. There are obvious liver function abnormalities and signs of decompensation, such as serum albumin <35g/L, A/G <1.0, obvious jaundice, bilirubin >35μmol/L, elevated ALT and AST, and prothrombin activity <60 %. Patients may present with ascites, hepatic encephalopathy and significant varices or ruptured bleeding in the esophageal and fundic veins due to portal hypertension. Based on the inflammatory activity of the liver, cirrhosis can be distinguished as
a. Active cirrhosis
Clinical manifestations of chronic hepatitis remain, especially elevated ALT, jaundice, decreased albumin levels, hardened liver texture, progressive enlargement of the spleen, and signs of portal hypertension.
b. Quiescent cirrhosis
Normal ALT, no obvious jaundice, hard liver texture, large spleen with signs of portal hypertension, and low serum albumin level. Imaging diagnosis of cirrhosis: Ultrasound shows shrinking liver, obvious uneven, serrated or wavy liver surface, blunted liver edge, uneven and enhanced echogenicity of liver parenchyma with nodular shape, widened inner diameter of portal vein and splenic portal vein, thinning, twisted and uneven thickness of hepatic veins, and liquid dark area visible in the abdominal cavity.
Second, the pathogenic diagnosis
(A) Pathogenic typing
There are at least five types of pathogens of viral hepatitis, namely hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV) and hepatitis E virus (HEV).
The issue of pathogenicity of GBV-C/HGV and TTV is controversial; therefore, it is not appropriate to include GBV-C/HGV and TTV in routine laboratory testing for viral hepatitis.
(B) The pathogenic diagnostic basis of each type of viral hepatitis
1, hepatitis A: serum anti-HAV IgM positivity in patients with acute hepatitis can confirm the diagnosis of recent HAV infection. In patients with chronic hepatitis B or autoimmune liver disease, serum positive for anti-HAV IgM should be used with caution to determine overlapping HAV infection, and rheumatoid factor (RF) and other causes of false positives must be excluded. About 8% to 20% of vaccinated patients can produce anti-HAV IgM 2 to 3 weeks after hepatitis A vaccination, so attention should be paid to differentiation.
2. Hepatitis B: A diagnosis of current HBV infection can be made with any of the following positives.
①Serum HBsAg positivity;
②Serum HBV DNA positive;
③Serum anti-HBc IgM positive;
④ Positive intrahepatic HBcAg and/or HBsAg, or positive HBV DNA.
(1) Diagnosis of acute hepatitis B: must be differentiated from an acute attack of chronic hepatitis B. The diagnosis of acute hepatitis B can be made with reference to the following dynamic indicators.
① HBsAg titer from high to low, anti-HBs positive after the disappearance of HBsAg;
(2) High anti-HBc IgM titers and negative or low levels of anti-HBc IgG in the acute phase.
(2) Chronic hepatitis B diagnosis: clinically consistent with chronic hepatitis and positive for more than one marker of presenting HBV infection.
(3) Chronic HBsAg carrier diagnosis: those without any clinical signs and symptoms, with normal liver function and persistent positive HBsAg for more than 6 months.
3. Hepatitis C.
(1) Acute hepatitis C diagnosis: clinically consistent with acute hepatitis, positive serum or intrahepatic HCV RNA; or positive anti-HCV, but no acute infection markers for other types of hepatitis viruses.
(2) Diagnosis of chronic hepatitis C: clinically consistent with chronic hepatitis, except for other types of hepatitis, positive serum anti-HCV, or positive serum and/or intrahepatic HCV RNA.
4. Hepatitis D.
(1) Diagnosis of acute hepatitis D.
(1) Acute HDV, HBV co-infection In patients with acute hepatitis, in addition to positive markers of acute HBV infection, positive serum anti-HDV IgM, positive anti-HDV IgG low titer; or positive serum and/or intrahepatic HDVAg and HDV RNA.
(2) HDV, HBV overlap infection Chronic hepatitis B patients or chronic HBsAg carriers with positive serum HDV RNA and/or HDVAg, or positive anti-HDV IgM and anti-HDV IgG, positive intrahepatic HDV RNA and/or intrahepatic HDVAg.
(2) Diagnosis of chronic hepatitis D: clinically consistent with chronic hepatitis, persistent high titers of serum anti-HDV IgG, persistent positive HDV RNA, positive intrahepatic HDV RNA and/or HDVAg.
5. Hepatitis E: serum anti-HEV positive or low to high titers in patients with acute hepatitis, or anti-HEV positive >1:20, or positive serum and/or fecal HEV RNA by speckle hybridization or reverse transcription polymerase chain reaction (RT-PCR). The detection reagents for anti-HEV IgM are not yet standardized and continue to be investigated, but the anti-HEV IgM test can be used as a reference for the diagnosis of acute hepatitis E.
(C) Establishing the diagnosis The diagnosis is confirmed in all cases with clinical diagnosis of acute, chronic, heavy, biliary hepatitis or hepatitis cirrhosis, when a particular type of hepatitis is identified by pathogenic or serologically specific methods. The co-infection of two or more hepatitis viruses is called co-infection. Infection with another type of hepatitis virus on top of an existing hepatitis virus infection is called super-infection.
The naming of confirmed hepatitis cases is based on a combination of clinical typing and pathogenic typing, with the results of liver histopathological examination attached. Examples include.
(1) Viral hepatitis, type A (or type A and type B co-infection), acute jaundice (or acute jaundice-free type).
(2) Viral hepatitis, type B (or overlapping type B and D infection), chronic (moderate), G2 S3 (degree of inflammatory activity 2; degree of fibrosis 3).
(3) Viral hepatitis, type C, subacute heavy, ascites, early (or intermediate or late) stage.
(4) HBsAg carriers with recent infection with another type of hepatitis virus may be named as follows.
(1) viral hepatitis, type A (or type E), acute jaundice type ;
② HBsAg carriers.
For the five types of hepatitis A, B, C, D, E virus markers are negative can be diagnosed as: acute hepatitis, pathogenic undetermined; or chronic hepatitis, pathogenic undetermined.
Histopathological diagnosis
Histopathological examination plays an important role in the diagnosis, classification and prognosis of liver diseases, and is the gold standard for definite diagnosis, measuring the inflammatory activity and degree of fibrosis as well as determining the efficacy of drugs. To avoid difficulties in proper diagnosis due to too small puncture tissue, aim to use a thick needle puncture, and the specimen must be more than 1 cm in length (1.5 to 2.5 cm). At least 3 or more confluent areas should be included microscopically. Liver puncture specimens should be serially sectioned and routinely stained for HE and reticulocytes and/or Masson trichrome to accurately determine intrahepatic inflammation, structural changes in liver tissue, and the degree of fibrosis. In situ examination of viral antigens or nucleic acids in liver tissues can be performed as needed to help determine the pathogen and viral replication status. The pathologist should strengthen the basic training of liver lesions, strive for correct characterization of lesions and proper delineation, and closely integrate with clinical practice to ensure the accuracy of histopathological diagnosis.
(A) Acute hepatitis
Acute hepatitis is a lobular lesion, mainly manifested by swelling of hepatocytes, watery degeneration and ballooning, interspersed with eosinophilia, apoptotic vesicle formation and scattered dotted and focal necrosis, while the surviving hepatocytes show regeneration, nuclei increase, binuclei increase or appear multinucleated; sinusoidal blast cells proliferate, sinusoidal lymphocytes and monocytes increase; the confluent area shows a mild to moderate inflammatory response; there is no obvious fibrosis in the liver. In some cases, bile sludge was seen in the liver tissue, and bile emboli and foci of necrosis were formed in the hepatic capillary bile ducts and phagocytic aggregates containing xanthophylls in the sinusoids. These changes are more obvious in jaundiced patients.
(B) Chronic hepatitis
1, the basic lesions of chronic hepatitis: in addition to varying degrees of hepatocyte degeneration and necrosis in the lobules, inflammation around the confluent and confluent areas is often more pronounced, often accompanied by varying degrees of fibrosis, the main lesions are inflammatory necrosis and fibrosis.
(1) Inflammatory necrosis: common points, focal necrosis, fusion necrosis, debris necrosis and bridging necrosis, the latter two are closely related to the prognosis, is an important morphological index to determine the degree of inflammatory activity.
It is characterized by infiltration of single nucleated cells, necrosis of hepatocytes in the junctional zone, proliferation of hepatic stellate cells, and local collagen deposition and fibrosis. According to the degree of lesion, it is classified as mild, moderate or severe, which is one of the important indicators to determine the activity of lobular inflammation. a. Mild Occurring in part of the confluent area, with a small extent of plate destruction and limited interface hepatitis; b. Moderate Most of the confluent area is involved, with up to 50% plate destruction and significant interface hepatitis; c. Severe Inflammation causing enlargement of the confluent area, with extensive PN and inflammatory necrosis reaching deep into the middle lobular zone, resulting in severe lobular border The collagen deposition around the confluent area can be more extensive.
(2) Bridging necrosis (BN) is a more extensive fusion necrosis, which is divided into 3 categories according to the necrosis connection site: a. confluent zone – confluent zone (P-P) BN mainly formed by the development of inflammation and PN in the confluent zone; b. confluent zone – central lobular zone (P-C) BN along the central lobular zone of hepatic alveoli 3 and confluent zone inflammation and necrosis fused with each other, often resulting in the destruction of lobular structures; c. central – central (C-C) BN BN fusion of necrosis in the central zone of two lobules. bn often leads to bridging fibrosis, which is closely related to prognosis. the amount of bn is one of the important bases for the diagnosis of moderate and severe chronic hepatitis.
(2) Fibrosis: refers to excessive collagen deposition in the liver, which is divided into stages 1 to 4 (S1-4) according to the extent of damage to liver structure, degree and impact on liver microcirculation.
①S1 includes confluent area, fibrosis around confluent area and restricted perisinusoidal fibrosis or intrafollicular fibrous scar, both of which do not affect the integrity of the lobular structure.
②S2 Fibrous septum, that is, bridging fibrosis (bridging fibrosis), mainly developed from bridging necrosis, S2 although there is formation of fibrous septum, but most of the lobular structure is still preserved.
S3 A large number of fibrous septa separate and destroy the lobules of the liver, resulting in disturbance of the lobular structure, but no cirrhosis yet. At this stage, some patients may develop portal hypertension and esophageal varices.
S4 Early cirrhosis with extensive destruction of liver parenchyma, diffuse fibrous hyperplasia, regeneration of separated hepatocyte masses and pseudobullet formation in varying degrees. At this stage, inflammation is mostly still ongoing, and the fibrous septa are wide and lax. The remodeling is not yet adequate. This is different from cirrhosis, in which the fibrous septum is wrapped around the pseudobullet, and the collagen and elastic fibers in the septum are modified and arranged in parallel around the pseudobullet.
2, grading and staging of chronic hepatitis lesions (see Table 2): the inflammatory activity and fibrosis degree are classified as grade 1-4 (G) and stage 1-4 (S), respectively. Inflammatory activity was graded according to the degree of inflammation in the confluent area, around the confluent area and within the lobules, and when the two were inconsistent, the total inflammatory activity (G) was determined as the higher.
Table 2 Criteria for grading and staging of chronic hepatitis
Inflammatory activity (G)
Degree of fibrosis (S)
Grade
Convergence zone and surrounding
Intralobular
stage
Degree of fibrosis
0
No inflammation
No inflammation
0
None
1
Inflammation in the confluence area
Degeneration and foci of fractional dots and focal necrosis
1
Enlarged fibrosis in the confluent area, limited perisinus and intralobular fibrosis
2
Mild PN (mild CAH)
Degeneration, punctate, focal necrosis or eosinophilic vesicles
2
Fibrosis around the confluent area, formation of fibrous septa, preservation of lobular structures
3
Moderate PN (medium CAH)
Degeneration, fusion necrosis or see BN
3
Fibrous septum with distortion of lobular structure (distortion), no cirrhosis
4
Severe PN (heavy CAH)
Extensive BN, involving multiple lobules (multilobular necrosis)
4
Early cirrhosis
3, the degree of chronic hepatitis: chronic hepatitis is divided into mild, moderate and severe according to the inflammatory activity (G). If S>G, it should be specially labeled.
(1) Mild chronic hepatitis (including the original chronic migratory hepatitis and light chronic active hepatitis): G1-2, S0-2.
(1) Hepatocyte degeneration, point and focal necrosis or apoptotic vesicles;
(ii) Confluent area with (without) inflammatory cell infiltration, enlargement, with or without focal debris necrosis (interface hepatitis);
(③) lobular structure is intact.
(2) Moderate chronic hepatitis (equivalent to original medium-sized chronic active hepatitis): G3, S1-3.
(1) Inflammation in the confluent area is obvious with moderate debris necrosis;
②Severe inflammation in the lobules with fusion necrosis or with few bridging necrosis;
(3) Fibrous septum formation, with most of the lobular structures preserved.
(3) Severe chronic hepatitis (equivalent to former heavy chronic active hepatitis): G4, S2-4.
(1) Severe inflammation or severe debris necrosis in the confluent area;
②Bridge necrosis involving most of the lobules;
③ A large number of fibrous septa, disorganized lobular structure, or formation of early cirrhosis.
4, histopathological diagnosis of chronic hepatitis: histopathological diagnosis includes etiology (determined by the results of hepatitis virology testing of serum or liver tissue), degree of lesion and grading and staging results. For example: viral hepatitis, type B, chronic, moderate, G3/S4; viral hepatitis, type B + C, chronic, severe, G4/S3.
(C) Heavy viral hepatitis
1, acute heavy hepatitis: hepatocytes are necrotic at once, necrosis area > 2/3 of the liver parenchyma, or submassive necrosis, or bridging necrosis, with severe degeneration of surviving hepatocytes; necrosis > 2/3, more can not survive; conversely, hepatocytes retain more than 50%, although hepatocytes have degeneration and dysfunction, through the acute stage, hepatocytes regenerate rapidly and can be expected to recover. If diffuse vesicular steatosis occurs, the prognosis is often poor.
2, sub-acute heavy hepatitis: liver tissue new and old varying sub-bulk necrosis (extensive Zone 3 necrosis); older necrotic areas of reticular fiber collapse, and may have collagen fiber deposition; residual hepatocytes proliferate into clusters; visible a large number of small bile duct hyperplasia and siltation.
3, chronic heavy hepatitis: lesions characterized by the presence of massive (all lobular) or submassive fresh liver parenchymal necrosis on the background of lesions of chronic liver disease (chronic hepatitis or cirrhosis).
(IV) Cirrhosis of the liver
1, Active cirrhosis: cirrhosis with marked inflammation, including inflammation within the fibrous septum, peripseudobulbar debris necrosis and inflammatory lesions within regenerative nodules.
2.Static cirrhosis: clear borders around pseudobullets, few inflammatory cells in the septum and mild inflammation in the nodules.
Differential diagnosis
1.Acute liver injury.
The main diseases with acute liver injury as the main manifestation are viral hepatitis and drug-related hepatitis. The main points of differentiation between drug-related hepatitis and viral hepatitis are.
(1) drug hepatitis generally has one or more primary diseases that require treatment and a history of drug use, which develops 5 days to 3 months after drug use;
(2) Liver damage is often accompanied by other clinical manifestations of drug allergy such as rash and fever;
(3) Hepatitis virology tests are often negative;
(4) A positive macrophage or leukocyte movement inhibition test with the suspected drug as antigen indicates that the patient is allergic to the drug;
(5) Liver function impairment improves quickly after discontinuation of the drug.
The clinical manifestations of acute fatty liver in pregnancy are similar to those of acute heavy hepatitis, but there are mostly varying degrees of edema, proteinuria and hypertension, with abdominal pain at the onset, often prone to severe hypoglycemia and hypoproteinemia, complicated by acute pancreatitis, severe jaundice, but with negative urinary bilirubin, insignificant reduction of liver borders, typical fatty liver wave pattern visible on ultrasound, and severe steatosis of hepatocytes on viral examination while hepatocyte necrosis The hepatocytes are severely fatty but the hepatocyte necrosis is not obvious.
Some systemic diseases can cause acute liver injury. For example: typhoid fever, malaria, leptospirosis, severe infections, infectious mononucleosis, acute cholecystitis, etc. However, regardless of the severity of their liver damage, are accompanied by obvious systemic symptoms, while viral hepatitis only at the beginning of the disease with 3 to 5 days of fever.
2. Chronic liver damage.
In addition to chronic viral hepatitis, diseases with chronic liver damage as the main manifestation include autoimmune hepatitis, hepatomegaly, alcoholic liver disease, fatty liver and certain liver parasitic diseases. Autoimmune hepatitis is most often seen in women and is often associated with extrahepatic manifestations, accelerated sedimentation, markedly elevated serum globulins, positive autoantibody tests, detection of lupus cells in 30% of patients, often negative hepatitis virology, and effective treatment with adrenocorticosteroids and immunosuppressive agents.
Patients with hepatomegaly have a significant decrease in copper orchid protein, urinary copper excretion is significantly higher than normal, there is significant steatosis on liver pathology, and slit lamp examination of the corneal K-F ring is an important sign of the disease. Patients with alcoholic liver disease have a history of long-term heavy drinking, mostly accompanied by alcoholic peripheral neuropathic damage, significantly elevated serum γ-GT, elevated AST/ALT, significant alcohol withdrawal reaction, and improvement of liver disease after quitting alcohol.
Fatty liver can also cause abnormal liver function, but both lipids and ultrasound can assist in the diagnosis. In the case of coexisting hepatitis virus infection, the possibility of the presence of fatty liver is also noted in the presence of persistent abnormal liver function. The possibility of liver parasitosis should be thought of in patients who have lived in parasitic infected areas such as schistosomes.
Common diseases that can be associated with chronic liver damage include cardiogenic jaundice, hyperthyroidism, and certain autoimmune diseases. However, all of these diseases have distinctive primary manifestations, and liver function improves with control of the primary disease. It is important to note that because viral hepatitis is a multifactorial disease in China, it is often possible to be infected with hepatitis viruses at the same time as some chronic diseases. Therefore, a comprehensive serum virological examination is necessary along with the detection of liver damage.
Principles of treatment of viral hepatitis
There are no satisfactory therapeutic drugs and methods for viral hepatitis. The principle of treatment is to differentiate according to different pathogens, different clinical types and histological damage.
I. General treatment
(a) Rest In the early stage of acute hepatitis, hospitalization or local isolation treatment and bed rest should be provided; in the recovery period, activities should be gradually increased, but avoid overwork to facilitate recovery. The active period of chronic hepatitis should be rested properly, and after the condition improves, attention should be paid to the combination of movement and rest, and overwork is not advisable. From acute hepatitis or chronic hepatitis turn heavy should be bed rest, hospitalization.
(B) Nutrition Patients with viral hepatitis should eat high protein, low fat, high vitamin food, carbohydrate intake should be moderate, not too much, in order to avoid the occurrence of fatty liver. Avoid over-eating during the recovery period. Absolute prohibition of alcohol, no alcoholic beverages, nutrients and drugs.
Second, drug treatment
When patients with various types of hepatitis have obvious loss of appetite, frequent vomiting and jaundice, in addition to rest and nutrition, intravenous infusion of 10%-20% glucose solution and vitamin C, etc. can be used. According to different conditions, the corresponding Chinese herbal medicine treatment can be used.
(A) Acute hepatitis
1, hepatitis A: unchanged chronic, mainly take supportive and symptomatic treatment. Closely observe the condition of elderly, pregnant, post-surgical or immunocompromised patients, and if the condition turns serious, it should be promptly treated as heavy hepatitis.
2, hepatitis B: should be distinguished from acute hepatitis B inhibited is an acute attack of chronic hepatitis B, the former treatment with hepatitis A, the latter according to the treatment of chronic hepatitis B.
3, hepatitis C: those diagnosed with acute hepatitis C should strive for early antiviral treatment see “Annex”.
4, hepatitis D: the same as the treatment of hepatitis B.
5, hepatitis E: the same as hepatitis A.
(II) chronic hepatitis
Anti-viral, immune adjustment, hepatocyte protection, improvement of liver function, anti-fibrosis and psychological treatment measures should be taken according to the specific conditions of the patient. It is currently believed that the formation of chronic hepatitis is mainly due to persistent viral infection, therefore, antiviral treatment should be emphasized for chronic hepatitis. Antiviral treatment is shown in the Annex.
(C) Heavy hepatitis
The main measures of comprehensive therapy are to enhance care, monitoring and close observation of the disease. Strengthen supportive therapy; maintain water-electrolyte balance, replenish fresh blood or blood products, multiple amino acids containing high branched chain amino acids, inhibit inflammatory necrosis and pro-hepatocyte regeneration drugs. Improve liver microcirculation, reduce endotoxemia, prevent and treat various complications (such as hepatic encephalopathy, cerebral edema, hemorrhage, renal insufficiency, secondary infection, electrolyte disorders, ascites and hypoglycemia, etc.). Research on artificial liver support system and liver transplantation can be conducted in conditional units. (See Annex II for details)
(D) chronic hepatitis B and C virus carriers
They can work as usual, but should be reviewed regularly, followed up and observed, and mobilized for liver aspiration for further diagnosis and corresponding treatment.