Lecture of acute viral hepatitis

2021-03-23 12:00 AM

Because there are different types of hepatitis viruses, these viruses belong to different virus families, different routes of transmission, pathogenicity, disease progression, and so on.


Acute viral hepatitis is a common acute infectious disease caused by the hepatitis viruses (HAV, HBV, HCV, HDV, HEV, ...). The disease is characterized by a general clinical feature of severe intoxication that causes fatigue, enlarged liver, jaundice and mucosal necrosis, leading to increased serum GOT and GPT (or AST and ALT) enzymes. ...

Research history

From the 5th century (BCE), the disease was recorded. But it was not until 1893 that Botkin (Russia) was identified as a systemic infection. In 1937, Findley and Callum (USA) and then 1940, Sergieb et al. (Russia) determined that the disease was caused by a viral etiology. In 1947, researchers divided the disease into two categories: infectious hepatitis (gastrointestinal infection) and serum hepatitis (blood sugar transmission).

In 1964, Blumberg discovered in the serum of some patients with viral hepatitis there is an antigen that is able to agglutinate with the serum of Aboriginal people in Australia and named "Australia antigen" (then people is known to be the hepatitis B virus surface antigen or HBsAg). In 1975, Dane discovered the "corpus Dane", later known as the hepatitis B virus, denoted as HBV (Hepatitis B virus).

In 1973, Feinstone et al discovered the hepatitis A virus (HAV).

1977, Rizzetto (Ytalia) and colleagues discovered the delta virus, later called HDV.

1989, Chou et al. Discovered the hepatitis C virus after blood transfusion, named hepatitis C virus (HCV).

1991, Benhamau found HEV spreads the gastrointestinal tract.

It is thought that it is likely that there are still other hepatitis viruses yet to be discovered. In 1994, hepatitis F virus (HFV) was reported, but the agent is currently considered a mutation of HBV in Japan. After that, other viruses were detected such as: Hepatitis G virus (HGV), TT virus (TTV, discovered in 1997), SANBAN virus, TLMV (mini virus similar to TTV), SEN virus (SENV, letter SEN is the abbreviated name of the patient infected with the virus), the Sentinel virus (SNTV) ... However, whether these viruses have the ability to cause hepatitis or have been considered hepatitis viruses, it still takes time to confirm. concentration.


Due to the different types of hepatitis viruses (HAV, HBV, HCV, HDV, HEV), these viruses belong to different virus families, with different routes of transmission, pathogenicity, disease progression, etc. . Therefore, epidemiological characteristics are also different.







Viruses family









Diameter (nm)










K hip

27 -  28

Positive single helix RNA





anti- HAV




42 - 45


DNA, 1 part twisted pair wire






anti - HBs

anti - HBe

anti - HBc






Positive single helix RNA





anti- HCV






Single helix, negative RNA







Is not



Positive single helix RNA







Path of infection

Feces-mouth (Digestive)

Blood sugar

Blood sugar

Blood sugar


Mechanism of pathogenesis and pathology

Mechanism of pathogenesis

Up to now, there have been many studies on viral hepatitis. But many points in the pathogenesis mechanism are still not clear. However, the pathogenesis can be divided into the following periods:

Period of virus penetration: With viruses A and E penetrating the digestive tract. Viruses B, C, D penetrate through the bloodstream.

Period of viral replication: At the organs of the gastrointestinal tract and later mesenteric lymph nodes, the virus is multiplied. Due to the effect of the virus on these organizations, it increases the permeability of cells, degeneration - necrosis of the organization and produces nonspecific changes, especially in the lymph nodes (in the two periods above, there is no manifest pathological symptoms).

Period of primary viral infection (corresponding to the period of clinical onset): Viruses from the lymph nodes into the blood cause a reaction of the body manifested by fever.

Period of organization spread: Viruses from the blood penetrate all organs, but mainly the liver. The most important during this period is the virus that causes liver damage. Liver damage manifests itself in three aspects: liver parenchymal cell destruction, damage to the medullary cells and congestion of bile fluid. Clinically, this period corresponds to the full-blown period of the disease.

Period of secondary blood virus infection: Viruses return from the liver to the blood causing flare-ups, allergic poisoning phenomenon, arising complications and recurrence.

Pathological anatomical injury

The macroscopic picture of the liver on laparoscopy shows "large, red liver". In cases of prolonged development, the dark red color will gradually fade into "large, white" or pale yellow liver. Gallbladder and gallbladder are empty because there is no bile fluid. In the case of prolonged development, cholestasis will see the gallbladder enlarge and contain bile fluid. Organizational changes are found in both hepatocytes, glial tissue, endothelial retinal system and biliary tract.

The hepatocytes are enlarged and then necrotic: At first enlargement followed by pitting degeneration or cytoplasmic coagulation and cell necrosis. The study of organizational changes over time can be seen through the following periods:

At week 1 a characteristic feature is proliferation of Kupffer cells and hepatocellular necrosis.

In the 2nd week, hepatocellular necrosis develops strongly and forms necrotic necrosis and associated organ proliferation appears.

In the 3rd week hepatocellular necrosis is maximized but regeneration begins with signs of increased division of hepatocellular mitochondria.

In the next period, the necrotic process gradually decreases with the proliferation of regenerated liver cells. However, scattered necrotic necrosis may persist depending on the disease.

Cases of cholestatic jaundice often appear to form lumps in the biliary tract and dilate the biliary tract. There is an infiltrating inflammation around the bile ducts.


Divide the clinical form

There are many ways to divide the disease clinical depending on the meaning set.

According to the pathogen

 According to the name of the hepatitis virus. For example: Hepatitis virus caused by HAV, HBV, HCV ...

According to clinical manifestations that are mainly symptoms of jaundice

 Jaundice (typical form), non-jaundice (atypical form), less symptomatic form, hidden form.

According to progress

The acute form (less than 3 months), the prolonged form (3-6 months), the chronic form (more than 6 months).

According to the level

Mild, moderate, severe, malignant (acute yellow liver atrophy).

The typical common form of acute viral hepatitis is the presence of jaundice, a full range of periods and symptoms, acute progression and resolution within 1-2 months.

Incubation period

There are no clinical symptoms, depending on the type of hepatitis virus:

Hepatitis A

 Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E

1-6 weeks

(15-45 days)

1-6 months

(30-120 days)

1-6 months

(30-150 days)

1-3 months

(20-90 days)

1-2 months

(20-50 days)

 Onset (also known as pre-jaundice)

The onset of viral hepatitis is varied. Suvalopva EP divides the following types of triggers:

Gastrointestinal disturbances: Patient has anorexia, fear of fat, nausea, vomiting, abdominal pain, and sometimes bowel disturbances; These symptoms appear with mild or moderate fever, lasting for 1 week.

Arthritis: Painful joints, but no change in shape in joints.

Type of exudate inflammation (also known as fake flu): The patient has a runny nose, sore throat, dry cough with fever.

Type of neurasthenia: Fatigue, dizziness, sleep disturbance (possibly in a state of inhibition or arousal).

Mixed type: Including many mixed symptoms of the above types of onset.

However, there are 3-5% cases of jaundice virus hepatitis without an onset period.

All of these onsets are usually accompanied by mild or moderate fever for a few days to a week, pain in the right lower rib. Especially during this period is the fatigue disproportionately with the fever. Although the patient has a mild fever, short-term, some patients do not have a fever, but he feels a lot tired, does not want to walk, does not want to do even light work ...

During the onset period, most patients can see an enlarged liver (90-95%). Most patients at this point see dark yellow urine; Urine test appeared urobilinogen (+).

Full-blown period (jaundice)

 Starting at jaundice, most patients have a fever. In mild and moderate levels, patients often feel better, eat, relieve joint pain ... On the contrary, with severe patients entering jaundice, symptoms develop and become severe. Up: liver enlargement, pain, some cases have enlarged spleen, anorexia, fatigue, digestive disorders ... Testing shows that the enzyme transaminase increases, especially SGPT (or ALT), Bilirubin in whole blood increases. but mainly direct bilirubin, alkaline phosphatase increases in cases of biliary obstruction, urine urobilinogen is from (+) converted to (-) calculated. Tests for blood count are less variable.

This stage of jaundice develops very quickly, usually reaching a maximum within 2-5 days. Jaundice reaches its maximum level and stays stable for a few days to a few weeks (usually 2-4 weeks). During these period clinical and subclinical symptoms increase to their maximum. In patients with severe jaundice, the stools are white like stools (discoloured stools), the urine is small and dark like a thick water, the patient is very itchy, so there are many scratches on the skin.

Retreat and recovery phase

Usually begins with a polyuria (called a polyuria). Clinical symptoms along with biochemical disorders began to decrease.

The patient feels comfortable, the symptoms of the disease gradually disappear, eat and sleep, clear urine, liver gradually return to normal, the tests of transaminases, bilirubin and other biochemical indicators gradually return to normal. However, the feeling of fatigue and pressure in the liver, especially after eating, can be prolonged.

Implementing the quadrants

Clinical basis

The disease usually progresses through 2 distinct periods: The onset usually has a fever and a jaundice period with the end of the fever. Other symptoms: Liver is large, soft, jaundice, very tired ... The disease progresses in cycles and lasts for 1-2 months.

Test basis

Enzyme transaminase (SGOT, SGPT) increases, in which SGPT is usually higher than SGOT, De Ritis index <1; Increased blood bilirubin (mainly direct Bilirubin).

To diagnose the etiology can look for antigens or antibodies (markers) of the hepatitis virus.

Prehistoric, epidemiological basis

How to record diagnosis: Must show: Name of disease, form of disease, ethology, stage, degree,.

Example: "Acute hepatitis B, common jaundice, full-stage, moderate".

Differential diagnosis

Depending on the period of viral hepatitis that needs differential diagnosis with some other diseases such as:

Fever onset period therefore requires differential diagnosis from influenza or acute respiratory viral infection. In patients with diarrhoea, epigastric pain should be differentiated from bacterial infection, intoxication or acute gastritis ...

Jaundice stage: It is necessary to distinguish between other jaundice such as intravascular haemolytic jaundice, chemical or drug jaundice, Leptospirosis disease, etc.

Progression and complications of acute viral hepatitis

Depending on the virus that causes hepatitis, the disease may have different progression and complications. Viruses can cause complications of cholangitis, malignant hepatitis ... HEV hepatitis in pregnant women easily leads to malignant hepatitis and high mortality. Acute hepatitis caused by HBV, HCV and HDV superinfection in chronic HBsAg carriers is more likely to lead to chronic hepatitis and cirrhosis and hepatocellular carcinoma (HCC).


Like many other viral diseases, viral hepatitis so far has not had an effective specific treatment. However, some antiviral drugs have been used for the treatment of hepatitis B and C, but their effectiveness is not high. Therefore, the general principles of treatment for viral hepatitis can be generalized as follows:

General treatment principles

Bed rest and resting mode during onset and full burst, then gentle activity. In the lying position, the amount of blood through the liver will increase by 25-30% compared to the standing position, helping the liver to be more perfused. Upon discharge, patients are exempt from heavy labor for 6-12 months depending on disease severity.

Diet rich in protein, sugar, vitamins, reducing animal fat, especially fried and fried dishes. Increase your intake of fresh fruits and yogurt.

Abstain from alcohol and beer and limit the use of drugs and chemicals that are toxic to the liver.

Use drugs to treat symptoms as needed: gum, fluid, diuretic when there is dark jaundice; vitamin K in the presence of haemorrhagic syndrome; B vitamins

Some medications

Diuretics, bile benefits

In patients with viral hepatitis there is fluid accumulation (in the fulminant phase) due to decreased hepatic Aldosterone destruction. Therefore, the diuretics used are anti-aldosterone drugs (such as Aldactone, Spironolactone ...). You can use diuretics of plant origin such as: grass roots, psyllium, corn stubble ...

Bile gums are used when jaundice occurs: Commonly used drugs are bile drugs containing magnesium, sorbitol or botanicals such as conifer, bodhi, gardenia, artichoke ... The Institute of Medicinal Materials, the Ministry of Health has extracted and prepared Abin tablets (from gymnosperms) and Abilin tablets (from the linden tree) which have been effectively used for treatment.

The drug works to protect liver cells, reduce enzyme transaminases such as: BDD (Biphenyl Dimetyl Dicarboxylate, there are many brand names: Fortec, RB25, Nissel, Omitan ...)

Some drugs are used in special cases

Corticoids are used in cases of malignant hepatitis or cases of chronic cholestatic jaundice. However, it is necessary to consider carefully because of prolonged use of corticosteroids, creating conditions for the virus to thrive.

Antiviral drugs: Lamivudin, Adfovir, Entecavir, Ribavirin, Famciclovir ... are used for hepatitis B and C patients. At present, these drugs are rarely indicated for acute viral hepatitis, which are commonly used in chronic hepatitis B and C hepatitis.


Non-specific preventive measures

For gastrointestinal hepatitis (HAV and HEV) viruses, it is important to keep food and water hygienic. Manage and disinfect the patient's stool to avoid spreading.

Infusion-transmitted hepatitis viruses (HBV, HCV, HDV) need to ensure good disinfection of intravenous and surgical instruments. Use of blood and blood products should be closely monitored for the elimination of hepatitis viruses. Hepatitis B virus can be sexually transmitted so you must have protective equipment like HIV / AIDS during sex.

Specific disease prevention

For hepatitis A

Urgent prevention with immune Gamma globulin, the protective effect is only 4-6 months. The inactivated vaccine with Formalin (Havrix) is effective for prevention but has not been widely used. Recently, the Central Institute of Hygiene and Epidemiology has successfully produced Hepatitis A Vaccines.

For hepatitis B

 Hepatitis B vaccine has been used quite widely and has been part of the extensive immunization program in our country.

Currently, there are 3 types of hepatitis B vaccine: Hepatitis B vaccine is made from plasma infected people (at present this vaccine is inexpensive but is rarely used because it is not safe); hepatitis B vaccine recombinant AND polypeptide synthetic hepatitis B vaccine. The vaccine is indicated for children and people at risk of infection.

For hepatitis caused by other viruses, research for vaccine production is underway.