Hepatitis B is an infectious liver disease that occurs in various clinical variants (from asymptomatic carrier to destruction of the hepatic parenchyma). In hepatitis B, liver cell damage is autoimmune in nature. Sufficient concentration of the virus for infection is found only in the biological fluids of the patient. Therefore, hepatitis B infection can occur parenterally during hemotransfusion and various traumatic procedures (dental manipulations, tattoos, pedicures, piercings), as well as sexually. In the diagnosis of hepatitis B, the detection of HBsAg antigen and HbcIgM antibodies in the blood plays a crucial role. Treatment of viral hepatitis B includes basic antiviral therapy, mandatory diet, detoxification and symptomatic treatment.
Hepatitis B virus – DNA-containing, belongs to the genus Orthohepadnavirus. In infected individuals, three types of viruses are detected in the blood, differing in morphological characteristics. Spherical and filamentous forms of viral particles do not have virulence, infectious properties are manifested by Dein particles – two-layer rounded full-structured viral forms. Their blood population rarely exceeds 7%. The hepatitis B virus particle has a surface antigen HBsAg, and three internal antigens: HBeAg, HBcAg and HbxAg.
The resistance of the virus to environmental conditions is very high. In the blood and its preparations, the virus remains viable for years, can exist for several months at room temperature on underwear, medical instruments, objects contaminated with the patient’s blood. Inactivation of the virus is carried out during processing in autoclaves when heated to 120 ° C for 45 minutes, or in a dry-burning cabinet at 180 ° C for 60 minutes. The virus dies when exposed to chemical disinfectants: chloramine, formalin, hydrogen peroxide.
The source and reservoir of viral hepatitis B are sick people, as well as healthy virus carriers. The blood of people infected with hepatitis B becomes contagious much earlier than the first clinical manifestations are noted. In 5-10% of cases, chronic asymptomatic carrier develops. Hepatitis B virus is transmitted by contact with various biological fluids (blood, semen, urine, saliva, bile, tears, milk). The main epidemiological danger is represented by blood, semen and, to some extent, saliva, since usually only in these fluids the concentration of the virus is sufficient for infection.
Transmission of infection occurs mainly parenterally: during blood transfusions, medical procedures using non-sterile instruments, during therapeutic manipulations in dentistry, as well as during traumatic processes: tattooing and piercing. There is a possibility of infection in nail salons during an edged manicure or pedicure. The contact path of transmission is realized during sexual contacts and in everyday life with the joint use of personal hygiene items. The virus is introduced into the human body through micro-injuries of the skin and mucous membranes.
The vertical transmission pathway is implemented intranatally, during normal pregnancy, the placental barrier for the virus is not passable, however, in case of placental rupture, transmission of the virus before delivery is possible. The probability of infection of the fetus increases many times when HBeAg in addition to HBsAg is detected in a pregnant woman. People have a fairly high susceptibility to infection. With transfusion transmission, hepatitis develops in 50-90% of cases. The probability of developing the disease after infection directly depends on the received dose of the pathogen and the state of general immunity. After the transfer of the disease, a long-lasting, probably lifelong immunity is formed.
The vast majority of people with hepatitis B are people aged 15-30 years. Among those who died from this disease, the proportion of drug addicts is 80%. People who inject narcotic substances have the greatest risk of contracting hepatitis B. Due to frequent direct contact with blood, medical workers (surgeons and operating nurses, laboratory assistants, dentists, employees of blood transfusion stations, etc.) are also at risk for viral hepatitis B.
Hepatitis b symptoms
The incubation period of hepatitis B varies quite widely, the interval from the moment of infection to the development of clinical symptoms can range from 30 to 180 days. It is often impossible to estimate the incubation period of the chronic form of hepatitis B. Acute viral hepatitis B often begins similarly to hepatitis A, but its pre-jaundice period can also occur in an arthralgic form, as well as in an asthenovegetative or dyspeptic variant.
The dyspeptic variant of the course is characterized by loss of appetite (up to anorexia), incessant nausea, episodes of causeless vomiting. The flu-like form of the clinical course of the pre-jaundice period of hepatitis B is characterized by fever and general intoxication symptoms, usually without catarrhal signs, but with frequent, mainly night and morning, arthralgias (while the joints are not visually changed). After movement in the joint, the pain usually subsides for a while.
If during this period there is arthralgia, combined with rashes of the type of urticaria, the course of the disease promises to be more severe. Most often, such symptoms are accompanied by fever. In the pre-jaundice phase, there may be pronounced weakness, drowsiness, dizziness, bleeding gums and episodes of nosebleeds (hemorrhagic syndrome).
When jaundice appears, there is no improvement in well-being, more often the general symptoms worsen: dyspepsia, asthenia increases, itching appears, hemorrhages increase (in women, hemorrhagic syndrome can contribute to the early onset and intensity of menstruation). Arthralgia and exanthema disappear in the jaundice period. The skin and mucous membranes have an intense ochre hue, petechiae and rounded hemorrhages are noted, urine darkens, feces become lighter until complete discoloration. The liver of patients increases in size, its edge protrudes from under the costal arch, painful to the touch. If, with intense ictericity of the skin, the liver retains its normal size, this is a harbinger of a more severe course of infection.
In half or more cases, hepatomegaly is accompanied by an enlargement of the spleen. From the cardiovascular system: bradycardia (or tachycardia with severe hepatitis), moderate hypotension. The general condition is characterized by apathy, weakness, dizziness, insomnia is noted. The jaundice period can last a month or more, after which a period of convalescence occurs: first, dyspeptic phenomena disappear, then there is a gradual regression of jaundice symptoms and normalization of bilirubin levels. The return of the liver to normal size often takes several months.
In the case of a tendency to cholestasis, hepatitis can acquire a sluggish (torpid) character. At the same time, intoxication is weakly expressed, steadily increased bilirubin levels and liver enzyme activity, feces are acolic, urine is dark, the liver is steadily increased, body temperature is kept within subfebrile limits. In 5-10% of cases, viral hepatitis B occurs in a chronic form and contributes to the development of viral cirrhosis of the liver.
The most dangerous complication of viral hepatitis B, characterized by a high degree of lethality, is acute liver failure (hepatargia, hepatic coma). In the case of massive death of hepatocytes, significant loss of liver functionality, severe hemorrhagic syndrome develops, accompanied by toxic effects of substances released as a result of cytolysis on the central nervous system. Hepatic encephalopathy develops, going through the following stages sequentially.
- Precoma I: the patient’s condition deteriorates sharply, jaundice and dyspepsia (nausea, repeated vomiting) worsen, hemorrhagic symptoms manifest, patients have a specific hepatic odor from the mouth (nauseatingly sweet). Orientation in space and time is disturbed, emotional lability is noted (apathy and lethargy are replaced by hyperexcitation, euphoria, increased anxiety). Thinking is slowed down, there is an inversion of sleep (at night patients cannot fall asleep, during the day they feel irresistible drowsiness). At this stage, violations of fine motor skills are noted (blunders during a finger test, distortion of handwriting). In the liver area, patients may notice pain, body temperature rises, pulse is unstable.
- Precoma II (threatening coma): disorders of consciousness are progressing, it is often confused, complete disorientation in space and time is noted, short-term outbursts of euphoria and aggressiveness are replaced by apathy, intoxication and hemorrhagic syndromes are progressing. At this stage, signs of edematous ascitic syndrome develop, the liver becomes smaller and hides under the ribs. Note a small tremor of the limbs, tongue. The stages of precoma can last from several hours to 1-2 days. In the future, neurological symptoms are aggravated (pathological reflexes, meningeal symptoms, respiratory disorders of the type of Kussmul, Cheyne-Stokes may be noted) and the hepatic coma itself develops.
- The terminal stage is coma, characterized by depression of consciousness (stupor, sopor) and in the future its complete loss. Initially, reflexes (corneal, swallowing) are preserved, patients can react to intense irritating actions (painful palpation, loud sound), later reflexes are suppressed, the reaction to stimuli is lost (deep coma). The death of patients occurs as a result of the development of acute cardiovascular insufficiency.
In the severe course of viral hepatitis B (lightning coma), especially in the case of its combination with hepatitis D and hepatitis C, hepatic coma often develops early and ends fatally in 90% of cases. Acute hepatic encephalopathy, in turn, contributes to secondary infection with the development of sepsis, and also threatens the development of renal syndrome. Intense hemorrhagic syndrome can cause significant blood loss in internal bleeding. Chronic viral hepatitis B develops into cirrhosis of the liver.
Diagnosis is carried out by detecting specific virus antigens in the blood of patients in the blood serum, as well as immunoglobulins to them. With the help of PCR, it is possible to isolate the DNA of the virus, which allows you to determine the degree of its activity. The detection of HBsAg surface antigen and HbcIgM antibodies plays a crucial role in the diagnosis. Serological diagnostics is performed with the help of ELISA and RIA.
To determine the functional state of the liver in the dynamics of the disease, regular laboratory tests are performed: biochemical analysis of blood and urine, coagulogram, ultrasound of the liver. A significant role is played by the value of the prothrombin index, a drop of which to 40% or lower indicates a critical condition of the patient. According to individual indications, a liver biopsy may be performed.
Complex therapy of viral hepatitis B includes dietary nutrition (a liver-sparing diet No. 5 is prescribed in variations depending on the phase of the disease and the severity of the course), basic antiviral therapy, as well as pathogenetic and symptomatic agents. The acute phase of the disease is an indication for inpatient treatment. Recommended bed rest, heavy drinking, categorical refusal of alcohol. Basic therapy involves the appointment of interferons (alpha interferon is the most effective) in combination with ribavirin. The course of treatment and dosages are calculated individually.
Detoxification solutions are used as auxiliary therapy (in severe cases, infusions of crystalloid solutions, dextran are carried out, corticosteroids are prescribed according to indications), means for normalizing the water-salt balance, potassium preparations, lactulose. To relieve spasms of the biliary system and the vascular network of the liver – drotaverine, eufillin. With the development of cholestasis, UDCA preparations are indicated. In case of severe complications (hepatic encephalopathy) – intensive therapy.
Prognosis and prevention
Acute viral hepatitis B rarely leads to death (only in cases of severe lightning-fast course), the prognosis worsens significantly with concomitant chronic liver pathologies, with combined hepatitis C and D viruses. Death of hepatitis B infected more often occurs after several decades as a result of chronic course and development of cirrhosis and liver cancer.
General prevention of viral hepatitis B implies a set of sanitary and epidemiological measures aimed at reducing the risk of infection during blood transfusion, monitoring the sterility of medical instruments, the introduction into mass practice of disposable needles, catheters, etc. Individual prevention measures imply the use of individual personal hygiene items (razors, toothbrushes), prevention of injury to the skin, safe sex, drug withdrawal. Vaccination is indicated for persons belonging to the occupational risk group. Immunity after vaccination against hepatitis B persists for about 15 years.