Toxic liver damage is understood as pathological structural changes in the tissue (reversible and irreversible) under the influence of damaging chemicals. The ICD 10 code for toxic hepatitis is K71.
Etiology
The reasons for the development of chronic hepatitis are: medicines, alcohol, household, plant and industrial poisons.
- Drug toxic liver damage. Symptoms of it can occur with a single administration of a large dose or prolonged use of small cumulative doses of some drugs. For example, with the use of "Tetracycline", "Paracetamol." Some substances can inhibit hepatocyte enzymes. These are such as, for example: "Erythromycin", "Rifampicin", "Clarithromycin", alcohol, smoking, antifungal and antiretroviral drugs, penicillins. Antiepileptic substances such as Oxacillin, Flucloxacillin, Amoxicillin Clavulonate (Amoxiclav), sulfonamides, Co-trimaxazole, Sulfosalazin, Nifurantoin, Isoniazid have toxic effects. "," Ftivazide ", anticonvulsants. The general ICD code 10 for toxic hepatitis of medicinal genesis is K71. Further, it is indicated depending on the morphological changes of the organ.
- Alcohol, narcotic substances. The general ICD code 10 for toxic hepatitis of alcoholic origin is K70.
- Industrial poisons. Pesticides, arsenic, phosphorus, insecticides, phenols, aldehydes, chlorinated hydrocarbons, etc.
- Plant poisons. Gorchak, the godson, mushroom poisons, etc. The general ICD code 10 for toxic hepatitis caused by chemical or plant poisons is also K71.
Pathogenesis
One of the functions of the liver is barrier. It neutralizes a toxic chemical substance, forming an inactive form from it.
- When a hepatotoxic substance enters the body, active metabolites are formed in the liver that can have a direct toxic effect on the cell or immune-mediated (determined by the mechanism of hypersensitivity). Both of these processes cause cytolysis, hepatocyte necrosis. Acute or chronic hepatitis develops.
- Also, drugs and their metabolites can reduce mitochondrial oxidation in the cell and transfer the metabolism in it to the anaerobic pathway. The synthesis of low density lipoproteins is impaired, and triglycerides accumulate in the hepatocyte. The patient develops fatty liver. A large number of fatty inclusions in the cell leads to its steatonecrosis.
- The functions of enzymes and transport proteins in the cell can also be impaired without damage to the hepatocyte itself, hyperbilirubinemia and an increase in gamma glutamyl transferase occur. Other functional liver tests do not change.
- Blockade of transport enzymes, damage to hepatocytes cause cholestasis, impaired synthesis or transport of bile. Bile is formed in the hepatocyte from bile acids, bilirubin, cholesterol. Then it enters the bile duct. Intrahepatic cholestasis is intralobular and extralobular. There is also extrahepatic cholestasis, characterized by difficulty in the flow of bile in the extrahepatic bile ducts.
Thus, a toxic substance can cause acute liver damage with massive death of hepatocytes and chronic - with multiple doses of small doses of a poisonous substance.
- With hepatocyte necrosis without the occurrence of autoimmune processes and cholestasis, AST, ALT will be increased.
- If hepatocellular cholestasis joins, then up to 2 norms of alkaline phosphatase, ALT, AST, GGTP are raised.
- With ductular cholestasis with cell necrosis, the picture is the same, but alkaline phosphatase increases by more than 2 norms.
- In autoimmune processes, an increase in immunoglobulins of more than 1.5 times is added.
Clinic
If toxic damage to the liver has occurred, symptoms can develop both acutely and slowly (chronically). The patient complains of pain and heaviness in the right hypochondrium, nausea, lack of appetite, weakness. It may be itchy skin, loose stools, bleeding. The patient is inhibited. On examination, the skin and sclera are icteric in color. With cholestasis, the color of the urine darkens, the stool becomes light. An increase in the liver and spleen is detected. Possible ascites, fever. Symptoms of toxic hepatitis and treatment depend on the activity of the inflammatory process.
Diagnostics
If toxic hepatitis is suspected, the diagnosis is made on the basis of clinical, medical, laboratory, instrumental data. A general analysis of blood and urine, a biochemical analysis are prescribed: liver tests, protein levels, coagulation system, lipid profile are studied. An analysis is also prescribed for immunoglobulins, ultrasound of the abdominal organs, endoscopy, MRI, liver biopsy.
Treatment
The main drugs used to treat liver damage include:
- Ursodeoxycholic acid UDCA (Ursofalk, Ursosan, Ursodez). It reduces cholestasis (stagnation of bile), enhances the excretion of bile acids, has a membrane stabilizing effect (protecting the cell wall from toxins), as well as hepatoprotective, immunomodulating, anti-inflammatory (prednisone-like), hypocholesterolemic, anti-apoptotic (slowing down the aging of hepatocytes), litholytic stones (dissolves with cholelithiasis), antifibrotic (slows the progress of cirrhosis, prevents its occurrence), cardioprotective, increases insulin sensitivity, improves etabolizm lipids and glucose in the liver acts as a vasodilator.
- Essential phospholipids ("Essential") restore the integrity of cell membranes, have an antifibrotic effect.
- S-ademeteonin ("Heptral") increases the amount of substances in the cell that fight toxins, reduces cholestasis and lipid peroxidation.
- Alpha lipoic acid preparations (Berlition, Thioctacid) fight the development of liver steatosis.
- Artichoke preparations have a choleretic effect.
- Silymarin preparations (Karsil, Legalon) have a direct antifibrotic effect.
Assignment algorithm
So what is toxic hepatitis? Symptoms and treatment what are it? Add some clarifications. According to clinical recommendations for toxic hepatitis, if GGTP, alkaline phosphatase are elevated (there is cholestasis), and AST and ALT are normal or rise no higher than two norms, then UDCA is prescribed at a dose of 15 mg per kg (750 - 1000 mg per day in two doses) for three months or longer. If more than two norms (3 - 5), then Heptral joins intravenously at 400 - 800 mg daily for 10 - 15 days.
With a normal level of alkaline phosphatase (no cholestasis) and an increase in ALT and AST to 5 norms, UDCA of 10 mg per kg is prescribed. Assigned for 2-3 months, "Essential", "Berlition", depending on the causes of the disease.
If AST, ALT, bilirubin is more than 5 norms, then glucocorticoids join. "Prednisolone" is administered intravenously to 300 mg per day for up to 5 days, with subsequent transfer to a tablet and a gradual dose reduction. UDCA and Heptral are prescribed according to the scheme above (where alkaline phosphatase is elevated). Plus vitamins B1, B12, B6, PP are needed.