What Is Fulminant Hepatitis?

Fulminant hepatitis is also called acute necrotizing hepatitis, which is also clinically called acute severe hepatitis. Its early onset is mostly similar to acute jaundice hepatitis, but the condition deteriorates rapidly, the liver shrinks progressively, and jaundice rapidly deepens. With the advancement and development of medicine, after 1978, the outbreak of hepatitis is no longer used as a clinical name in clinical practice, and the standard name in clinical cases has been defined as acute severe hepatitis or acute liver failure.

Fulminant hepatitis

Fulminant hepatitis is also called acute necrotizing hepatitis, which is also clinically called acute severe hepatitis. Its early onset is mostly similar to acute jaundice hepatitis, but the condition deteriorates rapidly, the liver shrinks progressively, and jaundice rapidly deepens. With the advancement and development of medicine, after 1978, the outbreak of hepatitis is no longer used as a clinical name in clinical practice, and the standard name in clinical cases has been defined as acute severe hepatitis or acute liver failure.

Explosive hepatitis symptoms

Often accompanied by bleeding symptoms such as bleeding gums, nosebleeds, subcutaneous bruising, vomiting, and blood in the stool. The patient was irritable, confused, lethargic or unconscious. Some patients developed bloating, ascites, edema, and oliguria or anuria. White blood cells are normal or slightly elevated, serum bilirubin is usually above 171 micromoles / liter (10 mg%), and liver function is severely damaged. Alanine aminotransferase (transaminase for short) rises initially, then decreases or even normal, with obvious enzyme bile separation; prothrombin activity gradually or rapidly drops below 30%, and some patients' blood ammonia increases, and blood ammonia is the decisive The direct factor of the degree of liver coma, blood sugar reduction, pathological changes are massive liver necrosis and bridging necrosis.
Most of the acute severe hepatitis is caused by chronic hepatitis. In clinical practice, chronic + acute severe hepatitis is often distinguished from acute severe hepatitis, or it is directly distinguished from chronic severe hepatitis, especially acute hepatitis caused by hepatitis B is the most common, because For acute severe hepatitis caused by hepatitis, antiviral treatment must be performed at the initial stage, which can greatly control the development of the disease and restrict the deterioration of the disease caused by the replication of the hepatitis virus. Interferon is generally not recommended. If necessary, interferon should be used. A small dose of interferon should be used, and the dose should be gradually increased according to the tolerance of the patient.

Evidence for the diagnosis of fulminant hepatitis

The main reasons doctors diagnose the disease are:
(1) The course of disease is within 10 days.
(2) Sudden onset with severe symptoms of poisoning.
(3) Progressive liver shrinkage, accompanied by deepening of liver odor and progressive jaundice.
(4) Bleeding tendency with prolonged prothrombin time and sharp decrease in activity.
(5) Ascites signs appear in a short time.
(6) Sudden mental disorder and coma after mania.
(7) The liver function test and transaminase were abnormal.
(8) Little or no urine.
The diagnosis should be distinguished from diseases such as toxic liver necrosis, fatty liver during pregnancy and severe bile duct infection.

Outbreak Hepatitis Treatment

(1) Albumin and fresh plasma. Supplementing albumin is beneficial for preventing and treating ascites and hepatic encephalopathy and maintaining blood volume. There are a large number of coagulation factors, blood platelets and immunoactive substances in fresh plasma, which is conducive to the prevention of bleeding and the promotion of liver cell regeneration. The daily input of 100-200ml is the most important measure in supportive therapy.
(2) Branched chain amino acids. It helps to increase the branched chain amino acid and correct the branch / aromatic ratio, and has certain effects on improving liver function and preventing and treating hepatic encephalopathy.
(3) Hepatocyte growth factor (HGF). For heavy liver treatment, it can increase the survival rate. It is reported that the mortality rate after comprehensive treatment is 44% -47%. On the basis of adding HGF, the mortality rate is reduced to 37.5%.
Usage: intravenous drip 1-2 times a day. If necessary, hepatotrophin is 160 mg each time, or Gan Le Ning 80 mg, which has a similar effect to hepatotrophin, is added to a 5% glucose injection 150 ml intravenously, once a day.
(4) Prostaglandin E1 (PGE1). The heavy liver collaboration group reported that the addition of PGE1 on the basis of comprehensive treatment has a fatality rate of 33.3%, similar to HGF. PGE1 is now believed to have the following effects: The PGE1 receptor on the liver cell membrane can bind to PGE1, and PGE1 can be reduced by The concentration of cAMF in liver cells reduces liver glycogen breakdown and hepatocyte catabolism. PGE1 has a strong vasodilator effect, improves blood circulation, promotes liver cell regeneration and protects liver cells. It can prevent the disorder of protein and fat metabolism in liver cells and promote protein synthesis. protect the capillary bile duct and benefit the bile effect. Improve microcirculation, inhibit platelet aggregation and prevent DIC and bleeding. It has antagonistic effects on renin, angiotensin aldosterone system, and diuretic and diuretic. It can fight against the excessive secretion of gastric acid and the formation of peptic ulcer caused by glucocorticoids.
Usage: PGEl 100-200ug is slowly added to the glucose solution. May have side effects such as high fever.
Calf blood deproteinization has similar efficacy and no side effects, and can be used instead of prostaglandin E1 as appropriate.
(5) Immune regulation. Thymosin is 10-20 mg daily, and large doses can be used up to 100 mg, which is conducive to correcting the immune dysfunction of patients with heavy liver, reducing complications and improving survival rate.
The above-mentioned blood products, PGE1 therapy, branched-chain amino acid and thymosin therapy are the main contents of basic comprehensive treatment for patients with heavy liver, and can also be used in conjunction with the liver to be healthy.
(6) Antiviral therapy. When antiviral treatment is considered when the condition is stable and the situation permits, matrine injection or lamivudine can be used, and interferon is generally not used. Because severe hepatitis is a large amount of HBv clearance response in some sense, many patients turn HBv-DNA to negative when severe liver disease, and no antiviral treatment is needed.

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