Hepatic encephalopathy: causes

Acute diseases and liver damage.

1. Acute viral hepatitis A, B, C, D, E, G.
2. Acute viral hepatitis caused by herpes viruses, infectious mononucleosis, Coxsackie, measles, cytomegalovirus.
3. Jaundice leptospirosis (Vasiliev-Weil disease).
4. Lesion of the liver with rickettsiosis, mycoplasmal, fungal infections (in severe course with generalized lesion of all organs).
5. Septicemia with liver abscess and purulent cholangitis.
6. Rey's syndrome is a liver damage with the development of hepatic insufficiency in children aged 6 weeks to 16 years 3-7 days after a virus infection of the upper respiratory tract.
7. Alcohol intoxication.
8. Medical hepatitis.
9. Liver involvement with industrial and industrial toxins, mixed toxins, aflatoxins.
10. Acute violations of the hepatic circulation (acute thrombosis of the hepatic vein).
11. Acute fatty liver of pregnant women (Shikhen's syndrome).
12. Heart failure.
13. Poisoning by poisonous mushrooms.

Chronic liver diseases.

1. Chronic hepatitis (with a high degree of activity).
2. Cirrhosis of the liver (late stages of the disease).
3. Hereditary disorders of bile acid metabolism (progressive intrahepatic cholestasis - Biehler's disease, hereditary lymphedema with recurrent cholestasis, cerebrohepatorenal syndrome, Tseveveger's syndrome).
4. Hemochromatosis.
5. Hepatolenticular degeneration (Wilson-Konovalov's disease).

Malignant tumors of the liver.

Factors that provoke the development of hepatic encephalopathy include:

• the use of alcohol and drugs that have hepatotoxic and cerebro-toxic effects (hypnotics, sedatives, tuberculostatic, cytostatic, analgesic, etc.);
• anesthesia;
• surgical operations;
• the formation of portocaval anastomosis - in this case ammonia and other cerebro-toxic substances come from the intestine directly into the bloodstream, bypassing the liver;
• exo- and endogenous infection - this leads to an increase in catabolic reactions, which leads to the accumulation of endogenous nitrogen, to the enhanced synthesis of ammonia; In addition, hyperthermia and hypoxia, which are manifestations of infection, contribute to intoxication;
• gastrointestinal bleeding - spilled blood is a substrate for the formation of ammonia and other cerebro-toxins; In addition, hypovolemia, shock, hypoxia worsen the nitrogen excretory function of the kidneys and, thus, contribute to an increase in the blood ammonia content;
• the intake of excess protein from food, which is a substrate for the synthesis of ammonia and other cerebrotoxins;
• paracentesis with the evacuation of a large amount of ascitic fluid - the loss of electrolytes and proteins provokes and aggravates hepatic encephalopathy;
• excessive use of diuretics, copious diuresis accompanied by a decrease in blood circulation of vital organs, hypovolemia, hypokalemia, alkalosis, prerenal azotemia; spontaneous azotemia occurs in connection with an increase in enterohepatic circulation of urea;
• kidney failure;
• metabolic alkalosis, which increases the active diffusion of non-ionized ammonia through the blood-brain barrier;
• constipation - the synthesis and absorption of ammonia and other cerebro-toxins in the intestine are increased due to the development of dysbacteriosis and digestive disorders;
• development in patients with cirrhosis of the liver portal vein thrombosis, accession of peritonitis, a significant activation of the pathological process in the liver.

Other factors contributing to the development of encephalopathy

Patients with hepatic encephalopathy are extremely susceptible to sedatives, so whenever possible, avoid their use. If a patient assumes an overdose of such drugs, then it is necessary to introduce an appropriate antagonist. If the patient can not be kept in bed and it is necessary to calm him, prescribe small doses of temazepam or oxazepam. Morphine and paraldehyde are absolutely contraindicated. Chlordiazepoxide and hemineurin are recommended for patients suffering from alcoholism with an impending hepatic coma. Patients with encephalopathy are contraindicated with drugs that are known to cause hepatic coma (eg, amino acids and diuretics for oral administration).

The lack of potassium can be filled with fruit juices, as well as effervescent or slowly soluble potassium chloride. In case of emergency therapy, potassium chloride can be added to solutions for intravenous administration.

Levodof and bromocriptine

If portosystemic encephalopathy is associated with impairment in dopaminergic structures, replenishment of dopamine stores in the brain should improve the condition of the patients. Dopamine does not pass through the blood-brain barrier, but this can be done by its predecessor - levodopa. In acute hepatic encephalopathy, this drug may have a temporary activating effect, but it is effective only in a small number of patients.

Bromocriptine is a specific dopamine receptor agonist with a prolonged action. Assigned in addition to a low protein diet and lactulose, it leads to an improvement in the clinical state, as well as psychometric and electroencephalographic data in patients with chronic port-systemic encephalopathy. Bromocriptine can be a valuable drug for individual patients with poorly treatable chronic portal encephalopathy, resistant to protein restriction in diet and lactulose, developed against a backdrop of sustained liver function compensation.

Flumazenil

This drug is a benzodiazepine receptor antagonist and causes a temporary, unstable but distinct improvement in the condition in approximately 70% of patients with hepatic encephalopathy associated with FPN or liver cirrhosis. Randomized studies have confirmed this effect and have shown that flumazenil may interfere with the action of ligands, benzodiazepine receptor agonists that are formed in situ in the brain in liver failure. The role of this group of drugs in clinical practice is currently being studied.

Amino acids with a branched chain

The development of hepatic encephalopathy is accompanied by a change in the ratio between the branched chain amino acids and aromatic amino acids. For the treatment of acute and chronic hepatic encephalopathy, infusions of solutions containing a high concentration of amino acids with a branched chain are used. The results obtained are extremely contradictory. This is probably due to the use in such studies of various types of amino acid solutions, different routes of administration and differences in patient groups. The analysis of controlled studies does not allow to unequivocally speak about the effectiveness of intravenous introduction of amino acids with a branched chain in hepatic encephalopathy.

Given the high cost of amino acid solutions for intravenous administration, it is difficult to justify their use in hepatic encephalopathy in cases where the level of amino acids with a branched chain in the blood is high.

Despite some studies showing that branched-chain amino acids that are administered internally are successfully used in hepatic encephalopathy, the effectiveness of this costly method remains controversial.

Occlusion of shunts

Surgical removal of the porto-cheval shunt can lead to regression of severe portosystemic encephalopathy, which developed after its application. In order to avoid repeated bleeding, before performing this operation, you can resort to crossing the mucosa of the esophagus. On the other hand, the shunt can be blocked by means of X-ray surgical methods with the introduction of a balloon or a steel spiral. These methods can also be used to close spontaneous splenorenal shunts.

Application of artificial liver

In patients with cirrhosis of the liver, who are in a coma, do not resort to complex methods of treatment with the use of artificial liver. These patients are either in a terminal state, or come out of a coma without these methods. Treatment with artificial liver is discussed in the section on acute hepatic insufficiency.

Liver transplantation

This method can be the final solution to the problem of hepatic encephalopathy. One patient suffering from encephalopathy for 3 years, during 9 months after transplantation, there was a noticeable improvement. In another patient with chronic hepatocerebral degeneration and spastic paraplegia, the condition improved significantly after orthotopic liver transplantation.

Factors contributing to the development of acute hepatic encephalopathy in patients with cirrhosis of the liver

Violations of electrolyte balance

• Diuretics
• Vomiting
• Diarrhea

Bleeding

• Varicose veins of the esophagus and stomach
• Gastroduodenal ulcers
• Tears in the Mallory-Weiss syndrome

Preparations

• Discontinuation of alcohol intake

Infections

• Spontaneous bacterial peritonitis
• Urinary tract infections
• Bronchopulmonary infection

Constipation

Protein-rich food

Gastrointestinal bleeding, mainly from the dilated esophagus, is another common factor. The development of a coma is promoted by protein-rich food (or blood with gastrointestinal bleeding) and oppression of liver function caused by anemia and decreased hepatic blood flow.

Patients with acute encephalopathy badly suffer surgical operations. Exacerbation of violations of the liver is due to blood loss, anesthesia, shock.

Acute alcoholic excesses contribute to the development of coma due to the suppression of brain function and due to the addition of acute alcoholic hepatitis. Opiates, benzodiazepines and barbiturates suppress brain activity, the duration of their action is prolonged due to the slowing down of the processes of detoxification in the liver.

The development of hepatic encephalopathy can be facilitated by infectious diseases, especially when they are complicated by bacteremia and spontaneous bacterial peritonitis.

A coma may occur due to the consumption of protein-rich foods or prolonged constipation.

Transgular intrahepatic portosystemic shunting with the help of stents (TSSH) promotes the development or enhances hepatic encephalopathy in 20-30% of patients. These data vary depending on patient groups and selection principles. As for the influence of the shunts themselves, the probability of encephalopathy is greater, the larger their diameter.

[1], [2]