Hepatic Insufficiency Syndrome

Hepatic insufficiency syndrome is a symptom complex characterized by a violation of one or many liver functions due to acute or chronic damage to its parenchyma. There are acute and chronic hepatic insufficiency and its 3 stages: stage I-initial (compensated), stage II-expressed (decompensated) and stage III-terminal (dystrophic). The terminal stage of hepatic failure ends with a hepatic coma.

Etiology, pathogenesis. Acute liver failure may occur in severe forms of viral hepatitis, industrial poisoning (compounds of arsenic, phosphorus, etc.), plant (inedible fungi) and other hepatotropic poisons, certain medicines (male fern extract, tetracycline, etc.), transfusion of other blood and In a number of other cases. Chronic liver failure occurs with the progression of many chronic liver diseases (cirrhosis, malignant tumors, etc.).

Hepatic insufficiency is due to the dystrophy and widespread necrobiosis of hepatocytes and (in chronic forms) the massive development of portocaval anastomoses, through which a significant part of the blood from the portal vein enters the hollow and then into the arterial bed, bypassing the liver (which further reduces its participation in detoxification of harmful substances , Absorbed in the intestine). The most antitoxic function of the liver suffers, and its participation in various types of metabolism (protein, fat, carbohydrate, electrolyte, vitamin, etc.) also decreases.

Symptoms, the course depends on the nature of the liver damage, the severity of the course of the process. In Stage 1, clinical symptoms are absent, but tolerance of the organism to alcohol and other toxic effects is reduced, positive results of loading hepatic tests (with galactose, sodium benzoate, bilirubin, especially vofavordin) are positive. Stage II is characterized by clinical symptoms: unmotivated weakness, decreased ability to work, dyspeptic disorders, the appearance and progression of jaundice, hemorrhagic diathesis, ascites, and sometimes hypoproteinemic edema. Laboratory tests show significant deviations from the norm of many or all of the hepatic samples; The content in blood of albumin, prothrombin, fibrinogen, cholesterol is lowered. Usually the blood levels of aminotransferases are increased, especially alanine aminotransferase, anemia, an increase in ESR is often observed. The degree of impaired liver function can also be determined by the method of radioisotope hepatology. In the III stage, there are profound metabolic disorders in the body, dystrophic phenomena not only in the liver, but also in other organs (CNS, kidneys, etc.); With chronic liver disease expressed cachexia. There are signs of an approaching hepatic coma.

Coma hepatic (hepatarga). In the development of the hepatic coma, the stages of precoma, threatening coma and to whom, are singled out. Distinguish also hepatic-cell (endogenous) coma arising from massive necrosis of the parenchyma, portocaval (bypass, shunt, exogenous), caused by the significant exclusion of the liver from metabolic processes due to the presence of pronounced portocaval anastomoses, and mixed coma, which occurs mainly in cirrhosis of the liver.

In the pre-coma period, progressive anorexia, nausea, diminished liver size, jaundice, hyperbilirubinemia, an increase in bile acid in the blood are usually noted.

In the future, growing neuropsychic disorders, slowing thinking, depression, and sometimes some euphoria. The mood is unstable, irritability; Memory is broken, sleep is upset. On the EEG, slow delta and tetra waves are recorded. The tendon reflexes increase, the small tremor of extremities is characteristic. Azotemia develops. Under the influence of active therapy, patients can get out of this condition, but more often with severe irreversible changes of the liver coma occurs.

In the period of coma, excitation is possible, which is then replaced by oppression (stupor) and progressive impairment of consciousness until it is completely lost. Meningeal phenomena develop, pathological reflexes, motor anxiety, convulsions. Distressed breathing (such as Kussma-ul, Cheyne-Stokes); Pulse-small, arrhythmic; Hypothermia of the body takes place. The face of the patient is drained, the limbs are cold, from the mouth, and also the characteristic sweetish liver odor emanates from the skin, hemorrhagic phenomena (skin hemorrhages, nosebleeds, gums, varicose-dilated esophagus veins, etc.) intensify. Increased ESR, the level of residual nitrogen and ammonia in the blood serum, hypokalemia occurs and often hyponatremia, metabolic acidosis. In the terminal phase, the EEG curve flattened.

Acute liver failure develops rapidly, for several hours or days, and with timely therapy can be reversible. Chronic liver failure develops gradually over a period of several weeks or months, but the addition of provoking factors (alcohol intake, esophageal-gastric bleeding from esophageal varices, intercurrent infection, physical overfatigue, the administration of large doses of diuretics or the simultaneous removal of a large amount of ascites fluid and Etc.) can quickly provoke the development of the hepatic coma. The prognosis, especially with chronic hepatic insufficiency, is unfavorable, but in some cases the hepatic coma (portocaval form) can regress and recur for a number of months.

Treatment. Patients with acute hepatic insufficiency (irrespective of its stage) are immediately hospitalized (with viral hepatitis, leptospirosis and other infectious diseases, into infectious hospitals, with toxic liver damage - into poisoning centers). With acute hepatic insufficiency and hepatic coma it is very important to support the life of the patient during a critical period (several days), by counting on the significant regenerative capacity of the liver. The main disease is treated, with toxic hepatoses - measures aimed at removing the toxic factor. Assign laxatives, enemas. For the purpose of binding ammonia accumulating in the body, 10-20 ml of 1% solution of glutamic acid (preferably in a 5% solution of glucose dropwise) is injected intravenously intravenously 2-3 times per day for several days (from the ammonia and glutacic acid there is no toxic effect of glutamine , The latter also increases the excretion of ammonia in the form of ammonium salts). Enter a large amount of glucose solution in / in (up to 3 liters of a 10% solution with predkomatoznyh states), cocarboxylase (50-150 mg / day), vitamins B6, B12, panangin (inside or intramuscularly), lipoic acid. Carry out oxygen therapy, hyperbaric oxygenation.

With the development of a hepatic coma, a solution of sodium hydrogencarbonate (in metabolic acidosis) or potassium chloride (0.4-0.5% solution in a 5% glucose solution in an amount up to 500 ml intravenously drip, carefully) is administered; Through the nasal catheter, they let you breathe moistened oxygen. With a decrease in venous and arterial pressure, polyglucin and albumin are injected intravenously. In case of massive bleeding, appropriate measures are taken to stop them, pour fresh single-group blood, inject drugs containing clotting factors. With expressed signs of disseminated intravascular coagulation, heparin is administered. To combat renal failure, peritoneal hemodialysis, plasmapheresis is performed. To eliminate psychomotor effects and seizures apply diprazine, haloperidol, sodium oxybutyrate. When the patient is withdrawn from the coma, an intensive therapy of the underlying disease is subsequently carried out.

In chronic liver failure, the main disease and symptomatic therapy are treated. Limit the supply of protein with food, lactic acid products are useful, prescribe laxatives and enemas in order to remove from the intestine products of protein decay; Courses prescribe antibiotics inside.

Intravenously injected solutions of glucose, glutamic acid, parenteral vitamins B1, B6, B12, liver hydrolyzates - sireppar (2-3 ml IV or IM once a day, up to 60 injections per course), vitohepat (in / M to 1-2 ml per day). In the presence of hemorrhagic phenomena, appoint Vikasol, with pronounced hypoproteinemia and hypoproteinemic edema, pour plasma, albumin. Strictly forbid the reception of alcoholic beverages, drugs, barbiturates. Patients with chronic liver diseases, complicated by liver failure, are disabled and need to be transferred to a disability.

Prevention of acute liver failure is reduced to the prevention of infectious and toxic liver damage. Prophylaxis of chronic liver failure is a timely treatment of liver diseases, which can serve as its cause. Great importance is the fight against alcoholism.