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Severe acute and chronic liver diseases due to severe dystrophy and death of hepatocytes, despite the significant compensatory capabilities of this organ, are accompanied by profound impairments of its many functions that are extremely important for the body, which clinicians designate as liver failure syndrome. Depending on the nature and severity of the disease affecting the liver, acute and chronic liver failure are distinguished and its three stages: 1) initial, compensated, 2) severe, decompensated, and 3) terminal, dystrophic, which ends with a hepatic coma and the death of the patient. insufficiency occurs in severe forms of viral hepatitis (Botkin’s disease), hepatotropic poisoning (i.e., having a toxic effect primarily on the liver) poisons: industrial, plant, some with other medicines, etc. (compounds of phosphorus, arsenic, large doses of alcohol, pale grebe, stitches, fly agaric and other inedible mushrooms containing poisonous substances - amanitotoxin, gelvelic acid, maskarin, etc., extract of male fern, etc.). Acute liver failure develops rapidly - within a few hours or days. Chronic liver failure occurs in many chronic liver diseases (cirrhosis, tumor lesions, etc.) and is characterized by a slow, gradual development. The development of hepatic insufficiency is based on pronounced dystrophy and necrobiosis of hepatocytes, accompanied by a significant decrease in all liver functions and the formation of abundant collaterals between the portal and vena cava systems, which arise when it is difficult to receive blood from the portal vein into the liver for any liver lesions. Through them, a large amount of blood containing toxic substances absorbed in the intestine enters the large circle of blood circulation bypassing the liver. Manifestations of liver failure are explained by complex disorders of various metabolic processes in which the liver is involved, a disorder of bile formation and bile secretion, and a violation of the antitoxic function of the liver.

The pathogenesis of hepatic coma is reduced to severe self-poisoning of the body due to the almost complete cessation of liver activity. Poisoning is caused by uninjured intestinal (bacterial) protein breakdown products, end products of metabolism, and especially ammonia. Normally, most of the ammonia is captured by hepatocytes and, when incorporated into the ornithine cycle, is converted to urea, then excreted by the kidneys. Phenols also have a toxic effect, which are normally inactivated in the liver by combining them with glucuronic and sulfuric acids. With liver failure, other toxic substances accumulate in the blood, electrolyte metabolism is disturbed, in severe cases, hypokalemia, alkalosis occur. To aggravate the severity of liver failure and provoke the occurrence of hepatic coma, alcohol, barbiturates, narcotic analgesics (morphine, promedol, etc.), excessive use of protein by patients with liver lesions, which leads to increased rotting processes in the intestine, and increased formation of absorption of toxic products into the bloodstream, massive bleeding from the digestive tract, often complicating portal cirrhosis of the liver, the appointment of large doses of diuretic agents, simultaneous removal of a significant amount of ascitic fluid, severe diarrhea, joining severe infectious diseases.

Clinical manifestations of liver failure are usually combined with symptoms of underlying liver disease. The stagedness of the increase in symptoms is most clearly observed with the progression of chronic liver failure (in patients with cirrhosis of the liver, its tumor lesions and other diseases).

At the earliest stage, there are no clinical symptoms of liver failure, however, there is a decrease in the body's tolerance to alcohol and other toxic effects, and the indicators of laboratory “stress” liver tests have been changed. Then, already in the second stage, there are clinical manifestations of liver failure: first, mild and then more pronounced “unmotivated” weakness, increased fatigue during the performance of usual physical work, poor appetite, often dyspeptic symptoms (poor tolerance of fatty foods, flatulence, rumbling and pain in the abdomen, impaired stool), which are explained by a violation of bile secretion and digestion in the intestine. Violation of the assimilation of vitamins explains the signs of polyhypovitaminosis. Often observed in liver failure, fever can be due to both the underlying disease and the violation of the inactivation of some pyrogenic substances by the liver by the liver. Common signs of liver failure are jaundice and hyperbilirubinemia with the accumulation of free (indirect) bilirubin in the blood.
At the same time, due to disorganization of the liver structure and cholestasis, bilirubinglucuronide (direct bilirubin) can accumulate in the blood of patients. Due to impaired synthesis of albumin in the liver and severe hypoalbuminemia, hypoproteinemic edema may appear and ascites often existing in patients with chronic liver lesions may progress. Violation of the synthesis of certain factors of the blood coagulation system by the liver (fibrinogen, prothrombin, proconvertin, etc.), as well as a decrease in the blood platelet count (due to hypersplenism associated with many chronic liver lesions) lead to hemorrhagic diathesis - the appearance of skin hemorrhage, nosebleeds, digestive tract, etc. Lack of inactivation of estrogen hormones in the liver affected by chronic diseases leads to the appearance of endocrine changes (gynecomastia in men m, violation of the menstrual cycle in women, etc.). In the second stage of liver failure, laboratory “liver tests” already produce significant changes. A characteristic decrease in the content of substances produced by the liver: albumin, cholesterol, fibrinogen, etc. Significant impairment of liver function is also detected by radioisotope hepatography. The third, final, stage of liver failure is characterized by even deeper metabolic disorders in the body, dystrophic changes expressed not only in the liver, but also in other organs; in patients with chronic liver diseases, depletion develops. Neuropsychiatric disturbances appear, precursors of coma: decreased intelligence, slowed thinking, some euphoria, sometimes depression and apathy. Often there is an instability of mood - irritability, followed by bouts of melancholy and doom, sleep disturbance. In the future, disorders of consciousness increase with a loss of orientation with respect to time and place, memory failures, speech disturbances, hallucinations, drowsiness occur. A characteristic minor tremor is noted along with a large trembling of the muscles of the upper and lower extremities. The precoma period can last from several hours to several days and even weeks, after which patients can sometimes completely get out of this condition, but more often coma occurs. The clinical picture of the hepatic coma is characterized at first by excitement, and then general depression (stupor) and progressive impaired consciousness ( stupor) until it is completely lost (coma). The curve of the electroencephalogram is flattened. Reflexes are reduced, however, hyperreflection and the appearance of pathological reflexes (grasping, sucking, etc.) are sometimes noted. Characterized by motor anxiety, clonic convulsions due to hypokalemia, muscle twitching, tremor of the extremities (rhythmic and irregular twitching of the fingers and toes). The rhythm of breathing is disturbed: the breathing of Kussmaul develops (less often Cheyne - Stokes). There is an incontinence of urine and feces. From the patient’s mouth, as well as from urine and sweat, a sweetish hepatic smell (“hepatic stench”) is felt, associated with the release of methyl mercaptan, resulting from impaired methionine metabolism; often when examined, signs of hemorrhagic diathesis (nosebleeds, gums, skin hemorrhages) attract attention. The patient's body temperature in the terminal period is below normal. The liver may remain enlarged or diminished. Jaundice intensifies. Laboratory studies show moderate anemia, leukocytosis, increased ESR, low platelet count, fibrinogen, prolonged thrombin time, a sharp violation of liver function tests, increased bilirubin levels; the content of residual nitrogen and ammonia in the blood serum increases, which indicates secondary damage to the kidneys (hepatic-renal syndrome). Hyponatremia, hypokalemia, metabolic acidosis develop. As a rule, a hepatic coma ends in death. However, in some cases, recovery is possible.

Treatment for acute renal failure aims at intensive therapeutic measures (infusion of plasma, polyglucin, a solution of glutamic acid that binds ammonia, oxygen therapy, correction of water-salt disorders, etc.) to support the patient's life for a critical period (several days), counting on a significant regenerative ability of the liver. In chronic liver lesions, in addition to treating the underlying disease, complicating factors (esophageal-gastric bleeding, concomitant infectious disease) are also being eliminated, a low protein diet is prescribed, antibiotics are used to suppress putrefactive processes in the intestines and reduce absorption of protein breakdown products. Correction of electrolyte disorders, the fight against hemorrhagic phenomena. Healthy liver transplant methods are being developed for patients with liver failure.
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    Acute liver failure is a syndrome manifested by a sharp deterioration in the state of the body due to impaired liver function. Hepatic encephalopathy is a condition that includes a spectrum of neuropsychiatric disorders that develop with liver failure and / or cirrhosis. Pathophysiology Acute liver failure develops in two cases: in patients with acute
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