Beginning >> Diseases >> Digestion diseases >> Liver failure

Liver failure

The liver failure is an insufficiency of metabolic function of a liver with damage of a brain and clinical manifestations in the form of hepatic encephalopathy and a hepatic coma.

On a current allocate an acute and chronic liver failure. The acute liver failure develops in connection with massive necroses of a parenchyma of a liver of various etiology, is shown by a sudden heavy abnormal liver function. Most often the acute liver failure arises at an acute viral hepatitis, is more rare — medicinal, alcoholic and other toxic damages of a liver.

Liver necroses are the reasons of a chronic liver failure at chronic hepatitis and cirrhosis, extensive fibrosis of a liver, and also existence of an anastomosis between portal and hollow veins.

Pathogeny of a liver failure

The leading value in a pathogeny of a liver failure has disturbance of the neutralizing function of a liver and toxic damage of a brain products of an exchange of nitrogenous substances (ammonia, phenols, at - aminobutyric acid and other amino acids, mercaptan and fatty acids).

On a pathogeny distinguish the endogenous, exogenous and mixed forms of a liver failure.

The endogenous liver failure is caused by death more than 80% of a parenchyma of a liver (at an acute viral hepatitis, toxic damages of a liver), actually pechenochnokletochny insufficiency with disturbance of disintoxication function of a liver.

The exogenous liver failure is connected with intake of toxic substances from intestines in blood on a porto-caval anastomosis, passing a liver that is observed at cirrhosis and operations of shunting for portal hypertensia.

The mixed form of a liver failure arises at a combination of necroses of a parenchyma of a liver and a porto-caval anastomosis at cirrhosis.

The pathogeny of a liver failure cannot be reduced only to a giperammoniyemiya. The metabolic acidosis, electrolytic disturbances, in particular, a hypopotassemia promoting disturbance of a metabolism of ammonia in kidneys are important.

Provocative factors of development of a porto-caval liver failure are: increase of protein content in food, gastric bleeding (big intake of protein in intestines), use of sedatives and alcohol. At patients with an edematous and ascitic syndrome development of a coma is promoted by the heavy electrolytic disturbances caused by use of high doses of diuretics, a paracentesis, and also vomiting and a diarrhea.

Symptoms of a liver failure

In a clinical picture of a liver failure it is necessary to allocate syndromes of a pechenochnokletochnoa of insufficiency and hepatic encephalopathy.

Pechenochnokletochny insufficiency is characterized by increase of syndromes of jaundice, hemorrhagic, edematous and ascitic, dispepsichesky, abdominal pains, fever, reduction of the sizes of a liver, weight loss are possible. There is a hepatic smell from a mouth caused by release of methyl mercaptan in connection with disturbance of processes of demethylation in a liver.

Laboratory signs of pechenochnokletochny insufficiency are the progressing decrease in proteinaceous and synthetic function of a liver, increase of concentration of bilirubin, phenols and ammonia in blood serum. Decrease before a superactivity of aminotransferases in dynamics, reduction of cholesterol and cholinesterase is observed.

Hepatic encephalopathy is characterized by disturbance of mentality (emotional instability, feeling of alarm, apathy, are possible the delirious states which are followed by excitement, aggression; disturbance of orientation, a dream, etc.) and neuromuscular frustration (disturbances of the speech, the "clapping" tremor of fingers of hands, disturbance of the letter, increase of reflexes, an ataxy).

Hepatic coma

In development of a hepatic coma allocate two phases — preky and to whom.

Prekoma is characterized by sharp disturbance of consciousness, a stupor. The long dream, slackness which are replaced short-term awakening, sometimes excitement are observed; fibrillar twitchings of muscles and a spasm, the expressed tremor, rigidity of skeletal muscles, pathological reflexes, an involuntary urination.

At a coma the consciousness is absent, the person maskoobrazno, reaction to painful irritants disappears. Gradually reinforced reflexes begin to die away, reaction of pupils to light disappears, pupils extend. Arterial pressure decreases, breath at first becomes frequent, then breath like Kussmaul or Cheyna-Stokes appears. In this state patients, as a rule, perish.

Treatment of a liver failure

Depending on weight of a liver failure protein content in food is regulated: at hepatic encephalopathy the amount of protein is reduced to 35 — 50 g a day; at a prekoma and a coma of squirrels it is completely excluded, food is provided with introduction through a gastric tube or intravenously 5 — 20% of solution of glucose.

Drug treatment is directed to elimination of ammoniac intoxication and an azotemia.
For this purpose appoint the high cleansing enemas and drugs suppressing the putrefactive processes in intestines and also reducing ammonia absorption.

The greatest application was found by Neomycinum sulfate (2-6 g a day inside) suppressing intestinal microflora and lactulose (portalak) which reduces rn intestinal contents, slows down formation of ammonia bacteria in a large intestine, reduces absorption it and other toxic products. Lactulose is accepted on 30 — 40 g by each 4 h to easy aperient effect. At a coma lactulose is entered through a nazogastralny probe or rektalno.

In blood apply glutaminic acid to neutralization of already soaked up ammonia, ornitsetol which is given preference. Ornitsetol (and - an ornithine ketogluconate) connects ammonia, is appointed to 15-20 g/days intravenously in 5% glucose solution.

With the disintoxication purpose enter intravenously kapelno 5% glucose solution with vitamins and solutions of electrolytes. Per day about 2,5-3 l of liquid under diuresis control are entered.
Correction of a hypopotassemia is carried out. Glucocorticoids at hepatic encephalopathy against cirrhosis are contraindicated in connection with high risk of complications and side effects (increase of an azotemia, development of gastrointestinal ulcers with bleedings).

In specialized hospitals carry out a hemodialysis, perfusion of blood through a liver of the person, a pig, transplantation of a liver.

"Round ulcer of a gullet   Postcholecystectomy syndrome"