Hepatic coma
Last reviewed: 23.04.2024
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The hepatic coma is the most severe condition diagnosed in hepatic encephalopathy (PE). PE is understood as the whole spectrum of neuropsychic disorders developing in hepatic-cell insufficiency or portosystemic shunting of blood.
How does the hepatic coma develop?
In the pathogenesis of encephalopathy and hepatic coma, two main mechanisms have been identified, the effect of endogenous neurotoxins and the amino acid imbalance, leading to the development of edema and functional disorders of astroglia. Among the neurotoxins, ammonia, formed with a decrease in the synthesis of urea and glutamine in the liver, as well as in portosystemic shunting of blood, is of great importance. Non-ionized ammonia penetrates through the BBB into the brain, inhibiting the synthesis of ATP, and stimulates the transport of aromatic amino acids. These changes lead to an increase in the affinity of postsynaptic 5-HT1-serotonin receptors.
Amino acid imbalance is characterized by an increase in the content of aromatic amino acids (phenylalanine, tyrosine) in the blood and a decrease in the level of amino acids with a branched side chain (valine, leucine, isoleucine). Penetration of aromatic amino acids in the brain causes the formation of false transmitters structurally similar to noradrenaline and dopamine (beta-phenylethanolamine and octopamine).
Symptoms of the hepatic coma
Clinical signs of a hepatic coma are the absence of consciousness and reactions to sound signals, pain stimuli, and the absence of pupillary reaction to light.
Treatment of the hepatic coma
Non-drug treatment
Patients suffering from liver failure to reduce ammonia formation and provide sufficient energy value [130-150 kcal / (kghsut)] are recommended to follow a diet with protein restriction to 0.6 g / kg per day. Implementation of medical recommendations leads to a decrease in the intensity of catabolism and, consequently, to a decrease in the severity of hyperammonemia.
In the absence of contraindications to enteral nutrition (absence of gastrointestinal bleeding and varicose veins of the esophagus IV degree), probe insertion of the mixtures (Hepatic Aid, Stresstein, Travasorb Hepatic and some others) is used.
Parenteral nutrition should include solutions containing branched amino acids (for example, aminostearyl-H-hepa, aminoplasmal-hepa, hepasol A).
Drug treatment for hepatic coma
The basis for the treatment of hepatic coma is the implementation of a common set of therapeutic measures aimed at maintaining vital body functions, and taking medications that reduce the formation of ammonia, improving its neutralization and binding.
Lactulose is the most well-known and widely used drug that helps to reduce the formation of ammonia in the large intestine (treatment regimen - see treatment of hepatic encephalopathy). If it is not possible to administer the drug inwardly, enemas with lactulose 1-2 times a day are prescribed (doses for enema and ingestion are the same). One part of the lactulose syrup is added to three parts of the water.
Antibacterials of a broad spectrum of action in standard therapeutic doses are prescribed to reduce the formation of toxins, including ammonia, in the large intestine.
Ornithine-aspartate (OA) (hepa-merz) and ornithine-a-ketoglutarate (ornithine-a-KG) enhance the clearance of ammonia in the liver Hepa-Mertz is given at a dose of 2-6 g / day intramuscularly or 2-10 g / day intravenously struyno, or 10-50 g / day intravenously drip (the drug is previously diluted in 500 ml infusion solution, the maximum infusion rate is 5 g / h).
Sodium benzoate binds ammonia in the blood to form hippuric acid, and also activates the exchange of glutamate for benzoate in perivennous hepatocytes. Assign inside the dose of 250 mg / kg per day, adults 2-5 g / day in 3-6 receptions. Often additionally used sodium phenylacetate, which also has the ability to bind ammonia, at a dose of 250 mg / kg per day in 3-6 receptions, the maximum dose of the drug is 100 ml.
Flumazenil provides a reduction in inhibitory processes in the central nervous system. With a hepatic coma, the drug is administered intravenously with a jet at a dose of 0.2-0.3 mg, then drip at 5 mg / h followed by a 50 mg / day dose of ingestion.
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