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Liver coma
Last reviewed: 07.07.2025
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Hepatic coma is the most severe condition diagnosed in hepatic encephalopathy (HE). HE is understood to mean the entire spectrum of neuropsychiatric disorders developing in hepatocellular insufficiency or portosystemic shunting of blood.
How does hepatic coma develop?
In the pathogenesis of encephalopathy and hepatic coma, two main mechanisms are distinguished: the effect of endogenous neurotoxins and amino acid imbalance, leading to the development of edema and functional disorders of astroglia. Among neurotoxins, ammonia is of great importance, formed when the synthesis of urea and glutamine in the liver decreases, as well as during portosystemic shunting of blood. Non-ionized ammonia penetrates 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 blood content of aromatic amino acids (phenylalanine, tyrosine) and a decrease in the level of amino acids with a branched side chain (valine, leucine, isoleucine). The penetration of aromatic amino acids into the brain causes the formation of false transmitters structurally similar to norepinephrine and dopamine (beta-phenylethanolamine and octopamine).
Symptoms of hepatic coma
Clinical signs of hepatic coma are lack of consciousness and reactions to sound signals, pain stimuli, as well as lack of pupillary response to light.
Treatment of hepatic coma
Non-drug treatment
Patients with liver failure are recommended to follow a diet with protein restriction to 0.6 g/kg per day to reduce ammonia formation and ensure sufficient energy value [130-150 kcal/(kg x day)]. Compliance with medical recommendations leads to a decrease in the intensity of catabolic processes and, consequently, to a decrease in the severity of hyperammonemia.
In the absence of contraindications to enteral nutrition (absence of gastrointestinal bleeding and grade IV esophageal varices), tube administration of mixtures is used (Hepatic Aid, Stresstein, Travasorb Hepatic and some others).
Parenteral nutrition should include solutions containing branched-chain amino acids (eg, aminosteryl-H-hepa, aminoplasmal-hepa, hepasol A).
Drug treatment of hepatic coma
The basis of treatment for hepatic coma is the implementation of a general set of therapeutic measures aimed at maintaining vital functions of the body, and taking medications that reduce the formation of ammonia, improve its neutralization and binding.
Lactulose is the most well-known and widely used drug that helps reduce the formation of ammonia in the colon (for instructions, see treatment of hepatic encephalopathy). If it is impossible to administer the drug orally, lactulose enemas are prescribed 1-2 times a day (the doses for enemas and oral administration are the same). One part of lactulose syrup is added to three parts of water.
Broad-spectrum antibacterial drugs in standard therapeutic doses are prescribed to reduce the formation of toxins, including ammonia, in the colon.
Ornithine aspartate (OA) (hepa-merz) and ornithine-a-ketoglutarate (ornithine-a-KG) enhance the detoxification of ammonia in the liver. Hepa-merz is prescribed at a dose of 2-6 g/day intramuscularly or 2-10 g/day intravenously by jet stream, or 10-50 g/day intravenously by drip (the drug is pre-diluted in 500 ml of infusion solution, the maximum infusion rate is 5 g/h).
Sodium benzoate binds ammonia in the blood to form hippuric acid and activates the exchange of glutamate for benzoate in perivenous hepatocytes. It is prescribed orally at a dose of 250 mg/kg per day, for adults 2-5 g/day in 3-6 doses. Sodium phenylacetate, which also has the ability to bind ammonia, is often additionally used at a dose of 250 mg/kg per day in 3-6 doses, the maximum dose of the drug is 100 ml.
Flumazenil reduces inhibitory processes in the central nervous system. In hepatic coma, the drug is administered intravenously by jet stream at a dose of 0.2-0.3 mg, then by drip at 5 mg/hour, followed by a transition to oral administration at a dose of 50 mg/day.
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