Causes of development
The syndrome can have an acute onset or be the consequence of a prolonged chronic disease.
Acute liver injury is caused by:
- Acute viral hepatitis.
- Toxic effects of medications.
- Industrial poisons (lead, phosphorus, arsenic, carbon tetrachloride).
- Poisoning by poisonous mushrooms.
Chronic failure most often becomes the endpoint of liver cirrhosis.
Even with a stable course of cirrhosis, there are triggers that can sharply worsen the condition and provoke a coma:
- Toxins and nutrition: alcohol consumption, excess dietary protein (increases ammonia load), intake of certain drugs (barbiturates, opiates, thiazide diuretics).
- Hemodynamic shifts: gastrointestinal bleeding (blood breaks down in the intestine, releasing protein and toxins), shock, collapse.
- Metabolic disruptions: potassium deficiency due to vomiting, diarrhea, or active diuresis.
- Infections.
Pathogenesis and portosystemic shunting
Normally, blood from the intestine, rich in toxins (protein breakdown products), passes through the portal vein into the liver, where hepatocytes cleanse it.
In liver failure, this mechanism breaks down. An important role is played by portosystemic shunting — the formation of bypass pathways. Blood from the portal vein is shunted into the general circulation, bypassing the liver. As a result, toxins from the intestine enter the systemic circulation directly.
The main "culprit" of intoxication is ammonia. Accumulating along with other nitrogenous compounds, it disrupts the amino acid balance. This leads to edema and dysfunction of brain astroglia, triggering neurological disorders.
Furthermore, due to hepatocyte death, synthetic functions decline:
- Production of blood clotting factors decreases, leading to hemorrhagic syndrome.
- Albumin levels drop (oncotic pressure decreases), leading to edematous-ascitic syndrome.
Clinical presentation
The classic tetrad of the syndrome includes:
- Hepatic encephalopathy (HE).
- Hemorrhagic syndrome.
- Progressive edematous-ascitic syndrome.
- Progressive jaundice.
The central link is hepatic encephalopathy, a potentially reversible disorder of mental and neurological functions. It progresses through four stages:
- Stage I (Prodromal): unstable mood (ranging from euphoria to depression), behavioral oddities. Sleep inversion is characteristic — the person sleeps during the day and suffers from insomnia at night.
- Stage II: inappropriate behavior and persistent lethargy. A specific neurological symptom appears — asterixis ("flapping" hand tremor).
- Stage III (Precoma): consciousness is depressed to stupor, speech is slurred (dysarthria), asterixis intensifies, and pathological reflexes appear. Respiration rhythm changes (Kussmaul or Cheyne-Stokes breathing). A sweetish fetor hepaticus (hepatic fetor) emanates from the mouth. Physical examination reveals the "shrinking liver" phenomenon — its size rapidly decreases. Jaundice intensifies (without itching), hemorrhages occur, and fever is possible.
- Stage IV (Coma): consciousness is completely absent, reflexes fade (areflexia).
Laboratory diagnostics and treatment
Blood tests in hepatocellular failure reveal:
- Decreased levels of albumin, prothrombin, and cholesterol (reflecting a decline in synthetic function).
- Elevated bilirubin levels.
Treatment of precoma aims to reduce intoxication by ammonia entering from the intestine:
- Diet: strict protein restriction (down to 20 g per day) during the acute period. As improvement occurs, the protein quota is gradually increased.
- Intestinal decontamination: laxatives (lactulose) and antibiotics (metronidazole, neomycin) are prescribed. This is necessary to suppress intestinal flora, reduce protein putrefaction, and block the absorption of toxins into the blood.
Briefly: answers to topical questions
How does the activity of liver enzymes (ALT, AST) change in hepatocellular failure?
In the cited sources, a specific change in ALT and AST specifically as a laboratory profile of hepatocellular failure is not listed: for it, hypoalbuminemia, hyperbilirubinemia, and a decrease in prothrombin and cholesterol are named.
Elevated ALT and AST are described as a sign of cytolytic syndrome: it reflects hepatocyte necrosis and the release of enzymes into the blood. The level of transaminases is directly proportional to the activity of the inflammatory process.
- ALT is localized in the cytoplasm of hepatocytes and has high specificity for liver tissue; in most liver pathologies, the increase in ALT exceeds the increase in AST.
- AST is localized in the mitochondria and has low specificity; a significant increase indicates deep damage — cell necrosis.
In alcoholic etiology, AST activity increases more than ALT. Maximum transaminase values are described in acute viral and drug-induced hepatitis — a 50–100-fold increase.
What scales and criteria are used to assess the severity of liver failure and cirrhosis in clinical practice?
To assess the functional state of the liver and the severity of liver cirrhosis, the sources indicate the following scales and indices:
- Child-Pugh scale (Child — Turcotte — Pugh) — a scale for assessing the functional state of the liver; used to objectify the severity of the condition in patients with liver cirrhosis and to determine treatment tactics.
- MELD (Model for End-stage Liver Disease) — a scale developed to determine the priority for liver transplantation; also used to assess the severity of liver cirrhosis. The higher the index value, the more severe the liver disease.
- MELD-Na — a modification of MELD, a more accurate method for assessing severity and liver transplantation priority; additionally takes into account serum sodium levels.
- ALBI score — a grade of liver function impairment specified in the source on hepatocellular carcinoma.
What is the mechanism of development of hemorrhagic syndrome in hepatocyte damage?
Hemorrhagic syndrome in liver dysfunction is associated with two main mechanisms:
- Impaired synthesis of blood clotting factors by the liver, primarily prothrombin. In liver failure, the synthesis of plasma coagulation factors decreases; standard tests predominantly reveal signs of hypocoagulation — an elevated INR and a decreased prothrombin index.
- Thrombocytopenia, often secondary to hypersplenism.
Clinically, this manifests as fine petechiae, ecchymoses, and bleeding from the oral mucosa and nose.
The PEJO syndrome tetrad: P — hepatic encephalopathy, E — edematous-ascitic syndrome, J — jaundice, O — oozing/bleeding (hemorrhagic syndrome).
Class and exam questions
What is asterixis?
This is a specific "flapping" tremor of the fingers of outstretched hands, which appears in stage II of hepatic encephalopathy and indicates profound damage to the nervous system by toxins.
Why are laxatives prescribed in liver failure?
Laxatives (e.g., lactulose) accelerate bowel evacuation, preventing toxins (primarily ammonia) from being absorbed into the systemic bloodstream.
What else to study on this topic
- Mechanism of ammonia's toxic effect on astroglia
- Differential diagnosis of types of coma
- Assessment of liver cirrhosis severity (Child-Pugh score)
- Types of portosystemic shunts
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