Portal hypertension

Clinical presentation and leading syndromes

In internal medicine, the development of portal hypertension is accompanied by prominent symptoms. A key manifestation is hepatosplenic syndrome—the simultaneous enlargement of the liver and spleen.

Pay attention to the patient's complaints of severe meteorism: abdominal distension is very frequently a harbinger of free fluid accumulation in the abdominal cavity.

The diagnosis is confirmed by the presence of the classic triad of signs:

• Accumulation of transudate in the abdominal cavity (ascites).
• Pathological enlargement of the spleen (splenomegaly).
• Varicose veins (primarily localized in the esophagus and rectum).

Terminal period and complications

Regardless of the etiological cause that led to the development of liver cirrhosis, the final stage of the disease is characterized by common, extremely severe features. The main causes of mortality in such patients are gastrointestinal bleeding and hepatic coma, which is a natural outcome of progressive functional insufficiency of the organ.

Pathogenesis and manifestations of bleeding:

1. Source: Most commonly, rupture of thinned varices located in the lower third of the esophagus or in the stomach occurs.
2. Symptoms: Massive bleeding clinically manifests as bloody vomiting (haematemesis) and tarry, black stools (melena).
3. Consequences: Even if the bleeding does not lead to immediate mortality, it triggers a vicious cycle. Severe posthemorrhagic anemia develops, which leads to hepatocyte hypoxia. Oxygen deficiency fatally exacerbates hepatocellular insufficiency.

Laboratory diagnostics

The laboratory picture strictly depends on the stage of the disease (compensation or decompensation). In compensated cirrhosis, parameters often remain within the normal range; only a slight increase in cytolysis markers (transaminases) or cholestasis (GGT) is permissible.

At the decompensation stage, clear laboratory syndromes form:

• Hypersplenism syndrome: manifests as pancytopenia (anemia, leukopenia, thrombocytopenia) due to the destruction of blood cells in the enlarged spleen.
• Cholestasis syndrome: characterized by an elevated bilirubin level.
• Mesenchymal-inflammatory syndrome: detected by an elevated $\gamma$-globulin fraction.
• Hepatocellular insufficiency syndrome: reflects impaired synthetic function of the liver, which manifests as a decrease in the concentration of albumin, prothrombin, and cholesterol.
• Cytolysis syndrome: accompanied by a sharp increase in transaminase activity due to hepatocyte destruction.

Instrumental methods and principles of treatment

Ultrasound and CT are used to visualize changes. Ultrasound allows the evaluation of the size of the liver and spleen, detection of structural heterogeneity of the parenchyma, and recording of signs of portal hypertension. Computed tomography (CT) serves as a more informative and accurate method. Final morphological verification (clarification of the lesion variant and fibrosis stage) is achieved using percutaneous liver biopsy.

Therapeutic tactics: Treatment directly depends on the activity of the process and the developed complications.

• In low-grade activity, general regimen measures, strict exclusion of any provoking factors (alcohol consumption, intake of hepatotoxic drugs, occupational hazards), as well as correction of concomitant pathologies are indicated.
• In active disease, etiotropic therapy is required.

To relieve edema-ascites syndrome, a diet with strict restriction of dietary salt and fluid intake comes to the first place. In later stages, diuretics are used medically. The drugs of choice in this case are aldosterone antagonists (spironolactone) and potassium-sparing diuretics (such as triamterene and amiloride).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Etiotropic therapy in active disease
• Morphological verification: evaluation of liver biopsy specimens
• Mechanisms of hypersplenism development
• Differential diagnosis of the causes of hepatic coma

Other topics in the section "Liver, Biliary Tract, and Spleen"

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