Mechanism of action
The drug is a synthetic precursor of vitamin $K$ (vitamin $K_3$). Upon entering the body, menadione sodium bisulfite is transformed into the active form of vitamin $K$. In the liver, it triggers a critical biochemical process — the synthesis of plasma blood clotting factors: prothrombin (factor II), proconvertin (factor VII), Christmas factor (IX), and Stuart-Prower factor (X), as well as the anticoagulant protein $C$.
In addition to hepatobiliary action, vitamin $K$ is involved in extrahepatic processes, in particular the synthesis of the bone calcium-binding protein osteocalcin.
Pharmacological effects
The main pharmacological effect of the drug is its hemostatic action. Clotting factors have a short half-life and rapidly degrade; vitamin $K$ deficiency impairs their synthesis, leading to hemorrhage. Administration of Vikasol restores the plasma pool of clotting factors, normalizes coagulogram parameters, and prevents hemorrhagic complications.
Indications for use
The primary goal of prescribing the drug is to arrest hemorrhagic syndrome associated with hypoprothrombinemia. Key clinical indications include:
- Liver and biliary tract pathologies: hepatitis, liver cirrhosis (impaired factor synthesis), obstructive jaundice (impaired vitamin $K$ absorption due to lack of bile).
- Absorption disorders: malabsorption syndrome, obstructive jaundice.
- Drug-induced causes: overdose of indirect anticoagulants (vitamin $K$ antagonists).
- Prophylactic use: preparation for major surgical interventions to prevent bleeding.
Side Effects and Characteristics
When using the drug, allergic reactions may occur: skin rash, pruritus, erythema, and bronchospasm. Intravenous administration carries a risk of anaphylactoid reactions.
A specific characteristic of vitamin $K_3$ (vicasol) is the risk of hemolytic anemia and hyperbilirubinemia in newborns, which is why naturally occurring phylloquinone (vitamin $K_1$) is preferred for the prevention of hemorrhagic disease of the newborn.
Administration and dosing details
The drug is available as 0.015 g tablets and a 1% solution in 1 ml ampoules.
- Orally: 1–2 tablets 1–2 times a day. The maximum single dose is 0.03 g, and the maximum daily dose is 0.06 g.
- Parenterally (intramuscularly): 0.01–0.015 g 2–3 times a day. The parenteral route is particularly important in malabsorption syndromes and obstructive jaundice, when bile flow to the intestine—necessary for the absorption of fat-soluble forms—is impaired.
Vicasol is vitamin Koagulation (K3): Koagulates blood, activates Kρισtmas factor and Konvertin in the liver.
Class and exam questions
Which clotting factors depend on vitamin K?
The vitamin is essential for the synthesis of factors II (prothrombin), VII (proconvertin), IX (Christmas factor), and X (Stuart-Prower factor), as well as protein C.
Why is vitamin K action impaired in obstructive jaundice?
Vitamin K is a fat-soluble compound, and an adequate flow of bile is critically required for its normal intestinal absorption. In obstructive jaundice, bile does not enter the intestinal lumen, causing a deficiency of the vitamin.
What is the role of Vicasol in anticoagulant overdose?
Vitamin K preparations act as specific antagonists of indirect anticoagulants, helping to restore clotting factor synthesis during bleeding.
What else to study on this topic
- Differences between phylloquinone (K1), menaquinones (K2), and menadione (K3)
- Pathogenesis of hemorrhagic disease of the newborn and the role of prophylaxis
- Interaction of indirect anticoagulants (warfarin) and vitamin K antagonists
- The role of extrahepatic osteocalcin synthesis in bone tissue
- Pharmacokinetics of water-soluble synthetic analogues versus fat-soluble forms
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