Vikasol 15 mg 20 tablets

Hemorrhagic syndrome associated with hypoprothrombinemia, vitamin K deficiency (including in cases of obstructive jaundice, hepatitis, liver cirrhosis, prolonged diarrhea).
Bleeding after wounds, injuries, and surgical interventions; as part of combination therapy for dysfunctional uterine bleeding, menorrhagia.
Hypoprothrombinemia due to decreased levels of factors II, VII, IX, X against the background of the use of certain medications (coumarin and indandione derivatives, salicylates, some antibiotics).

Vikasol is administered orally for 3-4 days, followed by a four-day break before repeating the course. The daily dose may be divided into 2-3 doses. The maximum single dose for adults is 30 mg, and the maximum daily dose for adults is 60 mg.
In surgical procedures with a risk of significant parenchymal bleeding, it is prescribed for 2-3 days prior to the operation. In pediatrics:
- 3 to 5 years - 7.5 mg/day;
- 5 to 14 years - 15 mg/day;
- over 14 years - 30 mg/day.

Active ingredient: Vikasol (menadione sodium bisulfite) - 15 mg.
Excipients: sugar, potato starch, sodium pyrosulfite, silicone emulsion, talc, stearic acid.

tablets of white or almost white color, flat-cylindrical shape with a bevel.

Increased sensitivity to the components of the drug. Increased blood coagulability, thromboembolism.
With caution - glucose-6-phosphate dehydrogenase deficiency, liver failure, pregnancy.
In cases of obstructive jaundice, the injectable form of the drug should be preferred.

In cases of hemophilia, von Willebrand disease, and Werlhof's disease, the drug is ineffective.
In diseases that lead to impaired bile flow, parenteral administration is recommended.
Prophylactic administration of vitamin K in the third trimester of pregnancy is ineffective due to the low placental permeability for it.

Allergic reactions: facial hyperemia, skin rash (including erythematous, urticaria), skin itching, bronchospasm.
Hematological system: hemolytic anemia, hemolysis in newborns with congenital glucose-6-phosphate dehydrogenase deficiency.
Others: hyperbilirubinemia, jaundice. Rarely - dizziness, transient decrease in blood pressure, profuse sweating, tachycardia, weak pulse filling, alteration in taste sensations.

In case of overdose, hypervitaminosis K may occur, manifested by hyperprothrombinemia, hyperbilirubinemia; seizures may rarely occur in children.

Reduces and blocks the anticoagulant effect of neodicumarin and phenindione. Does not affect the anticoagulant activity of heparin.
Antacids reduce absorption due to the precipitation of bile acid salts in the initial section of the small intestine.
Simultaneous administration with broad-spectrum antibiotics, quinidine, quinine, high-dose salicylates, and antibacterial sulfonamides requires an increase in the dose of vitamin K.
Cholestyramine, colestipol, mineral oils, sucralfate, and dactinomycin reduce the absorption of vitamin K, necessitating an increase in its dose.

Synthetic water-soluble analogue of vitamin K, it promotes the synthesis of prothrombin and proconvertin, increases blood coagulation by enhancing the synthesis of factors II, VII, IX, and X of coagulation.
It has a hemostatic effect (in vitamin K deficiency, increased bleeding occurs).
In the blood, prothrombin (factor II) in the presence of thromboplastin and calcium ions, with the participation of proconvertin (factor VII), factors IX (Christmas factor), X (Stuart-Prower factor) converts to thrombin, under the influence of which fibrinogen is transformed into fibrin, forming the basis of the blood clot (thrombus). It substrate-stimulates vitamin K reductase, activating vitamin K and ensuring its participation in the hepatic synthesis of vitamin K-dependent plasma coagulation factors.
Onset of effect - 7-12 hours after oral administration.

After intramuscular administration, it is easily and rapidly absorbed. It accumulates in tissues in small amounts. After undergoing a cycle of metabolic activation, it is oxidized to the diol form in the liver. It is excreted by the kidneys (up to 70%) and with bile almost exclusively in the form of metabolites. High concentrations of vitamin K in the feces are due to its synthesis by intestinal microflora.