Vitamin K1. Haemostatics. Antagonist of indirect anticoagulants
ATC code: B02BA01 (Phytomenadione (vitamin K1))
Brand names
Konakion MM, Mephyton, Phytonadione USP
Vitamin K1 (phylloquinone) is a cofactor for hepatic γ-glutamyl carboxylase, which activates clotting factors II (prothrombin), VII, IX, X, and the natural anticoagulants proteins C, S, Z. Without vitamin K, the liver synthesises inactive precursors of these factors, manifesting as prolonged prothrombin time and bleeding. The intramuscular effect develops within 4–6 hours, intravenous within 1–2 hours. After oral intake, coagulation parameters normalise over 12–24 hours. Vitamin K1 is fundamentally different from vitamin K3 (menadione sodium bisulfite, Vikasol): K3 acts more slowly and weakly, and in neonates causes haemolytic anaemia and kernicterus. International practice does not use K3 for VKDB or anticoagulant reversal – only K1.
First line
Vitamin K1 is first-line for vitamin K-deficient coagulopathy in cholestatic liver disease, malabsorption syndromes (cystic fibrosis, coeliac disease, short bowel syndrome), and long-term parenteral nutrition. Doses: 5–10 mg IM or subcutaneously daily for 3 days, then guided by INR. In children with cholestasis: 1–2 mg/kg. In patients with severe coagulopathy and bleeding: 10 mg slow IV with concurrent PCC or FFP transfusion.
First line
First-line agent for reversing excessive warfarin anticoagulation per ACCP recommendations. Dose and route depend on the situation. INR 4.5–10 without bleeding: hold 1–2 warfarin doses without vitamin K or 1–2.5 mg oral. INR above 10 without bleeding: 2.5–5 mg oral. Any significant warfarin-associated bleeding: 5–10 mg slow intravenous (over 30 minutes – rapid administration causes anaphylactoid reactions) plus prothrombin complex concentrate (4F-PCC) or fresh frozen plasma. The intravenous effect develops over 1–2 hours, oral over 12–24 hours. Vikasol (K3) is not used for this purpose – it acts more slowly and weakly.
First line
Global paediatric standard: vitamin K1 1 mg intramuscularly once within the first 6 hours of life for term newborns; 0.4 mg/kg for preterm under 1,500 g, 0.5–1 mg for preterm above 1,500 g. , NG194, and 2022 unanimously recommend the intramuscular route. Alternative oral regimens (3 doses of 2 mg on days 1, 4–7, and 28) are acceptable when parents refuse injection, but efficacy is lower: late VKDB rate is 1.2–6.4 per 100,000 live births with oral regimens versus 0.25 per 100,000 after IM. Without prophylaxis, late VKDB causes intracranial haemorrhage with up to 20 % mortality and severe disability. K1 (phytomenadione) is used for this purpose, not K3 (Vikasol) – K3 causes haemolytic anaemia in neonates.
Sources
Not recommended
— Anti-aging and longevity: International guidelines do not list vitamin K1 as an anti-ageing agent. Supplement marketing sometimes positions phytomenadione as a «vitamin for vessels and bones», borrowing the K2 narrative. K1 has not shown a systemic effect on bone mineral density or vascular calcification in RCTs – that activity belongs to K2-dependent tissue Gla proteins (osteocalcin, matrix Gla protein). K1 above dietary intake provides no clinical benefit in healthy individuals.
FDA category C. Used in pregnancy for anticoagulant- or deficiency-related coagulopathy. Phytomenadione transfers across the placenta poorly, so newborn prophylaxis via maternal third-trimester intake is less effective than post-delivery injection of the infant.
Breast milk contains little vitamin K (1–4 µg/L), so maternal K1 intake is insufficient to prevent VKDB in the infant. Standard practice: direct K1 injection to the newborn. Maternal K1 intake is compatible with breastfeeding.
phytomenadione is evaluated for the following indications with varying evidence strength: Coagulopathy in cholestasis and malabsorption (evidence tier A), Reversal of warfarin anticoagulant effect (evidence tier A), Vitamin K deficiency bleeding (VKDB) prevention in newborns (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of phytomenadione (≥ 1 in 100): Injection-site pain and erythema, Facial flushing, sensation of warmth (after intravenous administration). See the Safety section for uncommon and serious reactions.
FDA category C. FDA category C. Used in pregnancy for anticoagulant- or deficiency-related coagulopathy. Phytomenadione transfers across the placenta poorly, so newborn prophylaxis via maternal third-trimester intake is less effective than post-delivery injection of the infant.
Breast milk contains little vitamin K (1–4 µg/L), so maternal K1 intake is insufficient to prevent VKDB in the infant. Standard practice: direct K1 injection to the newborn. Maternal K1 intake is compatible with breastfeeding.
phytomenadione is contraindicated in: Hypersensitivity to phytomenadione; Severe hepatic failure with markedly reduced synthetic function (K1 effect is minimal). Full list in the Safety section.
intramuscular K1 1 mg in the first hours of life is the unanimous recommendation of AAP, NICE, WHO, and Russian normal-pregnancy guidelines. Without prophylaxis, the late VKDB risk with intracranial haemorrhage is 4–7 per 100,000 live births. Oral regimens are acceptable when injection is refused but are less effective.
Vikasol is K3 (menadione sodium bisulfite), a synthetic molecule. In newborns, K3 causes haemolytic anaemia and kernicterus risk. AAP, ESPGHAN, and NICE explicitly state that only K1 (phytomenadione) is used for VKDB. International paediatric practice has not used K3 for decades. Russian package inserts still list Vikasol as a «vitamin K» drug – this is outdated practice.
this hypothesis came from a single Golding et al. 1992 paper. Subsequent large epidemiological studies (Roman 2002, Fear 2003, McKinney 2003) did not confirm the association. AAP in its position statement explicitly rejects the hypothesis. Refusing K1 prophylaxis based on this myth raises real VKDB risk.
different molecules, different target tissues, different indications. K1 (phytomenadione) acts on hepatic clotting factors – the only form for VKDB and warfarin reversal. K2 (menaquinone) acts on tissue Gla proteins – marketed for bones and vessels with weak clinical basis. They do not substitute for each other across indications.
in a healthy adult, vitamin K is not deficient and clotting factors synthesise normally. Supplemental K1 without a clinical indication has no effect. In patients on warfarin, supplemental K1 is dangerous – it disrupts anticoagulation.