Vitamin K Dosing in Liver Disease
Vitamin K administration in liver disease has limited efficacy and is NOT routinely recommended for correcting coagulopathy caused by hepatic synthetic dysfunction; when indicated for specific situations (cholestatic disease, malnutrition, or diagnostic trial), the dose is 10 mg administered intravenously by slow injection. 1, 2
Understanding Why Vitamin K Usually Doesn't Work in Liver Disease
- Coagulopathy in liver disease reflects impaired hepatic synthesis of clotting factors, not vitamin K deficiency—the liver cannot produce these proteins regardless of vitamin K availability 1, 3
- Vitamin K takes more than 12 hours to begin correcting hemostatic defects and typically has only minimal impact on prothrombin time in cirrhotic patients 1, 2
- Research demonstrates that subcutaneous vitamin K does not modify coagulation parameters in liver disease, and intravenous vitamin K shows minimal effect except in cholestatic conditions 1, 4
- A 2017 study found that 62.3% of cirrhotic patients failed to achieve even a 10% decrease in INR after vitamin K administration, with only 16.7% meeting effectiveness endpoints 5
Specific Situations Where Vitamin K May Be Indicated
Cholestatic Liver Disease or Malabsorption
- Parenteral vitamin K supplementation (10 mg IV or oral) is recommended for jaundiced patients or those with cholestatic liver disease where true vitamin K deficiency exists from fat malabsorption 1, 2
- Vitamin K can be effective when patients have experienced prolonged antibiotic therapy, severe malnutrition, or malabsorption—conditions creating true vitamin K deficiency rather than synthetic dysfunction 1, 2
Diagnostic Trial to Distinguish Deficiency from Synthetic Dysfunction
- Administer a single dose of 10 mg vitamin K (IV or oral) with INR reassessment after 12-24 hours 1, 2
- Improvement in INR by ≥0.5 within 24-72 hours confirms a vitamin K deficiency component 1, 2
- No improvement indicates pure hepatic synthetic dysfunction where further vitamin K is futile 1, 3
Life-Threatening Bleeding on Vitamin K Antagonists
- For VKA-associated life-threatening bleeding: administer four-factor prothrombin complex concentrate PLUS 10 mg IV vitamin K by slow injection 6, 1
- This is the only major bleeding scenario where vitamin K is recommended in liver disease patients 6
Dosing and Administration Details
Standard Dose
- 10 mg is the recommended dose, administered either orally or intravenously 1, 2, 7
- For major bleeding on anticoagulants: 5-10 mg IV vitamin K by slow injection 6
- IV administration should not exceed 10 mg per dose to avoid creating a prothrombotic state 1
Route and Safety Considerations
- Administer IV vitamin K by slow injection (not to exceed 10 mg per dose) to minimize risk of anaphylactoid reactions 1, 2
- Anaphylactoid reactions occur in approximately 3 per 100,000 doses and can cause bronchospasm and cardiac arrest 1
- Dilute in preservative-free 0.9% Sodium Chloride, 5% Dextrose, or 5% Dextrose and Sodium Chloride Injection 7
What NOT to Do
- Do NOT routinely administer vitamin K to correct elevated INR in cirrhotic patients without active bleeding—this practice lacks evidence and is ineffective 1, 3
- Do NOT use vitamin K doses exceeding 10 mg, as higher doses create a prothrombotic state and prevent re-anticoagulation for days 1
- Do NOT use INR as a guide for bleeding risk in cirrhosis—it reflects synthetic function rather than hemostatic capacity 1
- Do NOT assume vitamin K will correct coagulopathy before invasive procedures in patients with hepatic synthetic dysfunction 1, 2
Alternative Management Strategies
For Invasive Procedures
- No correction is needed when platelet count is >50 × 10⁹/L or when local hemostasis is possible 1, 2
- For high-risk procedures where local hemostasis is impossible and platelets are 20-50 × 10⁹/L, consider platelet concentrates or TPO-R agonists on a case-by-case basis 1, 2
For Active Bleeding
- Consider targeted blood product replacement with thresholds: hematocrit ≥25%, platelets >50 × 10⁹/L, fibrinogen >120 mg/dL 1, 2
- Prothrombin complex concentrates provide more rapid INR correction than fresh frozen plasma but carry thrombotic risk (5.5% thromboembolic events) and are off-label in liver failure 1, 2
- Avoid volume overload from excessive fresh frozen plasma transfusions, which substantially increases portal pressure 1
Clinical Pitfalls to Avoid
- Patients with advanced cirrhosis (Child-Pugh B or C) and low fibrinogen (<100-150 mg/dL) have hepatic synthetic dysfunction, not vitamin K deficiency 1
- Despite abnormal coagulation tests, clinically significant spontaneous bleeding is rare in liver failure and often relates to portal hypertension rather than coagulopathy 1
- Routine correction of elevated INR with vitamin K is not supported by evidence in the absence of active bleeding 1, 3