Synopsis
Differentiate correctable vitamin K deficiency from the rebalanced haemostasis of liver disease, investigate bleeding by phenotype, and use vitamin K, components or anticoagulation without treating INR as a complete measure of risk.
- Vitamin K deficiency typically prolongs PT first because factor VII has the shortest half-life; severe deficiency can prolong both PT and APTT and cause mucosal, gastrointestinal, operative or intracranial bleeding.
- First-line assessment is medication and nutrition history, FBC and film, PT, APTT, fibrinogen, renal and liver profiles, bilirubin pattern and evaluation for cholestasis, malabsorption, antibiotics, warfarin, DIC and active bleeding.
- A prompt PT improvement after phytomenadione supports deficiency, whereas non-correction suggests hepatocellular failure, ongoing VKA effect, consumption or another defect; do not delay emergency haemostasis to use this as a diagnostic test.
- Cirrhosis creates rebalanced haemostasis: INR measures selected procoagulant factors but not reduced natural anticoagulants, high VWF, platelet function or fibrinolysis and does not reliably predict procedure bleeding.
- Do not give plasma merely to normalise INR in stable non-bleeding liver disease. Treat the bleeding source and correct clinically relevant platelets or fibrinogen under a procedure or major-haemorrhage protocol.
- For severe or life-threatening VKA-related bleeding, use four-factor PCC at the product-specific weight and pretreatment-INR dose plus phytomenadione 5–10 mg by slow intravenous injection.
- For suspected nutritional or cholestatic deficiency without life-threatening bleeding, oral or slow intravenous phytomenadione is selected by urgency and absorption; recheck PT and address the cause.
- Patients with cirrhosis still need VTE risk assessment. Use mechanical or pharmacological prophylaxis and therapeutic anticoagulation from individual thrombosis, platelet, bleeding, renal and variceal risk, not from INR alone.
Key red flags
Haematemesis or melaena with cirrhosis is a portal-hypertensive emergency until endoscopy establishes the source; correcting INR must not delay vasoactive therapy, antibiotics and endoscopic haemostasis.
New confusion, severe headache, focal deficit or reduced consciousness with coagulopathy requires urgent intracranial imaging and reversal or haemostatic support based on the actual cause.
Jaundice, hypoglycaemia, rapidly rising INR, encephalopathy, lactate elevation or kidney injury may represent acute liver failure and requires immediate specialist liver-centre discussion.
New encephalopathy with jaundice, coagulopathy, hypoglycaemia or lactate elevation needs urgent liver-centre and critical-care escalation.
Investigation priorities
Define the pattern, consequences and possible consumption alongside clinical bleeding.
Separate impaired synthesis from malabsorption and identify modifiers of bleeding and medicine clearance.
Management branches
PT or INR is newly prolonged with or without bleeding.
- Verify sampling, review warfarin and interacting medicines, nutrition, antibiotics, diarrhoea, cholestasis, alcohol and known hepatic disease.
- Check FBC, film, APTT, fibrinogen, liver and renal profiles and D-dimer when DIC is clinically plausible.
- Give vitamin K when deficiency is likely, repeat PT at an urgency-appropriate interval and investigate persistent or mixed abnormalities.