Vitamin K Deficiency Causes Bleeding, Not Clotting
Vitamin K deficiency is a bleeding disorder that results from impaired synthesis of functional clotting factors, leading to hemorrhage rather than thrombosis. 1
Mechanism of Bleeding
Vitamin K functions as an essential cofactor for the post-translational carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X. 2, 3 Without adequate vitamin K, the liver produces undercarboxylated (non-functional) versions of these proteins called PIVKA (Protein Induced by Vitamin K Absence), which cannot properly bind calcium and participate in the coagulation cascade. 1, 3
The deficiency impairs clot formation, not clot breakdown, resulting in prolonged bleeding times and hemorrhagic complications. 1, 2
Clinical Manifestations of Bleeding
Severity Spectrum
- Mild deficiency causes prolongation of prothrombin time (PT) with impaired clotting, confirmed by response to vitamin K administration. 1
- Clinically significant bleeding manifests as:
High-Risk Populations
- Newborns are at highest risk due to limited placental transfer, low hepatic stores, and sterile gut (no bacterial vitamin K synthesis). 5, 3, 4
- Critically ill hospitalized patients with inadequate diet, malabsorption, antibiotic therapy, or hepatic dysfunction can develop life-threatening coagulopathy. 6
Laboratory Findings
Vitamin K deficiency produces a characteristic pattern of prolonged PT/INR and possibly aPTT, with normal platelet count and fibrinogen levels. 1, 7
Key Diagnostic Features
- PIVKA-II (undercarboxylated prothrombin) is the most sensitive and specific marker for vitamin K deficiency. 1, 7, 3
- Factor V levels remain normal (Factor V is NOT vitamin K-dependent), which helps distinguish pure vitamin K deficiency from liver synthetic dysfunction. 7
- Therapeutic trial: Administration of 10 mg vitamin K with reassessment after 12-24 hours shows significant PT/INR correction if deficiency is the primary cause. 7, 8, 2
Common Causes
- Fat malabsorption syndromes (celiac disease, cystic fibrosis, short bowel syndrome, cholestatic liver disease) 1
- Malnutrition and inadequate dietary intake 1, 6
- Prolonged antibiotic therapy (disrupts gut bacterial synthesis) 1, 6
- Warfarin/anticoagulant therapy 1
- Newborn status (physiologic deficiency) 1, 5, 3, 4
Treatment and Prevention
Vitamin K administration rapidly corrects the bleeding tendency, with detectable improvement within 1-2 hours IV and hemorrhage control within 3-6 hours. 2
Dosing Guidelines
- Newborns: 1 mg intramuscular at birth prevents both classic and late VKDB (vitamin K deficiency bleeding). 5, 3, 4
- Adults with deficiency: 10 mg IV (slow injection) or oral, with reassessment after 12-24 hours. 1, 7, 8
- Cystic fibrosis patients: 0.3-1 mg/day for infants; 1-10 mg/day for older children and adults. 1
Critical Safety Considerations
- IV administration must be by slow injection to avoid rare anaphylactoid reactions (3 per 100,000 doses) that can cause bronchospasm and cardiac arrest. 1, 8, 2
- Do not exceed 10 mg per dose, as higher doses can create a prothrombotic state. 8
- Minimum 1-2 hours required for measurable PT improvement; immediate effect should not be expected. 2
Important Clinical Pitfalls
Vitamin K deficiency does NOT cause thrombosis—it exclusively causes bleeding. Any suggestion that vitamin K deficiency leads to clotting is fundamentally incorrect based on the mechanism of action. 1, 2, 3
Common Misdiagnoses
- Disseminated intravascular coagulation (DIC) is frequently misdiagnosed when vitamin K deficiency is the actual cause, particularly in critically ill patients. 6
- Mixed pathology can occur—patients with chronic liver disease may have BOTH hepatic synthetic dysfunction AND vitamin K deficiency, requiring careful distinction. 7, 8
When Vitamin K Won't Help
- Established liver synthetic dysfunction: Vitamin K has minimal efficacy when hepatic function is severely impaired, as the liver cannot produce clotting factor precursors regardless of vitamin K availability. 8, 2
- Heparin anticoagulation: Phytonadione does not counteract heparin's anticoagulant action. 2