Vitamin K Deficiency and Acquired Coagulopathies
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Direct answer
Vitamin K deficiency and acquired coagulopathies cause bleeding through reduced synthesis of vitamin K dependent factors II, VII, IX and X, through impaired hepatic synthesis, or through consumption of clotting factors and platelets. Vitamin K deficiency and warfarin both prolong the prothrombin time and correct with vitamin K, whereas liver failure impairs synthesis of all factors and fibrinogen and corrects only partly. Disseminated intravascular coagulation consumes fibrinogen and platelets, producing low fibrinogen and platelets with raised D-dimer, a combination that distinguishes it from the other two.
What you must remember
- Vitamin K dependent proteins: factors II, VII, IX and X, together with protein C and protein S; deficiency leads to production of abnormal PIVKA proteins.
- Warfarin: inhibits vitamin K epoxide reductase, so the PT rises first; urgent reversal uses four-factor prothrombin complex concentrate with intravenous vitamin K.
- Neonatal prophylaxis: vitamin K given at birth prevents haemorrhagic disease of the newborn, while late-onset disease is linked to cholestasis or exclusive breastfeeding.
- Liver disease: prolonged PT with low fibrinogen in severe disease, and factor VIII usually normal or raised because it is made by endothelium.
- DIC: prolonged PT and aPTT, low fibrinogen, low platelet count, raised D-dimer and fibrin degradation products, often with schistocytes on the smear.
- Malabsorption: cholestasis, coeliac disease and prolonged antibiotic use can all cause vitamin K deficiency.
- DIC management: treat the trigger, and give blood components for bleeding or procedures rather than prophylactically.
A worked case: three prolonged PTs
Three patients have a prolonged prothrombin time, and the fibrinogen, the response to vitamin K and the blood film decide the diagnosis.
- Cirrhosis with partial correction: A 58-year-old man with alcohol-related cirrhosis has a PT of 22 seconds, raised bilirubin, mildly low fibrinogen and platelets of 60,000. An intravenous vitamin K trial corrects the PT only partly, which points to hepatic synthetic failure rather than deficiency alone.
- Warfarin with bleeding: A 62-year-old on warfarin for atrial fibrillation has an INR of 6 with a major gastrointestinal bleed. Reversal uses prothrombin complex concentrate with intravenous vitamin K, reserving fresh frozen plasma for when it is unavailable.
- DIC with sepsis: A septic 50-year-old with DIC shows prolonged PT and aPTT, fibrinogen of 0.9 g/L, platelets of 40,000, raised D-dimer and schistocytes on the smear. Treatment targets the sepsis first, and blood products follow bleeding criteria.
- Track the trend: Repeating the coagulation profile after treatment shows whether the process is improving, which matters more than a single abnormal value.
Where the examiner sets the trap
Four traps recur in coagulation questions.
- Trap: confusing obstructive jaundice with hepatocellular failure Correct: the PT is prolonged by vitamin K malabsorption and corrects with parenteral vitamin K, which distinguishes it from hepatocellular failure.
- Trap: assuming a normal fibrinogen rules out liver failure Correct: fibrinogen is often only mildly reduced in early disease, so it must be read together with the rest of the profile.
- Trap: expecting vitamin K deficiency or warfarin to lower fibrinogen Correct: fibrinogen is not vitamin K dependent, so neither lowers it.
- Trap: naming the lab pattern in DIC without its cause Correct: name the trigger, such as sepsis, malignancy or an obstetric emergency, because a pattern alone loses the point in the viva.
Frequently asked questions
How does vitamin K deficiency differ from liver failure on coagulation tests?
Both prolong the PT, but vitamin K deficiency corrects with parenteral vitamin K within a day or two, whereas liver failure usually corrects only partly because the liver cannot synthesise the factors. The response to a vitamin K trial is therefore the key bedside distinction.
Which coagulation pattern identifies disseminated intravascular coagulation?
Disseminated intravascular coagulation shows prolonged PT and aPTT, low fibrinogen, low platelet count and raised D-dimer or fibrin degradation products, often with schistocytes on the smear. This combination reflects consumption of clotting factors and platelets triggered by sepsis, malignancy or an obstetric emergency.
Why is prothrombin complex concentrate used to reverse warfarin?
Prothrombin complex concentrate supplies vitamin K dependent factors rapidly in life-threatening bleeding on warfarin, while intravenous vitamin K restores hepatic production over a longer period. Fresh frozen plasma is an alternative but needs a larger volume.
Why is fibrinogen usually normal in vitamin K deficiency?
Fibrinogen is not a vitamin K dependent factor, so its level is not lowered by vitamin K deficiency or warfarin. A low fibrinogen therefore suggests severe liver failure, disseminated intravascular coagulation or consumption rather than vitamin K deficiency alone.