PA20.1-2 | DIC & Vitamin K Deficiency — Summary & Reflection

REFLECT

Before moving to the summary, take 3-4 minutes to answer these questions in your notes without looking back:

1. A patient presents with bleeding from IV sites, thrombocytopenia, prolonged PT and aPTT, low fibrinogen, and markedly elevated D-dimer. You identify schistocytes on the blood film. Write down the diagnosis and three possible triggers you would immediately investigate.

1. A neonate on day 3 of life presents with bleeding from the umbilical stump. The mother exclusively breastfed and did not consent to the neonatal vitamin K injection at birth. Predict the laboratory panel and explain why the PT is disproportionately prolonged compared to the aPTT.

1. Explain in two sentences why factor VIII level helps distinguish DIC from liver disease — where is factor VIII made, and how does each condition affect it differently?

KEY TAKEAWAYS

DIC — key points:
• Always secondary — treat the trigger, or treatment fails.
• Mechanism: TF release → thrombin burst → microthrombi + consumption of platelets, fibrinogen, factors V/VIII/II → secondary fibrinolysis → FDPs + D-dimer inhibit further haemostasis.
• Lab panel: ↓platelets, ↑PT, ↑aPTT, ↓↓fibrinogen, ↑↑↑D-dimer, schistocytes on film.
• Acute DIC = bleeding; chronic DIC = thrombosis (Trousseau).
• Key distinguisher from liver disease: factor VIII (↓ in DIC, normal/↑ in liver disease).

Vitamin K deficiency — key points:
• Required for γ-carboxylation of factors II, VII, IX, X (and protein C/S).
• PT prolongs first (factor VII shortest half-life), then aPTT — platelets and fibrinogen stay normal.
• Causes: neonatal (HDN), malabsorption (fat-soluble vitamin), antibiotics, warfarin.
• Corrects with parenteral vitamin K; failure to correct → liver disease.

The three-way differential: