Vitamin K Deficiency
The most likely cause of bleeding in this patient is vitamin K deficiency (Answer C). The clinical presentation of ecchymoses and epistaxis after three weeks of broad-spectrum antibiotic therapy, combined with the specific coagulation profile—markedly prolonged PT/INR, prolonged aPTT, isolated factor VII deficiency, and normal factor V, factor VIII, fibrinogen, and platelet count—is pathognomonic for vitamin K deficiency.
Diagnostic Reasoning Based on Laboratory Pattern
Why Vitamin K Deficiency is the Answer
The isolated decrease in factor VII with normal factor V is the key discriminating finding. Factor VII has the shortest half-life (4-6 hours) of all vitamin K-dependent clotting factors (II, VII, IX, X), making it the first to become deficient when vitamin K stores are depleted 1. This explains why the PT/INR (which is highly sensitive to factor VII) is disproportionately prolonged relative to the aPTT in early vitamin K deficiency 1.
Broad-spectrum antibiotics eliminate gut flora that synthesize vitamin K2 (menaquinone), leading to deficiency after 2-3 weeks of therapy 2. This timeline matches perfectly with the patient's three-week antibiotic course for pneumonia 3, 4.
The normal factor V definitively excludes liver disease 1. Factor V is synthesized in the liver but is NOT vitamin K-dependent, so it remains normal in vitamin K deficiency but decreases in hepatic synthetic dysfunction 1.
Normal fibrinogen (275 mg/dL) and normal platelet count (300,000/μL) exclude DIC 1. DIC characteristically causes consumption of fibrinogen (typically <150 mg/dL) and thrombocytopenia (<100,000/μL), neither of which is present 1.
Why the Other Options Are Incorrect
Liver disease (Option A) is excluded by the normal factor V. In hepatic dysfunction, both vitamin K-dependent factors (II, VII, IX, X) AND factor V would be decreased because the liver cannot synthesize any clotting factors adequately 1. The isolated factor VII deficiency with preserved factor V synthesis indicates the liver's synthetic machinery is intact—only the vitamin K-dependent carboxylation step is impaired 1.
Congenital factor VII deficiency (Option B) is incompatible with the acute presentation. A lifelong bleeding disorder would have manifested much earlier in life with prior bleeding episodes during childhood procedures, dental extractions, or minor trauma 1. The sudden onset after antibiotic therapy in an adult with no prior bleeding history makes this diagnosis untenable 3, 4.
Disseminated intravascular coagulation (Option D) is ruled out by normal fibrinogen and normal platelet count 1. DIC is a consumptive coagulopathy characterized by:
- Fibrinogen <150 mg/dL (this patient has 275 mg/dL)
- Thrombocytopenia <100,000/μL (this patient has 300,000/μL)
- Elevated D-dimer and fibrin degradation products
- Microangiopathic hemolytic anemia with schistocytes 1
None of these features are present in this case.
Mechanism of Antibiotic-Induced Vitamin K Deficiency
Broad-spectrum antibiotics deplete intestinal bacteria that produce vitamin K2, while simultaneously the patient's dietary intake during acute pneumonia is often inadequate 2. Certain cephalosporins (cefazolin, cefmetazole, latamoxef, cefoperazone) have additional direct anticoagulant effects through N-methylthiotetrazole side chains that inhibit vitamin K epoxide reductase, but any prolonged broad-spectrum antibiotic course can cause deficiency through gut flora suppression 2.
- The PT/INR becomes prolonged first (within 2-3 weeks) because factor VII has the shortest half-life 1.
- The aPTT becomes prolonged later as factors IX and II (half-lives 24 hours and 60 hours, respectively) decline 1.
- Factor X deficiency contributes to prolongation of both PT and aPTT 1.
Clinical Confirmation and Management
The diagnosis is confirmed by rapid normalization of PT/INR within 30 minutes to 6 hours after intravenous vitamin K1 (phytonadione) administration 3, 4. Cessation of bleeding typically occurs within 6-24 hours 4.
- Administer vitamin K1 10 mg intravenously slowly over 20-30 minutes (to avoid anaphylactoid reactions) 3, 4.
- Recheck PT/INR 6-12 hours after vitamin K administration to document correction 1.
- If life-threatening bleeding is present, administer 4-factor prothrombin complex concentrate (PCC) or fresh frozen plasma for immediate factor replacement while awaiting vitamin K effect 1.
Common Pitfalls to Avoid
Do not assume liver disease based solely on prolonged PT/INR—always check factor V to distinguish hepatic synthetic dysfunction from vitamin K deficiency 1. This is a critical diagnostic step that prevents unnecessary hepatic workup and delays in appropriate vitamin K replacement 1.
Do not overlook medication history—any patient on prolonged antibiotics (especially cephalosporins), with malabsorption syndromes, or with inadequate dietary intake is at risk for vitamin K deficiency 2, 5. The three-week timeline in this case is classic 3, 4.