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The usual presentation of vitamin K deficiency is a hospitalized patient who is found to have a prolonged PT/INR, rarely with bleeding manifestations.


  1. The most common cause of vitamin K deficiency is inadequate oral intake.

  2. Patients who have been hospitalized and need to start warfarin therapy may require smaller than expected doses to achieve therapeutic levels, because they may be unduly sensitive as a result of baseline vitamin K deficiency.

  3. Vitamin K deficiency can also occur with the recent use of antibiotics that alter the gut flora’s ability to convert ingested vitamin K to its absorbable form.


  1. As with liver disease, patients with vitamin K deficiency have PT/INR levels disproportionately longer than aPTT levels.

  2. This is due to factor VII having the shortest half-life of the vitamin K–dependent factors (II, VII, IX, and X), thus making the factor VII–dependent PT/INR more sensitive to vitamin K alterations.

  3. The aPTT will also go up eventually, as the levels of factors II, IX and X, with much longer half-lives, fall.


  1. Vitamin K repletion, either orally or parenterally, is the treatment of choice.

    1. If parenteral treatment is chosen, it should be administered subcutaneously or intravenously—not intramuscularly.

    2. Intramuscular injections should be avoided in patients with coagulopathies, in order to avoid the development of hematomas in muscles that can lead to neuropathy if a major nerve traverses the area.

  2. Vitamin K administration takes 18–24 hours to have its effect, so if a patient with vitamin K deficiency is bleeding, fresh frozen plasma or four-factor prothrombin complex concentrate, which contains factors II, VII, IX, and X, may be required.

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