Vitamin K Deficiency
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You are rounding on your patient, a 64 y/o M with C.Diff after treatment with antibiotics for CAP. He has had poor PO 2/2 nausea. He is on PO Vanc, Unasyn, and SQH. In the am, you are notified of prolonged bleeding thing from his PIVs, bruising, and see the above on exam. Labs show:
APTT WNL
PT Prolonged
HGB 12 (PRIOR 12.8)
PLT 190
LFT AND Factor VIII, V are WNL
What is the most likely etiology of your patient's bleeding? How will you intervene?
Vitamin K Deficiency
Let’s walk through this one! Last week Dr. Espinoza gave a great Fellow’s Friday on Bleeding Disorders. Refer back to that video under Distance Learning tab if you missed it.
Any patient with prolonged bleeding merits laboratory work up to evaluate their hemostasis with a prothrombin time (PT) and an activated partial thromboplastin time (aPTT). As you work through this bleeding patient’s coagulation studies, utilize the coagulation cascade to guide you.
There are three arms of the coagulation cascade: the intrinsic (aPTT; factors XII, XI, IX, VIII), extrinsic (PT; factor VII), and the common pathway (aPTT/PT; additional factors X, V, II).
Recall that Heparin use inhibits the intrinsic pathway and Coumadin use inhibits the extrinsic pathway. Recall that Vitamin K dependent factors are FX, IX, VII, II, protein C & S (bonus mnemonic: “1972 was the disco era”).
Our patient had a normal aPTT, prolonged PT, normal PLT count, and factors VIII and V were wnl.
Let’s walk through this one! Last week Dr. Espinoza gave a great Fellow’s Friday on Bleeding Disorders. Refer back to that video under Distance Learning tab if you missed it.
Any patient with prolonged bleeding merits laboratory work up to evaluate their hemostasis with a prothrombin time (PT) and an activated partial thromboplastin time (aPTT). As you work through this bleeding patient’s coagulation studies, utilize the coagulation cascade to guide you.
There are three arms of the coagulation cascade: the intrinsic (aPTT; factors XII, XI, IX, VIII), extrinsic (PT; factor VII), and the common pathway (aPTT/PT; additional factors X, V, II).
Recall that Heparin use inhibits the intrinsic pathway and Coumadin use inhibits the extrinsic pathway. Recall that Vitamin K dependent factors are FX, IX, VII, II, protein C & S (bonus mnemonic: “1972 was the disco era”).
Our patient had a normal aPTT, prolonged PT, normal PLT count, and factors VIII and V were wnl.
The normal aPTT makes a deficiency / inhibitor along the intrinsic pathway unlikely – ruling out common etiologies like Hemophilia A (FVIII) or Hemophilia B (IX), vWD (VIII), those factor inhibitors, or heparin use. If the common pathway was involved, we would expect both aPTT and PT to be abnormal so we also can rule out problems with FX, V, and II.
The PT was prolonged so we should focus more on this side of the cascade. Our differential can include FVII deficiency/inhibition (Coumadin use, vitamin K deficiency), DIC, or liver disease.
For DIC or liver disease, we would expect the PLT count to be low and for factor VII to be low. If both of those values had been low, we could’ve then used factor VIII to differentiate between DIC or liver disease. In DIC, the coagulation cascade is activated and consumed meaning that all factors we test for should be low. In liver disease, all factors that are synthesized by the liver should be low. Factor VIII is a helpful test though because it is not only produced by the liver but also synthesized by endothelial cells. FVIII will therefore be normal in liver failure (or even elevated).
Looking at the clinical context: Our patient is not on Coumadin. He has been hospitalized with pneumonia and c.diff, on multiple antibiotics, and has had poor nutrition through all of this. Our leading diagnosis is therefore vitamin K deficiency.
Although vitamin K is found in many foods (think leafy greens), actually most of your vitamin K is derived from colonic bacteria. Low dietary intake alone is rarely the cause for severe deficiency. His recent antibiotics likely wiped out his normal bacteria and his active diarrhea likely decreased is absorption from eating. Add in the poor appetite… And presto.
So why did the PT prolong, but the aPTT was normal? The PT is most sensitive and earliest sign of a decrease in vitamin-K dependent factors and PT will be prolonged out of proportion to the aPTT which will be normal or only mildly elevated. In severe vitamin K deficiency both PT and PTT will prolong.
Treatment options: IV vitamin K 10 mg is sufficient to restore normal clotting factor levels within <10 hours. If a patient has ongoing bleeding or need for immediate correction before an invasive procedure, then FFP or PCC is your answer. In an asymptomatic patients without active bleeding or high risk, enteric vitamin K is sufficient.
