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An 83-year-old man with a history of paroxysmal atrial fibrillation status post ablation, and chronic constipation, presents to the emergency department with his oldest son who endorses that his father has worsening leg swelling. He believes that, although his legs have gotten larger over the past several weeks, his hands and face have gotten thinner. His medications include a stool softener and a baby aspirin that he has been taking for years. He states that his wife of 50 years died of breast cancer 2 years ago, and she had always done most of the cooking. He states that he often has trouble sleeping, engages in no social activities with his friends, and cries often without any precipitating events. He denies tobacco or alcohol use. His physical examination reveals stable vital signs and is remarkable only for bitemporal wasting and symmetrically edematous legs with 2+ pitting. ECG shows no irregularities or evidence of any ischemic changes. Laboratory studies show:
WBC count: 5900/mm³
Hematocrit: 39%
Platelet count: 312,000/mm³
Alanine aminotransferase: 21 U/L
Aspartate aminotransferase: 20 U/L
Total bilirubin: 0.6 mg/dL
Albumin: 2.5 g/dL
Partial thromboplastin time: 27 seconds
Prothrombin time: 25 seconds
International Normalized Ratio: 1.7
A 1:1 mixing study corrects the prothrombin time.
Which of the following is the most likely cause of this man's coagulopathy?
127150 : handeep
A.Antiphospholipid antibody
B.Dietary vitamin K deficiency
C.Disseminated intravascular coagulation
D.Hepatic cirrhosis
E.Warfarin administration
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The correct answer is B. .
The evaluation of a patient with elevated clotting times should start with establishing the pattern of coagulopathy (ie, elevated prothrombin time [PT], elevated partial thromboplastin time [PTT], or both), as the differential diagnosis can be simplified from this step. The patient has an elevated PT, which is a marker of the extrinsic pathway that is most strongly determined by factor VII levels and activity. Disease states that would decrease factor VII activity include decreased production, increased consumption, or inhibition of the factor. The classic next step is a coagulation mixing study to look for inhibitors or specific factor deficiencies, although clues from the patient's history are frequently present. Given signs of profound malnutrition (likely from poorly controlled depression and poor self-care skills) with hypoalbuminemia and muscle wasting, the most likely source of his coagulopathy is nutritional vitamin K deficiency. Additional considerations for a diagnosis of vitamin K deficiency include antibiotic exposure or signs of liver dysfunction as they are predominantly implicated in the synthesis of vitamin K and gamma-carboxylation of vitamin K factors, respectively.
A is not correct. 5% chose this.
Antiphospholipid antibodies are a possible cause of an acquired coagulopathy. However, the 1:1 mixing study correctly points to a factor deficiency as opposed to an inhibitor (which would prevent correction of the PT). Furthermore, individuals with antiphospholipid syndrome conventionally have a prolonged PTT and classically present with history of thrombophilia.
C is not correct. 3% chose this.
Although disseminated intravascular coagulation (DIC) can cause consumptive coagulopathy and thus prolong the PT, this patient has no clinical signs of a marked inflammatory state or malignancy to drive such a process. Furthermore, the normal platelet count and preserved PTT argues against DIC. Along with serologic markers including a D-dimer, fibrinogen, and lactate dehydrogenase, a peripheral smear should be ordered to assess for RBC fragmentation (ie, schistocytes), which are classically present in DIC.
D is not correct. 11% chose this.
Hepatic dysfunction is a reasonable consideration in the work-up of coagulopathy as gamma-carboxylation of vitamin K coagulation factors (II, VII, IX, X) takes place in the liver. However, the absence of any clinical signs or serologic evidence inclusive of transaminitis or hyperbilirubinemia precludes this as a viable cause of his coagulopathy. Although his albumin is low, this is most likely a consequence of nutritional impairment as suggested by muscle wasting, and a prealbumin would corroborate this suspicion.
E is not correct. 18% chose this.
Warfarin is a very common cause of prolongation of the PT because of its actions of inhibition of epoxide reductase and subsequently impaired gamma-carboxylation of factor VII (along with II, IX, and X), and following the PT or International Normalized Ratio is the gold standard for monitoring therapeutic levels of warfarin. Although the patient does carry a diagnosis of paroxysmal atrial fibrillation, which is an indication for warfarin therapy, his low CHADS-2 score (Congestive heart failure, Hypertension, Age >75 years, Diabetes mellitus, Stroke [2 points]) precludes initiation of warfarin and thus is an unlikely cause of his coagulopathy.
Bottom Line:
Isolated prolongation of the PT is either due to warfarin, low vitamin K intake, antibiotics suppressing vitamin K production, liver dysfunction, or disseminated intravascular coagulation.
