Clinical manifestations of brodifacoum poisoning include vaginal bleeding,9,22 epistaxis,7,27,30,34 hematuria,7,8,19,26- 34 bleeding from the gums,20,25,31 gastrointestinal bleeding,8,30- 32 ecchymosis,6,19,34 spontaneous abortion,22 hemoptysis,23,25 abdominal pain,20 and intracranial hemorrhage.18,30,34 Sixteen of the 24 reported cases presented with hematuria. Ecchymosis was present in 6 of the 24 cases. Workup of brodifacoum poisoning is not a problem in cases of acute poisoning but may be challenging in patients with suspected Munchausen syndrome. We advise physicians confronted with cases of brodifacoum poisoning to determine the PT of the patient on initial exposure and at 48 hours.35 Any prolongation in PT indicates that poisoning has occurred. We also suggest that for patients with possible Munchausen syndrome, a mixing study of the patient's plasma with control plasma should be performed. Normalization of the PT and APTT after mixing studies implies the presence of factor deficiency and the absence of an inhibitor. Furthermore, we advise physicians to obtain samples of a few of the vitamin K–dependent factors (II, VII, IX, and X) and factor V, which is produced in the liver but is not vitamin K dependent. Although not usually necessary, one can determine the vitamin K1 epoxide–reduced vitamin K ratio. A deficiency of vitamin K–related factors plus a very high vitamin K1 epoxide–reduced vitamin K1 ratio is consistent with warfarin or superwarfarin poisoning.36,37 Vitamin K1 epoxide is a product of vitamin K metabolism and is the inactive form of vitamin K (Figure 1). The presence of warfarin or superwarfarin in the blood confirms warfarin or superwarfarin exposure or poisoning. Usually none is detected. If Munchausen syndrome is suspected and the patient's blood is negative for warfarin, a specific assay for brodifacoum (Talon) and other superwarfarins should be performed. In our first case, levels of all the vitamin K–dependent factors were low and the factor V level was normal, which is consistent with a lack of vitamin K1 or inhibition of its activity by warfarin or superwarfarin. After transient resolution, repeated and continuous treatment with large doses of vitamin K1 was necessary to correct the coagulopathy. The vitamin K1 epoxide–reduced vitamin K ratio confirmed the presence of a warfarin-type compound while assays for warfarin were being performed. Results of the original screening test for superwarfarin were reportedly negative, but brodifacoum was later detected at a concentration of 78 ng/mL.