Case Presentation: A 46-year-old man with diabetes mellitus presented with gingival bleeding and gross hematuria for one week. He had no prior bleeding episodes or infectious symptoms. He was not using anticoagulants, drugs, or alcohol. His family history was unremarkable except for his mother’s death during childbirth. Initial exam revealed gingival bleeding, upper extremity ecchymosis and hematuria. Admission labs showed hemoglobin of 13.4 g/dL, activated partial thromboplastin time (aPTT) 129 seconds (normal: 25-35 seconds), D-dimer 363 ng/mL (< 230 ng/mL), fibrinogen 558 mg/dL (200-393 mg/dL), Factor VIII 397% (50-150%), von Willebrand factor 390% (42-176%) and Factor IX 6.8% (65-150%). Serial prothrombin time (PT) and INR were unmeasurably high. Additional tests for hemolysis and TEG platelet studies were normal. Imaging revealed an occluded left renal artery. After administering 10 mg of intravenous (IV) vitamin K aPTT decreased to 71.8 seconds, PT to 94.3 seconds, and INR to 8.2. Factors II, VII, and X were also low. Further investigation revealed that the patient had encountered rats in his building, and his landlord frequently applied rat poison to kitchen surfaces. An anticoagulant poisoning panel was positive for brodifacoum, a superwarfarin used in rodenticides. Initially, the patient received 10 mg of IV vitamin K daily, leading to normalization of INR; however, follow-up labs showed an INR rise to 15. He was then transitioned to 30 mg of oral vitamin K three times daily, and PT and INR normalized. A repeat anticoagulant panel three weeks later still detected brodifacoum, necessitating a gradual taper of vitamin K over months. His discharge was complicated by the unavailability of oral vitamin K at the outpatient pharmacy, with costs exceeding $2000 per month.
Discussion: Bleeding disorders can be inherited or acquired. Common inherited causes include Von Willebrand disease and hemophilias. Acquired causes include cirrhosis, presence of inhibitory factors of the coagulation cascade due to autoimmune or paraneoplastic processes and the use of anticoagulants such as warfarin. Warfarin and superwarfarins inhibit vitamin K epoxide reductase (VKOR), disrupting the synthesis of vitamin K-dependent coagulation factors (factor II, VII, IX, and X, protein C, and protein S). This impairs clotting and increases the risk of spontaneous bleeding, easy bruising, and bleeding from minor injuries. Additionally, they can cause paradoxical thrombosis due to initial reductions in protein C and S, which may explain our patient’s renal artery thrombosis. The anticoagulant effect of coumarins can be reversed with vitamin K1 (phytonadione) which bypasses VKOR. Due to brodifacoum’s long half-life (15-62 days) and stronger VKOR binding, patients require significantly higher doses of vitamin K. Our patient initially required 90 mg of vitamin K daily for a week, followed by a slow taper over months. Discharge planning for cases of superwarfarin toxicity often includes addressing the high cost of vitamin K and ensuring the environment is cleared of rodenticides.
Conclusions: Clinicians should always inquire about potential environmental exposures, such as rodenticides in patients presenting with unexplained bleeding. In cases of suspected anticoagulant poisoning, timely vitamin K administration is crucial, with dosages tailored to the patient’s INR and clinical status.