A 67-year-old male was hospitalized for right lower extremity skin abscess with cellulitis complicated by methicillin sensitive Staphylococcus Aureusbacteremia. The patient received piperacillin/tazobactam (pip/taz) and vancomycin over the first 5 days of hospitalization which was de-escalated to cefazolin at discharge. Thirty-six hours after discharge, the patient was readmitted with expanding area of erythema, calor and dolor. Vancomycin and pip/taz were reinitiated. On hospital day 3, a critical platelet count of zero/μL (admission platelet count = 242,000/μL) was reported on two consecutive blood samples, confirmed by microscopy without evidence of platelet clumping. Diagnoses of heparin-induced thrombocytopenia (HIT), disseminated intravascular coagulation (DIC), and drug induced thrombocytopenia were entertained. Heparin flushes and enoxaparin were discontinued and the antimicrobial regimen was converted to daptomycin. Heparin-induced platelet antibodies, serotonin release assay, and DIC panel were unremarkable. Serum samples were tested for vancomycin-dependent and piperacillin/tazobactam-dependent anti-platelet antibodies. Two doses of platelets were transfused resulting in an increased platelet count to 2,000/μL. Following 2 doses of intravenous immune globulin and 6 more doses of platelets over hospital days 3 and 4, a platelet count above 40,000/μL was sustained. Serum samples returned positive for presence of vancomycin-dependent platelet-reactive IgG antibodies supporting a diagnosis of vancomycin-induced immune thrombocytopenia (VIT). Vancomycin was added to the patient’s allergy list prior to discharge home on hospital day 7 with platelet count recovery to 158,000/μL.
Discussion:
Thrombocytopenia is a common hematologic condition seen in hospitalized patients. However, quickly determining an exact etiology may be challenging given the numerous potential causes. The incidence of drug induced thrombocytopenia is not well delineated given the difficulty in establishing a direct link between this condition and the multitude of prescribed drugs that can be associated. Moreover, vancomycin may be overlooked as a potential etiology in patients with bacterial sepsis and patients receiving heparin products.
Previous reports suggest VIT results in nadir platelet counts 8 days following vancomycin initiation with a median nadir 93% below baseline. A platelet count return to at least 150,000/μL was reported an average of 7.5 days following vancomycin discontinuation. To our knowledge, this case is the first report of VIT to demonstrate a decline to undetectable platelet counts.
Conclusions:
Vancomycin-induced thrombocytopenia may have life threatening consequences. Prompt recognition and rapid discontinuation of vancomycin results in earlier diagnosis and decreased duration of severe thrombocytopenia. The availability of confirmatory diagnostic testing allows hospitalists to better inform patients and prevent vancomycin re-exposure.