Case Presentation: A 71-year-old woman who initially presented with sepsis from MSSA bacteremia was found to have an acute splenic infarct as well as a splenic artery pseudoaneurysm that was managed by coil embolization. She was discharged on a 4-week course of cefazolin for the treatment of her MSSA bacteremia. Two weeks later, she was re-hospitalized in the setting of worsening tachycardia. Workup identified a splenic abscess with splenic vein thrombosis as well as newly diagnosed paroxysmal atrial fibrillation. She was initially started on apixaban with lead-in dosing for the treatment of venous thromboembolism. Two days after initiation, the patient began endorsing generalized pruritis. Physical exam revealed a progressive non-blanching palpable purpura with highest density on the lower back, with extension to the posterior thighs and calves bilaterally, as well the upper extremities and face. A comprehensive workup to evaluate for infectious etiology, malignancy and connective tissue diseases was unrevealing. As the patient had already been on cefazolin for 2 weeks prior to symptom development, the likelihood of cefazolin-mediated drug reaction was low. Thus, apixaban was discontinued and a skin punch biopsy was performed, demonstrating early leukocytoclastic vasculitis. The skin lesions resolved almost fully three days after discontinuation of apixaban without additional treatment. The patient was subsequently transitioned to rivaroxaban without any complications or recurrence of rash.
Discussion: Leukocytoclastic vasculitis describes a small vessel immune-mediated vasculitis that presents with palpable purpura. Cases in association with oral anticoagulants have been well documented, but only a handful related specifically to apixaban have been identified. Those cases demonstrated a variable interval between exposure to apixaban and onset of rash, typically ranging from 7-21 days. In our case, apixaban was the only new medication to have been started within a two-week interval, so suspicion was high that it was the cause of an apixaban-mediated reaction. In more complex cases than the one presented here, however, leukocytoclastic vasculitis may be more difficult to identify early. As apixaban use continues to increase, it is important that clinicians consider underreported complications of apixaban, like leukocytoclastic vasculitis, which could allow for earlier diagnosis and management.
Conclusions: Given the increasing use of apixaban in the primary care setting, it is important for general internists to recognize unusual complications, such as leukocytoclastic vasculitis.