Clinical Course
We present the case of a 71-year-old male who was admitted for hyperkalemia and symptomatic bradycardia from a missed hemodialysis session due to occlusion of his arteriovenous fistula. He was also diagnosed with Enterobacter bacteremia and started on Cefepime. Shortly before this, he was recently admitted for five days for atrial fibrillation with rapid ventricular rhythm and treated with intravenous amiodarone loading followed by oral maintenance dose. He was discharged three days before the aforementioned admission. On day 2 the labwork revealed worsening thrombocytopenia of 37 K/mm3 was noted (compared to 62 K/mm3 upon previous discharge) and was presumed to be in the context of sepsis. Amiodarone was restarted for atrial fibrillation, and anticoagulation was held due to thrombocytopenia.  On day 3, blood culture showed no growth and all signs of sepsis resolved. Yet, the platelet count went down to 14 K/mm3 at which point, 1 unit of platelet was transfused. Fortunately, there was no evidence of bleeding. Response to transfusion was modest and temporary. Platelet count again decreased to 25 K/mm3 at which point, the hematology team was consulted.
Pseudothrombocytopenia, alcohol abuse, nutritional deficiencies (Vitamin B12 deficiency, folate deficiency), HIV, HCV were ruled out. Heparin induced thrombocytopenia antibody testing by ELISA was negative (O.D. 0.112). Review of peripheral blood smear showed decreased platelet count, but no platelet clumping or schistocytes and few giant platelets were notable. The latter, in addition to mild reactive neutrophilia pointed against the possibility of bone marrow suppression from sepsis. Giant platelets on peripheral blood smear and elevated immature platelet fraction at 20.1% pointed at rapid bone marrow turnover of platelets in the peripheral circulation. Abdominal imaging with CT scan ruled out splenomegaly; liver echotexture supported a functioning liver. Given that platelet count dropped below 20 K/mm3 despite resolution of sepsis, drug induced immune thrombocytopenia secondary to amiodarone was entertained as a working diagnosis. He was on chronic hemodialysis for end stage renal disease and was perceived to be at higher risk of bleeding due to functional coagulopathy from uremia11. Meanwhile, since AITP was a rare possibility, we were reluctant to stop amiodarone immediately for lack of better alternatives and risk of hemodynamic compromise.  Hence, two doses of intravenous immunoglobulin (IVIG) 1mg/kg were administered on Day 11 followed by 1mg/kg oral prednisone maintenance. Amiodarone was eventually discontinued on Day 17 considering AITP as a working diagnosis when platelet nadir reached 14 K/mm3. Platelet recovery occurred in parallel to a peak of 76 K/mm3 on Day 26.
On Day 25, the patient experienced hemodynamic instability in the setting of tachyarrhythmias for which he was cautiously restarted on oral amiodarone due to lack of a better alternative. Two days later, platelet count started worsening and continued to do so until amiodarone was safely weaned off 11 days after restarting it. Thrombocytopenia started recovering the following day lending more credibility to earlier suspicion of an immune mediated amiodarone dependent platelet destruction process. Unfortunately, the patient succumbed to a cardiac arrest before his platelet count could recover fully.