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.