LAUSR

Introduction: In this case we describe an uncommon eosinophilic predominant ALL that presented with a hypereosinophilic infiltrative myocarditis. Description: An 11 year old male presented to the ED with vomiting, altered mental status and fevers to 102 F for 4 days. He was intubated for airway protection and started on an epinephrine drip for fluid refractory shock. Labs significant for WBC 103 with 82% eosinophils, platelets 22, potassium 5.7 mEq/L, phosphorus 6.7 mg/dL, and LDH 1178 IU/L. Received cefepime, rasburicase, FFP, platelets, and transferred to PICU. A central line, dialysis catheter, and arterial line were placed. Plasmapheresis was started due to hyperviscosity concerns. Bone marrow biopsy revealed B-cell ALL with 90% cellularity, 64% blasts and 26% eosinophils. High dose steroids were initiated. CT chest revealed abnormal cardiac enhancement with presence of a 1 cm aneurysm near the apex of the left ventricle and a small thrombus in the right ventricle. Echocardiogram revealed low-normal systolic function (EF 56%) with stippled myocardium, consistent with a diffuse infiltrative process. EKGs showed persistent Right Bundle Branch Block, global low voltages, and diffuse ST depression. Troponin peaked at 64 ng/ml, and downtrended with improvement in hypereosinophilia. Milrinone was initiated as an adjunct to epinephrine for afterload reduction and increased lusitropy. Patient was extubated on hospital day (HD) 11 and transferred to floor on HD 15. Anthracyclines were not administered given his tenuous cardiac function. He was discharged home on HD 44 and is doing well. He continues on chemotherapy with the potential to add anthracyclines in the future if his cardiac status permits. Discussion: ALL with hypereosinophilia is reported in < 1% of ALL cases and hypereosinophilic myocarditis at presentation is very uncommon. Eosinophilic infiltration can lead to myocardial inflammation, cell death, and fibrosis; consequences include systolic and diastolic dysfunction, and restrictive hemodynamics. This patient required vasoactive support to maintain cardiac output, and ultimately had improvement in myocardial function with reduction in hypereosinophilia. This diagnosis should be considered in patients presenting with symptoms of impaired cardiac contractility who have peripheral eosinophilia.