WATERSHED INFARCTION DUE TO ACUTE HYPEREOSINOPHILIA

Abstract

Hypereosinophilia typically results from a parasitic, neoplastic, vasculitic, or allergic cause. However, when elevated blood eosinophil levels (≥1500/μL) persist beyond 6 months and show evidence of organ involvement (other than skin) without identifiable cause, the criteria for idiopathic hypereosinophilia are met. Idiopathic hypereosinophilia can affect multiple organ systems. Up to 65% of patients have neurologic manifestations, including peripheral neuropathy, encephalopathy, or thromboembolic infarction.1 Previously reported thromboembolic events have involved large, intracranial vessels2 and were attributed to the hyperviscous, hypercoaguable state, often accompanied by cardiac dysfunction. We report a patient with acute, severe hypereosinophilia complicated by extensive watershed infarction. Possible mechanistic causes include (1) local thrombus formation from a hyperviscous state or (2) distant microthromboemboli. ### Case report. A 16-year-old, previously healthy male was hospitalized after 2 weeks of cough and 4 days of fever. The initial examination revealed decreased air entry bilaterally. Blood work noted leukocytosis 77.4 × 109/L, with eosinophils 55.3 × 109/L, neutrophils 6.6 × 109/L, and no blasts. Hemoglobin was 115 g/L, and platelets were 154,000 × 109/L. His electrolytes, calcium, phosphorus, uric acid, and renal and liver function tests were normal. Neck and chest CT revealed lymph nodes (≤1.5 cm) and patchy “ground-glass” areas in the …