2025 – Abstract 11

by | Sep 24, 2025 | 2025 Abstracts

Abstract 11
Category: Clinical Science

At the end of the session, participants will be able to:

  1. Define the classification scheme of hypereosinophilic syndrome (HES).
  2. List the potential central and peripheral nervous system manifestations of HES.
  3. Discuss the potential pathologic findings in ischemic infarcts associated with HES.

COI Disclosure:

None to disclose.

Presenter

Karina Martin is a PGY-5 Neuropathology Resident at the University of British Columbia.

Karina C. Martin MD1, Dan Straathof MD2, Chi Lai MD3, Harry V. Vinters MD4

  1. Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC
  2. Fraser Health Department of Laboratory Medicine & Pathology, Royal Columbian Hospital, New Westminster, BC
  3. Providence Health – St. Paul’s Hospital, University of British Columbia, Department of Pathology & Laboratory Medicine, Vancouver, BC
  4. Departments of Pathology and Laboratory Medicine (Neuropathology) and Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1763, USA

Target Audience:
Pathologists, Residents, Medical Students

CanMEDS:
Medical Expert (the integrating role), Collaborator, Scholar, Professional

Ischemic stroke in hypereosinophilic syndrome: a clinicopathologic study of two cases

Abstract

Ischemic stroke is a rare complication of hypereosinophilic syndrome (HES). Manifestations of stroke in HES have been described mainly in the radiologic literature; however the pathologic characterization of central nervous system (CNS) involvement in HES is limited. We describe two patients who presented to hospital with systemic symptoms and were found to have peripheral blood hypereosinophilia. Thorough investigations for primary and secondary etiologies of hypereosinophilia were negative. Both patients subsequently suffered catastrophic strokes and died despite therapy and resuscitative efforts. Pertinent general autopsy findings in both cases included the presence of intraventricular cardiac thrombi. Post-mortem neuropathologic examination demonstrated a multi-territorial embolic infarct pattern in Patient 1 and a watershed infarct pattern in Patient 2. Microscopic features included the presence of microabscesses consisting of a disproportionately large number of eosinophils and infarcts associated with blood vessels showing occlusive thrombi with surrounding eosinophils. In summary, we present two post-mortem neuropathologic examinations of patients exhibiting CNS infarcts associated with HES, discuss potential pathomechanisms, and review the literature on this rare entity.