Abstract 12- 1500-1515
Category: Clinical

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

  1. Description of brain pathological features in patients with CHD
  2. Cerebral hypoperfusion is the main cause of the brain pathology in CHD patients

 

Presenter

Dr. Alturkustani is a Neuropathologist in King Abdulaziz University, Jeddah, Saudi Arabia

Authors

Murad A. Alturkustani 1,2,3, Linda J. Szymanski 2

1 King Abdulaziz University, Jeddah, Saudi Arabia

2 Children’s Hospital Los Angeles, Los Angeles, USA

3 Western University, London, ON, Canada

Target Audience:
Pathologists, Residents, Medical Students

CanMEDS:
Medical Expert (the integrating role), Health Advocate, Scholar

Brain pathology in patients with congenital heart disease

Abstract

Brain pathology in patients with congenital heart disease (CHD) are associated with neurodevelopmental delay. Imaging studies support vascular etiology for both white and gray matter lesions. In this retrospective study, we describe the pathological changes in the brains of patients with CHD. The last 20 autopsy cases in patients with CHD at our institution were retrieved and the clinical and the autopsy report were reviewed. The available H&E, special, and immunostains were evaluated and at least one section from each case was stained with GFAP, APP, and HLA-DR. Five control cases included telencephalic leukoencephalopathy (3) and no significant pathological changes (2). The following histological features were assessed: necrotic cells in cortex, hippocampus and the cerebellum; APP and GFAP staining pattern, and presence of focal lesions and amphophilic globules. Twenty patients (10 males, 10 females) were identified with age range of 2 weeks – 19 years. The pathological findings are as follow: 8 cases had changes consistent with acute global hypoperfusion, 5 cases showed features consistent with chronic global hypoperfusion, 3 cases showed focal white matter lesions (1 secondary, to septic emboli), 4 cases with only widespread gliosis, one case with only old focal neuronal loss in dentate gyrus, and one with no significant changes. Subarachnoid hemorrhages were present in 5 cases and germinal matrix hemorrhage in 3 cases. In conclusion, most of the pathological changes could be explained by cerebral hypoperfusion and better techniques to improve the cerebral perfusion are warranted in the management of these patients.