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In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
Published on: June 8, 2017
Perfusion abnormalities in children with cerebral malaria and malarial retinopathy
Nicholas A V Beare1, Simon P Harding, Terrie E Taylor
1St. Paul's Eye Unit, Royal Liverpool University Hospital, Prescot Street, Liverpool, United Kingdom. nbeare@btinternet.com
Insights
Retinal angiography in children with cerebral malaria (CM) reveals impaired perfusion in most cases, indicating hypoxia and ischemia are key to CM's development. Findings suggest interventions to improve blood flow could benefit patients.
Area of Science:
- Ophthalmology
- Neurology
- Infectious Diseases
Background:
- Cerebral malaria (CM) affects the central nervous system microvasculature.
- Retinal angiography offers in vivo study of this microvasculature.
- Pathophysiology of CM requires investigation.
Purpose of the Study:
- To examine retinal perfusion in children with CM using fluorescein angiography.
- To investigate the pathophysiology of CM through retinal microvasculature assessment.
Main Methods:
- Fluorescein angiography performed on 34 children with CM.
- Angiograms correlated with funduscopic findings.
- Study conducted at Queen Elizabeth Central Hospital, Malawi.
Main Results:
- Impaired retinal perfusion identified in 82% of patients.
- Capillary nonperfusion (CNP) observed in 76%, correlating with retinal whitening.
- Vessel occlusion and intravascular abnormalities noted in 26%.
Conclusions:
- Impaired retinal perfusion is common in pediatric CM, highlighting hypoxia and ischemia.
- Vessel occlusion and filling defects suggest sequestration of infected erythrocytes.
- Interventions improving perfusion or reducing hypoxic injury may benefit CM treatment.
Background:
In patients with cerebral malaria (CM), retinal angiography allows the study of infected central nervous system microvasculature in vivo. We aimed to examine retinal perfusion in children with CM by use of fluorescein angiography to investigate the pathophysiology of CM.
Methods:
We performed fluorescein angiography on children with CM admitted to Queen Elizabeth Central Hospital, Malawi. We related angiograms to funduscopic findings.
Results:
Fluorescein angiography was performed for 34 patients with CM, and impaired perfusion was identified in 28 (82%). Areas of capillary nonperfusion (CNP) were seen in 26 patients (76%). Multiple, scattered areas of CNP were typical and topographically matched to retinal whitening. Larger retinal vessels were occluded in 9 patients (26%) who had associated ischemia. These vessels appeared white on ophthalmoscopy. Intravascular abnormalities were seen in 9 patients (26%), including filling defects and mottling of the blood column. Limited fluorescein leakage occurred in 15 patients (44%) and was not related to angiographic intravascular abnormalities or visible vessel discoloration.
Conclusions:
Impaired perfusion occurs in the retinal microvasculature of most children with CM. This is evidence for hypoxia and ischemia as important components in the pathogenesis of CM. Vessel occlusion and filling defects are likely to be due to sequestration of infected erythrocytes. Interventions which improve perfusion or limit hypoxic injury may be beneficial in CM.
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