April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Abnormalities of Fundus Fluorescein Angiography in Cerebral Malaria - A Sequence of Vascular Changes
Author Affiliations & Notes
  • S. J. Glover
    College of Medicine, Blantyre, Malawi
  • T. Taylor
    Blantyre Malaria Project, Blantyre, Malawi
  • M. E. Molyneux
    College of Medicine/ Malawi-Liverpool-Wellcome-Trust, Blantyre, Malawi
  • Footnotes
    Commercial Relationships  S.J. Glover, None; T. Taylor, None; M.E. Molyneux, None.
  • Footnotes
    Support  the Wellcome Trust provided a grant to buy the digital camera system and other support
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 5415. doi:
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      S. J. Glover, T. Taylor, M. E. Molyneux; Abnormalities of Fundus Fluorescein Angiography in Cerebral Malaria - A Sequence of Vascular Changes. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5415.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To study the retinal circulation in children with malarial coma. The brain and retina are embryologically and structurally related. Previous studies in children with cerebral malaria have shown retinal changes to be prognostic and diagnostic. Study of the retina is the only way to visualise an infected CNS microvasculature in vivo.

Methods: : With parental informed consent we performed fluorescein angiograms within 6 hours of admission on comatose children admitted with a clinical diagnosis of cerebral malaria during the malaria high transmission season jan-june 2008. Angiography was repeated if the child remained unconscious for 24 hours.

Results: : We studied 52 patients. In 2 patients vessel changes occurred in a sequence. On or soon after admission there were orange vessels the correlate of which on the angiogram was filling defects, which are lesions attached to the vessel wall and occupying part of the vessel lumen. By day 2 the orange vessels resolved leaving behind white vessels which were more limited in extent, the correlate of these white vessels was complete non perfusion of the vessel. Areas of retinal whitening present on day 1 became more obvious by day 2, these correlated to retinal non perfusion. By day 4 the retinal non perfusion had almost totally resolved. 4 unusually old patients had atypical retinal vessel whitening affecting the vessel wall along long segments. 3 of these 4 patients were HIV positive and the 4th had lost their mother and all siblings suggesting HIV (testing declined). The appearance in these 4 patients was similar to retinal vessel changes associated with syphilis in HIV positive adults, but reliable syphilis serology was not available. 2 patients had cystoid macular oedema [CMO] associated with multiple small leaks resolving in 2 days. 3 patients with gross leaking all died.

Conclusions: : We suggest that intravascular filling defects represent parasitized red blood cells adhering to blood vessel walls [ sequestration]. The resolution of areas of retinal non perfusion raises the possibility that patients may be at risk of re-perfusion injury. A similar process within the brain could contribute to the neurological sequelae that occur in some patients. This risk applies to all survivors with significant areas of retinal whitening, not just those with the sequence of events detailed above. This possibility warrants further study, as protective agents given early in cerebral malaria could prevent later reperfusion injury. Additional infections, should be considered in patients with extensive vessel-wall whitening.

Keywords: retina • blood supply • edema 

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