AJTMH Transactions of the Royal Society of Tropical Medicine and Hygiene
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Am. J. Trop. Med. Hyg., 80(2), 2009, pp. 171
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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Malarial Retinopathy in Cerebral Malaria

Nicholas A. V. Beare*, Simon J. Glover, AND Malcolm Molyneux
St Paul’s Eye Unit, Royal Liverpool University Hospital, Liverpool, United Kingdom; Department of Anatomy, College of Medicine, Blantyre, Malawi; Malawi-Liverpool-Wellcome Trust Clinical Research Programme, College of Medicine, Blantyre, Malawi

A 2.5-year-old Malawian child was admitted in coma and fitting with Plasmodium falciparum infection. He was treated with intravenous quinine, anti-convulsants, and transfused for severe anemia. Ophthalmoscopy revealed discolored retinal vessels within zones of whitening of the retina (Figure 1AGo). Malarial retinopathy is common in African children with cerebral malaria in whom it has diagnostic and prognostic value. One of its specific manifestations is whitening of retinal vessels. The fluorescein angiogram demonstrates that these vessels are occluded (Figure 1BGo). The resultant area of retinal non-perfusion corresponds to the area of retinal whitening.


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  		    FIGURE 1. Panel A is a fundus photograph of the peripheral retina of a child with cerebral malaria showing whitened blood vessels within a zone of whitening of the retina. Panel B is the corresponding fluorescein angiogram demonstrating occlusion of the white blood vessels and resulting ischemia of the retina. This figure appears in color at www.ajtmh.org.

 
Erythrocytes parasitized by P. falciparum cytoadhere to vascular endothelium and each other, sequestering in the microvasculature of the brain, retina, and other organs. Sequestration appears to occlude retinal vessels, and small vessels in the brain at histologic examination. The resultant zones of retinal non-perfusion were unusually large in this child involving much of the peripheral retina. The whitening of the normally transparent retina is thought to be a result of oncotic cellular swelling induced by hypoxia. He remained in coma for 72 hours. A left-sided weakness resolved before discharge with a full recovery and no apparent ill-effects on vision.

Received November 17, 2008. Accepted for publication November 21, 2008.

* Address correspondence to Nicholas A.V. Beare, St Paul’s Eye Unit, Royal Liverpool University Hospital, Prescot Street, Liverpool, L7 8XP, UK. E-mail: nbeare{at}btinternet.com Back

Authors’ addresses: Nicholas A. V. Beare, St Paul’s Eye Unit, Royal Liverpool University Hospital, Prescot Street, Liverpool, L7 8XP, UK, Tel: +44 (0) 151 706-3997, Fax: +44 (0) 151 706-5905, E-mail: nbeare{at}btinternet.com. Simon J. Glover, Department of Anatomy, College of Medicine, Blantyre, Malawi, Tel: +265 (0) 995-0590, Fax: +265 (0) 167-5774, E-mail: simonglover{at}doctors.org.uk. Malcolm Molyneux, Malawi-Liverpool-Wellcome Trust Clinical Research Programme, College of Medicine, Blantyre, Malawi, Tel: +265 (0) 676-444, Fax: +265 (0) 675-774.





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