To report a case of bilateral malarial retinopathy secondary to uncomplicated Plasmodium vivax malaria. A 45-year-old male patient presented with sudden onset of diminution of vision both eyes and was treated for P. vivax malaria 1 week before the ocular symptoms. Dilated fundus examination revealed multiple intraretinal (dot-blot, flame shaped) hemorrhages, cotton-wool spots, and areas of retinal whitening predominantly involving the posterior pole both eyes, with features being more severe in left eye. Optical coherence tomography revealed bilateral subfoveal neurosensory detachments. Retinopathy is typically rare in the settings of P. vivax malaria, albeit commonly seen in patients with cerebral malaria (Plasmodium falciparum).
[Ophthalmic Surg Lasers Imaging Retina. 2021;52:50–51.]
A 45-year-old male presented to us with the complaints of sudden onset painless diminution of vision both eyes (left more than right) for more than 10 days. Medical records revealed that 2 weeks prior to the onset of ocular symptoms, he was treated with intramuscular injection Arteether (3 days) for high-grade fever secondary to Plasmodium vivax malaria (based on microscopy and rapid diagnostic test positivity). Blood reports denoted a normal haemoglobin, total platelet count, blood sugar, coagulation profile, and serum glucose-6-phosphate dehydrogenase (G6PD) enzyme levels. Blood pressure at presentation was 122/78 mm Hg and there was no history of hypertension. Best-corrected visual acuity at presentation was 20/20p in the right eye (OD) and counting finger at 1m in the left eye (OS). Intraocular pressures were 16 mm Hg in both eyes (OU), with unremarkable anterior segments under slit-lamp. Dilated fundus examination revealed multiple intraretinal hemorrhages (dot-blot, flame shaped), cotton-wool spots, and areas of retinal whitening predominantly involving the posterior pole OU (Figures 1a and 1b). Retinal whitening was more pronounced in OS surrounding fovea along with segmentation of blood columns (cattle trucking of veins) in the superior arcade vessels. (Figure 1b, inset) Optical coherence tomography passing through fovea showed inner retinal hyper reflectivity and thickening with subfoveal neurosensory detachment OU. (Figures 1c and 1d) Based on clinical and investigational finding a diagnosis of both eyes malarial retinopathy was made and patient was planned for OU intravitreal triamcinolone injection.
Color fundus photo of right eye (a) shows multiple intraretinal (dot-blot, flame shaped) hemorrhages, cotton-wool spots, and areas of retinal whitening predominantly involving the posterior pole in both eyes. In addition, left eye (b) also shows severe retinal whitening in the macular area. On close look, segmentation of blood columns (cattle trucking of veins) in the superior arcade vessels (inset) can be noted. Optical coherence tomography (horizontal line scan) of both eyes (c, d) shows hyperreflectivity of inner retinal layers and neurosensory detachment at fovea, features being more pronounced in the left eye (d).
Malaria retinopathy is typically seen in patients with cerebral malaria primarily caused by Plasmodium falciparum, predominantly affecting children. The pathological mechanism which precipitates retinopathy in the setting of severe malaria is the sequestration of parasitized erythrocytes in the retinal microvasculature causing hypoxia and secondary ischemic retinopathy.1 Beare et al. in 2006 described retinopathy signs in malaria that comprise four main components: a) retinal whitening (macular or peripheral); b) vessel changes (manifest as discoloration of retinal vessels to orange or white, mainly in the peripheral fundus, either discrete sections of vessels, or peripheral trees; white or orange tramlining within larger vessels in continuous or interrupted manner, delineating an apparently narrowed blood column; whitening of retinal capillaries and post-capillary venules), C) retinal hemorrhages (typically white-centered, intra-retinal, blot hemorrhages), and D) papilledema (not specific to malaria, generally accompanies retinal features of cerebral malaria in a proportion of cases).2,3 The most remarkable finding in the setting of P. vivax malaria is reported to be the presence of retinal hemorrhages.4,5 The presence of retinal signs in vivax malaria is reported to be associated with female sex, anemia, and jaundice.5 The incumbent case report challenges the established paradigm of P. vivax causing benign disease with evidence suggesting that P. vivax itself can cause severe retinopathy. Although retinal toxicity has been reported with antimalarial agents like hydroxychloroquine (outer retinal damage) and quinine poisoning (ganglion cell layer damage) there are no reports of Artemisinin related retinopathy in literature hitherto.
Our case is unique in the sense that the patient did not have any cerebral involvement and the causative species was Plasmodium vivax. Other possible explanation of retinopathy is development of hemolytic anaemia, which could be due to the hemolysis by the parasite per se or in patients with deficient serum G6PD enzyme, where antimalarials precipitates hemolysis.
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