A late presentation of ocular quinine toxicity managed with a combination of vasodilatory treatments

Vusirikala, Bharati; Williams, Tranettea; Ram, A R Raghu

doi:10.1038/sj.eye.6701631

Cited by 6 publications

(2 citation statements)

References 6 publications

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“…Other techniques like forced acid diuresis, charcoal column haemoperfusion, haemodialysis and exchange transfusion or techniques attempting to reverse retinal vasoconstriction like intravenous sodium nitrite, carbon dioxide inhalation, retrobulbar vasodilators, anterior chamber paracentesis and Stellate ganglion block have been unsuccessful. Vascular dilatation therapy and use of steroids have shown variable results [6]. We thus used steroids and nifedipine (as vasodilator) in our patient, though it may not have contributed to the improvement.…”

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confidence: 84%

A Case of Quinine Induced Blindness

Sagar

Mukherji

2010

Medical Journal Armed Forces India

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confidence: 84%

A Case of Quinine Induced Blindness

Sagar

Mukherji

2010

Medical Journal Armed Forces India

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“…In early 2007, the US Food and Drug Administration restricted the use of quinine solely to the treatment of malaria. Quinine has long been known to be toxic to the eye even at therapeutic levels, causing symptoms such as loss of vision, reduced color vision, and reduced visual fields 3,4. Most visual symptoms occur after a quinine dose greater than 4 g and death can occur with doses exceeding 8 g 5…”

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confidence: 99%

Optical coherence tomography findings of quinine poisoning

Christoforidis

Ricketts

Loizos

et al. 2011

OPTH

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PurposeTo report a case of acute quinine poisoning, document acute and chronic macular changes with optical coherence tomography imaging and fluorescein angiography (FA), and to review the literature on ocular toxicity of quinine.MethodsA 32-year-old white female presented to our Emergency Department after ingesting over 7.5 g of quinine. She underwent a complete ophthalmologic examination, fluorescein angiography, Stratus time-domain optical coherence tomography (OCT), and electroretinography at 72 hours and 15 months postingestion. Stratus time-domain and Cirrus spectral-domain OCT, fundus autofluorescence, and FA were obtained at 28 months postingestion.ResultsFluorescein angiography at 72 hours postingestion revealed normal filling times and vasculature. OCT showed marked thickening of the inner retina bilaterally. At 15 and 28 months follow-up, fundus photography and fluorescein angiography demonstrated optic nerve pallor, severely attenuated retinal vessels while OCT showed inner retinal atrophy. Fundus autofluorescence did not reveal any retinal pigmentary abnormalities.ConclusionsQuinine toxicity as seen by OCT reveals increased thickness with inner retinal hyperreflectivity acutely with development of significant retinal atrophy in the long-term. Fundus autofluorescence reveals an intact retinal pigment epithelial layer at 28 months. These findings suggest that quinine poisoning may produce a direct toxic effect on the inner retina in the acute phase resulting in long-term retinal atrophy.

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Chloroquine and Quinine

Jones¹

2017

Critical Care Toxicology

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A late presentation of ocular quinine toxicity managed with a combination of vasodilatory treatments

Cited by 6 publications

References 6 publications

A Case of Quinine Induced Blindness

A Case of Quinine Induced Blindness

Optical coherence tomography findings of quinine poisoning

Chloroquine and Quinine

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