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Year : 2022  |  Volume : 2  |  Issue : 4  |  Page : 926-928

A case of presumed bilateral central retinal artery occlusion following methanol poisoning

1 Department of Ophthalmology, Habib Thameur Hospital, Tunis, Tunisia
2 Department of Medical Assistance, CAMU Hospital, Tunis, Tunisia

Date of Submission02-Feb-2022
Date of Acceptance24-Jun-2022
Date of Web Publication11-Oct-2022

Correspondence Address:
Dr. Maamouri Rym
3, Rue Ali Ben Ayed, 1089 Montfleury, Tunis
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_344_22

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It is well established that methanol poisoning induces commonly acute toxic optic neuropathy. Herein, we describe a case of unusual ocular manifestation. A 35-year-old male presented with painless, bilateral, and simultaneous sudden onset of severe visual loss following methanol poisoning. The visual acuity was 20/200 in the right eye and limited to a finger count in the left eye. Fundus color photography showed a bilateral sub-total central retinal artery occlusion (CRAO). A methanolemia carried out following the hemodialysis returned to 0.2g/l. To the best of our knowledge, this is the first case reporting CRAO after methanol poisoning. Our report under-scores the importance of early ophthalmic examination of patients with acute methanol poisoning and suggests that it could induce acute CRAO because of retinal artery vasospasm.

Keywords: Methanol poisoning, sub-total central retinal artery occlusion, young adult

How to cite this article:
Rym M, Hela M, Nozha B, Monia C. A case of presumed bilateral central retinal artery occlusion following methanol poisoning. Indian J Ophthalmol Case Rep 2022;2:926-8

How to cite this URL:
Rym M, Hela M, Nozha B, Monia C. A case of presumed bilateral central retinal artery occlusion following methanol poisoning. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Nov 27];2:926-8. Available from: https://www.ijoreports.in/text.asp?2022/2/4/926/358169

Methanol poisoning, most of the time, leads to variable optic nerve damage ranging from alterations of the visual field and retrobulbar neuritis to a complete optic atrophy. However, ocular damage generally takes the second place as the vital prognosis is at stake with neurological damage. We report a case where bilateral central retinal artery occlusion (CRAO) was the presenting manifestation of methanol poisoning.

  Case Report Top

A 35-year-old patient with no previous history was hospitalized in intensive care for acute methanol poisoning. When questioned, the patient reported chronic methanol poisoning and had neither a history of visual impairment nor ocular symptoms and never consulted before. For the current episode, the patient had drunk one liter of methanol not associated with other toxic substances, in particular, without ethanol or cocaine. This ingestion was followed by painless, sudden bilateral and severe blindness, followed by an agitation and a coma for which he was intubated and ventilated. An emergency assessment was made, and metabolic acidosis with an increased anion and osmol gap was found with the pH at 7.18 and lactate at 5.6 mmol/l [Table 1]. Management of metabolic acidosis was performed initially with sodium bicarbonate; then, hemodialysis was performed in emergency. A methanolemia was carried out following the hemodialysis and returned to 0.2g/l. Blood and urine toxicity tests came back negative, notably ethanol and cocaine. A cerebral computed tomography scan was performed and returned normal. He received enteral ethanol to competitively inhibit the metabolic breakdown of methanol to formic acid and received adjuvant folate therapy. The patient was then referred to an ophthalmological examination 4 days after the intoxication. In the right eye, the visual acuity was 20/200 and limited to a finger count in the left eye. The slit lamp examination showed a calm anterior segment and eye tone at 14 mmHg in the right eye and 12 mmHg in the left eye. The pupil was reactive to direct and consensual light. Extra-ocular motility was normal. Fundus color photography showed bilateral retinal whitening associated to a bilateral macular cherry red spot; the optic nerve and the peripheral retina were normal [Figure 1]. Fundus fluorescein angiography (FFA) showed normal choroidal filling, the absence of the cilioretinal artery and normal angiographic features supporting a spastic and non-vaso occlusive mechanism corresponding to a transient CRAO [Figure 2]. Optical coherence tomography (OCT) showed a bilateral hyper-reflective macular thickening of the inner layers related to ischemic edema corresponding to a “sub-total” form of CRAO as was categorized by Seong JA et al.[1] [Figure 3]. Echocardiography made in emergency was without any abnormality. The patient was discharged after the improvement of his clinical condition but was lost to follow-up.
Figure 1: Fundus color photography showing retinal edema (ischemic retinal whitening) with a macular cherry red spot on both eyes with a normal-sized vessel

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Figure 2: FFA demonstrating reperfusion and the presence of a mild hyperfluorescence in the center of the foveal avascular zone (white arrow)

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Figure 3: Swept source OCT (DRI Triton, Topcon) scans of right (a, top row) and left eyes (b, bottom row) showing (a and b) marked hyper-reflectivity of the inner retinal layers with a relatively preserved layer-by-layer structure in the inner retina, with a foveolar prominent IS/OS junction – ellipsoid portion and external limiting membrane (indicated by a white arrow) and the sub-retinal fluid. (c and d) Photographic images of fundus with grid graph measurements, indicating an increase of macular thickness. (e and f) Macular thickness map images showing diffuse thickening predominating at the nasal part

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Table 1: Values of different investigations performed at initial presentation in the intensive care unit

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  Discussion Top

In Tunisia, since the first wave of coronavirus disease 2019 and the generalized lockdown, we have seen an increasing number of collective methanol poisoning. In this case, we describe a bilateral central retinal artery occlusion developed as manifestation of methanol poisoning, which to our knowledge has not been previously reported.

Over 162 years after the first case of CRAO described by Albrecht von Graefes in 1859,[2] several publications have been made. The most encountered etiologies are the results of emboli from the carotid origin with an underlying arteriosclerosis disease in older patients.[3] On the other hand, in young adults, the etiologies that have been found are cardiac valvular disease, coagulation abnormalities or embolic conditions such as the example of sickle cell hemoglobinopathies, use of oral contraceptives, systemic lupus erythematosus, vasculitis, hyperhomocysteinemia, hyperlipidemia, and homocystinuria.[4],[5],[6] Its bilateral involvement is unusual. The toxic substance which causes CRAO has been reported for intravenous drug abuse, especially with cocaine.[7] Methanol poisoning, on the other hand, most often leads to a cascade of metabolic events that give rise to formic acid that disturbs the mitochondrial functioning mainly in the retrolaminar or retrobulbar portion of the optic nerve.[8] An anion gap and a low pH (<7.22) were associated to increased mortality,[9] and the visual acuity was correlated with the degree of initial acidosis.[10] Acute methanol poisoning was associated to basal ganglia necrosis, particularly in the putamina documented through brain imaging causing central nervous complications, notably cerebral strokes.[11],[12] The hypothesis of methanol-induced cerebral vasospasm was highlighted by Li et al.,[13] reporting that higher concentrations of methanol raised rapidly and largely the intracellular Ca2+ in cerebral vascular smooth cells that could explain possible cerebral and retinal infracts.

The acute poisoning induces typically a toxic optic neuropathy,[14] but other ocular impairments could be observed, such as a sluggish pupillary reaction, a relative afferent pupillary defect, disc hyperemia, edema, pallor or atrophy, a dilated retinal vessel, and a retinal edema.[9] Our patient did not appear to have any another condition known to cause an acute bilateral CRAO, and most importantly, the decrease of his visual acuity was followed by the ingestion of methanol and concomitant with the comatose phase.

  Conclusion Top

Our report illustrates that methanol poisoning could cause a bilateral central retinal artery vasospasm, and we suggest early ophthalmic examination for patients with acute methanol poisoning. We also suggest that optic atrophy following severe acute methanol poisoning could be secondary to a CRAO not diagnosed promptly because of the lack of early ophthalmic examination and this is understandable because the vital prognosis for these patients is at stake.


The authors have no relevant financial or non-financial interests to disclose.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Seong JA, Se JW, Kyu HP, Cheolkyu J, Jeong-Ho H, Moon-Ku H. Retinal and choroidal changes and visual outcome in central retinal artery occlusion: An optical coherence tomography study. Am J Ophthalmol 2015;159:667-76.  Back to cited text no. 1
Von Graefes A. Ueber Embolie der Arteria centralis retinae als Ursache plotzlicherErblindung. Arch Ophthalmol 1859;5:136-57.  Back to cited text no. 2
Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: Associated systemic and ophthalmic abnormalities. Ophthalmology 2009;116:1928-36.  Back to cited text no. 3
Brown GC, Magargal LE, Shields JA, Goldberg RE, Walsh PN. Retinal arterial obstruction in children and young adults. Ophthalmology 1981;88:18-25.  Back to cited text no. 4
Greven CM, Slusher MM, Weaver RG. Retinal arterial occlusions in young adults. Am J Ophthalmol 1995;120:776-83.  Back to cited text no. 5
Ratra D, Dhupper M. Retinal arterial occlusions in the young: Systemic associations in Indian population. Indian J Ophthalmol 2012;60:95-100.  Back to cited text no. 6
[PUBMED]  [Full text]  
Michaelides M, Larkin G. Cocaine-associated central retinal artery occlusion in a young man. Eye (Lond) 2002;16:790-2.  Back to cited text no. 7
Liesivuori J, Savolainen H. Methanol and formic-acid toxicity-biochemical-mechanisms. Pharmacol Toxicol 1991;69:157-63.  Back to cited text no. 8
Coulter CV, Farquhar SE, McSherry CM, Isbister GK, Duffull SB. Methanol and ethylene glycol acute poisoning- predictors of mortality. Clin Toxical (Phila) 2011;49:900-6.  Back to cited text no. 9
Desai T, Sudhalkar A, Vyas U, Khamar B. Methanol poisoning: Predictors of visual outcomes. JAMA Ophthalmol 2013;131:358-64.  Back to cited text no. 10
Gaul HP, Wallace CJ, Auer RN, Fong TC. MR findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783-6.  Back to cited text no. 11
Lukman FO, Okezie OE, AbdulRazeq AR, Raafat ES, Hanem E, Bappa A. Methanol induced stroke: Report of cases occurring simultaneously in two biological brothers. J Community Hosp Intern Med Perspect 2020;10:265-8.  Back to cited text no. 12
Li W, Zheng T, Wang J, Altura BT, Altura BM. Methanol elevates cytosolic calcium ions in cultured canine cerebral vascular smooth muscle cells: Possible relation to CNS toxicity. Alcohol 1999;18:221-4.  Back to cited text no. 13
Nurieva O, Diblik P, Kuthan P, Sklenka P, Maliska M, Bydzovsky J, et al. Progressive chronic retinal axonal loss following acute methanol-induced optic neuropathy: Four-Year prospective cohort study. Am J Ophthalmol 2018;191:100-15.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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