Ethambutol Effect on Retinal and Optic Nerve Structural Changes in Toxic Optic Neuropathy Case: A Literature Review

Introduction: Ethambutol (EMB) is one of the first-line antituberculosis drugs that reported to cause toxic effects on the eye structure. This study aims to elucidate the histological mechanism of retinal and optic nerve damage in toxic optic neuropathy cases.Reference Sources: The literature search was conducted in the PUBMED and MEDLINE databases using the latest publication of the 2012-2022 series.Studies Selection: The observational and randomized controlled trial studies analyzing the effect of ethambutol on retinal nerve fiber layer, retinal ganglion layer, inner cell plexiform layer thickness, optic nerve tissue, best-corrected visual acuity (BCVA), color perception, visual evoked response, and patients' visual field were included.Data Extraction Method: Articles that met the inclusion criteria underwent a specific evaluation, whereby the main focus was the ethambutol on retinal and optic nerve tissue.Results: The results showed that ethambutol affects the thinning of the Retinal Nerve Fiber Layer (RNFL), decreasing the amount of Ganglion Cells and changing the optic nerve's histological function by damaging the mitochondria and axonal fiber.Conclusion: It was concluded that ethambutol has adverse effects on retinal and optic nerve tissue due to several mechanisms and significantly affects the patient's visual outcome.

Toxic Optic Neuropathy Caused by Chlorfenapyr Poisoning

PURPOSE: To report a case of toxic optic neuropathy caused by chlorfenapyr ingestion accompanied by central nervous system involvement. CASE SUMMARY: A 44-year-old female visited our clinic complaining of reduced visual acuity in both eyes for 7 days. She had ingested a mouthful of chlorfenapyr for a suicide attempt 2 weeks prior to the visit. Gastric lavage was performed immediately after ingestion at the other hospital. Her best-corrected visual acuity was finger count 30 cm in the right eye and hand motion in the left eye. Both pupils were dilated by 5.0 mm and the response to light was sluggish in both eyes. A relative afferent pupillary defect was detected in her left eye. Funduscopy revealed optic disc swelling in both eyes. Magnetic resonance imaging of the brain showed a symmetric hyper-intense signal in the white matter tract including the internal capsule, corpus callosum, middle cerebellar peduncle, and brainstem. The patient was diagnosed with toxic optic neuropathy induced by chlorfenapyr ingestion, and underwent high-dose intravenous corticosteroid pulse therapy. Three days later, the best-corrected visual acuity was no light perception in both eyes. Three months later, optic atrophy was observed in both eyes. Optical coherence tomography revealed a reduction in the thicknesses of the retinal nerve fiber layer and ganglion cell and inner plexiform layer in the macular area. CONCLUSIONS: Ingestion of even a small amount of chlorfenapyr can cause severe optic nerve damage through the latent period, despite prompt lavage and high-dose steroid treatment.

Baseline retinal nerve fiber layer thickness and visual outcomes of eyes with ethambutol toxic optic neuropathy

Objectives@#To determine the retinal nerve fiber layer thickness (RNFL) in eyes with ethambutol-induced toxic optic neuropathy (ETON) at the time of diagnosis and to describe the visual outcomes at 1, 3, and 6 months after discontinuation of ethambutol@*Methods@#This was a retrospective chart review of 8 patients (15 eyes) diagnosed with ETON that had RNFL thickness measurements using Cirrus® spectral-domain optical coherence tomography (OCT) at the time of diagnosis. Visual function was measured on initial visit and at 1, 3, and 6-month follow-up. Snellen visual acuity was converted to logMAR. Color vision was measured using Ishihara 14-plate test chart. @*Results@#The mean duration from commencement of ethambutol intake to onset of visual symptoms was 16 weeks (range: 8-24). While, the mean duration from onset of visual symptoms to discontinuation of ethambutol was 4 weeks (range: 2-14). The mean global RNFL thickness at time of diagnosis was 101.2 ± 17.0 microns. Mean RNFL in the temporal, superior, nasal, and inferior sectors were as follows: 79.2 ± 15.4, 119.7 ± 27.9, 71.7 ± 9.2, and 136.7 ± 25.8 microns. Global and sectoral RNFL thicknesses were either normal or thick when compared to age-matched normal database. No eye displayed global or sectoral RNFL thinning. Mean baseline visual acuity and color vision were logMAR 1.2 and 5 plates, respectively. At 1, 3, and 6 months after discontinuation of ethambutol, mean visual acuity and color vision were 0.96 and 6, 0.63 and 11, and 0.44 and 13, respectively.@*Conclusion@#Patients with early ETON have normal or thick RNFL at time of diagnosis. They display good visual recovery 6 months following discontinuation of ethambutol.

A Case of Optic Neuropathy Associated with Methyl Bromide Intoxication

PURPOSE: In this study, a case of toxic encephalopathy and optic neuropathy due to methyl bromide poisoning is reported. CASE SUMMARY: A 31-year-old male presented with dysarthria, gait disturbance and bilateral visual impairment. He was treated with intravenous methylprednisolone for bilateral optic neuritis 1 year prior. He previously worked in a fumigation warehouse and was exposed to methyl bromide in the past 3 years. His corrected visual acuity was 20/30 in both eyes. The patient had reduced color vision and enlarged central scotoma in both eyes. His mentality was alert but exhibited slow response, ataxia and dysarthria. Brain magnetic resonance imaging (MRI) revealed high signals in the brainstem, cerebellum and midbrain. His serum and urine methyl bromide concentrations were significantly elevated. The patient was treated with intravenous methylprednisolone 1.0 g/day for 5 days. MRI showed resolution of the multiple brain lesions observed previously. Ten days after steroid therapy, his visual acuity was 20/20 in both eyes and his neurologic manifestations were completely recovered at 2 months after treatment. CONCLUSIONS: Taking a detailed occupational history is necessary in patients with optic neuropathy. The probability of toxic optic neuropathy should be considered when patients are exposed to toxic materials.

Toxic optic neuropathy: An unusual cause.

A 60‑year‑old woman with a history of chronic alcoholism and tobacco use presented with the complaint of a painless decrease in vision in both eyes. She lost vision first in the left eye then in the right eye. She admitted consuming at least one 16 ounce bottle of over the counter mouthwash daily and denied consumption of any other alcohols, methanol, or antifreeze. She stated that her vision had been continuing to deteriorate in both eyes. Her best‑corrected visual acuity was 4/200 in each eye. Color vision was nil in each eye. Her pupils were sluggish bilaterally, and her optic discs were flat and hyperemic with peripapillary hemorrhages. Her visual fields revealed central scotomas bilaterally. The magnetic resonance imaging of the brain and lumbar puncture were within normal limits. Antinuclear antibody, human leukocyte antigen‑B27 genotyping, and B12 were normal; serum thiamine was low. While continuing to ingest mouthwash, her vision decreased to count fingers at 2 feet, and maculopapillary bundle pallor developed. She was started on folate and thiamine supplementation. Once she discontinued mouthwash, her vision improved to 20/400 bilaterally, and her central scotomas improved. This case demonstrates an alcoholinduced toxic optic neuropathy from mouthwash ingestion with some visual recovery after discontinuation of the offending agent.

A rare case of toxic optic neuropathy secondary to consumption of neem oil.

A 35-year-old female was referred to our hospital with bilateral loss of vision of two days duration. She gave history of consumption of about 150 ml of neem oil five days back. Examination revealed no perception of light in both eyes. Both pupils were dilated and sluggishly reacting to light. Her fundus examination showed bilateral hyperemic, edematous discs and also edema extending along the superior and inferior temporal vascular arcade. Magnetic resonance imaging (MRI) scan showed bilateral putaminal regions with altered signal, hypointensities in T1-weighted images, hyperintensities on T2-weighted, images and hyperintense on Fluid Attenuation Inversion Recovery (FLAIR) images suggestive of cytotoxic edema due to tissue hypoxia. Her vision improved to 20/200 in both eyes with treatment after two months. This is the first case report of such nature in the literature to the best of our knowledge.

Toxic optic neuropathy.

Toxic optic neuropathy (TON) is a disease entity which is not only underdiagnosed, but also often diagnosed at a stage when recovery of vision is not possible. This article gives an overview of common causes, clinical features, and management of TON.

Evaluation of VEP in Optic Nerve Diseases and Amblyopia

We performed full field pattern reversal VEP using UTAS-E 2000, in 87 eyes of the 70 patients with amblyopia(14 eyes) and optic nerve diseases; optic neuritis(21 eyes), optic nerve atrophy(23 eyes), toxic optic neuropathy(15 eyes) and optic nerve injury(14 eyes) from December 1993 to July 1994. This study was carried out to evaluate the relationship of the visual acuity with P1 amplitude, P1 latency, and to compare the latency of P1, and P1-N2 amplitude to each disease group and the normal groups. There was no correlation between the visual acuity and P1 latency, but significant correlation between the visual acuity and P1 amplitude(p<0.01). In the P1 implicit time, optic neuritis, optic nerve atrophy and toxic optic neuropathy patients presented marked delay and amblyopia patients presented moderate delay, but there was no other significant difference in each disease group. Over 50% of each disease group except amblyopia presented P1 destruction. Therefore, the authers concluded that P1 amplitude might not be good parameter in diagnosis of the optic nerve disease because of its variability to the visual acuity, but P1 latency and P1 destruction could be good parameter.