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Abstract
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 in-gested 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.
References
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Figure 1.
Ocular findings at initial presentation: fundus photographs, optical coherence tomography (OCT), and pattern visual evoked potential (VEP). (A) Optic disc swelling is observed in both eyes on color fundus photography. (B) OCT shows optic disc swelling and thinning of the ganglion cell and inner plexiform layers in both eyes. (C) Pattern VEP shows delayed P100 latency in the right eye and decreased P100 amplitude in the left eye. ONH = optic nerve head; RNFL = retinal nerve fiber layer; OD = oculus dexter; OS = oculus sinister; OU = oculus uterque; TEMP = temporal; SUP = superior; NAS = nasal; INF = inferior; S = superior; N = nasal; I = inferior; T = temporal; IPL = inner plexiform layer; C/D = cup/disc; GCL = ganglion cell layer.
Figure 2.
Orbit and brain magnetic resonance image at initial presentation. (A) Edematous optic nerve, especially optic nerve sheath enhancement is demonstrated in axial T1-weighted fat-suppressed gadolinium-enhanced image and coronal T2-weighted fat-suppressed image. (B) Axial diffusion-weighted image shows hyperintense signal in white matter tract including internal capsule, corpus callosum, middle cerebellar peduncle and brainstem.
Figure 3.
Ocular findings at 3 months after the initial presentation: fundus photographs, optical coherence tomography and flash visual evoked potential (VEP). (A) Color fundus photography shows both optic discs presenting atrophic change. (B) The thickness of superior and inferior retinal nerve fiber layer is decreased, and ganglion cell and inner plexiform layer thinning is observed in all sectors. (C) Flash VEP shows low P100 amplitude in both eyes. ONH = optic nerve head; RNFL = retinal nerve fiber layer; OD = oculus dexter; OS = oculus sinister; OU = oculus uterque; TEMP = temporal; SUP = superior; NAS = nasal; INF = inferior; S = superior; N = nasal; I = inferior; T = temporal; IPL = inner plexiform layer; C/D = cup/disc; GCL = ganglion cell layer.
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