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A section examined from the optic nerve showed mild edema. No demyelination or axonal necrosis was identified in the sections examined (Hematoxylin and eosin stain, magnification: 400x).
Source publication
Aims and objective
This study describes postmortem and histopathological findings to understand the internal progression of methanol poisoning. The study also aims to examine clinical, biochemical, and histological changes seen with methanol poisoning.
Materials and methods
The study describes the methanol poisoning tragedy that occurred in Februar...
Contexts in source publication
Context 1
... pH and bicarbonate levels among hospital deaths were 6.61 mmol/l and 6.18 mmol/l, respectively. Biochemical investigations revealed features of acute renal failure among those who died in the hospital (Tables 1, 2). ...
Citations
... Recent outbreaks of mass methyl alcohol poisoning were observed in Tehran, Saudi Arabia, and India [25][26][27]. The descriptions of these poisonings differ primarily in the ratio of poisoned women to poisoned men. ...
... The descriptions of these poisonings differ primarily in the ratio of poisoned women to poisoned men. The outbreak we described included 3 women out of 19 dead, while in a similar case in India, only men were poisoned [27]. In the case of the outbreak in Saudi Arabia, there were almost as many women (4) as men (5) [26]. ...
Methanol poisonings caused by drinking industrial alcohol remain a severe problem worldwide. Education on types of alcohol and their harmfulness and legal regulations limiting the industrial alcohol trade seem to be the keys to reducing the number of poisonings. Methanol distribution in different tissues after absorption is not well understood. This research aimed to quantify the methanol and formic acid distribution in body fluids and tissue material in post-mortem samples collected from 19 fatal victims of massive intoxication with industrial alcohol in the Silesia Region (Poland) who died between April and June 2022. The samples were analyzed using a gas chromatography–flame ionization detector (GC-FID), and correlation coefficients for methanol and formic acid were determined. The results show a wide distribution of methanol and formic acid in human post-mortem biological fluids (blood, urine, vitreous humor, bile, and cerebrospinal fluid) and tissues (muscle, kidney, liver, spleen, lung, and brain). The strongest correlation for methanol concentration in blood and body fluids/tissues was obtained in the cerebrospinal fluid (r = 0.997) and for formic acid in muscle tissue (r = 0.931). The obtained results may be a valuable tool in toxicological analysis and improve medical standards of early diagnosis and targeted treatment.
... Terefore, methanol-induced optic neuropathy belongs to acquired mitochondrial optic neuropathy, although other mechanisms, including oxidative stress and proinfammatory cytokines, are also reported. Optic nerve histopathology showed mild edematous changes [23] and degeneration of axons and glial cells [2]. Demyelination or axonal necrosis changes are inconsistent in diferent studies [23,24]. ...
... Optic nerve histopathology showed mild edematous changes [23] and degeneration of axons and glial cells [2]. Demyelination or axonal necrosis changes are inconsistent in diferent studies [23,24]. Accompanying damage to the retina may involve all its layers [2]. ...
Purpose:
To show the clinical characteristics, identify the magnetic resonance imaging (MRI) and optical coherence tomography (OCT) features, and observe the visual outcome of methanol-induced optic neuropathy.
Methods:
Clinical data were retrospectively collected from in-patients diagnosed with methanol-induced optic neuropathy in the Neuro-Ophthalmology Department of the Chinese People's Liberation Army General Hospital from January 2016 to January 2021.
Results:
Eight patients were included in this study. The exposure time was 6-34 h for ingestion, 3-4 months for inhalation, and more than ten years for skin absorption. All patients demonstrated bilateral acute visual impairment. Seven of eight patients had other accompanying systemic symptoms. Seven of eight patients demonstrated optic nerve lesions in MRI, and five presented with a hyperintense T2 signal in a "central" type. OCT showed the macular ganglion cell layer and inner plexiform layer (mGCL-IPL) thinning before the peripapillary retinal nerve fiber layer (pRNFL) thinning. The visual improvement was achieved transiently for seven of eight patients after treatment. One patient with a mitochondrial DNA mutation maintained a bilateral no-light perception (NLP) from the onset to the last visit. All patients had poor visual prognoses, with either light perception or NLP.
Conclusions:
Methanol-induced optic neuropathy is a rare bilateral optic neuropathy with a poor visual outcome. A centrally hyperintense T2 signal of the optic nerve is common in methanol-induced optic neuropathy. The thinning of the mGCL-IPL is more sensitive than that of the pRNFL for early diagnosis. A mitochondrial genetic defect may be a predisposing factor for methanol-induced optic neuropathy.
