Toxins in Neuro-Ophthalmology
Vivek Lal in A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Clinical features of methanol intoxication include nausea, vomiting and abdominal pain. The CNS effects of methanol result from accumulation of formic acid within the optic nerve and leads to flashes of light. It progresses further to scotomas and scintillations. Vision loss is probably caused by interruption of mitochondrial function in the optic nerve which results in hyperemia, edema and optic nerve atrophy. Pupillary response to light is compromised and subsequently lost. Confirmation of diagnosis is by serum methanol level with gas chromatography (>20 mg/dL). Serum levels peak after 60–90 min of ingestion, but these do not correlate with the level of toxicity. Accumulation of formate leads to decrease in pH (<7.2 is a severe intoxication). Imaging findings may be suggestive with bilateral enhancing optic nerves and putaminal necrosis.
Diseases of the Nervous System
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Acute toxicity of methanol is connected with headache, acidosis, circulatory collapse, respiratory failure, and blindness.380,521 Chronic toxicity starts with a decrease of the pupillary light reflex followed by pupil dilatation.399 Subsequently, a loss of acuity occurs. The optic disc and surrounding retina become edematous. Experimentation with monkeys showed accumulation of mitochondria in optic nerve axons. Intracranial pressure is increased in relation to stasis of axonal transport. The ocular action of methanol is associated with its metabolism to formic acid.380,381 When formate is administered to monkeys, gross and microscopic changes in the visual system showed the same changes as seen in human cases of methanol poisoning.
Miscellaneous poisons
Jason Payne-James, Richard Jones in Simpson's Forensic Medicine, 2019
Like ethanol, methanol can cause fatal central nervous system (CNS) depression. Methanol intoxication is an uncommon but serious poisoning. Its adverse effects are due primarily to the impact of its major metabolite formic acid and lactic acid resulting from cellular hypoxia. All of these processes occur in the liver. Formic acid (formate) is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level. Symptoms including abdominal pain and loss of vision can appear a few hours to a few days after exposure, reflecting the time necessary for accumulation of the toxic byproduct. Methanol also causes metabolic acidosis. Methanol poisoning most often occurs after drinking windscreen-washer fluid, but methanol is also used in copy machines and can be found in many other products, even embalming fluid. Methanol poisoning still remains a well-known consequence of ‘moonshine’ liquor ingestion, although this practice is increasingly uncommon. When paediatric poisoning occurs, it is usually the result of having ingested methanol-containing household products. Ingestion of even small amounts of methanol, in addition to causing profound metabolic acidosis, may lead to blindness or even multiorgan failure and death.
Pediatric hand sanitizer exposures reported to United States poison centers, 2017–2021
Published in Clinical Toxicology, 2023
Varun Vohra, Karima Lelak, Mark I. Neuman, Michael S. Toce, Liying Zhang, Steven J. Korzeniewski, Samantha Bauer, Robert D. Welch, Usha Sethuraman
Reports of increased exposure to household cleaning and disinfectant products emerged following the onset of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. To mitigate the spread of SARS-CoV-2, the United States Centers for Disease Control and Prevention (US CDC) responded by reinforcing the importance of hand hygiene and recommended handwashing with alcohol-based hand sanitizers containing at least 60% volume/volume ethanol or isopropanol if soap and water were unavailable [1]. The ensuing increase in hand sanitizer sales has paralleled an increase in both product accessibility and exposures in children. Pediatric cases involving hand sanitizer products are associated with significant health risks [2]. Moreover, when faced with untenable public demand in the US and globally, alternative manufacturing sources were permitted. Consequently, reports surfaced of the detection of methanol in various hand sanitizers, highlighting the risks associated with the manufacturing processes of these products. Subsequently, reports described serious adverse events secondary to exposures to methanol-containing products in some states, including at least one death [3–5]. Out of concern for methanol contamination, a byproduct during ethanol production, US poison centers began tracking reported cases. Methanol exposure can result in significant clinical effects, including visual impairment, permanent blindness, seizures, permanent damage to the nervous system, and death. Hence, this raises significant product quality control and public health concerns warranting surveillance.
Severe methanol intoxication with atypical symptoms and imaging changes: a fatal case report
Published in British Journal of Neurosurgery, 2023
Jiaqi Chen
Methanol is a highly toxic alcohol. It is most commonly found in adulterated spirits, windshield-washer fluid and other industrial products.1 A potentially lethal dose of pure methanol is 20 millilitres in adults.2 Acute methanol intoxication can occur as accidental ingestion, which causes metabolic acidosis from the production of formic acid leading to permanent visual damage, severe neurological dysfunction and even death.3,4 The symptoms of methanol intoxication may be atypical and delays in diagnosis increase the risk of irreversible organ damage and death. Bilateral putaminal necrosis and diffuse white matter involvement are often recognized radiologically in methanol intoxication,5,6 but extensive subarachnoid hemorrhage is rare. We report a patient with high anion-gap metabolic acidosis because of severe methanol intoxication who presented with atypical symptoms and rapidly developed extensive subarachnoid hemorrhage and diffuse cerebral edema and died within several days.
Effects of adenosine triphosphate on methanol-induced experimental optic nerve damage in rats: biochemical and histopathological evaluation
Published in Cutaneous and Ocular Toxicology, 2020
Erel Icel, Halis Suleyman, Gulce Naz Yazici, Nuri Bakan, Mukadder Sunar
Methanol is a widely used organic solvent. Acute methanol exposure leads to systemic intoxication and toxic optic neuropathy. Methanol poisoning is associated with serious visual and central nervous system (CNS) damage1. In methanol poisoning, methanol transforms into formic acid which is highly toxic and inhibits the mitochondrial functions causing a depletion of ATP in cells. Accumulation of formic acid results in metabolic acidosis with lactacidemia, visual impairment, and damage to basal ganglia. The ocular retina and the retinal ganglion cells are highly vulnerable to hypoxia caused by formic acid because of their high-energy dependence. Acute demyelination of the optic nerve and axonal degeneration are the main toxic effects of formic acid. Besides acute effects, long-term visual sequelae are also seen in 30–40% of patients after methanol poisoning2. In the treatment of methanol poisoning some antidotes, such as ethanol are in use, to prevent the formation of the toxic metabolites, formic acid or formate anions3,4. However, as yet, an exact treatment method for methanol-induced toxic optic neuropathy has not been defined with satisfactory results.
Related Knowledge Centers
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