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Toxins in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Treatment of methanol poisoning consists of supportive and specific therapy. Supportive therapy starts with airway management, correction of electrolytes and adequate hydration. Gastric lavage is beneficial within 2 h of ingestion of methanol. Metabolic acidosis needs correction with buffer like sodium bicarbonate. Hemodialysis can be done further to correct the acidosis and remove both methanol and formate. Antidote of methanol is ethanol which delays methanol metabolism to facilitate its elimination from the system by either naturally or by dialysis. Ethanol, like methanol, gets metabolized by ADH, and the enzyme has 10–20 times higher affinity for ethanol compared with methanol [18]. Fomepizole is also metabolized by the same enzyme, but it does not cause CNS depression like ethanol. But high cost and lack of availability act as limiting factor. Ethanol is commonly used and is given intravenously (IV) as a 10% solution in 5% dextrose. A loading dose of 0.6 g/kg is given followed by an IV infusion of 0.07–0.16 g/kg/h.
Miscellaneous poisons
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
The initial symptoms of methanol intoxication include CNS depression, with headache, dizziness, nausea, lack of coordination and confusion. Large doses quickly lead to unconsciousness and death. Once the initial symptoms have passed, a second set of symptoms can be observed 10–30 hours after the ingestion. These include blindness and worsening acidosis. These secondary symptoms are caused by accumulating levels of formate in the bloodstream. The process may progress to death by respiratory failure.
Alcohols and Aldehydes
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Methanol (methyl alcohol, wood alcohol, Columbian spirits) is readily available at various concentrations in numerous industrial and household products, including windshield washer fluid and paint thinner. It is also used in the manufacture of formaldehyde and methyl t-butyl ether. Exposure to methanol commonly occurs in the workplace and in the household, and it is often intentionally ingested by alcoholics.
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
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.