Single center experience of managing methanol poisoning in the hilly state of uttarakhand: A cross sectional study

Methanol-induced optic neuropathy (Me-ION) is a serious condition that may result in long-term or irreversible visual impairment or even blindness secondary to damage and loss of function of the optic nerve and retina. Me-ION shows a tendency to occur as mass poisonings around the world with a clear predilection for poor societies in developing countries. The main mechanism underlying the molecular basis of Me-ION is the inhibition of the mitochondrial oxidative phosphorylation process through the binding of the toxic metabolite of methanol—formic acid—with the key enzyme of this process—cytochrome c oxidase. However, other mechanisms, including damage to the eye tissues by oxidative stress causing the intensification of the oxidative peroxidation process with the formation of cytotoxic compounds, as well as an increase in the synthesis of pro-inflammatory cytokines and influence on the expression of key proteins responsible for maintaining cell homeostasis, also play an important role in the pathogenesis of Me-ION. Histopathological changes in the eye tissues are mainly manifested as the degeneration of axons and glial cells of the optic nerve, often with accompanying damage of the retina that may involve all its layers. Despite the development of therapeutic approaches, persistent visual sequelae are seen in 30–40% of survivors. Thus, Me-ION continues to be an important problem for healthcare systems worldwide.

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Methanol-induced optic neuropathy: a still-present problem

Liberski

Kałużny

Kocięcki

2022

Arch Toxicol

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Prognostic factors in acute poisoning with central nervous system xenobiotics: development of a nomogram predicting risk of intensive care unit admission

Sharif

Kasemy

Alshabibi

et al. 2022

Toxicology Research

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Background Acute intoxication with central nervous system (CNS) xenobiotics is an increasing global problem. Predicting the prognosis of acute toxic exposure among patients can significantly alter the morbidity and mortality. The present study outlined the early risk predictors among patients diagnosed with acute exposure to CNS xenobiotics and endorsed bedside nomograms for identifying patients requiring intensive care unit (ICU) admission and those at risk of poor prognosis or death. Methods This study is a 6-year retrospective cohort study conducted among patients presented with acute exposure to CNS xenobiotics. Results A total of 143 patients’ records were included, where (36.4%) were admitted to the ICU, and a significant proportion of which was due to exposure to alcohols, sedative hypnotics, psychotropic, and antidepressants (P = 0.021). ICU admission was associated with significantly lower blood pressure, pH, and HCO3 levels and higher random blood glucose (RBG), serum urea, and creatinine levels (P < 0.05). The study findings indicate that the decision of ICU admission could be determined using a nomogram combining the initial HCO3 level, blood pH, modified PSS, and GCS. HCO3 level < 17.1 mEq/L, pH < 7.2, moderate-to-severe PSS, and GCS < 11 significantly predicted ICU admission. Moreover, high PSS and low HCO3 levels significantly predicted poor prognosis and mortality. Hyperglycemia was another significant predictor of mortality. Combining initial GCS, RBG level, and HCO3 is substantially helpful in predicting the need for ICU admission in acute alcohol intoxication. Conclusion The proposed nomograms yielded significant straightforward and reliable prognostic outcomes predictors in acute exposure to CNS xenobiotics.

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Secondary Dysfunction of the Intestinal Barrier in the Pathogenesis of Complications of Acute Poisoning

Ivnitsky

Schäfer²,

Rejniuk³

et al. 2022

J Evol Biochem Phys

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The last decade has been marked by an exponential increase in the number of publications on the physiological role of the normal human gut microbiota. The idea of a symbiotic relationship between the human organism and normal microbiota of its gastrointestinal tract has been firmly established as an integral part of the current biomedical paradigm. However, the type of this symbiosis varies from mutualism to parasitism and depends on the functional state of the host organism. Damage caused to the organism by external agents can lead to the emergence of conditionally pathogenic properties in the normal gut microbiota, mediated by humoral factors and affecting the outcome of exogenous exposure. Among the substances produced by symbiotic microbiota, there are an indefinite number of compounds with systemic toxicity. Some occur in the intestinal chyme in potentially lethal amounts in the case they enter the bloodstream quickly. The quick entry of potential toxicants is prevented by the intestinal barrier (IB), a set of structural elements separating the intestinal chyme from the blood. Hypothetically, severe damage to the IB caused by exogenous toxicants can trigger a leakage and subsequent systemic redistribution of toxic substances of bacterial origin. Until recently, the impact of such a redistribution on the outcome of acute exogenous poisoning remained outside the view of toxicology. The present review addresses causal relationships between the secondary dysfunction of the IB and complications of acute poisoning. We characterize acute systemic toxicity of such waste products of the normal gut microflora as ammonia and endotoxins, and demonstrate their involvement in the formation of such complications of acute poisoning as shock, sepsis, cerebral insufficiency and secondary lung injuries. The principles of assessing the functional state of the IB and the approaches to its protection in acute poisoning are briefly considered.

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Single center experience of managing methanol poisoning in the hilly state of uttarakhand: A cross sectional study

Cited by 6 publications

References 16 publications

Methanol-induced optic neuropathy: a still-present problem

Methanol-induced optic neuropathy: a still-present problem

Prognostic factors in acute poisoning with central nervous system xenobiotics: development of a nomogram predicting risk of intensive care unit admission

Secondary Dysfunction of the Intestinal Barrier in the Pathogenesis of Complications of Acute Poisoning

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