Title: A Case Report of Non Food Grade Ethyl Alcohol Toxicity

Authors: Dr Snigdha Gannamraju, Dr K. Sai Abhinandan, Dr A. Rama Ratnam, Dr Prachee Nagrale

 DOI: https://dx.doi.org/10.18535/jmscr/v10i1.10

Abstract

 

Introduction

Ethanol is a highly water soluble and low molecular weight compound that rapidly crosses cell membrane.

Absorption– occurs mainly in proximal intestinal tract i.e stomach 70%, duodenum 25%, small percentage in remaining intestinal tract.(1)

Metabolism– gastric alcohol dehydrogenase (ADH) is responsible for 10% of alcohol metabolism i.e first pass metabolism. Remaining 90% of ingested alcohol is metabolised to acetaldehyde along 3 liver enzymatic pathways i.e liver ADH, microsomal ethanol oxidising system (MEOS) and catalase.(2)

Food or fluid in the gastric lumen dilutes ethanol concentration and reduces the efficiency of absorption. Caloric density and composition of a meal influence rate of gastric emptying.(3)

Distribution– completely miscible in water, insoluble in fat. Volume of distribution is proportional to lean body mass because adipose tissue contains little water. Therefore females have smaller volume of distribution.(4)

Elimination– 95-98% of ingested ethanol is metabolised in the liver first by enzyme alcohol dehydrogenase to acetaldehyde and then by the enzyme aldehyde dehydrogenase to acetic acid which dissociates to carbondioxide and water.(5)

Case Report

A 45 year old male patient presented to ophthalmology department with history of sudden painless diminution of vision both eyes since 4 days. No history of trauma and ocular surgery. No other ocular complaints. No known systemic illness.

On ocular examination visual acuity PL (+) PR inaccurate in both eyes with mid dilated non-reactive pupils in both eyes. Anterior segment findings were unremarkable and IOP recorded as 13mm hg in RE and 16mm hg in LE with AT. Extra ocular movements free and full range in all directions.

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