Alcohol intoxication
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Alcohol toxicity:
Alcohol toxicity 2:
Ethylalcohol (Ethanol)[edit | edit source]
Find more details on: Abusus of alcohol, Ethanol.
Ethylene glycol[edit | edit source]
- A colorless syrupy liquid with a sweet taste and is used to make antifreeze products (Fridex® for car radiators, brake fluid).
Etiopathogenesis[edit | edit source]
- By the same enzymes as alcohol , it is biotransformed → into glycoaldehyde → oxalic acid ,
- damages renal tubules by forming calcium oxalate crystals → acute renal failure and MAC ,
- osmolarity rises significantly,
- the maximum concentration in plasma is 1–4 h after ingestion, the elimination half-life is short,
- lethal dose - about 100 ml (with timely treatment, the ingestion of 2 liters was also survived).
Clinical picture[edit | edit source]
- Neurotoxic stage – transient drunkenness, vomiting , drowsiness, then development of MAC , hyperosmolarity, convulsions, convulsions, coma (secondary brain edema).
- Cardiopulmonary stage – zin 12–24 h, dysrhythmia, severe acidosis, hyperventilation ( Kussmaul breathing ), circulatory collapse, hypocalcemia → convulsions, edema of lungs , brain, cardiopulmonary arrest.
- Renal stage – 24–72 h – hematuria , albuminuria , oliguria , oxaluria , acute tubular necrosis , anuria , renal function never returns to normal.
Treatment[edit | edit source]
- The antidote is ethanol - orally or in a 5% glucose infusion, the level is maintained at 1 per thousand . Ethanol has a 100x greater affinity for alcohol dehydrogenase , unconverted ethylene glycol is then excreted in the urine,
- dwe also administer vitamin B 1 and folic acid ,
- possibly hemodialysis ,
- ideal drug – fomepizole ( Antizol® ) – alcohol dehydrogenase inhibitor – very expensive.
Methyl alcohol[edit | edit source]
- Formerly "wood spirit", most often mistaken for alcohol,
- it is well absorbed by the lungs and skin (it is also possible to become intoxicated),
- 30–60% is exhaled unchanged through the lungs , the rest is oxidized to formaldehyde and formic acid,
- folic acid is involved in the metabolism of formic acid, its decomposition is slow, there is a risk of accumulation, there is a risk of severe MAC and vision damage ,
- vision disorders – up to 24 h latency - initially blurred vision, flashes of light, feelings of glare, loss of field of vision, fundus - there is hyperemia and edema in the disc , in addition to the nerve , it damages the retina by blocking cytochrome oxidase → hypoxia ,
- blindness – 15 ml each
- death – 30-240 ml each
Treatment[edit | edit source]
- As in ethylene glycol.
Investigation[edit | edit source]
- Methanol in the urine ( BET ), in the case of intoxication in the blood, it is more reliable to measure formic acid in the urine (as a metabolite), but this is not usually done.
Source[edit | edit source]
- BENEŠ, Jiří. Studijní materiály [online]. [cit. 24.02.2010]. <http://jirben.wz.cz>.
References[edit | edit source]
- PELCLOVÁ, Daniela. Nemoci z povolání a intoxikace. 2. edition. Praha : Karolinum, 2006. 207 pp. ISBN 80-246-1183-X.