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]

Ethylenglycol
Oxalic acid
  • 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 glycoaldehydeoxalic 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]

  1. Neurotoxic stage – transient drunkenness, vomiting , drowsiness, then development of MAC , hyperosmolarity, convulsions, convulsions, coma (secondary brain edema).
  2. Cardiopulmonary stage – zin 12–24 h, dysrhythmia, severe acidosis, hyperventilation ( Kussmaul breathing ), circulatory collapse, hypocalcemia → convulsions, edema of lungs , brain, cardiopulmonary arrest.
  3. 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]

Metabolism of methyl alcohol
  • 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]


References[edit | edit source]

  • PELCLOVÁ, Daniela. Nemoci z povolání a intoxikace. 2. edition. Praha : Karolinum, 2006. 207 pp. ISBN 80-246-1183-X.

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