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Wednesday, June 27, 2007

Ethanol,Methanol and Ethylene glycol poisoning

Ethanol
Overdose of ethanol (ethyl alcohol or"alcohol") is very common. Alcohol potentiates the CNS-depressant effect of many drugs. It initially causes disinhibition and later ataxia, dizziness, dysarthria, and drowsiness. In severe poisoning may be coma with respiratory depression, hypotension, hypothermia, and a metabolic acidosis. Hypoglycemia is a particular problem in a children and may occur after some hours. Death may result from respiratory failure or aspiration of vomit.

For an adult, the fatal dose of ethanol alone is 300-500ML absolute alcohol. Whisky and gin usually contain 40-50% ethanol. Rarely alcohol intoxication cause lactic acidosis (Especially with the patient with liver diseases or taking biquanide hypoglicaemic drug) or ketoacidosis (due to dehydration and hypoglicaemia in alcohol).

Treat Supportively:
  • Maintain clear airway and adequate ventilation
  • Check blood glucose every 1-2 hours in severe poisoning
  • Emergency measurement of blood ethanol is rarely helpful
  • Correct hypoglicaemia with glucose not with glucagon
  • Look sign for injury, especially head injury
  • Gastric lavage and activated charcoal are ineffective in ethanol intoxication
  • Do not give fructose
Mehanol Poisoning
Methanol is used as a solvent and in antifreeze. Ingestion of >60ML of methanol (in Adult) may cause fatal poisoning, the toxic effect due to the metabolites formaldehide and formid acid. Methylated spirits is a mixture of ethanol and water with only 5% ethanol and toxicity is almost entirely due to ethanol.

Clninical features
Methanol initially cause only mild transient drowsiness. Serious toxicity develops after a latent period of 8-36 hours with vomiting, abdominal pain, headache, dizziness, blurring of vision and drowsiness leading to coma. There is a severe metabolic acidosis, hyperglicaemia, and increase serum amylase. survivor may be blind due to optic nerve damage and Parkinsonian Problem.

Management
  • Provide gastric lavage less than 1 hour since ingestion
  • Measure ABG (Analys Blood Gas), U&E, blood glucose, and plasma methanol
  • correct metabolic acidosis to keep arterial pH > 7,2 large amount of bicarbonate may be needed and hypernatremia may be occur.
  • Give methanol orally as whisky, gin or vodka (adult 125-150mL, child 2mL/kg) and then intravenous infusion (dose as for ethylene glycol)
  • Give folinic acid (30 mg IV every 6 hours)
  • In severe poisoning refer to ITU for haemodialysis and possibly IPPV
Ethylene glycol poisoning
Ethylene glicol is used mainly as antifreeze. The minimum fatal dose adult=100mL. Toxic effect due to metabolites, including glycolaldehyde and oxalid acid. ethanol blocks metabolism of ethylene glycol, preventing toxicity.

Clinical Features
In the first 12 hours after ingestion the victim look drunk, but does not smell of alcohol. Aaxia, disarthria, nausea, vomiting, and sometimes haematemesis occur, followed by convulsion, coma and severe metabolic acidosis. From 12-24 hours post ingestionthere is hyperventilation, tachycardia, pulmonary oedema, cardiac arrhythmias and cardiac failure. Hypocalcaemia may be severe. Acute tubular necrosis and renal failure occur at 24-72 hours. Cranial nerve palsies may be develop.

Management
  • Perform gastric lavage
  • Measure ABG, U&E, calcium and plasma ethylene glycol
  • Correct metabolic acidosis to keep arterial pH >7.2 large amount of bicarbonate may be needed and hypernattraemia may occur
  • Give ethanol orally as whisky, gin, or vodka (adult 125-150mL, child 2ml/kg) followed by intravenous infusion (IVI)of ethanol, preferably as 5% solution in dextrose, initial IV adult dose is 12g ethanol per hour, increase for alcoholic during haemodialysis and adjusted to maintain blod ethanol at 1gr/lt
  • correct severe hypocalcaemia with calcium gluconate (10mL of 10% slowly IV)
  • In severe poisoning, haemodialysis is required, with frequent measurement of blood ethlylene glycol and ethanol concentrations.
  • Ventialation may be needed if pulmonary oedema develops

Source
Oxford Handbook of Accident and emergency medicine

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