Poisoning by ethyl alcohol

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I- INTRODUCTION :

  • Ethyl alcohol or ethanol is a dangerous poison because the alcoholic harms not only his health, his antisocial reactions disturb the family peace and public order.
  • Professionally, the alcohol also has an effect on the yield and quality of work and even on worker safety.
  • Alcoholism is a cause of organic degeneration, psychic and a powerful criminogenic.
  • The most common poisoning worldwide :

– acute => intoxication,
– chronic => alcoholism

  • Origin ethanol :

– carbohydrate fermentation => wine, beer, cider,…
– drinks obtained after enrichment by distillation / calvados, liqueur,… ”

  • Disorders and accidents attributed to alcohol => scourge

II- etiologies :

  • occupational exposure :

– chronic intoxication with broad absorption pulmonary tract, cutaneous
– uses : solvent, laboratory reagent, in the pharmaceutical industry, dyes, the perfumes,….”

  • Suicide attempts : alcohol / psychotropic, alcohol / toxic gases / CO”
  • accidental poisoning (household) Infant : transcutaneous (frictions)
  • Excessive alcohol consumption :

– duration (chronicity)
– quality (title alcohol)

  • Average consumption in the world: 8 liters of pure alcohol / person / year

III- METABOLISM :

  • primarily gastrointestinal absorption : passive (20 % in the stomach 80 % the duodenum)
  • Depends : type beverage (title), quickly swallowed, digestive emptiness, individual (alcoholic, gastrectomie,…)
  • Distribution : diffusion in the circulating blood and in the intracellular and extracellular fluids and all organs including brain,
  • lung, foie => total resorption 2 – 6h.
  • Crosses the placenta, diffuse into the CSF and milk
  • Elimination :

– unchanged (2 at 10%)
– breath (2 at 3%) : Q / alveolar air 21 = Q / lml blood
– urine : from 1 g/1, low despite an increase in urine output
– Breastmilk, sweat, saliva, tears

  • Catabolisme :

– hepatic oxidation (80% ethanol absorbed)
– minor oxidation in other tissues
– oxidation capacity depending on the amount

  • Excess alcohol => tissue => direct effects

ethanol

acetaldehyde
↓ ALDH
Acetate
↓ Thiokinases (peripheral tissues
Acetyl-CoA

Cycle de Krebs
CO2 + H2O + E

  • Many oxidation pathways developing during alcoholism increasing metabolic tolerance
  • toxic metabolites :

– = Very oxidizing acetaldehyde, electrophilic
+ oxide proteins : necrosis
+ nucleic acids : cancer risk

IV- TOXICITY :

  • The toxicity of ethanol is due :

– Toxic itself : achievement of neural structures (membrane anesthetic power, Central depressant, impairment of consciousness, coma)
– acetaldehyde (effet antabuse) :
+ intolerance reactions (vasodilatation, hypotension, headaches, vomiting…)
+ mitochondrial alterations, hepatocyte injury

  • The increase of NADH H + / NAD + induced :

– increased lactate / pyruvate in blood and hepatocytes
– hyperlactacidémie : disturbance in the urinary excretion of uric acid -> gout and stimulates hepatic biosynthesis of collagen
– an increase in the concentration of glycerophosphate promoting the synthesis of triglycerides
– decrease in fatty acid catabolism
– decrease gluconeogenesis → hypoglycemia

V- SYMPTOMATOLOGY :

  • clinical effects due to : ethanol, metabolites (acetaldehyde), metabolic consequences

1- acute intoxication :

  • Clinical signs Correlation / BAC
  • interindividual variability

a- Phase excitation or facilitation (1 g/l) :

euphoria, loquacity, disinhibition, incoordination motrice, delay reflexes.

b- depressive phase, phase of intoxication characterized (1 at 2 g/l) :

Reactions increasingly slow, incoordination stronger =>risk of accidents, peripheral vasodilatation with risk of cerebral ischemia in case of cooling

  • special forms : furious, delirious, hallucinatory

c- Phase paralysis or comatose stage (3 g/l) :

Paralysis resulting coma, but especially the inhibition of cardiac and respiratory centers

  • Biology : metabolic acidosis, hyperlactacidémie, hypertriglycéridémie, hypoglycemia, hyper uricémie
  • Complications : respiratory failure, CCV, hypothermia, visceral / pancreatitis and acute hepatitis, subarachnoid hemorrhage and digestive.
  • Drink driving = Effects driver

– Tunnel vision
– Increased sensitivity to glare
– Altered appreciation of distances
– Decreased reflexes
– euphoric effect => overestimation of abilities
– Risk of accident x 2
– Algerian legislation > 0,2g/l

2- chronic intoxication :

  • Multiorgan
  • Addiction + tolerance

– SNC : tremors,
– SNP : paralysis, cramps, polyneuropathy
– Foie : steatosis, cirrhosis, alcoholic hepatitis
– Digestive tract : esophageal cancer
– Pancreas : acute pancreatitis
– cardiovascular : HTA, cardiomyopathie
– Eye : optic neuritis
– skeletal muscle : rhabdomyolyse

  • Withdrawal Complications => Delirium tremens
  • Clinical signs

– Mental confusion, disorientation spatiotemporal
– Tremor of the extremities, insomnia agitation.
– general signs : hyperthermia, sweats,
– tachycardia, HTA, diarrhea.

  • Treatment : medical emergency, Rehydration and bustle of sedation

WE- ANALYTICAL TOXICOLOGY :

  • Sample : ambiant air, breath, sang, urine, saliva, sweat, liquid or gastric contents

1- blood test :

  • Interest : clinique, professional, médicolégal (driving while intoxicated, toxic death)
  • Terms sampling : venipuncture, disinfectant without oxidizing substance or reducing (alcohol, ether) => Dakin, anticoagulant = NaF,
  • Forensic Expertise : 2 sealed tubes
  • Assays :

– chemical methods (Method Cordebard) : official method, separation of the alcohol by distillation in the presence of hot pi cove acid, oxidation by dichromate (nitrochromique mixture), excess dichromate determined iodometrically by return
– = physical method or electrochemistry

2- Dosage in other biological media :

  • Urine, sweat (epidemiological interest)
  • Saliva (Correlated with the amount of alcohol in blood)
  • gastric lavage (control the wash)
  • gastric contents (diagnostic toxic death)