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Alcohol poisoning Asmaa A

Asmaa A - TIU

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Page 1: Asmaa A - TIU

Alcohol poisoningAsmaa A

Page 2: Asmaa A - TIU

Ethanol (Ethyl Alcohol)

Pure ethanol is a clear and colourless volatile liquid with a characteristic fruityodour and sweetish browning taste. It is usually obtained by enzymaticfermentation of CHO (sugar).

• Absolute alcohol refers to 99% ethanol.

• Industerial or methylated or denatured spirit contains 95% ethanol and 5 to 10%methanol.

• Surgical spirit refers to methylated spirit which contains in addition, smallamounts of castor oil and wintergreen (methyl salicylate).

• Proof spirit referes to standard mixture of alcohol and water (57.10% byvolume)

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Mechanism of action

Ethanol is a CNS depressant (though initially there is suppression of inhibitorneurons causing paradoxical CNS stimulation).The frontal lobes are sensitive to lowconcentrations (resulting in mood changes) followed by the occipital lobe (visualdisturbance) and cerebellum (loss of coordination).

Fatal dose

It is said that consumption of 1000 to 1500 ml of a strong, distilled spirit like whiskyor rum, over a short period of time can be lethal.

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Uses

1.Beverage

2.Solvent for perfumes, after shaves and colognes.

3.Medicinal (many medicinal preparations contain varying percentage of alcohol).

4.Preservative for viscera (in the form of rectified spirit).

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Acute poisoning (intoxication) there are 7 stages of intoxication of progressive severity culminating in death.

1.Stage of sobriety (Decent)

Blood alcohol: 10 to 50%

Behaviour apparently normal.

2. Stage of euphoria (Delighted)

Blood alcohol: 50 to 100%

Feeling of well-being

Talkativeness

Increase self-confidence

Lack of inhibitions

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• Stage of excitement (Delirious)

Blood alcohol: 100 to 150%

Emotional instability

Increase reaction time

Mild muscular incoordination.

• Stage of confusion (Dazed)

Blood alcohol 150 to 200% Visual disturbance

Disorientation Muscular incoordination

Mental confusion Staggering gait

Vertigo Slurred speech

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• Stage of stupor (Dejected)

Blood alcohol: 200 to 300%

Diminished response to stimuli

General inertia

Inability to stand or walk

Vomiting

Loss of consciousness

• Stage of coma (Dead drunk)

Blood alcohol: 300 to 500% Hypothermia

Deep unconsciousness Laboured breathing

Abolished reflexes

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• Stage of death (Dead)

Blood alcohol: over 500%

Death due to respiratory failure.

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Chronic Poisoning (Alcohol addiction) there are 5 types of alcoholism:

1.Alpha alcoholism: excessive and inappropriate drinking without loss of controlor ability to abstain.

2.Beta alcoholism: excessive and inappropriate drinking without clear dependencebut with physical complications such as cirrhosis, gastritis or pancreatitis.

3.Gamma alcoholism: c.c by physical dependence , tolerance and inability tocontrol drinking.

4.Delta alcoholism: seen in wine-drinking individual and c.c by inability toabstain, tolerance and with drawal symptoms but the quantity consumed can becontrolled.

5.Epsilon alcoholism: intermittent or spree drinking.

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• Deleterious effects of ethanol poisoning

1.Vitamine B1 (thiamine )deficiency resulting in Wernicke’s encephalopathy and beriberi.

2.Karsakoff’s syndrome.

3.Alcohol hepatitis and cirrhosis.

4.Chronic gastritis and peptic ulceration.

5.Chronic pancreatitis.

6.Cardiomyopathies (especially in heavy beer drinkers).

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7.Alcohol amblyopia (dimness of vision).

8.Endocrinal and metabolic disorders.

9.Mallory-Weiss syndrome (tears of the mucosa of lower esophagus with haemorrhaging).

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Mechanism of toxicity

• It binds directly to Gamma –aminobutyric acid (GABA) receptor in theCNS and cause sedative effects similar to those of benzodiazepines

• It also block the N- methyl-D- aspartate (NMDA) glutamate receptor

• It has direct effect on cardiac muscle, thyroid and liver.

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• Toxicokinetics

Ethanol is rapidly absorbed across both gastric mucosa and small intestines,reaching a peak concentration 20-60 min after ingestion.

Once absorbed, it is converted to acetaldehyde by enzyme alcohol dehydrogenase(ADH). Acetaldehyde is then converted to acetate which is converted to acetylCOA,and ultimately carbone dioxide and water

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Disulfiram it act by inhibiting oxidation of acetaldehyde to acetic acid(metabolite of ethanol) resulting in accumulation of former, producingunpleasant syndromes (flushing, headache, palpitation, vertigo, vomiting,abdominal and chest pain, hypotension, etc).These symptoms are actuallyproduced by a metabolite of disulfiram (carbone disulphide) and not byacetaldehyde.

Side effects: halitosis, garlicky taste, headache, confusion, ataxia, liver damage,etc.

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There are several drugs which when taken a long with alcohol can producedisulfiram like reaction. They include chloramphenicol, metronidazole,furazolidone, some cephalosporones and oral hypoglycemic agents

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• Treatment

1.50% dextrose (50-100 ml) IV repeated as required.

2.Activated charcoal in the usual dose.

3.Thiamine 100 mg IV.

4.Stomach wash.

5.Naloxone in reversing alcoholic coma.

6.Physostigmine salicylate.

7.Supportive measures.

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Methanol (Methyl alcohol, wood alcohol)

Methanol colourless, volatile liquid with characteristic odour

Uses

Methanol is widely used as a solvent and is present as a constituent of

1.Antifreeze

2.Shellac

3.Paints

4.Paint remover

5.Vanishes.

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Usual fatal dose

60 to 250 ml

Mode of action: Toxicity results from accumulation of two of its metabolite: formaldehyde and formic acid.

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Metabolism of Toxicity

Methanol

Formaldehyde

Formic acid

Metabolic acidosis

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Signs and Symptoms of toxicity

1.CNS: headache, neck stiffness, vertigo, confusion, coma.

2.Eye: Mydriasis, blurred vision, photophobia, optic neuritis, retinal oedemaand blindness.

3.GIT: Abdominal pain, vomiting, acute pancreatitis, etc.

4.Other symptoms: Acute tubular necrosis, profound metabolic acidosis, (producing deep, noisy respiration referred to as kussmaul respiration), haemolytic anemia, etc.

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Treatment

1.Induction of emesis or stomach wash.

2.Peritoneal or haemodialysis.

3.Ethanol is antidote for methanol since it blocks the formation offormaldehyde and formic acid by its preferential affinity for alcoholdehydrogenase. It is preferably given IV as 10% solution starting withloading dose of around 500 ml gives as an infusion and repeating required.

4. 4methyl pyrazole (4MP) or fomepizole. Up to 20 mg/kg of 4 MP individeddoses have been given for 5 days without any demonstrable toxicity.

5.IV soda bicarbonate to correct metabolic acidosis.

6.Supportive measures

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