L9: Alcohol Flashcards
Source of Ethyl Alcohol (Ethanol)
Sugar fermentation by living yeast.
Characters of Ethyl Alcohol (Ethanol)
- Volatile colorless liquid, highly inflammable
- Having characteristic odor and fiery taste.
Uses of Ethyl Alcohol (Ethanol)
Toxic action of Ethyl Alcohol (Ethanol)
what does CP of Acute Ethyl Alcohol (Ethanol) Toxicity depend on?
concentration of alcohol in the blood
Mode of poisoning of Ethyl Alcohol (Ethanol)
Consumption of alcoholic beverages.
when do symptoms of Acute Ethyl Alcohol (Ethanol) Toxicity manifest?
Symptoms of CNS depression start when blood ethanol reaches 1.50 mg/dl
CP of Mild intoxication: “50-150 mg” of ethanol
what does Acute Ethyl Alcohol (Ethanol) toxicity predispose for?
trauma
CP of Moderate intoxication: “150-250 mg” of ethanol
CP of Severe intoxication: “150-250 mg” of ethanol
Alcohol coma (dead drunk): “350-400 mg”
Causes of death by Acute Ethanol Toxicity
Death within 10 hours:
- Respiratory failure.
- Brain damage (irreversible hypoxia).
Delayed couses of death:
- Fatty degeneration of liver.
- Acute hemorrhagic pancreatitis
Hypoglycemia in Acute Ethanol Toxicity
- Hypoglycemia is Very common.
- it is caused by impaired gluconeogenesis in patients with depleted or low glycogen stores (particularly small children and poorly nourished persons).
Investigations in Acute Ethanol Toxicity
emergency TTT in Acute Ethanol Toxicity
Decontamination in Acute Ethanol Toxicity
Antidotes in Acute Ethanol Toxicity
No specific antidotes.
Enhanced elimination in Acute Ethanol Toxicity
Hemodialysis
Indications of Hemodialysis in Acute Ethanol Toxicity
- Blood ethanol level is above 500mg/dL with coma and respiratory failure.
- Clinical deterioration despite maximal supportive measures.
- Impaired hepatic function.
Alcohol & Driving
- Even at low doses, there is clear evidence that alcohol impairs driving performance.
Characters of Acute Methanol Toxicity
- Methanol acquired name wood alcohol because it was once produced chiefly as a by product of the destructive distillation of wood.
- Today, industrial methanol is produced in a catalytic process directly from carbon monoxide, carbon dioxide, and hydrogen.
Uses of Acute Methanol Toxicity
- As a solvent “In industry”
- As a source of heat in some burners
- Adulteration of Ethanol “in cheap alcoholics beverage”.
- Paint remover
- Household cleaners
Absorbtion in Acute Methanol Toxicity
Rapidly absorbed through:
- Gastrointestinal mucosa.
- Intact skin
- Pulmonary alveoli
Distribution in Acute Methanol Toxicity
- Methanol is quickly distributed to the body water.
- Methanol enters the vitreous humor extensively, because of its extremely aqueous nature (eye is more vulnerable to damage from even small amounts).
Metabolism in Acute Methanol Toxicity
- Methanol is slowly metabolized (at a rate about one tenth that of ethanol), by alcohol dehydrogenase to formaldehyde subsequently by aldehyde dehydrogenase to formic acid (formate)
significant levels can be found up to 7 days after ingestion.
Excretion in Acute Methanol Toxicity
- Only about 3% is excreted unchanged by kidneys, Less than 10 % through breath.
Toxic action of Acute Methanol Toxicity
CP of Acute Methanol Toxicity
Ocular Toxicity in Acute Methanol Toxicity
- Visual disturbances up to blindness.
- Patients describe the visual disturbance as blurred vision, haziness, or “like standing in a snowfield.
- Impaired visual acuity followed by permanent blindness after 2-6 days
what dose of metahnol may cause occular manifestations?
10 ml of pure methanol can affect vision, due to retinal affection.
Fundoscopy in Occular affection in Acute Methanol Toxicity
- Optic disc hyperemia or pallor, venous engorgement
- Retinal or optic disc edema.
Investigations in Acute Methanol Toxicity
Goals of TTT in Acute Methanol Toxicity
- Correction of metabolic acidosis by NaHCO3.
- Blockage of alcohol dehydrodenase (ADH) which inhibits formation of toxic metabolites by specific antidotes.
- Removal of parental alcohol by hemodialysis.
Emergency & Supportive TTT in Acute Methanol Toxicity
- Maintain airway and assist ventilation if needed “Intubation with Hyperventilation)”
- Treat metabolic acidosis with IV sodium bicarbonate guided by arterial blood gases.
- Treat coma and seizures if they occur.
Decontamination in Acute Methanol Toxicity
- Aspirate gastric contents if this can be performed within 30-60 minutes of ingestion.
- Activated charcoal is not likely to be useful.
Antidote of Acute Methanol Toxicity
- Alcohol dehydrogenase inhibiters (Ethanol or fomepizole)
- Leucoverin (folinic acid) and folic acid
Guidelines of using antidote of Acute Methanol Toxicity
- Only give ethanol therapy until hemodialysis. become available (Definite Treatment)
- Once hemodialysis is available immediate stop ethanol.
- Only Adjusted ethanol dose to maintain the Ethanol Level in (Desired Range. 100-150mg)
Indications of Alcohol dehydrogenase inhibiters (Ethanol or fomepizole)
- Blood methanol concentration >20 mg/dl
- History of significant methanol ingestion
- Significant metabolic acidosis
Leucoverin (folinic acid) and folic acid
For conversion of formic acid to CO2 and water
Enhanced Elimination in Acute Methanol Toxicity
Hemodialysis
…………….. is the definitive management Line of methanol intoxication.
Hemodialysis
Effect of hemodialysis in Acute Methanol Toxicity
- Rapidly removes both methanol (half-life reduced to 3-6 hours)
- And formate (half-life decreases to 1.5-3.1 hours)
- And (corrects acidosis).
Indications of Hemodialysis in Acute Methanol Toxicity
- Methanol poisoning with significant metabolic acidosis not correctable with bicarbonate.
- Serum methanol concentration ≥ 40 mg/di.
- Renal failure.
- Deteriorating vital signs
- Vision deficits.
Endpoint of Hemodialysis in Acute Methanol Toxicity
- Concentration of methanol is less than 20 mg/dL
- Correction of acidosis
- Signs of toxicity disappear
