EM Toxicology 15: Ethanol Flashcards
Remarks on alcohols
All alcohols cause clinical inebriation, with the strength of inebriating effects directly proportional to the alcohol’s molecular weight; hence, at the same concentration, isopropanol is more intoxicating than ethanol
ethanol and isopropanol are themost common alcohols ingested
differentiate ethanol & isopropanol vs methanol & ethylene glycol
Ethanol & Isopropanol
- primary toxicity is due to parent compound
- principal effects are GI irritation and intoxication
- do not in themselves produce a clinically relevant metabolic acidosis
Methanol & Ethylene Glycol
- primary toxicity is due to toxic metabolites
- toxic alcohols because they cause serious multi-system damage and metabolic acidosis
most frequently used and abused drug in the world
ethanol
- blood levels peak about 30-60 mins after ingestion
- presence of food in the stomach prolongs absorption and delays the peak blood levels
what may account for the fact that women usually develop a higher blood ethanol level than men after consuming the same dose per kilogram of body weight?
higher levels of gastric alcohol dehydrogenase in men than in women
This enzyme breaks down ethanol in the stomach, thereby lowering the amount available for absorption
death may occur in nonhabituated individuals at what concentrations
400-500 mg/dL
(death from respiratory depression)
impairment in driving a motor vehicle may occur with levels as los as
50 mg/dL, especially in nonhabituated individuals
remarks on metabolism of ethanol
major enz: alcohol dehydrogenase
at high ethanol conc’n: CYP2E1
Both alcohol dehydrogenase and CYP2E1 are inducible and thus are more active in chronic ethanol users. Therefore, rates of ethanol elimination from the blood vary from
15-20 mg/dL/hour in nonhabituated
**30 mg/dL/hour **in those with chronic alcoholism
hallmark of ethanol toxicity
clinical inebriation
mechanism of ethanol as CNS depressent
Enhances GABA receptors
Blocks NMDA receptors
Modulation of these systems leads to the development of tolerance, dependence, and a withdrawal syndrome
explain hypoglycemia and lactic acidosis in ethanol ingestion
- The metabolism of ethanol by alcohol dehydrogenase requires the presence of the oxidized form of nicotinamide adenine dinucleotide (NAD+), which is then converted to its reduced form (NADH).
- The metabolism of a significant amount of ethanol increases the NADH/NAD+ ratio
- This then promotes the conversion of pyruvate to lactate, diverting pyruvate away from the gluconeogenesis pathway
In isolated ethanol intoxication, what is the significance of the presence of horizontal gaze nystagmus?
has a sensitivity of 80-90% for blood ethanol levels of 100 mg/dL
Most common cause of an osmolar gap on serum electrolyte analysis
ethanol ingestion
remarks on ethanol and metabolic acidosis
Ethanol ingestion may be associated with a mild metablic acidosis, but a significant anion gap metabolic acidosis suggests the presece of
- lactic acidosis,
- ketoacidsois,
- methanol or ethylene glycol toxcitiy
General management of ethanol intoxication
- Observation until sobriety.
- IV dextrose 0.5 to 1 g/kg for hypoglycemia
**Fluid administration does not hasten alcohol elimination, so establishment of IV access for fluid administration alone is unnecessary in uncomplicated mild to moderate intoxication*
The prevalence of vitamin deficiencies in *acutely intoxicated ED patients is low and does not justify the routine use of IV vitamin-containing fluids
Wernicke’s encephalopathy
TRIAD
Altered mental status
Nystagmus
Ataxia
Requires daily treatment with thiamine 100 mg, until normal diet is resumed.