Alcohol Toxicity

Introduction
• Alcohol intoxication usually describes the acute toxic effects
following ingestion of a large amount of ethanol alcohol.
• In the United States, 20%-40% of persons admitted to emergency
departments are reported to have alcohol related disorders, of which
acute alcohol intoxication is the most common
• 1.2% of emergency department visits over a 1-year period in Belgium
reported to be due to alcohol intoxication
• 0.6%-6% of patients treated in emergency departments in Europe
have acute alcohol intoxication

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Alcohol
 Ethanol or Ethyl -The type of alcohol in
alcoholic beverages. Can be produced
synthetically or naturally by fermenting
fruits and grains
 Methyl : Highly Flammable material,
poisonous
 Isopropyl: also known as rubbing
alcohol, bad for the body

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Risk Factor
• Weight
• Higher percentage of alcohol in beverages
• Large volume of alcohol consumed over a short period of
time
• Binge drinking: The consumption of an excessive amount
of alcohol in a short period of time. Generally 5 or more
drinks in a row for men, 4 or more for females

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 Mechanism of Toxicity
 Alcohol is absorbed through the proximal
GI tract.
 Ethanol inhibits glutamate receptor
subset N-methyl-D-aspartate, (NMDA),
which diminishes excitatory actions
of glutamate and enhances inhibitory
action of GABA
 Initial alcohol exposure activates reward
pathway, which releases dopamine into
nucleus accumbens from deeper within
brain (intra-ventral tegmental area)
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 Mechanism of Toxicity
 Acute toxicity in CNS: Alcohol binds strongly to GABA receptors, activating the
inhibitory cascade, which results in sedation, cognitive dysfunction, and decreased
coordination
 With chronic use of alcohol, the number of GABA receptors is increased, requiring
more and more alcohol to create the same level of inhibition. This is a phenomenon
known as tolerance. This tolerance partly explains the alertness of chronic alcohol
users at blood alcohol levels that in others would cause coma or death.
 Alcohol also inhibits the primary excitatory neurotransmitter in the CNS, glutamate.
Patients with alcohol use disorder have increased numbers of NMDA receptors and
increased sensitivity of these receptors to glutamate. Due to the increased sensitivity
of these receptors, patients with alcohol use disorder are at risk for seizures and
hallucinations when alcohol is withdrawn

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 Diagnosis
 History: known or admitted ingestion of alcohol
(quantity and type, timing, circumstances,
injuries, previous episode, history of chronic
alcohol, ingestion of other subtances)
 Physical examination: change in behavior and
clinical sign

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Short Term Effects
Depending on how much is taken and the physical condition of the individual

● Slurred speech Hypoglicemia (peak serum

● Drowsiness (level ≥50 mg/dL =11 mmol/L)

● Vomiting Unconsciousness

● Diarrhea Coma

● Upset stomach Blackouts

● Headaches
● Breathing difficulties >respiratory depression
● Distorted vision and hearing
● Impaired judgment
● Decreased perception and coordination
● Nystagmus
Long Term Effects
Binge drinking and continued alcohol use in large amounts are associated with many health problems,
including:
● Alcohol poisoning
● High blood pressure, stroke, and
other heart-related diseases

● Liver disease-Cirrhosis
● Nerve damage
Diagnosis
 Blood alcohol content (BAC)
 Blood Alcohol Concentration (BAC) is the amount of
alcohol in the bloodstream or on one’s breath. BAC is
expressed as the weight of ethanol, in grams, in 100
milliliters of blood, or 210 liters of breath. BAC can be
measured by breath, blood, or urine tests.

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Diagnosis
 Serum osmolality (if BCA not available)
 Normal serum osmolality ranges from 285 to 290 mOsm/L
 Osmolal gap > 20 mOsm/L indicates accumulation of alcohol in the blood
(methanol, ethanol, isopropanol, ethylene glycol, propylene glycol, or
diethylene glycol)
 Osmolal gap can also be present with other disorders but the gap is usually
≤ 15-20 mOsm/L
 The absence of an osmolal gap does not exclude ethanol intoxication
as alcohol concentrations that produce laboratory abnormalities may not be
high enough to raise serum osmolality

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Others
• ECG: P wave and QTc prolongation may be the most common ECG
changes associated with acute alcohol intoxication
• Blood glucose (especially in infant and young children) >> limited
glycogen store
• Serum electrolyte determinations assess for electrolyte disturbance
and allow for calculation of the anion gap in the setting of likely
coingestants or evidence for metabolic acidosis
• Arterial or venous blood gas measurement combined with pulse
oximetry >> respiratory distress
• Liver function test

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Others
• Antiemetic : in patients with nausea and/or vomiting
• Metadoxine 300-900 mg IV has been used to reduce symptom duration by
accelerating ethanol elimination in patients with acute intoxication
• Metadoxine is the ion pair between pyrrolidone carboxylate and pyridoxine,
and has been reported to accelerate ethanol metabolism in both animal and
human studies.
• Pyrrolidone carboxylate involved in amino acid metabolism via the
glutathione pathway: facilitates de novo adenosine triphosphate (ATP)
synthesis, in animal studies, prevents ATP from decreasing in the brain
and liver following acute ethanol intoxication
• Pyridoxine increases metabolic degradation rate of alcohol, which can
reduce cell damage caused by acetaldehyde

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 Others
 Gastrointestinal decontamination: Because ethanol is rapidly absorbed,
often induces vomiting, and does not bind to activated charcoal, gastric
emptying (eg, gastric lavage, syrup of ipecac administration) or
gastrointestinal decontamination (administration of activated charcoal [AC])
do not prevent or lessen ethanol intoxication and pose a small but
definite risk of pulmonary aspiration
• Extracorporeal removal: Elimination of ethanol occurs three to four times
faster with hemodialysis. Possible candidates for hemodialysis include
patients with liver disease that significantly decreases ethanol metabolism or
those with blood ethanol levels greater than 450 mg/dL (100 mmol/L)

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CHILDREN

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Referensi
 Pitzele HZ, Tolia VM. Twenty per hour: altered mental state due to ethanol abuse and
withdrawal. Emerg Med Clin North Am. 2010 Aug;28(3):683-705Gummin DD, Mowry JB, Spyker
 Diamond I, Messing RO. Neurologic effects of alcoholism. West J Med. 1994 Sep;161(3):279-87
 Noble JM, Weimer LH. Neurologic complications of alcoholism. Continuum (Minneap Minn). 2014
Jun;20(3 Neurology of Systemic Disease):624-41
 Olson KR et al, 2018, Poisoning & Drug Overdose, 7th Ed, Lange, New York
 DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 - . Record No. T115687,
Alcohol Intoxication; [updated 2018 Nov 30, cited place cited date here]. Available from
https://www.dynamed.com/topics/dmp~AN~T115687.
• Baum CR, 2019, UpToDate Ethanol intoxication in children: Clinical features, evaluation, and
management

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