Transcript Alcoholoxicity.ppt

Alcohols
DR BABAK MASOUMI
ASSISTANT PROFESSOR OF
EMERGENCY MEDICINE
ESFAHAN UNIVERSITY OF MEDICAL SCIENCES
2011
Types of alcohol
Beer
 Wine
 Spirits
 Vodka
 Gin
 Whiskey
 Rum
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
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
Ethanol / Ethyl
alcohol
Methanol / Methyl
alcohol
Isopropanol /
Isopropyl alcohol
Ethylene glycol
Propylene glycol
Fusel oil
Ethanol
H
H
H
C
C
H
H
Ethyl Alcohol
OH
. The ethanol concentration in distilled spirits is traditionally listed in terms of proof. In the United States, this expression represents twic
PROOF:
The ethanol concentration in
distilled spirits is traditionally listed
in terms of proof.
 In the United States, this
expression represents twice the
percentage concentration; for
example, 80 proof is equivalent to
40% ethanol by volume.

Methanol
H
H
C
H
Methyl Alcohol
OH
Methanol Poisoning


A product of wood distillation, it is a
component of many paint removers, varnishes,
shellacs, windshield washing fluids, and
antifreeze formulations.
Methanol poisoning has resulted from the
consumption of contaminated whiskey,
accidental ingestion by desperate alcoholics, or
intentional ingestion during suicide attempts.
Methanol Poisoning
Methanol is also present in measurable
but small amounts in wine and distilled
spirits, accounting for the fact that low
levels may be detectable in the blood
after binge drinking.
 Methanol's toxicity is due to the
formation of two toxic metabolites,
formaldehyde and formic acid.

Methanol
Methanol
Ethylene glycol
Ethylene Glycol
Ethylene glycol has many commercial
uses as a coolant (antifreeze),
preservative, and glycerine substitute;
it has also been used in lacquers,
cosmetics, polishes, and detergents.
 Ethylene glycol's toxicity is the result
of the formation of two toxic
metabolites, Glycoaldehyde and Glycolic
acid.

Ethylene Glycol / Methanol
Ethylene Glycol
Isopropanol / Isopropyl
alcohol
Isopropanol / Isopropyl
alcohol
Isopropanol= isopropyl alcohol and
2+propanol.
 It is also used widely in industry as a
solvent and disinfectant ,component of
a variety of skin and hair products,
jewelry cleaners, detergents, paint
thinners, antifreeze. Poisoning usually
results from ingestion.

Isopropanol / Isopropyl
alcohol
May also occur after inhalation or
dermal exposure in poorly ventilated
areas—for example, during alcohol sponge
bathing.
 Its principal metabolite, acetone, does
not cause the eye, kidney, cardiac, or
metabolic toxicity caused by the
metabolites of methanol and ethylene
glycol.

Isopropanol / Isopropyl
alcohol
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Isopropanol is approximately twice as
potent as ethanol in causing central nervous
system depression and its duration is two
to four times that of ethanol.
After ethanol, it is the second most
commonly ingested alcohol.
Though more toxic than ethanol, it is
considerably less so than methanol or
ethylene glycol.
Propylene glycol
Production of Alcohol
Fermentation – Sugar to Alcohol
and Carbon dioxide
C6H12O6→ 2(CH3-CH2-OH) + 2CO2
ETHANOL

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Ethanol is the most frequently used and
abused intoxicant in the United States and
most other societies.
Nearly three-quarters of adult Americans
consume at least one alcoholic drink each year.
Beer ranks as the fourth most popular
beverage in terms of volume consumed, after
soft drinks, milk, and coffee.
Some Current Facts:
 7.4% of adult population in U.S.
alcoholic
 $185 Billion – cost of alcohol abuse in
U.S.
 100,000 deaths annual in U.S. related
to
 $1.2 Billion spent on wine, beer and
liquor advertisements in U.S.
ETHANOL
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One-quarter of the victims of interpersonal
trauma report alcohol use by their
assailants.
Alcohol abuse as reported by the injured
woman is the strongest predictor for acute
injury related to domestic violence.
The prevalence and lifelong risk of alcohol
abuse or dependence are 7 and 13 percent.
Ancient Awareness
"You will conceive and bear a son…now
then be careful to take no wine or
strong drink and to eat nothing
unclean".
Bible - Judges 13:3-4
‫>>شرب خمر در آيات قران كريم<<‬
‫متن آيه ‪ 43‬سوره نساء (ترجمه) ‪:‬‬
‫اى كـسـانى كه ايمان آورده ايد! در حال مستى به نماز نزديك نشويد‪ ،‬تا بدانيد چه‬
‫مـيـگـويـيـد‪.‬‬
‫متن آيه ‪ 92 - 90‬سوره مائده (ترجمه) ‪:‬‬
‫اى كسانى كه ايمان آورده ايد شراب و قمار و بتها و از الم (كه يكنوع بخت آزمائى بوده ) پليدند و از عمل‬
‫‪.‬شيطانند از آنها دورى كنيد تا رستگار شويد‪.‬‬
‫متن آيه ‪219‬سوره بقره (ترجمه) ‪:‬‬
‫درباره شراب و قمار از تو سؤال مى كنند‪ ،‬بگو‪« :‬در آن دو گناه و زيان بزرگى است; و منافعى (از نظر‬
‫مادى) براى مردم در بردارد; ولى گناه آنها از نفعشان بيشتر است‪ ».‬و از تو مى پرسند‪« :‬چه چيز انفاق‬
‫كنند؟» بگو‪« :‬از مازاد نيازمندى خود‪ ».‬اينچنين خداوند آيات را براى شما روشن مى سازد; شايد بينديشيد‪.‬‬
IN IRAN
Pharmacology and
Metabolism
Ethanol is a CNS depressant which
inhibits neuronal activity.
 Alcohol intoxication is associated with
the depression of the excitatory
neurotransmitter glutamate and alcohol
increases the inhibitory activity of the
neurotransmitters -aminobutyric acid
(GABA) and glycine.

Pharmacology and
Metabolism

The clinically observed crosstolerance that exists between ethanol
and other sedative-hypnotic agents,
including benzodiazepines and
barbiturates, appears related to the
similar affects that these agents
have on brain chemistry.
Pharmacology and
Metabolism
Ethanol absorption :
 In the mouth and esophagus to a
small extent.
 In the stomach and large bowel to a
moderate extent.
 In the proximal portion of the small
bowel chiefly absorbed.
Pharmacology and
Metabolism
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Approximately 2 to 10 percent of
ethanol may be excreted by the lungs,
in urine, or in sweat, the proportion
being dependent on blood
concentration.
The Reminder of ethanol metabolized
to acetaldehyde in the liver by one of
two pathways.
Pharmacology and
Metabolism
1)In the cell, cytosol alcohol
dehydrogenase with nicotinamide adenine
dinucleotide as a cofactor produces
acetaldehyde, which in turn is
metabolized by aldehyde dehydrogenase.
2) The second pathway, which is
clinically significant at high blood
ethanol concentrations and has increased
activity with repeated exposures to
ethanol, is a microsomal alcohol oxidizing
system.
Gender-related differences
in the metabolism
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Gender-related differences in the
metabolism of ethanol explain the
considerably higher blood ethanol levels in
women versus men after similar dosing on a
gram-per-kilogram basis.
Women have a smaller volume of distribution
(0.6 L/kg) for ethanol than men (0.7 L/kg)
and have decreased first-pass metabolism of
ethanol because their gastric walls contain
less alcohol dehydrogenase than do those of
men.
Opioid/Sedative/Ethanol
Toxidrome
 Common
Signs:
Coma,respiratorydepression,
miosis,hypotension,bradycardia,
hypothermia,pulmonary
edema,decreased Bs,
hyporeflexia.
Acute Effects
•
•
•
•
•
•
•
•
CNS Depressant
Depression of inhibitory control
Vasodilation, warm, flushed, reddish skin
Emotional outbursts
Decreased memory & concentration
Poor judgment
Decreased reflexes
Decreased sexual response
Clinical Features
 Symptoms
and signs of
ethanol intoxication include
slurred speech, nystagmus,
disinhibited behavior, central
nervous system depression
including coma, and
decreased motor coordination
and control.
Clinical Features

A lowering of blood pressure or even
hypotension with resultant reflex
tachycardia are common secondary to
a decrease in total peripheral
resistance or as a result of volume
loss. Changes in posture may result in
syncope. However, when hypotension
is present, other causes must be
considered.
Clinical Features
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Because of the phenomenon of tolerance,
blood alcohol levels correlate poorly with
degree of intoxication.
While death from respiratory depression
may occur in unhabituated individuals at
concentrations of 400 to 500 mg/dL, it is
not uncommon for some alcoholics to
appear minimally intoxicated at blood
concentrations as high as 400 mg/dL.
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Blood Ethanol Concentration(mg/dl)
=Volume Ingested(ml)× Ethanol
Concentration × /0.6 × Weight
Accordingly, each 1 ounce of 100 proof
whiskey, 12 ounces of beer, or 4 ounces of a
typical table wine consumed by a 70-kg man
should theoretically raise the blood ethanol
concentration by approximately 30 mg/dL.
Blood
Ethanol
Concentratio
n (mg/dL)
Manifestations Clinical
<30 Little demonstrable effect
Mild euphoria, minimal central nervous system effects,
30-50 subjective sensation of cutaneous warmth
Relaxation, jocularity, gregariousness, cutaneous flushing,
50-80 prolongation of reaction time
Statutory intoxication in many jurisdictions
80-100
Loquacity, animation, exuberance, exaggerated emotional
100- responses, uninhibited behavior, impaired judgment
200
Sedation interrupted by periods of boisterous or antisocial behavior,
200-
Clinical Features
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Although most states have adopted 80
or 100 mg/dL as the legal definition of
intoxication for the purposes of driving
a motor vehicle.
There is considerable evidence to
suggest that impairment may be seen
with levels as low as 5 mg/dL,
especially in unhabituated individuals.
Clinical Features
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A mild lactic acidosis may be seen.
However, significant acidosis should
never be attributed to alcohol
intoxication, and should prompt an
aggressive search for another cause.
In the presence of volume depletion, a
mild contraction alkalosis may be noted,
as may pre-renal azotemia.
Treatment
 Management
of acute ethanol
intoxication consists of attending
to associated injuries or medical
illness and observation until clinical
sobriety is attained.
 A careful examination should be
performed to evaluate for
complicating injuries or medical
conditions.
Treatment:
 Ethanol
levels are not necessarily
required for mild or moderate
intoxication when no other
abnormality is suspected. It is
appropriate in all patients with
depressed level of consciousness or
altered mental status.
 The most appropriate fluid is
D5NS.
Treatment
Hypoglycemia should be excluded by a
bedside glucose determination.
 In the event of severe depression of
mental status, causes other than
alcohol ingestion must be considered,
especially subdural hematoma, which
can occur in the absence of external
signs of trauma.

Treatment
 Fluid
administration does not hasten
alcohol elimination.
 Intravenous
access for fluid
administration alone is unnecessary
in uncomplicated cases of mild to
moderate intoxication unless clinical
signs of volume depletion are
present.
Treatment
 Any
alcoholic with CNS depression,
even if apparently attributable to
intoxication, should receive
thiamine.
 Folate
and other vitamins are
indicated only if there are clinical
signs or laboratory confirmation of
deficiency.
Treatment
 Ethanol
does not bind to
Activated charcoal, which should
be administered only if other
substances have been ingested
that are adsorbable.
Treatment
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Careful and serial observation is
crucial, as in the vast majority of
uncomplicated cases rapid improvement
occurs over a few hours.
Mental status that fails to improve
and any deterioration should be
considered secondary to other causes
and evaluated aggressively.
Treatment
 Respiratory
depression may result
in carbon dioxide retention, which
on rare occasion may require
intubation.
Treatment
 Unhabituated
patients eliminate
ethanol from the bloodstream at
a rate of 15 to 20 mg/dL per h.
 Alcoholics
average 25 to 35
mg/dL per h.
Treatment

Alcoholics should be questioned about
concomitant drug use.
In the past, ethylene glycol or methanol
was occasionally substituted for or
combined with ethanol.
Today Cocaine has clearly become the most
common concomitant drug used by
alcoholics.
Treatment
 The
risk of sudden death
among users of both drugs
simultaneously may be as high
as 20 times that with cocaine
alone.
Treatment
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Ethanol is the most common cause of an
osmolar gap .
The concomitant presence of an aniongap (AG) metabolic acidosis may help
characterize the presence of a
coingestant.
Methanol and ethylene glycol poisoning are
associated with significant widened AGtype acidosis.
Disposition
 Morbidity
and mortality in
association with acute
intoxication are predominantly
the result of injuries, often
motor vehicle collisions related to
ethanol-induced deficits in
judgment or physical capabilities.
Disposition
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Patients with acute ethanol intoxication
alone rarely require hospital admission.
Questions frequently arise over alcoholics
who appear clinically sober while still
having considerable blood ethanol
concentrations.
Medical judgment of mental competence
should not be confused with any particular
blood alcohol concentration level.
Disposition

Patients whose intoxication has resolved
to the extent that they do not
constitute a danger to themselves or
others, and who will not be responsible
for their own transportation, may be
discharged on their own recognizance or
preferably in the company of
responsible friends or relatives who can
assist them and take some
responsibility for their care.
Disposition
 Discharge
(after excluding
significant abnormal laboratory
values or suspected head injury)
can be considered if a concerned,
sober adult is willing to take
responsibility for and remain with
the patient for the next 24 to 48
hours.
Disposition

Patients who are to drive themselves
home should have ethanol levels close
to zero, not merely below a given
state's legal level for driving, as there
is the theoretical potential for
psychometric disability at very low
levels, and the potential liability for
the emergency physician is
unfortunately huge.