DR BABAK MASOUMI ASSISTANT PROFESSOR OF EMERGENCY MEDICINE ESFAHAN UNIVERSITY OF MEDICAL SCIENCES 2011 Alcohols

DR BABAK MASOUMIASSISTANT PROFESSOR OF

EMERGENCY MEDICINEESFAHAN UNIVERSITY OF MEDICAL SCIENCES

2011

Alcohols

Types of alcohol Beer Wine Spirits

Vodka Gin Whiskey Rum

Ethanol / Ethyl alcohol

Methanol / Methyl alcohol

Isopropanol / Isopropyl alcohol

Ethylene glycol Propylene glycol Fusel oil

Ethanol

CH

H

H

OH

Ethyl Alcohol

C

H

H

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.

. 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

CH

H

H

OH

Methyl Alcohol

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

Ethylene Glycol / Methanol



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.


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 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

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.

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.

Some Current Facts:

ETHANOL 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.

"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

Ancient Awareness

آيات >> در خمر شربكريم <<قران

آیه (43متن ترجمه ) نساء سوره : ! نزدیك نماز به مستى حال در اید آورده ایمان كه كـسـانى اى

مـیـگـویـیـد چه بدانید تا .نشوید،

آیه (92 - 90متن ( ترجمه مائده سوره :بخت ) یكنوع كه الم از و بتها و قمار و شراب اید آورده ایمان كه كسانى اى

شوید ( رستگار تا كنید دورى آنها از شیطانند عمل از و پلیدند بوده ..آزمائى

آیه (219متن ترجمه ) بقره سوره : « : زیان و گناه دو آن در بگو كنند، مى سؤال تو از قمار و شراب درباره

; ) ( ; آنها گناه ولى بردارد در مردم براى مادى نظر از منافعى و است بزرگى « : » « : ». از بگو كنند؟ انفاق چیز چه پرسند مى تو از و است بیشتر نفعشان از ; ». سازد مى روشن شما براى را آیات خداوند اینچنین خود نیازمندى مازاد

بیندیشید .شاید

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.


The clinically observed cross-tolerance 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.


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.


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.


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 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.

• CNS Depressant• Depression of inhibitory control• Vasodilation, warm, flushed,

reddish skin• Emotional outbursts• Decreased memory & concentration• Poor judgment• Decreased reflexes• Decreased sexual response

Acute Effects

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 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.

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 Concentration

)mg/dL) Manifestations Clinical <30 Little demonstrable effect

30-50 Mild euphoria, minimal central nervous system effects, subjective sensation of cutaneous warmth

50-80 Relaxation, jocularity, gregariousness, cutaneous flushing, prolongation of reaction time

80-100 Statutory intoxication in many jurisdictions

100-200 Loquacity, animation, exuberance, exaggerated emotional responses, uninhibited behavior, impaired judgment

200-300 Sedation interrupted by periods of boisterous or antisocial behavior, nausea, emesis, dysarthria, horizontal nystagmus, impaired visual pursuit, diplopia, ataxia

300-400 Unstable station and gait, incoherent speech, somnolence, impairment of protective airway reflexes, incontinence, obtundation, stupor

>400 Coma, loss of protective reflexes, respiratory depression, death

Clinical Features 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 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 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.

TreatmentThe risk of sudden death among users of both drugs simultaneously may be as high as 20 times that with cocaine alone.

Treatment Ethanol is the most common cause of an

osmolar gap . The concomitant presence of an anion-

gap (AG) metabolic acidosis may help characterize the presence of a coingestant.

Methanol and ethylene glycol poisoning are associated with significant widened AG-type 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 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.

Documents

DR BABAK MASOUMI ASSISTANT PROFESSOR OF EMERGENCY MEDICINE ESFAHAN UNIVERSITY OF MEDICAL SCIENCES 2011 Alcohols