ethanol intoxication1

7/28/2019 Ethanol Intoxication1

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ETHANOL

ACUTE andCHRONIC

INTOXICATION


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Epidemiological data

45 to 50% of adults are currentdrinkers

20% are former drinkers

30 to 35% are lifetime abstainers

Alcohol use as a risk for healthenormously contributes to the burdenof disease world-wide.


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For most drinkers, the frequency andamount of alcohol consumption doesnot impair physical or mental health orthe ability to safely carry out daily

activities.

Acute alcohol intoxication is a

significant factor in injuries. Alcohol isinvolved in about 40% of motor vehicleaccidents, 47-70% of homicides, 25-37% of suicides.


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Chronic abuse interferes with the ability

to socialize and work.

About 7 to 10% of adults meet criteriafor an alcohol use disorder (abuse ordependence) in any given year.

Binge drinking, defined as consuming

5 dr inks per occasion fo r men

4 dr inks per occasion fo r women

is a particular problem among youngerpeople.


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DEFINITIONS

At-risk drinking is defined solely by quantityand frequency of drinking:

> 14 drinks/wk or 4 drinks per occasion formen

> 7 drinks/wk or 3 drinks per occasion for

womenAlcohol abuse refers to a maladaptive

pattern of episodic drinking that results infailure to fulfill obligations, drinking in

physically hazardous situations (eg,driving, boating), legal problems, or socialand interpersonal problems withoutevidence of dependence.


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DEFINITIONS

Alcohol dependence refers to frequent consumption oflarge amounts of alcohol with 3 of the following:

Tolerance Withdrawal symptoms

Drinking larger amounts than intended

Persistent desire to reduce use without success

Substantial time spent obtaining, drinking, orrecovering from alcohol

Sacrifice of other life events for drinking

Continued use despite physical or psychologic

problems Alcoholism is often used as an equivalent term for

alcohol dependence, especially when drinkingresults in significant toxicity and tissue damage.


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One serving of alcohol (can of beer, glass of

wine, or glass of distilled liquor) contains10 to 15 g of ethanol.

Alcohol is absorbed into the blood mainlyfrom the small bowel, although some isabsorbed from the stomach.

Alcohol accumulates in blood becauseabsorption is more rapid than oxidation andelimination.

The concentration peaks about 30 to 90 minafter ingestion if the stomach waspreviously empty.

Pharmacological data


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Pharmacological data

About 5 to 10% of ingested alcohol isexcreted unchanged in urine, sweat, andexpired air; the remainder is metabolizedmainly by the liver, where alcohol

dehydrogenase converts ethanol toacetaldehyde.

Acetaldehyde is ultimately oxidized to

CO2 and water at a rate of 5 to 10 mL/h (ofabsolute alcohol);

Each milliliter yields about 7 kcal.


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Alcohol exerts its effects by several

mechanisms.

Alcohol binds directly to -

aminobutyric acid (GABA) receptorsin the CNS, causing sedation.

Alcohol also directly affects cardiac,hepatic, and thyroid tissue.


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Acu te effects -Symptoms progress

proportionately to the BAC.

20 to 50 mg/dL: Tranquility, mild

sedation, and some decrease in finemotor coordination

50 to 100 mg/dL: Impaired judgmentand a further decrease in coordination


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Acu te effects :

100 to 150 mg/dL: Unsteady gait,

nystagmus, slurred speech, loss ofbehavioral inhibitions, and memoryimpairment

150 to 300 mg/dL: Delirium andlethargy (likely)

Emesis is common with moderate to

severe intoxication; because emesisusually occurs with obtundation,aspiration is a significant risk


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Tox ic i ty or overdose:

In alcohol-naive people, a BAC of 300 to 400mg/dL often causes unconsciousness, and a

BAC 400 mg/dL may be fatal.

Sudden death due to respiratory depression

or arrhythmias may occur, especially when

large quantities are drunk rapidly.

Other common effects include hypotension

and hypoglycemia.


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On the other hand, low to moderate levels

of alcohol consumption ( 1 to 2drinks/day) may decrease the risk of death

due to cardiovascular disorders.

Numerous explanations, including

increased high density lipoprotein (HDL)

levels and a direct antithrombotic effect,have been suggested. Nonetheless,

alcohol should not be recommended for

this purpose.


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Diagnosis

acute intoxication

Usually clinical

BAC, evaluation to rule out hypoglycemiaand occult trauma

Confirmation by breath or blood alcohollevels is useful for legal purposes (eg, to

document intoxication in drivers or

employees who appear impaired).


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Diagnosis

acute intoxication

Finding a low BAC in patients who have altered

mental status and smell of alcohol is helpful

because it expedites the search for an alternate

cause.

Clinicians should not assume that a high BAC in

patients with apparently minor trauma accounts

for their obtuntation, which may be due tointracranial injury or other abnormalities. Such

patients should also have toxicology tests to

search for evidence of toxicity due to other

substances.


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Treatment

The stomach may be lavaged, but care mustbe taken to prevent pulmonary aspiration ofthe return flow.

Since ethanol is freely miscible with water,ethanol can be removed from blood byhemodialysis.


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Treatment a. Management is mainly supportive, with

observation predominant. Intubate and ventilate ifnecessary.

b. AdministerIV glucose 50 g and thiamine 100mg to all obtunded patients after serum glucoselevel is drawn.

c. Correct volume depletion as needed.

d. If the patient is violent or very agitated, usephysical restraints as needed. Sedation may be

necessary. e. Treatment of alcoholic ketoacidosis: Fluid

replacement with dextrose 5%/normal saline.

Observe for appearance of hypoglycemia,

hypophosphatemia, and hypokalemia.


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CHRONIC EFFECTS:

Tolerance to alcohol develops rapidly and it is

caused by adaptational changes of CNS cells and

by induction of metabolic enzymes.

Ethanol tolerance is incomplete, and considerable

intoxication and impairment occur with a large

enough amount.


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Chronic heavy alcohol intake typically leads to:

Liver disorders (eg, fatty liver, alcoholichepatitis, cirrhosis); the amount and duration

required vary.

Patients with a severe liver disorder often have

coagulopathy due to decreased hepatic synthesis

of coagulation factors, increasing the risk of

significant bleeding - alcohol abusers are at

particular risk of GI bleeding. Gastritis

Pancreatitis


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Cardiomyopathy, often accompanied by

arrhythmias and hypertension

Peripheral neuropathy Brain damage: Wernicke's encephalopathy,

Korsakoff's psychosis, Marchiafava-Bignami

disease, and alcoholic dementia Certain cancers (eg, head and neck, esophageal),

especially when drinking is combined with smoking

Indirect long-term effects include undernutrition,particularly vitamin deficiencies.


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Marchiafava-Bignami disease

is a rare condition characterized by

demyelination of the corpus callosum.

it is seen most often in patients withchronic alcoholism


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Wernicke's encephalopathy

Thiamine (vitamin B-1) deficiency

A triad of: acute mental confusion +

ataxia + ophthalmoplegia.

Korsakoff amnestic syndrome is a lateneuropsychiatric manifestation of

Wernicke encephalopathy with memory

loss and confabulation


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Administration of dextrose in the setting of

thiamine deficiency can be harmful because

glucose oxidation is a thiamine-intensive

process that may drive the insufficientcirculating vitamin B-1 intracellularly, thereby

precipitating neurologic injury.

Wernicke's encephalopathy


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Dupuytren's contracture of the palmar

fascia,

vascular spiders, in men, signs ofhypogonadism and feminization (eg, smooth

skin, lack of male-pattern baldness,

gynecomastia, testicular atrophy).

enlarged parotid glands.

CHRONIC EFFECTS:

Withdrawal


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Withdrawal

Withdrawal following chronic use produces

a number of signs and symptoms, including

anxiety, insomnia, tremulousness, nausea,

vomiting, tachycardia, hyperthermia,

delirium, hallucinations, and seizures.

The hallmark of delirium tremens is

significant alteration of the sensorium

(global confusion, hallucinations, delusions,disorientation) accompanied by autonomic

CNS hyperreactivity


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Delirum tremens

Begins 48 to 72 h after alcohol withdrawal;

anxiety attacks, increasing confusion, poor sleep

(with frightening dreams or nocturnal illusions),

profuse sweating, and severe depression also

occur.

Fleeting hallucinations that arouse restlessness,

fear, and even terror are common. Typical of the

initial delirious, confused, and disoriented state is areturn to a habitual activity; eg, patients frequently

imagine that they are back at work and attempt to

do some related activity.


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Delirum tremens

Mild delirium is usually accompanied by marked

diaphoresis, a pulse rate of 100 to 120 beats/min,

and a temperature of 37.2 to 37.8 C. Marked

delirium, with gross disorientation and cognitivedisruption, is accompanied by significant

restlessness, a pulse of > 120 beats/min, and a

temperature of >37.8 C; risk of death is high.


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Delirum tremens

During DT, patients are suggestible to manysensory stimuli, particularly to objects seenin dim light.

Vestibular disturbances may cause them tobelieve that the floor is moving, the walls arefalling, or the room is rotating.

Ataxia is marked; care must be taken to

prevent self-injury. Symptoms vary among patients but are

usually the same for a particular patient witheach recurrence.


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Diagnosis - chronic intoxication

clinical diagnose experimental markers of long-term use have

not proved sufficiently sensitive or specific for

general use.

heavy alcohol users may have a number of

metabolic derangements: CBC, electrolytes

(including Mg), liver function tests including

coagulation profile (PT/PTT), and serumalbumin

withdrawal: evaluation to rule out CNS injury

and infection


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Withdrawal

A. SEDATION

(1). Benzodiazepines: diazepam 510 mg IV/chlordiazepoxide 25100 mg IV or PO q6 h, orlorazepam 12 mg IV, IM, or PO

(2). Phenobarbital 260 mg slow IV, repeat as

needed to produce light sedation ifbenzodiazepines are ineffective, but respiratorydepression is a risk with concomitant use.

(3). Haloperidol: Begin with 0.51.0 mg IV or IM

q16 h, but much largerdoses may be required. Phenothiazinesand haloperidol are not recommended initiallybecause they may lower the seizure threshold.

(4). Propofol


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Withdrawal

B. THIAMINE 100 mg IV

c. If severe hypertension ortachycardia is present, administerCLONIDINE 0.10.2 mg q6 h.

d. Other agents that have been usedinclude beta-blockers, baclofen, and

carbamazepine.

e. The use of ethanol to controlwithdrawal is discouraged in thesetting of acute alcohol withdrawal.


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Alchool dependence

TREATMENT

Rehabilitation programs

Outpatient counseling

Self-help groups

Consideration of drugs (eg, naltrexone,disulfiram, acamprosate)


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Disulfiram the first drug available to prevent relapse in alcohol dependence interferes with the metabolism of acetaldehyde (an intermediary

product in the oxidation of alcohol) so that acetaldehydeaccumulates.

drinking alcohol within 12 h of taking disulfiramcauses facial flushing in 5 -15 min, then intense vasodilation of theface and neck with suffusion of the conjunctivae, throbbingheadache, tachycardia, hyperpnea, and sweating.

with high doses of alcohol, nausea and vomiting may follow in 30 to60 min and may lead to hypotension, dizziness, and sometimesfainting and collapse. The reaction can last up to 3 h.

is contraindicated during pregnancy and in patients with cardiacdecompensation.

it may be given on an outpatient basis after 4 or 5 days of abstinence.Adherence usually requires adequate social support, such asobservation of drinking.


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Acamprosate

a synthetic analogue of-aminobutyricacid

is given as 2 g po

decrease the relapse rate and number ofdrinking days in patients who relapse.


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Naltrexone

an opioid antagonist

decreases the relapse rate and number ofdrinking days in most patients who take it

consistently 50 mg po once/day is typically given, although

there is evidence that higher doses (eg, 100mg once/day) may be more effective in some

patients is contraindicated in patients with acute

hepatitis or liver failure and in those who areopioid dependent.


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Fetal alcohol syndrome (FAS)

Children born to alcoholic mothers display acommon pattern of distinct dysmorphologyknown as

fetal alcohol syndrom e(FAS).

The diagnosis of FAS typically is based on theobservance of a triad of abnormalities in thenewborn, including

(1) a cluster of craniofacial abnormalities,

(2) CNS dysfunction,

(3) pre- and/or postnatal stunting of growth.


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Fetal alcohol synd rome(FAS)

Important considerations of FAS that may affecttreatment rendered by dental clinicians include multiplefacial deformities contributing to mouth breathing andcorresponding dry mouth.

Mouth breathers tend to have a higher incidence of cariesand gingivitis due to loss of the buffering capacity ofsaliva and gingival irritation due to drying. In thesepatients, it is paramount to stress the importance ofimpeccable oral hygiene.

The orofacial manifestations that dentists should beconcerned with include CNS and oral/motor deficits, poortongue thrusting, temporomandibular joint (TMJ)

disorders, cleft lip/palate, and dental malocclusions.


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FAS


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FAS

Shakespeare


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Shakespeare

-scene ofMacbeth-

The Porter, awakened from an alcohol-induced sleep by Macduff, explains thecontradictory aspects of soaringoverconfidence with physical impairment.

Porter : s i r , i t provokes and unprovokes: i tpro vokes the desire but i t takes away theperformance.

ethanol intoxication1

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