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Alcohol: V Sem KMC Ic
Alcohol: V Sem KMC Ic
V Sem
KMC IC
ACUTE ETHANOL
INTOXICATION
• An increased reaction time,
• diminished fine motor control,
• impulsivity,
• and impaired judgment become evident when the
concentration of ethanol in the blood is 20 to 30
mg/dl.
• More than 50% of persons are grossly intoxicated
by a concentration of 150 mg/dl.
• In fatal cases, the average concentration is about
400 mg/dl.
• In the United States, most states set the ethanol
level defined as intoxication at 80 mg/dl.
• There is increasing evidence that lowering the
limit to 50 to 80 mg/dl can reduce motor vehicle
injuries and fatalities significantly.
• While alcohol can be measured in saliva, urine,
sweat, and blood, measurement of levels in
Treatment of acute alcohol
intoxication
• The treatment of acute alcohol
intoxication is based on the severity of
respiratory and CNS depression.
• Acute alcohol intoxication can be a
medical emergency,
• Patients who are comatose and who
exhibit evidence of respiratory depression
• Should be intubated to protect the airway
and to provide ventilatory assistance.
• The stomach may be lavaged, but care
must be taken to prevent pulmonary
aspiration of the return flow.
• Since ethanol is freely miscible with water,
• Acute alcohol intoxication is not always
associated with coma, and careful
observation is the primary treatment.
• Usual care involves observing the patient in
the emergency room for 4 to 6 hours while
the patient metabolizes the ingested
ethanol.
• Blood alcohol levels will be reduced at a
rate of about 15 mg/dl per hour.
• During this period, some individuals may
display extremely violent behavior.
• Sedatives and antipsychotic agents have
been employed to quiet such patients.
• Great care must be taken, however, when
using sedatives to treat patients who have
ingested an excessive amount of another
CNS depressant, i.e., ethanol, because of
synergistic effects.
• The use of alcohol to treat patients in
alcohol withdrawal or obstetrical
patients with premature contractions
is no longer recommended.
• Some medical centers continue to
use alcohol to prevent or reduce the
risk of alcohol withdrawal in
postoperative patients,
• but administering a combination of a
benzodiazepine with haloperidol or
clonidine may be more appropriate.
Methanol Poisoning
• Added to rectified spirit to render it
unfit for drinking
• No pharmacological relevence
• Highly toxic
Treatment consists of
• Keep patient in quiet,dark room:protect
eyes from light---even 15ml of methanol has
caused blindness
• Gastric Lavage with sodium bicarbonate to
combat acidosis,
• hemodialysis, and the
• Pot Chloride is needed only when
hypokalemia occurs
• administration of ethanol,
• Slows formate production by competing
with methanol
• For metabolism by alcohol dehydrogenase.
• Fomipezole – inhibits Alcohol Dh
• Folate therapy-Ca leucovorin reduces blood
formate levels
CLINICAL USES OF
ETHANOL
• Dehydrated alcohol may be injected in close
proximity to nerves or sympathetic ganglia
-to relieve the long-lasting pain related to
trigeminal neuralgia, inoperable carcinoma, and
other conditions.
• Epidural, subarachnoid, and lumbar paravertebral
injections of ethanol also have been employed for
inoperable pain.
• For example, lumbar paravertebral injections of
ethanol may destroy sympathetic ganglia
• and thereby produce vasodilation, relieve pain,
and
• promote healing of lesions in patients with
• Systemically administered ethanol is
confined to the treatment of
poisoning by methyl alcohol and
ethylene glycol.
• The ingestion results in
• formation of methanol's metabolites,
formaldehyde and formic acid .
• Formic acid causes nerve damage;
its effects on the retina and optic
nerve can cause blindness.
PHARMACOTHERAPY OF
ALCOHOLISM
• Currently, three drugs are approved
in the United States for treatment of
alcoholism: disulfiram (ANTABUSE),
naltrexone (REVIA), and
acamprosate.
• The goal of these medications is to
assist the patient in maintaining
abstinence.
Naltrexone
approved by the FDA for treatment of
alcoholism in 1994.
• opioid-receptor antagonist
• has higher oral bioavailability and a
longer duration of action.
• Animal research and clinical
experience suggested that
• blocks activation by alcohol of
dopaminergic pathways in the brain
that are thought to be critical to
reward.