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Barbiturates: Uses, Risks, and History

Barbiturates, developed in 1862, are used to treat conditions like anxiety, depression, and insomnia, but are also abused for their euphoric effects. They are addictive and can lead to severe toxicity, including respiratory depression and withdrawal symptoms. Management of barbiturate overdose focuses on supportive care, as there is no specific antidote, and gastrointestinal decontamination may be necessary in cases of large overdoses.

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Uroosa Jamil
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46 views23 pages

Barbiturates: Uses, Risks, and History

Barbiturates, developed in 1862, are used to treat conditions like anxiety, depression, and insomnia, but are also abused for their euphoric effects. They are addictive and can lead to severe toxicity, including respiratory depression and withdrawal symptoms. Management of barbiturate overdose focuses on supportive care, as there is no specific antidote, and gastrointestinal decontamination may be necessary in cases of large overdoses.

Uploaded by

Uroosa Jamil
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

BARBITURATES

By [Link]
HISTORY OF BARBITURATES
1862 - Barbiturates were developed by Adolph von Bayer in 1862.
1903 – Put to use for the first time in medical practices.
Since 1903 – Over 2,000 types of barbiturates have been manufactured using
Bayer’s original formula.
HOW ARE BARBITURATES
CONSUMED?
•Orally – In pill, tablet or liquid form
•Injection –
• Into the blood stream
• Into muscle tissue
• Directly under the skin
•Inserted into the body via
suppository. ( A form of medicine
contained in a small piece of solid
material, such as cocoa butter or
glycerin, that melts at body
temperature)
WHICH DRUGS ARE
BARBITURATES?
Amobarbital. This can treat insomnia, but it's only
effective in the short term. ...
Butalbital. This medication is part of many
combination medications, including aspirin,
acetaminophen, caffeine and codeine. ...
Methohexital. ...
Pentobarbital. ...
Phenobarbital. ...
Primidone. ...
Secobarbital.
WHY ARE BARBITURATES
USED
•Barbiturates are prescribed to treat several medical conditions.
• Anxiety
• Depression
• Insomnia
• AOD Withdrawal
•Barbiturates are also consumed to get “high”.
•Used by drug users to treat the unpleasant effects of other drugs.
Barbiturates are addictive, producing physical d
ependence
and a withdrawal syndrome that can be life-
threatening. While tolerance to the mood-altering
effects of barbiturates develops rapidly with
repeated use, tolerance to the lethal effects develops
more slowly, and the risk of severe toxicity
increases with continued use.
PRINCIPLES OF DISEASE
•Barbiturates depress the activity of all excitable
cells, especially those in the central nervous system
(CNS) by enhancing the activity of γ-aminobutyric
acid (GABA), the major central inhibitor.

• In acute overdose, barbiturates decrease neural


transmission in autonomic ganglia, the myocardium,
and the gastrointestinal tract and also inhibit the
response to acetylcholine at the neuromuscular
junctions.
There are separate receptor sites for barbiturates and fo
r
benzodiazepines and a third site that binds GABA, ethanol,
and meprobamate.
Although barbiturates and ethanol can directly increase Cl−
conductance, benzodiazepines require the presence of
GABA to affect Cl−flow, which may account for the relative
safety of benzodiazepines in comparison with barbiturates.
Barbiturates produce dose-related depressive effects, fr
om
mild sedation to coma and fatal respiratory arrest.
• In the early stages of intoxication, some patients
experience euphoria. Barbiturates have no analgesic effect
and can paradoxically increase the reaction to pain at low
Barbiturates act directly on the medulla to produce
respiratory depression.
Therapeutic oral doses of barbiturates produce only mil
d
decreases in pulse and blood pressure, similar to sleep.
• With toxic doses, more significant hypotension occurs
from direct depression of the myocardium along with pooling
of blood in a dilated venous system.
Barbiturates also decrease cerebral blood flow and
intracerebral pressure.
• higher doses can decrease gastrointestinal smooth
muscle tone and peristaltic contractions and delay gastric
emptying.
Barbiturates are classified according to their onset and
duration of action:
(1) ultrashort-acting (onset immediate after intravenous
dose, duration minutes),
(2) short-acting (onset 10–15 minutes after oral dose,
duration 6–8 hours),
(3) intermediate-acting (onset 45–60 minutes, duration 10–
12 hours), and
(4) long-acting (onset 1 hour, duration 10–12 hours).
Only long-acting preparations have anticonvulsant effects
in doses that do not cause sedation.
Barbiturates cross the placenta, with fetal levels approaching
those of the mother. They are also excreted in low concentration in
breast milk.
Use during pregnancy is associated with birth defects.
CLINICAL FEATURES
• Mild barbiturate toxicity mimics ethanol intoxication, presenting with
drowsiness, slurred speech, ataxia, unsteady gait, nystagmus,
emotional lability, and impaired cognition.

• In severe acute intoxication, CNS depression progresses from


stupor to deep coma and respiratory arrest. Although pupils are
usually normal or small and reactive, concomitant hypoxia can cause
pupils to be fixed and dilated.
Corneal and gag reflexes may be diminished or
absent, muscle
tone flaccid, and deep tendon reflexes diminished or
absent.
Flexor (decorticate) and extensor (decerebrate)
posturing can occur in patients comatose from
barbiturate intoxication. These neurologic signs are
variable and do not always correlate with severity of
intoxication or depth of coma.
A fluctuating level of consciousness is common
ly seen. High
barbiturate levels depress gastrointestinal motility,
delaying drug absorption. As the drug is metabolized
and blood levels drop, peristalsis and drug
absorption may increase, causing drug levels to rise.

• The life threat of severe barbiturate toxicity is


respiratory depression. Because respirations can be
rapid but shallow, the degree of hypoventilation may
not be apparent on clinical examination, but pulse
oximetry or capnography will detect the ventilation
compromise.
Hypotension is common in patients with severe intoxicati
on,
along with a normal or increased heart rate.
Barbiturate overdose has been associated with noncardiogenic
pulmonary edema.
Altered pulmonary capillary permeability can be caused by
hypoperfusion, hypoxia, or a direct effect of the drug. Pneumonia
may be delayed.
A barbiturate withdrawal syndrome includes tremors,
hallucinations, seizures, and delirium (similar to the delirium
tremens of ethanol withdrawal).
However, severe withdrawal occurs only following dependence
on short- or intermediate-acting barbiturates (e.g., pentobarbital,
secobarbital, amobarbital, or butalbital).
Because these drugs are not commonly used, this syndrome is
now rare.
DIAGNOSTIC STRATEGIES
• The therapeutic level of phenobarbital is 15 to 40 µg/mL (65–
172 µmol/L). A serum level greater than 50 µg/mL can be associated
with coma, especially in a patient who is not a chronic user.
Levels greater than 80 µg/mL are potentially fatal.
Serial phenobarbital levels may be helpful in monitoring effectiveness
of treatment.
Because barbiturates other than phenobarbital have high
volumes of distribution, serum levels do not accurately reflect CNS
concentrations or correlate with clinical severity.
• A positive urine screen establishes exposure to a barbiturate but
does not prove that the drug is present in toxic amounts and should
not be relied upon to explain decreased mental status.
Chest radiographs can detect noncardiogenic
pulmonary edema or pneumonia. Computed
tomography of the head should be obtained in comatose
patients with evidence of trauma, focal neurologic signs,
papilledema, or uncertain diagnosis.
Management • Since barbiturates have no specific
antidote, management is based on supportive care,
particularly with respect to the cardiovascular and
respiratory systems. Severely intoxicated patients are
unable to protect their airway adequately and have
decreased ventilatory drive. Supplemental oxygen may
suffice for patients with mild to moderate overdose, but
intubation is often required.
Careful fluid replacement should maintain a sy
stolic blood
pressure above 90 mm Hg and adequate urine
output.
Patients must be monitored for fluid overload and
pulmonary edema.
If vasopressors are necessary, dopamine is
preferable to norepinephrine because of its renal
vasodilating effects.
• Active warming should be initiated if the rectal
temperature is less than 30 degree C.
GASTROINTESTINAL DEC
ONTAMINATION
• Gastric emptying by lavage is not indicated.
• For large overdoses, there is evidence that clearance of
phenobarbital is markedly increased with multidose activated
charcoal (MDAC).
The dose of activated charcoal is 25 g every 2 hours in an
adult; the pediatric dose is 0.5 g/kg every 2 hours.
If vomiting occurs, a smaller dose or antiemetic should be
used.
MDAC can also be administered slowly through a nasogastric
tube.
Contraindications to MDAC include an unprotected airway, so
CLINICAL USES TOXICITY

Orally ___ hypnotic


 I/M ____
. GIT upset on oral adm
Mania 2. I/M adm – abscess formation
Alcohol withdrawal 3. Accidental I/V administration
Anticonvulsant Violent coughing
Status epilepticus Pulmonary edema
Tetanus
Eclampsia
Coma & sudden death
CONT…
4. Administration of expired drug (or drug exposed to sunlight)
Acetic acid & Acetaldehyde is formed Hypotension
Respiratory depression
Coma
5. Tolerance & addiction
CONT….
6. Over dosage toxicity
1. Acidosis
2. GIT Bleeding
3. Toxic hepatitis
4. Nephrosis
CONTRAINDICATION
 Hepatic & pulmonary impairment

 Never given to patients taking Disulfiram ( Aldehyde


dehydrogenase inhibitor)

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