This document discusses the poisoning and treatment of several substances: 1. Barbiturate poisoning can cause lethargy, slurred speech, coma and respiratory arrest. Treatment involves protecting the airway, treating coma/hypotension, and no specific antidote exists. 2. Morphine poisoning presents as stupor, flaccidity, shallow breathing, and pinpoint pupils. Treatment is respiratory support, naloxone antidote, and gastric lavage. 3. Organophosphate poisoning impacts the muscarinic, nicotinic and central nervous systems. Treatment includes atropine antidote, pralidoxime to restore nerve function, and supportive care.

1. Nem Kumar Jain
MS. (Pharm.) Pharmacology & Toxicology
Assistant Professor
School of Pharmacy
ITM University Gwalior
Specific drug poisoning and
Treatment

2. Barbiturate Poisoning
 Barbiturates have been used as hypnotic and sedative agents,
for the induction of anesthesia, and for the treatment of epilepsy
and status epilepticus.
Toxic dose: The toxic dose of barbiturates varies widely and
depends on the drug, the route and rate of administration, and
individual patient tolerance.
 In general, toxicity is likely when the dose exceeds 5–10 times
the hypnotic dose. Chronic users or abusers may have striking
tolerance to depressant effects.
 A. The potentially fatal oral dose of the shorter-acting agents
such as pentobarbital is 2–3 g, compared with 6–10 g for
phenobarbital.
 B. Several deaths were reported in young women undergoing

4. Barbiturate poisoning
Clinical presentation: The onset of symptoms depends on
the drug and the route of administration.
 A. Lethargy, slurred speech, nystagmus, and ataxia are
common with mild to moderate intoxication.
 With higher doses, hypotension, coma, and respiratory
arrest commonly occur. With deep coma, the pupils are
usually small or mid-position; the patient may lose all
reflex activity and appear to be dead.
 B. Hypothermia is common in patients with deep coma,
especially if the victim has been exposed to a cool
environment.
 Hypotension and bradycardia commonly accompany
hypothermia.

5. Treatment
 A. Emergency and supportive measures
 1. Protect the airway and assist ventilation if necessary.
 2. Treat coma , hypothermia , and hypotension if they occur.
 B. Specific drugs and antidotes. There is no specific
antidote.
 C. Decontamination . Administer activated charcoal orally if
conditions are appropriate. Gastric lavage is not necessary
after small to moderate ingestions if activated charcoal can be
given promptly.
 D. Enhanced elimination
 1. Alkalinization of the urine increases the urinary elimination of
phenobarbital but not other barbiturates. Its value in acute
overdose is unproven, and it may potentially contribute to fluid
overload and pulmonary edema.
 2. Repeat-dose activated charcoal has been shown to decrease
the half-life of phenobarbital and its metabolites, but data are
conflicting regarding its effects on the duration of coma, time on
mechanical ventilation, and time to extubation.
 3. Hemodialysis or hemoperfusion may be necessary for

6. Morphine Poisoning
 Accidental, suicidal or drug abuse.
 Dose: in none tolerant- 50 mg i.m. lethal dose
250 mg
 Clinical manifestations: extension of
pharmacological actions:
 stupor or coma, flaccidity, shallow and occasional
breathing, cyanosis, pinpoint pupil, fall in BP and
 shock
 Convulsions may be seen, pulmonary oedema
and respiratory failure- Death

7. Treatment
 Respiratory support and maintenance of BP (I.V.
Fluid and vasoconstrictors)
 Gastric lavage should be done with Potassium
permanganate to remove unabsorbed drug (both
cases oral and parenteral administration)
 Specific antidote: Naloxone 0.4-0.8 mg i.v. repeated
every 2-3 min till respiration picks up
 Short duration of action, should be repeated every
1-4 hours

8. Organophosphate poisoning
 Extensively used as agricultural and household insecticides,
accidental as well as suicidal and homicidal poisoning is
common
 Clinical manifestations:
 Local manifestation at the site of exposure (skin, GIT, eye) occur
immediately and are followed by complex systemic effects due
to muscarinic, nicotinic and central actions
 Irritation o eye, lacrimation, salivation, copius trachio-bronchial
secretions, miosis, blurring of vision, bronchospasm,
breathlessness, colic, involuntary defecation, and urination
 Fall in BP, Bradycardia or tachycardia, cardiac arrythmias,
vascular collapse
 Muscular fasciculations, weakness, respiratory paralysis (central
as well as peripheral)
 Irritability, disorientation, unsteadiness, tremor, ataxia,
convulsions, coma and death

9. Treatment
 Termination of further exposure to the poison: fresh air,
wash the skin and mucus membrnes with soap and water,
gastric lavage according to need.
 Maintain patent airway, positive pressure respiration if it is
failing
 Supportive measures: maintain BP, Hdration, control
convulsions with judicious use of diazepam
 Specific antidotes
 Atropine: counteract muscarinic symptoms, higher dose for
cns effects
 2mg i.v. must be promptly given and should be repeated
every 10 minutes till dryness of mouth or other signs of
atropinizations appear(almost 200 mg in a day)

10.  Pralidoxime (2-PAM): restores neuromuscular
transmission
 Should be started as early as possible
 Injected i.v. in a dose of 1-2 g (children 20-40 mg/kg)
 Another regimen: 30mg/kg i.v. loading dose and 8-10
mg/kg/h continuous infusion till recovery
 Doses may be repeated according to need
 Maximum 12 g in first 24 hour
 Lower doses according to symptoms may be
continued 1-2 weaks.
 2-PAM use is secondary to that of atropine

11. Arsenic Poisoning
 Source: Arsenic compounds are found in a select group
of industrial, commercial, and pharmaceutical products.
 Wood preservative, pesticides, herbicides (monosodium
methane arsonate (MSMA)), phynylarsenic as feed
additive for poultry and swine, arsenic trioxide as
anticancer drug, use of inorganic arsenic in metallurgy
and semiconductor and glass production
 Arsenical in folk remedy and homeopathy medicines
 Chemical warfare agent lewisite (dichloro[2-chlorovinyl]
arsine)

12.  Mechanism: arsenicals exert their toxic effects through
multiple mechanisms, including inhibition of enzymatic
reactions vital to cellular metabolism, induction of oxidative
stress, and alteration in gene expression and cell signal
transduction
 Toxic dose: The toxicity of arsenic compounds varies
considerably with the valence state, chemical composition,
and solubility.
 trivalent arsenic (As3+) is 2–10 times more acutely toxic
than pentavalent arsenic (As5+)
 Acute ingestion of as little as 100–300 mg of a soluble
trivalent arsenic compound (eg, sodium arsenite) can be

13. Clinical Manifestations Acute exposure: multisystem manifestations
 Git effects: hemorrhagic gastroenteritis, nausea,
vomiting, abdominal pain, and watery diarrhoea.
 Cardiovascular: hypotension, tachycardia, prolongation of
QT interval, shock and death.
 Neurological : lethargy, agitation or delirium, seizures
may occur, weakness and paralysis of feet
 Haematological: pancytopenia, mainly leucopoenia and
anaemia
 Dermatological: desquamation of palms and soles, a
diffuse maculopapular rash
 Chronic exposure: is also associated with multisystem
effects, which may include fatigue and malaise,
gastroenteritis, leukopenia and anaemia (occasionally
megaloblastic), sensory-predominant peripheral
neuropathy, hepatic transaminase elevation, noncirrhotic
portal hypertension, and peripheral vascular insufficiency.
Skin disorders and cancer may occur

14. Treatment
 Emergency and supportive measures
 Maintain open airway and assist ventilation
 Treat coma, arrhythmia and shock
 Treat hypotension and fluid loss
 Cardiac monitoring
 Decontamination: activated charcoal, for large ingestion gastric
lavage
 Enhance elimination: hemodialysis in case ofrenal failure
 Specific drugs and antidotes:
 Unithiol (2,3- dimercaptopropanesulfonic acid, DMPS, Dimaval)
a water soluble analogue of Dimercaprol (BAL), 3–5 mg/kg
every 4 hours by slow IV infusion over 20 minutes is a
suggested starting dose
 Dimercaprol (BAL, British anti-lewisite, 2,3-
dimercaptopropanol) is the chelating agent of second choice if
unithiol is not immediately available.
 The starting dose is3–5mg/kg by deep IM injection every 4–6