This document discusses common drug and plant poisonings. It provides an overview of frequently ingested drugs like acetaminophen, iron, and anti-convulsants. It describes the toxic effects, clinical features, investigations, and management for poisonings. It also discusses plant toxins including oleander, datura, and cleistanthus. The document is intended as an educational guide for medical students to learn about treating accidental or intentional overdoses.

1. COMMON DRUG AND PLANT
POISONING
DR.ZAHEEN ZEHRA
1ST YEAR MD PAEDIATRICS.

2. Topics of Discussion
• Drugs commonly used.
• Drugs of Abuse.
• Plant Poisoning.

3. PRE TEST
• What is the toxic substance which
Acetaminophen is metabolized into?
• What is the Antidote for Iron Poisoning?
• Where is Activated Charcoal contraindicated?
• Name some drugs or plant toxicity which
shows Anticholinergic effects.
• Antidote for yellow Oleander Poisoning.
• Toxic dose of Paracetamol.

4. Common Drug Poisoning
• Poisoning due to drug Ingestion has become
very common.
• One of the most common emergencies in
children presenting in the Emergency Room.
• Most of the drug poisoning is accidental and
trivial but it can be life threatening
sometimes.

5. Commonly Available Drugs
1. Acetaminophen.
2. Iron
3. Anticonvulsants.
5. AntiHistamines.
6. Beta Adrenergic Agonists.

6. OTHER COMMON DRUG POISONING
• Antipsychotics.
• Beta blockers.
• Benzodiazepines.
• Carbon monoxide.
• Clonidine.
• Calcium channel blockers.
• Isoniazid.
• Lead.
• Lithium.
• Drugs causing Methemoglobinemia.
• Oral Antidiabetic drugs

7. ACETAMINOPHEN
• Acetaminophen, N-acetyl-para-aminophenol
is the most common Antipyretic and
Analgesic.
• Therapeutic dose: 10-15mg/kg every 4 hours.
Max-60mg/kg/day.
• Toxic dose- 150mg/kg
• 150micrograms/mL at 4 hours after ingestion
is Hepatotoxic in 25% (therapeutic levels-10-
30micrograms/ml)

8. ACETAMINOPHEN-Pathophysiology
• 95% of acetaminophen gets metabolised in
Liver.
• PCM Liver Non Toxic Glucoronide and
Sulphate Conjugates.
• PCM Cytochrome P450 system NAPQI
• NAPQI+Glutathione Non Toxic Mercapturates
• In overdose situations, glutathione is
depleted, and the excess NAPQI is toxic to
hepatocytes, causing centrilobular necrosis.

9. • N-acetylcysteine (NAC) acts as a substitute for
glutathione, and binds with NAPQI, therefore
blocking hepatocellular toxicity if initiated
within 8–12 hours of ingestion.

10. CLINICAL FEATURES

11. INVESTIGATIONS
• Elevated Aspartate Aminotransferase, Alanine
Aminotranferase(AST & ALT), Bilirubin, PT
• Baseline Electrolytes and Glucose
• Blood Levels: The Rumack-Matthew
nomogram.

12. Only intended for use in
patients who present
within 24 hours of single
acute acetaminophen
ingestion with known
time of ingestion.

13. MANAGEMENT
Potentially toxic ingestions are defined as:
1) a level above the “possible toxicity”
nomogram line
2) the ingestion that is complicated by multiple
doses.
3) the time course is not defined if reliable.

14. Management
• Decontamination:
1. GI decontamination is indicated in the first 1-2
hours after potentially toxic ingestions.
2. Activated charcoal (AC)- High affinity
A single dose of AC 1g/kg orally or through
nasogastric tube is administered.
3. Gastric Lavage is indicated for multiple drug
ingestions- can be eliminated with early
decontamination.

15. Management
• Antidote Therapy:
1. N-Acetyl Cysteine-indicated in any potentially toxic
ingestion or with evidence of hepatic injury (elevated
AST/ALT,PT)
2. NAC is most effective in the first 24 hours post-ingestion,
even if activated charcoal has been given.
3. NAC is administered orally or through nasogastric tube in
140 mg/kg initial loading dose, then 70 mg/kg q 4 hours
for 18 total doses.
iv dose – dilute 20% NAC solution to a 3% solution with
5% dextrose
150 mg/kg over 60 minutes
50 mg/kg over next 4 hours
100 mg/kg over 16 hours

16. Management
• Liver Transplantation:
1. Increasing PT on day 4, pH <7.30, PT >100
seconds, creatinine >3.4 mg/dl or hepatic
encephalopathy at any time.
• Supportive Treatment:
1. Intergral Part of Management.
2.Rehydration and maintenance fluids are
indicated for the severely vomiting and/or
anorectic patient.
3. Mental health evaluation- Suicidal Attempt

17. IRON
• Leading causes of non-intentional ingestion
deaths in children.
• Readily available and bright coloured sugar
coating.
• >60mg/kg of elemental Iron is toxic.
• Persistent vomiting >4 times indicates serious
ingestion.

18. Pathophysiology
Two Mechanisms:
1. Direct caustic effects on the gastrointestinal
mucosa.
2. Iron also has a direct cytotoxic effect on
several tissues and organs, principally the
liver, heart and lungs.

19. • Toxicity of iron depends
on the elemental iron
ingested.
Eg: Ingestion of 20 tabs of
325 mg ferrous sulfate
in a 15 kg child = 20 X
[325 X 0.2 mg] = 1300
mg elemental Fe which
is equal to 87 mg/kg.
• Ferrous sulphate -20%
Ferrous gluconate -12%
Ferrous fumarate -33%
Ferric phosphate -37%
Ferric pyrophosphate-
12%
Ferroglycine sulfate -16%

20. • Toxicity of Iron by blood level:
Serum Iron
(mcg/dL)
Level of Toxicity
50 – 150 mcg/dL Normal serum iron concentration
<300 Non-toxic
300 – 500 Mild
500 – 1000 Moderate: Highly associated with Toxicity
>1000 Severe: Death if Untreated

21. CLINICAL FEATURES

22. INVESTIGATIONS
• CBC: Total leucocyte count more than 15,000
• CBG, Serial ABG.
• Serum iron levels.
•Radio opaque
material found in an x
ray within 2 hours of
ingestion.

23. MANAGEMENT
• Any symptomatic patient requires treatment.
• Decontamination:
1. Gastric Lavage.
2. Activated charcoal: does not bind iron.
3. Whole bowel irrigation is contraindicated with
severe GI haemorrhage or perforation.
4. Hemodialysis is not effective for free iron.

24. Antidote/Specific Therapy
1. Deferoxamine is an iron chelating agent
• Serum iron levels less than 300 mcg/dL usually
do not warrant therapy.
• A symptomatic patient with serum iron 300 –
500 μg/dL, needs chelation therapy.
• A level more than 500 mcg/dL should be
chelated even if asymptomatic.
IV dose is 15 mg/kg/hour for 4 – 6 hour or
until the patient stabilizes, then 6 mg/kg/hour.

25. • Vin Rose Urine:
Deferoxamine causes urine to change to
vin rose colour in presence of iron toxicity.

26. ANTICONVULSANTS
• Phenobarbital.
• Phenytoin.
• Carbamazepine.
• Valproic acid.

27. CLINICAL FEATURES
• Phenobarbital- Respiratory Depression,
Hypothermia, Vesicular rash.
• Phenytoin- Ataxia, Nystagmus.
• Carbamazepin- Anticholinergic effects.

28. INVESTIGATIONS
• ABG, CBC, electrolytes, urinalysis, hepatic
enzymes and CPK.
• Phenytoin sodium:
o Therapeutic levels: 10 – 20 μg/mL.
o Ataxia and nystagmus occur at >30μg/mL.
o Easily available OTC drug.
o Most Notorious Anticonvulsant.

29. INVESTIGATIONS
• Valproic acid: Therapeutic levels: 50–100
μg/mL.
• Phenobarbital: Therapeutic levels range from
15 to 40 μg/mL.
Sedation to coma is common above 70 μg/mL
level. Reversible “flat line” EEG may be seen
over 120 μg/mL.

30. MANAGEMENT
• Decontamination:
1. Gastric lavage is indicated for recent
ingestions.
2. Single dose charcoal is indicated for all.
Multidose charcoal is effective in
phenobarbital, phenytoin and carbamazepine
The first dose should be given in the dose
1g/kg NG or P.O. Repeat charcoal doses of 0.
5g/kg once in every 2-4 hours

31. ANTIHISTAMINES
• First generation antihistamines:
Diphenhydramine, Hydroxyzine,
Chlorpheniramine and many others.
• Second generation: Terfenadine, Astemizole,
Loratadine, Cetirizine and Fexofenadine

32. CLINICAL FEATURES
• Neurotoxicity.
• Anticholinergic effects.
• Arrhythmias- QT prolongation and Ventricular
arrhythmias.

33. MANAGEMENT
• Decontamination: Gastric lavage is indicated
for recent ingestions with potential for altered
mental status. Activated charcoal is used as
single dose for non-sustained release
preparations and multi-dose charcoal for
slowed gastric motility or sustained release
ingestions.
• Supportive Care.
• Physostigmine for severe anticholinergic
toxicity

34. Beta Adrenergic Agonist
• ß-adrenergic agonist toxicity is dose
dependent
• Ingestion of <1 mg/kg of salbutamol is non-
toxic.
• Up to 20 times the normal daily dose of
salbutamol has been ingested without serious
medical complications or death.
• Rapidly absorbed, and toxic effects are seen
within an hour of ingestion.

35. EFFECTS
• ß1 Receptors -found on the heart.
• ß1 effects-tachycardia, Increased cardiac
contractility, tremor, agitation, vomiting.
• Β2 Receptors - found in blood vessels, lungs
and pancreas.
• ß2 effects-peripheral vasodilatation,
tachycardia, widened pulse pressure, tremor,
hypokalemia and hyperglycemia.

36. BETA ADRENERGIC AGONIST
• GI decontamination is usually not necessary.
• Not needed if patient has already vomited.
• Activated charcoal may be used if child arrives
early.
• Use of ß-adrenergic blockers has been
suggested as helpful in patients with severe
toxicity, but rarely used.

37. Methemoglobinemia
• Hemoglobin with the iron oxidized to ferric
state from normal ferrous state.
• Consequences:
Decreased oxygen binding and impaired O2
transport to tissues.
Agents causing methemoglobinemia can
also cause hemolysis.
• Drugs causing methHb:
Chloroquine, dapsone, LA, High doses of
methylene blue, metoclopramide,
naphthalene, nitrites, toluidine.

38. METHEMOGLOBIN % CLINICAL FEATURES TREATMENT
<30% No symptoms ,mild
acrocyanosis
Observation ,no tretament
required
30-55% Poorfeeding , lethargy ,
irritability . The older child
maycomplain of fatigue ,
dizziness , headaches and
weakness
Iv methylene blue 1-2
mg/kg/30-60 minutes for
severe cyanosis(max
7mg/kg) or
methaemoglobin <30% or
clinically better
55-70% Respiratory depression,
cardiac arrhythmias,
seizures and coma.
Methylene blue as above
exchange transfusion,
hyperbaric oxygen.
>70% Potentially lethal Methylene blue, exchange
transfusion, hyperbaric
oxygen.

39. Common Antidotes
TOXIN ANTIDOTE
Benzodiazepines Flumazenil
Valproate Carnitine.
Opiates Naloxone
Beta-Blockers Glucagon
Calcium channel blockers Calcium, glucagon, insulin and glucose
Carbon monoxide Oxygen
Cyanide Amyl nitrate, sodium nitrate, sodium
thiosulfate
Lead EDTA (Ethylenediaminetetraacetic acid)
Digitalis F(AB) fragments.

40. COMMON PLANT POISONS
• Cleistanthus
• Oleander
• Datura
• Abrus precatorius.
• Jatropha
• Cerbera Odollam.
• Vasambu.

42. PLANT PART OF THE
PLANT
EFFECTS TREATMENT
Cleistanthus
(Oduvanthalei,
Nillipillai)
All parts Hypokalemia,
Persistent metabolic
aciosis,RTA
Supportive,
Correction of
electrolytes.
Yellow Oleander
(Arali)
Seeds Cardiac Toxicity Digoxin speific
antibody fragments.
Datura (Vellai
Umathai)
Seeds and Fruits Anticholinergic
effects
Physostigmine
Abrus precatorius
(Gundumani)
All parts.
Crushed Seeds
GI Toxicity Decontamination,
Supportive care.
Jatropa
(Kattamanakku)
Seeds (Sweet taste of
seeds)
GI symptoms (OPC) Decontamination,
Supportive care.

43. THANK YOU

44. • NAPQI
• Deferoxamine.
• Pesticides, Hydrocarbons, Acids, Alkali,
Alcohol, Iron, Lithium, Solvents.
Increased risk of aspiration: Absent gag reflex,
ileus, Intestinal Obstruction.
• Carbamazepine, Antihistamines, Datura.
• Digoxin speific antibody fragments
• >150mg/kg