1.
A farmer with history of handling insecticides is brought to the hospital with
convulsions, sweating & laboured breathing.
On examination he had pinpoint pupils, profuse salivation, pulse 50/min, rapid
breathing, rales & rhonchi all over the lungs.
a. What is the probable diagnosis?
b. Outline the management & the rationale for the drug chosen
ANSWER-
a. What is the probable diagnosis? – organophosphorus poisoning
b. Outline the management & the rationale for the drug chosen
Management
1. Remove stained clothes
2. Wash skin and mucus membrane with water
3. Gastric lavage
4. Maintenance of airway and circulation
5. Antidote – atropine
Atropine sulphate 2mg iv stat and repeated every 10-15min until
full atropinisation occur, which is assessed by degree of dilatation
of pupil, increase in heart rate, disappearance of crepitation
6. Pralidoxime (2-PAM)
1-2 given as slow iv infusion over 30minutes after dilution (5%
solution in 10ml normal saline)
It must be given before ageing of the enzyme occurs
2. Patients were admitted to the hospital with symptoms of vertigo, abdominal
pain, blurring of vision, motor restlessness after consumption of illicit liquor
Outline the management & give the rationale for the same
ANSWER:
It is metabolized to formaldehyde (by alcohol dehydrogenase) and finally to
formic acid (by aldehyde dehydrogenase). Accumulation of formic acid may
result in lactic acidosis (high anion gap metabolic acidosis), blindness and
death. Specific toxicity of formic acid is retinal damage leading to blindness.
Methanol poisoning can be treated by supportive measures, gastric lavage
and sodium bicarbonate (to treat acidosis). Ethanol is useful because it
competitively inhibits the conversion of methanol to formic acid.
Fomepizole (4-Methylpyrazole) can also be used in methanol poisoning
because it is a specific inhibitor of alcohol dehydrogenase. Folic acid or
folinic acid can also be used because folate dependent systems are
responsible for conversion of formic acid to CO2
3. A patient was admitted to the emergency ward with history of abdominal pain,
nausea, vomiting & anorexia. After a few hours the patient developed jaundice
with liver tenderness
On careful elicitation of history, the patient revealed of having consumed about
25 – 30 tablets of a pain-relieving drug, which the patient used to take frequently
for the relief of headache
a. What drug the patient has consumed in overdose?
b. How do you explain the above toxic manifestation and what is the dose at
which serious toxicity occurs?
c. What is the line of management?
ANSWER:
A. Acute paracetamol (acetaminophen) poisoning.
B. Toxic Manifestation:
Paracetamol is primarily metabolized in the liver via glucuronidation and
sulfation.
A small fraction is metabolized by cytochrome P450 enzymes (CYP2E1) to a
toxic metabolite called NAPQI (N-acetyl-p-benzoquinone imine).
Under normal doses, NAPQI is detoxified by conjugation with glutathione.
In overdose, glutathione stores are depleted, leading to accumulation of NAPQI,
which causes hepatic cell necrosis, particularly in the centrilobular (Zone 3)
region of the liver.
Toxic Dose:
Adults: Hepatotoxicity risk begins at >150 mg/kg (~10 grams or more in adults).
Ingestion of >25–30 tablets (500 mg each) = 12.5–15 g → highly hepatotoxic.
C. Management:
a. vomiting should be induced, or gastric lavage should be done.
b. to prevent further absorption - Activated charcoal is given
c. Specific antidote: N-acetylcysteine (150 mg/kg should be infused i.v. in
200 ml 5% glucose solution over 15 min, followed by the same dose given
i.v. over the next 20 hours)
It replenishes the glutathione stores of liver and prevents binding of the
toxic metabolite to other cellular constituents.
4. In a mass casualty caused by a chemical agent, patients declared as brought dead with
H/O exposure of large challenges of gas agent cyanide & died within minutes of
exposure
a. What is the mechanism of action of cyanide poisoning?
b. What are the clinical features of cyanide poisoning?
c. What is the antitode & its mechanism of action?
d. What is the difference between cyanide poisoning & nerve agent poisoning?
ANSWER:
a. Cyanide exerts its toxicity primarily by inhibiting cytochrome oxidase (cytochrome a₃)
in the mitochondrial electron transport chain (complex IV):
• It binds to the ferric ion (Fe³⁺) in cytochrome a₃
• Inhibits oxidative phosphorylation
• Results in cellular hypoxia despite adequate oxygenation
b. Early Signs:
•Headache, dizziness
• Anxiety, confusion
• Shortness of breath, hyperventilation
• Nausea and vomiting
Progression:
• Seizures
• Bradycardia → hypotension
• Cardiac arrhythmia
• Coma
• Bright red venous blood due to failure of O₂ extraction
• Death within minutes due to respiratory or cardiac arrest
c. Antitode: Sodium nitrite + Sodium thiosulfate
d.
Feature Cyanide Poisoning Nerve Agent Poisoning (e.g. Sarin, VX)
Target Mitochondrial cytochrome oxidase (Complex IV) Acetylcholinesterase enzyme (AChE)
Mechanism Inhibits cellular respiration (hypoxia) Accumulation of ACh → cholinergic overstimulation
Onset Seconds to minutes Seconds to minutes
Primary Symptoms Seizures, coma, bright red blood, hypoxia Miosis, salivation, lacrimation, bronchospasm
Pupils Usually normal or dilated Pinpoint (miosis)
Antidote Hydroxocobalamin, Sodium thiosulfate, Nitrites Atropine + Pralidoxime (2-PAM)
Effect on Respiration Central respiratory arrest Bronchorrhea, bronchospasm, diaphragm paralysis
5. A 27-year male brought to the hospital with history of snake bite over his left foot and
he had the complaints of headache, nausea, vomiting & drooping of both eyelids.
On examination patient had mild tachycardia, hypotension & ptosis of both
eyes.
a. What is the type of toxicity developed in this patient?
b. What are the types of systemic effects caused by venomous animals (snake,
scorpion, bees, wasps)?
c. What is the pre hospital first aid & treatment of the envenomation?
d. What is antivenom
e. What is the role of antivenom to reverse the toxicity?
ANSWER:
a) Neurotoxic envenomation — affects the neuromuscular junction.
Signs: Ptosis (early), ophthalmoplegia, bulbar paralysis, respiratory muscle paralysis
Mechanism: Blockade of neuromuscular transmission (either presynaptic or postsynaptic)
Krait venom (β-bungarotoxin): Presynaptic inhibition of ACh release
Cobra venom: Postsynaptic blockade of ACh receptors
b) 1. Elapid snakes (cobra, krait) - Neurotoxicity
2. Viperidae family (Russell’s viper, saw-scaled viper) - Hemotoxicity
3. Sea snakes- Myotoxicity
4. Bees / Wasps Allergic - Anaphylactic
5. Scorpions - Autonomic storm (Hypertension, sweating, pulmonary edema)
c) Pre-hospital first aid:
First Aid (Do’s):
Reassure and immobilize the patient
Apply a broad pressure bandage (only for neurotoxic bites like kraits/cobras)
Keep the limb at heart level
Remove any tight clothing/jewelry
Transport to hospital urgently
First Aid (Don’ts):
Do not cut or suck the bite
Do not apply tourniquets
Do not apply ice
Do not give alcohol or stimulants
Hospital Treatment:
Airway management (ventilation support if needed)
IV fluids for hypotension
Antivenom administration
Tetanus prophylaxis
Antibiotics if secondary infection suspected
Supportive care (e.g., dialysis if renal failure, antiemetics, etc.)
d) Anti-snake venom (ASV) is a medicine made from antibodies that neutralize snake venom.
It is produced by injecting small amounts of venom into animals (usually horses) and
collecting the antibodies from their blood
e) Role of antivenom to reverse toxicity:
Neutralizes circulating venom: Prevents further binding to tissues (e.g., neuromuscular junctions,
endothelium)
Reduces progression of systemic effects
Reverses early neurotoxicity if given before irreversible damage (e.g., respiratory muscle paralysis)
Stops coagulopathy and prevents DIC in hemotoxic bites
