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General Toxicology - Detailed Notes

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1. DEFINITIONS

Toxicology

• The word "toxicology" is derived from the Greek word "Toxon" (a bow used for shooting arrows); "toxeuma" meant an arrow, and "toxicos" referred to the poison placed on arrow tips to create more lethal weapons.
• Paracelsus (16th century), the "Father of Modern Toxicology," was the first to explain the dose-response relationship: "All things are poison and nothing is without poison. It is the dose that determines the poison."

Forensic Toxicology

Toxinology

Poison

• There is no sharp boundary between a medicine and a poison. A medicine in a toxic dose is a poison, and a poison in a small dose may be a medicine.
• In law, the real difference between a medicine and a poison is the intent with which it is given - if given to save life it is a medicine; if given to cause bodily harm, it is a poison.
• LD50 - The dose of a toxic substance that kills 50% of a test population (typically rats or similar surrogates).

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2. TYPES OF POISONING

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3. MECHANISM OF ACTION OF POISONS

• Neurotoxins / Nerve gases: Paralyze the nervous system within seconds (e.g., sarin, organophosphates)
• Mitochondrial poisons: Cyanide starves the body of energy by inhibiting cytochrome c oxidase and blocking ATP synthesis in mitochondria
• Cardiac poisons: Potassium chloride in excess eliminates the cell potential necessary for cardiac muscle contraction
• Liver-converted toxins: Some substances are not poisonous themselves but are converted to toxic compounds in the liver (e.g., methanol is converted to formaldehyde)
• Cumulative poisons: Lead, mercury, copper accumulate with repeated doses and cause chronic toxicity

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4. FACTORS MODIFYING THE ACTION OF POISONS

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5. MANNER OF POISONING

Comparison: Ideal Suicidal vs. Homicidal Poison

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6. CLASSIFICATION OF POISONS

I. Corrosives

• Inorganic (mineral) acids - sulphuric acid, nitric acid, hydrochloric acid
• Organic acids - carbolic acid, oxalic acid, acetic acid, salicylic acid

• Hydrates
• Carbonates of sodium and potassium

• Zinc chloride, potassium chloride, ferric chloride

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II. Irritants

• Metallic - arsenic, lead, mercury, copper, zinc, thallium
• Non-metallic - phosphorus, chlorine, bromine, iodine

• Vegetable poisons - castor oil seeds, croton oil, madar, semicarpus anacardium, calotropis, capsicum, aloes, Abrus precatorius
• Animal - cantharides, snake venom, insects, scorpions, spiders

• Powdered glass, diamond dust, chopped hair

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III. Neurotoxic

• Somniferous (sleep-inducing) - opium, barbiturates
• Inebriants - alcohol, ether, chloroform
• Deliriants - dhatura, belladonna, cannabis, hyoscyamus, cocaine

• Nux vomica, gelsemium

• Curare, conium

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IV. Cardiotoxic

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V. Asphyxiants

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VI. Miscellaneous

• Food poisons - food-borne botulism, etc.
• Agrochemicals - organophosphates, carbamates, organochlorine compounds (pesticides/insecticides); bipyridyl herbicides (paraquat, diquat)
• Narcotic drugs and psychotropic substances
• Medicines causing iatrogenic poisoning

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7. MEDICO-LEGAL DUTIES OF A DOCTOR IN POISONING CASES

1. A doctor is required by law to report all cases of poisoning to the police - failure to do so is an offence under Section 39 CrPC.
2. All articles should be preserved for chemical analysis; withholding evidence is an offence under Section 201 IPC.
3. In both suicidal and homicidal cases, the attending physician must divulge all information to police; providing wrong information is punishable under Sections 202 and 193 IPC.
4. In cases of dying patients, the doctor must record the dying declaration if the magistrate is not available.
5. In cases brought dead to the hospital, the doctor should not issue a death certificate but must send the body for autopsy.
6. In food poisoning, contaminated food must be collected and sent to the forensic science laboratory for chemical analysis, and the case must be reported to public health officials.

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8. TREATMENT OF POISONING

A. Stabilise the Patient (Life-Saving Measures - ABCD)

• (A) Airway: Clear the oral cavity and nostrils of secretions, vomit, or foreign bodies. Endotracheal intubation may be necessary.
• (B) Breathing: If arterial blood gases cannot be maintained, administer graduated supplemental oxygen (via ventimask or endotracheal tube). Give aminophylline 250-500 mg for severe bronchospasm; diuretics for pulmonary oedema.
• (C) Circulation: IV fluid administration may be life-sustaining. Monitor blood pressure.
• (D) Depression of CNS: Correct CNS depression. Place unconscious patients in the recovery position (lateral) to prevent aspiration. Most poisoning cases, conscious or unconscious, recover with supportive care alone.

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B. Removal of Unabsorbed Poison (Decontamination)

(1) Inhaled Poisons

• Remove patient to fresh air.
• Artificial respiration; oxygen at 6-8 liters/min.
• Keep air-passages free from mucus by postural drainage or aspiration.
• Nikethamide 2 mL IV if necessary.

(2) Injected Poisons (bite or injection)

• Apply a tight ligature immediately above the wound.
• Loosen for 1 minute every 10 minutes to prevent gangrene.
• Excise the wound, suck out the poison, neutralize with suitable chemical.
• Local vasoconstriction by injection of adrenaline.
• Immersion of the extremity in water at 10°C slows capillary blood flow and limits absorption.

(3) Contact Poisons (skin/mucous membrane)

• Remove contaminated clothes, contact lenses, and jewellery immediately.
• Wash skin with water for 30 minutes or neutralize with specific chemical.
• Irrigate eyes with normal saline for at least 15 minutes.

(4) Ingested Poisons

• Useful within 2 hours of ingestion.
• Performed using Ewald's or Boa's tube, or a soft non-collapsible rubber tube (1 cm diameter, 1.5 m length).
• About 250 mL warm water (35°C) is passed through; contents siphoned back.
• Repeat until the fluid is clear, colourless, and odourless.
• Leave a small amount of activated charcoal suspension (1 g/kg) and/or cathartic in the stomach at the end.
• Gastric lavage fluids used:

1. Laryngeal spasm
2. Aspiration pneumonitis
3. Perforation of stomach or oesophagus
4. Sinus bradycardia and ST elevation on ECG

1. Corrosive poisoning (except carbolic acid) - risk of perforation
2. Convulsant poisons
3. Comatose patient - risk of aspiration
4. Volatile poisons - risk of inhalation
5. Hypothermic patients

1. Oesophageal varices or alimentary tract diseases
2. Comatose patients
3. Ingestion of alkali
4. Advanced pregnancy
5. Haemorrhagic diathesis
6. Recent surgical operation history

• Avoid in corrosive poisoning, semicomatose states, convulsions, petroleum distillate ingestion.
• Copper sulphate (0.5 g in warm water) can act as an emetic but is itself toxic in large doses.

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C. Administration of Antidotes

(i) Mechanical / Physical Antidotes

• Fine, black, odourless, tasteless amorphous carbon prepared by destructive distillation of wood, coconut shell, bone, sucrose, or rice starch, followed by activation with steam or CO2.
• Surface area: 1000 m² per gram - gives extraordinary adsorptive capacity.
• Strongly adsorbs: acetaminophen, salicylates, barbiturates, tricyclic antidepressants.
• Dose: 1 g/kg body weight (50-100 g in adults; 10-30 g in children) as a suspension in 4-8 times water.
• Multi-dose activated charcoal: Initial loading dose 1-2 g/kg; repeat doses 0.5-1 g/kg every 4-6 hours. Significantly decreases the half-life of several drugs.
• Side effects: Vomiting, diarrhoea, constipation, pulmonary aspiration, intestinal obstruction.
• Contraindications: Ileus, small bowel obstruction, caustic or petroleum distillate ingestion.
• Charcoal haemoperfusion: Useful for highly protein-bound, lipid-soluble substances (barbiturates, salicylates, paraquat, phenytoin, theophylline, digitalis, glutethimide). Blood is circulated extracorporeally through a charcoal filter.

• Form protective coatings on gastric mucosa to prevent poison absorption.
• Examples: milk, egg white, starch, milk of magnesia, aluminium hydroxide gel.

• Bananas, boiled rice, or potatoes dilute the poison and reduce its contact with mucosa. Used particularly for glass powder ingestion.

• Composition: 2 parts activated charcoal + 1 part tannic acid + 1 part magnesium oxide.
• 15 g in half a glass of warm water.

(ii) Chemical Antidotes

1. Common salt - decomposes silver nitrate (forms insoluble silver chloride)
2. Albumin - precipitates mercuric chloride
3. Dialyzed iron - neutralizes arsenic
4. Copper sulphate - precipitates phosphorus
5. Potassium permanganate (1:5000) - oxidizes opium, morphine, strychnine, nicotine, physostigmine
6. Sodium thiosulphate - used in cyanide poisoning

(iii) Pharmacological / Physiological Antidotes

(iv) Chelating Agents

• Originally an antidote for Lewisite (an arsenic-containing war gas).
• Used in poisoning by: arsenic, mercury, lead, antimony, gold, thallium, and to some extent copper and bismuth.
• Mechanism: The SH (thiol) groups of BAL combine with heavy metals in tissues, dislodging them from their combination with sulphydryl radicals in tissue enzymes, thereby protecting enzyme function. The BAL-metal complex is excreted in urine.
• Dose: 3-4 mg/kg body weight deep IM; given every 4 hours for first 2 days, then thrice daily for 10 days.
• Contraindications: Cadmium poisoning (forms nephrotoxic compound), pre-existing liver disease.

• Used for lead, heavy metal poisoning.

• Orally active chelating agent for copper (Wilson's disease), lead, mercury, arsenic, gold.
• Side effects: Hypersensitivity reactions (skin rashes, nephrotoxicity), optic neuritis (pyridoxine deficiency), leucopenia, thrombocytopenia, agranulocytosis.

• Water-soluble oral agent; more effective and safer alternative to BAL. Used for mercury, lead, and arsenic poisoning.

• Effective for mercury, lead, and arsenic poisoning. Same dithiol chelating group as BAL.

• Water-soluble compound with great affinity for ferric ions.
• Used in acute iron poisoning and haemochromatosis.
• Removes iron from ferritin and haemosiderin (but NOT from haemoglobin or cytochromes).
• Doses: Oral 8-10 g in 80-100 mL distilled water; IM 1 g initially then 0.5 g twice/thrice daily; IV 1-2 g in 500 mL 5% dextrose saline (max 15 mg/kg/hour or 80 mg/kg in 24 hours).

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D. Elimination of Absorbed Poison by Excretion

1. Severe poisoning
2. Progressive deterioration despite full supportive care
3. High risk of serious morbidity or mortality
4. Normal excretion route impaired
5. Poison produces delayed but serious toxic effects

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9. POSTMORTEM FINDINGS IN POISONING

External Examination

• Normal: coppery red or purple
• Pink - carbon monoxide poisoning, hydrocyanic acid, burns
• Brown/chocolate - potassium chlorate, nitrites, aniline dyes (methaemoglobinaemia)
• Brick red - nitric acid

Internal Examination (Stomach Findings)

• Redness: In poisoning - patchy, more marked at cardiac end and greater curvature, involves mucosal ridges. In disease - uniform, ridges not involved.
• Softening: Corrosive acids and alkalis cause softening at greater curvature and cardiac end. Carbolic acid causes hardening/shrinkage.
• Ulcers: Corrosive/irritant ulcers are at the greater curvature, thin friable margins, surrounded by inflammation. Disease ulcers are at the lesser curvature with punched-out, indurated edges.
• Perforation: May occur in strong acid poisoning (sulphuric acid); stomach is black with extensively damaged mucosa.

Postmortem Examination Aims

1. Identify the type of poison
2. Determine time since death
3. Establish cause of death
4. Determine manner of death (suicide, accident, or homicide)
5. In infants - determine live birth and viability

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10. CHEMICAL ANALYSIS / TOXICOLOGICAL SCREENING

Common Colour Tests (Preliminary Screening)

Analytical Methods

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11. KEY CONCEPTS SUMMARY

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