Forensic Medicine & Toxicology
High-yield MBBS Forensic Medicine & Toxicology question bank — medical jurisprudence, identification, thanatology, injuries, asphyxia, forensic sexology and toxicology, at Reddy’s / Parikh depth.
12chapters144questions77High-Yield
Definition
Toxicology is the science of poisons; a poison is any substance which, when administered, produces harmful effects or death.
Definitions & Classification
- Forensic toxicology — medicolegal aspects; clinical toxicology — diagnosis and treatment
- Corrosives — strong acids and alkalis
- Irritants — inorganic (metallic, non-metallic), organic (vegetable, animal), mechanical
- Neurotics — cerebral (alcohol, opioids), spinal (strychnine), peripheral (curare)
- Cardiac (oleander, aconite), asphyxiants (carbon monoxide, cyanide), miscellaneous
- By mode: acute, chronic, subacute, fulminant
Duties of the Doctor
- In a private (clinical) case — treat the patient first; if poisoning is suspected, persuade the patient to inform the police
- Treatment always takes priority over legal formalities
- Preserve vomit, gastric lavage fluid, urine, blood and any suspicious material, properly labelled and sealed
- Maintain detailed contemporaneous records; note the smell, colour and residue
- In a suspected criminal or homicidal case, inform the nearest Magistrate or police — a legal duty
- Record a dying declaration if death appears imminent
- In hospital deaths, do not issue a death certificate — refer for medicolegal autopsy
Treatment first, evidence second, notification always. Class Example Corrosive Sulphuric acid Irritant Arsenic Neurotic Opioids Asphyxiant Carbon monoxide Applied
- Failure to inform in a suspected criminal case is punishable (Section 39 CrPC, Section 201 IPC)
- Sale of poisons is regulated by the Poisons Act and Drugs and Cosmetics Act
🔑KEY POINTS TO REMEMBER- Poisons are classified as corrosive, irritant, neurotic, cardiac and asphyxiant.
- Treatment always takes priority over legal formalities.
- The doctor must preserve samples and inform police in suspected criminal poisoning.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Diagnosis of poisoning rests on history, clinical features and laboratory analysis; management follows a standard sequence of resuscitation, decontamination and antidote.
Diagnosis
- In the living — sudden illness in a previously healthy person; several people affected together after a common meal
- Toxidromes — cholinergic (pinpoint pupils, salivation, bradycardia), anticholinergic (dilated pupils, dry hot skin, delirium), opioid (pinpoint pupils, respiratory depression, coma), sympathomimetic
- Characteristic odour — bitter almonds (cyanide), garlic (organophosphates, phosphorus, arsenic), kerosene, alcohol
- In the dead — smell, stains around mouth, colour of lividity (cherry-red in carbon monoxide, chocolate-brown in nitrites), unusual preservation of the body
- Chemical analysis of viscera is confirmatory
Management (in sequence)
- Resuscitation — airway, breathing, circulation; treat convulsions and hypoglycaemia
- Decontamination — remove clothing, wash skin and eyes; gastric lavage where indicated
- Activated charcoal — 1 g/kg, the most useful adsorbent; ineffective for metals, alcohols, corrosives
- Specific antidotes where available
- Elimination enhancement — forced alkaline diuresis, haemodialysis, haemoperfusion
- Supportive care — usually the most important element; psychiatric referral after recovery
Supportive care saves more lives than antidotes in most poisonings. Toxidrome Pupils Example Cholinergic Pinpoint Organophosphate Anticholinergic Dilated Datura Opioid Pinpoint Morphine Applied
- Most poisonings have no specific antidote — supportive care is the mainstay
- Preserve the first sample of gastric aspirate for analysis
🔑KEY POINTS TO REMEMBER- Diagnosis rests on history, toxidromes, odour and viscera analysis.
- Sequence: resuscitation, decontamination, antidote, elimination, supportive care.
- Activated charcoal is the most useful adsorbent but not for metals or corrosives.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Corrosives are substances that cause local destruction of tissue on contact, producing chemical burns of the skin and gastrointestinal tract.
Types & Mechanism
- Mineral (inorganic) acids — sulphuric, nitric, hydrochloric
- Organic acids — carbolic, oxalic, acetic
- Alkalis — sodium and potassium hydroxide, ammonia
- Acids cause coagulative necrosis — an eschar limits deeper penetration
- Alkalis cause liquefactive necrosis — penetrate deeper, so long-term damage is worse
- Sulphuric acid — blackish charring; nitric acid — yellow (xanthoproteic) staining; hydrochloric — greyish-brown
Features, Autopsy & Treatment
- Intense burning pain in mouth, throat and abdomen; dysphagia, vomiting of altered blood
- Corrosion of lips, mouth and chin with staining running downwards
- Complications: perforation, mediastinitis, peritonitis, shock; later oesophageal and pyloric stricture
- Autopsy: corroded, perforated stomach with characteristic staining; softening and perforation of the stomach wall
- Treatment: NEVER perform gastric lavage or induce vomiting (risk of perforation); no chemical neutralisation (exothermic); dilute with water or milk, analgesia, endoscopy, treat shock
- Manner: mostly accidental or suicidal; vitriolage (acid throwing) on the face is a homicidal act punishable under Sections 326-A and 326-B IPC
Alkalis penetrate deeper, so they cause worse long-term damage. Acid Stain Sulphuric Black, charred Nitric Yellow Hydrochloric Greyish-brown Applied
- Gastric lavage is absolutely contraindicated in corrosive poisoning
- Acid-attack survivors require reconstructive surgery and are entitled to compensation
🔑KEY POINTS TO REMEMBER- Acids cause coagulative necrosis; alkalis cause deeper liquefactive necrosis.
- Nitric acid stains yellow, sulphuric black, hydrochloric greyish-brown.
- Never lavage or neutralise — dilute with water or milk; vitriolage is punishable under 326-A IPC.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Arsenic is a metallic irritant poison, historically called the ‘king of poisons’ and ‘poison of kings’ because of its former use in homicide.
Acute Poisoning
- Gastrointestinal (choleraic) form — commonest; burning pain, profuse rice-watery diarrhoea and vomiting, closely simulating cholera
- Intense thirst, dehydration, cramps, garlicky odour of breath
- Narcotic form — stupor, delirium, convulsions, coma
- Death from circulatory collapse within 12–48 hours
- Fatal dose about 120–200 mg; fatal period 12–48 hours (standard textbook figures)
Chronic Poisoning, Autopsy & Treatment
- Chronic — ‘raindrop’ pigmentation, hyperkeratosis of palms and soles, Mees’ lines (transverse white nail bands), peripheral neuropathy, anaemia
- Chronic exposure through contaminated groundwater is a major public health problem in West Bengal and Bangladesh
- Carcinogenic — skin, lung and bladder cancer
- Autopsy — red velvety inflammation of gastric mucosa, subendocardial haemorrhage; arsenic delays putrefaction, so bodies are well preserved even after long burial
- Detection — Reinsch, Marsh and Gutzeit tests; hair and nails show arsenic for months (segmental analysis dates the exposure)
- Treatment — chelation with BAL (dimercaprol), DMSA (succimer), penicillamine; supportive care
Arsenic acts by inactivating sulphydryl-containing enzymes. Form Key feature Acute Rice-watery stools Chronic Mees’ lines, raindrop pigmentation Autopsy Red velvety gastric mucosa Applied
- Preserve hair and nails — they record chronic exposure long after death
- Because arsenic preserves the body, exhumation remains useful even years later
🔑KEY POINTS TO REMEMBER- Acute arsenic poisoning mimics cholera with rice-watery stools.
- Chronic features: raindrop pigmentation, hyperkeratosis, Mees’ lines, neuropathy.
- Arsenic delays putrefaction; treated by chelation with BAL or succimer.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Lead, mercury and copper are metallic irritant poisons producing characteristic acute and chronic syndromes.
Lead (Plumbism)
- Sources: paint, batteries, cosmetics (surma, sindoor), pottery glaze, contaminated water pipes
- Chronic is commoner: blue ‘Burtonian’ line on the gums, facial pallor, lead colic, constipation, wrist and foot drop (extensor paralysis)
- Basophilic stippling of red cells; anaemia; lead encephalopathy in children
- Lead lines at the metaphyses on X-ray in children
- Treatment: calcium disodium EDTA, BAL, penicillamine, DMSA
Mercury & Copper
- Mercury (acute) — corrosive gastroenteritis, metallic taste, bloody diarrhoea, acute kidney injury
- Mercury (chronic, hydrargyrism) — salivation, gingivitis, blue line on gums, mercurial tremors, erethism (shyness, irritability); Minamata disease from organic mercury in fish, causing neurological damage
- Copper — metallic taste, blue-green vomit, gastroenteritis, haemolysis, jaundice, kidney injury
- Wilson disease — inherited copper accumulation with Kayser-Fleischer rings
- Treatment: mercury — BAL, DMSA; copper — penicillamine, BAL
Each metal produces a recognisable clinical signature. Metal Hallmark Chelator Lead Burtonian line EDTA Mercury Erethism, tremor BAL/DMSA Copper Blue-green vomit Penicillamine Applied
- Lead poisoning in children causes irreversible cognitive impairment
- Occupational exposure is notifiable under factory legislation
🔑KEY POINTS TO REMEMBER- Lead: Burtonian gum line, colic, wrist drop, basophilic stippling; treat with EDTA.
- Mercury: salivation, tremors, erethism, kidney injury; Minamata disease from fish.
- Copper: blue-green vomit and haemolysis; treated with penicillamine.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
An antidote is a substance that counteracts the effects of a poison, acting physically, chemically or physiologically.
Classification
- Mechanical (physical) — prevent absorption: activated charcoal, demulcents (milk, egg white), bulky food
- Chemical — react with the poison to form a harmless compound: sodium thiosulphate for cyanide, tannic acid for alkaloids, chelating agents for metals
- Physiological (pharmacological) — produce opposing effects: atropine for organophosphates, naloxone for opioids, flumazenil for benzodiazepines
- Universal antidote — historical mixture; now obsolete and not recommended
- Antivenom and antitoxins — immunological antidotes
Important Specific Antidotes
- Organophosphate — atropine + pralidoxime
- Opioid — naloxone; Paracetamol — N-acetylcysteine
- Methanol / ethylene glycol — ethanol or fomepizole
- Cyanide — sodium nitrite + sodium thiosulphate, hydroxocobalamin
- Iron — desferrioxamine; Warfarin — vitamin K; Heparin — protamine
- Digoxin — digoxin-specific antibody; Methaemoglobinaemia — methylene blue
Antidotes supplement, never replace, supportive care. Poison Antidote Organophosphate Atropine + pralidoxime Paracetamol N-acetylcysteine Cyanide Thiosulphate Applied
- Most poisons have no specific antidote
- The universal antidote is obsolete and should not be used
🔑KEY POINTS TO REMEMBER- Antidotes are mechanical, chemical or physiological.
- Key pairs: organophosphate-atropine, opioid-naloxone, paracetamol-N-acetylcysteine.
- The universal antidote is obsolete; supportive care remains the mainstay.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Carbolic acid (phenol) is an organic corrosive poison; the resulting condition is called carbolism.
Features
- Used as a disinfectant; poisoning usually accidental or suicidal
- Characteristic smell of phenol in breath and vomit — a valuable diagnostic clue
- Corrosive effect — burning pain, white or greyish-white corrugated (leathery) patches in the mouth and throat, with little bleeding
- Local anaesthetic effect — pain may be surprisingly slight
- Systemic: giddiness, rapid unconsciousness, shallow respiration, hypotension, convulsions
- Carboluria — urine turns greenish-brown or smoky-green on standing, a classical sign
Autopsy, Treatment & Medicolegal Aspects
- Autopsy: hardened, corrugated, greyish-white gastric mucosa with a strong phenolic smell
- Kidneys congested; acute tubular necrosis
- Treatment — gastric lavage is generally avoided because of corrosion; dilute with water or milk; olive oil or castor oil may be given (phenol is fat-soluble); supportive care, treat kidney injury
- Skin decontamination with polyethylene glycol or copious water
- Fatal dose about 10–15 g; fatal period 3–12 hours (standard textbook figures)
- Historically used in ‘carbolic acid throwing’ — now punishable as an acid attack
Its local anaesthetic action means pain is a poor guide to severity. Sign Detail Mouth Greyish corrugated patches Urine Smoky-green (carboluria) Smell Phenolic Applied
- Carboluria is a simple bedside diagnostic pointer
- Phenol is absorbed rapidly through intact skin — decontaminate promptly
🔑KEY POINTS TO REMEMBER- Phenol produces greyish-white corrugated mouth patches with little pain.
- Carboluria — urine turning smoky-green on standing — is classical.
- Lavage is avoided; treat with dilution, skin decontamination and supportive care.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Oxalic acid is an organic corrosive and systemic poison, historically called the ‘acid of sugar’.
Features
- Found in bleaching powder, metal polish, rust removers, ink stain removers; naturally in rhubarb and some leafy vegetables
- Poisoning usually accidental or suicidal (mistaken for magnesium sulphate)
- Local corrosive action — burning pain, vomiting of dark ‘coffee-ground’ material; mouth and throat white and sodden
- Systemic action — binds calcium causing severe hypocalcaemia: tetany, carpopedal spasm, twitching, convulsions, cardiac arrhythmia
- Renal action — calcium oxalate crystals block the renal tubules → acute kidney injury, oliguria, haematuria
Autopsy, Treatment & Diagnosis
- Autopsy: corroded gastric mucosa with dark brown or black stomach contents
- Kidneys swollen; envelope-shaped (octahedral) calcium oxalate crystals in the renal tubules — characteristic
- Diagnosis: hypocalcaemia, oxalate crystals in urine, raised anion gap acidosis
- Treatment — avoid lavage if corrosion is marked; give calcium salts (calcium gluconate, calcium lactate or milk) as a chemical antidote to precipitate oxalate
- Intravenous calcium gluconate for tetany; fluids and dialysis for kidney injury
- Fatal dose about 15–20 g; fatal period 1–2 hours (standard textbook figures)
Calcium binding explains both the tetany and the renal damage. Effect Result Local Corrosion, coffee-ground vomit Systemic Hypocalcaemia, tetany Renal Oxalate crystals, AKI Applied
- Calcium is both antidote and treatment — milk is a useful first measure
- Envelope-shaped crystals in renal tubules are diagnostic at autopsy
🔑KEY POINTS TO REMEMBER- Oxalic acid acts locally as a corrosive and systemically by binding calcium.
- Causes tetany, convulsions and acute kidney injury from oxalate crystals.
- Calcium salts are the specific antidote; envelope-shaped crystals are diagnostic.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Gastric lavage is washing out the stomach with fluid to remove unabsorbed poison, and is also used to obtain a sample for analysis.
Technique & Indications
- Boas or Ewald tube passed orally; patient in the left lateral head-low position
- Warm water or normal saline, about 200–300 mL at a time, repeated until the return is clear
- First portion always preserved for chemical analysis
- Most useful within one hour of ingestion
- Indicated for recent ingestion of a significant amount of a life-threatening poison with a protected airway
Contraindications & Complications
- Corrosive acids and alkalis — risk of perforation
- Kerosene and other volatile hydrocarbons — risk of aspiration pneumonitis
- Unconscious patient without a cuffed endotracheal tube
- Convulsions, oesophageal varices, recent surgery, marked hypothermia
- Complications: aspiration pneumonia, oesophageal or gastric perforation, laryngospasm, electrolyte disturbance, arrhythmia
- Current evidence limits its routine use — activated charcoal is usually preferred
The first aspirate is the most valuable forensic sample. Aspect Detail Best within 1 hour Contraindicated Corrosives, kerosene Sample First portion preserved Applied
- Always protect the airway first in an unconscious patient
- Label and seal the sample; hand it to the police under receipt
🔑KEY POINTS TO REMEMBER- Gastric lavage is most useful within one hour of ingestion.
- Contraindicated in corrosive and kerosene poisoning and unprotected airway.
- The first portion must be preserved for chemical analysis.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
Chelating agents are compounds that bind metal ions to form stable, non-toxic, water-soluble complexes that are readily excreted in urine.
Principal Agents
- BAL (dimercaprol, British Anti-Lewisite) — for arsenic, mercury, gold, lead (with EDTA); given deep intramuscularly in peanut oil; painful
- Calcium disodium EDTA — the agent of choice for lead
- Penicillamine — oral; for copper (Wilson disease), lead, mercury
- DMSA (succimer) — oral, safer, fewer side effects; for lead, arsenic, mercury
- Desferrioxamine — for iron
- Dicobalt edetate — for cyanide
Principles & Precautions
- Chelator must have greater affinity for the metal than the body’s own binding sites
- The complex must be stable, non-toxic and readily excreted
- Start early — chelation cannot reverse established damage, especially neurological
- Adequate renal function is essential — the complex is excreted in urine
- Side effects: hypertension, nausea, nephrotoxicity (BAL), redistribution of metal to the brain if used inappropriately
- BAL is contraindicated in iron, cadmium and selenium poisoning — the complexes are more toxic
Renal function must be adequate for the complex to be eliminated. Metal Chelator Lead Calcium disodium EDTA Arsenic, mercury BAL / DMSA Copper Penicillamine Iron Desferrioxamine Applied
- Monitor renal function throughout chelation therapy
- DMSA is increasingly preferred for being oral and better tolerated
🔑KEY POINTS TO REMEMBER- Chelators form stable, non-toxic, water-soluble complexes excreted in urine.
- Lead-EDTA, arsenic and mercury-BAL/DMSA, copper-penicillamine, iron-desferrioxamine.
- Start early; adequate renal function is essential; BAL is unsuitable for iron.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
The Marsh test is a classical sensitive chemical test for the detection of arsenic in biological material, of great historical importance in toxicology.
Principle & Procedure
- Devised by James Marsh in 1836
- The suspected material is treated with zinc and sulphuric acid, generating hydrogen
- Any arsenic present is converted to arsine gas (AsH₃)
- The gas is passed through a heated glass tube, where it decomposes and deposits a brownish-black metallic mirror (arsenic mirror)
- Extremely sensitive — detects as little as about 0.02 mg of arsenic
Interpretation & Significance
- The arsenic mirror is soluble in sodium hypochlorite, whereas a similar mirror from antimony is not — this distinguishes the two
- Historical importance — first use of a scientific chemical test as courtroom evidence; used in the Lafarge case (1840), which established forensic toxicology as a discipline
- Ended the era in which arsenic was regarded as undetectable
- Other tests for arsenic: Reinsch test (copper foil turns grey-black) and Gutzeit test
- Now largely superseded by atomic absorption spectrophotometry and neutron activation analysis, which are quantitative
Solubility in hypochlorite distinguishes arsenic from antimony. Test Basis Marsh Arsenic mirror Reinsch Copper foil greys Gutzeit Stain on paper Applied
- Distinguishing arsenic from antimony is the key interpretive step
- Modern quantitative methods have replaced it in practice
🔑KEY POINTS TO REMEMBER- Marsh test converts arsenic to arsine gas, depositing an arsenic mirror.
- The mirror dissolves in sodium hypochlorite, unlike antimony.
- Historically established forensic toxicology; now superseded by AAS.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.Definition
An ‘ideal homicidal poison’ is a theoretical concept describing the properties that would make a poisoning difficult to detect — studied so that doctors know when to be suspicious.
Properties Described in Textbooks
- Cheap and easily available without arousing suspicion
- Colourless, odourless and tasteless — not detectable by the victim
- Highly potent in small amount
- Symptoms resembling a natural disease — so death is attributed to illness
- No characteristic postmortem appearance
- Not detectable by routine chemical analysis; rapidly destroyed or eliminated from the body
- No such perfect poison exists — every substance leaves some trace
Practical & Medicolegal Significance
- The concept exists to teach the doctor when to suspect poisoning, not as a guide to any substance
- Suspect poisoning when a healthy person has a sudden unexplained illness, when several people fall ill after a common meal, or when symptoms do not fit a recognised disease
- In India, poisons historically implicated in homicide include arsenic, aconite, oleander and abrus — all now readily detectable
- Modern analytical toxicology — gas chromatography-mass spectrometry, HPLC, atomic absorption — detects minute traces, so the concept is now largely of academic and historical interest
- Always preserve viscera when the cause of death is unclear
- Availability of poisons is restricted by the Poisons Act
The lesson is vigilance — modern analysis defeats the ‘ideal poison’ idea. Property Purpose in concept Tasteless Escapes victim Mimics disease Escapes clinician Not detectable Escapes analyst Applied
- No ideal homicidal poison exists in practice
- The doctor’s suspicion and preservation of viscera remain the decisive safeguards
🔑KEY POINTS TO REMEMBER- The ‘ideal homicidal poison’ is a theoretical concept, not a real substance.
- Described properties: cheap, tasteless, potent, mimicking disease, undetectable.
- Modern analytical methods detect trace amounts — the concept is now academic.
📚SOURCES: The Essentials of Forensic Medicine and Toxicology (K.S. Narayan Reddy); Textbook of Forensic Medicine and Toxicology (V.V. Pillay); Modi’s Textbook of Medical Jurisprudence and Toxicology.