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Arsenic Poisoning - FM Exam Notes

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1. Introduction

• Arsenic trioxide (As₂O₃) - white powder, most common
• Copper arsenite (Paris green) - insecticide
• Calcium/lead arsenate - pesticides
• Arsenic trisulphide (orpiment) - yellow
• Realgar (red arsenic sulphide)
• Arsine gas (AsH₃) - industrial setting

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2. Fatal Dose & Fatal Period

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3. Mechanism of Toxicity

1. Reversible combination with sulphydryl (-SH) groups - reacts with SH groups in tissue proteins (most important mechanism)
2. Interferes with enzyme systems essential for cellular metabolism
3. Capillary poison - dilates capillaries causing transudation
4. Fatty degeneration of liver
5. Hyperemia and haemorrhages in intestine
6. Renal tubular necrosis
7. Peripheral nerves: disintegration of axis cylinder (axonal neuropathy) with fragmentation and resorption of myelin

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4. Absorption, Distribution & Elimination

• Blood: < 4 mg/L (serious poisoning: > 1.5 mg/100 mL)
• Urine: < 0.03 μg/L (acute poisoning: > 100 μg/24 hr)
• Hair: < 0.05 mg/100 g (diagnostic if > 1 mg/100 g or 3 ppm)

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5. Acute Arsenic Poisoning - Signs & Symptoms

1. Metallic taste in mouth + garlic odour in breath + xerostomia + dysphagia
2. Nausea, vomiting (projectile, dark brown/yellow, contains blood + mucus)
3. Colicky abdominal pain + profuse diarrhoea
4. Stools: initially dark, bloody → later rice-water (colourless, odourless)
5. Tenesmus + anal irritation (distinguishes from cholera)
6. Increased salivation + intense thirst
7. Generalised vasodilation → severe hypovolemia/shock
8. Cyanosis, cold clammy extremities
9. Hypoxic encephalopathy, convulsions
10. Acute tubular necrosis - oliguria, proteinuria, haematuria
11. Hyperpyrexia + acute haemolysis
12. Cardiac: acute cardiomyopathy, subendocardial haemorrhages, prolonged QT interval, non-specific ST-T changes

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6. Chronic Arsenic Poisoning - Signs & Symptoms

Skin (hallmark)

• Earliest: persistent erythematous flushing
• Raindrop pigmentation - finely mottled brown, on skin flexures (temples, eyelids, neck, axilla) - classic
• Hyperkeratosis of palms and soles
• Desquamation, brittle nails
• Mees' lines (Aldrich-Mees lines) - transverse white lines on fingernails, appear 5-6 weeks after exposure, 1-2 mm wide (double lines if repeated exposure)
• Hair loss (alopecia)
• Bowen's disease - intraepidermal carcinoma; long-term complication; signals systemic neoplasm

Nervous System (hallmark)

• Symmetrical sensorimotor polyneuropathy - resembles Guillain-Barré syndrome
• Paresthesia, numbness, pain - especially soles of feet
• "Glove and stocking" distribution
• Wrist drop, inability to walk, muscle atrophy, ataxia
• Encephalopathy: headache, personality change, convulsions, coma

Other Systems

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7. Arsenic vs. Cholera (High-Yield Differentiating Table)

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8. Laboratory Diagnosis

• 24-hour urine arsenic - best test for recent/chronic exposure (> 100 μg/24 hr in acute poisoning)
• Hair and nail analysis - > 1 mg/100 g or > 3 ppm = diagnostic (can detect exposure years after death)
• Measuring distance of Mees' lines from nail base = estimates timing of exposure (nails grow ~1 mm/week; hair ~1 cm/month)
• Atomic absorption spectroscopy / Neutron activation analysis - modern gold standard
• Marsh's test and Reinsch's test - now obsolete (but may still be asked in exam)
• Basophilic stippling on peripheral smear (non-specific but consistent)
• Serum: elevated liver transaminases, alkaline phosphatase, bilirubin; urobilinogen in urine
• ECG: prolonged QT interval

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9. Treatment

General (Acute Oral)

1. Emetics (NOT tartar emetic, NOT copper sulphate - forms copper arsenite)
2. Stomach wash with freshly prepared ferric oxide solution (forms insoluble ferric arsenite) OR 1% sodium thiosulphate; repeated washes; gastric lavage
3. Whole bowel irrigation
4. Alkalis must NOT be given (increase solubility)
5. Butter/greasy substances prevent absorption

Antidote - Chelation Therapy

Note: BAL is NOT effective for arsine gas poisoning

Supportive

• IV saline for dehydration
• Morphine for pain
• Demulcents (ghee, barley water)
• Castor oil / magnesium sulphate (reduce intestinal absorption)
• Haemodialysis in renal failure

Arsine Gas Poisoning (different!)

• Fresh air + oxygen
• Exchange transfusion
• Haemodialysis
• Alkaline drinks
• Chelation INEFFECTIVE

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10. Postmortem (Autopsy) Findings

External

• Rigor mortis lasts longer than normal
• Body shrunken (dehydration)
• Eyeballs sunken
• Cyanosis of hands and feet
• Jaundice

Internal

• Mouth/pharynx/oesophagus: inflamed, ulcerated
• Stomach (main organ): mucosa swollen, congested, brownish-red/scarlet ("red velvet" appearance); petechial haemorrhages; sticky mucus with arsenic particles; inflammation most marked at greater curvature and cardiac end; ulceration, gangrene, perforation (rare)
• Small intestine: flabby, large flakes of mucus, submucosal haemorrhages, pale-violet mucosa
• Large intestine: seromucous discharge, glands swollen
• Lungs: congested, oedematous, subpleural ecchymoses
• Liver, spleen, kidneys: congested, enlarged, cloudy swelling, fatty change
• Heart: subendocardial petechial haemorrhages of ventricle (typical; present even when stomach shows little irritation)
• Brain: oedema, patchy necrosis, haemorrhagic encephalitis
• Arsenic delays putrefaction (important forensic point)

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11. Medico-legal Importance (Why Arsenic is Popular for Homicide)

1. Cheap and easily obtained
2. Colourless, odourless, tasteless
3. Small quantity causes death
4. Easily mixed with food/drink
5. Gradual onset; symptoms mimic cholera

1. Delays putrefaction - body preserved
2. Detectable in completely decomposed bodies
3. Found in bones, hair, nails for several years
4. Detectable in charred bones or ashes
5. Can be found in exhumed bodies

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12. Postmortem Imbibition (Exam Trap!)

• In exhumations, arsenic from soil may contaminate the body
• Arsenic introduced into stomach after death: transudation occurs into organs of the left side before the right
• No inflammation/ulceration if arsenic introduced post-mortem
• Soil arsenic is usually insoluble salt - differentiates from poisoning

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High-Yield One-Liners for Quick Revision

• Garlic odour in breath = arsenic (also phosphorus)
• Mees' lines = transverse white nail lines; appear 5-6 weeks post-exposure
• Raindrop pigmentation = chronic arsenic (pathognomonic skin sign)
• Red velvet stomach = arsenic PM finding
• Antidote = BAL (dimercaprol); DMSA/DMPS superior if available
• Arsine gas = BAL ineffective; causes haemolysis
• Hair diagnostic level = > 1 mg/100 g (or > 3 ppm)
• Mechanism = binds -SH groups → enzyme inhibition
• Neuropathy = hallmark of chronic poisoning; glove-and-stocking pattern
• Bowen's disease = chronic arsenic complication (skin carcinoma)
• Delays putrefaction = arsenic (forensic significance)
• Fatal dose = 200-300 mg As₂O₃
• Fatal period = 12-48 hours
• Arsenic replaces phosphorus in bone (stays for years)
• Tenesmus present in arsenic, absent in cholera

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Food Poisoning - FM Exam (Important Points Only)

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Definition

1. History of ingestion of a common food
2. Many persons attacked at the same time
3. Similarity of signs and symptoms in majority

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Classification

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High-Yield Comparison Table - All Major Organisms

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Organism-Wise Key Points

1. Salmonella Food Poisoning

• Most common species: S. typhimurium, S. enteritidis, S. cholera-suis
• Source: Farm animals, poultry, eggs, rats/mice (contaminate food via urine/feces)
• Mechanism: Organisms multiply in intestine → acute enteritis + colitis
• IP: 12-24 hours
• Symptoms: Sudden chills, fever, nausea, vomiting, profuse watery diarrhoea (lasts 2-3 days)
• Mortality: ~1%; convalescent carrier state possible

2. Staphylococcal Food Poisoning

• Most common food poisoning organism overall
• Agent: Enterotoxin A (most common); Enterotoxin B = pyogenic toxin, can be used as bioterrorism weapon (lethal dose 1.7 mcg/person)
• Toxin: Heat-stable (survives cooking; organisms may die but toxin remains)
• IP: 1-8 hours (short because preformed toxin)
• Symptoms: Sudden vomiting, abdominal cramps, mild diarrhoea, no fever, headache
• No fever = key distinguishing feature from Salmonella

3. Botulism (C. botulinum)

• Most serious, most fatal (kills 2/3 of victims)
• Agent: Exotoxin Type A, B, or E
• Source: Home-canned/preserved foods, smoked/pickled fish, home-made cheese (low-acid anaerobic foods). Name from botulus = Latin for sausage
• Toxin: Preformed in food; heat-labile (destroyed at 100°C for few minutes)
• IP: 18-36 hours
• Mechanism: Acts on parasympathetic nervous system → blocks ACh at NMJ
• Symptoms: Minimal GI symptoms; prominent neurological: dysphagia, diplopia, ptosis, dysarthria, blurring of vision, muscle weakness, quadriplegia. Fever absent, consciousness retained
• Death: 4-8 days from respiratory/cardiac failure
• Recovered patients do NOT develop antitoxin in blood
• Infant botulism: Due to gut infection (not preformed toxin); honey/sugar must NOT be fed to neonates
• Prevention: Boil home-preserved food at 120°C before consumption

4. Clostridium perfringens

• IP: 8-22 hours
• Source: Meat, poultry stews (reheated)
• Toxin formed in gut; spores survive normal cooking
• Symptoms: Diarrhoea > vomiting, little or no fever

5. Bacillus cereus

• Emetic form: Toxin = Cereulide (heat-stable); source = fried rice, pasta, noodles ("Fried Rice Syndrome"); IP = 1-5 hours; symptoms = nausea + vomiting
• Diarrheal form: Heat-labile toxin; source = meat, vegetables, milk; IP = 8-16 hours; symptoms = watery diarrhoea + abdominal pain
• Spores resistant to extreme temperature; found in natural soil

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Medicolegal Aspects (FM Exam Specific)

1. Most food poisoning cases are accidental unless questioned
2. 90% are domestic food poisoning; 4% hostel/restaurants; 2% food industry
3. 70% vegetarian diet, 17% meat, 13% fish
4. Botulinum toxin misused for biowarfare (causes paralysis of soldiers)
5. Ptomaines = cadaveric alkaloids from bacterial decomposition; once thought to cause food poisoning; now obsolete theory; NOT bacterial poisons; harmless except neurine and mydalein (resemble atropine poisoning)

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Food Poisoning vs. Cholera (Exam Table)

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Investigation of a Food Poisoning Outbreak

1. Secure list of all affected persons + questionnaire (foods eaten last 2 days, onset, symptoms)
2. Lab investigation: Stool/vomit/remnants for culture; aerobic + anaerobic; phage typing
3. Animal experiments: Feed rhesus monkeys; botulism - protection test in mice
4. Blood for antibodies (retrospective diagnosis)
5. Environmental study: Inspect kitchen, food handlers

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Treatment (General)

• ORS / IV Rehydration (Ringer's lactate)
• Antidiarrheal agents (Kaolin-pectin)
• Botulism = antitoxin (Type A, B, E)
• Antibiotics rarely needed (supportive usually sufficient)
• Do NOT feed honey/sugar to neonates (infant botulism prevention)

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One-Liners to Remember

• Shortest IP = Staph aureus (1-8 hrs) / B. cereus emetic (1-5 hrs) - preformed toxin
• Longest IP = Botulism (18-36 hrs)
• No fever = Staph aureus, Botulism
• Neurological symptoms only = Botulism
• Most fatal = Botulism
• Most common = Staphylococcus aureus
• Fried rice = B. cereus emetic form
• Home canned food = Botulism
• Heat-stable toxin = Staph aureus (toxin survives cooking)
• Heat-labile toxin = Botulism (destroyed at 100°C)
• Bioterrorism agent = Staph Enterotoxin B + Botulinum toxin
• 90% food poisoning = domestic