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Metallic poisons in forensic medicine.pptx
- 1. INORGANIC IRRITANT POISON METALLICPOISONS Dr Alok Kumar Maurya MBBS, MD Senior Resident Dept Of Forensic Medicine & Toxicology
- 2. Introduction • Classification ofPoisons • Many metallic elements in trace quantities are essential for various biological processes. • Excessive exposure(nutritional/ occupational or environmental) can lead to accumulation and toxicity resulting in serious consequences.
- 3. • Heavy metalpoisoning is a major cause for morbidity and mortality- worldwide and in India. • Hippocrates described abdominal colic in a man who extracted metals. • The pernicious effects of arsenic and mercury among smelters were known even to Theophrastus of Erebus (370-287 BC).
- 4. Common Metallic Poisons Common Arsenic (As) Lead (Pb) Mercury (Hg) Iron (Fe) Copper (Cu) Uncommon Aluminium Antimony Barium Beryllium Bismuth Cadmium Magnesium Potassium Silver Thallium Zinc
- 5. Types of Poisoning •Fulminant • Acute • Chronic • Subacute Detailed complete history of ingestion or exposure has to be taken
- 6. Arsenic Poisoning • Metallicarsenic - Non Poisonous • Insoluble in water • Poisonous – Exposed to air Commonest- ideal homicidal poison.
- 7. Arsenic Compounds Syonyms Physical Properties Uses Elemental Arsenic •Metallic Arsenic •GreyArsenic •Shiny Grey, Brittle, Metallic looking Substance In Alloys Arsine •Arsenic tri- hydride •Hydrogen Arsenide •Arseniuretted Hydrogen Colourless gas with garlicky odour Lead plating, soldering, galvanizing, and in electronic components Trimethyl arsine Gosio gas Colourless gas Present in sewage Arsenic trioxide, Arsenic oxide, white arsenic, arsenic sesqui- oxide, arsenious White powder(dissolves slowly in water to form arsenious Manufacture of glass, insecticide, rodenticide. Previously used in
- 8. Arsenic Compounds Syonyms Physical Properties Uses Arsenic trichlorideButter of arsenic Yellowish, oily liquid Pottery Sodium arsenite Meta-arsenite, arsenious acid sodium White or greyish powder Insecticide, wood preservative, veterinary use Arsenic pentoxide Arsenic acid, arsenic anhydride White powder(dissolves rapidly in water to form arsenic acid) Manufacture of coloured glass, insecticide, wood preservative Lead arsenate Acid lead arsenate Heavy, white powder Insecticide. Copper arsenite Scheele’s green Greenish powder Colouring agent for toys, wall paper, etc. Copper Paris or Emerald Greenish powder Insecticide
- 9. Arsenic oxide orArsenic trioxide • White Arsenic • Crystalline Powder or Solid mass • Transparent later porcelain in appearance • Odourless, Tasteless, Floats in water • Used in Calico Printing, Taxidermy, Wallpapers, Artificial flowers, Dyeing, Rodenticide, Preserving timbers.
- 11. Toxicokinetics and Modeof Action • Absorbed through all routes • Binds to sulphydryl group of tissue proteins • Interferes with cellular respiration – Cell death. • Affinity-Vascular endothelium • Replaces Phosphorus in bone – Remains for years and deposited in hair • Does not cross Blood – Brain barrier and Crosses
- 12. Signs and Symptoms TheFulminant Type ▫ Massive doses 3 – 5 gms, causes death in 1-3 hrs ▫ Shock and peripheral vascular failure ▫ Direct action on Heart muscle. ▫ GIT Symptoms Absent
- 13. Signs and Symptoms TheGastro-enteric Type ▫ Resembles Bacterial food poisoning ▫ Sweetish metallic taste ▫ Constriction in the throat, Difficulty in swallowing ▫ Burning & Colicky pain in Oesophagus, Stomach & Intestine. ▫ Intense thirst and severe vomiting ▫ Purging – Tenesmus, pain and irritation. ▫ Stools – Expelled frequently and involuntarily, dark coloured
- 14. Symptoms Arsenic PoisoningCholera Pain in the throat Before vomiting Not so Voice Not affected Peculiar, rough and whistling. Conjunctivae Inflamed Not so Vomited matter Contains mucus, bile and streaks of blood Is watery Purging Follows Vomiting Usually precedes vomiting Stools High coloured, Bloody faeculent, foetid and discharged with straining and tenesmus ‘Rice-water’, liquid whitish and discharge in an almost continuous and involuntary jet Laboratory Examination •Barium like radio-opaque shadow on X-Ray of abdomen •Arsenic detected on chemical analysis Cholera vibrio detected on microscopic examination of stools
- 15. Signs and Symptoms •Hepatic: Fatty infiltration • Renal: Oliguria, uraemia, Urine contains albumin, red cells and casts, pain during micturition. • CVS: Acute circulatory collapse with vasodilatation increased vascular permeability, ventricular tachycardia and ventricular fibrillation. • CNS: Headache, vertigo, hyperthermia, tremors, convulsions, coma, generalised paralysis. • Skin: Delayed loss of Hair, skin eruptions
- 16. Signs and Symptoms NarcoticForm • GIT – Symptoms • Giddiness, Formication, tenderness of muscles, delirium, coma and death.
- 17. Fatal Dose • 200– 300mg of arsenious oxide • Most toxic form ‘Arsine Gas’ Fatal Period • 12 – 48 hrs
- 18. Diagnosis • Urine level:24 hrs excretion exceeds 100µg indicative of toxicity. • Blood level: Less reliable because of short half life of arsenic in blood. • Hair level: Cannot discriminate external and toxic accumulation. • Atomic absorption spectroscopy – Biological samples, contaminated water.
- 19. Treatment • Supportive measures:Gastric lavage, IV Fluids, cardiac monitoring, etc • Chelating therapy: ▫ BAL (British Anti Lewisite) ▫ Dimercaprol, ▫ Penicillamine ▫ DMSA (Di Mercapto Succinic Acid), ▫ DMPS (Di Mercapto Propane Sulfonic Acid) BAL 3 – 5 mg/kg IM 4 hourly for 7 – 10 days. Penicillamine orally 100mg/kg/day 6 hourly for 5 days • Haemodialysis or Exchange transfusion ▫ Forced alkaline diuresis ▫ Exchange transfusion
- 20. Post Mortem changes •External Appearances ▫ Rigor mortis – Lasts longer ▫ Shrunken appearance ▫ Skin of hands and feet – cyanosed
- 21. Post Mortem changes •Internal Appearances • GIT ▫ Mouth pharynx and oesophagus inflamed. ▫ Stomach Mucosa swollen, oedematous, lines of redness along the walls. Petechiae scattered all over the mucosa. Red velvety mucosa. ▫ Ulceration or large erosions – Pyloric end ▫ Congestion – Marked along the crest of the rugae. ▫ Inflammation – Greater curvature , posterior part and cardiac end of stomach ▫ Small intestine – Flaccid and contains large flakes of mucus with little faecal matter.
- 22.
- 23. Post Mortem changes •Putrefaction – Yellow streaks in the sub-peritoneal layer of the stomach and intestines • Liver, spleen, kidney are congested, enlarged and show cloudy swelling and occasionally fatty change. • Lungs congested with subpleural ecchymoses • Haemorrhages – Abdominal organs, mesenteries. • Brian – Oedema, Patchy necrosis or Haemorrhagic encephalitis • Heart – Subendo cardial petechial haemorrhages
- 24. Chronic Poisoning • Smelting •Refining of ores • Subliming of white arsenic – Manufacture of sheep-dips, weed-killers, insecticides, paints, dyes, cosmetics and drugs.
- 25. Symptoms • First stage: ▫Loss of Weight ▫ Loss of appetite ▫ Salivation ▫ Colicky pain ▫ Constipation or Diarrhoea ▫ Vomiting ▫ Gums are red & soft ▫ Tongue – White, silvery fur ▫ Oedema of ankles and lower eyelids ▫ Increased temperature and pulse rate
- 26. Symptoms • Second stage ▫Cutaneous eruptions ▫ Catarrh – larynx and bronchial tree ▫ Voice - hoarse and husky ▫ Eyes – Photophobia and conjunctivitis ▫ Liver – Enlarged or cirrhotic ▫ Kidney may be damaged ▫ Skin – Generalised or localised, finely mottled pigmentation – “RAIN DROP TYPE” appears in skin flexures, temples, eyelids and neck. ▫ ALDRICH-MEES LINES – Bands of opacity in the fingernails, Hyperkeratosis of the palms and soles.
- 27.
- 28. Symptoms • Third stage ▫Sensory symptoms ▫ Impotence ▫ Bone marrow depression
- 29. Symptoms • Fourth Stage ▫Peripheral neurites and muscular atrophy ▫ Wrist drop ▫ Foot drop
- 30. Post Mortem Appearances •Stomach • Liver: Fatty change ,necrosis • Kidney: Tubular necrosis
- 31. Elimination • Mainly byKidney • Hair and Nails • Faeces • Bile • Sweat • Breast milk – does not contain significant amount of arsenic • Fixed in cancellous tissues and long bones
- 32. Medico-legal Aspects • Homicide ▫Cheap ▫ Easily obtained ▫ Colourless ▫ No smell ▫ No taste ▫ Small Quantity ▫ Gradual onset of symptom ▫ Simulates: Cholera
- 33. Medico-legal Aspects • Disadvantages ▫Delays putrefaction ▫ Detected in completely decomposed body, bones, hairs for several years. • Suicide: Rare • Accidental: Food, water • Abortion stick • Cattle poison
- 34. LEAD (pb) SHISHA •Heavy steel metal • All salts are poisonous • Principal salts which produce toxic effects 1.Lead acetate 2.Lead carbonate 3.Lead tetroxide 4.Lead sulphide 5.T E L
- 37. Metabolism • Through ingestion/inhalation/Throughskin • Plasma-equilibrates with E C F • Blood-95 to 99% is sequestered into RBC • Largest proportion is incorporated into skeleton • Half life of lead in blood is about 25days, soft tissues about 40 days and in bones >25 years • Excreted mainly in urine and in faeces
- 38. Mechanism • Interferes withmitochondrial oxidative phosphorylation and Na, K and Ca ATPases • Depresses the enzymes for haem synthesis –RBC life span • Blocks enzyme aminolevulinic acid(ALA) dehydrase • Inhibits ferrochelatase-raises F E P
- 39. ACUTE POISONING • Metallicastringent taste • Vomiting with colicky pain abdomen • Purging with constipation • Faeces are offensive and black • Cramps in legs and arthralgia • Collapse - death
- 40. Management-contd… • Fatal doses:10mgs/70 kg of Metallic salts 100mgs/kg of T E L • Remove unabsorbed poison • Ca gluconate-2g I V pain abdomen • EDTA-30 to 40 gm/kg • DMSA-30 mg/kg • BAL, Pencillamine
- 41. PLUMBISM(Chronic poisoning) • Inhalationof lead dust in factories • Ingestion through stored H2O, ghee stored in copper vessels lined by tin –lead oleate • Absorption through skin-Absorption of vermillion/sindhur • Licking and chewing by children
- 42. SIGNS AND SYMPTOMS •Facial pallor • Anemia, punctate basophilia • Lead line • Colic and constipation • Lead palsy • Encephalopathy • CVS and nephropathy • Reproductive system • Others system-lead osteopathy
- 44. DIAGNOSIS • History • Clinicalfeatures • Lab test Coproporphyrin-150mg/litre of urine ALAU-5 microgram Blood lead level more than 25 microgram/100ml
- 45. • X-ray radio-opaquebands at metaphyses • Basophilic stippling • Zinc protoporphyrin and free erythrocyte protoporphyin above 50 micrograms/100ml • X-ray abdomen
- 46. MANAGEMENT 1.With encephalopathy BAL-4mg/kg EDTA-75mg/kg/day D-pencillamine 10mg/kg/dayfor 20 days 2.Without encephalopathy BAL-12mg/kg/day EDTA-50mg/kg/day 3.Moderate poisoning EDTA 50mg/kg/day 4.Mild poisoning D-pencillamine 30 mg /kg/day 5.Supportive measures: Ca-gluconate,vitamin
- 47. Post Mortem Changes •Blue line • Stomach and intestines –ulcerative or haemorrhagic changes and contracted and thickened • Kidney and Liver –contracted • Brain-swollen • Paralysed muscles-fatty degeneration • Bone marrow –hyperplasia • Segmental demyelination
- 48. Cause of death •Acute poisoning-G -E with shock • Chronic poisoning-infection, malnutrition, liver failure, respiratory failure, renal failure and encephalopathy
- 49. Circumstances • Chronic –common •Cattle poison • Lead missiles • Pica • Lead water-Roman culture
- 52. INORGANIC IRRITANT POISON- METALLICPOISONS-II Dr B S Hugar, MD,DNB, MNAMS Associate Professor Dept Of Forensic Medicine
- 53. Mercury ( QuickSilver) • Physical Appearances ▫ Heavy, silvery liquid, non toxic as such ▫ Vapours – Toxic • Boiling point – 356.9° F • Melting Point - -38° F • 13.5 times denser than water • 1.2 times heavier than lead
- 54. • Two seriesof compound 1. Mercuric (Bivalent, i.e Hg++ ) Soluble and intensely poisonous 2. Mercurous(Monovalent, i.e. Hg+ ). Less soluble and less toxic.
- 55. Poisonous Compounds 1. Mercuricchloride (HgCl2 , Corrosive sublimate) 2. Mercuric oxide 3. Mercuric iodide 4. Mercuric cyanide 5. Mercuric sulphide ( cinnabar /sindhoor/vermilion) 6. Mercurous chloride 7. Mercuric nitrate 8. Mercuric sulphate
- 56. Uses • Thermometer • Ceramics •Dry cell batteries • Explosives and Fire works • Hat and glass industries • Electroplating powder • Fingerprint powder • Fluorescent and Mercury vapour lamps • Paints and • Pesticide
- 57. Action • Binds withsulphydryl group of enzymes and cellular proteins (NA/Mitochondria) • Readily absorbed by alveolar membrane and enters blood stream • CNS: Cerebellum, temporal lobe, basal ganglia and corpus callosum
- 58. Clinical Features • FirstPhase ▫ Metallic taste ▫ Constriction ▫ Hoarse voice ▫ Difficulty in breathing ▫ GIT – Corroded, swollen and greyish white coating ▫ Burning Pain ▫ Vomiting ▫ Diarrhoea ▫ Circulatory collapse
- 59. Clinical Features • SecondPhase ▫ Survives for 1 – 3 day ▫ Glossitis and ulcerative gingivitis: 24 – 36 hrs ▫ Severe infection, loosening of teeth and necrosis of jaw. ▫ In 2 – 3 days renal failure
- 60. Fatal dose • Mercuricchloride: 0.5 – 1g/70kg • Mercurous chloride: 1.5 – 2g/70kg Fatal Period • 3 – 5 days
- 61. Chronic Poisoning(Hydrargyrism) • Hydrargyrum(Hg)- latin word for mercury
- 62. Inhalation • Tremor ▫ Hatter’sshake or glass blower shake ▫ Concussio mercurialis • Ataxia • Metallic taste, anorexia, nausea, increased salivation • Gingivitis: blue line on gums
- 63. •Erethism ▫Mad hatter’s Syndrome •Mercurialentis •Renal damage
- 64.
- 65. •Acrodynia (Pink disease) • Anorexia, •Insomnia • Profuse sweating • Skin rash • Photophobia • Hands and feet ▫ Puffy, Pinkish, Painful, paraesthetic, Perspiring andpeeling ( the child pees!)
- 66. Diagnosis • X-Ray • Bloodmercury level • Urine Levels • Hair analysis
- 67. Treatment • Acute Poisoning ▫Inhalation ▫ Removal from source ▫ Laxatives ▫ Demulcents ▫ Stomach wash ▫ Chelation Therapy ▫ Supportive measures
- 68. Treatment Contd.. Chelation Therapy •BAL (British Anti Lewisite): 100mg IM every 4hrs for 48 hrs followed by 100 mg 8 hourly for 8 – 10 days OR • DMPS(Di Mercapto propane sulfonate): 5mg/kg IV, or 6 infusions of 250 mg/day followed by 100mg B D for 24 days OR • DMSA (Di Mercapto Succinic Acid or Succimer): 30mg/kg/day orally for 5 days followed by 20mg/day/14days OR • D-Penicillamine:250 mg QID for adults (20mg/kg/day)
- 69. Post Mortem Appearances •GIT- Mucosa of GIT appears greyish with softening and superficial corrosion • Large intestine –ulcerations • Renal -pale, reveals necrotic change in renal tubules • Liver
- 70. COPPER • Salts ofcopper are poisonous • Copper sulphate or blue vitriol and sub acetate or verdigris • Copper is powerful inhibitor of enzymes • Copper is a component of tyrosinases and cytochrome oxidase • 80% is bound to ceruloplasmin • Absorbed copper bound to metalothionein • Eliminated via bile, urine
- 71. Chemical name Commonname Copper acetoarsenite Paris green Copper arsenite Scheele’s green Copper carbonate Brunswick green Copper sub acetate verdigris Copper sulfate Blue vitriol
- 72.
- 73. ACUTE POISONING • Metallictaste in mouth, salivation and thirst • Nausea, vomiting, pain abdomen, diarrhoea • Vomitus -addition of NH4OH turns deep blue • Stools –liquid brown • Urine –scanty and inky • Jaundice • Renal failure • Convulsions and coma
- 74. MANAGEMENT • FATAL doses-10to 20 gm • Fatal period-12 to 24 hrs • Gastric lavage with potassium ferrocyanide to form cupric ferrocyanide • Albumin –copper albuminate • Pencillamine and calcium EDTA • Dimercaprol
- 75. P M CHANGES •Greenish blue froth • Blue or green gastric mucosa
- 76. CHRONIC POISONING • Occupationalexposure • Vineyard sparyer lung disease-histiocytic granulomatous • Wilsons disease • Chalcosis • Swimming pool with algicidal copper-green hair
- 77. KF Ring- wilson’sdisease
- 78. DIAGNOSIS • Diagnosis-increased bloodlevel of 1.5 mg/100ml • Reduced cerluplasmin of 35%
- 79. Autopsy • Yellowish discolourationof skin and conjunctiva • Greenish or bluish discolouration of stomach contents • Hepatic or renal necrosis
- 80. Circumstances of poisoning •Rarely homicide and suicide. • Accidental by eating food contaminated with VERDIGRIS (formed from action of vegetable acids on copper cooking vessels which are not properly tinned). • As a abortifacient. • Cattle poison.
- 81. Medico legal Aspects •Copper is used to keep vegetables green. • As an antidote in phosphorous poisoning. • Metallic copper is non poisonous. • Spiritual green water can cause toxicity.
- 82. Iron • Metallic ironusually harmless • Even if ingestion is more than requirement it is excreted • Iron toxicity is related in more circumstances to over dose of therapeutically administered iron salts • Green vitriol (ferrous sulfate)
- 83. Uses • Medicinal –treatment of iron deficiency • Industry – tanning, inks, dyes, pigments • General - photography
- 84. Mode of action •Massive post-arteriolar dilatation, venous pooling of blood • capillary permeability • Oxidation of ferrous to ferric releasing hydrogen ions • Inhibits mitochondrial function • Inhibits thrombin induced conversion of fibrinogen to fibrin • Has a direct corrosive action on GI mucosa
- 85. Clinical features • Vomiting,diarrhoea, abdominal pain, hypotension, pallor, lethargy, hypoglycemia • Multi organ failure • Convulsions, coma and death
- 87. Treatment • Gastric lavage •Magnesium hydroxide solution orally • Correction of hypovolemia and metabolic acidosis • Desferrioxamine
- 88. OTHER METALLIC POISONS •Thallium. • Zinc – Sulphate (white vitriol). Chloride (Butter of Zinc). • Barium. • Kmno4.
- 89. Metal Fume Fever •Previously known as Brass foundryman’s Ague. • Metals like copper, Manganese, Magnesium, Iron, Chromium, Cadmium, Nickel, Mercury, Cobalt, Lead, Silver, Antimony and Aluminium produces this conditions. • Symptoms are similar to Influenza. • Symptoms appear after the weekend hence called “Monday morning fever”, has good prognosis and symptoms improve by the end of working week.