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MERCURY POISONING.pptx
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- 7. Characteristics Liquid metal Bright silvery appearance Volatile at room temperature
- 8. Organic Salts Compounds Organic Salts Methyl mercury Dimethyl Mercury Ethyl Mercury Phenyl Mercury
- 9. Inorganic Salts Compounds Mercuric (Hg ++) Soluble & poisonous Mercuric chloride (corrosive sublimate) Mercuric cyanide (pharaoh’s serpent aka Diwali poison) Mercuric sulphide (Sindoor, Vermilion) Mercurous ( Hg+) Less soluble less poisonous Mercurous chloride ( Calomel )
- 10. Uses Medicine Disinfectant Dentalamalgam Purgative Thimerosal , a preservative (DTP., Hep B.) Industry Thermometer, Barometer, Calibration Instruments, Fluorescent And Mercury Vapor Lamp, Electrical Equipment, Explosives And Fireworks
- 11. Action Mercury bindswith sulfhydryl groups resulting in enzyme inhibition and pathological alteration of cellular membranes. Elemental mercury and methyl mercury are toxic to the CNS.
- 12. Action Metallic mercuryvapor is also a pulmonary irritant. corrosive to the skin, eyes and GIT, and nephrotoxic. contact dermatitis.
- 13. Absorption and Excretion It is absorbed through the GIT and respiratory tract. After absorption, mercury gets deposited in all tissues, particularly in the liver, kidneys, spleen and bones. When inhaled, the maximum concentration occurs in the brain.
- 14. Absorption and Excretion Mainly excreted through the kidneys (urine), liver (bile) and colonic mucous membrane (feces). It passes rapidly to the fetus through placental circulation.
- 15. Fatal dose andFatal period Fatal Dose : One to 2 g. of mercuric chloride. Fatal Period : Three to five days.
- 16.
- 18. Symptoms First phase Acridmetallic taste Constriction of throat, hoarse voice, difficulty in breathing Mouth, tongue and fauces corroded
- 19. Symptoms First phase Nauseaand vomiting with greyish-white coating, blood, slimy mucoid material and shreds of mucous membrane Blood stained diarrhoea Circulatory collapse
- 20. Symptoms Acute exposureto elemental mercury vapour Corrosive bronchitis Fever, chills and dyspnoea Progress to pulmonary oedema and fibrosis Nervous symptoms e.g. Ataxia, paresis, delirium etc.
- 21. Symptoms Second phase(if person survives) Begins in 1 to 3 days 24 to 36 hrs glossitis & ulcerative gingivitis Loosening of teeth, infection and necrosis of jaw 2 to 3 days Renal tubular necrosis Albuminuria, uraemia and acidosis
- 22. Symptoms Recovery mayoccur within 10- 14 days i.m. Inj. abscess with ulceration i.v. Inj. mecurialism (thrombophlebitis, granuloma, pulmonary embolism and hemoptysis)
- 23. Treatment Gastric lavage Milk Eggwhite 2-5 % sodium bicarbonate Activated charcoal – uncertain benefit Whole bowel irrigation – beneficial
- 25. Penicillamine Useful in Less severe mercury vapour poisoning Inorganic mercury poisoning Orally 100 mg every 6 hours for 5 days in children Orally 250 mg every 6 hours for 5 days in adults Chronic poisoning 25 to 40 mg twice a day in children 250 mg twice a day in adults Until URINARY mercury levels < 50 µg/l
- 27. BAL Chelating agentof choice 400 to 800 mg on first day every 6 hours 200 to 400 mg on second and third day, every 6 hours 100 to 200 mg 7 to 10 days 12 hourly OR until urine level < 50 µg in a 24 hour specimen
- 28. BAL BAL andpenicillamine not used together formation of toxic compound Urine must be kept alkaline High colonic lavage with 1:1000 solution of sulphoxylate twice daily Hemodialysis in renal failure
- 29. Post mortem appearances Mucosa of GIT Inflammation,Congestion,Coagulation,Corrosion If person survives Necrosis of large intestine due to re-excretion of mercury into large bowel Acute tubular and glomerular degeneration or haemorrhagic glomerular nephritis Liver congested and cloudy swelling or fatty change seen
- 30.
- 31. Chronic Poisoning (Hydrargyrism) 1. Continuousaccidental absorption by industrial workers 2. Excessive therapeutic use (ointment) 3. Recovery from acute poisoning by large dose
- 32. Triad of chronicpoisoning Elemental mercury causes triad of Gingivitis and salivation Tremors Neuropsychiatric changes
- 33. Clinical Features Salivation Inflammation of gums Blue line at junction of gums and teeth Sore mouth and throat Anaemia and anorexia Loss of weight Chronic renal inflammation uraemia
- 34. Tremors Danbury tremors /mercurial Tremors First in hands Progress to lips and tongue Static / intentional Later involves arms and legs Moderately coarse and interspersed by jerky movements
- 35. Tremors Hatter’s shakes Theadvanced condition is called hatter's shakes or· glass-blower's shakes unable to dress himself. write legibly or walk properly. They are common in persons working in glass- blowing and hat industries.
- 36. Tremors Concussio Mercurialis Themost severe form is known as concussio mercurialis, in which no activity is possible.
- 37. Mercurialentis Peculiar eyechange due to exposure to the vapour of mercury. Brownish deposit of mercury through the cornea on the anterior lens capsule
- 38.
- 41. Acrodynia or pinkdisease characterised by a generalised body rash hypersensitivity reaction particularly seen in children Hands and feet become puffy, pinkish,painful, paraesthetic with peeling of skin.
- 42. Treatment Removal ofpatient from further exposure. Demulcents. Saline purgatives Oral hygiene. Chelation therapy
- 43. Minimata disease Minimatadisease is a type of organic mercurial poisoning due to eating of fish poisoned by mercury. This disease occurred as a disaster in Japan in 1956 by eating contaminated fish from Minimata Bay.
- 45.
- 46. Poisonous iron salts Ironsulphate (ferrous sulphate) • Also known as green vitriol • Green monosymmetric crystals Ferric chloride (perchloride of iron) • It is water soluble and irritant • When water is evaporated, yellow crystals are formed.
- 47. Mechanism of Action In concentrated form it acts as corrosive and in dilute form act as irritant. It increases capillary permeability After absorption, when serum iron level exceeds the body’s binding capacity, the free iron produces an increase in reactive oxygen species (ROS) or free radicals.
- 48. Mechanism of Action cellular damage. It inhibits mitochondrial functions. It also causes hepatic damage, hypoglycemia and hypoprothrombinemia.
- 49. Clinical Features Four stagesare identified and are: Stage I: Stage of Gastrointestinal Toxicity Stage II: Stage of Apparent Stabilization or Quiescent Phase Stage III: Stage of Mitochondrial Toxicity and Hepatic Necrosis Stage IV: Stage of Recovery and/or Gastric Scarring
- 50. Stage I: Stageof Gastrointestinal Toxicity • Metallic taste • Vomiting and diarrhea • Abdominal pain • Pallor • Shock • Lethargy • Acidosis • Hematemesis • Black stool
- 51. Stage II: Stageof Apparent Stabilization or Quiescent Phase • Headache • Confusion • Delirium
- 52. Stage III: Stageof Mitochondrial Toxicity and Hepatic Necrosis • Hepatic failure • Hypovolaemia • Hypotension • Multiorgan failure • Coagulopathy • Hypoglycemia • Jaundice • Convulsions • Coma
- 53. IV: Stage ofRecovery and/or Gastric Scarring • Recovery may occur • Gastric scarring • Pyloric obstruction.
- 54. Fatal dose andFatal period Fatal dose: ferrous sulphate – 20 to 40 gm Fatal period: variable.
- 55. Management Gastric lavagewith normal saline Activated charcoal Whole bowel irrigation Chelation – Desferrioxamine is used as specific antidote..
- 57. Autopsy Findings Hemorrhagicnecrosis or corrosion of gastrointestinal mucosa In ferrous sulfate – greenish-blue colour of mucosa Hepatic and renal necrosis Jaundice Pyloric stenosis
- 58. Medicolegal Importance Accidentalpoisoning Homicide/suicide – rare Use to procure criminal abortion.
- 59.
- 60. Poisonous forms Antimonytartarum Antimony trioxide Antimony trichloride Antimony trisulphide
- 61. Clinical Features Vomiting Abdominal pain Diarrhea Hematemesis Dermatitis Renal failure and oliguria Hepatic failure
- 62. Management Gastric lavage Chelation with BAL Hemodialysis Supportive treatment
- 63. Fatal Dose andFatal period Fatal Dose • Antimony tartarum – 90 to 180 mg • Antimony trichloride – 8 to 12 ml Fatal period: 24 hours
- 64. Medicolegal Importance Accidentalpoisoning – common Suicide/homicide – rare
- 65.
- 66. Properties Thallium issoft and pliable metal Have tin-white colour but tarnishes the surface on exposure to air due to formation of black thallous oxide Thallium sulfate is odourless and tasteless.
- 67. Toxic Compounds ofThallium 1. Thallium sulfate 2. Thallium acetate 3. Thallium iodide 4. Thallium nitrate 5. Thallium carbonate.
- 68. Uses 1. Dye industry 2.Optical glass 3. Imitation jewelry 4. Rodenticide 5. Depilatory agent 6. Fire works.
- 69. Mechanism Exact mechanismis unclear but postulated that thallium results in ligand formation with protein sulphydryl group of enzymes and inhibits cellular respiration. It disrupts calcium homeostasis Interaction with riboflavin and riboflavin based cofactors
- 70. Clinical Features -Acute Poisoning • Pain in abdomen • Features of gastroenteritis • Hematemesis • Hematochezia • Headache • Confusion • Disorientation • Paraesthesia • Hallucinations • Convulsions • Retrobulbar neuritis • Ophthalmoplegia • Peripheral neuropathy
- 71. Clinical Features -Chronic Poisoning Chronic Poisoning Alopecia Skin rash Acneform eruptions Dystrophy of nails Ascending sensorimotor neuropathy Ataxia Optic neuropathy Encephalopathy Ptosis Nystagmus
- 72. Thallium triad Combinationof alopecia and skin rash, painful peripheral neuropathy mental confusion with lethargy
- 73. Fatal dose andFatal period Fatal dose: 12 mg/kg body weight Fatal period: 24 to 30 hours
- 74. Management Gastric lavagewith ferric ferrocyanide (Prussian blue). Prussian blue binds thallium in the intestine and enhances its fecal excretion. Hemodialysis Forced diuresis Supportive measures.
- 75. Autopsy Findings • alopecia •Stomatitis • Fatty degeneration of liver and heart • Tubular necrosis • Pulmonary edema • Cerebral edema
- 76. Medicolegal Importance Popularas ideal homicidal agent. Also consumed as suicidal agent.
- 80.
- 81. Physical properties Itis a heavy, white, tasteless, odorless powder and insoluble in water. Barium sulfate is used for the X-ray examination of the GIT (‘barium-meal’).
- 82. Toxic compounds Solublesalts are most toxic. These are barium chloride barium nitrate barium carbonate (rodenticide) barium sulphide
- 83. Action It actslocally as an irritant poison. After absorption it acts both on voluntary and involuntary muscles. Barium seems to act as potassium antagonist and calcium agonist
- 84. Absorption Toxicity ofbarium compounds depends on their solubility. The free ion is absorbed from the lungs and GIT, but barium sulfate remains unabsorbed. After absorption, it accumulates in the skeleton and in pigmented parts of the eye.
- 85. Signs and Symptoms Oningestion The most characteristic features are areflexia and paralysis (Ba2+ ion is a muscle poison). On inhalation Inhalation of barium sulfate dust causes a benign pneumoconiosis (‘baritosis’)
- 86. Fatal dose andFatal period Fatal dose: About 0.8–1 g of barium chloride/sulfide/ nitrate. Fatal period: Usually within 12 h.
- 87. Treatment Wash-out thestomach and give sulphate of soda or magnesium sulphate 10 ml. of 10% sodium sulphate i.v. every 15 minutes Purging with magnesium sulphate and repeated bowel wash. Symptomatic.
- 88. Postmortem findings Non-specific. Submucosal hemorrhages may be seen in the GIT.
- 89. Medico-legal Aspects Suicidalcases may be seen. Homicidal cases are rare. Accidental poisoning with barium sulfide may occur, if taken by mistake as barium sulfate for X- ray examination.
- 90.
Editor's Notes
- #83 In Kiating, China, a subacute form of barium poisoning (pa-ping) was endemic because of use of contaminated table salt.