Metalic (Cu,fe,th,mg) poisoning
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Transcript of Metalic (Cu,fe,th,mg) poisoning
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COPPER / TAMBA
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COPPER
• It is a brown colour metal• As a metal it is non poisonous• Important integral of enzymes
Action: – high affinity for sulphhydryl and amino groups.– May also target nucleic acids
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Toxic compounds and its uses:• Copper sulphate (CuSO4, blue vitriol, neela tutia):
– Large blue crystals, soluble in water and styptic taste
– Used in algaecides, fungicides, electroplating, leather tanning, hide preservation to impart rich green colour and for preservation of fruits and vegetables and also usedas emetic except in arsenic.
– It is used as an antidote in phosphorus poisoning where it forms cupric phosphide (non toxic substance).
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Copper sulphate
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• Copper subacetate (verdigris / zangal) :– Bluish green powder formed by the action of
vegetable acids on improperly tined copper cooking vessels.
– Used in arts and external medicine
• Copper carbonate– fungicide
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Exposure, Absorption and Excretion:
• Principal route of exposure is through – Ingestion, – Inhalation of fumes and dust and also – Exposure of skin
• Maximum absorption occurs in stomach and GIT and then transported to liver to bond with ceruloplasmin
• Excreted in feces, bile and urine
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• F.D.: copper subacetate: 15 gm copper sulphate: 20 gm
• F.P. : 1- 2 days.
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Signs and symptoms: Acute
• GIT: Metallic taste, ptyalism, thirst, colicky abdominal pain, nausea, eructation, repeated vomiting (blue/green). Diarrhea (brown) with much straining
• Hemolytic tendencies due to increased concentration of copper in the erythrocytes, resulting in haemetemesis and Melaena.
• Hepatic: jaundice
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– Renal: oliguria, haematuria, uraemia
– MS: cramps/spasm of legs, paralysis
– Inhalation of fumes: sore throat, cough; conjunctivitis; perforation of nasal mucosa
– Skin exposure: contact dermatitis
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Treatment :– No need to use emetic as vomiting occurs in 5-10 min– Gastric lavage 1% potassium ferrocyanide as it form
insoluble cupric ferrocyanide– Demulcents: egg white or milk– Castor oil– Chelating agents: D-pencillamine (2 gm / day in four
divided doses orally), EDTA or BAL– Morphine and diuretics– Symptomatic– For severe cases: cortisone 50- 100 mg thrice daily
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Post mortem findings:
– Skin yellow d/t jaundice
– Greenish blue froth from mouth
– Greenish blue tinge in the mucus membrane of GIT.– Liver : soft and fatty; shows centri-lobular necrosis
and biliary stasis– Kidneys : degenerative changes in proximal tubules,
Hb casts
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Chronic poisoning :• Seen in factory workers• It result from, preservation and cooking of food in
unclean copper utensils may result in poisoning as it is contaminated with verdigris.
• Chronic consumption of fruits and vegetables preserved and coloured with copper sulphate.
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– Greenish or purple line on gums at its junction with the teeth called Clapton’s line.
– Giddiness and headache– laryngitis and bronchitis– Metal fume fever– Progressive emaciation with anemia malaise and
debility– Conjunctivitis and corneal ulcers– Bronze diabetes m/b present
• Treatment: Symptomatic management
Signs and symptoms:
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PM findings
• Liver: fatty degeneration• Kidneys: degeneration of epithelial cells
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Medico Legal Aspects
– Suicide: common– Accidental: eating food coked in copper utensils,
children– Copper used in IUCDs and haemodailysis
equipment.– Copper is used as antidote in phosphorus
poisoning and wound debridement– Cattle poison– Homicide is rare
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IRON
– Incidence usually d/t overdose and in children less than 6 yrs of age
– M O A: taken up by parenchymal cells of liver, causes mitochondrial damage and cellular dysfunction l/t
• Metabolic acidosis and Necrosis, • Liver failure, • Hypoglycemia, • Coagulopathy and death.
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Signs and symptoms ( 4 stages)
• Phase 1: (30 min to few hrs)– vomiting, gastroenteritis, with grey or black vomitus and stool with
metallic odour l/t collapse and coma
• Phase 2: (6 - 24 hrs)– s/s alleviate finally progressing to next stage
• Phase 3: (12 to 48 hrs)- hepatic stage– severe lethargy, convulsions, shock, gastrointestinal hg, cv collapse,
metabolic acidosis, hepatic failure with hepatocellular necrosis, jaundice, hypoglycemia, Coagulopathy, pulmonary edema and renal failure.
• Phase 4: (2- 5 wks)– Formation of gastric strictures and pyloric stenosis, Hepatic cirrhosis
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Diagnosis and Treatment
– X-ray abdomen show iron tablets– Serum iron level more than 350 μg/dl– Blood glucose : > 150 µg/dl – Prothrombin time increased– Fatal dose: 20-40 gm of ferrous sulphate/ 150 mg of iron
A 325-mg tablet of ferrous sulfate has 65 mg of elemental ironferrous gluconate has 39 mg of elemental ironferrous fumarate has 107.25 mg of elemental iron
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Treatment:
– GL with sodium bicarbonate
– Demulscents
– Antidote: desferoxamine: iv at the rate of 15- 80 mg /kg BW/hr
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THALLIUM
– Heavy metal with lustrous colour on exposure to air form thallous oxide
– It is a cumulative poison– All salts as well as metal are poisonous.
• Toxic compounds and uses: Thallium acetate: depillatory creams, fire works,
rodenticides and insecticides Thallium sulphate: rodenticides and insecticides
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Absorption and Excretion
• Abs through all routes
• Deposited in epididymis, liver, kidneys, muscles and bones.
• Excreted through kidneys and in breast milk
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Signs and symptoms• Acute:
– Metallic taste, nausea vomiting, colic, diarrhoea, – Conjunctivitis, scotoma, blindness, – Polyneuritis, peripheral neuropathy- (burning feet
syndrome), ataxia coma, encephalopathy– Loss of hair, mees lines and deafness, – Maculo-papular skin eruptions on face with butterfly
distribution,
• F.D.: 1 gm• F.P.: 2-3 days
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Chronic Poisoning
• Alopecia• Skin rashes• Painful peripheral neuropathy• Mental confusion with lethargy
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Diagnosis and Treatment
• Eosinophilia
• Urine m/b green
• thallium > 40 μgm % in blood and > 150 μgm/l in urine
• Opacity in liver on X-ray
• Signs of gastric irritability and loss of hair.
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Treatment:– Stomach wash with 1% sodium or potassium
iodide
– Prussian blue (potassium ferric hexacyanoferrate) orally 250 mg/kg/day in 2-4 divided doses
– BAL and EDTA are contraindicated– Pilocarpine is physiological antidote– Hemodialysis/ peritoneal dialysis– Symptomatic
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MLI:
• Ideal homicidal poison: more prevalent in European countries.
• Chronic poisoning in industries.• Accidental poisoning d/t therapeutic over usage.
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MANGANESE • Important compounds are Potassium
permanganate and manganese dioxide.
• Potassium permanganate :• Dark purple slender crystals with astringent
taste. powerful antioxidant and disinfectant.• MOA: causes coagulation necrosis and brown
discolouration of mucus mb., paralysis of heart
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Signs And Symptoms:– Burning pain from mouth to stomach, thirst, colicky
abdominal pain, nausea, eructation, repeated vomiting, difficulty in swallowing, dyspnoea , stridor, cough.
– Discolouration initially purple brown but later changes to brown then coal black d/t formation of manganese dioxide
– F.D.: 10- 20 gm– F.P.: few hrs
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Treatment: • GL• Demulscents• Charcoal• Symptomatic
PM appearance:
• necrosis , Hg and corrosion• Liver and kidneys show degensrative changes
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MLI:
– Usually suicidal poisoning
– M/b accidental in case of children
– Abortificient: inserted into vagina- causes
ulceration ( acute, localised, punched out with
raised edges and granular black base)
– Fictious injury: when applied to skin for 10 -20
min causes ulcer resembling syphilis.