Metalic (Cu,fe,th,mg) poisoning

COPPER / TAMBA

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

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).

Copper sulphate

• 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

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

• F.D.: copper subacetate: 15 gm copper sulphate: 20 gm

• F.P. : 1- 2 days.

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

– 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

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

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

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.

– 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:

PM findings

• Liver: fatty degeneration• Kidneys: degeneration of epithelial cells

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

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.

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

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

Treatment:

– GL with sodium bicarbonate

– Demulscents

– Antidote: desferoxamine: iv at the rate of 15- 80 mg /kg BW/hr

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

Absorption and Excretion

• Abs through all routes

• Deposited in epididymis, liver, kidneys, muscles and bones.

• Excreted through kidneys and in breast milk

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

Chronic Poisoning

• Alopecia• Skin rashes• Painful peripheral neuropathy• Mental confusion with lethargy

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.

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

MLI:

• Ideal homicidal poison: more prevalent in European countries.

• Chronic poisoning in industries.• Accidental poisoning d/t therapeutic over usage.

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

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

Treatment: • GL• Demulscents• Charcoal• Symptomatic

PM appearance:

• necrosis , Hg and corrosion• Liver and kidneys show degensrative changes

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.