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ARSENIC
POISONING
BY:
Shaista sumayya
PharmD
INTRODUCTION
 Arsenic is thought to occur throughout the universe.
 It is the 20th most common element in the earth’s crust, having a
concentration of 1.8 ppm.
 Arsenic is today the commonest source of acute heavy metal poisoning,
and is second only to lead in the incidence of chronic toxicity
PHYSICAL APPEARANCE
 Arsenic is a metalloid i.e. it is an element which resembles a
metal in some respects, and is by itself not very toxic.
 However, almost all the salts are toxic to varying degree.
 Arsenic is a silver-grey or tin-white, shiny, brittle, crystalline
and metallic-looking element.
 It is rarely found in its isolated, elemental form.
 More commonly, it is present in mineral species, in alloys, or
as an oxide or other compound form.
INORGANIC AND ORGANIC
ARSENICALS
Chemical Name Synonyms Physical Properties Uses
Elemental arsenic Metallic arsenic
grey arsenic
Shiny grey, brittle, metallic-looking
substance
In alloys
Arsine Arsenic trihydride
hydrogen arsenide
arseniuretted hydrogen
Colourless gas with garlicky odour Lead plating, soldering, galvanising,
and in electronic components
Arsenic trioxide Arsenic oxide
white arsenic
arsenic sesquioxide
arsenious anhydride
White powder (dissolves slowly in
water to formarsenious acid)
Manufacture of glass, insecticide,
rodenticide. Previously used in
medicine for treating fever (e.g.
Fowler’s solution)
Arsenic pentoxide Arsenic acid
arsenic anhydride
White powder (dissolves rapidly in
water to form arsenic acid)
Manufacture of coloured glass,
insecticide, wood preservative
Copper arsenite Scheele’s green Greenish powder Colouring agent for toys,wall paper,
etc.
USUAL FATAL DOSE
 200 to 300 mg for arsenic trioxide.
 In general, the pentavalent form of arsenic (arsenate) is less toxic than the
trivalent form (arsenite) because it is less water soluble.
 The most toxic form is arsine gas - 25 to 30 ppm can be lethal in 30
minutes.
TOXICOKINETICS AND MODE OF
ACTION
 Arsenic is absorbed through all portals of entry including oral, inhalational,
and cutaneous routes.
 After absorption it is redistributed to the liver, lungs, intestinal wall, and spleen,
where it binds to the sulfydryl groups of tissue proteins.
 Arsenic replaces phosphorus in the bone where it may remain for years.
 It gets deposited also in hair.
 While arsenic does not cross the blood-brain barrier easily, it crosses the
placenta readily and can give rise to intrauterine death of the foetus.
 In less severe intoxications it can cause respiratory distress of the newborn due
to pulmonary haemorrhage and hyaline membrane formation.
CLINICAL FEATURES
HYPERKERATOSIS RAINDROP
PIGMENTATION
MEES’ LINES
LESIONS – ARSENIC POISONING
DIAGNOSIS
Urine level
 If the 24 hour excretion of arsenic
exceeds 100 mcg, it is indicative
of toxicity.
 However, ingestion of seafood
can interfere with interpretation
since considerable concentrations
of organic arsenicals such as
arsenobetaine and
arsenocholine may be present in
shellfish, cod, haddock, etc.,
although it is not associated with
toxic effects.
 In such cases, the analysis must
be repeated after 2 days of “no
fish” diet.
Blood level
 This is less reliable than urine
level because of short half-life
of arsenic in the blood.
 However, a blood level of
arsenic less than 7 mcg/100
mL (70 mcg/L) is generally
considered in the normal
range.
Hair level
 Although considered to be an
important diagnostic criterion,
it is actually virtually useless
since it cannot discriminate
between external deposition
and toxic accumulation.
 If hair is sent for arsenic
quantitation, pubic hair instead
of scalp hair should be sent
because of the possibility of
scalp hair being contaminated
with arsenic from the
environment.
Radiography
 Since arsenic is radiopaque,
abdominal x-ray may reveal its
presence in the gastrointestinal tract
in acute poisoning.
Additional investigations
 Monitor CBC, serum electrolytes,
urinalysis (for proteinuria, haematuria or
pyuria), liver and renal function tests.
 Obtain an ECG and institute continuous
cardiac monitoring in symptomatic
patients.
 Obtain a chest radiograph in patients
with severe poisoning or pulmonary
effects.
 Initial and periodic biological
monitoring and medical surveillance are
required for employees exposed to
arsenic.
TREATMENT
 SUPPORTIVE MEASURES:
 Gastric lavage
 Intravenous fluids
 Cardiac monitoring
CHELATION THERAPY
 BAL (British Anti Lewisite or dimercaprol):
 The usual agent employed is BAL at a dose of 3 to 5 mg/kg intramuscularly
every 4 hours until the urinary arsenic excretion dips below 50 mcg/24
hours. Usual duration of therapy is 7 to 10 days.
 PENICILLAMINE:
 In patients who are not allergic to penicillin, penicillamine can be given orally
at a dose of 100 mg/kg/day, 6th hourly for 5 days.
 DMSA (DIMERCAPTO SUCCINIC ACID), DMPS (DIMERCAPTO PROPANE
SULFONIC ACID):
 DMSA and DMPS said to be superior to BAL and penicillamine, are currently
not available in India.
PRINCIPLES OF CHELATION:
 Begin chelation therapy in symptomatic patients.
 The urine arsenic level which should prompt chelation in an asymptomatic
patient has been recommended as 200 mcg/litre.
 Repeat courses of chelation therapy should be prescribed in severe
poisonings until the 24-hour urine arsenic level falls below 50 mcg/litre.
 Observation for return of symptoms is strongly recommended.
 Chelation therapy is not very effective for chronic poisoning, and is totally
ineffective in arsine poisoning.
 The latter should be treated with emphasis on respiratory stabilisation and
haemodialysis.
CHRONIC POISONING
 Haemodialysis or exchange transfusion.
THANK YOU

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Arsenic poisoning - heavy metal poisoning - clinical toxicology

  • 2. INTRODUCTION  Arsenic is thought to occur throughout the universe.  It is the 20th most common element in the earth’s crust, having a concentration of 1.8 ppm.  Arsenic is today the commonest source of acute heavy metal poisoning, and is second only to lead in the incidence of chronic toxicity
  • 3. PHYSICAL APPEARANCE  Arsenic is a metalloid i.e. it is an element which resembles a metal in some respects, and is by itself not very toxic.  However, almost all the salts are toxic to varying degree.  Arsenic is a silver-grey or tin-white, shiny, brittle, crystalline and metallic-looking element.  It is rarely found in its isolated, elemental form.  More commonly, it is present in mineral species, in alloys, or as an oxide or other compound form.
  • 4. INORGANIC AND ORGANIC ARSENICALS Chemical Name Synonyms Physical Properties Uses Elemental arsenic Metallic arsenic grey arsenic Shiny grey, brittle, metallic-looking substance In alloys Arsine Arsenic trihydride hydrogen arsenide arseniuretted hydrogen Colourless gas with garlicky odour Lead plating, soldering, galvanising, and in electronic components Arsenic trioxide Arsenic oxide white arsenic arsenic sesquioxide arsenious anhydride White powder (dissolves slowly in water to formarsenious acid) Manufacture of glass, insecticide, rodenticide. Previously used in medicine for treating fever (e.g. Fowler’s solution) Arsenic pentoxide Arsenic acid arsenic anhydride White powder (dissolves rapidly in water to form arsenic acid) Manufacture of coloured glass, insecticide, wood preservative Copper arsenite Scheele’s green Greenish powder Colouring agent for toys,wall paper, etc.
  • 5. USUAL FATAL DOSE  200 to 300 mg for arsenic trioxide.  In general, the pentavalent form of arsenic (arsenate) is less toxic than the trivalent form (arsenite) because it is less water soluble.  The most toxic form is arsine gas - 25 to 30 ppm can be lethal in 30 minutes.
  • 6. TOXICOKINETICS AND MODE OF ACTION  Arsenic is absorbed through all portals of entry including oral, inhalational, and cutaneous routes.  After absorption it is redistributed to the liver, lungs, intestinal wall, and spleen, where it binds to the sulfydryl groups of tissue proteins.  Arsenic replaces phosphorus in the bone where it may remain for years.  It gets deposited also in hair.  While arsenic does not cross the blood-brain barrier easily, it crosses the placenta readily and can give rise to intrauterine death of the foetus.  In less severe intoxications it can cause respiratory distress of the newborn due to pulmonary haemorrhage and hyaline membrane formation.
  • 9. DIAGNOSIS Urine level  If the 24 hour excretion of arsenic exceeds 100 mcg, it is indicative of toxicity.  However, ingestion of seafood can interfere with interpretation since considerable concentrations of organic arsenicals such as arsenobetaine and arsenocholine may be present in shellfish, cod, haddock, etc., although it is not associated with toxic effects.  In such cases, the analysis must be repeated after 2 days of “no fish” diet. Blood level  This is less reliable than urine level because of short half-life of arsenic in the blood.  However, a blood level of arsenic less than 7 mcg/100 mL (70 mcg/L) is generally considered in the normal range. Hair level  Although considered to be an important diagnostic criterion, it is actually virtually useless since it cannot discriminate between external deposition and toxic accumulation.  If hair is sent for arsenic quantitation, pubic hair instead of scalp hair should be sent because of the possibility of scalp hair being contaminated with arsenic from the environment.
  • 10. Radiography  Since arsenic is radiopaque, abdominal x-ray may reveal its presence in the gastrointestinal tract in acute poisoning. Additional investigations  Monitor CBC, serum electrolytes, urinalysis (for proteinuria, haematuria or pyuria), liver and renal function tests.  Obtain an ECG and institute continuous cardiac monitoring in symptomatic patients.  Obtain a chest radiograph in patients with severe poisoning or pulmonary effects.  Initial and periodic biological monitoring and medical surveillance are required for employees exposed to arsenic.
  • 11. TREATMENT  SUPPORTIVE MEASURES:  Gastric lavage  Intravenous fluids  Cardiac monitoring
  • 12. CHELATION THERAPY  BAL (British Anti Lewisite or dimercaprol):  The usual agent employed is BAL at a dose of 3 to 5 mg/kg intramuscularly every 4 hours until the urinary arsenic excretion dips below 50 mcg/24 hours. Usual duration of therapy is 7 to 10 days.  PENICILLAMINE:  In patients who are not allergic to penicillin, penicillamine can be given orally at a dose of 100 mg/kg/day, 6th hourly for 5 days.  DMSA (DIMERCAPTO SUCCINIC ACID), DMPS (DIMERCAPTO PROPANE SULFONIC ACID):  DMSA and DMPS said to be superior to BAL and penicillamine, are currently not available in India.
  • 13. PRINCIPLES OF CHELATION:  Begin chelation therapy in symptomatic patients.  The urine arsenic level which should prompt chelation in an asymptomatic patient has been recommended as 200 mcg/litre.  Repeat courses of chelation therapy should be prescribed in severe poisonings until the 24-hour urine arsenic level falls below 50 mcg/litre.  Observation for return of symptoms is strongly recommended.  Chelation therapy is not very effective for chronic poisoning, and is totally ineffective in arsine poisoning.  The latter should be treated with emphasis on respiratory stabilisation and haemodialysis.
  • 14. CHRONIC POISONING  Haemodialysis or exchange transfusion.