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DR RUHULAMIN
DEPT O FMEDICINE
JRRMCH,SYLHET
03/28/161
ARSENICOSIS
Published BMJ 2003;326:466 ( 1 March )
doi:10.1136/bmj.c199. www.patient.co.uk
Last Updated: 21 Jan 200903/28/162
Arsenic
Poisoning
Arsenic Poisoning
03/28/163
Arsenic is a heavy metal that exists in 3 metallic forms:
 beta or black
 alpha or yellow
 gamma or grey
It also exists in compounds:
 organic (arsines)
 inorganic
Inorganic compounds are more toxic than organic compounds.
Elemental arsenic is least toxic..
03/28/164
Poisoning can occur by
 ingestion
 inhalation
 dermal absorption.
 Toxicity is due to arsenic's effect on many cell enzymes, which affect
metabolism and DNA repair.
 Arsenic is excreted in urine, but can also accumulate in many body
tissues.
03/28/165
 Arsenic has been used in medicines, as a pigment, a
pesticide, and as a weapon of murder.
 It shares many toxic features with the other heavy
metals like mercury and lead.
 It is used in the production of glass and
semiconductors.
 It is found in some water supplies and seafood, and
is used in various industries.
Epidemiology
03/28/166
In Victorian times arsenic was commonly used for
murder but nowadays it is used much less as it is more
difficult to acquire.
Contamination of water supplies has occurred in parts
of.
 Bangladesh and West Bengal, affecting millions of people.
 Chile, Argentina, Mexico and the USA.
 China, Taiwan, Thailand.
Etiology
03/28/167
Sources of arsenic poisoning include:
» Contaminated drinking water
» Pesticides
» Herbicides
» Fungicides
» Wood preservatives
Etiology (cont.)
03/28/168
» Ceramic enamels
» Paints
» Tobacco (6 mcg per pack)
» Burning of fossil fuels as arsenic is a contaminant.
» From the diet, as organic arsenic from fish and sea food.
Etiology (cont.)
03/28/169
Occupational exposure can occur in:
 The smelting industry (arsenic is a by-product of
ores containing lead, gold, zinc, cobalt and nickel).
 The microelectronics industry (as gallium arsenide).
 Coal power plants.
 Manufacture of glass and fireworks
 Use of pesticides.
 Contact with wood treated with arsenic as a
preservative.
Presentation
03/28/1610
A. History
 Arsenic exposure is usually occupational or
environmental, but can result from deliberate
poisoning.
 Exposure to arsine gas is usually the result of an
industrial accident.
 Take a work and travel history when a patient
presents with painful peripheral neuropathy.
03/28/1611
A. History (cont.)
 Other history:
 hobbies.
 unusual forms of alcohol or diet
supplements.
 herbal medicines.
 Many organ systems are involved.
Overview of acute poisoning
features
03/28/1612
Symptoms usually start within
30 minutes - 2 hours.
 Acute arsenic ingestion is typically follows :
 severe gastroenteritis,
 garlic Hypersalivation.
 odour
03/28/1613
Characteristic sequence of multi-organ
failure, with: neurological symptoms
(within hours) and cardiac features,
succeeded by adult respiratory distress
syndrome and renal/liver dysfunction.
03/28/1614
Marrow suppression develops after a few
days-weeks in survivors, as does alopecia
and an ascending motor neuropathy.
Details of acute poisoning
features
03/28/1615
Gastrointestinal:
 Hypersalivation.
 abdominal pain.
 vomiting, diarrhoea leading to hypovolaemic shock.
 Trivalent arsenic is corrosive - may cause oral
burns, dysphagia and G-I bleeding.
03/28/1616
Cardiovascular:
 Myocardial depression
 Dehydration, hypovolaemia or shock
 ECG changes including ST segment changes,
prolong QT interval, ventricular tachycardia, torsa
de pointes, & ventricular fibrillation .
 Gangrene of extremities
03/28/1617
Respiratory:
 Pulmonary oedema,
 Acute respiratory distress syndrome
 Acute respiratory failure
 Inhaled arsenic causes irritation, bronchospasm
and pulmonary oedema .
Renal :
 Haematuria
 haemoglobinuria (from acute haemolysis),
 proteinuria,
 acute tubular necrosis with acute renal failure.
03/28/16 18
03/28/1619
 hepatic:
 Jaundice,
 hepatomegaly,
 pancreatitis
 Haematological:
 Acute haemolysis
 Bone
03/28/1620
 Neurological:
 CNS depression
 Encephalopathy
 Seizures
 Coma
Skin:
 Rashes
03/28/16 21
Features of chronic arsenic
poisoning
 Skin lesions:
 Typically start about 10
years after first exposure
 Hyper pigmentation
(especially arms and upper
chest) - diffuse dark areas
or‘raindrop’ pigmentation
03/28/16 22
 Also exfoliative dermatitis,
alopecia, conjunctivitis,
corneal ulceration.
 Keratoses occurs on palms
and soles
03/28/16 23
Mees lines (transverse
white lines on nails)
03/28/16 24
03/28/1625
Gastro-intestinal:
Anorexia, abdominal pain, diarrhoea,
weight loss,
Jaundice, hepatomegaly
03/28/1626
 Cardiac/respiratory:
 Myocarditis, pericarditis
 Hypertension - increased risk
 Restrictive or obstructive lung disease
 Haematological:
 pancytopenia
 aplastic anaemia
03/28/1627
 Neurological:
 Peripheral neuropathy (sensory and motor at 1-3
weeks)
 Muscle fasciculation and wasting
 Ataxia
 Diabetes
 increased risk
Cancer –
 increased risk of
cancers:
 skin,
 lung,
 liver,
 bladder,
 kidney,
 larynx,
 lymphoid system.
03/28/16 28
Differential diagnosis
03/28/1629
 Other forms of poisoning e.g.
 Lead
 Mercury
 Botulism
 Gastroenteritis
 Haemolytic uraemic syndrome
 The skin lesions look like other forms of dermatitis
Investigations
03/28/1630
A. Acute poisoning
 Monitoring – for at least 4 hours after suspected ingestion:
pulse, blood pressure, respiratory rate, oxygen saturation and
ECG, urine output.
 Haematology, biochemistry and arterial blood gases – as for
any acutely ill patient.
 Urinalysis.
 ECG.
 Arsenic levels in blood and urine (Chest X-ray and plain x-ray
abdomen (inorganic arsenic compounds are radio-opaque).
Arsenic levels
Normal values
mcg/L
Note
whole blood
concentration
< 50 blood levels are of limited use, as the
half-life of inorganic arsenic in the blood
is short (approx 2 hours
24 hour urinary
excretion
<50
mcg/day
organic arsenical compounds found in the
urine are usually from food sources such as
shellfish, rather than arsenic toxicity. Ask if
shellfish have been eaten in the last few days,
and check whether the laboratory
differentiates organic from inorganic arsenic
compounds.
spot urinary arsenic
concentration
<30
03/28/16 31
Arsenic levels (cont.)
03/28/1632
Hair samples become positive 30 hours after
exposure but may give falsely high results. They do
not differentiate between ingestion and external
exposure.
03/28/1633
B. Chronic arsenic poisoning
 Urinary concentrations are useful in chronic exposure.
 Hair samples (as above).
 Arsenic levels in drinking water (high drinking water levels in
conjunction with relevant clinical features are useful for diagnosis
in some settings).
 Investigation and screening for complications may be appropriate
(e.g. look for diabetes, hypertension).
Management
03/28/1634
A. Management of acute arsenic
poisoning:
 Remove patient from source of arsenic; if
skin contamination wash with copious
water; seal contaminated clothing.
 Resuscitate (ABC principles).
03/28/1635
Management of acute arsenic poisoning (cont):
 Gastric lavage – consider if a significant amount ingested < 1
hour ago and patient has not vomited, or if plain x-ray indicates
arsenic present in the stomach. (Activated charcoal is unlikely to
be of benefit - it does not absorb arsenic.)
 Whole bowel irrigation with polyethylene glycol may be used, to
prevent arsenic absorption.
03/28/1636
Management of acute arsenic poisoning (cont):
 Supportive treatment:
 Oxygen (humidified for inhaled arsenic); bronchodilators if
bronchospasm; PEEP (positive end-expiratory pressure) for pulmonary oedema.
 Intravenous fluids for hypovolaemia; blood transfusion for GI
haemorrhage.
 Inotropes for myocardial depression.
 Torsa de pointes may be treated with magnesium sulphate, pacing or
isoprenaline.
 Treat seizures (diazepam, lorazepam +/- phenytoin).
 Analgesia.
03/28/1637
Management of acute arsenic poisoning (cont):
Renal impairment:
Maintain an alkaline urine using sodium bicarbonate over 2 hours and repeat as
necessary.
Haemodialysis does not reduce arsenic concentrations but may be needed for
renal failure.
 Bone marrow suppression: red cell and/or platelet transfusions.
 Burns (from skin contamination) are treated conventionally.
 Eye contact: treat as for a chemical eye burn
03/28/1638
Management of acute arsenic poisoning
(cont):
 Chelation:
Consider chelation therapy in patients who are symptomatic and/or
have urine concentration > 200 mcg/L.
DMPS is the chelation agent of choice. DMSA is an alternative (oral
preparation only, so unsuitable if patient is vomiting).
Dimercaprol (BAL) or penicillamine have also been used, but are
superseded by DMPS and DMSA.
Management of chronic arsenic
poisoning
03/28/1639
 Provide arsenic-free drinking water, to reduce the risk of
further disease developing.
 Chelation therapy may have a role, but its effectiveness is
uncertain. Also, it is of no use if exposure to arsenic
continues.
Management of chronic arsenic
poisoning (cont.)
03/28/1640
Micronutrients and antioxidants may be beneficial,
especially in undernourished populations. It is
recommended that all patients with skin lesions be given
multivitamins.
Certain plant compounds may help to remove arsenic
from tissues.
Skin care for keratoses and any associated bacterial or
fungal infections.
Management of chronic arsenic
poisoning (cont.)
03/28/1641
 Screen and treat for complications, e.g. diabetes,
hypertension.
 Other household members:
 Check other members of the family as they may also
have been exposed.
 Pregnancy and breastfeeding: arsenic is probably
transferred to the baby via the placenta and breast
milk
Prognosis
03/28/1642
 The prognosis varies with the amount and rate of arsenic
ingestion.
 Effects and complications can occur at different times after
exposure - from days to years later.
Staging
03/28/1643
 Arsenic poisoning has been classified into 4 stages, 7 grades,
and 20 sub grades but this is not common practice.
Prevention
03/28/1644
 Test all groundwater sources of drinking water for arsenic.
 Provision of uncontaminated water for all is essential, but
not yet achieved. Some plants have the ability to remove
arsenic from the environment.

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ArsenicOSIS

  • 1. DR RUHULAMIN DEPT O FMEDICINE JRRMCH,SYLHET 03/28/161 ARSENICOSIS
  • 2. Published BMJ 2003;326:466 ( 1 March ) doi:10.1136/bmj.c199. www.patient.co.uk Last Updated: 21 Jan 200903/28/162 Arsenic Poisoning
  • 3. Arsenic Poisoning 03/28/163 Arsenic is a heavy metal that exists in 3 metallic forms:  beta or black  alpha or yellow  gamma or grey It also exists in compounds:  organic (arsines)  inorganic Inorganic compounds are more toxic than organic compounds. Elemental arsenic is least toxic..
  • 4. 03/28/164 Poisoning can occur by  ingestion  inhalation  dermal absorption.  Toxicity is due to arsenic's effect on many cell enzymes, which affect metabolism and DNA repair.  Arsenic is excreted in urine, but can also accumulate in many body tissues.
  • 5. 03/28/165  Arsenic has been used in medicines, as a pigment, a pesticide, and as a weapon of murder.  It shares many toxic features with the other heavy metals like mercury and lead.  It is used in the production of glass and semiconductors.  It is found in some water supplies and seafood, and is used in various industries.
  • 6. Epidemiology 03/28/166 In Victorian times arsenic was commonly used for murder but nowadays it is used much less as it is more difficult to acquire. Contamination of water supplies has occurred in parts of.  Bangladesh and West Bengal, affecting millions of people.  Chile, Argentina, Mexico and the USA.  China, Taiwan, Thailand.
  • 7. Etiology 03/28/167 Sources of arsenic poisoning include: » Contaminated drinking water » Pesticides » Herbicides » Fungicides » Wood preservatives
  • 8. Etiology (cont.) 03/28/168 » Ceramic enamels » Paints » Tobacco (6 mcg per pack) » Burning of fossil fuels as arsenic is a contaminant. » From the diet, as organic arsenic from fish and sea food.
  • 9. Etiology (cont.) 03/28/169 Occupational exposure can occur in:  The smelting industry (arsenic is a by-product of ores containing lead, gold, zinc, cobalt and nickel).  The microelectronics industry (as gallium arsenide).  Coal power plants.  Manufacture of glass and fireworks  Use of pesticides.  Contact with wood treated with arsenic as a preservative.
  • 10. Presentation 03/28/1610 A. History  Arsenic exposure is usually occupational or environmental, but can result from deliberate poisoning.  Exposure to arsine gas is usually the result of an industrial accident.  Take a work and travel history when a patient presents with painful peripheral neuropathy.
  • 11. 03/28/1611 A. History (cont.)  Other history:  hobbies.  unusual forms of alcohol or diet supplements.  herbal medicines.  Many organ systems are involved.
  • 12. Overview of acute poisoning features 03/28/1612 Symptoms usually start within 30 minutes - 2 hours.  Acute arsenic ingestion is typically follows :  severe gastroenteritis,  garlic Hypersalivation.  odour
  • 13. 03/28/1613 Characteristic sequence of multi-organ failure, with: neurological symptoms (within hours) and cardiac features, succeeded by adult respiratory distress syndrome and renal/liver dysfunction.
  • 14. 03/28/1614 Marrow suppression develops after a few days-weeks in survivors, as does alopecia and an ascending motor neuropathy.
  • 15. Details of acute poisoning features 03/28/1615 Gastrointestinal:  Hypersalivation.  abdominal pain.  vomiting, diarrhoea leading to hypovolaemic shock.  Trivalent arsenic is corrosive - may cause oral burns, dysphagia and G-I bleeding.
  • 16. 03/28/1616 Cardiovascular:  Myocardial depression  Dehydration, hypovolaemia or shock  ECG changes including ST segment changes, prolong QT interval, ventricular tachycardia, torsa de pointes, & ventricular fibrillation .  Gangrene of extremities
  • 17. 03/28/1617 Respiratory:  Pulmonary oedema,  Acute respiratory distress syndrome  Acute respiratory failure  Inhaled arsenic causes irritation, bronchospasm and pulmonary oedema .
  • 18. Renal :  Haematuria  haemoglobinuria (from acute haemolysis),  proteinuria,  acute tubular necrosis with acute renal failure. 03/28/16 18
  • 19. 03/28/1619  hepatic:  Jaundice,  hepatomegaly,  pancreatitis  Haematological:  Acute haemolysis  Bone
  • 20. 03/28/1620  Neurological:  CNS depression  Encephalopathy  Seizures  Coma
  • 22. Features of chronic arsenic poisoning  Skin lesions:  Typically start about 10 years after first exposure  Hyper pigmentation (especially arms and upper chest) - diffuse dark areas or‘raindrop’ pigmentation 03/28/16 22
  • 23.  Also exfoliative dermatitis, alopecia, conjunctivitis, corneal ulceration.  Keratoses occurs on palms and soles 03/28/16 23
  • 24. Mees lines (transverse white lines on nails) 03/28/16 24
  • 25. 03/28/1625 Gastro-intestinal: Anorexia, abdominal pain, diarrhoea, weight loss, Jaundice, hepatomegaly
  • 26. 03/28/1626  Cardiac/respiratory:  Myocarditis, pericarditis  Hypertension - increased risk  Restrictive or obstructive lung disease  Haematological:  pancytopenia  aplastic anaemia
  • 27. 03/28/1627  Neurological:  Peripheral neuropathy (sensory and motor at 1-3 weeks)  Muscle fasciculation and wasting  Ataxia  Diabetes  increased risk
  • 28. Cancer –  increased risk of cancers:  skin,  lung,  liver,  bladder,  kidney,  larynx,  lymphoid system. 03/28/16 28
  • 29. Differential diagnosis 03/28/1629  Other forms of poisoning e.g.  Lead  Mercury  Botulism  Gastroenteritis  Haemolytic uraemic syndrome  The skin lesions look like other forms of dermatitis
  • 30. Investigations 03/28/1630 A. Acute poisoning  Monitoring – for at least 4 hours after suspected ingestion: pulse, blood pressure, respiratory rate, oxygen saturation and ECG, urine output.  Haematology, biochemistry and arterial blood gases – as for any acutely ill patient.  Urinalysis.  ECG.  Arsenic levels in blood and urine (Chest X-ray and plain x-ray abdomen (inorganic arsenic compounds are radio-opaque).
  • 31. Arsenic levels Normal values mcg/L Note whole blood concentration < 50 blood levels are of limited use, as the half-life of inorganic arsenic in the blood is short (approx 2 hours 24 hour urinary excretion <50 mcg/day organic arsenical compounds found in the urine are usually from food sources such as shellfish, rather than arsenic toxicity. Ask if shellfish have been eaten in the last few days, and check whether the laboratory differentiates organic from inorganic arsenic compounds. spot urinary arsenic concentration <30 03/28/16 31
  • 32. Arsenic levels (cont.) 03/28/1632 Hair samples become positive 30 hours after exposure but may give falsely high results. They do not differentiate between ingestion and external exposure.
  • 33. 03/28/1633 B. Chronic arsenic poisoning  Urinary concentrations are useful in chronic exposure.  Hair samples (as above).  Arsenic levels in drinking water (high drinking water levels in conjunction with relevant clinical features are useful for diagnosis in some settings).  Investigation and screening for complications may be appropriate (e.g. look for diabetes, hypertension).
  • 34. Management 03/28/1634 A. Management of acute arsenic poisoning:  Remove patient from source of arsenic; if skin contamination wash with copious water; seal contaminated clothing.  Resuscitate (ABC principles).
  • 35. 03/28/1635 Management of acute arsenic poisoning (cont):  Gastric lavage – consider if a significant amount ingested < 1 hour ago and patient has not vomited, or if plain x-ray indicates arsenic present in the stomach. (Activated charcoal is unlikely to be of benefit - it does not absorb arsenic.)  Whole bowel irrigation with polyethylene glycol may be used, to prevent arsenic absorption.
  • 36. 03/28/1636 Management of acute arsenic poisoning (cont):  Supportive treatment:  Oxygen (humidified for inhaled arsenic); bronchodilators if bronchospasm; PEEP (positive end-expiratory pressure) for pulmonary oedema.  Intravenous fluids for hypovolaemia; blood transfusion for GI haemorrhage.  Inotropes for myocardial depression.  Torsa de pointes may be treated with magnesium sulphate, pacing or isoprenaline.  Treat seizures (diazepam, lorazepam +/- phenytoin).  Analgesia.
  • 37. 03/28/1637 Management of acute arsenic poisoning (cont): Renal impairment: Maintain an alkaline urine using sodium bicarbonate over 2 hours and repeat as necessary. Haemodialysis does not reduce arsenic concentrations but may be needed for renal failure.  Bone marrow suppression: red cell and/or platelet transfusions.  Burns (from skin contamination) are treated conventionally.  Eye contact: treat as for a chemical eye burn
  • 38. 03/28/1638 Management of acute arsenic poisoning (cont):  Chelation: Consider chelation therapy in patients who are symptomatic and/or have urine concentration > 200 mcg/L. DMPS is the chelation agent of choice. DMSA is an alternative (oral preparation only, so unsuitable if patient is vomiting). Dimercaprol (BAL) or penicillamine have also been used, but are superseded by DMPS and DMSA.
  • 39. Management of chronic arsenic poisoning 03/28/1639  Provide arsenic-free drinking water, to reduce the risk of further disease developing.  Chelation therapy may have a role, but its effectiveness is uncertain. Also, it is of no use if exposure to arsenic continues.
  • 40. Management of chronic arsenic poisoning (cont.) 03/28/1640 Micronutrients and antioxidants may be beneficial, especially in undernourished populations. It is recommended that all patients with skin lesions be given multivitamins. Certain plant compounds may help to remove arsenic from tissues. Skin care for keratoses and any associated bacterial or fungal infections.
  • 41. Management of chronic arsenic poisoning (cont.) 03/28/1641  Screen and treat for complications, e.g. diabetes, hypertension.  Other household members:  Check other members of the family as they may also have been exposed.  Pregnancy and breastfeeding: arsenic is probably transferred to the baby via the placenta and breast milk
  • 42. Prognosis 03/28/1642  The prognosis varies with the amount and rate of arsenic ingestion.  Effects and complications can occur at different times after exposure - from days to years later.
  • 43. Staging 03/28/1643  Arsenic poisoning has been classified into 4 stages, 7 grades, and 20 sub grades but this is not common practice.
  • 44. Prevention 03/28/1644  Test all groundwater sources of drinking water for arsenic.  Provision of uncontaminated water for all is essential, but not yet achieved. Some plants have the ability to remove arsenic from the environment.