2. Mercury poisoningMercury poisoning
- elemental- elemental
- inorganic- inorganic
- organic- organic
Each has a different toxicological profileEach has a different toxicological profile
There are 3 different forms of mercuryThere are 3 different forms of mercury
3. Sources of mercurySources of mercury
Elemental mercury:Elemental mercury:
– Sphygmomanometers, thermometers, barometersSphygmomanometers, thermometers, barometers
– Liquid at room temp – volatilises easilyLiquid at room temp – volatilises easily
Inorganic mercury:Inorganic mercury:
– Traditional remedies (ayurvedic, chinese)Traditional remedies (ayurvedic, chinese)
– Used in gold extraction, caustic sodaUsed in gold extraction, caustic soda
manufacturingmanufacturing
– RodenticidesRodenticides
Organic mercury:Organic mercury:
– Fungicides, seed dressingsFungicides, seed dressings
– Methylmercury in fish …Methylmercury in fish …
6. Organic mercuryOrganic mercury
poisoning:poisoning:
Rare … but severeRare … but severe• Exposure: ingestion, topical or inhalationExposure: ingestion, topical or inhalation
• CNS Toxicity:CNS Toxicity:
• poor concentration, fatigue, ataxia, tremor,poor concentration, fatigue, ataxia, tremor,
constricted visual fields,constricted visual fields,
• coma & convulsionscoma & convulsions
• BM suppressionBM suppression
• Renal toxicity - dealkylation to inorganic formRenal toxicity - dealkylation to inorganic form
• Poorer response to treatmentPoorer response to treatment
7. Inorganic mercuryInorganic mercury
poisoningpoisoning
Gastrointestinal phaseGastrointestinal phase:: HgHg2+2+
is a potent GI irritantis a potent GI irritant
– gingivitis, stomatitisgingivitis, stomatitis
- oesophageal, gastric, small and large boweloesophageal, gastric, small and large bowel
erosionserosions
- haematemesis, bloody diarrhoea, CVS collapsehaematemesis, bloody diarrhoea, CVS collapse
Systemic toxicitySystemic toxicity:: HgHg2+2+
inhibits sulphydryl enzymesinhibits sulphydryl enzymes
– hypotension, lactic acidosishypotension, lactic acidosis
NephrotoxicityNephrotoxicity: Hg: Hg2+2+
deposits in the tubulesdeposits in the tubules →→ ATNATN
– acute renal failureacute renal failure
- potentially leads to CRF in survivorspotentially leads to CRF in survivors
19. Diagnosis of MercuryDiagnosis of Mercury
poisoningpoisoning
Blood mercury:Blood mercury:
– only really useful acutelyonly really useful acutely
normal <10µg/lnormal <10µg/l
symptoms with blood mercury >150-200µg/lsymptoms with blood mercury >150-200µg/l
Urine mercuryUrine mercury
– probably the most reliable indicatorprobably the most reliable indicator
normal <10µg/lnormal <10µg/l
symptoms with urine mercury >100-150µg/lsymptoms with urine mercury >100-150µg/l
Radiology:Radiology: for elemental ingestion/aspiration/injectionfor elemental ingestion/aspiration/injection
20. Remove from sourceRemove from source
Supportive careSupportive care
– particularly important with inhalationparticularly important with inhalation
DMPS ChelationDMPS Chelation (2,3-Dimercapto-1-(2,3-Dimercapto-1-
propanesulphonate)propanesulphonate)
Chelation therapy of choice for mercuryChelation therapy of choice for mercury
For both acute and chronic mercury poisoningFor both acute and chronic mercury poisoning
For all forms of HgFor all forms of Hg (inorganic > metallic >> organic(inorganic > metallic >> organic))
- Indications:- Indications:
symptomatic patientssymptomatic patients
blood/urine mercury persistently > 100 - 150blood/urine mercury persistently > 100 - 150µµg/lg/l
Treatment of MercuryTreatment of Mercury
poisoningpoisoning
22. Clinical Effects of Acute ExposureClinical Effects of Acute Exposure
Ocular exposures:Ocular exposures: Eye exposureEye exposure
produces pain, itching, conjunctivitis,produces pain, itching, conjunctivitis,
blurred vision and burns.blurred vision and burns.
Dermal exposures:Dermal exposures: TetraethylleadTetraethyllead
is readily absorbed through intact skin.is readily absorbed through intact skin.
ItIt produces itching, burning andproduces itching, burning and
transient redness. On occasion, skintransient redness. On occasion, skin
may begin to look pale.may begin to look pale.
23. Inhalation exposures:Inhalation exposures:
InhalationInhalation is the major route ofis the major route of
exposure; however, symptoms ofexposure; however, symptoms of
tetraethyllead exposure cannot betetraethyllead exposure cannot be
separated from the also-toxic solventseparated from the also-toxic solvent
mixture it is associated with. Earlymixture it is associated with. Early
inhalation effects include sneezing,inhalation effects include sneezing,
irritation of the upper respiratory tractirritation of the upper respiratory tract
and mild systemic effects.and mild systemic effects.
24. Inhalation exposures:Inhalation exposures:
Mild systemic effects include anxiety,Mild systemic effects include anxiety,
lethargy, irritability, nausea, vomiting,lethargy, irritability, nausea, vomiting,
headache, tremors, slurred speech andheadache, tremors, slurred speech and
euphoria.euphoria.
Moderate effects include disorientation,Moderate effects include disorientation,
hyperreflexiahyperreflexia, spasmodic muscular, spasmodic muscular
contractions, spasticity, extreme fatigue,contractions, spasticity, extreme fatigue,
bradycardia, hypotension and nystagmus.bradycardia, hypotension and nystagmus.
Severe systemic effects include completeSevere systemic effects include complete
disorientation with hallucinations, facialdisorientation with hallucinations, facial
contortions, mania, psychotic behavior,contortions, mania, psychotic behavior,
violent seizures which terminate in coma,violent seizures which terminate in coma,
and death.and death.
25. Ingestion exposures:Ingestion exposures:
Poisonings from ingestions are rare.Poisonings from ingestions are rare.
Nausea, vomiting and diarrhea wouldNausea, vomiting and diarrhea would
be expected. It would be reasonable tobe expected. It would be reasonable to
conclude that the systemic effectsconclude that the systemic effects
noted in the inhalation exposuresnoted in the inhalation exposures
section would occur from ingestion.section would occur from ingestion.
Increased intracranial pressure andIncreased intracranial pressure and
pulmonary edema also have beenpulmonary edema also have been
reportedreported
26. Treatment of Exposures in aTreatment of Exposures in a
Health Care FacilityHealth Care Facility
Ocular exposures:Ocular exposures: Irrigate exposedIrrigate exposed
eyes with lukewarm, low-pressureeyes with lukewarm, low-pressure
water or room-temperature 0.9 percentwater or room-temperature 0.9 percent
saline solution. Obtain an ophthalmicsaline solution. Obtain an ophthalmic
exam after irrigation.exam after irrigation.
27. Treatment of ExposuresTreatment of Exposures
in a Health Care Facilityin a Health Care Facility
Dermal exposures:Dermal exposures: First, flood theFirst, flood the
skin with water. Mandatory soap andskin with water. Mandatory soap and
water washings will be necessary towater washings will be necessary to
remove the chemical completely fromremove the chemical completely from
the skin. Due to the rapid absorption ofthe skin. Due to the rapid absorption of
this chemical through intact skin,this chemical through intact skin,
patients may require chelation therapypatients may require chelation therapy
for increasing blood lead levels.for increasing blood lead levels.
28. Treatment of ExposuresTreatment of Exposures
in a Health Care Facilityin a Health Care Facility
Inhalation exposures:Inhalation exposures: Maintain theMaintain the
patient’s airway. Ventilation may bepatient’s airway. Ventilation may be
required. Bronchospasms may berequired. Bronchospasms may be
treated with beta2 agonists.treated with beta2 agonists.
Chelation therapy will be required forChelation therapy will be required for
patients with blood lead levels greaterpatients with blood lead levels greater
than 45 mcg/dl. Treat seizures first withthan 45 mcg/dl. Treat seizures first with
the benzodiazepines. If not controlled bythe benzodiazepines. If not controlled by
the benzodiazepines, second-linethe benzodiazepines, second-line
therapy is phenobarbital.therapy is phenobarbital.
29. Treatment of Exposures in aTreatment of Exposures in a
Health Care FacilityHealth Care Facility
Ingestion exposures:Ingestion exposures: If a large ingestion hasIf a large ingestion has
occurred, stomach decontamination should be considered.occurred, stomach decontamination should be considered.
These ingestions must be treated as an ingestion ofThese ingestions must be treated as an ingestion of
organic solvents, and pulmonary aspiration may occur. Theorganic solvents, and pulmonary aspiration may occur. The
airway must be protected.airway must be protected.
Aspiration must be avoided. Emesis is not recommended.Aspiration must be avoided. Emesis is not recommended.
Whole bowel irrigation should be considered. ChelationWhole bowel irrigation should be considered. Chelation
therapy will be required for patients with blood lead levelstherapy will be required for patients with blood lead levels
greater than 45 mcg/dl. Chelation therapy is controversial,greater than 45 mcg/dl. Chelation therapy is controversial,
as alkylleads are not chelatable, and the therapy probablyas alkylleads are not chelatable, and the therapy probably
does not influence central nervous system symptoms.does not influence central nervous system symptoms.
31. Manganese poisoningManganese poisoning
A type of heavy metal poisoning causedA type of heavy metal poisoning caused
by excessive exposure to manganese.by excessive exposure to manganese.
34. Main risks and targetMain risks and target
organsorgans
Acute toxic effects include centralAcute toxic effects include central
nervous systemnervous system depression, peripheraldepression, peripheral
neuropathy and cardiovascularneuropathy and cardiovascular collapse.collapse.
Dyspnoea and respiratory failure mayDyspnoea and respiratory failure may
occuroccur following exposure to highfollowing exposure to high
concentration. Carbonconcentration. Carbon disulphidedisulphide isis
irritant to eyes and skin and may causeirritant to eyes and skin and may cause
corneal erosionscorneal erosions and chemical burnsand chemical burns
respectively. Chronic exposure mayrespectively. Chronic exposure may
causecause neuropsychiatric disorders,neuropsychiatric disorders,
peripheral neuropathies andperipheral neuropathies and increasedincreased
35. Summary of clinical effectsSummary of clinical effects
Acute carbon disulphide poisoning isAcute carbon disulphide poisoning is
rare but very dangerous. Absorptionrare but very dangerous. Absorption
occurs through the skin, by ingestionoccurs through the skin, by ingestion
or by inhalation. In severe poisoning,or by inhalation. In severe poisoning,
the patient rapidly becomes comatosethe patient rapidly becomes comatose
and death occurs in a few hours,and death occurs in a few hours,
usually due to respiratory depressionusually due to respiratory depression
and convulsions.and convulsions.
36. CClinical effectslinical effects
In less severe cases local irritation,In less severe cases local irritation,
nausea, vomiting and abdominal painnausea, vomiting and abdominal pain
are followed by headache, euphoria,are followed by headache, euphoria,
hallucinations, manic delirium,hallucinations, manic delirium,
paranoid reactions and suicidalparanoid reactions and suicidal
tendencies.tendencies.
37. CClinical effectslinical effects
Chronic occupational exposure is more common. After 10 -15Chronic occupational exposure is more common. After 10 -15
years it may cause sensory and motor neuropathy,years it may cause sensory and motor neuropathy,
neuropsychiatric changes and parkinsonism. Atherosclerosis,neuropsychiatric changes and parkinsonism. Atherosclerosis,
in particular coronary heart disease, impaired visionin particular coronary heart disease, impaired vision
(perception of coloured rings around lights and retinal(perception of coloured rings around lights and retinal
changes), renal and hepatic damage, and permanentchanges), renal and hepatic damage, and permanent
impairment of reproductive function also occur after long-termimpairment of reproductive function also occur after long-term
exposures. In addition, sleep disturbance, fatigue, anorexiaexposures. In addition, sleep disturbance, fatigue, anorexia
and weight loss are common complaints among exposedand weight loss are common complaints among exposed
workers. Local contact may result in irritation, burningworkers. Local contact may result in irritation, burning
sensation, blistering or deep burns. Conjunctivitis, pain andsensation, blistering or deep burns. Conjunctivitis, pain and
blurred vision result from exposure of the eyes to the vapour,blurred vision result from exposure of the eyes to the vapour,
and severe irritation or burns occur after direct contact.and severe irritation or burns occur after direct contact.
38. DiagnosisDiagnosis
The diagnosis is made on the history of exposureThe diagnosis is made on the history of exposure
and the presence of clinical effects. In acuteand the presence of clinical effects. In acute
poisoning by ingestion, there may be nausea,poisoning by ingestion, there may be nausea,
vomiting and abdominal pain followed by headache,vomiting and abdominal pain followed by headache,
euphoria, hallucinations, manic delirium, dyspnoea,euphoria, hallucinations, manic delirium, dyspnoea,
cyanosis, peripheral vascular collapse,convulsionscyanosis, peripheral vascular collapse,convulsions
and coma.and coma.
Carbon disulphide can be measured in blood, urineCarbon disulphide can be measured in blood, urine
and breathand breath
but this is not useful in the management of poisoning.but this is not useful in the management of poisoning.
Dithiocarbamine (DTS) may also be measured inDithiocarbamine (DTS) may also be measured in
urine.urine.
In chronic occupational exposure, the diagnosis isIn chronic occupational exposure, the diagnosis is
made from the presence of sensory and motormade from the presence of sensory and motor
neuropathy, neuropsychiatric changes, parkinsonism,neuropathy, neuropsychiatric changes, parkinsonism,
renal and hepatic damage, sleep disturbance,renal and hepatic damage, sleep disturbance,
fatigue, anorexia and weight loss.fatigue, anorexia and weight loss.
39. First-aid measures andFirst-aid measures and
management principlesmanagement principles
Remove patient to fresh air if carbon disulphide isRemove patient to fresh air if carbon disulphide is
inhaled. In cases of ingestion do not induceinhaled. In cases of ingestion do not induce
vomiting.vomiting.
Perform gastric aspiration or lavage if the toxin wasPerform gastric aspiration or lavage if the toxin was
recently ingested. Wash contaminated skin withrecently ingested. Wash contaminated skin with
soap and water. Irrigate contaminated eyessoap and water. Irrigate contaminated eyes
copiously with water.copiously with water.
In case of severe poisoning, support respiration,In case of severe poisoning, support respiration,
administeradminister
oxygen and monitor cardiovascular function.oxygen and monitor cardiovascular function.
There is no specific antidote. Give symptomatic andThere is no specific antidote. Give symptomatic and
supportive treatment as required.supportive treatment as required.