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Treatment of Mercury
Intoxication
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This information was provided by EMedicine. http://emedicine.com/...emerg&topicid=813
| Toxicity,
Mercury |
 |
Authored by Barry Diner, MD, Chief
Resident, Department of Emergency Medicine, The Brooklyn
Hospital Center
Co-authored by Barry Brenner, MD, PhD,
Director, Division of Research, Associate Clinical
Professor, Department of Emergency Medicine, Weill
College of Medicine, Cornell University, The Brooklyn
Hospital Cen
Barry Diner, MD is a member of the following medical
societies: American College of Emergency Physicians
Edited by Michelle Ervin, MD, Chair,
Department of Emergency Medicine, Howard University
Hospital; John T. VanDeVoort, PharmD, ABAT,
Clinical Assistant Professor, Pharmacy Manager, Regions
Hospital Pharmacy, University of Minnesota College of
Pharmacy; Fred Harchelroad, MD,
Director, Medical Toxicology Treatment Center, Associate
Professor of Emergency Medicine, Department of Emergency
Medicine, Allegheny General Hospital; John
Halamka, MD, Executive Director, Center for
Quality and Value, Instructor, Division of Emergency
Medicine, Beth Israel Deaconess Medical Center; and Raymond
J. Roberge, MD, MPH, Vice-Chair, Clinical
Associate Professor, Department of Emergency Medicine,
Western Pennsylvania Hospital
Background: Throughout the
centuries, there have been several incidents of reported
mercury toxicity. As early as 1500 BC we know that the
Egyptians used mercury, as it was found in their tombs.
In the late 18th century, antisyphilitic agents
contained mercury. It was during the 1800s that the
phrase, "mad as a hatter" was coined due to
the chronic mercury exposure felters faced.
In the 1940s and 1950s, mercury became known as the
product that caused acrodynia, also known as Pink
Disease. The manifestations of acrodynia included pain
and erythema of the palms and soles, irritability,
insomnia, anorexia, diaphoresis, photophobia, and a skin
rash.
Some of the more recent exposures include Minamata
Bay in Japan (1960), mercury contaminated fish in
Canada, methylmercury-treated grain in Iraq (1960 and
1970) and, in the U.S. (1996), a beauty cream product
from Mexico called "Crèma de Belleza-Manning."
For centuries, mercury was an essential part of many
different medicines, such as diuretics, antibacterial
agents, antiseptics, and laxatives. More recently, these
drugs have been substituted and drug-induced signs of
mercury toxicity are rare. Mercury toxicity in
environmental pollution is a major concern because of
increased usage of fossil fuels and agricultural
products, both of which contain mercury.
Mercury poisoning usually is misdiagnosed due to the
insidious onset, nonspecific signs and symptoms, and
lack of knowledge within the medical profession.
Mercury is found in many industries, such as battery,
thermometer, and barometer manufacturing. Mercury can be
found in fungicides used in the agricultural industry.
Prior to 1990, paints contained mercury as an antimildew
agent. In medicine, mercury is used in dental amalgams
and various antiseptic agents.
On July 7, 1999 a joint statement by the American
Academy of Pediatrics (AAP) and the US Public Health
Service (USPHS) was issued alerting clinicians and the
public of thimerosal, a mercury containing preservative
used in some vaccines.
Pathophysiology: Mercury is the only
metal that is a liquid at room temperature. Its symbol
is Hg, which is derived from the Greek word hydrargyrias
meaning "water silver." Mercury is found in
both organic and inorganic forms. The inorganic form can
be further divided into elemental mercury and mercuric
salts. Organic mercury can be found in long and short
alkyl and aryl compounds.
Mercury in any form is toxic. The difference lies in
how it is absorbed, the clinical signs and symptoms, and
the response to treatment modalities. Mercury poisoning
can result from vapor inhalation, ingestion, injection,
or absorption through the skin.
Elemental mercury (Hg) is found as a liquid form,
which easily vaporizes at room temperature and is well
absorbed (80%) through inhalation. Its lipid soluble
property allows for easy passage through the alveoli
into the bloodstream and red blood cells (RBCs). Once
inhaled, elemental mercury is mostly converted to an
inorganic divalent or mercuric form by catalase in the
erythrocytes. This inorganic form has similar properties
to inorganic mercury (eg, poor lipid solubility, limited
permeability to the blood brain barrier, and excretion
in feces). Small amounts of nonoxidized elemental
mercury continue to persist and account for central
nervous system toxicity.
Elemental mercury as a vapor has the ability to
penetrate the CNS, where it is ionized and trapped,
attributing to its significant toxic effects. Elemental
mercury is not well absorbed by the GI tract and,
therefore, when ingested (eg, thermometers), is only
mildly toxic.
Inorganic mercury, found mostly in the mercuric salt
form (eg, batteries), is highly toxic and corrosive. It
gains access to the body orally, or dermally, and is
absorbed at a rate of 10% of that ingested. It has a
nonuniform mode of distribution secondary to poor lipid
solubility and accumulates mostly in the kidney, causing
significant renal damage. Although poor lipid solubility
characteristics limit CNS penetration, slow elimination
and chronic exposure allow for significant CNS
accumulation of mercuric ions and subsequent toxicity.
Chronic dermal exposure to inorganic mercury may also
lead to toxicity.
Excretion of inorganic mercury, as with organic
mercury, is mostly via feces. Renal excretion of mercury
is considered insufficient and attributes to its chronic
exposure and accumulation within the brain, causing CNS
effects.
Organic mercury can be found in 3 forms, aryl and
short and long chain alkyl compounds. Organic mercurials
are absorbed more completely from the GI tract than are
inorganic salts because of intrinsic properties, such as
lipid solubility and mild corrosiveness (though much
less corrosive than inorganic mercury). Once absorbed,
the aryl and long chain alkyl compounds are converted to
their inorganic forms and possess similar toxic
properties of inorganic mercury. The short chain alkyl
mercurials are readily absorbed in the GI tract (90-95%)
and remain stable in their initial forms. Alkyl organic
mercury has high lipid solubility and is distributed
uniformly throughout the body, accumulating in the
brain, kidney, liver, hair, and skin. Organic mercurials
also cross the blood brain barrier and the placenta and
penetrate erythrocytes, attributing to neurological
symptoms, teratogenic effects, and high blood to plasma
ratio, respectively.
Methylmercury has a high affinity for sulfhydryl
groups, which attributes to its effect on enzyme
dysfunction. One enzyme that is inhibited is choline
acetyl transferase, which is involved in the final step
of acetylcholine production. This inhibition may lead to
acetylcholine deficiency, contributing to the signs and
symptoms of motor dysfunction.
Excretion of alkyl mercury occurs mostly in the form
of feces (90%), secondary to significant enterohepatic
circulation. The biological half-life of methyl mercury
is approximately 65 days. Organic mercury is found most
commonly in antiseptics, fungicides and industrial
run-off.
Frequency:
 | In the U.S.: The 1998 annual
report of the American Association of Poison Control
Centers' toxic exposure surveillance system noted
4,039 exposures to mercury. Of these, 1,039 were in
children younger than 6 years, and 1,385 were older
than 19 years. Overall, 68 patients were reported to
have moderate effects, 12 patients had major
effects, and 3 patients died as a result of mercury
exposure. |
Race: There is no scientific
evidence that demonstrates any difference in outcome
following exposure to mercury that is attributable to
race.
Sex: There is no scientific evidence
that demonstrates any difference in outcome following
exposure to mercury that is attributable to gender.
History: The clinical presentation
of mercury toxicity can manifest in a variety of ways
depending on the nature of the exposure, the intensity
of the exposure, and the chemical form. Acute toxicity
usually is related to the inhalation of elemental or
ingestion of inorganic mercury. Exposure to organic
mercury leads to chronic toxicity and, occasionally,
acute toxicity.
| Acute exposure due to inhaled elemental mercury
can lead to pulmonary symptoms. Initial signs and
symptoms, such as fever, chills, shortness of
breath, metallic taste, and pleuritic chest pain,
may be confused with metal fume fever. Other
possible symptoms could include stomatitis,
lethargy, confusion, and vomiting. |
| Recovery is usually without sequela, but pulmonary
complications of inhaled toxicity may include
interstitial emphysema, pneumatocele, pneumothorax,
pneumomediastinum, and interstitial fibrosis. Fatal
ARDS has been reported following elemental mercury
inhalation. |
| Chronic and intense acute exposure causes
cutaneous and neurological symptoms. The classic
triad found in chronic toxicity is tremors,
gingivitis, and erethism (ie, a constellation of
neuropsychiatric findings that includes insomnia,
shyness, memory loss, emotional instability,
depression, anorexia, vasomotor disturbance,
uncontrolled perspiration and blushing). |
| Additional findings may include headache, visual
disturbance (eg, tunnel vision), peripheral
neuropathy, salivation, insomnia, and ataxia. |
| Without a complete history, mercury toxicity,
especially in the elderly, can be misdiagnosed as
Parkinson's disease, senile dementia, metabolic
encephalopathy, depression, or Alzheimer's disease. |
| Elemental mercury has poor GI absorption and,
therefore, oral or rectal exposure to elemental
mercury from a thermometer should have no toxic
effect. Dental amalgams also contain elemental
mercury. Dental professionals who are in contact
with amalgam must follow specific guidelines in
order not to be exposed to toxic amounts of
aerosolized elemental mercury. Patients with dental
amalgam fillings have slightly elevated levels in
their urine, but these findings have not correlated
with any systemic disease. |
| Inorganic mercury or mercuric salt exposure mainly
occurs through the oral and GI tract. Its corrosive
properties account for the majority of the acute
signs and symptoms. The acute presentation can
include ashen-gray mucous membranes secondary to
precipitation of mercuric salts, hematochezia,
vomiting, severe abdominal pain, and hypovolemic
shock. Systemic effects usually begin several hours
after ingestion and may last several days. These
effects include metallic taste, stomatitis, gingival
irritation, foul breath, loosening of teeth, and
renal tubular necrosis leading to oliguria or anuria. |
| Batteries contain inorganic mercury but are rarely
the cause of systemic symptoms. Ingestion of
batteries by pediatric patients is a common problem,
and its complications are related to local corrosive
complications. |
 | Patients who ingest mercury-containing batteries
should receive chelation therapy if symptoms of
mercury toxicity are present. |
| The use of cathartics and water-soluble enemas
is useful for increasing transit time of released
mercury, but is not indicated for intact
batteries. |
| Chronic exposure usually results from prolonged
occupational exposure to elemental mercury that is
converted into the inorganic form, topical
application of mercurial salves, and the chronic use
of diuretics or cathartics. |
| Chronic exposure results in renal failure,
dementia, and acrodynia. |
| Acrodynia, known as pink disease and is
considered to be a mercury allergy, presents with
erythema of the palms and soles, edema of the
hands and feet, desquamating skin rash, hair loss,
pruritus, diaphoresis, tachycardia, hypertension,
photophobia, irritability, anorexia, insomnia,
poor muscle tone, constipation, or diarrhea. |
| Acrodynia does not present in everyone who is
exposed to inorganic mercury, but is an indicator
of widespread disease. |
| Organic mercury poisoning usually results from
ingestion of contaminated food. The long chain and
aryl forms of organic mercury have similar
characteristics of inorganic mercury toxicity. |
| The onset of symptoms usually is delayed
(days-to-weeks) after exposure. |
| Organic mercury targets enzymes and the
depletion of these enzymes must take place prior
to the onset of symptoms. |
| Symptoms related to toxicity typically are
neurological, such as visual disturbance (eg,
scotomata, visual field constriction), ataxia,
paresthesias (early signs), hearing loss,
dysarthria, mental deterioration, muscle tremor,
movement disorders, and, with severe exposure,
paralysis and death. |
| There are specific sights in the brain that
organic mercury targets, including the cerebral
cortex (especially visual cortex), motor and
sensory centers (pre-and postcentral cortex),
auditory center (temporal cortex), and cerebellum. |
| All forms of mercury are toxic to the fetus, but
methylmercury most readily passes through the
placenta. Even with an asymptomatic patient,
maternal exposure can lead to spontaneous abortion
or retardation. |
Physical: The physical examination
should be focused on the areas most commonly affected.
| Perform a complete neurological examination,
including a detailed cerebellar exam. Do full visual
field evaluation. |
| Perform abdominal and rectal exams, with stool
guaiac testing, and include documentation of a skin
exam. |
Causes:
| The causes of elemental mercury toxicity include
barometers, batteries, bronzing, calibration
instruments, chloralki production, dental amalgams,
electroplating, fingerprinting products, fluorescent
and mercury lamps, infrared detectors, jewelry
industry, manometers, neon lamps, paints, paper pulp
production, photography, silver and gold production,
semiconductor cells, and thermometers. |
| The causes of inorganic mercury toxicity include
antisyphilitic agents, acetaldehyde production,
chemical laboratory work, cosmetics, disinfectants,
explosives, embalming, fur hat processing, ink
manufacturing, mercury vapor lamps, mirror
silvering, perfume industry, photography,
spermicidal jellies, tattooing inks, taxidermy
production, vinyl chloride production, and wood
preservation. |
| The causes of organic mercury toxicity include
antiseptics, bactericidals, embalming agents,
farming industry, fungicides, germicidal agents,
insecticidal products, laundry/diaper products,
paper manufacturing, pathology/histology products,
seed preservation, and wood preservatives. |
| Another cause is thimerosal, an additive
preservative that is used in vaccines to prevent
bacterial contamination. The most commonly used
vaccines that contain Thimerosal are DTP(whole
cell), HIB, and Hepatitis B. |
Acute Respiratory Distress Syndrome
Amyotrophic Lateral Sclerosis
Dermatitis, Exfoliative
Disk Battery Ingestion
Gastroenteritis
Myasthenia Gravis
Pediatrics, Bronchiolitis
Pediatrics, Fifth Disease or Erythema Infectiosum
Renal Failure, Acute
Toxicity, Arsenic
Toxicity, Carbon Monoxide
Toxicity, Iron
Toxicity, Phenytoin
Toxicity, Theophylline
Other Problems to be Considered:
Elemental mercury toxicity
Adverse effects of therapeutic medication (eg, lithium,
theophylline, phenytoin)
Alzheimer's disease
Cerebellar degenerative disease or tumor
Delayed neuropsychiatric sequela of carbon monoxide
poisoning
Ethanol or sedative hypnotic drug withdrawal
Lacunar infarction
Metabolic encephalopathy
Parkinson's disease
Senile dementia
Inorganic mercury toxicity (mercury salts)
Acid ingestion
Alkali ingestion
Arsenic toxicity
Iron toxicity
Phosphorus toxicity
Similar to the causes of acute gastroenteritis
Organic mercury toxicity
Cerebral palsy
Intrauterine hypoxia
Teratogenic effects in the embryo
Lab Studies:
| The diagnostic approach to the patient with
suspected mercury toxicity starts with a thorough
history, including occupation(s), hobbies, and
degree of seafood intake. All toxic presentations,
whether acute, chronic or subacute, are difficult
diagnoses because the multiple organ systems
affected (eg, CNS, kidney, mucous membranes) can
mimic a variety of other diseases. If no such
history exists, clinical suspicion can be confirmed
by laboratory analysis. |
| Complete blood count and serum chemistries: To
assess possible anemia secondary to GI hemorrhage,
determine the onset of acute and chronic renal
failure and rule out the possibility of electrolyte
abnormality.
| Pregnancy testing should be considered in
women of childbearing ages. |
|
| Whole blood mercury levels are normally < 2
mcg/dL in unexposed individuals (exceptions are
those individuals with a high dietary intake of
fish). Methylmercury concentrates in erythrocytes;
therefore, its levels in blood will remain high in
acute toxicity. The blood level correlation with
chronic methylmercury toxicity is more variable.
Methylmercury exhibits a blood-to-plasma ratio of
20:1, a characteristic of inorganic mercury. This
higher ratio may be of utility in determining if
organic or inorganic mercurials have poisoned the
patient. Aryl mercury compounds accumulate in RBCs
but are metabolized to inorganic mercury more
rapidly, thus demonstrating lower blood-to-plasma
ratios than that seen with methyl mercury
exposures. Following high exposure to inorganic
mercury salts, the blood-to-plasma ratio ranges
from a high of 2:1, to 1:1. Paraesthesias are
expected if blood mercury levels are > 20 mcg/dL.
Inorganic mercury redistributes to other body
tissue and its levels in the blood only are
accurate after an acute ingestion. In general,
blood levels of mercury are helpful for recent
exposures, as well as determining if the toxicity
is secondary to organic or inorganic mercury, but
they are not useful for a guide to therapy.
|
| Urine mercury levels (normally < 10-20 mcg/L):
Excretion of mercury in urine is a good indicator of
inorganic and elemental mercury exposure but is
unreliable for organic mercury (methylmercury),
since elimination occurs mostly in the feces. There
is no absolute correlation between the levels in the
urine and the onset of symptoms, but levels above
300 mcg/L are associated with overt symptoms.
Mercury levels in the urine can also be used to
gauge the efficacy of chelation therapy. For workers
chronically exposed to mercury compounds, urinary
excretion > 50 mcg/L is associated with an
increased frequency of tremor. |
| Hair has a high sulfhydryl content. Mercury forms
covalent bonds with sulfur and, therefore, it can be
found in abundance in hair samples. The rate of
false positives is high with hair analysis secondary
to environmental exposure. Hair analysis should not
be used solely as a means to confirm mercury
toxicity or exposure. |
Imaging Studies:
| Obtain a flat plate radiograph of the abdomen in
order to visualize ingested elemental mercury, which
is radiopaque. |
Prehospital Care: Prehospital
management includes gathering information on the time,
type and mode of exposure.
| Initial assessment (ABCs) |
| Oxygen |
| IV access |
Emergency Department Care: Supportive
care begins with the ABCs, especially when dealing with
inhalation of elemental mercury and the ingestion of
caustic inorganic mercury, both of which may cause the
onset of airway obstruction and failure. The next step
in supportive care is the removal of contaminated
clothing and copious irrigation of exposed skin. The
need for aggressive hydration may be required for acute
inorganic mercury poisoning due to its caustic
properties.
| Do not induce emesis if the compound ingested is
of the caustic inorganic form.
| Gastric lavage is recommended for organic
ingestion, especially if the compound is seen on
the abdominal x-ray series. Gastric lavage with
protein-containing solutions (eg, milk, egg
whites, salt-poor albumin) or 5% sodium
formaldehyde sulfoxylate solution may bind
gastric mercury and limit its absorption. |
| Activated charcoal is indicated for GI
decontamination, as it will bind both inorganic
and organic mercury compounds to some extent. |
| Whole bowel irrigation may be used until
rectal effluent is clear and void of any
radiopaque material. However, it is doubtful to
be efficacious in decreasing the GI transit time
of elemental mercury because of the high density
of elemental mercury and the low density of the
whole bowel irrigant solutions. Likewise, whole
bowel irrigation has no adsorptive effect on any
type of mercury within the GI tract. |
| Use chelating agents if the patient is
symptomatic, if systemic absorption is
anticipated, or if increased blood or urine
levels are present. Chelating agents all contain
thiol groups, which compete with endogenous
sulfhydryl groups. |
| Hemodialysis is used in severe cases of
toxicity when renal function has declined.
Regular hemodialysis' ability to filter out
mercury is limited because of mercury's mode of
distribution between erythrocytes and plasma.
However, hemodialysis, with L-cysteine compound
as a chelator, has been successful. |
| Neostigmine may help motor function in
methylmercury toxicity. This toxicity often
leads to acetylcholine deficiency.
Polithiol is a nonabsorbable resin that can
help in facilitating the removal of
methylmercury (short chain alkyl organic
mercury), which is then excreted in the bile
after enterohepatic circulation.
|
Consultations: Consultation with
the regional poison control center or your local
medical toxicologist (certified through the American
Board of Medical Toxicology and/or the American
Board of Emergency Medicine) may provide additional
information and patient care recommendations.
| Recommendation: The American Academy of
Pediatric and US Public Health Service states
that the use of products containing thimerosal
is preferable to withholding vaccinations, which
protect against diseases that represent
immediate threat to young infants (ie, pertussis,
Haemophilus Infuenzae). For the
hepatitis B vaccine, adjustments in timing
within the ranges proposed in the immunization
schedule provide additional opportunities to
minimize exposure of small infants to thimerosal.
If thimerosal-free vaccine is not available
Hepatitis B virus vaccination should be
initiated in infants aged 6 months. |
The use of chelating agents should be instituted
if the patient is symptomatic, systemic absorption
is anticipated or increased blood or urine levels
present.
Drug Category: Chelating
Agents - The thiol groups in the
chelating agent compete with endogenous sulfhydryl
groups.
-
| Drug Name |
BAL (British
Anti-Lewisite) - BAL is used only in
acute ingestion. BAL(dimercaprol in an
oil solution) is contraindicated for use
in organic (methylmercury) toxicity
because it can raise levels in the brain
causing further neurotoxicity. |
| Adult Dose |
3-5 mg/kg/dose deep IM
injection q4h the first 2 d; followed by
2.5-3 mg/kg/dose IM q6h for 2 d; then
2.5-3 mg/kg/dose IM q12h for 1 wk |
| Pediatric Dose |
Administer as in
adults |
| Contraindications |
Methylmercury
toxicity; G-6-PD deficiency, unless a
life-threatening situation exists;
Severe peanut allergy, as the excipient
for the dimercaprol is peanut oil. |
| Pregnancy |
C - Safety for use
during pregnancy has not been
established. |
| Precautions |
Caution with patients
that are G-6-PD deficient, as it may
produce hemolysis. Side effects include
abdominal pain, nausea, vomiting,
headache, elevated blood pressure,
tachycardia, burning sensation to the
lips and throat, constricting feeling of
the throat, conjunctivitis,
blepharospasm, lacrimation, rhinorrhea,
salivation, burning sensation to the
penis and urticaria (some side effects
responsive to diphenhydramine cotherapy). |
-
| Drug Name |
Penicillamine (Cuprimine
, Depen) - PCN (D-penicillamine) forms a
complex with mercury and is excreted in
the urine; therefore, it should not be
used in renal failure. It cannot be
considered a first line agent because of
the safer and more efficacious agent,
dimercaptosuccinic acid. |
| Adult Dose |
15-40 mg/kg/d, up to a
maximum of 250-500 mg PO q6h ac
(Continue 1 wk until decline in urine
mercury levels) |
| Pediatric Dose |
20-30 mg/kg/d PO once
or twice daily before meals (ac) |
| Contraindications |
Avoid in patients with
penicillin allergy. |
| Interactions |
Antacids, digoxin,
iron |
| Pregnancy |
D - Unsafe in
pregnancy |
| Precautions |
Side effects include
GI disturbances, rash, leukopenia,
thrombocytopenia and proteinuria.
Use in caution during renal
insufficiency. Therapy with d-penicillamine
may be dangerous since the main route of
elimination of this complex is renal. |
-
| Drug Name |
DMSA
(2,3-dimercaptosuccinic acid, Succimer,
Chemet) - DMSA (2,3-dimercaptosuccinic
acid) is used in both inorganic and
organic mercurials. It is considered
superior to PCN. DMSA is an oral
medication that has fewer side effects
than do PCN and BAL. Because of its ease
of use, good efficacy and safety,
initiate treatment with this agent if
there is good evidence that significant
absorption will occur, as mercury levels
may not be readily available. |
| Adult Dose |
10 mg/kg PO tid for 5
d, followed by 10 mg/kg PO bid for 14 d |
| Pediatric Dose |
10 mg/kg or 350 mg/m2
PO q8h for 5 d, followed by 10 mg/kg PO
bid for 14 d |
| Contraindications |
Hypersensitivity to
Succimer |
| Pregnancy |
C - Safety for use
during pregnancy has not been
established. |
| Precautions |
Side effects include
mild GI disturbances and a transient
rise in liver enzymes. The product has a
strong sulfur smell.
Thrombocytosis, eosinophilia, and
neutropenia have all been reported with
therapeutic use, and all are reported to
resolve when therapy ends. |
Prognosis:
| Outcome depends on the form of the mercury
compound and the severity of the exposure. Mild
exposure to inorganic (ie, elemental, mercuric
salt) and organic compounds can result in a
complete recovery. Death is usually the result
of a severe exposure to mercuric salt. Most
organic mercury exposures leave a neurological
sequela. Very minimal dermal exposure to
dimethyl mercury has resulted in progressive
neurologic deterioration and death, with initial
symptoms delayed for several months. |
Medical/Legal Pitfalls:
| Failure to obtain a history of exposure to
mercury compounds in a patient with significant
historical features of the signs and symptoms of
mercury exposure. |
| Failure to initiate treatment in a patient
with significant exposure, and symptoms, prior
to receiving the confirmatory laboratory
analysis (which may be delayed for a week.) |
| Failure to consult your local medical
toxicologist or regional poison control center
for updated information on this rare poisoning. |
Special Concerns:
| Significant oral ingestion of elemental
mercury may lead to significant environmental
contamination as the mercury is passed,
essentially unabsorbed, through the GI tract,
and expelled in the feces. |
CME Question 1: The mother of a
7-year-old male presents to the ED in rural Ohio and
states that her son drank an unknown amount of
liquid from a bottle in their shed. She brings the
bottle with her; it is a fungicide that contains
methylmercury. The patient is complaining of
difficulty seeing, has trouble walking, and senses a
funny feeling in his hands. Presuming that this is
an organic mercury poisoning, which of the following
chelating agents is contraindicated?
A: DMSA (2,3-dimercaptosuccinic
acid)
B: Calcium disodium
ethylenediaminetetraacetic acid
C: PCN (D-penicillamine)
D: Dimercaprol
E: None of the above
The correct answer is D: Dimercaprol (BAL)
is contraindicated for use in organic mercury
toxicity because it can raise the mercury levels in
the CNS causing further neurotoxicity. Calcium
disodium ethylenediaminetetraacetic acid is
indicated for the treatment of acute lead and
cadmium poisoning, not mercury poisoning; however,
it is not specifically contraindicated.
CME Question 2: The parents of
an 8-year-old female run into the ED screaming,
"My daughter is going to die. She has been
poisoned with mercury from the thermometer that
broke in her mouth." Which of the following is
the next appropriate step?
A: Begin GI decontamination.
B: Start chelating therapy.
C: Reassure parents that their
child will be okay and send them home.
D: Call poison control.
E: Begin hemodialysis.
The correct answer is C: Elemental mercury
is very poorly absorbed by the GI tract and,
therefore, is only mildly toxic. Certainly, the
physician should examine the oropharynx of the
patient to assess any intra-oral lacerations from
the glass.
Pearl Question 1: How does
chronic elemental mercury poisoning present?
The correct answer is : Tremors,
gingivitis, and erethism (ie, insomnia, shyness,
decreased memory, uncontrollable sweating, blushing)
Pearl Question 2: What are the
most common causes of elemental mercury ingestion?
The correct answer is : Batteries and
thermometers
Pearl Question 3: What medical
condition can mercury toxicity simulate?
The correct answer is : Parkinson`s
disease
Pearl Question 4: What are
common causes of inorganic mercury poisoning?
The correct answer is : Fur hat
production, embalming, ink manufacturing, and
tattooing.
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Arch Environ Health 1970; 21: 717-727. |
| Taueg C, Sanfillipo DJ, Rowens B, et al:
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30: 63-67. |
| Young J: Mercury.
Goldfrank's Toxicology Emergencies 1994; 74:
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| NOTE: |
| Medicine
is a constantly changing science and not all
therapies are clearly established. New
research changes drug and treatment
therapies daily. The authors, editors, and
publisher of this textbook have used their
best efforts to provide information that is
up-to-date and accurate and is generally
accepted within medical standards at the
time of publication. However, as medical
science is constantly changing and human
error is always possible, the authors,
editors, and publisher or any other party
involved with the publication of this text
do not warrant the information in this text
is accurate or complete, nor are they
responsible for omissions or errors in the
text or for the results of using this
information. The reader should confirm the
information in this text from other sources
prior to use. In particular, all drug doses,
indications, and contraindications should be
confirmed in the package insert. |
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Dental
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