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NEUROTOXICOSIS
Bodnar R.Ya.
PLAN
NEUROTOXICOSIS
Mercury poisoning
 Industrial uses.
 Pathogenesis of
Mercury poisoning.
 Clinical picture. Diagnosis.
 Treatment.
Tetraethyllead poisoning
 Industrial uses.
 Pathogenesis
of Tetraethyllead
poisoning.
 Clinical picture. Diagnosis.
 Treatment.
Manganese poisoning
 Industrial uses.
 Pathogenesis of
Manganese poisoning.
 Clinical picture.
Diagnosis.
 Treatment.
MERCURY
POISONING
MERCURY POISONING
Mercury has been used commercially and
medically for centuries.
 In the past it was a common constituent of
many medications. It is still used in hospitals in
thermometers and blood-pressure cuffs and
commercially in batteries, switches, and
fluorescent light bulbs.
 Large quantities of metallic mercury are
employed as electrodes in the electrolytic
production of chlorine and sodium hydroxide
from saline.
 These uses still give rise to accidental and
occupational exposures.
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MERCURY POISONING
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Today, however, exposure of the general population
comes from three major sources: fish consumption,
dental amalgams, and vaccines.
Each has its own characteristic form of mercury and
distinctive toxicologic profile and clinical symptoms.
Dental amalgams emit mercury vapor that is inhaled
and absorbed into the bloodstream.
Dentists and anyone with an amalgam filling are
exposed to this form of mercury.
Liquid metallic mercury (quicksilver) still finds its way
into homes, causing a risk of poisoning from the vapor
and creating major cleanup costs.
Humans are also exposed to two distinct but related
organic forms, methyl mercury (CH3Hg+) and ethyl
mercury (CH3CH2Hg+).
MERCURY POISONING
Fish are the main if not the only source of methyl
mercury, since it is no longer used as a fungicide.
 In many countries, babies are exposed to ethyl
mercury through vaccination, since this form is the
active ingredient of the preservative thimerosal used
in vaccines.
 Whereas removal of certain forms of mercury, such as
that in blood-pressure cuffs, will not cause increased
health risks, removal of each of the three major
sources described in this article entails health risks
and thus poses a dilemma to the health professional.

MERCURY POISONING
Exposure to mercury from dental amalgams
and fish consumption has been a concern for
decades, but the possible risk associated with
thimerosal is a much newer concern.
 These fears have been heightened by a recent
recommendation
by
the
Environmental
Protection Agency (EPA) that the allowable or
safe daily intake of methyl mercury be reduced
from 0.5 μg of mercury per kilogram of body
weight per day, the threshold established by
the World Health Organization in 1978, to 0.1
μg of mercury per kilogram per day.

The Global Cycle of Mercury
In nature, mercury vapor (Hg0), a
stable monatomic gas, evaporates from
the earth’s surface (both soil and water)
and
is
emitted
by
volcanoes
Anthropogenic sources include emissions
from coal-burning power stations and
municipal
incinerators.
After
approximately one year, mercury vapor is
converted to a soluble form (Hg2+) and
returned to the earth in rainwater. It may
be converted back to the vapor form both
in soil and in water by microorganisms
and reemitted into the atmosphere. Thus,
mercury may recirculate for long periods.
Mercury attached to aquatic sediments is
subject to microbial conversion to methyl
mercury (MeHg), whereupon it enters the
aquatic food chain. It reaches its highest
concentrations in long-lived predatory
fish, such as sharks.
The Global Cycle of Mercury

Panel
indicates
the
routes of
transformation
to methyl
mercury
as
originally
The Global Cycle of Mercury
Panel depicts the
increase in mercury
concentrations in
feathers of fish-eating
birds in Sweden.
 The period covered
by these data
corresponds
approximately to the
growth of
industrialization in
Sweden.
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Acute MERCURY poisoning
Acute mercury poisoning occurs rarely.
 It arises up after contact with large
quantities of mercury.
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Acute MERCURY poisoning
The main symptoms of the acute poisoning are
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hypersalivation,
inflammation and formation of ulcers of mucous
of the mouth,
swelling of salivary glands,
increase of submandibular lymph nodes,
inflammation of gums,
nausea,
vomiting,
diarrhea,
tenesmus,
intestinal colic.
Acute MERCURY poisoning
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Necrotizing nephrosis with acute renal failure
often develops.
acute bronchitis,
pneumonia.
Very often liver, nervous system are affected.
In blood: hemolysis, leukocytosis, increase of ESR
(to 30-50 mm/h), increase of blood protein,
nitrogen.
Mercury poisoning
Necrotizing nephrosis
Acute MERCURY poisoning
After the acute poisoning:
 a chronic diseases of kidneys,
 chronic colitis,
 hepatitis
 astheniс syndrome.
 After the treatment may be complete
recovery.
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Chronis MERCURY poisoning
Occurs after contact with mercury during
8-10 years.
 Clinical symptoms develop gradually and
are characterized by affection of the
NERVOUS SYSTEM.
 According to the degree of expressiveness
of pathological process chronic poisoning
is divided into 3 stages: INITIAL
(FUNCTIONAL), MODERATE AND SEVERE.
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MERCURY POISONING
DIAGNOSIS
Early typical symptoms:
irritability,
 weakness,
 Gingivitis
 stomatitis.
Confirmation of diagnosis is mercury
determination in urine and feces.
Presence of mercury in urine without
proper clinical symptoms indicates a
“mercury carriage”.
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MERCURY POISONING
Treatment
-To destroy mercury and excrete it from organism
antidotes are recommend: Unitiol, Sucsimer,
sodium thiosulphate.
- Most effective is Unitiol (sodium 2,3dymercaptopropansulfonat) - 5% 5-10 ml (0,05 g
or 5% 1 ml per 10 kg of patient’s weight). 1 day
- 2-4 injections, next 6-7 days –1 injection/ day.
- Its sulfhydryl groups form untoxic complexes
with poison and are excreted with urine.
MERCURY POISONING
Treatment
Sodium thiosulphate 30% 5-10 ml i/v
slowly.
 Drugs which improve metabolism and
blood supply of brain (Pyracetam,
Stugeron).
 Glucose 40% 20 ml + Vit. C,
 Vit.B 1, B 12, B 6.
 Tranquilizers.
 Symptomatic therapy.
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TETRAETHYLLEAD
POISONING
TETRAETHYLLEAD POISONING
TEL is an oily transparent liquid which
contains a 64,07 % of lead,
 well dissolves in organic solvents (ether,
alcohol, benzol, petrol and other) and in
fats.
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TETRAETHYLLEAD POISONING
ТЕL is applied as antidetonate.
 A dangerous contact with TEL may occur
-at its producing,
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- mixing with a fuel,
- at cleaning of petrol cisterns.
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Tetraethyllead
poison.
is
a
strong
neurotrop
TETRAETHYLLEAD POISONING
MODE OF ABSORPTION
INHALATION
SKIN
INGESTION
TETRAETHYLLEAD POISONING
TYPE
of POISONING
ACUTE
SUBACUTE
CHRONIC
TETRAETHYLLEAD POISONING
 Tetraethyllead
Poisoning is
characterized by neurological
symptoms.
Toxic affection of cerebral neurocytes
ACUTE TETRAETHYLLEAD
POISONING
in 1-3 hours after a contact with ТЕL the
first symptoms of the acute poisoning
appear.
 According to the degree of expressiveness
of clinical manifestations there are three
STAGES of the acute poisoning by ТЕL:
- INITIAL,
- PRECULMINATION,
- CULMINATION.
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CHRONIC
TETRAETHYLLEAD
POISONING
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is observed in workers who worked in contact
with ТЕL during long period.
A clinic develops gradually and can be poorly
expressed.
According
to
the
degree
of
expressiveness
of
clinical
manifestations there are three STAGES of the
chronic poisoning:
I-st (initial),
II-nd
III-rd.
ACUTE TEL POISONING
Treatment
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To wash up skin (with warm water and soap), to
make gastric washing, to use absorbents.
Patients with acute TEL poisoning need
complete rest, hypnotic medicines from the
group of barbituratus (phenobarbital, barbital
sodium or etaminal sodium).
At hyperexcitability barbamil (i/m or i/v) or
hexenal are prescribed.
hypertensive solution of glucose i/v, Vitamine
therapy.
Warm baths are recommended before sleep.
CHRONIC TEL POISONING
Treatment
Treatment of patients with the chronic form of
TEL poisoning is appointed taking into account
expressiveness of clinical manifestations.
 For such patients
- drugs which influence on a tissue metabolism
(glutamine acid, glucose, vitamins C, B1, B2,
ATF, riboxin),
- tranquilizers (Diasepam, Tazepam) are
recommended.
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MANGANESE
POISONING
Manganese poisoning
The
occupational manganese poisoning occurs among
workers who work
- on the manganese mines,
- in metallurgical industry at steel making ,
-special alloys producing (ferromanganese – to 80 %
of manganese, mirror cast-iron – to 15 % of manganese),
- at making of electrodes and gumboils which are
used for the electric welding,
- in chemical and lacquer-paint industry,
- in agriculture (stain of seed for stimulation of plant
growth),
- in rubber industry.
- Most dangerous is ground and sifting of pound ore,
because a lot of small disperse dust of manganese appear.
VARIANTS OF CLINICAL COURSE
Ways of
Manganese poisoning
Respiratory
system
Gastrointestinal
tract
Skin
Manganese poisoning
- The oxides of manganese are quickly
absorbed.
- In blood manganese circulates as an
unsteady complex with plasma proteins.
- Manganese is deposited in bones,
cerebrum, parenchyma organs.
- It is excreted from the organism with
feces and urine.
- Manganese may cause bronchial
asthma and eczema because of its allergic
influence.
Manganese poisoning
Pathogenesis
Manganese, as a microelement, takes part in
biological processes of organism.
 It influences on metabolic processes, depresses
cholinesterase activity, affects metabolism of
serotonin.
 At the protracted and systematic getting into the
organism it has a direct influence on nervous
tissue, and causes vascular violations, increase
capillary permeability.
 It changes activity of enzymes of nervous cells,
depresses the biosynthesis of catecholamines,
intensifies protein metabolism.
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Manganese poisoning
Pathogenesis
The action of manganese is divided
into two phases.
 I phase – cholinergic – is characterized by
predominance of cholinergic influence.
 II phase – phase of areactivity – injury of
acetylcholinoreactive structures.
 A manganese influences on the function of
thyroid,
cardiovascular
system,
gastrointestinal tract, liver and other.
Acute Manganese poisoning
In industry acute manganese poisoning occurs
rarely.
 It arises up at breathing in large quantities of
dust which contains manganese.
 Manganese poisoning causes severe disorders of
blood circulation, dyspnea, frequent syncopes.
 In easy cases of poisoning irritation of the
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mucous of respiratory
headache are observed.
tracts,
cough,
and
CHRONIC MANGANESE
POISONING
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Clinical picture of the chronic manganese
poisoning is characterized by three stages.
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!!! The special feature of clinical course of
chronic manganese poisoning is inclination
to its progress after stopping contact with
a metal.
MANGANESE POISONING
DIAGNOSIS
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Special attention is paid to early diagnosis of
chronic manganese poisoning.
It’s necessary to find out a professional route,
sanitary description of labor conditions
(manganese concentration in the workplace,
duration of contact during work day, experience
of work, influence of other harmful professional
factors),
to analyse results of biochemical investigations
(level of manganese in blood, urine, saliva,
milk).
MANGANESE POISONING
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A decline of patient activity, dormancy of
psychical processes, insufficient critical
relation to the state of organism
predetermine the late appeal of patients
for medical help.
Handwriting in different stages of
manganese poisoning
MANGANESE POISONING
Treatment
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Glucose 40 % + Vit.C (300-500 mg) i/v,
vitamin B1 (40-50 mg),
0,25 % novocaine 10-15 ml (15-20 injections).
At appearance of Parkinsonism signs it is
necessary
to
prescribe
antiparkinsonism
cholinolytics
(Cyklodol,
Norakin,
Amedin,
Tropacin, tab. “Korbella”).
Tropacinum – is effective antiparkinsonism
cholinolytical drug (10-20 mg 1-2 times per a
day after meal). “Karbella” decrease tremor and
diminish tonus of muscles (1 tablet before
sleep).
MANGANESE POISONING
Treatment
medical gymnastics
 bath (36-37C, duration - 20 minutes,
course of treatment - 10 baths)
 Application of ozocerite on spine (20-25
minutes 7-10 days)).
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