Transcript 1. Pneumoconiosis. Silicosis. Silicatosis. Vibration disease

Internal medicine department №2
Pneumoconiosis. Silicosis. Silicatosis.
Vibration disease
Asist. O.S. Kvasnitska
Introduction
•Recent decades have seen a marked
increase in concern about the
adverse health effects of hazardous
exposures in the workplace and
elsewhere in the environment
•Endless array of hazardous
substances in industrial and
agriculture sectors
•The lung – with its extensive
surface area, high blood flow and
thin alveolar epithelium– – is an
important site of contact with these
substances in the environment
• Occupational lung diseases are a
broad group of diagnoses caused by the
inhalation of dusts, chemicals, or
proteins
• “Pneumoconiosis” is the term used for
the diseases associated with inhaling
mineral dusts
• The severity of the disease is
related to the material inhaled and the
intensity and duration of the exposure
• Individuals who do not work in the
industry can develop occupational
disease through indirect exposure
• These diseases have been
documented as far back as ancient
Greece and Rome; the incidence of the
disease increased dramatically with the
development of modern industry.
Importance of occupational lung
diseases
Knowledge of cause may affect patient
management and prognosis and may prevent
further disease progression in the affected
person
 Establishment of cause may have significant
legal, financial and social implications for
the patient
 The recognition of occupational and
environmental risk factors can also have
important public health and policy
 Occupational and environmental lung
diseases can also serve as important
disease models

Industrial dust
• Inorganic dust (consists of particles of
minerals and metals)
• Organic dust (contains particles of
plant and animal origin, and also
microorganisms that are on them, and their
waste products)
• Mixed dust
Inorganic dust
Asbestos fibers under
the electron microscope
Talc - hydrated aluminum silicate
Сoal dust of mining enterprises
Organic dust
Dust generated during processing of raw cotton
Moldy hay
Classification
1996 year, The Russian Academy of Medical Sciences
Research institute of Health Medicine
1. Pneumoconiosis, which develops by influence moderately and highly
fibrogenic dust (with containing free silica more than 10 %) – silicosis,
antracosilicosis, silicosiderhosis, silicisilicatosis
2. Pneumoconiosis, which develops by influence mild fibrogenic dust (with
containing free silica less than 10 % or not containing it) – silicatosis
(asbestosis, talcosis, caolinosis, olivinosis, nephelinosis, pneumoconiosis from
exposure to cement dust) – carboconiosis (anthracosis, graphitosis, blacklung carbon disease etc.), polisher’s and emery’s pneumoconiosis,
metalloconiosis or pneumoconiosis from exposure radiopaque dusts
(siderosis, including of aerosol electric welding or gas cutting iron products,
baritoz, stanioz, manganokonioz etc).
3. Pneumoconiosis, which develops by influence toxic-allergic aerosols (dust,
which containing metals-allergens, plastic and other polymeric material
compounds, organic dust etc) – berylliosis, aluminosis, farmer's lung and
other hypersensitivity pneumonitis
International Labour organization, Geneva.
List of occupational Diseases (2002)
1. Diseases caused by agents
1.1 Chemical agents ( 32 items)
1.2 Physical agents ( 8 items )
1.3 Biological agents ( infectious and parasitic
diseases contracted in an occupation where there is a
par contracted in an occupation where there is a
particular risk of contamination )
2. Diseases by target organ systems
2.1 Occupational respiratory diseases
2.2 Occupational skin diseases
2.3 Occupational musculoskeletal disorders
International Labour organization, Geneva.
List of occupational Diseases (2002)
3. Occupational cancer ( 15 items )
(Asbestos, Benzidine and compounds,
Bischloromethylether, chromium and compounds,
coal tar, beta-naphthylamine,Vinylchloride, Benzene,
Toxic nitro and amino derivatives of benzene,
Ionizing radiations, Tar, pitch bitumen, mineral oil, and
related compounds, coke oven emission, coke oven
emission, wood dust ).
4. Other diseases
4.1 Miner’s nystagmus
2.1 Occupational respiratory diseases
2.1.1 Pneumoconioses caused by sclerogenic mineral dusts
2.1.2 Bronchopulmonary disease caused by hard-metal dust
2.1.3 Bronchopulmonary disease caused by cotton, flax, hemp or
sisal dust
2.1.4 Occupational asthma
2.1.5 Extrinsic allergic alveolitis
2.1.5 Siderosis
2.1.6 Chronic obstructive pulmonary diseases
2.1.7 Diseases caused by aluminium
2.1.9 Upper airways disorders
2.1.10 Any other respiratory disease not mentioned in the
proceeding items caused by an agent where the casual
relationship is established
Basic principles of occupational lung diseases
Certain principles apply broadly to the full range of
occupational respiratory disorders
 While a few environmental and occupational lung
diseases may present with pathognomonic
features, most are difficult to distinguish from
disorders of nonenvironmental origin
 A given substance in the workplace or
environment can cause more than one clinical or
pathologic entity
The etiology of many lung diseases may be
multifactorial and occupational factors may
interact with other factors
 The dose of exposure is an important
determinant of the proportion of people affected
or the severity of disease
 Individual
differences in susceptibility to
exposures do exist
 The effects of a given occupational or
environmental lung exposure occur after the
exposure with a predictable latency interval

Pathogenesis
The effects of an inhaled agent depend on
many factors
 its physical and chemical properties
 the susceptibility of the exposed person
 the site of deposition within the bronchial
tree
Physical properties
• physical state (solid particulates,
mist, vapor and gases)
• solubility
• size, shape and density
• concentration
• penetrability
• radioactivity
Chemical properties
• alkalinity and acidity
• fibrogenicity
• antigenicity
Susceptibility of exposed person
• Integrity of local defense
mechanisms
• Immunological status ( atopy, HLA
type)
• Airway geometry
Site of deposition
• When airborne particles come in
contact with the wall of the conducting
airway or a respiratory unit they do not
become airborne again
• Governs the lung response
substantially
• Mechanisms of dust deposition:

Sedimentation

Inertial impaction

Diffusion

Interception

Electrostatic precipitation
Pathogenesis
Size of Dust
10- 5 μ Upper Respiratory tract
5-3μ
Mid respiratory tract
3-1μ
Alveoli
Clinical approach to the
patient
There are two important phases in the workup of any
patient with a potential occupational or
environmental lung disease.
1. General approach: To define and characterize the
nature and extent of the respiratory illness,
regardless of the suspected origin
 A detailed history
 Physical examination
 Appropriate diagnostic tools
2. To determine the extent to which the disease or
symptom complex is caused or exacerbated by an
exposure at work or in the environment
Occupational and environmental history – single
most helpful tool in the diagnostic workup
1. Employment details
 Job title
 Type of industry and specific work
 Name of employer
 Years employed
2. Exposure information
 General description of job process and overall
hygiene
 Materials used by worker and others
 Specific workplace exposures
 Ventilation / exhaust system
 Use of respiratory protection
 Industrial hygiene informations provided by
the employer to the employee
3. Environmental nonoccupational factors
 Smoking
 Diet
 Hobbies
4. Details about past employments in chronological
order
5. Other details
 Does the patient think symptoms / problem is
related to anything at work?
 Are other workers affected?
 Work absenteeism
 Prior pulmonary problems and medications
used
Physical examinations
Generally unrevealing about specific cause
 It is most helpful in ruling out
nonoccupational causes of respiratory
symptoms or diseases (cardiac problems
or connective tissue disorders)

Chest radiography - is the most important
diagnostic test for occupational lung diseases
Limitations:
The chest radiographic findings can be
nonspecific.
 „„Conventional chest radiography is
insensitive, missing as many as 10 to 15
percent of cases with pathologically
documented disease.
 „„Interpersonal variations

ILO – International Classification of
radiographs of pneumoconiosis,1971, 2002
1. Film quality : Grades I to IV
2. Small opacities:
 round opacities:
p (<1.5mm)
q (1.5 –3mm)
r (3 - 10mm)
 Irregular opacities:
s (<1.5mm)
t (1.5 – 3mm)
u (3 – 10mm)
ILO – International Classification of
radiographs of pneumoconiosis,1971,
2002
 Profusion:
Category 0: small rounded opacities absent or less
profuse than in category 1
Category 1: small rounded opacities definitely present
but few in number
Category 2: small rounded opacities numerous. The
normal lung markings are still visible
Category 3: small rounded opacities very numerous.
The lung markings are partially or totally obscured
ILO – International Classification of
radiographs of pneumoconiosis,1971,
2002
Large opacities
Category A: one or more large opacities not
exceeding a combined diameter of 5 cm
Category B: large opacities with combined
diameter greater than 5 cm but does not
exceed the equivalent of the right upper
zone
Category C: bigger than B

ILO – International Classification of
radiographs of pneumoconiosis,1971, 2002
Pleural Abnormalities:
 Location
 width
 extent
 degree of calcification
Other abnormal features
Computed tomography
•Conventional and HRCT scanning are highly sensitive for
diagnosis of pleural diseases and useful for improved
visualization of parenchymal abnormalities.
•„„HRCT findings are usually non specific, but occasionally
certain features and distribution pattern may suggest a
specific cause and may help narrow the differential diagnosis
Silicosis
Silica is silicon dioxide, the oxide of silicon, chemical
formula SiO2
SiO2 is the most abundant mineral on earth; comprises
large part of granite, sandstone and slate.
Silicosis is lung disease caused by inhalation of fine silica
dust; the dust causes inflammation and then scarring of the
lungs. Scarring shows up on chest x-ray.
Silicosis is one type of pneumoconiosis, the medical term
for lung scarring from inhaled dust. Pneumoconiosis can
also occur from inhaled asbestos (asbestosis), coal (coal
workers’ pneumonconiosis), beryllium (berylliosis), and
other respirable dusts.
There is no effective treatment for any pneumoconiosis,
including silicosis
Silica Dust Exposure – Risk Factors
Any work that exposes
silica dust:
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◦
◦
mining
stone cutting
quarrying
road and building
construction
work with abrasives
glass manufacturing
sand blasting
also, some hobbies can
involve exposure to silica
(sculptor, glass blower)
Silicosis - Sandblasting
Silicosis – Foundry work

Silicosis - Stone cutting
Silicosis – Glass Factory
Workers
Sumathi, 19, admitted to
Government Hospital,
Pondicherry, India, suffers
from severe silicosis. She
worked in the sand plant
(where silica is sieved) of a
glass-container
manufacturing plant.
Silicosis - Tunnel construction
Worst single incidence of silicosis in U.S. –
Came to national attention 1930-1931 with construction of Hawk’s
Nest Tunnel in Gauley Bridge, West Virginia. Called “the worst industrial
accident in U.S. history.” At least 764 tunnel workers died from silicosis.
Hawk’s Nest disaster led to Congressional hearings in 1936, and new
laws protecting workers in many states
Silicosis – history
Full description by
Bernardino Ramazzini
(1633-1714) in early 18th
century. “...when the
bodies of such workers
are dissected, they have
been found to be stuffed
with small stones.”
Diseases of Workers (De
Morbis Artificum Diatriba,
1713).
Pathology
Fibrotic nodules develop
by a particular process in
which fibrous tissue is
laid down in concentric
rings around a central
core of silica particles as
an onion
Healthy lung
Silicosis
Manifestions
Symptoms
 shortness of breath while
exercising
 fever
 occasional bluish skin at
ear lobes or lips
 fatigue
 loss of appetite
Three ‘types’ of silicosis

Simple chronic silicosis From long-term exposure
(10-20 years) to low amounts of silica dust. Nodules of
chronic inflammation and scarring, provoked by the silica
dust, form in the lungs and chest lymph nodes. Patients
often asymptomatic, seen for other reasons.
 Accelerated silicosis (= PMF, progressive massive
fibrosis) Occurs after exposure to larger amounts of silica
over a shorter period of time (5-10 years). Inflammation,
scarring, and symptoms progress faster in accelerated
silicosis than in simple silicosis. Patients have symptoms,
especially shortness of breath.
 Acute silicosis From short-term exposure to very large
amounts of silica dust. The lungs become very inflamed,
causing severe shortness of breath and low blood oxygen
level.
Simple Silicosis
normal chest x-ray
simple silicosis
Accelerated Silicosis
(= Progressive Massive Fibrosis)
normal chest x-ray
PMF
Accelerated Silicosis (PMF)
chest x-ray
CT scan
Eggshell calcification –
almost exclusively silicosis
Silicosis – associated risks
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Having silicosis increases risk of contracting
tuberculosis & lung cancer.
Degree of increased risk is highly variable; depends
on several OTHER factors, including immune
system & exposure history (for TB), and amount of
lung scarring, age & smoking history (for cancer).
Silicosis also strongly associated with scleroderma
and rheumatoid arthritis.
Other associations less well established: lupus,
systemic vasculitis, end-stage kidney disease.
Diagnosis of silicosis
•Abnormal chest X-ray or chest CT scan
•History of significant exposure to silica dust
•Medical evaluation to rule out other causes of
abnormal x-ray
•Pulmonary function tests
•Lung biopsy rarely used
Silicosis can be mis-diagnosed
as something else
Silicosis can mimic:
◦ Sarcoidosis (benign inflammation of unknown cause)
◦ Idiopathic pulmonary fibrosis (lung scarring of unknown
cause)
◦ Lung cancer
◦ Several other lung conditions (chronic infection, collagenvascular disease, etc.)
Can usually make right diagnosis with
detailed history (occupational & medical)
or, rarely, a lung biopsy.
Treatment
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Early revealing and change of occupation to
industry without dust.
Oxygen therapy to improve lung ventilation.
Corticosteroids are used in the period of fast
progression, in Rheumatoid Silicosis.
Treatment of Heart failure
Treatment of Complication (Pleuritis,
Pneumonia, Tuberculosis)
Symptomatic Therapy.
Silicatosis (Asbestosis)
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Parenchymal lung fibrosis with or without pleural involvement due to
inhalation of asbestos fibres.
5- 20 years to develop
Inflammation from fibres causes scarring (fibrosis) and stiffening of the
lung. This causes less oxygen exchange. Damage leads to bronchitis,
bronhiectasis.
Damage leads to pleural changes (pleuritis, spikes, enlargement of lymph
nodes at the lung hila (containing asbestos).
It is more dangerous than silicosis as it predisposes to bronchogenic
carcinoma and mesothelioma of the pleura and peritoneum
Symptoms – shortness of breath, a dry, persistant cough , chest tightness,
deformed, club-shaped fingers
Asbestos fibers
Diagnosis of Asbestosis
Chest X- Ray :
Interstitial
pneumoscelerosis
Diagnostic Particularities:
a) In sputum - asbestos
bodies
b) In skin - asbestos Warts
(containing asbestos)
Typical dumbbell shaped ferruginous bodies seen in a bronchial washing specimen
asbestos warts
Complications
Bronchogenic carcinoma
 Mesothelioma

A
B
65-year-old asymptomatic man who had been employed in construction and demolition for over forty years
Radiologic Findings PA (A) and lateral (B) chest radiographs demonstrate the presence of bilateral, relatively
symmetric, multi-focal, discontinuous areas of pleural thickening and calcification primarily distributed along
the anterolateral and posterolateral chest wall and domes of each hemidiaphragm. The apices
and costophrenic angles are spared. Lesions seen en face on the frontal exam (A) exhibit scalloped
morphology, whereas those seen in profile on the lateral exam (B) appear more linear confirming the lesions
change morphology from one orthogonal plane to the next and are therefore pleural-based.
Diagnosis:Asbestos-Related Pleural Plaques
Coal Worker's Pneumoconiosis
(CWP)
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CWP is a lung disease that results from
breathing in dust from coal, graphite, or manmade carbon over a long period of time
Necessary to differentiate from silicotuberculosis, disseminated tuberculosis,
metastatic lung cancer, and other diffuse
infiltrative pulmonary diseases
The disease is divided into 2 categories:
simple CWP and complicated CWP or
progressive massive fibrosis (PMF)
Particularities
 Slow
growth, benign character of current,
active phagocytosis, saved lung protective
mechanism.
 Causes chronic bronchitis, lung
emphysema
 Radiological investigation – interstitial or
interstitial nodular fibrosis of the lung.
Symptoms and Diagnosis
Simple CWP:
 It is said to exist in the presence of
radiological opacities < 1cm in diameter.
 It is benign disease if no complications.
 Cough, expectoration and dyspnea are
frequently present.
 Slight decrease in FVC and FEV1/FVC
Simple CWP
Minute opacities are diffusely
scatterred throughout both
lung fields, providing a crude
measure
of
excessive
exposure.
Early
pneumoconiosis
is
essentially a focal disorder and
may
produce
little
physiologycal disorders
Complicated CWP (PMF):
 Is diagnosed when large opacity of 1cm or more in
diameter is observed in the chest X-ray.
 Pathologically it is characterized by large masses of black
colored fibrous tissue.
 The large lesions may cavitate as a result of ischemic
necrosis or infection (T.B)
 The severe stages of PMF cause cough and often disabling
shortness of breath.
 Pulmonary function test reveals decreased FVC,
FEV1/FVC and increased residual volume
These pictures show complicated coal workers
pneumoconiosis. There are diffuse, small, light areas (more than 1
cm) in all areas on both sides of the lungs. There are large light
areas which run together with poorly defined borders in the upper
areas on both sides of the lungs.
If coal worker's pneumoconiosis occurs
with rheumatoid arthritis it is called
Caplan syndrome.
Caplan's syndrome (or Caplan's disease)
is a combination of rheumatoid arthritis and
pneumoconiosis that manifests as
intrapulmonary nodules, which appear
homogenous and well-defined on chest Xray
Caplan's syndrome presents with
 Cough, shortness of breath
 features of rheumatoid arthritis (painful joints and morning
stiffness)
 Examination should reveal tender, swollen MCP
joints and rheumatoid nodules
 Auscultation of the chest may reveal diffuse rales that do
not disappear on coughing or taking a deep breath.
Other types of occupational lung
disease
Byssinosis
 Byssinosis is a narrowing of the airways
caused by inhaling cotton, flax, or hemp
particles.
 The substance or substances in the
material that cause the disease are not
known, but it is believed that the protein
component rather than the cellulose or
mineral constituents is responsible
Other types of occupational lung
disease
Hypersensitivity Pneumonitis

Hypersensitivity Pneumonitis (also referred to as
“extrinsic allergic alveolitis”) is an immunologicinduced, non-IgE mediated inflammatory
pulmonary disease. It affects primarily the
interstitium, alveoli, and terminal airways, and is
caused by prolonged, repeated inhalation of
organic dusts or certain chemicals (Farmer’s lung,
Bagassosis etc.)
Other types of occupational lung
disease
Occupational Asthma
 Reversible airflow obstruction caused by
workplace exposures
 With latency period (sensitization)
 Without latency period (irritant)
 Causes: a broad group of vegetable, animal
products, chemicals, metals-referred to as
“asthmagens”
“New” Occupational Lung
Diseases
Popcorn workers lung
 Obstructive airways disease, some with
bronchitis obliterans
 Caused by a ketone (diacetyl) in the artificial
butter flavoring used in microwave popcorn
processing
Kreiss et al., NEJM 2002; 347: 330-8
Prevention of occupational
lung diseases

Respirators
Prevention of occupational
lung diseases
Ventilation and exhaust systems
Occupational disease,
caused by influence
physical factors.
Vibration disease
Vibration disease - an
occupational disease caused by
exposure to vibration. This
pathology was first described by
Lörig in 1911 as a syndrome of
stonecutters dead fingers, and in
1955 it was named vibration
disease
OCCUPATIONAL VIBRATION A SHORT HISTORY
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1839 - Pneumatic tools were first used in French mines
1862 - Primary Raynaud's Phenomenon (Raynaud's
Disease) identified.
1911 - Professor Loriga first described vascular spasm
in the hands of Italian miners using pneumatic tools.
1918 - Alice Hamilton studied miners using drills in
limestone quarries describing spastic anaemia of the
hands.
1930-40s - Cases of white finger were identified
studies in fettlers, riveters, boot and shoe industry
workers and users of electrical powered rotating tools
1950s - Research links signs and symptoms in nerves,
bones, joints and muscles with vibrating tools.
1968-69 - After 12-14 years of continuous chain saw
use widespread complaints of VWF (Vibration white
WHAT IS VIBRATION?
Frequency
Amplitude
Acceleration
TYPES OF
VIBRATION
 low-frequency (8 – 15 Hz)
 medium-frequency (16 – 64 Hz)
 high-frequency (more than 64 Hz)
Dangerous for the development of
disease is the vibration with the
frequency 16 – 250 Hz.
EXPOSURE
Segmental (Local) Vibration
‘Segment of body’ such as hand-transmitted
vibration (known as hand-arm vibration or HAV)
Whole Body Vibration
Vibration transmitted through the seat or
feet (known as whole-body vibration or
WBV)
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TRANSMITTED TO THE
WHOLE BODY THROUGH
THE SUPPORTING AREA
Industry
Type of
Vibration
Common Source of
Vibration
Agriculture
Whole body
Tractors
Construction
Whole body
Local
Forestry
Whole body
Local
Heavy equipment vehicles
Pneumatic tools,
Jackhammers
Tractors
Chain saws
Furniture
manufacture
Local
Pneumatic chisels
Machine tools
Local
Vibrating hand tools
Textile
Local
Sewing machines, Looms
Transportation
Whole body
Vehicles
Mining
Whole body
Local
Vehicle operation
Rock drills
LOCAL EFFECTS
These effects occur under the influence of
afferent impulses in the spinal cord neurons,
sympathetic ganglia, and the reticular
formation of the brain, including the levels of
autonomic-vascular centers.
The state of regional circulation disturbs,
there are specific manifestations of
vasospasm. The greater the altered vibration
sensitivity, so vasospasm is significant.
Direct mechanical damage and irritation of
smooth muscle cells of blood vessels is
expressed, which contributes to their spasm
or atony. Further dystrophic changes
PATHOGENESIS: CENTRAL EFFECTS
In parallel with the progressive decline
in the perception of vibration in vibration
disease pain, tactile and thermal
sensitivity disturbed.
Vibrational excitation irradiating to
neighboring areas, especially in the
vasomotor
center,
changing
the
functional state of the peripheral vessel.
Later irritation radiating to vasomotor,
PATHOGENESIS
Defeat of
 Cardiovascular system
 Nervous system
 Locomotor system
 Metabolism
Decreasing of
 Vibrational sensitivity
 Algesthesia (pain sensitivity)
 Tactile sensitivity
 Thermoesthesia (temperature sensitivity)
DISEASE
 Vibration disease from local
vibration impact
 Vibration disease from general
vibration impact
 Vibration disease from combine
vibration (local and general) impact
CLASSIFICATION
Initial stage (mild manifestation)
II. Moderately expressed (dystrophic
disorders)
III. Expressed (irreversible organic
changes)
IV. Generalized (very rare)
I.
MAIN SYNDROMES IN
VIBRATION DISEASE
Angiodistonic syndrome
2. Angiospastic syndrome
3. Syndrome of vegetative polyneuritis
4. Syndrome of vegetative myofascitis
5. Syndrome of somatic neuritis (cubital,
median), plexitis, radiculitis
6. Diencephalic syndrome with
neurocirculatory disturbance
1.
SYNDROME
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
Vegetative-vascular disease in
the limbs, impaired capillary
blood circulation (atonic or
spastic-atonic state)
At high-frequency vibration
and overall in the early stages,
with the midrange - in
elementary and moderate
stages, the low-frequency
vibrations - in all stages
SYNDROME
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
White finger attack, spasms of
the capillaries, skin
temperature violation,
marked reduction of vibration
sensitivity preferentially
localized to the hands and
feet
At high-frequency vibration in
severe stages, and the stage
of generalization, with a total
of vibration - in the initial
stages and marked
VEGETATIVE
POLYNEURITIS
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
Pain phenomena, violation of
skin sensitivity, reduced skin
temperature, vegetative
symptoms
At low-frequency vibrations in the initial stages, with a
total of vibration - in the initial
stages
VEGETATIVE
MYOFASCITIS
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
Painful phenomena, vascular
disorders, changes in
sensitivity by peripheral or
segmental type
At low-frequency vibration
(especially in the presence of
static stress and significant
return impact) and less
frequently in middle
frequency vibration in various
stages
NEURITIS
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
Electoral amyotrophy,
impaired of sensitivity and
reflex areas
Low-frequency vibration,
combined with significant
blowback, with emphasis
trauma tool in severe stages
NEUROCIRCULATORY
DISTURBANCE
Main symptoms
The nature of vibration and
the stage of disease at which
a given syndrome
Generalized vascular disorders At high-frequency vibration
and crises (cerebral,
(local and general) in the
coronary), metabolic
terminal stage
endocrine disorders
LOCAL VIBRATION
(HAND ARM
VIBRATION,
VIBRATION
WHITE FINGER)
HAND ARM
VIBRATION
WHAT IS HAV?
HAV is vibration transmitted from work
processes into workers’ hands and
arms. It can be caused by operating
hand-held power tools such as road
breakers, hand-guided equipment such
as lawn mowers, or by holding materials
being processed by machines such as
pedestal grinders.
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WHEN IS IT HAZARDOUS?
Regular and frequent exposure to high
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VIBRATION
WHAT SORT OF TOOLS AND EQUIPMENT CAN
CAUSE VIBRATION INJURY?
 Chainsaws
 Concrete breakers/road drills
 Hammer drills
 Hand-held grinders
 Hand-held sanders
 Nut runners
 Pedestal grinders
 Power hammers and chisels
 Powered lawnmowers
 Riveting hammers and bolsters
 Strimmers/brush cutters
 Swaging machines.
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HAND ARM VIBRATION
High vibration
Moderate vibration
 impact wrenches
chain saws
93
 percussive tools
• jack hammers
• scalers
• riveting or chipping hammers
 grinders
 sanders
 jig saws
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HAND ARM VIBRATION
- CAUSES & EFFECTS
Neurological
component
Vascular component
Muscular and soft tissue
component
HAND ARM VIBRATION
- CAUSES & EFFECTS
WHAT INJURIES CAN HAV
CAUSE?
Regular exposure to HAV can cause
a range of permanent injuries to
hands and arms including damage
to the:
Blood circulatory system (e.g.
vibration white finger)
Sensory nerves
Muscles
CLASSIFICATION
І — initial manifestations:
 1) Peripheral angiodystonic syndrome of the
upper extremities, including fingers with rare
angiospasm;
 2) neuro-sensory upper limb polyneuropathy
CLASSIFICATION
II — mild manifestations:
1) Peripheral angiodystonic syndrome of
the upper extremities with frequent
fingers angiospasm;
2) neuro-sensory polyneuropathy
syndrome of upper extremities with:
a) frequent fingers angiospasm;
b) persistent vegetative and trophic
disorders on the hands;
c) with degenerative disorders device
support and movement of the upper limbs
CLASSIFICATION
III - pronounced symptoms:
1) sensory motor polyneuropathy syndrome of
the upper extremities;
2) Encephalopolineuropathy syndrome;
3) syndrome polineuropathy with generalized
angiospasm.
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VASCULAR
COMPONENT
Stage
Grade
0
Description
No attacks
1v
Mild
Occasional attacks affecting
only the tips of one or more
fingers
2v
Moderate
Occasional attacks affecting
distal and middle (rarely also
proximal)
phalanges of one or more
fingers
3v
Severe
Frequent attacks affecting all
phalanges of most fingers
SENSORINEURAL
COMPONENT
Stage
Grade
0
Description
Vibration-exposed but no
symptoms
1sn
Mild
Intermittent numbness with
or without tingling
2sn
Moderate
Intermittent or persistent
numbness, reduced sensory
perception
3sn
Severe
Intermittent or persistent
numbness, reduced tactile
discrimination
and/or manipulative dexterity
Numerical scoring of vascular symptoms
of HAVS (after Griffin, 1982)
VIBRATION INDUCED GANGRENE
DURING VIBRATION
DISEASES
DIAGNOSIS OF HAVS
History of symptoms
History of vibration exposure
Various clinical tests to exclude other disorders
Objective measurement of vascular, neurological and
musculoskeletal function:
Vascular tests:
 Finger systolic blood pressures
 Rewarming time after cold provocation
Neurological tests:
 Clinical tactile threshold tests
 Thermal thresholds
 Vibrotactile thresholds
 Nerve conductive velocity
Musculoskeletal function:




VASCULAR TESTS
 Finger systolic blood pressures
 Rewarming time after cold provocation
TESTS
 Clinical tactile threshold tests
 Thermal thresholds
 Vibrotactile thresholds
 Nerve conductive velocity
MUSCULOSKELETAL
FUNCTION
 Finger dexterity
 Hand grip force
FROM EXPOSURE TO
LOCAL VIBRATION
 The
typical additional signs of vascular disorders
1. Symptom of "white spot". You ask a patient
to clench firmly the first of hand and through 5
sec quickly unclench it. In a norm the white spots
which appeared have to vanish in 5 sec. If spots
do not disappear quickly – the test is positive
2. Pile’s symptom. A pulse is found on both radial
arteries, and then by rapid motion lift up the hands
of patient. Thus a pulse can vanish on a few
seconds. Such test is positive.
3. Test on reactive hyperemia. You impose a cuff
on a shoulder and pump a pressure 180 - 200 mm
FROM EXPOSURE TO
LOCAL VIBRATION
 The
typical additional signs of vascular disorders
4. Boholyepov’s test. A patient stretches both hands
with the unbended fingers ahead. At that you pay
attention on colouring of skin, state of veins and
capillary net of nail bed of fingers. Then a patient
lifts a right hand up, and put down a left on 30
sec. After it, returns hands in previous position.
We look after the change of vein and capillary
circulation of blood. Normally, the changes of
blood filling are normalized in 30 sec. At
insufficiency of circulation of blood, pallor or
FROM EXPOSURE TO
LOCAL VIBRATION
 The
typical additional signs of vascular disorders
5. Cold test. The hands of explored are dipped into
a cold water (+10°С) on 5 min. At albication of
fingers the test is considered positive. Pay
attention on prevalence and intensity of the
process, mark the time of renewal of skin
temperature after cooling. Normally it does not
exceed 20 min. At patients with vibration disease
there is an acute deceleration of renewal of skin
temperature.
8–Channel Temperature Monitor
CAPILLAROS
COPE
DURING VIBRATION
DISEASE
DURING VIBRATION
DISEASE
TREATMENT
Therapeutic interventions
 Pharmaceutical agents for the
treatment of HAVS
1. Calcium antagonists
2. Alpha-adreno receptor antagonists
3. Antifibrinolytics
4. Prostaglandin analogues
 Surgical interventions for HAVS

WHOLE BODY
VIBRATION
І
— initial manifestation:
 1) angiodystonic syndrome (cerebral or
peripheral);
 2) neuro-vestibular syndrome;
 3) sensory syndrome (neuro-sensory)
polyneuropathy of the lower extremities.
WHOLE BODY
VIBRATION
II - moderate symptoms:
1) cerebro-peripheral angiodystonic syndrome;
2) sensory syndrome (neuro-sensory)
polyneuropathy in combination:
 a) polyradiculoneuropathy syndrome;
 b) secondary lumbosacral radicular syndrome
(due to degenerative disc disease of the lumbar
spine);
 c) with functional disorders of the nervous
system (neurasthenia syndrome).
WHOLE BODY
VIBRATION
III - pronounced symptoms:
 1) sensorimotor polyneuropathy syndrome;
 2) dyscirculatory encephalopathy syndrome in
combination with peripheral neuropathy
syndrome (encephalopolineuropathy)
FROM
THE INFLUENCE OF
GENERAL VIBRATION
Syndromes of vibration disease conditioned
by general vibration:
- cerebral-peripheral,
- angiodistonic,
- vegetative-vestibular,
- vegetative-sensory polyneuropathy.
BY THE PERIPHERAL
TYPE
Roentgenograms can reveal ossific
formations and centers of osteosclerosis. In
a spinal column, the changes in
intervertebral disks and joints prevail,
mainly
of
degenerative-dystrophic
character.

PROPHYLAXIS
The contra-indications to the
employment on the work related with
influence of vibration are

chronic diseases of the peripheral nervous
system

obliterating endarteritis

Raynaud's disease

angina pectoris, arterial hypertension of ІІ III stages,

endocrine disease (diabetus mellitus)

ulcer disease

ON
Development of HAV is dose related,
meaning that effective control
procedures should be:
• reducing the intensity of the vibration
• reducing the duration of the exposure
to vibration
• early recognition of signs and
symptoms
CONTROLS
Buy lower vibration
A link to the European
tools Hand Arm
Vibration Database is in the
Links and References
at the end of this presentation
Tape
existing
handles with
vibration
dampening
tape
Use full
fingered antivibration
gloves
Suspend tools
from tool
balancers to
reduce hand
grip force
Regularly
maintain
and
balance
hand
tools
OPERATOR VIBRATION
EXPOSURE - ZERO
VIBRATION REDUCED
BREAKER
Keep the moil point
sharp
Break a little at a time
Don’t get jammed
Don’t force antivibration handles
Stop breaker before
pulling out
MECHANISATION
REMOVES THE RISK
MACHINE-MOUNTED PICK
REPLACES HAND-OPERATED
BREAKERS
Thanks for attention!