16.Pneumoconiosis

Pneumoconiosis. Silicosis. Silicatosis. Vibration disease

Asist. O.S. Kvasnitska
Internal medicine department №2

Recent decades have seen a marked increase in concern about the adverse health effects of hazardous exposures in the workplace and elsewhere in the environmentEndless array of hazardous substances in industrial and agriculture sectorsThe 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 Introduction


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 dustsThe severity of the disease is related to the material inhaled and the intensity and duration of the exposureIndividuals who do not work in the industry can develop occupational disease through indirect exposureThese 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

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
Industrial 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, silicisilicatosis2. 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, black-lung 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 diseases4.1 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


10- 5 μ - Upper Respiratory tract 5 - 3 μ Mid respiratory tract 3 - 1 μ Alveoli Pathogenesis Size of Dust

Clinical approach to the patient

There are two important phases in the workup of any patient with a potential occupational or environmental lung disease. 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:

ILO – International Classification of radiographs of pneumoconiosis,1971, 2002 1. Film quality : Grades I to IV2. 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

Silicosis
Silica is silicon dioxide, the oxide of silicon, chemical formula SiO2SiO2 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: 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 – 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 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, collagen-vascular disease, etc.) Can usually make right diagnosis with detailed history (occupational & medical) or, rarely, a lung biopsy.

Treatment

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)

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 peritoneumSymptoms – shortness of breath, a dry, persistant cough , chest tightness, deformed, club-shaped fingers

Asbestos fibers

Chest X- Ray : Interstitial pneumoscelerosis Diagnostic Particularities: a) In sputum - asbestos bodies b) In skin - asbestos Warts (containing asbestos)
Diagnosis of Asbestosis

Typical dumbbell shaped ferruginous bodies seen in a bronchial washing specimen

asbestos warts

Complications

Bronchogenic carcinoma Mesothelioma

A
B

Coal Worker's Pneumoconiosis (CWP)

CWP is a lung disease that results from breathing in dust from coal, graphite, or man-made carbon over a long period of time Necessary to differentiate from silico-tuberculosis, 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.

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 PneumonitisHypersensitivity Pneumonitis (also referred to as “extrinsic allergic alveolitis”) is an immunologic-induced, 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 AsthmaReversible airflow obstruction caused by workplace exposuresWith latency period (sensitization)Without latency period (irritant)Causes: a broad group of vegetable, animal products, chemicals, metals-referred to as “asthmagens”


“New” Occupational LungDiseases 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

OCCUPATIONAL VIBRATION - A SHORT HISTORY
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 finger) in operators. 1975 - Scale for assessing the extent of vascular injury associated with vibration white finger published by Taylor-Pelmear 1985 - VWF becomes a prescribed disease for Industrial Injuries Disablement Benefit purposes 1987 - Stockholm scale for assessment of VWF published. Standard for measurement of vibration published in BS 6842.

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.

* VIBRATION 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)

 ACTING DIRECTIONS OF THE MECHANICAL VIBRATIONS 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
Heavy equipment vehicles Pneumatic tools, Jackhammers
Forestry
Whole body Local
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

PATHOGENESIS: 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 develops. Pathological process is in general has character of angiotrophoneurosis that at some stage has a tendency to generalize. However, trophic disorders relate primarily to the neuromuscular and musculoskeletal system, especially the shoulder girdle muscles, bones and joints.

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, pain and temperature centers if the disease development of vibration centers in stagnant excitation (parabiosis).
PATHOGENESIS: CENTRAL EFFECTS

PATHOGENESIS

Defeat of Cardiovascular system Nervous system Locomotor system Metabolism Decreasing of Vibrational sensitivity Algesthesia (pain sensitivity) Tactile sensitivity Thermoesthesia (temperature sensitivity)

TYPES OF VIBRATION 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) Moderately expressed (dystrophic disorders) Expressed (irreversible organic changes) Generalized (very rare)

MAIN SYNDROMES IN VIBRATION DISEASE

Angiodistonic syndrome Angiospastic syndrome Syndrome of vegetative polyneuritis Syndrome of vegetative myofascitis Syndrome of somatic neuritis (cubital, median), plexitis, radiculitis Diencephalic syndrome with neurocirculatory disturbance Vestibular syndrome

ANGIODISTONIC 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

ANGIOSPASTIC 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

SYNDROME OF 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

SYNDROME OF 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

SYNDROME OF SOMATIC 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

DIENCEPHALIC SYNDROME WITH NEUROCIRCULATORY DISTURBANCE

Main symptoms
The nature of vibration and the stage of disease at which a given syndrome
Generalized vascular disorders and crises (cerebral, coronary), metabolic endocrine disorders
At high-frequency vibration (local and general) in the terminal stage

VESTIBULAR SYNDROME

Main symptoms
The nature of vibration and the stage of disease at which a given syndrome
Vertigo, nystagmus, ataxia
With the overall of vibration, at least - with high local vibration



VIBRATION DISEASE FROM THE ACTION OF 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. WHEN IS IT HAZARDOUS?Regular and frequent exposure to high levels of vibration can lead to permanent injury. This is most likely when contact with a vibrating tool or process is a regular part of a person’s job.

* HAND ARM 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.

* HAND ARM VIBRATION

Moderate vibration
High vibration
impact wrenches chain saws percussive tools jack hammers scalers riveting or chipping hammers
grinders sanders jig saws

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 Bones Joints

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 and their zone (miofibrosis, periartrosis, arthritis);d) cervical-brachial plexopathy;e) with cerebral angiodystonic syndrome.

CLASSIFICATION

III - pronounced symptoms: 1) sensory motor polyneuropathy syndrome of the upper extremities; 2) Encephalopolineuropathy syndrome; 3) syndrome polineuropathy with generalized angiospasm.

*

STOCKHOLM WORKSHOP SCALESVASCULAR COMPONENT

Stage
Grade
Description
0
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
4v
Very severe
As in stage 3, with trophic changes in the fingertips


STOCKHOLM WORKSHOP SCALESSENSORINEURAL COMPONENT
Stage
Grade
Description
0
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

ATROPHY OF MUSCLES 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: Finger dexterity Hand grip force

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

Finger dexterity Hand grip force

DIAGNOSIS OF VIBRATION DISEASE FROM EXPOSURE TO LOCAL VIBRATION

The typical additional signs of vascular disorders1. 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 positive2. 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 of Hg. Then ask to lift hands up, in 2 min. to put hands down, take cuff off and write down time of hand’s reddening. In a norm the reddening begins in 1,5 - 2 sec. and passes in 15 sec. Lengthening of this time testifies to the spasm of vessels, and shortening - about their atony


DIAGNOSIS OF VIBRATION DISEASE FROM EXPOSURE TO LOCAL VIBRATION
The typical additional signs of vascular disorders4. 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 cyanosis, which arose up disappear slower, than the more expressed is a disorder of peripheral circulation of blood.

DIAGNOSIS OF VIBRATION DISEASE FROM EXPOSURE TO LOCAL VIBRATION

The typical additional signs of vascular disorders5. 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

CAPILLAROSCOPE

DIAGNOSTIC OF SENSORY DURING VIBRATION DISEASE

DIAGNOSTIC OF SENSORY DURING VIBRATION DISEASE

TREATMENT
Therapeutic interventions Pharmaceutical agents for the treatment of HAVS Calcium antagonists Alpha-adreno receptor antagonists Antifibrinolytics 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)

VIBRATION DISEASE FROM THE INFLUENCE OF GENERAL VIBRATION

SENSORY DECREMENT 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 systemobliterating endarteritisRaynaud's diseaseangina pectoris, arterial hypertension of ІІ -III stages,endocrine disease (diabetus mellitus)ulcer diseaseneuritis, polyneuritisstable hearing loss of any aetiology, otosclerosis chronic gynecological diseases

PREVENTION

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 identifying vibration sensitive individuals

CONTROLS

Buy lower vibration tools
A link to the European Hand Arm Vibration Database is in the Links and References at the end of this presentation
Tape existing handles with vibration dampening tape
Regularly maintain and balance hand tools
Use full fingered anti-vibration gloves
Suspend tools from tool balancers to reduce hand grip force

REMOTE CONTROL VIBRATORY PLATEOPERATOR VIBRATION EXPOSURE - ZERO

VIBRATION REDUCED BREAKER
Keep the moil point sharpBreak a little at a timeDon’t get jammedDon’t force anti-vibration handlesStop breaker before pulling out

MECHANISATION REMOVES THE RISKMACHINE-MOUNTED PICK REPLACES HAND-OPERATED BREAKERS

Thanks for attention!