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Internal medicine department № 2 Pneumoconiosis. 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, 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 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, 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: ØSedimentation ØInertial impaction ØDiffusion ØInterception ØElectrostatic 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: Ø round opacities: p (<1. 5 mm) q (1. 5 – 3 mm) r (3 - 10 mm) Ø Irregular opacities: s (<1. 5 mm) t (1. 5 – 3 mm) u (3 – 10 mm)
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 ØSilica is silicon dioxide, the oxide of silicon, chemical formula Si. O 2 ØSi. O 2 is the most abundant mineral on earth; comprises large part of granite, sandstone and slate. ØSilicosis 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. ØSilicosis 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. ØThere 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 - 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 18 th 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, collagenvascular disease, etc. ) Can usually make right diagnosis with detailed history (occupational & medical) or, rarely, a lung biopsy.
Treatment Ø Ø Ø 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) Ø Ø Ø 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
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
Complications Bronchogenic Mesothelioma carcinoma
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) 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 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 Ø Slow growth, benign character of current, active phagocytosis, saved lung protective mechanism. Ø Causes chronic bronchitis, lung emphysema Ø Radiological investigation – interstitial or interstitial nodular fibrosis of the lung.
Symptoms and Diagnosis Simple CWP: Ø It is said to exist in the presence of radiological opacities < 1 cm in diameter. Ø It is benign disease if no complications. Ø Cough, expectoration and dyspnea are frequently present. Ø Slight decrease in FVC and FEV 1/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): Ø Is diagnosed when large opacity of 1 cm or more in diameter is observed in the chest X-ray. Ø Pathologically it is characterized by large masses of black colored fibrous tissue. Ø The large lesions may cavitate as a result of ischemic necrosis or infection (T. B) Ø The severe stages of PMF cause cough and often disabling shortness of breath. Ø Pulmonary function test reveals decreased FVC, FEV 1/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 Ø Byssinosis is a narrowing of the airways caused by inhaling cotton, flax, or hemp particles. Ø 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 (also referred to as “extrinsic allergic alveolitis”) is an immunologicinduced, non-Ig. E 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 Ø Reversible airflow obstruction caused by workplace exposures Ø With latency period (sensitization) Ø Without latency period (irritant) Ø Causes: a broad group of vegetable, animal products, chemicals, metalsreferred 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 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 -40 s - Cases of white finger were identified studies in fettlers, riveters, boot and shoe industry workers and users of electrical powered rotating tools 1950 s - 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? v. Frequency v. Amplitude v. 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 transmitted through the seat or feet (known as whole-body vibration or WBV) 73
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 develops.
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, pain and
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, coronary), (local and general) in the metabolic endocrine disorders terminal stage
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 91
VIBRATION WHAT SORT OF TOOLS AND EQUIPMENT CAN CAUSE VIBRATION INJURY? v Chainsaws v Concrete breakers/road drills v Hammer drills v Hand-held grinders v Hand-held sanders v Nut runners v Pedestal grinders v Power hammers and chisels v Powered lawnmowers v Riveting hammers and bolsters v Strimmers/brush cutters v Swaging machines. 92
HAND ARM VIBRATION High vibration Moderate vibration v impact wrenches vchain saws 93 v percussive tools • jack hammers • scalers • riveting or chipping hammers v grinders v sanders v jig saws Cons ultne t Limi ted ©
HAND ARM VIBRATION - CAUSES & EFFECTS ØNeurological component ØVascular component ØMuscular 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: v. Blood circulatory system (e. g. vibration white finger) v. Sensory nerves v. Muscles
CLASSIFICATION І — initial manifestations: Ø 1) Peripheral angiodystonic syndrome of the upper extremities, including fingers with rare angiospasm; Ø 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: Øa) frequent fingers angiospasm; Øb) persistent vegetative and trophic disorders on the hands; Øc) 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 1 v Mild 2 v Moderate 3 v Severe Occasional attacks affecting only the tips of one or more fingers Occasional attacks affecting distal and middle (rarely also proximal) phalanges of one or more fingers Frequent attacks affecting all phalanges of most fingers
SENSORINEURAL COMPONENT Stage Grade 0 Description Vibration-exposed but no symptoms 1 sn Mild Intermittent numbness with or without tingling 2 sn Moderate Intermittent or persistent numbness, reduced sensory perception 3 sn 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 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
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 ØІ — initial manifestation: Ø 1) angiodystonic syndrome (cerebral or peripheral); Ø 2) neuro-vestibular syndrome; Ø 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: Øa) polyradiculoneuropathy syndrome; Øb) secondary lumbosacral radicular syndrome (due to degenerative disc disease of the lumbar spine); Øc) with functional disorders of the nervous system (neurasthenia syndrome).
WHOLE BODY VIBRATION III - pronounced symptoms: Ø 1) sensorimotor polyneuropathy syndrome; Ø 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 Hand Arm tools 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 v. Keep the moil point sharp v. Break a little at a time v. Don’t get jammed v. Don’t force antivibration handles v. Stop breaker before pulling out
MECHANISATION REMOVES THE RISK MACHINE-MOUNTED PICK REPLACES HAND-OPERATED BREAKERS
Thanks for attention!