PNEUMOCONIOSIS

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PNEUMOCONIOSIS

• Conf. Dr. Brandusa Constantin

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• Definition "Pneumoconiosis is the accumulation
  of mineral dust in the lung and the tissue
  reaction to its presence".
• Classification
• Collagenous pneumoconiosis is characterized by
• - permanent alteration or destruction of alveolar
  architecture
• - collagenous stromal reaction of moderate to
  maximal degree
• - permanent scarring of lung.
• Examples silicosis, asbestosis.

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• Complicated coalworkers' pneumoconiosis or
  progressive massive fibrosis (PMF) is an altered
  tissue response to a relatively non-fibrogenic
  dust.
• Non-collagenous pneumoconiosis is caused by a non
  fibrogenic dust ("inert" dust) and has the
  following characteristics
• - the alveolar architecture remains intact
• - the stromal reaction is minimal and consists
  mainly of reticulin fibres
• - the lesion is potentially reversible examples
  are those caused by pure dusts of barium sulphate
  (barytosis), kaolinite, titanium dioxide, ferric
  oxide, glass
• - iron dust if inhaled in sufficient quantities
  can lead to pneumoconiosis - known as siderosis.
  The disease is seen in metal polishes,
  arc-welders, but above all among iron mines. In
  some iron mines, the presence of free silica
  leads to mixed-dust pneumoconiosis. Siderosis is
  observed after long exposure 15-25 years. The
  radiological appearance of siderosis is discrete,
  we may find punctiform images, rarely
  micronodular and never macronodular or
  pseudotumoral after exposure has ceased, the
  images are seen to precede somewhat in the course
  of the years.

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SILICOSIS

• Silicosis is a pulmonary fibrosis caused by the
  inhalation of dust containing free silica.
• It is the most common and severe of all
  pneumoconiosis.
• Silicosis remains a difficult problem for the
  entire world.

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Etiology

• Silicosis is caused by the inhalation of free
  crystalline silica (SiO2).
• In nature, free silica is found in a variety of
  forms, the most important and widespread being
  quartz. Even in its normal state quartz is highly
  silicogenic but, when heated to temperatures in
  excess of 100o C it is converted to, its
  allotropic forms, trydimite and cristobalit,
  which are even more pathogenic.

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• The silicosis hazard is encountered in a wide
  variety of occupations
• underground mining and tunneling in
  quartz-bearing rock
• extraction and cutting of quartzite, granite and
  slate
• manufacture of refractory materials and silicous
  abrasives
• foundry operations sand preparation,
  knocking-out, fettling and sand-blasting).

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• The level of risk depends on 3 factors
• - concentration of dust in the atmosphere
• - the percentage of free silica in the dust
• - the exposure time.
• The dangerous free silica particles are those
  with a diameter of less than 3 ?m called
  "respirable fraction".
• The retention maximal in the alveoli is for
  particles with a diameter of 1-2 ?m the
  retention break down for particles of less than 1
  ?m and it is null for particles of 0.3-0.5 ?m
  that have a Brownian movement. For smaller
  particles of less than 025 ?m, the retention
  grows and become 100 through the diffusion
  mechanism.
• The retention and absorption of free silica
  particles depend to the integrity of the
  mechanisms of elimination of dust - out of
  alveoli.

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Pathogenie

• Whereas the aetiology of silicosis is well
  defined, its pathogenesis still has to be
  elucidated. There are many hypothesis, but the
  immunological theory by Pernis and Vigliani is
  recognised being the best.
• the free silica particles are phagocytised by the
  macrophages.
• the death of macrophages release, arise the
  proliferation of fibroblasts and collagenous
  fibres
• the plasma cells proliferation and gamma globulin
  synthesis. It is a specific antibody autoimmune
  response to tissue antigens (the rest of protein
  macrophages become "non self") or a heteroimmune
  response to different antigens arrived to the
  interstitial with macrophages.

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Pathology

• The silicotic nodule has an unmistakable
  histological appearance, being rounded. The
  centre is composed of fibro-hyaline tissue either
  whorled or resembling a ball of wool, and
  sometimes aggregated to a homogenous form. The
  rim consists of a cellular halo, often clearly
  delimited from the hyaline centre, that contains,
  in varying proportions, reticular fibres,
  macrophages, fibroblasts and immunocytes (plasma
  cells and lymphocytes) at varying stages of
  maturity. The cellular halo may be very large,
  the larger the halo, the more active, that is
  progressive, the lesion sclero-hyaline nodules
  with virtually no cell haloes can be regarded as
  inactive.

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• The nodules may aggregate to form round masses
  ranging from a few millimetres to 1 cm in
  diameter in more serious cases a number of
  nodules coalesce or form large hyaline masses.
  The coalescing of several nodules is almost
  always caused by additional factors, of which
  infection, often tubercular, or rheumatoid factor
  seem to be the most important.
• The pulmonary parenchyma between the aggregated
  silicotic nodules and between the silicotic
  masses invariably displays a high degree of
  emphysema.

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• Symptoms at the beginning of this century (in
  Romania at 1950-1960 years), fatal cases of
  silicosis with a rapid evolution (1-3 years)
  so-called "acute silicosis" were not uncommon
  among workers who inhaled enormous quantities of
  dust with a high quartz content (for example the
  mining Lesu-Ursului with 90-96 silica free in
  atmosphere).
• Now, this rapidly evolving form has been
  replaced by slowly developing silicosis (12-15-20
  years or more). But still exist the case with
  small exposure - 5-7years, that occurs especially
  in foundry.
• The symptoms are untypical.
• The first symptom of silicosis is dyspnoea on
  exertion. In serious cases, the dyspnoea occurs
  even on very slight exertion or when the patient
  is at rest. Cough with sputum is an indication of
  bronchitis and chronic bronchitis is frequently
  associated with advances silicosis.

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Complications

• Pulmonary tuberculosis is, even today, still the
  cause of death in a quarter of cases and is the
  most frequent complication. It has recently been
  proved that tubercle bacilli grow and multiply
  far more actively in macrophages that have
  phagocytised silica particles than in those that
  have not done so, perhaps because the former have
  suffered a loss of vitality and are no longer
  capable of destroying the tubercle bacilli.
• Respiratory insufficiency is largely due to
  massive emphysematous and fibrotic changes. These
  are sometimes accompanied by chronic obstructive
  pulmonary disease resulting by the destruction of
  a large part of the vascular bed and spasm of the
  pulmonary capillaries brought about by hypoxemia.
• Acute broncho-pulmonary infection is often
  epiphenomenal of chronic bronchitis associated
  with advanced silicosis.

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• Diagnosis is based on
• medical and occupational history,
• clinical examination,
• radiology and
• respiratory tests-function.
• The radiographic examination must be carried out
  using a suitable technique.

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Differential diagnosis

• Tuberculosis especially in its disseminated
  miliary form.
• Endogenous hemosiderosis due to mitral stenosis
• Boeck's sarcoidosis, especially in nodular form.
• Some forms of pulmonary metastasis of carcinoma
• Idiopathic interstitial pulmonary fibrosis
  (seaman Rich type)
• Some collagen diseases (scleroderma rheumatoid
  arthritis).

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• The radiographs are classified in 4 level of
  quality
• 1. Good 2. Acceptable 3. Mediocre 4.
  Unacceptable.
• It is accompanied by a new set of 22 standard
  radiographs selected after international trials.
  It is mandatory to read the film comparatively
  with standard films.
• The short classification
• - film quality
• - small opacities rounded
• Profusion. Category
• 0 - absent
• 1 - small opacities present, but relatively few
  in number
• 2 - small opacities - numerous
• 3 - small opacities - very numerous
• Type
• p - rounded opacities up to about 1.5 mm diameter
• q - rounded opacities exceeding about 1.4 mm and
  up to about 3 mm diameter
• r - rounded opacities exceeding about 3 mm and
  up to about 10 mm diameter

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• Small opacities irregular
• Profusion. Category 1, 2, 3
• Type
• s - fine irregular or linear opacities
• t - medium irregular opacities
• u - coarse (blotchy) opacities
• Large opacities
• A - an opacity with greatest diameter between 1
  cm and 5 cm or several such opacities the sum of
  whose greatest diameters does not exceed 5 cm
• B - one or more larger or more numerous than
  thosse in category A, whose combined area
  does not exceed one-third of the area of the
  right lung
• C - one or more large third of the area of the
  right lung

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Obligatory symbols

• Plc - pleural calcification
• pl - pleural thickening
• ax - suspect coalescence of small rounded
  opacities
• bu - bullae
• ca - suspect cancer of lung or pleura
• cn - calcification in small opacities
• co - abnormality of cardiac size of shape
• cp - suspect COPD
• cv - cavity
• di - marked distortion of the intrathoracic
  organs
• ef - epanchement pleural
• em - marked emphysema
• es - eggshell calcifications
• fr - fracture of rim fracture
• tu - marked enlargement of hilar shadows
• ho - honey comb lung
• id - diaphragm ill defined
• kl - Kerley line
• od - other significant disease

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The stages in silicosis

• I 1p, 1q, 1r stage
• I/II 2p, 2q, 2r stage
• II 3p, 3q, 3r stage
• II/III 3p, 3q, 3r ax
• III A, B, C

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Treatment

• Etiologic interruption of the occupational
  exposure to free crystalline SiO2
• Pathogenic it does not exist because the
  ethiopathogenical mechanism is not known

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• Symptomatic
• bronchodilators
• expectorants
• respiratory gymnastics
• respiratory infection prevention
• chemoprophylaxis with HIN 15 mg/body,6 months.
• Silico-tuberculosis treatment lasts at least 3
  years.
• Complications (silico-tuberculosis, chronic
  obstructive pulmonary disease) treatment
• Aerosols
• Vitamins

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