Transcript PNEUMOCONIOSIS - UMF IASI 2015

Conf. Dr. Brandusa Constantin
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.
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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.
 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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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 quartzbearing 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).
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".
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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.
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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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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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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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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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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
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- 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
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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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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
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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
pi - pleural thickening of
interlobare scissure of
mediastin
px - pneumothorax
rp - rheumatoid
pneumoconiosis
tb - tuberculosis
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I/II
II
II/III
III
1p, 1q, 1r stage
2p, 2q, 2r stage
3p, 3q, 3r stage
3p, 3q, 3r ax
A, B, C
 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:
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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