PENYAKIT PARU AKIBAT

KERJA

dr. Sultan Buraena, MS, SpOk.

RSUP Dr. Wahidin Sudirohusodo/ FK. Univ
Hasanuddin
MAKASSAR

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 BATASAN

Penyakit Paru Akibat Kerja  peny/

kelainan paru yang disebabkan oleh
pemajanan faktor-faktor risisko di tempat
kerja  a.l. debu, gas, dan uap.

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 INTRODUCTION
The following case histories are quite
representative of the spectrum of
occupational respiratory disease that may
be encountered by :
general practitioner
chest physician
occupational physician
the doctor in the accident
emergency unit
the medical ward
 EPIDEMIOLOGY
 Statistics on occupational respiratory diseases
vary from country to country depending on the
type of industries, stage of industrialisation or
economic development, notification and
compensation system of industrial diseases,
research interests of doctors and institutions.
 In the industrialized countries, e.g. the United
Kingdom and Canada, occupational asthma is
the most common occupational respiratory
disorder.
 In the developing countries such as China,
silicosis is the leading occupational lung
disease.
 EPIDEMIOLOGY
Newer occupational respiratory diseases
such as occupational asthma and other
acute lung injuries are due to a variety of
chemicals, the list of which is continually
increasing.
the increase in manufacturing activity
the increasing use of chemicals
a greater awareness
 EPIDEMIOLOGY
The more traditional occupational lung
diseases such as as the silicosis and
asbestosis are on the decline use of silica
and asbestos is increasingly restricted or
controlled.
Today, occupational respiratory diseases
are still relevant as our workers are
exposed to a complex variety of
inhalable contaminants in the
workplace.
 Clinical tools useful in the
investigation of respiratory disorders :
History
Physical Examination
Chest X-Ray
Pulmonary Function Test
Methacholine/Histamine
Inhalational Testing
 HISTORY
 A complete history should include a careful
review of respiratory symptoms, the
smoking history, history of atopic and
allergies including family history and
occupational and environmental
exposures.
 Review of symptoms should include
questions on cough, sputum production,
shortness of breath, chest tightness,
wheezing, and chest pain.
 HISTORY
 For occupational asthma, it is particularly
useful to ask if the symptoms improve
during periods away from work, and
recur when back at work.
 For chronic diseases such as silicosis and
asbestosis, a detailed and accurate
occupational history starting from the very
first job is important to document possible
exposure to silica or asbestos. Both the
intensity and duration of exposure should
be documented useful to ask whether other
workers have been similarly affected.
 PHYSICAL EXAMINATION
 In most cases there is a relative absence of
physical signs :
A general observation of the patient may
reveal a patient who is dyspnoe at rest or
after performing a lung function test.
There may be clubbing of the digits in a
case of asbestosis, berylliosis or lung
cancer.
Auscultation of the lungs may reveal fine
crepitations at the lung bases of a
patient with asbestosis. There may be
wheezing and ronchi in a patient with work-
related asthma.
 CHEST X-RAY
 A chest X-ray is always useful in a worker
with chronic respiratory symptoms, e.g
cough, breathlessness to screen for
tuberculosis, other infections, or
malignancy.
 A full sized chest X-ray of good quality is
important, especially in the diagnosis of
early asbestosis or silicosis.
 The diagnosis of silicosis or asbestosis
should not be based on a single film, it is
usually based on at least two consistent
films several months a part
 CHEST X-RAY
 Comparison with the standard films for
pneumoconiosis, is very helpful when
looking for evidence of nodular or linear
profusions suggesting silicosis or
asbestosis.
 Hilar lymph node calcifications, i.e.
“eggshell calcifications” may be seen in
some cases of silicosis.
 Asbestos exposed workers may show
evidence of pleural thickening or
calcifications or effusions, e.g. blunting
of costo-phrenic angle.
 PULMONARY FUNCTION
TESTS
The evaluation of lung function provides
information on the functional status. It
helps determine the degree of fitness or
impairment.
The most basic of these tests are :
Forced Vital Capacity (FVC)
Forced Expiratory Volume in the first second
(FEV1)
the ratio of these two measurements
(FEV1/FVC)
 PULMONARY FUNCTION
TESTS
The FVC is the total volume of air which
can be forcefully expelled from the lungs
after a maximum inspiration.
The FEV1 is the volume of air expelled
during the first second of the manoeuvre.
The manoeuvre requires the patient to
start from total lung capacity (TLC) before
blowing out.
 PULMONARY FUNCTION
TESTS
 The test can be performed on a spirometer
in a physician’s consultation room or in the
lung function laboratory of a large hospital.
 The values of these tests differ between
males and females, and vary with age,
height and race.
 The individual results must be interpreted by
comparison with predicted normal values for
someone of the same sex, age, height, and
race.
 PULMONARY FUNCTION
TESTS
 A FVC or FEV1 which is 80% or more of the
predicted value is generally considered as
normal.
 The FEV1 is affected more than the FVC, and the
ratio of FEV1 to FVC, which is normally more
than 70 – 75%, is reduced. This is refferred to as
an obstructive defect.
 The obstructive defect in asthma can be
distinguished from that of chronic bronchitis or
emphysema by the immediate improvement in
FEV1 by 15 – 20% or more.
 PULMONARY FUNCTION
TESTS
Diseases which cause inflammation and
thickening of alveolar walls such as
fibrosing alveolitis, asbestosis, and
hypersensitivity pneumonitis cause
stiffening of the lungs with impairment
of gas transfer.
 PULMONARY FUNCTION
TESTS
 Increased stiffness of the lungs reduce the
volume of air which can be taken into the
rate at which air can be expelled.
 The FEV1/FVC ratio is often greater than
normal ( > 90% ), because FVC is reduced
to a greater degree than FEV1.
 The supranormal flow rates may be due to
the increased elastic recoil that characterises
interstitial lung disease. This is described as
a restrictive defect.
Measurement of forced exoiratory volume in one second, FEV1, and
forced vital capacity, FVC. In obstructive disease, such as asthma, the
FEV1 is reduced much more the FVC, giving a low FEV1/FVC%. In
restrictive disease such as pulmonary fibrosis, both the FEV1 and FVC are
reduced but characteristically, the FEV1/FVC% is normal or increased.
 METHACHOLINE/
HISTAMINE INHALATION
TESTING
 The presence and degree of non-specific
bronchial hyperreactivity can be
documented by measuring the
concentration or dose of histamine or
methacholine that causes a 20% fall in
the pretest FEV1.
 For the patient’s safety, the test is normally
done only when the FEV1 is at least 60% of
the predicted values.
 In the appropriate clinical setting, a positive
test is strongly suggestive of asthma.
 METHACHOLINE
CHALLENGE TEST
 KELAINAN
AKUT
KRONIK :
– P.P. INTERSTITIAL
– UDEMA PARU
– PENYAKIT PLEURA  ASBES
– BRONKITIS
– ASMA
– KARSINOMA BRONKUS
– PENYAKIT INFEKSI.
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 Peny. Paru interstitial
Asbes
Batu bara
Silika
Berylium
Jamur
Antigen burung (hepersensitif
pneumonitis)

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UDEMA PARU :
ASAP
NITROGEN, SO2
FOSGEN

BRONKITIS :
DEBU TEPUNG
DEBU BERAT
(PEKERJA TAMBANG BATU BARA)

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 ASMA :

BULU BINATANG
TOLUEN DIISOSIANAT
GARAM PLATINA
TEPUNG DAN DEBU KAPAS

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KARSINOMA BRONKUS

URANIUM
ASBES
KROMNIKEL
METIL ETER

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PENYAKIT INFEKSI :

ANTHRAKS
COCCODIOMYCOSIS
ACHOCOCCOSIS
PSITACHOSIS

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 DIAGNOSIS
ANAMNESIS
– RIWAYAT PEKERJAAN
– KELUHAN PENYAKIT
– RIWAYAT PENYAKIT
– RIWAYAT KEBIASAAN
PEM FISIK
– KEADAAN UMUM
– PEM PULMONOLOGIK
PEM PENUNJANG
– RUTIN & KHUSUS
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 RIWAYAT PEKERJAAN
CATAT PEKERJAAN TETAP DAN PART
TIME  KRONOLOGIS
IDENTIFIKASI BAHAN BERBAHAYA
DITEMPAT KERJA
HUBUNGAN ANTARA PAJANAN DAN
GEJALA :
– WAKTU ANTARA MULAI BEKERJA DAN GEJALA I
– URUT-URUTAN & PERKEMBANGAN GEJALA
– PERUBAHAN GEJALA PD WAKTU LIBUR

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 KELUHAN PENYAKIT
Batuk
Dahak  pagi/siang/ malam/terus-
menerus
Napas pendek
– Wkt jalan cepat
– Wkt berjalan 100m/1,5 km
Nyeri dada

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 RIWAYAT PENYAKIT
Batuk  lama, sifat, wkt batuk, bertambah
Dahak  lama, wkt, bertambah
Napas pendek  wkt terbangun 12 bln
terakhir
Mengi (wheezing)  kapan, disertai napas
pendek/ tidak.
Nyeri dada  kapan/ berapa lama
Penyakit lain  kecelakaan/ operasi dada,
ggn jantung, bronkitis, pneumoni, pleuritis,
tb paru, asma bronkial,ggn dada lain
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 RIWAYAT KEBIASAAN 
MEROKOK
jumlah batang rokok/ hari
Lama merokok
Cara isap rokok  dangkal, sedang,
dalam
Umur mulai merokok teratur
Jenis rokok  buatan pabrik/sendiri, ada
filter, tipe besar/kecil, ganti-ganti rokok,
kretek/putih.
kontuinitas
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PEMERIKSAAN PENUNJANG
Rutin
– Lab  darah, urin.
– Foto toraks  PA & lateral
– Spirometri
Khusus
– Uji allergi pd kulit
– Uji provokasi bronkus
– Sputum BTA, sitologi
– Bronkoskopi
– PA  biopsi
– Radiologi  tomogram, bronkografi,CT-scan.

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 REAKSI RESPIRASI AKUT 
TERHADAP GAS IRITAN
Pemajan konsentrasi tinggi gas irirtan 
iritasi sistim pernfasan bgn atas

Chemical pneumonitis, udema paru,

kadang kematian bila pemejanan massif.
Kematian  Akibat dari brochiolitis
obliterans 4 – 6 minggu kemudian
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 BAHAN PENYEBAB
Chlorin, ammonia, sulphur dioxida, ozone,
nitrogen oksida
Gamb klinis 
– udema epiglottic, iritsi mata, hidung &
tenggorokan
– Dosis tinggi  bronchospasma
– Chest x-ray  normal  kecuali udema paru
– Broncho-constriction

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 PENATALAKSANAAN
Penderita dipindahkan dan oksigen
diberikan bila tersedia.
Rawat inap  utk menghindari komplikasi
Pengobatan suppotif yg penting :
– Menjamin cukup ventlasi,
– Steroid, bronchodilatator,diuretik

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 REAKSI SISTEMIK
Penyebab  metal fume, polymer fumes
& debu organik
Gamb klinis
– Demam akut + myalgia,
– Menggigil, sakit kepala,
– Batuk Chest discomfort, dispneu
– Berkeringat, mual-muntah, kolik abd.

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Diagnosis
Gamb klinis
Gejala berhubungan dg pajanan khusus
Polymorph leukositosis
Foto dada  normal
Tes fungsi paru  obstruksi ringan tapi
biasanya normal

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Penatalaksanaan

Tdk ada pengobatan khusus

Istirahat 1 hari  perbaikan.
Komplikasi  pneumonitis & udema paru.

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 PNEUMOKONIOSIS
Paru yang berdebu
Keadaan yang menyebabkan perubahan
menetap pada arsitektur paru setelah
menghirup debu.
Debu :
– Silika(atau kuarsa)
– Batu bara, dan
– asbes

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 SILIKOSIS
Terjadi setelah menghirup silika bebas :
– Penghancuran batu, pertambangan,
pembuatan terowongan (tambang emas)
– Penggerindaan, Penyemprotan pasir
– Pembuatan gelas, pemotongan & pengukiran
batu,
– Pengecoran & industri keramik.

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4 Jenis silikosis
Noduler  lesi hialin dan kolagen paru
Fibrosis debu campuran  lesi fibrotik tdk
beraturan
Diatomik  mirip alveolitis fibrosans
Akut  lipoproteinosis alveoli.

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Penatalaksanaan

Simptomatis
Infeksi tb  diobati cepat
Penyakit mungkin msh berlangsung
walaupun penderita tidak lagi terpajan.

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 BISSINOSIS
Dianggap sejenis asma kerja  > rumit
Debu kapas  sesak napas akut + batuk
+ obstruksi sal napas yg reversible.
Masa inkubasi 5 tahun atau lebih
Gejala  hari pertama minggu pertama 
mereda kambuh lg bbrp hari pada
minggu selanjutnya`
Masuk kerja hr senin (perasaan hari
senin) sesak siang  sore redah
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Diagnosis
Dini  perasaan hari senin  Monday
fever
Pem klinis, lab & ro  tdk ada kelainan
Lanjut  bronchitis khronis dan
emphysema (tdk khas) + perasaan hari
senin
Cacat paru  bekerja tdk normal lagi

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DERAJAT BERATNYA PENYAKIT
½  Kdg rasa berat/ sempit di dada hari
pertama msk kerja
1  Keluhan rasa berat dd + sesak napas
hr I msk kerja
2  derajat I + hari-hari lain
3  derajat 2 + ggn paru menetap

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Pencegahan/pengendalian
Ketatarumah tanggan yang baik  pabrik
tekstil
Pembersihan mesin  pompa hampa
udara
Ventilasi umum  hisap
Pem kes sebelum kerja + uji fungsi paru
Pem kes berkala
Pekerja sakit  dipindahkan.
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 ASBESTOSIS
Fibrosis interstitial khronis dari parenchym
paru disebabkan karena menghirup debu
asbes.
Terpajan pada pekerja: pengolahan
abses, penenunan & pemintalan asbes,
reparasi tekstil, penggunaan asbes pd
pembangunan,dll
Merangsang fibrosis yg berat dan
irriversibel dlm jaringan tubuh.

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Gamb klinis
Kelainan paru diffus + penebalan pleura +
ephysema
Sesak napas, batuk + banyak riak
Cyanotis, pelebaran ujung-2 jari
Krepitasi halus pd dasar paru 
auskultasi
Ludah  ada kelompok-2 badan asbestos
Ro  ground glass appearance
Batas jantung & diaphragma  tdk jelas 49
Pengendalian
Kadar debu diudara diturunkan.
Pertambangan asbes  basah
Industri tekstil  ventilasi setempat
APD
Penyuluhan

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 ASMA
Sebab  berbagai jenis debu  reaksi
segera (bbrp menit kemudian) & tipe
lambat (setelah 4 – 24 jam)
2-15% dari seluruh asma.
Pengobatan  penderita pindah,
pengobatan non-spesifik.

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Allergan
Gabah, tepung, debu tembakau
Kumbang, kerang, kecoa, kutu padi.
Tikus & mencit di lab
Bulu burung, amuba, jamur
Aneka jenis kayu, logam & garamnya
Formalin dll

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Pengendalian
Higene yang ketat di tpt kerja.
Substitusi bahan
APD
Mengenali pekerja yang berisisko
Pem kesehatan berkala

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Penyebab dan mekanisme asma
Mekanisme allergi :
– Hair, dender, urine animal/insect, bird 
animal handlers, veterinaries laboratory
workers, poultry breeders
– fish
Mek Farmakologis
Mek irritasi
Mek mungkin allergi

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 BATUBARA
Riwayat terpapar debu batubara
Bekerja minimal 10 thn
Kelainan foto toraks
Simple coal worker’s pneumokoniosis  tdk ada
gejala, jarang sesak napas (obstruksi khronik),
bercak kecil pd foto, tdk ada hub kel rad dan faal
paru
Complicated pneumokoniosis (fibrosis massif
progressif)  bayangan > 1 cm + ggn respirasi
berat + proses berlanjut tanpa paparan lg

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 FITNESS TO WORK
Penyebab utama ketidk mampuan 
chronic bronchitis, emphysema & asthma
Jarang  pulmonary fibrosis 
keterbatasan paru memenuhi kebutuhan
kegiatan fisik
Dokter  kemampuan kerja pekerja dan
pekerjaan yg cocok.

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 PENILAIAN PENDERITA
Penderita dlm keadan stabil  tdk dlm
keadaan sakit dan minum obat
Derajat ketidak mampuan paru  FEV1,
FVC
60-80%  mild impairment
50-60%  moderate impairment
< 50%  severe impairment

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 PENILAIAN PEKERJAAN &
KONDISI
Kondisi fisik T.K.  komponen ada hub
kemampuan indvidu pekerja  lifting,
carrying, walking, upstairs
Istirahat dlm pekerjaan, pemeliharaan alat,
menggunakan respirator?
Tempat jg di nilai  paparan  debu,
fume, gas

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 PERTIMBANGAN KHUSUS
Pekerja alleri khusus & hipersensitif 
dipindahkan  mis asthma
Penyakit respirasi progressif  Kapasitas
kerja terbatas  secara periodik diperiksa
Merokok dihentikan

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