BENIGN PLEURAL DISEASE DO

TO ASBEST EXPOSURE

Feni Fitriani Taufik

Department of Pulmonology and Respiratory Medicine
Faculty of Medicine University of Indonesia
Persahabatan Hospital - Jakarta
 ASBES, KANKER PARU & MESOTELIOMA

 Asbes dibagi atas 2 kelompok besar :

serpentine dan amphibole

 Efek terhadap kesehatan :

 Asbestosis, kanker paru dan mesotelioma
 Reaksi pleura jinak lain seperti
efusi pleura, plak pleura (fibrosis lokal pada pleura
parietal) , fibrosis difus serta rounded atelectasis.
 Asbestos

Serpentine group
Chrysotile (white
asbestos)

Amphibole group
amosite (brown
asbestos), crocidolite
(blue asbestos),
anthophyllite, actinolite,
tremolite
Risiko terpajan asbes
 Sheet metal workers  Automotive and other
 Pipe fitters repair shops
 Shipyards (all jobs)
 Custodian/Handyman
 Asbestos plant workers
 Hotels
 Steamfitters
 Telephone (installation/repair)  Asbestos
 Boiler Makers workers/Insulators/Laggers
 Hospitals  Steel Workers (plants and
 Railroad workers construction)
 Laborers  Firefighters
 Glass factory workers
 Heating and Air Conditioning
 Chemical Plants
 Asbestos-related pleuro-
pulmonary diseases
Non malignant respiratory diseases
• Benign pleural disease
- pleural plaques (parietal pleura)
- pleural effusion
- diffuse pleural thickening (visceral pleura)
• Asbestosis

Malignant respiratory diseases

• Lung cancer
• Mesothelioma

Limits exposure : 0,1 fiber/ cm3 (USA)

Asbestos-related Pleural Disease

 Benign asbestos pleural effusion (10-20 year

latency)
 Pleural plaques (20-30 year after latency)
 Diffuse pleural fibrosis
 Rounded atelectasis
 Mesothelioma (30-40 year latency)
3 respons pleura terhadap inhalasi asbes
 Fibrosis parenkim paru  septal lines,
intralobular line dan honeycomb
 Fibrosis yang melibatkan pleura viseral 
Diffuse pleural thickening
 Fibrosis pleura parietal  Pleural plaques
Respons ini dipengaruhi oleh
 Tipe serat asbes
 Dosis kumulatif
 Migrasi serat ke pleura
 Periode laten
 Faktor individu
Patogenesis

 Teori serat asbes migrasi ke rongga pleura  kontroversi

 Kerusakan pleura : akibat langsung fiber dalam rongga
pleura atau akibat tidak langsung sitokin atau toksin
metabolik yang dilepaskan parenkim paru akibat deposit
serat asbes
 Serat asbes terutama ditemukan di klj limfe dan pleural
plaques daripada parenkim  bersihan melalui sal limfe
 Inhalasi asbes  akumulasi di limfatik  blockade 
backflow ke saluran limfe di pleura parietal
 Ditemukan distribusi serat asbes yang heterogen di pleura
Patofisiologi

 Bersihan mukosilier  >> serat dibersihkan

 Sedikit serat sampai ke interstitium
 Overload effect  inisiasi  sel inflamasi 
fibrosis parenkim
 Interstitium  serat msk aliran limfatik 
terkonsentrat di pleura parietal (melewati
ruang interpleural )
 Dosis rendah, pajanan intermitten pleural
plaques
 Dosis besar Asbestosis
 Antara pleural plaques dan Asbestosis 
Diffuse pleural thickening & rounded
atelectasis
 Amphibole (amosite, crocidolite, tremolite) :
efek fibrosis paru > chrysotile
 Asbes diinjeksi Intra pleura makrofag
pleura >>  pleural plaque
 Pleural plaque : < 20 tahun
 Pleural effusion : 1 tahun  Diffuse pleural
thickening
PLEURAL PLAQUES
PLEURAL PLAQUES

 Paling sering ditemukan

 Setelah pajanan > 20 tahun
 50% pekerja terpajan asbes
 Low dose exposure
 Intermittent
 Ditemukan secara kebetulan
PLEURAL PLAQUES

 Discrete, dense, pleural

linear structure which
may have a smooth or
nodular inner surface
Penelitian di Scotland (autopsi)
 Pekerja galangan kapal (shipyards) :
 plaques pada 51.2% laki-laki usia > 70 tahun
 Pajanan extremely slow rate  plaques
 Pleural and diaphragmatic
plaques.
 Perubahan ukuran dan
proses kalsifikasi terjadi
sangat lambat.
.
 CT scan (pasien berbeda)

 Penebalan pleura dan

kalsifikasi di berbagai sisi
(kiri bawah) dan diafragma
(kanan bawah)
 Edge
Pajanan asbes pada 425 pekerja : risiko
kematian kanker paru 2x lipat bila terdapat
plaque
 Harber
Tidak ada hubungan plaque, asbes dan
kanker pada 1500 pekerja asbes (follow up 4
thn)
Left: Punctate calcification in a chest wall plaque.
Right: Serrated edge of a chest wall plaque
PLEURAL EFFUSION
PLEURAL EFFUSION

 paling cepat 1 tahun

 Akut : demam, pleuritis, nyeri
 Asimptomatik dan membaik spontan
 Unilateral , sering di kiri
 Waktu lama : pada sisi berlawanan
 Eksudat
 Sequele: diffuse pleural thickening, rounded
atelectasis dan parenchimal band
Kriteria spesifik

 Riwayat terpajan asbes

 Eliminasi penyebab efusi lain
 Keganasan tidak ditemukan 3 thn setelah
onset efusi muncul
DIFFUSE PLEURAL THICKENING
Diffuse pleural thickening

 Extensive fibrosis of the visceral pleura with

areas of adhesion with the parietal pleura and
consequent obliteration of the pleural space
 margins are ill defined and it frequently
involves the costophrenic angles, apices, and
interlobar fissures
Diffuse Pleural thickening

Keluhan
 Sesak saat beraktivitas
 Nyeri dada (kronik dan berat)
 Progresif  Restriksi terutama bila sudut
costofrenikus mengalami obliterasi
 Gagal napas hiperkapnik
 Home NIV
 Bedah ?
Diffuse pleural thickening

 Diawali dengan Benign pleural effusion

 Tidak spesifik terhadap pajanan asbes

 Ambang batas serat asbes pada

pasien DPT berada antara ambang
pleural plaque dan asbestosis

 Biasanya unilateral
 Diffuse pleural thickening

Epidemiology

 Data  minimal
 Sering diragukan dg pleural plaques
 Frekuensi lebih jarang daripada plural plaques
Studi kohort 18.943 pekerja konstruksi, shipyard and asbestos
industry (Koskinen, 1998)
- pleural plaques : 27 %
- DPT : 7%

Klinis

 Sering berhubungan dengan nyeri dada

 Gangguan fungsi paru : Restriktif

Left, A: Diffuse pleural thickening or pleural fibrosis. Note the costophrenic angle blunting,
the interlobar pleural thickening, and the extension of the pleural fibrosis into the apex on the left side.
Center, B: Very extensive pleural plaques with calcification of the pleura on the lateral chest wall, in the
minor fissure and on the diaphragm. The costophrenic angle is spared. Right, C: Close-up view of the
lower half of the right hemithorax of center, B.
Diffuse pleural thickening

Contagious pleural
thickening
 more than 5cm wide,
 more than 8 cm in
craniocaudal extent
 and more than 3 cm
thick
Diffuse pleural thickening
ROUNDED ATELECTASIS
 folded lung,
 Blesovsky syndrome,
 Gambaran radiologis: the comet tail sign.
 Frekuensi jarang
 Dd/ Tumor paru perifer
 Rounded atelectasis
 Lokasi di paru dan berhubungan dg Diffuse Pleural Thickening

 Bentuk kolaps paru yang tidak spesifik

 Kadang terlihat pada foto toraks PA

 Seringkali berhubungan dengan parenchymal bands

 4 tanda utama :
-massa bulat atau oval yg berkontak dg permukaan pleura
- penebalan pleura
-Struktur bronkovaskular melingkupi bagian dalam massa
(« comet tail »)
-hilangnya volume paru
Formation of rounded atelectasis. A possible mechanism whereby this occurs is a low-grade
inflammatory pleural reaction at one site, fusion of the two pleural surfaces with progressive thickening
at the fused region. This results in compression of the underlying lung and bronchial occlusion that
renders the underlying lung airless. The bronchus and adjacent blood vessels contribute the “tail” or
comet sign of this unusual form of pleural fibrosis.
Rounded atelectasis

 Mass related to an area of

pleural thickening
associated with a partial
interposition of lung
between pleura and mass,
and with a visible “comet
tail” of vessels and bronchi
sweping into the lateral or
medial and lateral aspect of
the mass
 Rounded
atelectasis
 Rounded
atelectasis
 Rounded
atelectasis
Terima Kasih