PANITIA PELATIHAN HIPERKES DAN KESELAMATAN KERJA BAGI DOKTER IKATAN ALUMNI UNIVERSITAS INDONESIA PASCA SARJANA KEDOKTERAN KERJA D E N G A N

PANITIA PELATIHAN HIPERKES DAN KESELAMATAN KERJA BAGI DOKTER IKATAN ALUMNI UNIVERSITAS INDONESIA PASCA SARJANA KEDOKTERAN KERJA DENGAN

BALAI HIPERKES DAN KESELAMATAN KERJA DKI JAKARTA DINAS TENAGA KERJA DAN TRANSMIGRASI PEMERINTAH PROPINSI DAERAH KHUSUS IBUKOTA JAKARTA JL. JENDRAL AHMAD YANI 69-70 JAKARTA 10510. PHONE: (+62).21.4209820. FAX: (+62) 21 4240284

Dr. S. Widodo PELATIHAN HIPERKES & KESELAMATAN KERJA BAGI DOKTER DAN PERAWAT JAKARTA, 10 September 2007

Cakupan • Definisi • Diagnosa • Cacat dan penaksiran • Kasus kasus yang banyak terjadi: Debu dan Paru, Dermatosis, Mata. • Sistem pelaporan

DEFINISI

Penyakit yang disebabkan oleh Pekerjaan dan/atau lingkungan kerja (Permen.Nakerstrans No. PER.01/MEN/1981)

Penyakit Yang Timbul Karena Hubungan Kerja. (Keppres No. 22 Th. 1993)

Occupational Disease = Maladie Proffesionelle =

PENYAKIT AKIBAT KERJA

DUA ASPEK P A K Pencegahan Penyakit Akibat Kerja (UU No. 1 Th. 1970 dan peraturan pelaksanaannya)

Jaminan Kecelakaan Kerja (UU No. 3 Th. 1992)

DATA KECELAKAAN KERJA

DATA KECELAKAAN KERJA (Rata Rata per Tahun)

¾ 100.000 kecelakaan kerja; ¾ Kerugian Rp. 100 – 200 milyar; ¾ Meninggal : 1500 - 2000 orang; ¾ 70 juta hari kerja hilang; ¾ 500 juta jam kerja hilang

(khusus tahun 2000 )

DATA PENYAKIT AKIBAT KERJA

TEMUAN PENELITIAN

P.A.K.

Tahun

Peneliti

1964

Suma’mur & Karimuddin

Diperiksa 111 dari 1082 tenaga kerja pemintalan

1% bisinosis dan 40% keluhan pernafasan

Karimuddin & Suma’mur

976 tenaga kerja pertambangan

0.5% silikosis (murni atau campuran TBC paru)

1968

Suma’mur

48 dari 167 penenun

8,3% mill fever

1971

Suma’mur

20 tenaga kerja blowers dan carders

10% bronkhitis kronis; 15% kelainan paru lain

1974

Suma’mur

1559 tenaga kerja pabrik rokok

4,7% bronkhitis kronis

457 tenaga kerja pabrik beras

5% bronkhitis kronis

54 pekerja pompa bensin

16,7% dermatosis akibat kerja 16,7% dermatosis akibat kerja; 47,2% iritasi kulit; 38,9% kerusakan lapisan tanduk kulit

1978/ 1979

Jumlah sampel dan populasi

Suma’mur & Susianti Wenas

36 pengecer kerosen

Temuan

Tahun 1984 1984/ 1985 1984/ 1985 1986 1989/ 1990 1989/ 1990

1992/ 1993 1993

Peneliti

Jumlah sampel dan populasi

Suma’mur

518 dari 982 tenaga kerja pabrik aki Suma’mur, 113 penyemprot hama Tjepi Aleuwi & industri perkayuan Tjipto Pranowo Suma’mur, 99 petani penyemprot Bunandir & hama Tjipto Pranowo Sugeng Budiono 347 tenaga kerja terpapar pestisida Karnen Garna Baratawidjaja

250 tenaga kerja pabrik tekstil; 1375 tenaga kerja pabrik tekstil Retno Widowati 230 tenaga kerja pabrik cat Subaryo 80 tenaga kerja bengkel pengecatan mobil 4000 tenaga kerja pabrik semen 200 tenaga kerja bangunan Eddy Charles 425 tenaga kerja terpapar kepada debu; 518 kepada asbes Santoso 372 tenaga kerja batik tradisional

Temuan

7,9% timah hitam darah 800 mikrogram/L atau lebih 48,7%% kadar kolin-esterase 62,5% atau kurang 6% penurunan kolin-esterase darah 35,7% keracunan ringan; 20,2% keracunan sedang; 3,4% keracunan berat 2,8% obstruksi paru akut; 3,2% obstruksi paru kronis 24,8% bisinosis; obstruksi paru akut 1,7% dan 0,2% kronis 0,9% dermatosis akibat kerja 2,5% dermatosis akibat kerja 0,2% dermatosis akibat kerja 3% dermatosis akibat kerja 10,8% restriksi paru; 2% obstruksi paru 11,8% paru obstruktif; 7,8% restriktif dan 1,1% campuran

Hasil penelitian kronologis dari tahun 1964 sampai dengan 1993 (oleh: Suma’mur, Karimudin, Susianti Wenas, Tjepy F. Aleuwi, Tjipto Pranowo, Bunandir, Sugeng Budiono, Karnen Garna Baratawidjaja, Retno Widowati Soebaryo, Santoso, dll) dan pada tahun tahun selanjutnya, mengindikasikan bahwa prevalensi penyakit akibat kerja cukup tinggi.

Dari banyak temuan penelitian tersebut diatas dapat disimpulkan bahwa Penyakit Akibat Kerja memang ada dan diderita oleh tenaga kerja dan sering banyak jumlahnya!

Penyakit Akibat Kerja : Data Jamsostek pada tahun 2001 : Terhimpun 104,852 kasus Kecelakaan Kerja. Sudah termasuk 78 kasus Penyakit Akibat Kerja, Atau kurang lebih HANYA 0,07% dari semua kasus.

SANGAT MINIM Mengapa??

KEPPRES. No. 22 Th.1993 (BERDASARKAN UU No. 3 TH. 1992) o

31 JENIS PENYAKIT AKI BAT KERJA (FAKTOR KIMIA; FISIK; BIOLOGIS; ERGONOMIS)

o o

TIAP JENIS ADALAH KELOMPOK PENYAKIT

o

JENIS KE 26 ^ 27: MENGENAI KULIT

o

JENIS KE 31 (SEMUA BAHAN KIMIA)

JENIS KE 1 – 5 & 28 : MENGENAI SALURAN PERNAPASAN.

PENYAKIT AKIBAT KERJA (Lampiran Keppres No. 22 Tahun 1993)

1. Pnemokoniosis yang disebabkan debu mineral pembentuk jaringan parut(silikosis, antrakosilikosis, asbestosis) dan silikotuberkulosis yang silikosisnya merupakan faktor utama penyebab cacat dan kematian.

2. Penyakit paru dan saluran pernafasan (bronkhopulmoner) yang disebabkan oleh debu logam keras.

3. Penyakit paru dan saluran pernafasan(bronkhopulmoner) yang disebabkan oleh debu kapas, vlas, henep dan sisal (bissinosis).

4. Asma akibat kerja yang disebabkan oleh penyebab sensitisasi dan zat perangsang yang dikenal yang berada dalam proses pekerjaan.

5. Alveolitis allergika yang disebabkan oleh faktor dari luar sebagai akibat penghirupan debu organik.

PENYAKIT AKIBAT KERJA

(Lampiran Keppres No. 22 Tahun 1993)

6. Penyakit yang disebabkan oleh berillium

(=atau persenyawaannya yang beracun).

7. Penyakit yang disebabkan oleh kadmium

8. Penyakit yang disebabkan fosfor

, dst , dst

, dst 9. Penyakit yang disebabkan oleh krom , dst 10. Penyakit yang disebabkan oleh mangan , dst 11. Penyakit yang disebabkan oleh arsen , dst 12. Penyakit yang disebabkan oleh raksa , dst


Penyakit yang disebabkan oleh timbal , dst Penyakit yang disebabkan oleh fluor atau , dst Penyakit yang disebabkan oleh karbon disulfida. Penyakit yang disebabkan oleh derivat halogen dari persenyawaan hidrokarbon alifatik atau aromatik yang beracun. 17. Penyakit yang disebabkan oleh benzena atau homolognya yang beracun. 18. Penyakit yang disebabkan oleh derivat nitro dan amina dari benzena dan hoimolognya yang beracun. 19. Penyakit yang disebabkan oleh nitrogliserin atau ester asam nitrat lainnya. 13. 14. 15. 16.


20.Penyakit yang disebabkan oleh alkohol, glikol atau keton. 21.Penyakit yang disebabkan oleh gas atau uap penyebab asfiksia atau beracunan seperti karbon monoksida, hidrogen sianida, hidrogen sulfida, atau derivatnya yang beracun, amoniak seng, braso dan nikel. 22.Kelainan pendengaran yang disebabkan oleh kebisingan. 23.Penyakit yang disebabkan oleh getaran mekanis (kelainan-kelainan otot, urat, tulang persendian, pembuluh darah tepi atau saraf tepi). 24.Penyakit yang disebabkan oleh pekerjaan dalam udara yang bertekanan lebih. 25.Penyakit yang disebabkan oleh radiasi elektromagnetis dan radiasi yang mengion.


26. Penyakit kulit(dermatosis) yang disebabkan oleh penyebab fisik, kimiawi atau biologis. 27. Penyakit kulit epitelioma primer yang disebabkan oleh ter, pic, bitumen, minyak mineral, antrasena atau persenyawaan, produk atau residu dari zat tsb. 28. Kanker paru atau mesotelioma yang disebabkan oleh asbes. 29. Penyakit infeksi yang disebabkan oleh virus, bakteri atau parasit yang didapat dalam suatu pekerjaan yang memiliki risiko kontaminasi khusus. 30. Penyakit yang disebabkan oleh suhu tinggi atau rendah atau panas radiasi atau kelembaban udara tinggi. 31. Penyakit yang disebabkan oleh kimia lainnya termasuk bahan obat.

ICD

International Classification of Diseases. = Klasifikasi Internasional untuk berbagai Penyakit.

CONTOH Keppres No. 22

ICD

JENIS No. 1; PNEUMOKONIOSIS

PENYAKIT SALURAN PERNAFASAN: J60-65

JENIS No. 6,7,9,10,12, 13

KERACUNAN LOGAM: T56-

JENIS No. 22

PEMAPARAN BISING: W42-

JENIS No. 26

DERMATOSIS AKIBAT KERJA: L23-24

JENIS No. 29

INFEKSI VIRUS; MIKOSIS;PENYAKIT YANG BERKAITAN DENGAN PROTOZOA DAN PARASIT

metoda Diagnosis Anamnesis tentang riwayat penyakit dan riwayat pekerjaan; Pemeriksaan klinis; Pemeriksaan laboratoris; Pemeriksaan pendukung, misalnya pemeriksaan sinar tembus; Pemeriksaan tempat / ruang kerja = workplace inspection: - management: peraturan, tanda; - machine: peralatan; - man : cara kerja.

Diagnosis Dasar untuk mempunyai hak atas Jaminan:

Biaya pengangkutan; Biaya pemeriksaan, pengobatan, dan/atau perawatan; Biaya rehabilitasi; Santunan berupa uang: – santunan sementara tidak mampu bekerja; – santunan cacat sebagian untuk selamalamanya; – santunan cacat total untuk selama lamanya, baik fisik maupun mental; – dan santunan kematian.

CACAT (KARENA KECELAKAAN KERJA DAN PENYAKIT AKIBAT KERJA)

KEADAAN HILANG, ATAU BERKURANGNYA FUNGSI ANGGOTA BADAN YANG SECARA LANGSUNG ATAU TIDAK LANGSUNG MENGAKIBATKAN HILANG ATAU BERKURANGNYA KEMAMPUAN UNTUK MENJALANKAN PEKERJAAN

Cacat anatomis : Keadaan hilang anggota badan. Cacat fungsi: Berkurangnya fungsi anggota badan. Anggota badan : Bagian/organ tubuh seperti tangan, kaki, hidung, telinga, mata, kulit, alat kelamin, paru, jantung, usus, otak, dsbnya)

CACAT (JENIS) (KARENA KECELAKAAN KERJA ATAU PENYAKIT AKIBAT KERJA)

Tabel Lampiran II PP. No.14 Tahun 1993 (KETENTUAN NORMATIF)

A. Cacat anatomis B. Cacat fungsi C. Cacat mental (CATATAN KHUSUS) 9Aspek kemampuan bekerja 9Aspek estetika 9Aspek mental-psikologis



DUA MACAM: I. MACAM CACAT TETAP SEBAGIAN II. MACAM CACAT-CACAT LAINNYA



I. MACAM CACAT TETAP SEBAGIAN 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Lengan kanan dari sendi bahu ke bawah; Lengan kiri dari sendi bahu ke bawah; Lengan kanan dari atau dari atas siku ke bawah; Lengan kiri dari atau atas siku ke bawah; Tangan kanan dari atau dari atas pergelangan ke bawah; Tangan kiri dari atau dari atas pergelangan ke bawah; Kedua belah kaki dari pangkal paha ke bawah; Sebelah kaki dari pangkal paha ke bawah; Kedua belah kaki dari mata kaki ke bawah; Sebelah kaki dari mata kaki ke bawah; Kedua belah mata; Sebelah mata atau diplopia pada penglihatan dekat; Pendengaran pada kedua belah telinga; Pendengaran pada sebelah telinga;



I. MACAM CACAT TETAP SEBAGIAN (LANJUTAN)

15.

16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

Ibu jari tangan kanan; Ibu jari tangan kiri; Telunjuk tangan kanan; Telunjuk tangan kiri; Salah satu jari lain tangan kanan; Salah satu jari lain tangan kiri; Ruas pertama telunjuk kanan; Ruas pertama telunjuk kiri; Ruas pertama jari lain tangan kanan; Ruas pertama jari lain tangan kiri; Salah satu ibu jari kaki; Salah satu jari telunjuk kaki; Salah satu jari kaki lain.



II. MACAM CACAT-CACAT LAINNYA 1. Terkelupasnya kulit kepala (cacat anatomis); 2. Impotensi(cacat anatomis atau cacat fungsi); 3. Kaki memendek sebelah: kurang dari 5 cm; 5 – 7,5 cm; 7,5 cm atau lebih (cacat anatomis); 4. Penurunan daya dengar kedua belah telinga setiap 10 desibel (cacat fungsi); 5. Penurunan daya dengar sebelah telinga setiap 10 desibel (cacat fungsi); 6. Kehilangan daun telinga sebelah(cacat anatomis);



II. MACAM CACAT-CACAT LAINNYA (LANJUTAN)

7.

Kehilangan kedua belah daun telinga (cacat anatomis); Cacat hilangnya cuping hidung (cacat anatomis); Perforasi sekat rongga hidung (cacat anatomis); Kehilangan daya penciuman (cacat fungsi); Hilangnya kemampuan kerja fisik(cacat fungsi); Hilangnya kemampuan kerja mental tetap(cacat fungsi); Kehilangan sebagaian fungsi penglihatan; kehilangan efisiensi tajam penglihatan; kehilangan penglihatan warna; kehilangan lapangan pandang (cacat fungsi).


Tabel Lampiran II PP. No.14 Tahun 1993 (KETENTUAN NORMATIF) I.MACAM CACAT TETAP SEBAGIAN II.MACAM CACAT-CACAT LAINNYA DAPAT DIKELOMPOKKAN MENURUT SPESIALISASI BIDANG KEDOKTERAN: - Bidang Penyakit Paru; - Bidang Penyakit Kulit. - Bidang Penyakit Mata; - Bidang Penyakit THT; - Bidang Penyakit Ortopedi; - Bidang Penyakit Dalam; - Bidang Bidang Penyakit Radiasi; - Bidang Penyakit Psikiatri; - Bidang Penyakit Nerologi; - Bidang Penyakit Urologi;

PENILAIAN CACAT (KARENA KECELAKAAN KERJA ATAU PENYAKIT AKIBAT KERJA)

Tabel,Lp.II PP. No.:14 Tahun 1993 (KETENTUAN NORMATIF)

MACAM CACAT TETAP SEBAGIAN Macam cacat tetap sebagian Nilai%x upah 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Lengan kanan dari sendi bahu ke bawah Lengan kiri dari sendi bahu ke bawah Lengan kanan dari atau dari atas siku ke bawah Lengan kiri dari atau atas siku ke bawah Tangan kanan dari atau dari atas pergelangan ke bawah Tangan kiri dari atau dari atas pergelangan ke bawah Kedua belah kaki dari pangkal paha ke bawah Sebelah kaki dari pangkal paha ke bawah Kedua belah kaki dari mata kaki ke bawah Sebelah kaki dari mata kaki ke bawah Kedua belah mata Sebelah mata atau diplopia pada penglihatan dekat Pendengaran pada kedua belah telinga Pendengaran pada sebelah telinga

40 35 35 30 32 28 70 35 50 25 70 35 40 20



MACAM CACAT TETAP SEBAGIAN(Lanjutan) Macam cacat tetap sebagian Nilai%x upah 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

Ibu jari tangan kanan Ibu jari tangan kiri Telunjuk tangan kanan Telunjuk tangan kiri Salah satu jari lain tangan kanan Salah satu jari lain tangan kiri Ruas pertama telunjuk kanan Ruas pertama telunjuk kiri Ruas pertama jari lain tangan kanan Ruas pertama jari lain tangan kiri Salah satu ibu jari kaki Salah satu jari telunjuk kaki Salah satu jari kaki lain

15 12 9 7 4 3 4,5 3,5 2 1,5 5 3 1



MACAM CACAT-CACAT LAINNYA Macam cacat-cacat lainnya Nilai%x upah 1. Terkelupasnya kulit kepala(cacat anatomis) 10-30 2. Impotensi(cacat anatomis atau cacat fungsi) 30 3. Kaki memendek sebelah: kurang dari 5 cm; 5 – 7,5 cm; 7,5 cm atau lebih (cacat anatomis) 10,20,30 4. Penurunan daya dengar kedua belah telinga setiap 10 desibel(cacat fungsi) 6 5. Penurunan daya dengar sebelah telinga setiap 10 desibel(cacat fungsi) 3 6. Kehilangan daun telinga sebelah(cacat anatomis) 5 7. Kehilangan kedua belah daun telinga(cacat anatomis) 10



MACAM CACAT-CACAT LAINNYA Macam cacat-cacat lainnya Nilai%x upah 8. 9. 10. 11 12. 13.

Cacat hilangnya cuping hidung(cacat anatomis) 30 Perforasi sekat rongga hidung(cacat anatomis) 15 Kehilangan daya penciuman (cacat fungsi) 10 Hilangnya kemampuan kerja fisik(cacat fungsi) 40,20,5 Hilangnya kemampuan kerja mental tetap(cacat fungsi) 70 Kehilangan sebagaian fungsi penglihatan; kehilangan efisiensi tajam 7,10,7 penglihatan; kehilangan penglihatan warna; kehilangan lapangan pandang (cacat fungsi).


1. Cacat pada Penglihatan 2. Cacat pada Paru – Paru 3. Cacat pada kulit.

Cacat Penglihatan Parameter diagnostik fungsi indera mata: 1. Tajam penglihatan: bilangan pecahan, pembilang adalah jarak pemeriksaan (6m), dan penyebut adalah angka/huruf paling kecil yang masih bisa dibaca (N : 6/6) 2. Lapang pandang: membandingkannya dengan pemeriksa. 3. Binokularitas: penglihatan serentak dan fusi, stereopsis 4. Penglihatan warna.

Penentuan Cacat Penglihatan 1. 2. 3.

Mengingat komponen fungsi penglihatan Komponen ini dinilai masing masing mata dan kemudian diberi nilai dalam fungsi binokuler P.P 14/1993 terdapat:

Cacat tetap kedua mata (70% upah) Sebelah mata atau diplopia pada mata dekat (35% upah) Kehilangan penglihatan warna (10% upah) Setiap kehilangan lapang pandang 10% ( 7% upah) Setiap kehilangan efisiensi tajam penglihatan (7% upah)

Organ Dalam Beberapa organ dalam yang belum jelas fungsinya bila diambil dan tidak ada dampak pada tubuh khususnya untuk bekerja (misal, appendix, lymphnode spleen, ) kompensasinya masih debat.

Penurunan fungsi organ diketahui dengan pemeriksaan laboratorium terkait, contoh fungsi paru, fungsi ginjal, fungsi hati.

Cacatan Khusus Penetapan Cacat Azas confidential Bukan konsumsi informasi/interest publik Tidak sampai hitungan ekonomis/nominal, karena hanya sebatas impairment Professional judgment bebas, tidak boleh dipengaruhi apapun. Bersifat global, general.

KESIMPULAN 1. Sangat perlu dan penting mewujudkan kesepahaman dan pemahaman secara benar; 2. Urgensi sosialisasi; 3. Kesatuan bahasa dan kesamaan/konsistensi tindakan dokter pemeriksa atau dokter yang merawat,dokter penasehat dan pegawai pengawas ketenagakerjaan; 4. Penyakit akibat kerja adalah penyakit yang timbul karena hubungan kerja; tidak semua penyakit akibat kerja menimbulkan cacat; 5. Diagnosis penyakit akibat kerja adalah dasar penentu bagi adanya hak jaminan kecelakaan kerja untuk penyakit akibat kerja; 6. Pegawai pengawas ketenagakerjaan yang dokterlah yang menetapkan penyakit akibat kerja atau bukan.

PANITIA PELATIHAN HIPERKES DAN KESELAMATAN KERJA BAGI DOKTER IKATAN ALUMNI UNIVERSITAS INDONESIA PASCA SARJANA KEDOKTERAN KERJA BALAI HIPERKES DAN Dengan KESELAMATAN KERJA DKI JAKARTA DINAS TENAGA KERJA DAN TRANSMIGRASI PEMERINTAH PROPINSI DAERAH KHUSUS IBUKOTA JAKARTA JL. JENDRAL AHMAD YANI 69-70 JAKARTA 10510. PHONE: (+62).21.4209820. FAX: (+62) 21 4240284

Dr. Widodo PELATIHAN HIPERKES & KESELAMATAN KERJA BAGI DOKTER DAN PERAWAT JAKARTA, 28 MEI 2007

TUJUAN DOKTER mendalami Debu dan Penyakit Paru Kerja

Dokter diharapkan MAMPU untuk: Mengetahui jenis pekerjaan yang dulu dan sekarang yang berpotensi ikut berperan menyebabkan kelainan dan menjelaskan mengapa dapat terjadi demikian; Memilih, mengartikan dan menggambarkan gejala klinis tiap kelainan, memaparkan mekanisme patogenesis yang berperan untuk setiap gejala dan keluhan yang timbul; Melakukan tes spirometri dan mengartikan hasilnya; dan menterjemahkan hasil analisa tekanan gas darah sebagai indikator kelainan fungsi paru yang mungkin timbul dari kelainan tersebut; Mengenali dan menguraikan foto rontgen paru normal & pada foto rontgen abnormal, mengenali pola pola abnormal yang menjadi indikasi dari kelainan tersebut; Menentukan pemeriksaan yang sesuai untuk diagnosa dan pengelolaan lanjut, yang harus dimulai oleh dokter pada kontak pertama, untuk kelainan tersebut; Dalam keadaan klinis tertentu, membahas implikasinya dalam pekerjaan, paparan bahaya, sehat atau layak-tidaknya untuk kembali pada suatu jenis pekerjaan tertentu.

Pendahuluan Industrialisasi – ekonomi ↑ & sosial ↑. Limbah – bahan baku, proses, produk Hazard – potensi mencemari lingkungan Pekerja terpajan – inhalasi, kulit, oral Gangguan kesehatan – hampir semua organ Debu, gas, uap, fume; bila tidak dikendalikan – penyakit paru akibat kerja

Penyakit Akibat Kerja Paru – PAK-P • Di AS (American Lung Association): – Penyebab utama (cacat, absen & kematian). – Disebabkan oleh pajanan berulang dan lama – Rokok: memperparah PAK-P dan tingkatkan risiko Kanker.

• Di R.I.: – Penyakit Infeksi Saluran Pernapasan: peringkat atas untuk morbiditas & mortalitas – PAK-P & PPOK (rokok & polusi) bertambah – Perlu dipahami oleh dokter umum, terutama yang bekerja di tempat dengan resiko tinggi

Anatomi sistem pernafasan

Empat kompartemen

•

Naso-faringeal: nares s/d pita suara : saring,

•

Trakeobronkeal: s/d bronkiolus respirasi.

•

lembab, hangat.

Hantar udara. 0,25-0,5 μm. Proteksi. Parenkimal: s/d alveol. Ada 300juta! Luas 140m2, tebal 1 μm. Pertukaran gas, epitel erat berinteraksi dg vasa, saraf& sistem imunologi.

•

Rongga pleura.

Alveol.

Sel eptitel I/II, sitoplasma 0,1-0,2 μm, endotel, makrofag, fibroblast.

Fungsi Sistem Pernafasan Pertukaran gas Perisai terhadap toksikan Biotransformasi (C-P450) mis: parakuat & 4

ipomeanol membentuk radikal bebas & epoxi yang merusak sel paru.

Ekskresi toksikan – expirasi Atur kadar angiotensin, amin biogenik,

prostaglandin

Proses respirasi, 3 tahap: - ventilasi : inspirasi & expirasi. 12-18X/1’; 400-500mL/insp; 5-8L/1’

difusi : di dinding alveol & kapiler - perfusi : distribusi gas dlm paru, via aliran darah. -

Pertahanan Paru

Menghindari toksikan terinhalasi - PENGHIDU - BRONKO-KONSTRIKSI Deaktivasi toksikan - SEKRESI - ANTIBODI, ANTIOXIDAN, ANTIPROTEASE Membersihkan toksikan - BATUK - ESKALATORMUKOSILIAR - FAGOSITOSIS Mengambil toksikan - FAGOSITOSIS - JARINGAN IKAT

Faktor yang Mempengaruhi Respons Sistem Respirasi terhadap DEBU terinhalasi

Sifat fisik:

ukuran, densitas, bentuk, penetrabilitas, solubilitas, higroskopis

Sifat kimia:

asam, basa, efek lokal/sistemik, fibrogenisitas, antigenisitas

Faktor pejamu:

genetik, obat, rokok, alkohol, anatomi & fisiologi, status imunologi

BENTUK FISIK TOKSIKAN

GAS – substansi pd P&T kamar dlm fase gas. Mis. O2, CO2.

VAPOR – fase gas dari substansi cair. Mis. water vapor.

AEROSOL – substansi yang stabil dari partikel padat /

cair di udara. Termasuk: ¾ Dust : partikel solid hasil grinding. ¾ Fumes

: hasil pembakaran. Mis: lead fumes. ¾ Smoke : hasil pembakaran organik. Mis. rokok. ¾ Mist & Fog: hasil kondensasi cairan pada partikel. ¾ Smog : kompleks gas & partikel di udara (smoke+fog)

UKURAN PARTIKEL

INHALABLE PARTICULATE MASS (PM) Dapat terhisap ke saluran nafas. Median cut-off aerodynamic (=MCA) ∅ ± 30 μm THORACAL PM Terhirup masuk ke ronggga dada, zona penghantar & zona respirasi. MCA ∅ ± 10 μm RESPIRABLE PM Terhirup masuk zona respirasi MCA ∅ ± 3-4 μm

MEKANISME DEPOSIT

IMPAKSI ¾ TERBENTUR KRN ALIRAN LURUS ¾ DI CABANG BRONKUS BESAR ¾ ∅ 30 μm: 100%. > 5 μm: 95%.

SEDIMENTASI ¾ JATUH MENGENDAP ¾ DI BRONKUS SEDANG ¾ ∅ 1-5 μm

DIFUSI ¾ DI ALVEOL ¾ ∅ 1-5 μm ¾ ∅ <1 μm – GERAK BROWN.

PENYAKIT AKIBAT KERJA - PARU ¾ Pneumokoniosis ¾ Bronkitis industri ¾ Asma kerja ¾ Pneumonitis Hipersensitif ¾ Kanker paru akibat kerja

Risalah PAK-P

PNEUMOKONIOSIS ¾ Akumulasi debu dalam paru dan reaksi

jaringan terhadap keberadaan debu. ¾ Debu= aerosol mengandung partikel padat. ¾ Inflamasi & fibrosis; gen & lingkungan ¾ Asbestosis, silikosis, coal worker’s

pneumokoniosis

Standard diagnosis ILO (Radiologis)

. Alat: high KV & mA . Side-by-side comparison ≅ ILO standard films. . 2 pembaca + 1 penentu . Kerapatan perselubungan: 1, 2, 3 / A, B, C. . Bentuk reguler: p, q, r. Bentuk ireguler; s, t, u.

CHEST RADIOGRAPH EVALUATION OF PNEUMOCONIOSIS PARENCHYMES PLEURAL abnormalities CALCIFICATIONS PARENCHYMAL abnormalities:

ILO DIAGRAMS

OPACITIES: small and large. SMALL lesions, < 1 cm in diameter

REGULAR=Rounded-shaped: Types: p (<1.5 mm), q (1.5-3 mm),

r (3-10 mm)

IREGULAR-shaped: width of fine linear opacities: Types s (< 1.5 mm), t (1.5-3 mm), u ( 3-10 mm). LARGE opacities: A : > 1.5 cm. B : > 5 cm, not larger than right upper lobe. C : combined areas exceeds the volume encompassed by the right upper lobe. PROFUSION Readings: 0, 1, 2, 3. The readings must be written in two separate numbers, side-by-side. Left: the reading; Right: the comparison. Left : the category felt by the reader/s) to be most representative of the standard ILO film. Right: the major category which was considered to be similar to the film being read, but not eventually chosen. Example of final reading: 3 / 2. The 3: it most resembles standard category 3; while the 2: a similarity to a standard film of category 2 was seriously considered. The Final readings is one of the 12-point system.

PLEURAL abnormalities Include: Pleural effusion, calcification, diffuse pleural thickening, and pleural plaques or circumscribed pleural thickening. Readings: Type, anatomic location, approximate size

CALCIFICATIONS: Readings: present, absence. THICKENING. Readings: by site.

CHEST RADIOGRAPH EVALUATION OF PNEUMOCONIOSIS ILO GUIDELINES FEATURE

CLASSIFICATION

No Pneumoconiosis Pneumoconiosis Rounded small PARENCHYMAL OPACITIES

0

Profusion Type Extent Irregular small PARENCHYMAL OPACITIES

1, 2, 3

Profusion Type Extent Large PARENCHYMAL OPACITIES Size Type PLEURAL THICKENING Diaphragmatic outline (costophrenic areas) Cardiac outline (cardiophrenic areas) PLEURAL CALCIFICATIONS

1, 2, 3

p, q (m), r (n) Zones

s, t, u Zones A, B, C Well-defined / ill-defined By site Ill-defined: right, left Ill-defined 1, 2, 3 By site and extent

The 1, 2, 3 profusion groups can be extended to a 12-point system:

0/-, 0/0, 0/1, 1/0, 1/1, 1/2, 2/1, 2/2, 2/3, 3/2, 3/3, 3/4

ASBESTOSIS Pekerja

asbes dan handling Fibrosis interstisial difus parenkhim paru Ferruginous bodies. Penebalan pleural viseral; kadang kalsifikasi Tanpa gejala → cor pulmonal Kanker mesotelioma

SILIKOSIS Penambang logam, batu bara, penggali terowongan, pemotong batu, keramik, penuang besi/baja, pabrik amplas & gelas. 3 bentuk klinis: Simpel, Terakselerasi, Akut. Tanpa gejala →sesak, cor-pulmonal Kronik & progresif, nir-pulih Silicotic nodules. Egg Cell Calcifications

BISINOSIS

Peny saluran nafas akut & kronik pd pekerja kapas, linen & serat rami Perasaan dada tertekan, mengi & sesak waktu kembali ke tempat kerja “Monday sickness”. Pemberat: durasi, perokok Foto thorax normal, FEV1 pd permulaan hari kerja; gejala respirasi derajat 0 - 3. ¾ Grade 0 ¾ Grade RTI 1 ¾ Grade RTI 2 ¾ Grade RTI 3

: no symptoms : cough associated with dust exposure. : persistent phlegm, initiated/exacerbated by dust exposure : persistent phlegm (initiated/made worse by dust exposure) either with exacerbations of chest illness or persisting for 2 years or more.

BRONKITIS INDUSTRI

Pajanan debu kadar tinggi & lama Pekerja tambang batu bara, tepung, wool, kapas, keramik, dll. Paralisis silia, hipertrofi & hiperplasi kelenjar mukus → batuk produktif kronik. FEV1 ↓

ASMA KERJA

Penyakit obstruksi saluran nafas yg reversibel, oleh iritasi zat di lingkungan kerja Hanya mengenai sebagian dari pekerja yang terpajan Masa latent yang berbeda Tumbuhan, hewan, enzim, kimia, obat Uji provokasi = pharmacologic challenge test: - using histamin, methacholin, or prostaglandin D2 or F2Alpha

PNEUMONITIS HIPERSENSITIF

Kumpulan peny paru alergi akibat sensitisasi & pajanan debu organik Difus, inflamasi mononuklear parenkim paru di bronkiolus terminalis & alveoli Diagnosis paru umum + uji imunologis

Kanker Paru

Asbes, arsen, nikel, krom, arang, ter, batu bara, silica I l u s t r a s i Pneumoconiosis

Penilaian Cacat Paru Derajat sesak

VEP 1

0

> 2,5 L

% Cacat fungsi -

1 RINGAN

1,6 – 2,5 L

25%

2 SEDANG

1,1 – 1,5 L

50%

0,5 – 1 L

75%

< 0,1 L

100%

3 BERAT 4 SANGAT BERAT

REFERENSI UNTUK PENELUSURAN LEBIH DALAM:

DR. Dr. Suma’mur PK, MSc., Sp.Ok: (berbagai penelitian dan paparan). Prof. DR. Dr. Tjipto Suwandi, MOH., Sp.Ok: (berbagai penelitian dan paparan). Fishman’s Manual of Pulmonary Diseases and Disorders, McGraw Hill – 2002 ILO: Guidelines For The Use of The ILO International Classification of Radiograph of Pneumoconioses, Revised Edition - 2000. Occupational Lung Dsease – D.E. Banks; Chapman & Hall Medical – 1998 Occupational Medicine, Carl Zenz; Mosby Third Edition, 1994 Merck’s Manual on Occupational Lung Diseases, 2002 Guidelines For Equipment And Technology, Y.Hosoda, Et Al, Dokkyo University, Tochigi, Japan - 1996

Beberapa

alamat Websites tentang Occupational Medicine: – New York State Occupational Health Clinic Network: – http://www.health.state.ny.us/nysdoh/environ/occupate.htm

– American Lung Association : http://www.lungusa.org/occupational/ – Environmental Protection Agency Asthma and Indoor Environments: – http://www.epa.gov/iaq/asthma/index.html – Occupational Safety and Health Administration: http://www.osha-slc.gov/index.html – Dan lain lain.

PANITIA PELATIHAN HIPERKES DAN KESELAMATAN KERJA BAGI DOKTER IKATAN ALUMNI UNIVERSITAS INDONESIA PASCA SARJANA KEDOKTERAN KERJA dengan BALAI HIPERKES DAN KESELAMATAN KERJA DKI JAKARTA DINAS TENAGA KERJA DAN TRANSMIGRASI PEMERINTAH PROPINSI DAERAH KHUSUS IBUKOTA JAKARTA

JL. JENDRAL AHMAD YANI 69-70 JAKARTA 10510. PHONE: (+62).21.4209820. FAX: (+62) 21 4240284

PELATIHAN HIPERKES & KESELAMATAN KERJA BAGI DOKTER DAN PERAWAT JAKARTA, 10 SEPTEMBER 2007

CONTENTS

The Competency of the Doctor Historical Aspects Kedudukan Perundangan The Skin The Dermatoses The Diagnosis, and The Prognosis Special Work Problems Treatment Disability and Compensation Rehabilitation Prevention Conclusions and Recommendations Selected References and Further Readings Occupational Skin Cancer Appendices

The Competency : Doctors will be able to

Work History : indicate aspects of a past or present occupation which have a potential to contribute to the cause, or aggravation, of the disorder and explain why this might be so; A case: describe and interpret the appearance of the skin lesions, and describe the pathogenetic mechanisms responsible for those lesions; and Description of Occupational Situation: state whether a person should be precluded from pursuing that occupation, or should be advised against it and, in a given clinical situation, discuss the implications for employment, exposure to risk, or fitness to a specified job.

Historical and Public Health Aspects. Occupational diseases of the skin historically have paralleled industrial development. Occupational Dermotoses are one of the most common types of occup.disease. 1985, in the US, accounted for no less than 65-70% of all reported Occ.Diseases. Later on, statistics collected by the United States Department of Labor indicated a drop in frequency to approximately 42%. In 1997, OSD constituted 13.5% of all Occup. Illnesses reported. In 1999 and later the numbers were still decreasing gradually. ¾The annual estimated costs of OSD in the US: $1 billion. ¾From 1990 through 2000, 11,084 skin disorder state fund claims were accepted by the Washington State workers' compensation system. ¾The cumulative cost of all skin disorder claims was $7.5 million. ¾Industries with the highest claims incidence rate are Agriculture, Forestry and Fishing and Manufacturing. Jamsostek? Compiled 104,852 occupational accident cases in 2001, with 78 cases of occupationally related diseases; that is a mere fraction of 0.07%. Government of Indonesia issued UU no. 1, 1970 on Work Safety, and UU no. 3, 1992 on Jaminan Sosial Tenaga Kerja (Jamsostek). The recent directives on above laws issued, one was: Kep.79/MEN/2003 on Pedoman Diagnosis Dan Penilaian Cacat Karena Kecelakaan Dan Penyakit Akibat Kerja.

Kedudukan Perundangan: Keppres No. 22 Tahun 1993 Lampiran: 31 Penyakit Akibat Kerja

1. 2. Dst 26. Penyakit Kulit (dermatotis) yang disebabkan oleh penyebab fisik, kimiawi atau biologis. 27. Dst. 31.

Structure, Function, and Occupational Disorders of the Skin. STRUCTURE

FUNCTION

OCCUPATIONAL DISORDER

Stratum corneum

Barrier against chemical diffusion and microorganisms

Chapping from low humidity, chemical stains

Squamous and basal cells of epidermis

Cell regeneration, synthesis of stratum corneum, corneum, wound repair

Infection, contact dermatitis, dermatitis, neoplasms

Melanocytes and melanin

Absorption of ultraviolet radiation

Toxic vitiligo, vitiligo, melanoma, hyperpigmentation

Langerhans’ Langerhans’ cells, lymphatics, lymphatics, dermal macrophages

Immune regulation and surveillance

Delayed hypersensitivity reactions

Merkel cells, nerve tissue elements

Perception of environment

Toxic neuropathies

Blood vessels, mast cells

Thermoregulation, nutrition of tissue

Heat stroke, contact and systemic urticaria, urticaria, flushing reactions, vibration “white” white” finger

Connective tissue

Mechanical protection against trauma, wound repair

Infection, granulomatous reactions, scleroderma, solar elastosis, elastosis, scar

Eccrine sweat glands

Thermoregulation, buffering of skin surface

Miliaria, Miliaria, “rusting” rusting”

Sebaceous glands

Synthesis of skin surface lipids, chemical barrier against microorganisms

Oil acne, chloracne

Hair, follicles

Insulation and protection, secondary sensory organs, social appearance

Folliculitis, Folliculitis, traumatic or toxic alopecia

Nails

Grasping and manipulation of small objects

Paronychia, Paronychia, dystrophy, oncholysis

The Dermatoses What is occupational dermatoses? it is one of the most widespread causes of ill health and affects people working in many employment sectors, including hairdressing/beauty, catering, housekeeping/cleaning. signs can be redness, itching, scaling and blistering to the skin. as it gets worse the skin can crack and bleed and it can spread all over the body. It can be a very painful condition. dermatoses basically involves a loss of moisture from your skin, for example when hands are constantly immersed in water or if they come into contact with detergents/solvents. Employees in all jobs are entitled to protection from this foreseeable condition: it should never be looked upon as acceptable. if it is spotted early and adequate precautions are taken, most people can recover and this is why it is so important for employers to firstly have preventative measures in place and proactive management systems to identify potential problems and deal with them effectively. once someone develops dermatoses, they can become sensitized to what ever caused the condition, which basically means that any future contact can cause an acute and severe reaction. For this reason some employees even have to change jobs. dermatoses is not infectious: it cannot be passed from one person to another.

How is dermatoses caused? z

z

z

z

It is caused by the skin coming into contact with certain substances at work and because of this it is sometimes referred to as occupational dermatoses. It usually affects the hands or forearms, the places most likely to touch the substances. 40% of occupational dermatoses cases in the catering industry are caused by contact with foods, such as flour/dough, fish and sea foods, meat and poultry. Dermatoses can also be caused by immersion in water for prolonged periods of time. Once a person has become sensitized to a substance, the dermatoses can spread to parts of the body that haven't even been in contact with it. How quickly a person gets dermatoses depends on a number of things: - the substance - the strength or potency - how long in contact with the skin - how often it touches the skin

Contact dermatoses are by far the most common occupational dermatoses. The term refers to the induction of cutaneous changes, usually accompanied by inflammation, from direct skin exposure to exogenous chemical or physical substances. Skin disease may be characterized by discrete elevated lesions, patchy rashes that bear a limited geographic resemblance to the area of external assault and distinct localized irritation, which, usually, is a faithful replica of the area of injury. Occupational dermatoses or skin inflammation is provoked by either (or both) of two mechanisms: irritation or allergy, and therefore it may be broadly divided into two groups:

Primary Irritant Contact Dermatoses.

Allergic Contact Dermatoses.

Primary Irritant Contact Dermatoses

Nearly three-quarters ( ± 75%) of all occupational dermatoses are of this type. The irritants produce a direct effect on the skin with which they come into contact and the effect will be more dependent on the dose and duration of exposure than on any inherent response emanating from the individual. For example, concentrated sulphuric acid splashes on to the face of anybody will produce skin reaction. Soap and water are more variable but these seemingly harmless materials can cause irritation in non-allergic subjects The inflammatory cutaneous changes that occur from skin irritation result from a direct, local, toxic effect on cellular elements in the skin, leading to cell death, release of lysosomal enzymes and soluble inflammatory mediators, recruitment of inflammatory cells, and further tissue destruction. Although substantial tissue destruction may quickly occur following relatively brief skin exposure to strong caustic or corrosives (i.e., chemical burns), the majority of cases of irritant contact dermatoses result from cumulative and repetitive exposures to “weak” irritants, substances that are not likely to produce visible cutaneous injury following only brief or limited exposure.

Allergic Contact Dermatoses

Sensitizing eczemas account for 15-20% of all occupational dermatoses. The response is usually specific to one agent but may be delayed for a week or more after contact. The initial sensitizing episode may need to be of several hours’ duration but could be up to life long: even though subsequent reactions can be provoked by the most transient exposures. – Refractory Phase The mechanism of the response is a delayed hypersensitivity reaction. The allergen (hapten) combines with protein in the epidermis and is engulfed in skin macrophages and transported in the lymphatics. At the regional lymph nodes, circulating antibody is produced which is then ‘ready’ to react locally with any further contact with the hapten-protein complex. This could take from 4 days to several weeks. – Induction Phase. The acute effect is erythema, eruption, vesiculation, oozing and desquamation. In a chronic form, this leads to thickened fissured skin. The development of allergic contact dermatoses requires that the affected individual first become immunologically sensitized to the offending substance. The sensitization process involves delayed hypersensitivity mechanism, which require a period of 1 to 3 weeks following first exposure before sensitization can occur. Generally, the allergenic substance must first complex with skin tissue protein, following which this hapten–protein conjugate is processed by circulating Tlymphocytes to regional lymph nodes, where further antigen processing and cell proliferation occur. Once sensitized, an affected individual will react within several hours to 1 to 2 days following cutaneous re-exposure to extremely low concentrations of the offending substance. - Elicit Phase. Effector cells may stay for life and able to recognize the specific Hapten and yield inflammation. – Persistent Phase Unlike irritant contact dermatoses, allergic contact dermatitis frequently extends to other body surfaces remote from the primary site of direct skin contact with the allergen.

THE THE DIAGNOSIS DIAGNOSIS EVALUATION 0N EMPLOYEE

WORKPLACE INSPECTION

EVALUATION EVALUATION ON ON EMPLOYEE EMPLOYEE I. History / Anamnesis

In the course of taking the history from a patient who may have work-related skin disease, the following should be obtained: an accurate chronologic sequence of events surrounding the onset of the skin disease, its subsequent clinical course, and associated work activities; a description of the skin lesions and their initial anatomic locations and spread to other body sites; disability caused by the skin disease; Identification of all relevant work exposures; Presence of similar skin disease in co-workers; and Response to previous medical treatment. A thorough history should properly determine the presence of important risk factors, such as personal or family history of atopic allergies; antecedent skin disease or reactions, such as dermatoses from jewelry, cosmetic preparations, or hair dyes; and potential causative exposures in the domestic environment.

The Diagnosis II. PHYSICAL EXAMINATION Particular attention should be paid not only to the morphological appearance of individual skin lesions but also to their distribution on the body surface. The search for a causative agent should be directed at chemical, physical, or biologic exposures actually occurring at the principal site(s) of involvement.

Dermatoses that is confined only to palmar surfaces usually indicates that endogenous factors are probably operative. The physical examination must help to differentiate occupational from endogenous dermatoses, principally psoriasis, atopic dermatoses, and dyshidrotic and various other forms of eczema. The entire skin surface should be examined for the presence of other characteristic skin lesions, particularly the feet. It is not unusual for an affected worker to deny the presence of skin lesions on covered parts of the body, especially if these other lesions are asymptomatic. If the entire skin surface is not properly examined, the correct diagnosis may be overlooked.

The Diagnosis III. LABORATORY: Virtually any diagnostic procedure (blood tests, potassium hydroxide [KOH] examinations, skin biopsies) may be utilized in an evaluation of a suspected occupational dermatoses, Patch testing the patch test is the most frequently employed. A great deal of confusion and misunderstanding surrounds this remarkably simple but useful test. The fundamental purpose of the patch test is to establish a diagnosis of allergic (not irritant) contact dermatoses. Interpretation of the patch test rests on the assumption that a suspected allergen will cause a localized eczematous reaction, resembling the clinical eruption under evaluation, when occluded against the skin of a sensitized individual; no reaction should occur on the skin of a nonsensitized person. Details of the methodology may be found in appropriate textbooks or manuals on the subject. The patch test should not be used to diagnose irritant contact dermatoses since the conditions of the test (total occlusion against the skin for 48 hours) seldom approximate the actual conditions under which exposure is occurring. The complications of patch testing include scarring, pigmentary alterations, infections, and accidental induction of sensitization, which did not exist prior to the test procedure.

TREATMENT = MANAGEMENT

General: Prevention. The first step of safety measure is the engineering system: the elimination of the toxic materials causing the dermatoses. When this is not practicable, then the substances should be substituted with a less toxic ones. From personal side the worker should wear PPE – Personal Protective Equipment, such as proper clothing, hand gloves of appropriate materials, safety helmet, safety glasses/goggles or face mask, etc. More details are elaborated in Prevention. Specific: Systemic: Antihistamin, antibiotics, corticosteroid (if the disease is extensive), and vitamin supplement. Topical: when wet, apply open compress with KMnO4 solution. If it is dry, apply thinly the corticosteroid cream. (calon) Pekerja.

Prognosis • Irritant dermatoses, acne and infective dermatoses are usually cured when the causative agents are eliminated. The prognosis of allergic eczema would depend on the characteristic of the allergens and the duration of exposure. • If employee can be excluded from the exposure earlier, or exposure is limited within work environment, the prognosis is good. • However, if the allergen exposure is large, such as chromium or detergent, or if there is a secondary allergic reaction to bacterial infection on eczematous lesion, the skin disease might be long life.

SPECIAL WORK PROBLEMS, restrictions, or needs caused by skin conditions.

Certain type of works may be considered unsuitable from the point of view of the employer, the insurer, or the safety engineer, though skin conditions rarely pose a safety concern. Public health considerations in healthcare, catering, and pharmaceutical industries, may preclude or delay the employment of certain applicants, for example those with untreated hand eczema, otitis externa, or scalp psoriasis. People working with ionizing radiation may not be considered suitable for work in areas of potential contamination if they have widespread skin lesions since these may provide a portal of entry and can present difficulties if decontamination becomes necessary.

Occupational Skin Cancer

Penilaian Cacat Kulit Kep.79/MEN/2003:

Pedoman Diagnosis Dan Penilaian Cacat karena Kecelakaan Dan Penyakit Akibat Kerja: Cacat Kulit Tidak mudah untuk ditetapkan.

Lampiran PP No. 14 Tahun 1993. ¾ Masih perlu pemahaman yang lebih mendalam. ¾ Cacat kulit dirujuk kepada cacat anatomis atau fungsi anggota badan. Contoh: ¾ Cacat tetap pada kulit yang menyebabkan hilangnya seluruh fungsi lengan kanan, dari atas siku kebawah, nilai kecacatannya adalah: 35% x upah. ¾ Cacat tetap pada kulit yang menyebabkan hilangnya fungsi telunjuk tangan kanannya, nilai kecacatannya adalah 9 %x upah.

Penilaian Cacat Kulit Penetapan cacat: cacat pada kulit dapat terjadi baik karena keloid / cicatrix, hipo atau hiperpigmentasi, papul yang keras dsb. yang mengganggu fungsi organ (cacat fungsi) Cacat kulit aesthetica sejauh ini masih belum dapat ditetapkan. Penetapan cacat tergantung pada gangguan fungsi organ yang tertutup kulit yang cacat.

Rehabilitation

Rehabilitation of people with occupational dermatoses rarely requires special facilities. Patients need not necessarily achieve complete clearance of their dermatitis before returning to work, especially if they can temporarily be offered alternative work away from the offending irritant or allergen. Too often employees are advised to stay off work until all traces of abnormality is gone, causing unnecessary emotional and financial strain and endangering the patient’s eventual chance of returning to their original jobs. Such action, although taken for what is thought to be the best of motives, can hinder rather than help recovery. The aim of rehabilitation in occupational dermatology is to keep the patient in the same job if at all possible, but this can be irretrievably jeopardized by prolonged sickness absence.

The foundations of successful rehabilitation are close working relationships between general

practitioners, dermatologists, occupational physicians, occupational hygienists, and employers; maintenance of contact between the patient and the place of work during any periods of sickness absence; and monitoring the employees’ progress on their return to work.

Prevention (continued)

Work-related dermatitis is preventable. Engineering controls, personal protective equipment, and employer/employee education are all potential strategies that can be used to prevent this serious illness.

Awareness of various types of occupational dermatoses and the agents that may cause them is essential to many successful preventive programs. Exposures, which may cause occupational skin disease within various occupational settings, are listed in Appendix – Potential Occupational Exposures (see separate text provided).

Protective measures that contain the industrial process and reduce workers’ exposures have been the traditional preventive measures for reducing the incidence of occupational skin disease. Protective clothing, such as gloves, boots, and aprons, are available in a number of fabrics or materials; these should be carefully selected with regard to chemical and physical resistance to workplace exposures, and workers should be cautioned concerning entrapment and occlusion of potentially noxious substances against the skin beneath protective clothing.

GOOD SKIN HYGIENE and CLEANSING are other important measures, but workers must be instructed not to clean or wash excessively with harsh substances. BARRIER CREAM have been highly touted as effective deterrents, but from a scientific viewpoint, hard evidence of efficacy is lacking. Commercially available barrier creams may be divided into four general categories: - vanishing creams that simply facilitate skin cleansing; - water-repellent barrier creams that contain film-forming, hydrophobic substances (silicone, stearates, waxes, oils); - oil-and solvent-repellent barrier creams, which contain beeswax or lanolin to repel oil, or tragacanth and acacia to repel solvent; - ionic exchangers that contain acidic or alkaline bases to buffer the effects of acids and alkalis.

Prevention (continued) In summary, Prevention of dermatitis in the workplace should ideally be accomplished through total elimination of cutaneous exposure to hazardous substances. Often, this is not feasible. Mathias sets forth the main elements of a multidimensional approach to prevention that have been identified. These elements include:

RECOGNITION of potential cutaneous irritants and allergens ENGINEERING CONTROLS or chemical substitution to prevent skin exposure PPE = with appropriate clothing or barrier creams personal and environmental hygiene REGULATIONS of potential allergens and irritants within the workplace EDUCATION: efforts to promote awareness of potential allergens and irritants motivational TECHNIQUES to promote safe work conditions and practices

Prevention (continued) MEX – Medical Examination : PE-MEX (preemployment medical examination) and P-MEX (periodic medical examination). Must cover questionnaire on medical history, and physical examination with emphasis on all body surface area, screening out for sign of eczema and /or atopy. Patch test is not recommended for screening on otherwise healthy candidate. P-MEX(Periodic Medical Examination ). In essence it is the same as PE-MEX, conducted at least annually.

Conclusions and Recommendations Thorough dermatological investigation. Walk through survey Medical advice is subject to error. Prompting an overcautious approach should be resisted in a rational manner, which can be legally defended. Emphasize on accurate identification that have genuine implications for employment. Disclosing medical report should be supplied only with the patient’s written consent, after due consideration.

Selected References and Further Readings.

Adams RM: Occupational Dermatology, ed 2, New York, 1990, Grune & Stratton. Champion, RH, Burton JL, Burns DA, Breathnach SM (ed) Textbook of Dermatology, 6th edition, pp. 144-145, Oxford, Blackwell, 1998. Cox, R.A.F., Edwards F.C., Palmer, K, Fitness For Work, The Medical Aspects, Oxford Medical Publications, Third Edition, 2000. Deteksi Dini Penyakit Akibat Kerja, Terjemahan dari Early Detection of Occupational Disease, World Health Organization, EGC, 1993. Dr. Zulmiar Yanri, PhD: Kebijakan Pemerintah Tentang Penyakit Akibat Kerja, Pertemuan Ilmiah Dermatosis Akibat Kerja II, 24-25 Agustus 2002. Posch A, Chen Z, Raulf-Heimsoth M, Baur X, latex allergens. Clin Exp Allergy 1998;28:134-140. Prof. Dr. R.S. Siregar DTM & H: Saripati Penyakit Kulit, Atlas Berwarna, Penerbit Buku Kediokteran, EGC,1996. Suma’mur P.K.: Pandangan Hiperkes Mengenai Dermatosis Akibat Kerja, Simposium Dermatosis Akibat Kerja. Jakarta, 19 Juli 1986. Zenz, Carl, O. B. Dickerson, E.P. Horvarth, Jr: Occupational Medicine, Third Edition, 1996. Keputusan Menteri Tenaga Kerja dan Transmigrasi Tentang Pedoman Diagnosis Dan Penilaian Cacat Karena Kecelakaan Dan Penyakit Akibat Kerja Menteri Tenaga Kerja Dan Transmigrasi, Maret 2003. Open sources in Web sites on related subjects.

PANITIA PELATIHAN HIPERKES DAN KESELAMATAN KERJA BAGI DOKTER IKATAN ALUMNI UNIVERSITAS INDONESIA PASCA SARJANA KEDOKTERAN KERJA D E N G A N

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