LAPORAN KASUS MORBUS HANSEN
Pembimbing: dr. Sri Adila Nurainiwati, Sp.KK dr. DN Pravitasari, Sp.KK
Oleh : Imron Rosyadi 201420401011117
SMF KULIT DAN KELAMIN RSUD JOMBANG FAKULTAS KEDOKTERAN UNIVERSITAS MUHAMMADIYAH MALANG 2016
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KATA PENGANTAR
Assalamu’alaikum warahmatullahi wabarakatuh Segala puji bagi Allah SWT atas segala rahmat dan hidayah-Nya, shalawat serta salam terlimpahkan kepada Nabi Muhammad SAW, keluarga dan para sahabatnya. Syukur Alhamdulillah, penulis dapat menyelesaikan laporan kasus yang berjudul “MORBUS HANSEN”. Dalam penyelesaian laporan kasus ini penulis ingin mengucapkan terima kasih yang tak terhingga kepada : 1. dr.Andri Catur Jatmiko, Sp.KK, dr. Sri Adila Nurainiwati, Sp.KK dan dr. DN Pravitasari, Sp.KK. 2. Seluruh tenaga medis maupun non-medis RSUD Kabupaten Jombang khususnya bagian instalasi kulit dan kelamin. 3. Seluruh teman-teman dokter muda di RSUD Kabupaten Jombang, atas dukungan serta doanya. Laporan kasus ini masih jauh dari kesempurnaan. Dengan kerendahan hati penulis mohon maaf yang sebesar-besarnya dan mengharapkan saran serta kritik yang membangun. Semoga laporan kasus ini dapat menambah wawasan dan bermanfaat bagi semua pihak. Wassalamu’alaikum Wassalamu’alaikum warahmatullahi wabarakatuh
Jombang, 28 Agustus 2016
Penulis
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DAFTAR ISI
HALAMAN JUDUL ................................. ....................................................... ............................................ .............................. ........ i KATA PENGANTAR ............................................................... .................................................................................. ................... ii DAFTAR ISI ................................................ ....................................................................... ............................................. .......................... .... iii BAB I TINJAUAN PUSTAKA ........................................... .................................................................. ....................... 1 1.1 Pendahuluan ............................................ .................................................................. ............................................ ........................ 1 1.2 Definisi ............................................. ................................................................... ............................................ .............................. ........ 1 1.3 Epidemiologi ........................................... ................................................................. ............................................ ........................ 1 1.4 Etiologi ........................................... ................................................................. ............................................ ............................................. ........................... .... 4 1.5 Patogenesis ........................................... .................................................................. ............................................. .......................... .... 3 2.6 Gejala klinis .......................................... ................................................................. ............................................. ............................................ .......................... .... 5 2.7 Diagnosis .......................................... ................................................................. ............................................. ............................................ .......................... .... 6 2.8 Diagnosis Banding .......................................... ................................................................. ............................................. ............................................ .......................... .... 8 2.9 Penatalaksanaan .......................................... ................................................................. ............................................. ............................................ .......................... .... 9 2.10 Prognosis .......................................... ................................................................. ............................................. ............................................ .......................... .... 10
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2.1 Identitas Penderita ............................................. ................................................................... .......................... .... 12 2.2 Anamnesis .......................................... ................................................................ ......................................... ................... 12 2.3 Pemeriksaan Fisik ............................................. ................................................................... .......................... .... 13 2.4 Pemeriksaan Penunjang .......................... ................................................. ...................................... ............... 15 2.5 Resume ...................... ............................................ ............................................ ............................................ ........................ 16 2.6 Diagnosis ......................................... ............................................................... ............................................ ........................ 16 2.7 Diagnosis Banding.......................................... ................................................................ .............................. ........ 16 2.9 Planning ............................................... ..................................................................... ......................................... ................... 16 2.10 Prognosis ........................................... ................................................................. ......................................... ................... 17 BAB III PEMBAHASAN .......................................... ................................................................ .................................. ............ 18 BAB IV KESIMPULAN ............................................................... .............................................................................. ............... 21 DAFTAR PUSTAKA .......................................... ................................................................ ......................................... ................... 23
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BAB I TINJAUAN PUSTAKA
1.1 Pendahuluan
Penyakit Morbus Hansen atau di masyarakat lebih sering dikenal dengan sebutan lepra atau kusta adalah sebuah penyakit infeksi kronik dan penyebabnya adalah Mycobacterium Leprae (M. Leprae) yang bersifat intraselula r obligat.1 Penyakit kusta juga disebut dengan penyakit Hansen, yaitu suatu penyakit infeksi kronik yang bermanifestasi terhadap kulit dan kelainan nervus perifer. Manifestasi dari penyakit kusta ini berbeda dari seseorang atau dengan yang lain tergantung imune system di system di penderita. Diagnosis penyakit kusta didasarkan pada beberapa parameter klinik, yaitu pemeriksaan lesi di kulit dan pemeriksaan saraf perifer. Dan ditemukannya bakteri berbentuk basil yang tahan asam yang didapatkan dari kerokan jaringan kulit melalui pemeriksaan Ziehl- Neelsen’s Neelsen’s yang merupakan pemeriksaan penunjang penyakit kusta. 2 1.2 Definisi
Penyakit Morbus Hansen atau di masyarakat lebih sering dikenal dengan sebutan lepra atau kusta adalah sebuah penyakit infeksi kronik dan penyebabnya adalah Mycobacterium Leprae ( M. M. Leprae) Leprae) yang bersifat intraselular obligat. Saraf perifer sebagai afinitas pertama lalu kulit, dan mukusa traktus respiratorius bagian atas, kemudian dapat ke organ lain kecuali susunan saraf pusat. 1 1.3 Epidemiologi
Penyakit kusta menyebar di seluruh dunia mulai dari Afrika, Amerika, Asia Tenggara, Mediterania Timur dan Pasifik Barat. Dapat menyerang semua umur, frekwensi tertinggi pada kelompok umur antara 30-50 tahun dan lebih sering mengenai laki-laki daripada wanita. Sementara itu di regional Asia Tenggara distribusi kasus kusta bervariasi berdasarkan penemuan kasus baru dan prevalensi seperti terlihat dalam tabel dibawah ini :
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Tabel 1.1 Situasi Kusta di wilayah WHO-SEARO pada tahun 2011 4 Jumlah kasus baru yang ditemukan ( case ) detec detecti ti on r ate
Jumlah kasus kusta terdaftar (prevalensi) awal tahun 2012
3.970
3.300
23
29
Data tidak tersedia
Data tidak tersedia
India
127.295
83.187
Indonesia
20.023
23.169
Maladewa
14
2
Myanmar
3.082
2.735
Nepal
3.184
2.410
Sri Lanka
2.178
1.565
Thailand
280
678
Timor Leste
83
72
160.132
117.147
Negara
Bangladesh Bhutan Korea Utara
Total
Dari data-data tersebut di atas dapat disimpulkan bahwa penyakit kusta masih menjadi masalah di Indonesia yang menempati urutan ke 4 di Asia Tenggara. Di Indonesia penderita kusta terdapat hampir pada seluruh propinsi dengan pola penyebaran yang tidak merata. Meskipun pada pertengahan tahun 2000 Indonesia secara nasional sudah mencapai eliminasi kusta namun pada tahun tahun 2002 sampai dengan tahun 2006 terjadi peningkatan penderita kusta baruPada tahun 2006 jumlah penderita kusta baru di Indonesia sebanyak 17.921 orang. Propinsi terbanyak melaporkan penderita kusta baru adalah Maluku, Papua, Sulawesi Utara dan Sulawesi Selatan dengan prevalensi lebih besar dari 20 per 100.000 penduduk. Pada tahun 2010, tercatat 17.012 kasus baru kusta di
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tahun 2011, tercatat 19.371 kasus baru kusta di Indonesia dengan angka prevalensi 8,03 per 100.000 penduduk 1.4 Etiologi
Kuman penyebab adalah Mycobacterium adalah Mycobacterium leprae yang leprae yang ditemukan oleh G.A. HANSEN pada tahun 1874 di Norwegia, yang sampai sekarang belum juga dapat dibiakkan dalam media artificial. artificial. M. leprae berbentuk basil dengan ukuran 38Umx0,5Um, tahan asam dan alkohol serta Gram positif. 1
1.5 Patogenesis
Sebenarnya M. leprae mempunyai patogenitas dan daya invasi yang rendah, sebab penderita yang mengandung kuman lebih banyak belum tentu memberikan
gejala
yang
lebih
berat,
bahkan
dapat
sebaliknya.
Ketidakseimbangan antara derajat infeksi dengan derajat penyakit, tidak lain disebabkan oleh respon imun yang berbeda. 5 Meskipun cara masuk M. leprae belum diketahui secara pasti, tetapi beberapa penelitian
memperlihatkan bahwa yang tersering melalui kulit yang
lecet pada bagian tubuh yang bersuhu dingin dan melalui mukosa nasal (secar a inhalasi). Pengaruh M. leprae terhadap kulit bergantung pada faktor imunitas seseorang, kemampuan hidup M. leprae pada suhu tubuh yang rendah, waktu regenerasi yang lama, serta sifat kuman yang avirulen dan nontoksis.5 Pada kusta tipe LL terjadi kelumpuhan sistem imunitas seluler, dengan demikian makrofag tidak mampu menghancurkan kuman sehingga kuman daapat bermultiplikasi dengan bebas, yang kemudian dapat merusak jaringan. ja ringan. Sedangkan
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Klasifikasi kusta didasarkan berbagai criteria yaitu manifestasi klinis, bakteriologis, imunologis dan histopatologis. Manifestasi berupa lesi kulit dan gejala neurologi adalah yang terpenting.5 Tabel 1.2 Bagan Diagnosis Klinis Menurut WHO 1 Sifat
Kusta Pausibasiler (PB)
Lesi Kulit Makula datar, papul yang meninggi, nodus
Kusta Multibasilar (MB)
1-5 lesi
>6 lesi
Hipopigmentasi/eritema
Distribusi lebih simetris
Distribusi tidak simetris Hilangnya sensasi yang jelas
Hilangnya sensasi kurang jelas
Hanya satu cabang saraf
Banyak cabang saraf
Kerusakan saraf Menyebabkan hilangnya sensasi/kelemahan otot yang dipersarafi oleh saraf yang terkena
Sedangkan klasifikasi kusta menurut Ridley-Jopling adalah sebagai berikut : Tabel 1.3 Klasifikasi Kusta Ridley-Jopling6 Resistensi tinggi TT
Lesi
Satu / dua
Un stabl e r esi esi stan ce
Tidak resisten
BT
BB
BL
LL
Sedikit
Sedikit / beberapa, asimetris
Banyak
Banyak dan simetris
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Gambar 1.1. Penderita Kusta Tipe Tuberkuloid & Bordeline
Gambar 1.2.Penderita Kusta Tipe Lepramatosa
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Gambar 1.4. Penderita Kusta Tipe B.B dan B.T.
1.7 Gejala Klinis
Gejala klinis pada morbus hansen dapat dilihat berdasarkan kelainan saraf tepi dan kelainan kulit dan organ lainnya seperti berikut 7 :
1. Kelainan saraf tepi Kerusakan saraf tepi bisa bersifat sensorik, motorik, autonomik. Sensorik biasanya berupa hipoestesia ataupun anastesia pada kulit yang
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Kelianan kulit bisa hipopigmentasi ataupun eritematus dengan adanya g angguan estesi yang jelas. Bila gejala lanjut dapat timbul gejala akibat banyaknya kuman, 7
yaitu :
a. Facies leonina (gejala infiltrasi difus di muka) b. Penebalan cuping telinga c. Madarosis (penipisan alis bagian lateral) d. Anastesi simetris pada kedua tungkai. 1.8 Diagnosis
Untuk menetapkan diagnosis penyakit kusta perlu dicari tanda-tanda utama atau tanda kardinal, yaitu4 : A. Lesi (kelainan) kulit yang mati rasa. B. Penebalan saraf tepi yang disertai dengan gangguan fungsi saraf. C. Ditemukannya M. leprae pada pemeriksaan bakteriologis Pemeriksaan Klinis yang lengkap dan lengkap sangat penting dalam menegakkan diagnosis kusta. Pemeriksaan tersebut meliputi :
a. Anamnesis Pada anamnesis ditanyakan lengkap mengenai riwayat datangnya keluhan8
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3. Karakteristik lesi kulit : bercak kusta tidak gatal dan biasanya tidak nyeri. Rambut rontok biasanya ada pada kulit yang terdapat bercak. 4. Keringat : area lesi di kulit biasanya tidak berkeringat 5. Riwayat rekuren : lesi yang hilang timbul atau musiman biasanya bukan kusta -
Pertanyaan yang lain : 1. Apakah kulit menjadi lebih kering di sekitar bercak? 2. Apakah tangan dan kaki menjadi lemah? 3. Apakah merasakan hilang rasa raba atau rasa yang abnormal di tangan atau kaki? Apakah ada masalah ketika memegang, menggerakkan, atau mengangkat benda atau saat aktifitas?
-
Kelainan yang lain :
Mulai kapan terjadinya, lama keluhan tersebut dan perkembangannya? perkembangannya?
-
Riwayat pengobatan : Pengobatan apa yang telah dilakukan, nama obat yang didapatkan
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Pemeriksaan sensibilitas suhu dilakukan dengan cara tes panas dingin.
Terhadap rasa nyeri digunakan jarum pentul
Terhadap raba digunakan kapas.
2. Pemeriksaan fungsi saraf perifer Gangguan fungsi saraf tepi ini biasanya akibat dari peradangan kronis pada saraf tepi (neuritis perifer). Pemeriksaan dilakukan pada saraf-saraf tepi yang paling sering terlibat dalam penyakit kusta, dan dapat diraba, seperti4 :
Tempat terjadinya kerusakan saraf Pada umumnya, kerusakan saraf tepi yang sering terkena seperti gambar di bawah ini 8:
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Kehilangan fungsi sensorik : di area yang di suplai oleh nervus, misalnya dengan tes fungsi sensorik.
Kekuatan otot (VMT) : menilai kekuatan gerakan dari Otot Voluntar.
Tabel 2.4 Fungsi Saraf Perifer 4
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Gangguan otonomik terhadap kelenjar keringat dilakukan guratan tes (lesi digores dengan tinta) penderita exercise, exercise, bila tinta masih jelas, maka tes menunjukkan positif (Gunawan Test). 7
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Gambar 2.3 Pengambilan kerokan di lesi dan cuping telinga 9
Bentuk-bentuk kuman kusta yang dapat ditemukan dalam lapangan mikroskop 4 :
Bentuk utuh (solid) a. Dinding sel tidak putus b. Mengambil zat warna secara merata c. Panjang kuman 4 kali lebarnya
Bentuk pecah-pecah ( fragmented ) a. Dinding sel terputus mungkin sebagian atau seluruhnya b. Pengambilan zat warna tidak merata
Bentuk granular ( granulated ) Kelihatan seperti titik-titik tersusun garis lurus atau berkelompok
Bentuk globus Beberapa BTA utuh atau fragmented atau granulated mengadakan ikatan atau kelompok. Kelompok kecil 40-60 BTA.
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Tabel 2.5 Indeks Bakteri (IB) 4,9 Jumlah Bakteri
0
0 BTA dalam 100 LP, hitung 100 lapangan pandang
1+
1-10 BTA dalam 100 LP, hitung 100 lapangan pandang
2+
1-10 BTA dalam 10 LP, hitung 100 lapangan pandang
3+
1-10 BTA dalam rata-rata 1 LP, hitung 25 lapangan pandang
4+
10-100 BTA dalam rata-rata 1 LP, hitung 25 lapangan pandang
5+
100-1000 BTA dalam rata-rata 1 LP, hitung 25 lapangan pandang
6+
>1000 BTA atau 5 clumps ditemukan dalam rata-rata 1 lapangan
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saraf sensoris sulit dilakukan, juga pada lesi dini contohnya pada tipe interminate, serta untuk menentukan klasifikasi yang tepat. 5 Biopsy seharusnya diambil dari tepi lesi yang aktif dan diambil secara luas sampai ke jaringan subkutan. Pemeriksaan histologist dari penyakit Hansen berkorelasi dengan gejala klinis penyakit. Adanya kelainan saraf merupaan karakteristik dari penyakit Hansen dan histological perineural dan kelainan saraf meningkatkan kemungkinan adanya penyakit Hansen. 6 Ada beberapa kegunaan dalam pemeriksaan histopatologi dari pasien penyakit kusta, yaitu 10: a.
Untuk menegakkan diagnosis penyakit kusta
b.
Untuk mengetahui klasidikasi lesi pada penyakit kusta
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Hasil pemeriksaan histology histology BB hampir sama yaitu yaitu adanya sel epitheloid dan macrofag tanpa membentuk granuloma
yang jelas.
Limphosit sedikit dan tersebar dan giant cell mulnitucleat tidak ada, hal ini yang membedakan dengan histology dari BT. 10 d. Borderline Lepromatous Leprosy (BL) Leprosy (BL) Pada hasil pemeriksaan histology BL, terdapat bentukan histiosit, lebih banyak daripada sel epitheloid. Limphosit bisa ada di dalam granuloma.6 e. Lepramatous Leprosy (LL) Leprosy (LL) Makrofag granuloma pada LL besar dan terdapat foam cells dengan jumlah limfosit yang jarang. Basil yang solid tertumpuk membentuk seperti rokok dan terlihat sebagai globi. 10
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terbentuk dapat bersifat spesifik terhadap M. leprae yaitu antibodi anti phenolic glycolipid (PGL-1) dan antibodi antiprotein 16 kD serta 35 kD.1 Sedangkan antibodi yang tidak spesifik antara lain antibodi antilipoarabinomanan (LAM) yang juga dihasilkan oleh kuman M. Tuberculosis1. Kegunaan pemeriksaan serologik ini ialah dapat membantu diagnosis kusta yang meragukan karena tanda klinis dan bakteriologik tidak jelas. Disamping itu dapat membantu menentukan kusta subklinis, karena tidak didapati lesi kulit misalnya pada narakontak serumah. Macam-macam pemeriksaan serologik kusta lainnya adalah 1:
Uji MLPA (mycobacterium leprae particle aglutination)
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-Lamprene 50mg/hari -DDS 100mg/hari Pengobatan dilakukan secara teratur sebanyak 12 dosis (bulan) dan diselesaikan dalam waktu maksimal 18 bulan. Setelah selesai 12 dosis dinyatakan RFT, meskipun secara klinis lesiya masih aktif dan BTA(+).
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BAB 2 TINJAUAN KASUS
2.1 Identitas Penderita
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2.2.4Riwayat Penyakit Keluarga: -
Saat ini tidak ada keluarga yang sakit seperti ini.
2.2.5Riwayat 2.2.5 Riwayat Sosial: -
Sebelumnya pasien berada bekerja sebagai tukang las di Surabaya.
2.2.6 Riwayat Alergi
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