http://www.ascp.org/pdf/SneekPeekPracDiagofHemDisorders.aspx http://www.kalbemed.com/Portals/6/04_194CMEPendekatan%20Klinis%20dan%20Diagnosis%20Anemia.pdf
BAB I PENDAHULUAN
Anemia merupakan masalah medik yang paling sering dijumpai di klinik di seluruh dunia, di samping sebagai masalah kesehatan utama masyarakat, terutama di Negara berkembang. Kelainan ini merupakan penyebab debilitas kronik (chronic debility) yang mempunyai dampak besar terhadap kesejahteraan sosial dan ekonomi serta kesehatan fisik. Oleh karena frekuensinya yang demikian sering, anemia terutama anemia ringan seringkali tidak mendapat perhatian dan dilewati oleh para dokter di praktek klinik. Berdasarkan data WHO tahun 2005, penderita anemia di Indonesia >40% dari total populasi, dimana sebagian besar merupakan anak-anak dan wanita hamil.WHO. hamil.WHO. Worldwide prevalence of anemia 1993-2005. 2005. Atlanta: CDC. Anemia didefinisikan sebagai berkurangnya 1 atau lebih parameter sel darah merah: konsentrasi hemoglobin, hematokrit atau jumlah sel darah merah. Menurut kriteria WHO anemia adalah kadar hemoglobin di ba bawah 13 g% pad pada pria dan di bawah 12 g% pad pada wanita. Berdasarkan kriteria WHO yang direvisi/ kriteria National Cancer Institute, anemia adalah kadar hemoglobin di bawah 14 g% pada pria dan di bawah 12 g% pada wanita. Kriteria ini digunakan untuk evaluasi anemia pada penderita dengan keganasan. Schrier SL. Approach to the adult patient with anemia. January 2011. [cited 2011, June 9 ]. Available from: www.uptodate.com Pendekatan Klinis dan Diagnosis AnemiaAmaylia OehadianSubbagian Hematologi Onkologi Medik, CDK-194/ vol. 39 no. 6, th. 2012 Anemia bukanlah suatu kesatuan penyakit tersendiri (disease entity), tetapi merupakan gejala berbagai macam penyakit dasar (underlying disease). Oleh karena itu, dalam diagnosis anemia tidaklah cukup hanya sampai kepada label anemia tetapi harus dapat ditetapkan penyakit dasar yang menyebabkan anemia tersebut. Hal ini penting karena seringkali penyakit dasar tersebut tersembunyi, sehingga apabila hal ini dapat diungkap akan menuntun para klinisi kearah penyakit berbahaya yang tersembunyi. tersembun yi. Penentuan penyakit dasar juga penting dalam pengelolaan kasus anemia, karena tanpa mengetahui penyebab yang mendasari anemia tidak dapat diberikan terapi yang tuntas pada kasus anemia an emia tersebut.
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Pendekatan terhadap terhadap pasien anemia memerlukan pemahaman tentang pathogenesis dan patofisiologi anemia serta keterampilan dalam memilih, menganalisis serta merangkum hasil anamnesis, pemeriksaan fisik, pemeriksaan laboratorium dan pemeriksaan penunjan g lainnya. Bakta, Prof. Dr. I. Made. 2007. Hematologi Klinik Ringkas Ringkas.. Jakarta: Penerbit Buku Kedokteran EGC.
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BAB II TINJAUAN PUSTAKA
2.1 Sistem Hematopoesis 2.1.1 Tahapan hematopoesis
Sistem hematopoetik mempunyai karakteristik berupa pergantian sel yang konstan dengan konsekuensi untuk mempertahankan populasi leukosit, trombosit dan eritrosit. Sistem 1
hematopoetik dibagi menjadi 3, yaitu : 1. Sel stem (progenitor awal) yang menyokong hematopoesis 2. Colony forming unit (CFU) (CFU) sebagai pelopor yang selanjutnya berkembang dan berdiferensiasi dalam memproduksi sel 3. Faktor regulator yang mengatur agar sistem berlangsung beraturan
Perkembangan sistem vaskuler dan hematopoesis dimulai pada awal kehidupan embrio dan berlangsung secara paralel/bersamaan sampai masa dewasa. Perkembangan ini mempunyai hubungan dengan lokasi anatomi yang menyokong hematopoesis tersebut. Secara garis besar perkembangan hematopoesis dibagi menjadi 3 periode: 1. Hematopoesis yolk sac (mesoblastik atau primitif) Sel darah dibuat dari jaringan mesenkim 2-3 minggu setelah fertilisasi. Mula-mula sel tersebut dibentuk dalam pulau-pulau darah (blood (blood islands) islands) dari yolk sac yang merupakan pelopor
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IL-3, IL-6, dan faktor sel stem. Sel induk hematopoesis (blood (blood borne pluripotent hematopoetic progenitors) progenitors) mulai berkelompok dalam hati janin pada masa gestasi 5-6 minggu. Pada masa gestasi 8 minggu blood islands mengalami islands mengalami regresi. 2. Hematopoesis hati (definitif) Hematopoesis hati berasal dari sel stem pluripoten yang berpindah dari yolk sac. Hematopoesis terbentuk dalam hati saat masa gestasi 9 minggu. Hematopoesis dalam hati yang terutama adalah eritropoesis, namun masih ditemukan pula sirkulasi granulosit dan trombosit. Hematopoesis hati mencapai puncaknya pada masa gestasi 4-5 bulan kemudian mengalami regresi perlahan-lahan. Pada masa pertengahan kehamilan, tampak pelopor hematopoetik terdapat di limpa, thymus, kelenjar limfe, dan ginjal. Dalam limpa dibentuk eritropoesis dan leukopoesis sampai bulan kelima kehidupan fetus. Limpa terutama membentuk sistem limfosit. Timus terutama membentuk limfosit, sedikit mielosit dan eritroblas. 3. Hematopoesis medular Merupakan periode terakhir dalam sistem hematopoesis dan dimulai sejak masa gestasi 4 bulan. Ruang medular terbentuk dalam tulang rawan dan tulang panjang dengan proses reabsorpsi. Mula-mula sel eritropoetik terutama dibuat dalam hati sedangkan sel leukosit dalam sumsum tulang. Namun dalam perkembangan selanjutnya fungsi pembuatan sel darah diambil alih oleh sumsum tulang dan hepar tidak berfungsi lagi untuk membuat sel darah. Pada masa gestasi 32 minggu sampai lahir semua rongga sumsum tulang diisi jaringan hematopoetik yang aktif dan sumsum tulang penuh berisi sel darah. Sel mesenkim yang mempunyai kemampuan untuk membentuk sel darah menjadi berkurang namun tetap ada dalam sumsum tulang, hati, limpa, kelenjar getah bening, dan dinding usus. Sel-sel ini dikenal secara umum sebagai sistem retikuloendotelial. Pada bayi dan anak, hematopoesis yang aktif terutama terdapat pada sumsum tulang, termasuk bagian distal tulang panjang. Sedangkan pada dewasa sistem hematopoetik terbatas pada vertebra, tulang iga, sternum, pelvis, skapula, tulang tengkorak, dan jarang berlokasi pada tulang panjang.
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Gambar 1. Tahapan hematopoesis Sumber: http://www.medscape.com/viewarticle/497032_2
2.1.2 Eritropoesis Eritropoesis adalah suatu proses dimana terjadi pembentukan/produksi dari sel darah
merah/eritrosit. Proses ini distimulasi oleh berkurangnya oksigen dalam sirkulasi. Rendahnya kadar oksigen dalam darah dideteksi oleh ginjal, yang kemudian mensekresikan hormon eritropoetin. Hormon ini menstimulasi proliferasi dan diferensiasi dari prekursor sel darah merah, yang kemudian mengaktivasi sistem eritropoesis pada sistem hematopoetik. Dalam proses maturasi sel darah merah, sel tersebut mengalami suatu rangkaian diferensiasi. Hemositoblas merupakan suatu stem cell hematopoetik yang pluripoten. Sel ini kemudian berdiferensiasi menjadi common myeloid progenitor dan common lymphoid progenitor . Sel darah merah sendiri dibentuk dari diferensiasi dari common myeloid progenitor , sedangkan common lymphoid progenitor merupakan prekursor dari sel limfosit. Common
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normoblast menghilang dan menjadi polychromatic erythrocyte (retikulosit). Retikulosit dilepaskan dari sum-sum tulang dan masuk ke dalam sirkulasi, sebelum kemudian menjadi eritrosit matur setelah 1-2 hari berada dalam sirkulasi. Dalam sirkulasi darah dapat ditemukan kurang lebih 1% retikulosit. Dalam proses maturasi sel darah merah ini dibutuhkan dua vitamin, yaitu vitamin B12 dan asam folat. Defisiensi dari salah satu vitamin ini menyebabkan kegagalan maturasi sel darah merah, yang bermanifestasi sebagai retikulositopenia.
Gambar 2. Sistem hematopoetik Sumber: http://upload.wikimedia.org/wikipedia/commons/thumb/a/a1/Hematopoietic_growth_factors.png /350px-Hematopoietic_growth_factors.png
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Gambar 3. Maturasi sel darah Sumber: http://www.irvingcrowley.com/cls/hemchart.gif
2.2 Hemoglobin 2.2.1 Susunan hemoglobin Hemoglobin merupakan kompleks protein yang terdiri dari heme, yang mengandung besi,
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A. Hemoglobin embrional Selama masa gestasi 2 minggu pertama, eritroblas primitif dalam yolk sac membentuk rantai globin-epsilon ( ( ) dan zeta (Z) yang akan membentuk hemoglobin primitif Gower-1 (Z2 (Z22). Selanjutnya mulai sintesis rantai mengganti rantai zeta, rantai mengganti rantai di yolk sac, yang akan membentuk Hb-Portland (Z2 (Z22) dan Gower-2 ( (22). Hemoglobin yang terutama ditemukan pada masa gestasi 4-8 minggu adalah Hb Gower-1 dan Gower-2 yaitu kira-kira 75% dan merupakan hemoglobin yang disintesis di yolk sac, tetapi akan menghilang pada masa gestasi 3 bulan. B. Hemoglobin fetal Migrasi pluripoten sel stem dari yolk sac ke hati, diikuti dengan sintesis hemoglobin fetal (22) dan awal dari sintesis rantai . Setelah masa gestasi 8 minggu, Hb F merupakan hemoglobin yang paling dominan dan setelah janin berusia 6 bulan, Hb F merupakan 90% dari keseluruhan hemoglobin. Kadar Hb F akan berkurang bertahap. Pada saat lahir, ditemukan kirakira 70% Hb F dalam sirkulasi. Sintesis Hb F menurun secara cepat setelah bayi lahir. Setelah usia bayi 6-12 bulan, hanya sedikit ditemukan Hb F dalam sirkulasi. C. Hemoglobin dewasa Pada masa embrio telah dapat dideteksi HbA1 (22) karena telah terjadi perubahan rantai sintesis rantai menjadi dan selanjutnya globin meningkat. Pada masa gestasi 6 bulan ditemukan 5-10% HbA , sedangkan pada waktu lahir mencapai 30%. Pada saat bayi berusia 6-12
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Gambar 4. Hemoglobin prenatal-postnatal
Sumber: http://www.blackwellpublishing.com/korfgenetics/jpg/300_96dpi/Fig13-1.jpg
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Gambar 5. Struktur hemoglobin Sumber: http://gassama.myweb.uga.edu/hemoglobinmolecule.gif
2.2.2 Fungsi hemoglobin Hemoglobin merupakan protein yang berfungsi mengangkut oksigen dari paru-paru ke
jaringan, serta mengangkut karbon dioksida dari jaringan kembali ke paru-paru.
Gambar 6. Fungsi hemoglobin Sumber: http://images.lifescript.com/images/ebsco/images/si55551170.jpg
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molekul asam - amino- levulinat ( (-amino levulinic acid), disingkat menjadi -ALA. Dua molekul -ALA ini bersenyawa untuk membentuk porfobilinogen yang mempunyai struktur pirol. Empat molekul porfobilinogen akhirnya membentuk ikat porfirin (protoporfirin IX) dan setelah mengikuti Fe++ dibentuklah hem. Peristiwa ini terjadi dalam mitokondria sel tubuh atau sel darah muda. Dengan globin yang telah terbentuk tersebut, hem membentuk hemoglobin. Penghancuran sel darah merah terjadi dalam sistem retikuloendotelial, yaitu dalam hati dan limpa. Rantai porfirin dipecah oleh suatu proses oksidasi pada jembatan -metan, sedangkan Fe tetap terikat pada ada persenyawaan dan globin pun tetap tidak terputus. Persenyawaan ini disebut verdo-hemoglobin. Kemudian Fe dan globin lepas dan terbentuklah biliverdin. Dalam tubuh manusia, biliverdin ini cepat diubah menjadi bilirubin. Fe yang dilepaskan diikat oleh protein dalam jaringan dan melalui plasma diangkut untuk dipergunakan kembali, sedangkan globin yang dilepaskan selanjutnya akan dipecah menjadi asam amino lagi. Bilirubin yang dibentuk (tidak larut dalam air) diikat oleh albumin dan diangkut dalam plasma dari tempat penghancuran hemoglobin tersebut ke hati. Dalam hati bilirubin ini bersenyawa dengan asam glukoronat dengan bantuan enzim glukoronil transferase. Bilirubin yang belum bersenyawa dengan asam glukoronat disebut bilirubin indirek. Sedangkat bilrubin yang telah bersenyawa dengan asam glukoronat disebut bilirubin direk. Bilirubin direk ini akan keluar dari hati dan masuk ke dalam saluran pencernaan. Oleh bakteri dalam usus bilirubin direk ini akan diubah menjadi urobilinogen. Selanjutnya urobilinogen akan dioksidasi menjadi urobilin yang akan dikeluarkan bersama-sama tinja (disebut sterkobilin). Sebagian dari urobilinogen yang terdapat
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Gambar 7. Heme
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Wanita tidak hamil ( ( 15 tahun)
12
Wanita hamil
11
Pria ( ( 15 tahun)
13
Tabel 1. Batas nilai hemoglobin berdasarkan usia dan gender
Berikut ini merupakan prevalensi global dari anemia berdasarkan data WHO yang dikumpulkan dari tahun 1993 hingga 2005.
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Sindrom Fanconi yang biasanya disertai kelainan bawaan lain seperti mikrosefali, strabismus, anomali jari, kelainan ginjal, dan sebagainya. a.2 Faktor didapat 1. Bahan kimia, seperti benzene, insektisida, dan lain-lain 2.
Obat-obatan,
seperti
kloramfenikol,
mesantoin
(antikonvulsan),
piribenzamin
(antihistamin), obat sitostatika (myleran, methotrexate, vincristine, dan sebagainya) 3. Radiasi 4. Idiopatik
b. Anemia defisiensi Anemia defisiensi adalah anemia yang disebabkan oleh kekurangan satu atau beberapa bahan yang diperlukan untuk pematangan eritrosit.
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Anemia defisiensi vitamin B12 dapat terjadi pada vegetarian, sebab vitamin B12 banyak terkandung pada produk hewani (telur, daging, susu). Selain itu defisiensi vitamin B12 juga dapat terjadi pada kasus gangguan absorpsi vitamin B12 karena defisiensi faktor intrinsik, yaitu protein yang esensial untuk absorpsi vitamin B12 di ileum. Keadaan ini sering disebut anemia pernisiosa. Terjadi destruksi autoimun terhadap sel parietal dari lambung yang memproduksi faktor intrinsik sehingga terjadilah malabsorpsi vitamin B12.
c. Anemia karena penyakit kronis c.1 Penyakit ginjal Ginjal memproduksi hormon eritropoetin (EPO) yang akan menstimulasi sum-sum tulang untuk memproduksi sel darah merah. Pada keadaan gangguan ginjal, ginjal tidak dapat memproduksi EPO dalam jumlah yang adekuat sehingga produksi sel darah merah pun akan terganggu.
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Keadaan ini berbeda dari anemia aplastik, dimana pada pure red cell aplasia aplasia ini produksi 7
leukosit dan trombosit normal . PRCA dapat disebabkan oleh kelainan congenital, infeksi virus, atau karena penggunaan obat-obatan tertentu (Azathioprine, kloramfenikol, tiamfenikol, isoniazid, dll).
2. Penghancuran Terjadi akibat penghancuran (hemolisis) eritrosit yang berlebihan. Anemia hemolitik dapat terjadi akibat kelainan intrasel (proses hemolisis terdapat dalam eritrosit sendiri) ataupun ekstrasel. Proses hemolisis intrasel umumnya disebabkan oleh kelainan bawaan (congenital (congenital ), ), sedangkan hemolisis ekstrasel umumnya disebabkan oleh faktor yang didapat (acquired (acquired ). ). a. Faktor intrasel Sickle cell anemia, talasemia, anemia, talasemia, sferositosis congenital, defisiensi enzim eritrosit (G-6PD, piruvat kinase, glutation reduktase).
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Perdarahan yang bersifat kronis dapat disebabkan oleh perdarahan gastrointestinal, misalnya karena ulkus peptikum. Selain itu juga dapat disebabkan oleh proses keganasan, seperti kanker kolon, walaupun jarang terjadi pada anak-anak. Perdarahan yang bersifat kronis ini akan menyebabkan defisiensi zat besi. 2.3.3 Patofisiologi Pada keadaan normal, ketika tubuh mengalami hipoksia, akan terjadi dua mekanisme
untuk mengatasi keadaan hipoksia ini yaitu peningkatan ekspresi eritropoetin dan penurunan ekspresi hepcidin. Hepcidin sendiri merupakan hormon peptida yang diproduksi oleh liver yang berfungsi untuk mengatur homeostasis zat besi dalam tubuh. Hepcidin menginhibisi transport zat
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menstimulasi liver untuk mensekresikan hepcidin sehingga terjadi penurunan absorpsi zat besi dan peningkatan sekuestrasi zat besi. Semua mekanisme tersebut akan berujung pada keadaan anemia. Defisiensi nutrisional dan inflitrasi sum-sum tulang juga akan menyebabkan anemia akibat menurunnya respon sum-sum tulang terhadap EPO.
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terjadi gangguan pertumbuhan anak karena adanya metabolisme seluler yang terganggu. Biasanya hal ini disertai dengan keadaan anoreksia dan maturasi seksual yang terlambat.
2.3.5 Diagnosa Diagnosa dapat ditegakkan dari anamnesis, pemeriksaan fisik, dan pemeriksaan
penunjang. 2.3.5.1 Anamnesis
Anamnesis harus dilakukan dengan teliti agar dapat ditemukan kelainan yang mendasari
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menunjukkan adanya trombositopenia atau gangguan pendarahan yang lain. Hal ini dapat mengindikasikan bahwa lebih dari 1 sistem hematopoetik sumsum tulang yang terlibat, atau dapat juga menunjukan bahwa koagulopati merupakan penyebab anemia karena adanya perdarahan. Gali adanya gejala-gejala yang dapat menunjukkan adanya penyakit lain yang mendasari, seperti penyakit jantung, liver, dan ginjal, ataupun infeksi kronis.
2.3.5.2 Pemeriksaan Fisik
Pertama-tama perhatikan habitus pasien. Amati adanya habitus yang tidak normal, seperti
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1. Pemeriksaan darah lengkap dan zat besi Untuk menegakkan diagnosis anemia, diperlukan pemeriksaan darah lengkap, yang mencakup kadar hemoglobin, hematokrit, leukosit, dan trombosit, serta mean corpuscular
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Pada anemia mikrositik hipokrom, dapat dilakukan pengukuran kadar zat besi dalam serum ( serum serum iron), iron), total-iron binding capacity capacity (TIBC), dan feritin serum atau zat besi dalam
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Tabel 4. Anemia mikrositik hipokrom (MCV < 83 fl; MCHC < 31%) 31%) Total Iron-
Bone
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