LEUKEMIA KRONIK
ETIOLOGI
Penyebab penyakit tidak diketahui secara pasti. Sama seperti tipe leukemia yang lainnya, leukemia berasal dari mutasi yang terjadi pada spesifik protein yang disebut juga dengan gen yang mengkontrol perkembangan dan pertumbuhan dari sel darah. Akibatnya sel berkembang dan bertumbuh tidak terkontrol.
LEUKEMIA LIMFOBLASTIK KRONIK
Leukemia limfoblastik leukemia (LLK) adalah gangguan pada monoklonal yang dikarakteristikkan dengan adanya proliferasi limfosit B meskipun proliferasi dari limfosit T terjadi tetapi sangat jarang. Pada leukemia ini limfosit diproduksi tetapi tidak berfungsi, dan berakumulasi di dalam darah, sumsum tulang dan jaringan limfa. Setiap individu berbeda dalam jumlah akumulasi. Biasanya leukemia ini banyak terjadi di negara-negara eropa. Jenis lainnya yang dapat dimasukkan ke dalam kategori LLK adalah sindroma sezary (merupakan fusi leukemia dari mikosis fungoides) dan leukemia sel berambut (menghasilkan sejumlah besar sel darah putih yang memiliki tonjolan khas seperti rambut bila dilihat dibawah mikroskop).
GAMBARAN KLINIS
Leukemia limfoblastik kronik mempunyai bermacam-macam jenis. Banyak pasien yang tidak menunjukkan gejala menderita LLK. Gambaran klinis diantaranya letih lesu, infeksi, hilangnya berat badan, keringat malam, limfadenopati dan hepatosplenomegali. Gambaran klinis yang lain diantaranya adalah Infeksi, fatigue, limfadenopati (80%), hepatomegali/splenomegali (50%). LLK biasanya dimulai dengan limfositosis diikuti dengan limfadenopati dan kegagalan pada sumsum tulang, 10% adanya Coomb test. Adanya limfositosis adalah merupakan ciri khas dari LLK. Biasanya 75% hingga 98% sel yang beredar didalam darah adalah limfosit. Jumlah limfosit lebih dari 5000/mm3. Bentuk dari limfosit biasanya kecil dan sudah dewasa. Jumlah sel darah putih meningkat lebih dari 20.000/mm3. Sedangkan jumlah hematokrit dan trombosit biasanya normal. Lebih dari 30% limfosit menginfiltrasi sumsum tulang.
STADIUM DAN KLASIFIKASI
Menegakkan klasifikasi atau fase dari LLK sangat penting karena berguna dalam pengambilan keputusan apakah harus diterapi atau tidak serta dalam menegakkan prognosa. Ada 2 sistem yang dipergunakan dalam pengklasifikasian stadium LLK yang berdasarkan karakteristik dari sel yaitu klasifikasi RAI dan BINET. Klasifikasi RAI lebih populer dipergunakan di Amerika, klasifikasi ini mengkategorikan LLK menjadi resiko rendah, sedang dan tinggi. Sedangkan Klasifikasi Binet lebih populer di Eropa, klasifikasi ini berdasarkan jumlah jaringan limfosit yang terganggu, anemia dan trombositopenia. Klasifikasi ini sangat simpel dan berkorelasi dengan survival.
Klasifikasi RAI
Stadium Penemuan Survival
0 Hanya limfositosis
>120 bulan
I Limfositosis plus limfodenopati
95 bulan
II Limfositosis plus spleenomegali atau hepatomegali atau keduanya
72 bulan
III
Limfositosis plus anemia 30 bulan
IV
Limfositosis plus trombositopenia 30 bulan
Klasifikasi BINET
Stadium Penemuan Survival
A Hb> 10, trombosit >100 , <3 area yang terpengaruh
>120 bulan
B Hb> 10, trombosit >100 , >3 area yang terpengaruh
84 bulan
C Hb< 10, trombosit <100 , <3 area yang terpengaruh termasuk cervical, nodul axila atau inguinal, spleen atau hati.
24 bulan
DIAGNOSA
Diagnosa ditegakkan berdasarkan pemeriksaan darah biasanya ditemukan secara tidak sengaja dengan hitung limfosit yang sangat tinggi atau disebut juga limfositosis. Menurut Mulligan (2008), penegakkan diagnosa dapat disimpulkan dari fitur pemeriksaan klinis dan fitur pemeriksaan laboratorium.
I. Fitur Pemeriksaan Klinis.
Ditemukan adanya limfadenopati dan hepatosplenomegali yang mengakibatkan infeksi, autoimunitas dan transformasi.
II. Fitur Pemeriksaan Laboratorium.
a. Morfologi – pada pemeriksaan hitung darah lengkap mungkin ditemukan adanya abnormalitas pada ukuran dan bentuk dari sel darah. Hitung sel darah merah, sel darah putih dan trombosit juga menunjukkan adanya perbedaan. Trombositopenia dan anemia biasanya terjadi pada penyakit yang sudah lanjut. Lebih dari 90% bentuk dari limfosit berukuran kecil atau sedang.
b. Fenotipe – adalah test yang dipergunakan untuk mendeteksi antigen yang ditemukan pada permukaan disekitar sel (surface). Antigen sering diidentifikasikan sebagai Cluster Differentiation (CD), diikuti oleh nomer. Contohnya adalah CD19, CD20, CD5 dan CD23. Test ini sebaiknya dilakukan incase jumlah limfosit rendah pada waktu penegakkan diagnosa LLK. Imunofenotipe menunjukkan adanya limfosit B, CD19, CD20 dan CD5.
c. Pemeriksaan sumsum tulang – pemeriksaan sumsum tulang dengan biopsi yang mengkonfirmasikan diagnosa dari LLK. Translokasi jarang terjadi, tetapi yang lebih sering terjadi adalah delesi. Kromosom yang terganggu adalah 13q (berkisar 55%), 11q (18%), trisomi 12q (16%), 17p (7%), 6q (6%) dan normal sitogenetik sekitar 18%. Delesi kromosom 11q dan 17p berhubungan dengan prognosa yang buruk dan berkembang pesat. Sedangkan delesi kromosom 13q berhubungan dengan prognosa yang baik serta survival yang lama. Prognostik Marker CD38, menunjukkan LLK yang agresif.
Pemeriksaan lain yang dibutuhkan dan cukup bermanfaat adalah:
1. Direct Antiglobulin Test (DAT) – pemeriksaan ini sangat penting pada semua pasien anemik dan sebelum terapi dilaksanakan.
2. Hitung Retikulosit
3. Fungsi ginjal dan hati
4. Serum protein elektroporesis – adanya peningkatan. Tingkat serum imunoglobulin dalam darah – Hipogammaglobulinemia, hampir setengah populasi menderita, pada stadium lanjut hampir semua pasien menderita. Bila seseorang tingkat antibodinya rendah, orang tersebut dapat lebih mudah menderita sakit. Oleh karena itu transfusi imunoglobulin mungkin bermanfaat bagi pasien. Adanya mutasi pada imunoglobin rantai berat (heavy chain) - prognosa buruk.
5. Meningkatnya jumlah limfosit 2 kali lipat dalam satu tahun mempunyai surival yang lebih rendah dibandingkan dengan meningkatnya limfosit 2 kali lipat lebih dari 1 tahun
6. Pemeriksaan Xray pada paru-paru
7. Biopsi nodul limfa – dalam beberapa kasus pemeriksaan biopsi pada limfa mungkin dibutuhkan untuk membedakannya dengan limfoma atau bila dicurigai telah bertransformasi ke limfoma.
8. CT (Computerisec Axial Tomography) Scan – berguna bila dicurigai adanya splenomegali pada pemeriksaan fisik untuk mengkonfirmasikannya.
PROGNOSA
Prognosa tergantung dari area yang terpengaruh serta hasil pemeriksaan sel darah merah dan trombosit. Stadium A, merupakan stadium awal tidak memperlihatkan gejala, nil terapi. Stadium B dan C membutuhkan terapi. Sepertiga dari LLK tidak membutuhkan terapi dan dapat hidup lebih dari 10 tahun, sedangkan sepertiga lagi berproses ke stadium berikutnya dan membutuhkan terapi, sisanya agresif dan membutuhkan terapi setelah didiagnosa. Tidak ada terapi dapat menyembuhkan LLK. Tujuan utama adalah mengkontrol simptom dan kemungkinan memperpanjang usia. Berkisar 5% Penderita LLK berkembang menjadi Large Cell Lymphoma yang sangat agresif. Prognosa pada pasien ini buruk dan hanya 5 bulan survival.
Baik Buruk
Jenis Kelamin
Perempuan Laki-laki
Stadium
A B, C
Limfosit waktu doubling
> 1 tahun < 6 bulan
ZAP 70
Negative Positive
Mutasi Somatik
Mutasi Germline
Sitogenetika
13q delesi Trisomi 12, delesi p53
PENATALAKSANAAN LEUKEMIA LIMFOSITIK KRONIK
Terapi pada Leukemia Limfositik Kronik tergantung dari stadium dari penyakitnya, mulai dari hanya mengobservasi hingga kemoterapi dan transplantasi sumsum tulang. Pada stadium awal (RAI I & II serta BINET A) tindakan hanya mengobservasi. Terapi dimulai ketika pasien mulai mengalami simptom dari penyakitnya. Pada stadium lanjut (RAI III & IV serta BINET A & B) dibutuhkan terapi. Terapi termaksud kemoterapi baik single maupun kombinasi, monoklonal antibodi, transplantasi sumsum tulang dan dosis rendah radioterapi. Pada pasien ini imun sistem mungkin terganggu, oleh karena itu antibiotik dan anti jamur mungkin dibutuhkan. Selain itu penggunaan immunoglobulin juga diberikan untuk meningkatkan sistem imunitas dan mencegah infeksi.
Chlorambucil(Leukeran)
Adalah kemoterapi oral jenis alkylating yang mana dipergunakan lebih dari 40 tahun dalam mengobati LLK.
Fludarabine
Adalah terapi standar yang dipergunakan untuk mengatasi LLK yang berprogresif.
Alemtuzumab (Campath)
Adalah recombinant antibodi monoklonal yang secara langsung melawan CD52. CD52 adalah ekspresi normal pada lapisan luar (surface) limfosit B dan T yang malignan, sel natural killer, monosit.
Rituximab
recombinant antibodi monoklonal yang secara langsung ke reseptor CD20.
Terapi radiasi
Pada dosis rendah, radiasi pada spleen menolong mengkontrol simptom dari LLK dari beberapa bulan hingga beberapa tahun.
Transplantasi sumsum tulang
Pasien yang berusia lebih muda mungkin mendapatkan manfaat dari terapi ini dengan memungkinkan untuk sembuh total, baik dengan regim mieoblatif maupun non mieoblatif.
Contoh Protokol Leukemia Limfositik Kronik
Chlorambucil 6mg/m2 D1-7 PO
Chlorambucil 4-5mg/m2 D1-14 PO
+/- Prednisone 5-25mg/hari D1-14 PO
FC
Fludarabine 25mg/m2 D1-5 IV diberikan lebih dari 30 menit
Cyclophosphamide 600-750mg/m2 D1 IV diberikan lebih dari 1 jam
Diberikan setiap 4 minggu sesuai dengan kebutuhan
Fludarabine 25mg/m2 D1-5 IV diberikan lebih dari 30 menit
Diberikan setiap 4 minggu untuk 4-6 siklus
FMD
Fludarabine 25mg/m2 D1-5 IV diberikan lebih dari 30 menit
Mitozantrone D1 IV diberikan lebih dari 1 jam
Dexamethasone
Alemtuzumab (Campath)
Alemtuzumab 30mg 3 x seminggu S/C
Berikan Diphenhydramine 50mg per oral dan Paracetamol 1gr per oral 30menit sebelum pemberian Alemtuzumab.
FMC
Fludarabine 25mg/m2 D1-3 IV diberikan lebih dari 1 jam
Mitozantrone 8mg/m2 D1 IV diberikan lebih dari 15 menit
Cyclophosphamide 200mg/m2 D1-3 IV diberikan lebih dari 1 jam
LEUKEMIA MIEOBLASTIK KRONIS
Leukemia mieloid kronis adalah gangguan yang tidak hanya meningkatnya sel mieloid di dalam darah tepi (periperal), tetapi juga meningkatnya sel eritrosit dan trombosit (keping darah).
Lebih dikenal dengan gangguan mieloproliferatif yang ditandai dengan meningkatnya neutrofil dari para prekursornya, akibatnya granulosit didalam sumsum tulang meningkat. Lebih dari 95% dari pasien mempunyai kromosom Philadelphia.
PATOGENESIS
Patogenesis dari LMK berhubungan dengan adanya kromosom yang abnormal yaitu adanya translokasi atau pertukaran antara 2 kromosom panjang 9 dan 22 yang disebut juga t(9;22). Translokasi mungkin terjadi pada tingkat sitogenetik atau pada tingkat molekul. Konsekuensi dari molekular dari translokasi ini menyebabkan terjadinya fusi protein BCR-ABL. Gen ini membuat kode protein 210-kDa yang membuat aktifitas tyrosine Kinase meningkat.
Fusi protein ini merupakan sitoplasmik aktif tyrosine kinase yang memediasi transformasi leukemia. Tyrosine Kinase sendiri adalah enzyme yang berpengaruh dalam tranduksi signal sellular. Gen Abl terletak di kromosom 9 dan diterima di tempat yang spesifik di kromosom 22 Bcr (Breakpoint cluster). Dalam kondisi normal protein Abl berpengaruh dalam proses perkembangan dan diferensiasi dari sel dan apoptosis (sel mati secara normal). Sedangkan fungsi dari protein Bcr secara normal tidak diketahui secara pasti. Pada LMK fusi dari Bcr dan Abl menyebabkan Abl tyrosine kinase menjadi aktif terus menerus tanpa dapat terkontrol oleh regulasi normal dari mekanisme sel.
GAMBARAN KLINIS
Gambaran klinis tergantung dari fase LMK. Pada fase kronik, tanda dan gejala diantaranya letih dan lesu, hilangnya berat badan, keringat, anoreksia dan pallor, serta spleenomegali yang menyebabkan nausea dan kembung. Bahkan 20% pasien tidak ada tanda dan gejala pada saat didiagnosa.
KLASIFIKASI DAN FASE PENYAKIT
Tidak ada klasifikasi yang spesifik pada LMK, hanya dapat dikategorikan dalam 3 fase perkembangannya.
Fase Kronik Indolent, kurang dari 5% sel blast dan pro mielosit (imatur granulosit) didalam darah dan sumsum tulang.
Fase Akselerasi Fase dimana pasien bertambah sakit. Sel blast berkisar 5 hingga 30% pada sumsum tulang atau darah tepi.
Basofil dalam darah lebih dari 20%
Trombositepenia tetap persisten, yang mana bukan diakibatkan oleh efek samping dari terapi.
Fase Krisis atau fase blast Fase paling berat. Lebih dari 30% sel blast didalam darah dan sumsum tulang. Pada fase ini LMK mungkin akan berubah menjadi LMA (70%) atau LLA (30%). Bila tidak ditangani akan berakibat fatal.
DIAGNOSA
Biasanya dari hasil pemeriksaan darah sudah dapat dilihat gambaran penyakitnya dengan mengevaluasi jumlah sel darah. Pada pemeriksaan darah peripheral didapati meningkatnya jumlah sel darah putih khususnya granulosit yang sudah dewasa. Konfirmasi LMK biasanya didapatkan dari pemeriksaan sumsum tulang. Sel blast atau sel leukemia ditemukan lebih dari 30% dari seluruh nukleus sel di sumsum tulang. Dengan pemeriksaan FISH serta PCR, sel leukemia dapat dideteksi yang mungkin dengan analisa mikroskopik tidak terdeteksi. Pemeriksaan ini dapat mendeteksi fusi protein BCR-ABL.
Pemeriksaan imunofenotipe dipergunakan untuk mendiagnosa dengan mempergunakan antibodi-antibodi monoklonal untunk mengidentifikasi sel surface antigen yang spesifik yang biasanya ditemukan pada tipe sel leukemia yang spesifik.
Antigen-antigen tersebut membantu dalam membedakan dari garis mana sel leukemia berkembang. Sel yang sering ditemukan pada LMA diantaranya adalah CD13, CD33 (mioblast dan monoblast), CD14 (monoblast). Pemeriksaan sitogenetik pada sumsum tulang menunjukkan adanya kromosom Philadelphia dan 95% penderita menderita kromosom ini.
PROGNOSA
Angka harapan hidup cukup rendah sebelum terapi imatinib ditemukan.
PENATALAKSANAAN LEUKEMIA MIELOBLASTIK KRONIK
Tujuan terapi pada LMK dapat dibagi menjadi 3 tingkatan respon:
1. Respon hematologi –> semua hitung sel darah dalam keadaan normal atau kembali ke normal.
Respon hematologi komplit : hitung trombosit < 450 x 10 9/L. Hitung sel darah putih <10 x 10 9/L. Pada diferensial tidak ditemukan adanya sel granulosit yang imatur dan basofil , 5%
2. Respon Sitogenetika –> menghilangkan atau menurunkan kromosom philadelphia dari sumsum tulang. Respon sitogenetika komplit artinya metafase philadelphia positive 0%. Sedangkan 1-35% meruapkan respon sitogenetika sebagian diikuti oleh minor (36-65%) dan minimal (66-95%).
3. Respon Molekul –> mengeliminasi fusi protein Bcr- Abl hingga tidak terdeteksi lagi pada test PCR. Didapatkannya respon molekul berhubungan dengan survival dari pasien. Respon molekular komplit artinya tidak terdeteksi adanya transkripsi pada DNA, sedangkan respon molekular major sekitar 0,1%.
Respon terhadap sitogenetik dan molekul berhubungan dengan panjangnya waktu remisi. Terapi tergantung fase dari penyakit, umur, status kesehatan dan tersedianya donor sel stem. Pada fase kronik, tujuan utama adalah mengkontrol penyakit, memperpanjang fase ini dan memperlambat komplikasi dan simptom. Pada orang dewasa standar praktek LMK adalah penggunaan Imatinib 400 mg per hari. Imatinib (Glivec), adalah inhibitor yang spesifik pada tyrosine kinase yang membuat encode Bcr-Abl.
Selain itu radioterapi pada limfa berguna untuk mengurangi jumlah sel leukemia. Sedangkan Splenektomi juga berguna untuk mengurangi rasa tidak nyaman pada abdomen.
Hydroxyurea
Sebelum ditemukannya imatinib, hydrosyurea merupakan salah satu terapi konvensional pada LMK. Kemoterapi ini diberikan secaral oral. Berguna dalam mengkontrol jumlah sel darah putih dan mengecilkan spleen yang membesar akibat dari LMK, juga berguna menghilangkan simptom akibar dari LMK.
Walaupun hydroxyurea dapat mengkontrol jumlah sel darah putih dan splenomegali, tetapi tidak merubah respon sitogenetka. Akibanya setiap tahun 25% dari fase kronik menjadi fase blast dengan median survival 4 tahun.
Alfa Interferon
Dibandingkan dengan hydroxyurea, alfa interferon dapat memperpanjang fase kronik dan memperpanjang survival. Bila dikombinasikan dengan kemoterapi, dapat lebih efektif, tetapi respon sitogenetika dan respon molekular masih jarang dicapai dengan terapi ini, bahkan tidak efektif dalam fase akselerasi dan krisis (fase blast).
Imatinib Mesylate (Gleevec)
Imantinib adalah terapi target, yang artinya bekerja langsung ke target yang diinginkan. Terapi merupakan inhibitor pada BCR-Abl tyrosine kinase dan dipergunakan sebagai standard dari terapi. Imatinib merupakan pilihan pertama dan yang terbaik untuk terapi LMK pada saat sekarang ini. Terapi ini menggantikan Hydroxyurea dan Alfa-Interferon. Diberikan secara oral dengan dosis 400mg pada fase kronik, dan 600mg pada fase akselerasi dan krisis.
Bila pasien tidak mendapatkan respon hematologik selama 3 bulan, atau respon sitogenetika selama 6 bulan atau respon sitogenetika komplit selama 9 bulan, dosis dapat ditingkatkan ke 600mg perhari. Bila tetap tidak ada respon selama 3 bulan dosis dapat ditingkatkan ke 800mg perhari (400mg dua kali sehari) atau penggunaan alternatif terapi.
Dengan terapi ini survival lebih dari 5 tahun meningkat dari 50% menjadi 90% (Fuerst, 2009).
Penggunaan transplantasi sumsum tulang secara allogeneik pada pasien dibawah umur 50 tahun, pada saat sekarang ini masih dalam investigasi yang mana sebelumnya merupakan terapi standard.
Bila pasien gagal dalam awal terapi dengan Imatinib, beberapa hal yang dapat dilakukan yang direkomendasikan oleh British Committe for Standard in Haematology adalah:
1. Tingkatkan dosis dari Imatinib.
2. Ganti ke generasi terbaru dari TKI’s seperti Dasatinib, Nilotinib, Bosutinib atau MK-0457.
3. Transplantasi sumsum tulang secara Allogenik.
4. Kemoterapi seperti, Cytarabine, Hydroxyurea, Busulphun.
5. Tindakan Ekperimental.
6. Transplantasi sumsum tulang secara Autograft, yang mana sel stem diambil pada saat pasien dalam remisi komplit.
7. Imunoterapi.
Adanya resistensi terhadap imatinib mungkin diakibatkan oleh terjadinya mutasi genetik pada BCR-ABL, meningkatnya produksi BCR-ABL atau terjadinya aktifasi BCR-ABL secara independent (Baver & Romvari, 2009). Generasi terbaru TKI’s, Nilotinib dan dasatinib mempunyai respon sitogenetika lebih cepat dibandingkan generasi sebelumnya (Fuerst, 2009). Dasatinib sudah disetujui untuk terapi LMK yang resisten terhadap imatinib. Nilotinib, lebih potent dari imatinib, pada fase kronik dan akselerasi bila resistent terhadap imatinib (Baver & Romvari, 2009). Belum ada solusi yang terbaik untuk mutasi T3151 (Fuerst, 2009).
Contoh protokol terapi pada LMK
Hydroxyurea 0.5 – 3 gram dua kali sehari PO Hentikan bila hitung sel darah putih kurang dari 10x10.9/L.
Imatinib 400 mg/hari pada fase kronik PO -
Imatinib 600 mg/hari pada fase akselerasi PO -
Cytarabine dosis 20mg/m2 S/C D1-10, diberikan setiap 28 hari
Showing posts with label Haematology. Show all posts
Showing posts with label Haematology. Show all posts
Friday, 31 December 2010
Sunday, 17 June 2007
ACUTE LYMPHOBLASTIC LEUKEMIA
QUESTION 1
Select a patient in your clinical setting and provide a brief descriptive profile outlining their age, diagnosis, disease stage and general treatment plan.
WT is a seventeen years old boy who was referred to Emergency Department by a GP with two weeks of legs petechia rash, hematuria, bilateral lower leg pain and general lethargic. It was also noted that he had a bruising and bleeding easily over last few days, tachycardic, and haematomesis. There were no epistaxis or melena presents.
From blood test showed that his blood counts were abnormal.
Haemoglobin: 110 l
White Cell Count: 268.5 c
Neotrhophills: 21.6 h
Platelets: 17 c
Circulating Blast Cells: 198.5 c
Lymp: 35.6 h
Mono: 8.9 h
RBC: 3.77 l
HCT: 0.33 l
Microscopy MSU:
WBC: >100 x 10,000,000
RBC: >100 x 6
Epi: <10
Chemistry: Positive of ketones, protein,
From blood test’s result, Tom was suspected with Acute Leukemia. Tom was then referred to haematology ward for further investigations after stayed overnight at children’s ward. These investigations include Bone Marrow Aspirate, CT Abdoment, Chest Xray, HIV V2V HSU serology and routine blood test such as FBC, EUC, CRP, LFT, Co agulation, & C3 nephritic factor.
After investigations were performed, Tom was finally diagnosed with Acute Lymphacytic Leukemia (ALL). The treatment plan for him includes:
To commence induction chemotherapy by using BFM 95 protocol.
Tissue typing of the family if allogenic stem cells transplant required in the future.
Sperm Banking.
Further Bone Marrow Biopsy and other test to view the response to induction therapy.
To understand leukemia, it is important to understand the process of blood formation. The formation of blood cells started in bone marrow which called haematopoiesis. Leukemia is a type of blood cancer affecting the bone marrow. Bone marrow is the spongy center of the bone that produces blood cells. All mature blood cells are originated from a pluripotent stem cell which is produced in bone marrow. Stem cell can be divided into two lineages, myeloid lineage and lymphoid lineage. These are a type of mature myeloid and lymphoid cells, including white cells or leukocytes (help the body fight against infection and other disease), red blood cells or erythrocytes (carry oxygen from the lungs to the body’s tissues and take carbon dioxide from the tissue back to the lungs), and Platelets (help form blood clots that control bleeding). These cells are normally produced in an orderly controlled way when the body needs them, but with leukemia that process gets out of control.
Leukemia means white blood. In leukemia the marrow produces too many immature white blood cells, which is called blasts. These immature white blood cells are abnormal shaped and cannot carry out their normal duties. These blasts are multiplying and crowding the bone marrow, as they interfere the production of other type of blood cells. Red cells, platelets and mature white cells will be affected. When they circulate in the body, they can be stayed in different places causing swelling or pain. Leukemia has a sudden onset and rapid progression of symptoms and disease.
Acute leukemia can be classified into acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). AML develops when maturation and proliferation of myeloid stem cell are abnormal, and ALL is established when abnormalities in maturation and proliferation of the lymphoid stem cells are occurred. In other word lymphocytic leukemia that affects the white blood cells called lymphocytes, which is the overproduction of the immature lymphocytes. Lymphocytes control the body’s immune response by finding and destroying foreign substances.
ALL is common occurred in children by two third (Cremer et al. 2002, 6). As the abnormal white blood cells cannot help the body fights against infection, frequent infections and flu-like symptoms such as fever and chills will occur. As the abnormal cells keep multiplying and move out into the body, they are tend to be collected in the lymph nodes organs such as liver or spleen or joints.
QUESTION 2
Outline the role of diagnosis and staging in the evaluation of your patient’s disease and its relevance to the general treatment plan.
Untreated ALL shows the presence of abnormal white blood count, haematocrit, haemoglobin, platelets counts, bone marrow (more than 5% blast) as well as the presents of signs and symptoms of the disease. The diagnosis can be made by performing full physical examination, blood test, bone marrow aspirate/biopsy and other additional tests. The physical examination is to find out the swelling in the liver, the spleen, and the lymph nodes under the arms, groin and the neck. From Tom’s physical examination were found that he had swelling under the arms, groin and the neck. He also had an enlarged spleen.
Blood test is performed to see what the cells look like under the microscope and compare the number of abnormal cell with the normal cells. Tom’s blood test showed that he had excessive white blood cells count (268.5) and circulating blast cells (198.5). There is no blasts should be circulating in the blood.
Bone marrow aspirate is a procedure by taking a sample of bone marrow using needle inserted into large bone, usually hip. Sometimes a small cykindrical piece of bone and marrow are also needed, this procedure is called bone marrow biopsy. This procedure will confirm weather or not the leukemia is present. The ALL can be established when 25% more of nucleated cells in the marrow contain lymphoblast.
There is no clear cut staging system for ALL according to Pui and Evans (1998, 2). They also noted that the diagnosis of ALL is depending on immunophenotyping. Unlikely AML which can be identified by the presence of auer rods, myelophoblastic leukemia, or monocyte associated esterases, ALL is lack of specific morphologic or cytochemical features (Pui & Evans, 1998, 2).
World Health Organisation (WHO) classified the types of leukemia in respect to where the cell formation is disruptive and with prognosis of outcomes. Cytogenetics can confirm the diagnosis and favourable or unfavourable outcomes.
Leukemic cell characteristic such as morphological features cytocemistry, immunologic cell surface and biochemical markers and cytogenic characteristics are important when diagnosing leukemia. However cellular classification using French, American and British (FAB) classification is limited for ALL, it is still used. The FAB classification classified ALL into three morphology types including L1 T-cell and B-cell in children, L2 T-cell and B-cell in adult, and L3 B-cell (Burkitt cell types). L1 morphology occurred in 84% of children with ALL, and 80% of Adult ALL have L2 morphology.
Immunophenotyping is more relevant to ALL when makes diagnose or prognosis. Immunophenotyping can be studied by flow cytometry. Flow cytometry and the use of monoclonal antibodies allow detecting cell surface antigents. Antigens are identified by cluster differentiation (CD) number.
The treatment plan for Tom is to commence induction chemotherapy with Vincristine, Daunorubicin, and Asparaginase without methotraxate.
QUESTION 3
Considering your answer to question 2, review the current literature and rationalize the treatment regime your patient is currently receiving.
The course of therapy for ALL can be divided into three stages:
1. Induction therapy.
2. CNS propylaxis.
3. Post remission therapy.
The aim of induction chemotherapy therapy is to achieve complete remission. Complete remission is defined by restoration of normal haematopoesis including less than 5% of blast cells present on bone marrow and no circulating blast cells.
Front-line therapy for children with ALL is mostly similar in all developed countries including Australia.
Induction chemotherapy used for Tom included:
Prednison 60 grams/m2/day per oral from day 1 to day 29.
Vincristine 1.5 grams/m2 per intravenous on day 8, 15, 22, 29. Daunorubicin 30 milligrams /m2 per intravenous on day 8 & 15. Asparaginase 5000 units/m2 per intravenous on day 12, 15, 18, 21, 24, 27, 30, 33.
It is called BFM 95 protocol with modification. For his treatment, metotraxate was not used.
The side effect of Asparaginase is quite significant. For some patients, coagulopathies, pancreatitis and allergic reaction could occur. Therefore, a test dose of 100 units of asparaginase subcute is required 45 minutes prior to the therapy. APPT, PT, Fibronogen level and Pancreatic Lipase test should be taken prior to asparaginase. If fibrinogen level <1.0 g/l or Lipase level are rising, a specialist has to be contacted. When pancreatitis is present, no further dose is to be given (RNSH Hematology Department, 2001).
Gated heart pool scan cardiac echo needs to be considered to rule out ventricular dysfunction if further dose of daunorubicin required, as this chemotherapy is toxic to the heart at cumulative dose of 400 mg/m2. For high risk ALL, additional dose might be added on day 22 and 29 (RNSH Hematology Department, 2001).
After normal hematopoesis was restored post induction therapy which is called in remissio, patient will be a candidate for intensification (consolidation) therapy. The treatment will commence shortly after the induction of remission. According to RNS Haematology Protocol for Chemotherapy (2001), the treatment protocol for Tom is called BFM 95 Protocol MCA which includes Methotrexate given in high dose, 6-mercaptopurine per oral plus Cytarabine. For High risk ALL, Etoposide and Asparaginase are added without 6-Mercaptopurine. This protocol is called BFM 95 Element HR-3.
Pui et al (p. 7) also suggested that intensive multi drug therapy commenced post induction of remission will make remission lasting-longer, especially in young adults. Cyclosphomide and Cytarabine might be benefit for patient’s with T-cell ALL. It was also suggested that Cytarabine with dose will improve the outcome of patient with standard, risk, or high risk ALL (Pui et al. p. 7).
Some suggestion made by Gaynon (2002, 1) that the progress of the treatment also can be achieved by improving the post induction therapy. Pui et al (p. 7) concluded that the successful cure of ALL depends on the development of more effective multi drugs regime on well designed clinical trial. Tom has not started with intensification therapy yet as he just commenced with induction therapy.
Most of the patient with ALL can be expected to attain complete remission status following appropriate induction therapy. According to Pui et al. (p.6) the rate of complete remission for ALL in children now ranges from 97 to 99 percent and lower in adult from 75 to 90 percent. All patients with ALL are at risk of developing central nervous system involvement during the course of their disease.
QUESTION 4
Identify two actual or potential complications that may confront your patient in light of their treatment regime or disease progression.
Nausea and vomiting was perceived by patients to be the most distressing side effect of chemotherapy (Coulbourne, 1995, p. 442; Potter & Schafer, 1999, p.2). Chemotherapy drugs have been cited to often cause nausea and vomiting within 1-2 hours. However, some drugs induce these symptoms several hours after treatment. Symptoms observed ranged between a mild to severe level of severity, depending on the types of the drugs and the doses used. Usually this condition was cited to resolve within 24 hours or over several days (Held-Warmkessel, 1998, p. 43).
Chemotherapy drugs were seen to have a potential inducing nausea and vomiting in a variety of ways. Drugs associated with pronounced nausea and vomiting were noted to be that of Camustine, Cisplatin, Cyclophosphomide, Cytarabine, Dacarbazine, Dactinomycin, Doxorubicin HCl, Lomustine, Mechlorethamine HCL, and Procarbazine HCl (Glick, Griffith & Mortimer, 1998, p. 50). According to RNSH Chemotherapy Patient Information Leaflet (2001), Asparaginase and Daunorubicin have a potential nausea and vomiting side effects. It is not only on early side effects, but also on late side effects. However, mild nausea might be expected in Vincristine.
Dodd, Onishi, Dibble & Larson (1996, p. 160) determined the differences in the side effects of nausea, vomiting and retching between younger and older patients receiving chemotherapy. This research reported that younger patients’ consistently had higher nausea, vomiting, and retching than older patients. Therefore, this finding suggested that older patients could be given more aggressive chemotherapy regimes, as they were seen to be able to tolerate them better than younger patients (Dodd et al., 1996, p. 160).
Fatigue was reported as the most common and debilitating response to chemotherapy treatment (Carrol-Johnson et al, p. 116; Held-Warmkessel, 1998, p. 42; Mast, 1998; Richardson, et al. 1998). Patients receiving chemotherapy for the treatment of cancer, frequently experience severe fatigue, which was seen to be highly distruptive and distressing (Richardson & Ream, 1997, p. 35). Fatigue will be expected for patients who are receiving Asparaginase, Vincristine, and Daunorubicin (RNSH Chemotherapy Patient Information Leaflet, 2001).
Fatigue was also cited to increase over the time that the patient receives chemotherapy treatment (Berger, 1998, p. 51-62; Carrol-Johnson, et al. 1998, p 116; Richardson, et al. 1998) and after treatment (Carrol-Johnson, et al. 1998, p 116). The level of fatigue was reported to occur frequently in the afternoon and early evening, and perpetuate throughout the day (Richardson, et al. 1998). It was cited that fatigue reverted to baseline levels before the next chemotherapy cycle, and persisted for years after treatment has been completed (Carrol-Johnson, et al. 1998, p 116).
Fatigue was cited to affect the general well-being of patients, by weakness, and negative effects such as their general well-being, their specific body parts, change in self image and their daily activities. There were reported to be varying degrees and dimensions of ‘being tired’. Tiredness was not only seen as physical in nature, but also mentally exhausting (Messias, Yeager, Dibble & Dood, 1997, p. 45). Medication, nutritional status, work, and other physical conditions were seen to implicate the cause of fatigue. Patients, who were viewed to have more energy, were reported to be less tired with a lower dose of chemotherapy or on the termination of treatment (Messias et al. 1997, p.46).
When it came to patients’ awareness and expectations, some persons were reported to not have prepared for the degree or the extent of fatigue that they may experience, while others recognized the invetability and the expectations of the fatigue on the bases of their prior knowledge (Messias et al. 1997, p.46). It was also reported that "patient express frustration, worry, concern, displeasure, fear, depression, and disappointment regarding their fatigue" (Messias et al. 1997, p.46). Some patients experience frustration by the extent and the dimension of their tiredness. Others reported being annoyed or bothered by the fatigue. Fatigue was also viewed to be associated with mood and energy levels. It was seen to diminish patients’ levels of functioning and slow their pace of operation, decrease their threshold for activity, and make the person totally disabled. Patients who were tired have been seen to have difficulty with sleeping, a need for increased sleep, and also observed to lack a desire to be active. As a result of the adverse reactions from chemotherapy, patients who had fatigue were cited to be working fewer hours, taking increased time off, experiencing diminished interest and productivity, and frequently expressing their concern about the possible negative effects of not working or not going to school (Messias et al. 1997, p.46).
Dimensions of fatigue were described as the extent of fatigue, distress caused by fatigue, the influence of fatigue on the ability to engage in social activities and impact of fatigue on work related activities. By knowing these dimensions of fatigue, the nurse will be able to provide more effective help for individual who experienced fatigue (Richardson et al. 1998).
Select a patient in your clinical setting and provide a brief descriptive profile outlining their age, diagnosis, disease stage and general treatment plan.
WT is a seventeen years old boy who was referred to Emergency Department by a GP with two weeks of legs petechia rash, hematuria, bilateral lower leg pain and general lethargic. It was also noted that he had a bruising and bleeding easily over last few days, tachycardic, and haematomesis. There were no epistaxis or melena presents.
From blood test showed that his blood counts were abnormal.
Haemoglobin: 110 l
White Cell Count: 268.5 c
Neotrhophills: 21.6 h
Platelets: 17 c
Circulating Blast Cells: 198.5 c
Lymp: 35.6 h
Mono: 8.9 h
RBC: 3.77 l
HCT: 0.33 l
Microscopy MSU:
WBC: >100 x 10,000,000
RBC: >100 x 6
Epi: <10
Chemistry: Positive of ketones, protein,
From blood test’s result, Tom was suspected with Acute Leukemia. Tom was then referred to haematology ward for further investigations after stayed overnight at children’s ward. These investigations include Bone Marrow Aspirate, CT Abdoment, Chest Xray, HIV V2V HSU serology and routine blood test such as FBC, EUC, CRP, LFT, Co agulation, & C3 nephritic factor.
After investigations were performed, Tom was finally diagnosed with Acute Lymphacytic Leukemia (ALL). The treatment plan for him includes:
To commence induction chemotherapy by using BFM 95 protocol.
Tissue typing of the family if allogenic stem cells transplant required in the future.
Sperm Banking.
Further Bone Marrow Biopsy and other test to view the response to induction therapy.
To understand leukemia, it is important to understand the process of blood formation. The formation of blood cells started in bone marrow which called haematopoiesis. Leukemia is a type of blood cancer affecting the bone marrow. Bone marrow is the spongy center of the bone that produces blood cells. All mature blood cells are originated from a pluripotent stem cell which is produced in bone marrow. Stem cell can be divided into two lineages, myeloid lineage and lymphoid lineage. These are a type of mature myeloid and lymphoid cells, including white cells or leukocytes (help the body fight against infection and other disease), red blood cells or erythrocytes (carry oxygen from the lungs to the body’s tissues and take carbon dioxide from the tissue back to the lungs), and Platelets (help form blood clots that control bleeding). These cells are normally produced in an orderly controlled way when the body needs them, but with leukemia that process gets out of control.
Leukemia means white blood. In leukemia the marrow produces too many immature white blood cells, which is called blasts. These immature white blood cells are abnormal shaped and cannot carry out their normal duties. These blasts are multiplying and crowding the bone marrow, as they interfere the production of other type of blood cells. Red cells, platelets and mature white cells will be affected. When they circulate in the body, they can be stayed in different places causing swelling or pain. Leukemia has a sudden onset and rapid progression of symptoms and disease.
Acute leukemia can be classified into acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). AML develops when maturation and proliferation of myeloid stem cell are abnormal, and ALL is established when abnormalities in maturation and proliferation of the lymphoid stem cells are occurred. In other word lymphocytic leukemia that affects the white blood cells called lymphocytes, which is the overproduction of the immature lymphocytes. Lymphocytes control the body’s immune response by finding and destroying foreign substances.
ALL is common occurred in children by two third (Cremer et al. 2002, 6). As the abnormal white blood cells cannot help the body fights against infection, frequent infections and flu-like symptoms such as fever and chills will occur. As the abnormal cells keep multiplying and move out into the body, they are tend to be collected in the lymph nodes organs such as liver or spleen or joints.
QUESTION 2
Outline the role of diagnosis and staging in the evaluation of your patient’s disease and its relevance to the general treatment plan.
Untreated ALL shows the presence of abnormal white blood count, haematocrit, haemoglobin, platelets counts, bone marrow (more than 5% blast) as well as the presents of signs and symptoms of the disease. The diagnosis can be made by performing full physical examination, blood test, bone marrow aspirate/biopsy and other additional tests. The physical examination is to find out the swelling in the liver, the spleen, and the lymph nodes under the arms, groin and the neck. From Tom’s physical examination were found that he had swelling under the arms, groin and the neck. He also had an enlarged spleen.
Blood test is performed to see what the cells look like under the microscope and compare the number of abnormal cell with the normal cells. Tom’s blood test showed that he had excessive white blood cells count (268.5) and circulating blast cells (198.5). There is no blasts should be circulating in the blood.
Bone marrow aspirate is a procedure by taking a sample of bone marrow using needle inserted into large bone, usually hip. Sometimes a small cykindrical piece of bone and marrow are also needed, this procedure is called bone marrow biopsy. This procedure will confirm weather or not the leukemia is present. The ALL can be established when 25% more of nucleated cells in the marrow contain lymphoblast.
There is no clear cut staging system for ALL according to Pui and Evans (1998, 2). They also noted that the diagnosis of ALL is depending on immunophenotyping. Unlikely AML which can be identified by the presence of auer rods, myelophoblastic leukemia, or monocyte associated esterases, ALL is lack of specific morphologic or cytochemical features (Pui & Evans, 1998, 2).
World Health Organisation (WHO) classified the types of leukemia in respect to where the cell formation is disruptive and with prognosis of outcomes. Cytogenetics can confirm the diagnosis and favourable or unfavourable outcomes.
Leukemic cell characteristic such as morphological features cytocemistry, immunologic cell surface and biochemical markers and cytogenic characteristics are important when diagnosing leukemia. However cellular classification using French, American and British (FAB) classification is limited for ALL, it is still used. The FAB classification classified ALL into three morphology types including L1 T-cell and B-cell in children, L2 T-cell and B-cell in adult, and L3 B-cell (Burkitt cell types). L1 morphology occurred in 84% of children with ALL, and 80% of Adult ALL have L2 morphology.
Immunophenotyping is more relevant to ALL when makes diagnose or prognosis. Immunophenotyping can be studied by flow cytometry. Flow cytometry and the use of monoclonal antibodies allow detecting cell surface antigents. Antigens are identified by cluster differentiation (CD) number.
The treatment plan for Tom is to commence induction chemotherapy with Vincristine, Daunorubicin, and Asparaginase without methotraxate.
QUESTION 3
Considering your answer to question 2, review the current literature and rationalize the treatment regime your patient is currently receiving.
The course of therapy for ALL can be divided into three stages:
1. Induction therapy.
2. CNS propylaxis.
3. Post remission therapy.
The aim of induction chemotherapy therapy is to achieve complete remission. Complete remission is defined by restoration of normal haematopoesis including less than 5% of blast cells present on bone marrow and no circulating blast cells.
Front-line therapy for children with ALL is mostly similar in all developed countries including Australia.
Induction chemotherapy used for Tom included:
Prednison 60 grams/m2/day per oral from day 1 to day 29.
Vincristine 1.5 grams/m2 per intravenous on day 8, 15, 22, 29. Daunorubicin 30 milligrams /m2 per intravenous on day 8 & 15. Asparaginase 5000 units/m2 per intravenous on day 12, 15, 18, 21, 24, 27, 30, 33.
It is called BFM 95 protocol with modification. For his treatment, metotraxate was not used.
The side effect of Asparaginase is quite significant. For some patients, coagulopathies, pancreatitis and allergic reaction could occur. Therefore, a test dose of 100 units of asparaginase subcute is required 45 minutes prior to the therapy. APPT, PT, Fibronogen level and Pancreatic Lipase test should be taken prior to asparaginase. If fibrinogen level <1.0 g/l or Lipase level are rising, a specialist has to be contacted. When pancreatitis is present, no further dose is to be given (RNSH Hematology Department, 2001).
Gated heart pool scan cardiac echo needs to be considered to rule out ventricular dysfunction if further dose of daunorubicin required, as this chemotherapy is toxic to the heart at cumulative dose of 400 mg/m2. For high risk ALL, additional dose might be added on day 22 and 29 (RNSH Hematology Department, 2001).
After normal hematopoesis was restored post induction therapy which is called in remissio, patient will be a candidate for intensification (consolidation) therapy. The treatment will commence shortly after the induction of remission. According to RNS Haematology Protocol for Chemotherapy (2001), the treatment protocol for Tom is called BFM 95 Protocol MCA which includes Methotrexate given in high dose, 6-mercaptopurine per oral plus Cytarabine. For High risk ALL, Etoposide and Asparaginase are added without 6-Mercaptopurine. This protocol is called BFM 95 Element HR-3.
Pui et al (p. 7) also suggested that intensive multi drug therapy commenced post induction of remission will make remission lasting-longer, especially in young adults. Cyclosphomide and Cytarabine might be benefit for patient’s with T-cell ALL. It was also suggested that Cytarabine with dose will improve the outcome of patient with standard, risk, or high risk ALL (Pui et al. p. 7).
Some suggestion made by Gaynon (2002, 1) that the progress of the treatment also can be achieved by improving the post induction therapy. Pui et al (p. 7) concluded that the successful cure of ALL depends on the development of more effective multi drugs regime on well designed clinical trial. Tom has not started with intensification therapy yet as he just commenced with induction therapy.
Most of the patient with ALL can be expected to attain complete remission status following appropriate induction therapy. According to Pui et al. (p.6) the rate of complete remission for ALL in children now ranges from 97 to 99 percent and lower in adult from 75 to 90 percent. All patients with ALL are at risk of developing central nervous system involvement during the course of their disease.
QUESTION 4
Identify two actual or potential complications that may confront your patient in light of their treatment regime or disease progression.
Nausea and vomiting was perceived by patients to be the most distressing side effect of chemotherapy (Coulbourne, 1995, p. 442; Potter & Schafer, 1999, p.2). Chemotherapy drugs have been cited to often cause nausea and vomiting within 1-2 hours. However, some drugs induce these symptoms several hours after treatment. Symptoms observed ranged between a mild to severe level of severity, depending on the types of the drugs and the doses used. Usually this condition was cited to resolve within 24 hours or over several days (Held-Warmkessel, 1998, p. 43).
Chemotherapy drugs were seen to have a potential inducing nausea and vomiting in a variety of ways. Drugs associated with pronounced nausea and vomiting were noted to be that of Camustine, Cisplatin, Cyclophosphomide, Cytarabine, Dacarbazine, Dactinomycin, Doxorubicin HCl, Lomustine, Mechlorethamine HCL, and Procarbazine HCl (Glick, Griffith & Mortimer, 1998, p. 50). According to RNSH Chemotherapy Patient Information Leaflet (2001), Asparaginase and Daunorubicin have a potential nausea and vomiting side effects. It is not only on early side effects, but also on late side effects. However, mild nausea might be expected in Vincristine.
Dodd, Onishi, Dibble & Larson (1996, p. 160) determined the differences in the side effects of nausea, vomiting and retching between younger and older patients receiving chemotherapy. This research reported that younger patients’ consistently had higher nausea, vomiting, and retching than older patients. Therefore, this finding suggested that older patients could be given more aggressive chemotherapy regimes, as they were seen to be able to tolerate them better than younger patients (Dodd et al., 1996, p. 160).
Fatigue was reported as the most common and debilitating response to chemotherapy treatment (Carrol-Johnson et al, p. 116; Held-Warmkessel, 1998, p. 42; Mast, 1998; Richardson, et al. 1998). Patients receiving chemotherapy for the treatment of cancer, frequently experience severe fatigue, which was seen to be highly distruptive and distressing (Richardson & Ream, 1997, p. 35). Fatigue will be expected for patients who are receiving Asparaginase, Vincristine, and Daunorubicin (RNSH Chemotherapy Patient Information Leaflet, 2001).
Fatigue was also cited to increase over the time that the patient receives chemotherapy treatment (Berger, 1998, p. 51-62; Carrol-Johnson, et al. 1998, p 116; Richardson, et al. 1998) and after treatment (Carrol-Johnson, et al. 1998, p 116). The level of fatigue was reported to occur frequently in the afternoon and early evening, and perpetuate throughout the day (Richardson, et al. 1998). It was cited that fatigue reverted to baseline levels before the next chemotherapy cycle, and persisted for years after treatment has been completed (Carrol-Johnson, et al. 1998, p 116).
Fatigue was cited to affect the general well-being of patients, by weakness, and negative effects such as their general well-being, their specific body parts, change in self image and their daily activities. There were reported to be varying degrees and dimensions of ‘being tired’. Tiredness was not only seen as physical in nature, but also mentally exhausting (Messias, Yeager, Dibble & Dood, 1997, p. 45). Medication, nutritional status, work, and other physical conditions were seen to implicate the cause of fatigue. Patients, who were viewed to have more energy, were reported to be less tired with a lower dose of chemotherapy or on the termination of treatment (Messias et al. 1997, p.46).
When it came to patients’ awareness and expectations, some persons were reported to not have prepared for the degree or the extent of fatigue that they may experience, while others recognized the invetability and the expectations of the fatigue on the bases of their prior knowledge (Messias et al. 1997, p.46). It was also reported that "patient express frustration, worry, concern, displeasure, fear, depression, and disappointment regarding their fatigue" (Messias et al. 1997, p.46). Some patients experience frustration by the extent and the dimension of their tiredness. Others reported being annoyed or bothered by the fatigue. Fatigue was also viewed to be associated with mood and energy levels. It was seen to diminish patients’ levels of functioning and slow their pace of operation, decrease their threshold for activity, and make the person totally disabled. Patients who were tired have been seen to have difficulty with sleeping, a need for increased sleep, and also observed to lack a desire to be active. As a result of the adverse reactions from chemotherapy, patients who had fatigue were cited to be working fewer hours, taking increased time off, experiencing diminished interest and productivity, and frequently expressing their concern about the possible negative effects of not working or not going to school (Messias et al. 1997, p.46).
Dimensions of fatigue were described as the extent of fatigue, distress caused by fatigue, the influence of fatigue on the ability to engage in social activities and impact of fatigue on work related activities. By knowing these dimensions of fatigue, the nurse will be able to provide more effective help for individual who experienced fatigue (Richardson et al. 1998).
Subscribe to:
Comments (Atom)