Jumat, 06 Mei 2011
Leukemia
Epidemiology
Leukemia Incidence in the United States is 13 per 100,000 population per year (Wilson, 1991). Leukemia in children ranging in 3-4 cases per 100,000 children / year. For ANLL incidence in the United States about 3 per 200,000 people per year. While in England, Germany, and Japan range from 2-3 per 100,000 population per year (Rahayu, 1993, cit Nugroho, 1998). In a study of leukemia at Dr. Soetomo / FK Unair during August-December 1996 recorded was 25 cases of acute leukemia from 33 patients with leukemia. With 10 people suffering from ALL (40%) and 15 people suffering from AML (60%) (Boediwarsono, 1998).
Etiology
The cause of leukemia as yet unclear, but several factors thought to be the cause of, among others:
1.Genetik
a.keturunan
a.1. The existence of Chromosome Irregularities
The incidence of leukemia is increased in patients with congenital abnormalities, such as in Down syndrome, syndrome, Bloom's, Fanconi's anemia, syndrome Wiskott-Aldrich syndrome, Ellis van Creveld syndrome, Kleinfelter, D-Trisomy syndrome, syndrome, von Reckinghausen, and neurofibromatosis (Wiernik, 1985; Wilson, 1991). Congenital abnormalities are associated closely with the change of gene information, eg on chromosome 21 or C-Trisomy group, or an unstable chromosome pattern, as in aneuploidy.
a.2. Sibling
Reported a high risk of acute leukemia in identical twins where cases of acute leukemia occurred in the first year of birth. This applies also in families with a very high incidence of leukemia (Wiernik, 1985).
Environmental b.Faktor
Several environmental factors known to cause chromosomal damage to earnings, eg radiation, chemicals, and drugs associated with an increased incidence of acute leukemia, particularly ANLL (Wiernik, 1985; Wilson, 1991).
2.Virus
In many experiments have found the fact that RNA viruses cause leukemia in animals including primates.
Research in humans found an RNA-dependent DNA polymerase in leukemia cells but not found in normal cells and the enzyme is derived from a virus which is a type C RNA viruses that cause leukemia in animals.(Wiernik, 1985). One of the viruses that are proven to cause leukemia in humans is the Human T-Cell Leukemia. Types of leukemia are caused by T-Cell Acute Leukemia. This virus was discovered by Takatsuki et al (Kumala, 1999).
3.Chemistry and Drug
a.Chemistry
Kromis exposure of chemicals (eg benzene) was associated with an increased incidence of acute leukemia, for example on the cobbler who are often exposed to benzene. (Wiernik, 1985; Wilson, 1991)
Besides benzene several other materials associated with high risk of AML, such as: product - petroleum products, paints, ethylene oxide, herbicides, pesticides, and electromagnetic fields (Fauci, et. Al, 1998).
b.drugs
Anti-neoplastic drugs (eg alkilator and topoisomere II inhibitors) can lead to chromosomal aberrations that cause AML. Chloramphenicol, phenylbutazone, and methoxypsoralen reported to cause bone marrow failure which gradually became AML (Fauci, et. Al, 1998).
4.Radiasi
Close relationship between radiation and leukemia (ANLL) was found in patients with ankylosing anxylosing who received radiation therapy, and in other cases, such as increased incidence of leukemia in the Japanese population that survived the atomic bomb explosion. Also found increased risk of leukemia in patients who received radiation therapy eg thymic enlargement, workers exposed to radiation and the radiological.
Secondary 5.Leukemia
Leukemia occurring after treatment of other malignancies disease called Secondary Acute Leukemia (SAL) or treatment related leukemia.Diseases including Hodgin, limphoma, myeloma, and breast cancer. This is because the drugs used include immunosuppressive groups other than cause can cause DNA damage.
definition of Acute Leukemia
Acute leukemia is a primary malignancy of bone marrow that result in abnormal blood components terdesaknya (blastocyst), accompanied by the spread to other organs. (Guidelines for Diagnosis and Treatment of Child Health. Airlangga University School of Medicine & dr Soetomo, 1994).
Pathogenesis of Acute Leukemia
Abnormal blastocyst fails to differentiate into mature forms and the division process continues. These cells urgent hemopoitik components resulting in failure of normal bone marrow function. In addition, the abnormal cells through the blood circulation to infiltration into the organs of the body.(Guidelines for Diagnosis and Treatment of Child Health. Airlangga University School of Medicine & dr Soetomo, 1994).
Clinical manifestations of acute leukemia patients due to the replacement of cells in the bone marrow by leukemik cells, causing disruption of red blood cell production. Depression of platelet production that caused purpura and bleeding tendency. The failure of cellular defense mechanism because the replacement of white blood cells by leukemik cells, which causes the high possibility of infection. Leukemik cells infiltration into vital organs like the liver and spleen by leukemik cells that can cause enlargement of these organs. (Cawson, 1982).
Classification of Acute Leukemia
Based on the classification of French American British (FAB), acute leukemia is divided into 2 (two), Limphocytic Acute Leukemia (ALL) and Acute Myelogenous Leukemia (AML).
ALL itself is divided into 3, namely:
L1
Leukemia cells consist of a homogeneous limfoblas and L1 is a lot of attacking the children.
L2
Composed of cells limfoblas more heterogeneous when compared with L1. ALL of this type is often suffered by adults.
L3
Limfoblas consists of a homogeneous, with the characteristics of Burkitt cells. Occur both in adults and children alike with a poor prognosis.
AML is divided into 8 types:
Mo (Acute Undifferentiated Leukemia)
Is the least mature forms of AML, also known as AML with minimal differentiation.
M1 (Acute Myeloid Leukemia without maturation)
It is a classic mieloblastik leukemia that occurred nearly a quarter of cases of AML. In AML there is a picture of this type of azurophilic granules and Auer rods. And leukemik cells are divided into 2 types, type 1 and type 2 without granules with granules, where type 1 is dominant in M1.
M2 (Acute Myeloid Leukemia)
Tues leukemik on M2 shows the maturity of a morphologically distinct, with the number of granulocytes from promielosit that turned into mature granulocytes amounted to more than 10%. The number of cells leukemik between 30-90%. But more than 50% of the total bone marrow cells in M2 is mielosit and promielosit.
M3 (Promyelocitic Acute Leukemia)
Leukemic cells in M3 mostly promielosit with heavy granulation, stain mieloperoksidase + strong. The nucleus varies in shape and size, sometimes berlobul. Cytoplasm contains large granules, and some promielosit contain granule-like dust. Disseminated intravascular presence coagulation (DIC) associated with these abnormal granule-granule.
M4 (Acute Myelomonocytic Leukemia)
Visible 2 (two) types of cells, namely granulositik and monositik, and leukemik cells more than 30% of the cells that are not eritroit. M4 is similar to M1, distinguished by the way 20% of cells are cells that are not eritroit monositik on track, with the stages of maturation different.
The number of monocytes in peripheral blood over 5,000 / uL. Another sign of the M4 is the increased proportion of eosinophils in bone marrow, more than 5% darisel non eritroit, called M4 with eoshinophilia. Patients with AML type M4 has good response to chemotherapy-induced standard.
M5 (Acute Monocytic Leukemia)
On the M5 there are more than 80% of the cells is not eritroit monoblas, promonosit, and monocytes. Divided into two, M5a which is dominant monocyte monoblas, being on M5b is promonosit and monocytes. M5a rarely occurs and results of treatment pretty well.
M6 (Erythroleukemia)
Bone marrow consists of more than 50% eritroblas with different degrees of morphological bizzare. Eritroblas has a picture of abnormal morphology in the form of a giant multinukleat. This megaloblastic changes associated with maturation are not consistent between the nucleus and cytoplasm. M6 called Myelodisplastic Syndrome (MDS) if the cell leukemik less than 30% of the cells that are not eritroit. M6 rare and usually relapse of chemotherapy-induced standard.
M7 (Acute Megakaryocytic Leukemia)
Some cells seemed shaped promegakariosit / megakariosit.
(Yoshida, 1998; Wetzler and Bloomfield, 1998).
Clinical manifestations of acute leukemia
Clinical symptoms most frequently encountered are:
Anemia: pale, easily tired, sometimes shortness of breath.
Leukopenia (due to decreased function): local or general infection (sepsis) with symptoms of body heat (fever) and decreased general condition.
Thrombocytopenia: bleeding skin, mucosa and other places.
As a result of infiltration to other organs:
Bone pain.
Enlarged lymph nodes.
Hepatomegaly and splenomegaly
(Guidelines for Diagnosis and Treatment of Child Health. Airlangga University School of Medicine & dr Soetomo, 1994).
Other symptoms such as Purpura, epistaxis (often), hematoma, infection oropharingeal, enlarged lymph nodes, weakness (weakness), pharyngitis, flu-like symptoms (flu-like syndrome) which is the initial clinical manifestations, lymphadenopathy, jaundice seizures to coma (Cawson 1982; De Vita Jr., 1985, Archida, 1987, Lister, 1990, Rubin, 1992).
examination and diagnosis of Acute Leukemia
Enforcement diagnosis of acute leukemia is based on a diagnose, clinical examination, blood tests and examination of bone marrow in some cases.
On examination of blood, white blood cells showed an increase in the amount of the declines, as well as normal.
Examination showed decreased number of platelets.
Examination showed decreased hemoglobin values (De Vita Jr., 1993).Examination of red blood cells showed reduced number and abnormal morphology (Cawson, 1982; De Vita Jr., 1993).
The presence of 5% leukemik cells is sufficient to diagnose blood disorders as leukemia, but is often used value of 25% or more (Altman JA, 1988 cit De Vita Jr., 1993).
Inspection with staining Sudan Black, PAS, and mieloperoksidase for AML and ALL distinction, (De Vita Jr., 1993; Boediwarsono, 1996; Yoshida, 1996).
Blood smear: normokrom, normositer, almost always found abnormal blastocyst.
Hiperseluler bone marrow, is almost always full with abnormal blastocyst, the normal hemopoitik recessive.
(Guidelines for Diagnosis and Treatment of Child Health. Airlangga University School of Medicine & dr Soetomo, 1994).
Diagnosis
When you find a collection of symptoms: anemia, bleeding, enlarged lymph nodes and hepatosplenomegaly, peripheral blood examination.
When the examination of peripheral blood there are suspicions of leukemia, bone marrow check.
Oral cavity abnormalities-Related Acute Leukemia
Abnormalities of the oral cavity here is abnormalities - abnormalities that arise in the oral cavity patients with acute leukemia, including:
Swollen gums
Swelling of gums in the form of swelling of the papilla and gum margins.The swelling is due to leukemik cell infiltration in the reticular layer of oral mucosa, the proven results biopsy and FNAB of the oral mucosa (Nugroho, 1991; Berkovitz 1995). Oral mucosa that experienced mucosal cell infiltration leukemik is often experienced minor trauma, such as along the line of occlusion mucosa, palate, tongue and corners of the mouth (Rusliyanto, 1986; Glickman, 1958 cit Berkovitz 1995). This phenomenon was found in 14.28% patients with leukemia (Archida, 1987) and typical of acute leukemia monositik and mielomonositik (Rusliyanto, 1980; Wiernik, 1985; Berkovitz, 1995). Enlargement of the gums is also allegedly caused by chronic inflammation caused by plaque, gingivitis, chronic form of inflammation due to a mild degree which is also found in clinically healthy gums (Widjaja, 1992; Moughal et al, 1991 cit Berkovitz 1995).
Bleeding
Bleeding in the cases of leukemia can be petekie, ekimosis or spontaneous bleeding (Lister, 1990). It often happens in cases of acute leukemia that accompanied decreased platelet count (thrombocytopenia) and morphology and platelet function abnormality (Widmann, 1995).Platelets are important components in the process of blood clotting, which serves to form a platelet plug. Platelet plug comes from the aggregation of platelets that cover torn blood vessels. Platelets also contribute to the activation of fibrinogen into fibrin which is a plug fixed in the process of blood clotting. Decrease in platelet count (thrombocytopenia) and morphology and platelet function abnormality will result in a tendency perdarahanan (Guyton, 1994; Ganiswara, 1995). Bleeding caused by damage to blood vessels as well. Damage to blood vessels caused by the rupture of capillaries. Increased blood viscosity due leukemik cells with high concentrations. This condition causes the intra-capillary blood pressure increase. blood flow to the side of low pressure should be blocked because of infiltration of cells that form leukemik embolism.Cessation of blood flow with viscosity and high pressure causes rupture capillary blood vessels (Wiernik, 1985). Poor oral hygiene, periodontal tissues are not healthy and local irritation is believed to be another cause of bleeding oral cavity (Wezler, 1991; Nugroho 1998). Local conditions poor oral cavity, can cause inflammation and lead to easy bleeding.
Ulceration
Ulceration in the oral cavity patients with acute leukemia allegedly caused by any failure of the body's defense mechanism. Neutrophil function in the form of decreased phagocytosis and migration failure. In these conditions even small trauma can cause ulcer (Rusliyanto, 1986).
The number of cells leukemik that many in peripheral blood can cause static small blood vessels, causing anemia (Burket, 1940 cit Berkovitz, 1995, Sinrod, 1957 cit Berkovitz, 1995; Bodey, 1971 cit Berkovitz, 1995; Segelman and Doku, 1977, cit Berkovitz , 1995) subsequent necrosis and ulceration (Rusliyanto, 1986).
Lymphadenopathy
lymphadenopathy in the form of enlarged lymph nodes, due to the infiltration of cells into lymph nodes leukemik (Lister, 1990; Rusliyanto, 1986; Berkovitz, 1995) and is also suspected to be a reactive lymphadenitis as the body's defense against the body against inflammation which is the body's physiological processes (Rubbins and Khumar, 1992). According to Guyton et. al. (1994) lymphadenopathy also occur due to the extra hematopoeisis medular in lymph nodes.Hematopoesis that in adulthood should occur in the bone marrow, perturbed by cell multiplication process leukemik of leukemik precursor cells have a longer life span, bone marrow and urged menginfiltasi normal cells. The statement is supported by W.F. Guyton Ganong (1995) which states that extra hematopoesis medular can occur in adulthood as a result of diseases that cause fibrosis or bone marrow damage. This enlargement can reach a size of chicken eggs (Pitojo S, 1992).
Infection
Infection is very common in patients with acute leukemia, both fungal infections, bacterial or viral infection. This condition is caused by the failure of the body's defense mechanisms to combat infection. In patients with acute leukemia occurred neutropenia (Barrett, 1986) and neutrophil itself has decreased function of the failure of phagocytosis and migration (Rusliyanto, 1986; Berkovitz, 1995). Fungal infections are most often found is a fungal infection of Candida Albicans which reached 60% in patients with ALL (Reskiasih, 2000). Candida fungal infections in clinical white lesions can be found as well as red lesions. White lesions in the form of a more white color than the surrounding tissue, higher than the surrounding, more rough or has a different texture than normal tissue around them.White lesions, this may be a lesion or non keratotik keratotik based on convenience or scrapings removed with gentle rubbing. Lesions that are difficult / can not be removed by gently rubbing or scrapings taken for involving thickening of the mucosal epithelium and perhaps as a result of lifting the thickness of the berkeratosis (hyperkeratosis) and called the lesion keratotik. The lesions are easily removed and often creates an area of rough or slightly reddish mucosa could be debris or inflammation in pseudomembranous oral mucosal lesions, called non keratotik. Lesions due to Candida yeast infection is often associated with inflammation in pseudomembranous mucosa or had a role in the etiology of the lesion hyperkeratotic white lesions although it can be accompanied by lesions hipokeratotik. Another fungal infection could be angular cheilitis, and median rhomboid glossitis (Brightment, 1993). Infection with gram-negative bacteria that cause pneumonia is very common. And the only common clinical signs are fever (Wiernik, 1985). Viral infections are often encountered Shingles is an infection that has a fairly high percentage of 40% in patients with acute leukemia type of AML and 30% of acute leukemia types ALL (Barrett, 1986). One of the complications of infection, namely sepsis is the leading cause of death in patients with acute leukemia who achieved 52.63% (Archida, 1987)
IMPLEMENTASI
Improve general condition:
Anemia: peacock blood cell transfusion solid (PRC) 10 ml / kg / dose, up to Hb 12 g / dl.
Bleeding: blood transfusion according to the number of missing, if necessary, can be given a transfusion of platelets (usually required if platelet count <10.000/mm3).
Secondary infection: when can do culture germs (from ulcer, urine, blood, spinal fluid serebro) and immediately start with broad-spectrum antibiotic / high dose, according to the allegations of causing germs.
Nutritional status should be noted / corrected.
Treatment sfesifik:
Protocol for ALL:
Remission induction phase.
Give a combination of 1 + 2 + 3a or 1 + 2 + 3b.
1.Vinkristin 1.5 mg/m2 (body surface area), 1 time a week I. V. for 6 weeks.
Mg/M2/24 2.Prednison 50 hours divided into three doses orally, every day for 6 weeks.
3.a. Daunomycin 45 mg/M2/dosis I. V. given only on days I, II, III or Adriablastin 40 mg/M2/dosis I. V. given only on days I, II, III or
3.b. Asparaginase (specific protocols).
Phase prevention of spread to the central nervous system.
Intrathecal methotrexate 10 mg/M2/dosis, 1 time a week, for 5 weeks.
Phase maintenance
Give a combination of
1.6 merkaptopurin 75 mg/M2/dosis orally 1 time a day.
2.Metotreksat 20 mg/M2/minggu orally, divided 2 doses (Monday + Thursday). Treatment continued until 2-3 tahin.
Protocol for the LMA:
For this type of LMA, the protocol that is used varies, consisting of various combinations of drugs, such as:
Cytosine arabinosid + + 6 tioguanin daunomycin.
Prednisone + vincristine + methotrexate + merkaptopurin.
complication
The most frequent complications found were:
Bleeding.
Sepsis.
prognosis
The prognosis is not good. High mortality rate.
NURSING DIAGNOSIS WHICH MAY ARISE AND ACTION PLAN
1.Resiko risk of infection associated with:
Inadequate secondary defenses
Impaired maturation of white blood cells
Increasing the number of immature lymphocytes
Immunosuppression
Bone marrow suppression (chemotherapy effects 0
Expected Results:
Infection does not occur,
Plan of action:
1.Tempatkan child in a special room. Limit visitors as indicated
Rational; Protecting children from potential sources of pathogens / infection
2.Berikan protocol for good hand washing for all staff officers
Rational: to prevent cross contamination and decrease the risk of infection
3.Warning temperature. Note the relationship between rising temperatures and treatment chemoterapi. Observations in connection with tachicardi fever, hiertensi
Rational: Hipertermi information occurs in several types of infection and fever occurs in most patients with leukemia.
4.Dorong often change position, breathe deeply, cough.
Rational; Prevent static respiratory secretions, lowering the risk atelektasisi / pneumonia.
5.Inspeksi oral mucous membrane. Clean mouth periodically. Gnakan soft toothbrush for oral care.
Rational: Oral cavity is a good medium for the growth of pathogenic organisms
6.laboratory tests: WBC, complete blood
Rational: The decrease in WBC normal / mature can be caused by the disease process or kemoterapo.
7.drugs as indicated, for example Antibiotics
Rational; Can be given a prophylaxis or treatment of infection in particular.
8.Hindari antipyretics that contain aspirin
Rational; of aspirin can cause stomach bleeding or a further decrease in platelet count
High 2.Resiko deficiency associated with body fluid volume:
Losing excess, eg, vomiting, bleeding
Decrease in fluid intake: nausea, anorexia.
Expected Results: The volume of adequate body fluids, characterized by TTV dbn, stable, palpable pulse, urine output, BJ and PH urine, dbn.
Action Plan:
1.inputs and expenditures. Calculate the invisible expenditure and fluid balance. Note the decrease in urine in adequate income. Measure urine specific gravity and pH of urine.
Rational; decrease secondary circulation of red blood cells and originators in renal tubules and / or the occurrence of kidney stones (due to elevated levels of uric acid) can cause urinary retention or renal failure.
2.BB each day.
Rationale: Measuring keadekuatan fluid replacement according to renal function. Revenue more than the output can indicate worsening / kidney obstruction.
3.TD and heart frequency
Rationale: The change to show the effects of hypovolemic (hemorrhagic / dehydration)
4.Inspeksi skin / mucous membranes to petike, ekimotik area, notice bleeding gums, blood warn rust or vague on the stool or urine; further bleeding from the puncture invesif.
Rational; Suppression marrow and platelet production of placing patients at risk of uncontrolled bleeding spntan.
5.Evaluasi skin turgor, capillary pengiisian and general condition of the mucous membranes.
Rational; direct indicator of fluid status / dehydration.
6.Implementasion action to prevent tissue injury / bleeding, ex: brush your teeth or gums with a soft brush.
Rational; Network fragile and mechanical disruption of freezing increases the risk of bleeding, although minor trauma.
7.soft diet.
Rational: It can help reduce irritation to the gums.
8.IV fluids as indicated
Rationale: Maintaining a balance of fluid / electrolyte in the absence of revenue through oral; reduce the risk of kidney complications.
9.Red blood cells, platelets or clotting factors
Raional: Fixing the number of red blood cells and O2 capacity to improve anemia. Useful to prevent / treat bleeding.
3.Nyeri (Acute) related to:
Fiscal agent; enlarged organs / lymph nodes, bone marrow dikmas with leukemia cells.
Chemical agents; antileukemia treatment.
Action Plan;
1.vital signs, pay attention to nonverbal clues, fussy, whiny, restless
Rational; It can help evaluate the verbal statement and the ineffectiveness of intervention.
2.quiet environment and reduce stress stimuli
Rational; improving the break.
3.in comfortable position and chock joints, extremities denganan pillow
Rational; Reduce discomfort bone / sensi
4.position periodically and give a gentle range of motion exercises.
Rational: Improve circulation and tissue mobilization of the joints.
5.action discomfort; eg: massage, compress
Rationale: Minimizes need for or increase the effects of the drug.
6.drugs as indicated.
REFERENCES
Carpenito, Lynda Juall. (1999). Nursing Care Plans & Documentation.Issue 2. (Translation). Medical book publishers EGC. Jakarata.
Carpenito, Lynda Juall. (2000.). Nursing Diagnosis Handbook. Edition 8.(Translation). Medical book publishers EGC. Jakarta.
Doenges, Marilynn E. (1999). Nursing care plan. Edition 3. (Translation).Medical book publishers EGC. Jakarta.
Engram, Barbara. (1998). Plan for Medical Surgical Nursing. Volume 2, (translation). Medical Book Publisher EGC. Jakarta.
Junadi, Purnawan. (1982). Capita Selekta Medicine, New York: Media Aesculapius Medical Faculty University of Indonesia.
Long, Barbara C. (1996). Medical Surgical Nursing. Volume I.(Translation). Nursing Education Alumni Association Foundation Pajajaran. Bandung.
Mansjoer, Arif & Suprohaita. (2000). Capita Slekta Medicine Volume II.Faculty of Medicine, UI: Media Aescullapius. Jakarta.
Matondang, S. Corry (2000) Physical Diagnosis in Children. Edition 2, PT.Sagung Seto. Jakarta.
Ngastiyah (1997). Child Care Hospital. Medical book publishers EGC.Jakarta.
John Rendle. (1994). Summary of Child Diseases, 6th edition. Binapura Script. Jakarta.
Santosa NI. (1989). Nursing I (Fundamentals of Nursing). MOH. Jakarta.
Santosa NI. (1993). Health care in the Context Keluarg. MOH. Jakarta.
Soeparman. (1987). Medicine Volume I Second edition. Publisher FKUI.Jakarta.
Soetjiningsih. (1995). Growth. Medical book publishers EGC, Jakarta.
Suharso Darto (1994). Guidelines for Diagnosis and Therapy. F.K.Airlangga University. Surabaya.
Sumijati M.E, et al, (2000). Nursing In Case of Illness That Commonly Occurred In Children. PERKANI. Surabaya.
Wahidiyat Iskandar (1985). Pediatrics. Issue 2. Info Medika, Jakarta.
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