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    CASE REPORT

    Acute Lymphoblastic Leukemia + Malnutrition(Marasmic Type) + Hyperuricemia

    Presentators: Imela Sari, S.Ked

    Akbar Husaini Angkat, S.Ked

    Day,date: Wednesday, August 28th 2013

    Supervisor: dr.Hakimi, Sp.A(K)

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    Acute Lymphoblastic Leukemia, form of

    leukemia, white blood cells cancer, characterized

    by excess malignant, immature overproducelymphblast.

    WHO estimates that 54% child mortality, 1 million

    children due to malnutrition. Measurement childs

    growth provide key information for malnutrition

    Hyperuricemia is a level of uric acid in blood thatabnormall hi h

    Background

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    ObjectiveOThe aim for this study is to

    explore more about the

    theoritical aspects on ALL,

    malnutrition, and hyperuricemia

    and also to integrate theory and

    application of these cases indaily life

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    Epidemiology

    The leukemiasmost common malignantneoplasms in childhood, about 41'% of all

    malignancies that occur in children

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    Acute lymphoblastic leukemia (ALL)accounts for about 77% of cases of

    childhood leukemia. And the second

    leading cause of death in children.

    It has a striking peak incidencebetween 2-6 yr of age and occurs

    more frequently in boys than in girls,

    at all ag

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    TREATMENT

    The choice of treatment of ALL based onthe estimated clinical risk of relapse inthe patient.

    Three of the most important predictivefactors : age at the time of diagnosis, the

    initial leukocyte, and the speed ofresponse to treatment.

    Leukocyte count < 50.000/l, agebetween 1-10 years are used to defineavera e risk.

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    Criteria for high risk patieninclude:

    Age < 1 ore > 10 years

    WBC > 50.000/mct

    T-cell phenotype

    Anterior mediastinal mass

    CNS disease

    Translocation t (4:11) or t(9;22)

    Slow response to inductio therapy

    Four phase of therapy

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    Chemotheraphy

    InitialCNS

    Intensification

    Continuation

    Nutritional

    Supportive care Psycological aspect.

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    Hyperuricemia in ALLUric acid is poorly soluble and must be

    excreted continuously to avoid toxic

    accumulations. Its not a specific diseasemarker so the cause of its elevation must

    be detemined.

    Its Elevated (>6 mg/dL in females and >7

    mg/dL in males) serum [UA] may

    predispose the patient to gouty attacks,

    nephrolithiasis, and hypertension

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    *Renal tubule excretion is greater in

    children than in adults, serum level isless reliable indicator of serum uric

    acid production in children,

    measurement of the level in urine isrequired.

    *In ALL patient its frequently caused byTumor Lysis Syndrome (TLS)

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    MALNUTRITION

    Th l f k f N P bl

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    Theoretical framework of Nutrition Problems.

    Nutrition problems

    Food intake Infect Disease directcauses

    Food availability Mother & child Health indirect

    in household caring service causes

    POOR FAMILY & EDUCATION, main

    FOOD STUFF & JOB OPPORTUNITY problem

    ECONOMIC & POLITIC CRISIS core

    problem

    Th l l f d t i t l d t t iti t t

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    Three level of determinants lead to nutrition statusImmediate :Inadequacy of dietary intake

    manifested :

    - PEM

    - Micronutr.deficiency

    - Diarrhea & worm disease

    - ARI

    Supply & coverage immuniz

    Immediate :Inadequacy of dietary intake

    manifested :

    -PEM

    - Micronutr.deficiency

    - Diarrhea & worm disease

    - ARI

    Supply & coverage immuniz

    Underlying :- Household food security

    - Access to PHC

    - Community of awareness &

    care for children & women

    Basic :- Socio-economic conditions

    (poverty & crisis)

    - Political factors

    - Traditional practices (infant

    feeding)

    - Environment & sanitation

    Intervention programs

    Supply side :- access : health care facilities

    - supplementation of food &

    micronutr.

    - immunization

    - quality: providersskill- information system: coverage

    of suplpement., fortification,

    surveillance, etc.

    Demand side:- empowerment

    - family awareness of nutrition

    - subsidies / health insurance

    Health &

    Nutrition

    Status of

    Children

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    PERMASALAHAN MEP :tmerupakan primadona masalah kesehatan gizi

    t

    berperan pd. morbiditas & mortalitas anakt deteksi dini dan tatalaksananya penting sebagai

    upaya pencegahan melanjutnya MEP

    t MEP berat perlu perawatan di intensif di RSt Berdampak jangka panjang thd. kualitas SDM

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    Klasifikasi Gizi Buruk :

    1. GOMEZ (195..) : BB/U

    2. MacLarren (196..) : Klinis + laboratoris3. The Wellcome : Klinis + antropometris

    Trust Party (1970)

    4. Waterlow (1973) : BB/TB

    5. WHO (1999) : Klinis + antropometris

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    Klasifikasi Gizi Buruk :Wellcome classification of severe forms of protein-energymalnutrition

    Percentage of

    standard weight for

    age

    Oedema present Oedema absent

    60-80 Kwashiorkor Undernourishedhment

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    Klasifikasi Gizi Buruk (WHO,1999) :Gizi kurang Gizi buruk

    Edema simetris -- +(oedematousmalnutrition)

    BB/TB -3< Z-score

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    Feature Kwashiorkor Marasmus

    Growth failure Present Present

    Wasting Present Present, marked

    Oedema Present (mild) Absent

    Hair changes Common Less common

    Mental changes Very common Uncommon

    Dermatosis, flaky-paint Common Does not occur

    Appetite Poor Good

    Anaemia Severe (sometimes) Present, less severe

    Subcutaneous fat Reduced but present Absent

    Face May be oedematous Drawn in, monkey-like

    Fatty infiltration of liver Present Absent

    Clinical Feature of Marasmus and Kwashiorkor

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    CASE REPORT

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    Name : ACH Age : 4 years 1 month Sex : Male Date of Admission : July, 29 th 2013

    Main Complaint : Pale

    History : A patient was admitted to H Adam Malik General Hospital with a

    main complaint of paleness since 5 months before admittion. Thepatient had no history of nosebleed and gum bleeding, but ahistory of bruise and fever. The patient also complained abdominalbloating since 6 months ago. No family history of the samedisease. The patient had normal urination and defecation.

    History of birth : Normal, assisted by a midwife, cried as soonas baby was born.

    History of previous illness: Patient had been treated to MurniTeguh Hospital and BMP inspection had been done with thediagnosis was ALL

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    Physical Examination

    BW = 12 kg , BH = 92 cm

    BW-for-Age: 75%

    BH-for-Age: 90% BW-for-BH: 85%

    Presens status

    Sens. Compos Mentis, Body temperature:37oC, Pulse: 100 bpm, Respiratory Rate:24 bpm.

    Localized status

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    Localized status

    Head : Face : Old man face (-), Eye : Light

    reflexes(+/+), isochoric pupil, pale inferiorconjunctivae palpebrae (+/+), icteric (-/-) ,Ear : Normal appereance , Mouth : Sianosis (-),Nose: Normal appereance.

    Neck : Lymph node enlargement (-)

    Thorax: Symmetrical fusiformis. Epigastrialretraction(-). HR: 100 bpm, reguler, murmur(-). RR: 24x/i, reguler. Crackles (-/-)

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    Abdomen: Expand. Liver palpable 4cmBAC. Peristaltic (+) normal. Spleen: SIII-

    IV

    Extremities: Pulse 100 bpm, regular,adequate pressure and volume, warmacral, CRT < 3. Baggy Pants (+).Decreased subcutaneous fat. Musclehypotrophy.

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    Differential Diagnosis

    ALL FAB L2 + Malnutrition ( Marasmic Type )+

    Hyperuricemia

    Working Diagnosis

    ALL FAB L2 + Malnutrition ( Marasmic Type ) +

    Hyperuricemia

    Plans:

    PRC Transfussion

    Chemotherapy Urinalisis / RF

    Fluid Balance

    July, 29th 2013 (1st day)

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    S: Pale (+) Fever (+). Bruise (+)

    O: Sens: CM, Temp: 37oC, Body weight: 12kg Head