TIMELINE

Januari 29th, March 3rd, March 4th, March 9th, March 11th,
2020 2020 2020 2020 2020

Patient came Initial Final

Observation Reporting
to Hospital B observation Observation
started
by candidate

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 PATIENT’S RECORD
Candidate : dr. Patricia Wonodihardjo.

I. IDENTITY
1.1. PATIENT’S IDENTITY
Registration number : 71.50.XX
Patient’s name : MP
Date of birth : October 4th, 2007 ( 12 years 3 months old )
Gender : Male
Nationality : Indonesia
Date of first admission : January 29th , 2020

1.2. PARENT’S IDENTITY

FATHER MOTHER
Name : HP DE
Age : 57 years old 49 years old
Occupation : Farmer Housewife
Education : Senior High School Senior High School

II. HISTORY
( alloanamnesis was taken from parents, physician, and based on medical
records on January 29th, 2020 at 10.00 AM in hemato-oncology sub division
ward )
 Chief complaint : Fever
 Additional complaint : Bone pain and pale

2.1. HISTORY OF PRESENT ILLNESS

Patient came to the hospital with chief complaint of fever felt on
palpation, which the patient already felt for 1 month before admission, even the
patient felt the fever, but the temperature was not measured by the parents.
The fever was recurrent, and decreased with the administration of antipyretic.
The fever itself was not accompanied by shivering, vomiting, or convulsion.

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 The patient also felt bone pain all over his body, which is recurrent since
1 month prior to admission. There were no complaints of swollen joints or
previous trauma history. The patient was brought to a general practitioner and
only received an antipyretic.
One month prior to admission, the patient also looked pale. Pale was
recognized by parents initially on the face, and then appeared on the soles of
feet and hands. Pale was not accompanied by bleeding signs. Bleeding
complaint such as nosebleed, gum bleeding or blackish-colored stool were
denied.
At this present admission, the patient has no fever, do not look pale and
there is no bone pain. He has good appetite. There is no complain of defecation
and urination. Patient is on the fourth week of induction phase chemotherapy.

2.2. HISTORY OF PREVIOUS ILLNESS

 Patient never suffered from these complaints before.
 History of using certain drugs like chloramphenicol and alkylating agents in
long term period or without doctor’s advice is denied.

2.3. HISTORY OF ILLNESS IN THE FAMILY

There was no other family who had blood malignancy or other disorder with the
same symptoms.

2.4 HISTORY OF FAMILY’S HEALTH

There was no exposure to ionizing radiation.

FAMILY TREE

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STRUCTURE OF FAMILY MEMBERS

No Name Relation Gender Age Information

1 HP Father M 57 years Healthy

2 DE Mother F 49 years Healthy

3 SS Brother M 20 years Brother

4 MP Patient M 12 years 3 months Patient

2.4. PERSONAL / SOCIAL HISTORY

A. HISTORY OF ANTENATAL CARE

Patient was the youngest child in the family. His mother had more than 8 times
antenatal examinations at primary health care. His mother received two doses of
tetanus toxoid (TT) immunization. During pregnancy, the patient’s mother was healthy
and never consumed any drugs, alcohol, and cigarette. She only took the vitamins
from the physician. History of X-ray, paints and gasoline exposure during pregnancy
was denied.

B. HISTORY OF LABOR
Patient was born spontaneously, term, with birth weight of 3,200 grams, birth length
was 48 cm, cried immediately. He was born at primary health center and was assisted
by midwife.

C. HISTORY OF POSTNATAL
Patient had never experienced any cyanotic or yellowish skin color. He was
breastfed and was routinely checked up to primary health care facility for vaccination.
Patient was never hospitalized until he was diagnosed with ALL.

D. HISTORY OF FEEDING
The patient was breastfed since birth until twelve months old, mixed with
formula milk from 6 months until two years old. Milk porridge was given at six months
old, then changed to strained porridge on eight months old.

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He ate soft rice from 9 months old then continued with home meals at 2 years old. He
eats three times daily, one plate consists of rice with fish, chicken, or eggs, vegetables
and fruits.

E. DEVELOPMENTAL MILESTONES
GROWTH
Growth and development examination was routinely examined at primary health care.
At this time the growth and development of this patient was normal.

DEVELOPMENTAL
Patient seemed to be able to roll over by the age of 5 months, could sit without
support at 6 months old and was able to say mama and papa at 8 months old. Patient
began to walk at 12 months old and run at 18 months old. At 2 years old, patient was
able to combine words and use spoon/fork to eat. At 3 years old, patient was able to
build tower of cubes and do toilet training. At 4 years old, he wore clothes without help
and was able to speak clearly. At 5 years old, patient was able to eat by himself. The
patient is currently in the six grade of elementary school. According to his parents, he
can follow the lesson given in school without any difficulty and his development is
same with his peers and he is able to socialize with others in school.
Conclusion: normal developmental milestone.

F. HISTORY OF IMMUNIZATIONS
The patient received Bacille Calmette Guerin (BCG) vaccine with scar (+) on
upper right arm, Polio immunization five times, Diphteria Pertussis Tetanus (DPT)
immunization four times, Hepatitis B five times, Measles immunization twice, DT
immunization once, Td immunization twice.
Conclusion : basic and booster immunization was appropriate for this age.

G. HISTORY OF BASIC NEEDS

Physic-biomedic:
The patient received adequate primary needs (clothes, food, and housing).
Patient eats three times daily. He also got enough recreations and sport activities.
When he got sick, his parents took him to the nearest health facility in the area.

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Mental stimulation :
Patient learns and plays like his peers. He has many friends and able to
socialize easily with new friend. Currently, patient is in six grade of elementary school
and able to follow all the lessons taught in school.
Conclusion: Patient received adequate affection, care, and attention from his family.

Emotional needs:
Affection was received from parents and family. The patient’s parents accepted
his illness condition. The patient gained enough care and love from his parents and
family for his recovery.
Conclusion: patient got adequate physic-biomedic, emotional needs and mental
stimulation.

2.5 SOCIO ECONOMIC AND ENVIRONTMENT CONDITIONS

Socio-economic
Patient’s father work as farmer and his mother as a housewife. Healthcare
expenses are covered national insurance class III.
Environment
The patient lives with his parents in their house with tin roof, concrete wall, tiles
floor. Ther house consists of two bedrooms, lived by 4 people, 2 adults and 2 children.
The bathroom/restroom is inside the house, water source is from governmental water
company, and electricity source is from the government electric company. Waste is
handled by dumping outside the house.
The patient lives in the suburban area which is not densely populated. His
house is far from the road, not located near a cellphone transmitting tower or high
voltage electricity. There is no smoke exposure in the patient’s house.

PATIENT’S HOSPITAL ADMISSION SUMMARY

Prior to candidate’s initial observation (January 29th, 2020 – March 3rd , 2020)
The patient first admitted to hospital on January 29th, 2020, patient came by
himself and his family to the hospital with chief complaint of fever. When hospitalized,
the patient had fever, looked pale, and had bone pain.

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 On the first day in hospital, his weight was 38 kg and height was 149 cm (good
nutritional status according to CDC 2000 growth chart). The patient looked sick but his
awareness was compos mentis. In vital sign examination is found: blood pressure
110/70 mmHg, pulse 96 bpm (regular, full pulses), respiratory rates 25 cpm, and body
temperature 37,9°C. On head and neck examination, there was anemic conjunctiva
and there was multiple lymph nodes enlargement around the neck, with the smallest
size of lymph node was 0.5 cm and the biggest diameter of lymph node was 1 cm.
On chest examination, heart and lung were normal. The abdomen was flat, soft
on palpation, with normal bowel movement sound. There was liver enlargement 3 cm
below costal margin (BCM) and 3 cm below xiphoid process, with sharp edge, flat
surface, soft in consistency, and spleen was palpated measured as Schuffner II. The
extremities looked pale with capillary refill time (CRT) was <2 seconds.
On January 29th, 2020 when the patient hospitalized, this patient was evaluated
with laboratory examination showed a result of: hemoglobin 6.4 g/dL, hematocrit
20.5%, leukocyte 62,000/L, erythrocyte 2.54 x 106/L, platelet 135 x 103/L, sodium
137 mEq/L, potassium 4.17 mEq/L, chloride 100.2 mEq/L, AST 27 U/L, ALT 6 U/L,
ureum 14 mg/dl, dan creatinine 0.3 mg/dl, LDH 574 U/L, PT 14.6 seconds (control
13.8 seconds), INR 1.10 seconds (control 1.13 seconds), APTT 41.9 seconds (control
32.9 seconds). In urinalysis examination was found specific gravity 1.020, pH 7,
epithelial cells 1-2/lpf, RBC 0-1/hpf, WBC 0-1/hpf, ketone (-), protein (-), nitrite (-) and
the result of stool examination was: mushy consistency, brown color, erythrocyte (-),
epithelia (-), worm (-), bacteria (-), protozoa (-), fungus (-).
On January 31st 2020, the peripheral blood smear examination result was
normocytic normochromic erythrocyte, anisocytosis (+), macrocyte (+), microcyte (+),
with leukocytosis, differential count: eosinophil 0%, basophil 0%, stab neutrophil 5%,
segment neutrophil 22% lymphoblast 15%, lymphocyte 55%, monocyte 3%, with
conclusion suggestive of ALL. Following the result of laboratory examination, the
patient received a Packed Red Cell (PRC) transfusion, and was planned to have a
Bone Marrow Puncture (BMP) and immunophenotyping examination.
On February 5th 2020, the patient undergo Bone Marrow Puncture (BMP)
procedure and immunophenotyping examination. The result of BMP examination on
February 5th 2020, showed predominantly lymphoblast L2 with blast.

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 The result of immunophenotyping showed gating on the blast with positive with
HLA-DR, CD 10, CD 19, CD 34. The conclusion was B-Lineage. Patient was
diagnosed as High risk B-cell acute lymphoblastic leukemia.
Following the BMP procedure, the patient was controlled for the laboratory
examination and the result show hemoglobin 9.4 g/dL, hematocrit 26.8%, leukocyte
48,000/L, erythrocyte 3.35 x 106/L, platelet 94 x 103/L, MCH 28.0 pg, MCHC 35.0
g/dl, MCV 88.1 fL.
The patient was planned to start his chemotherapy by first completing the
comprehensive physical examination. Echocardiography result was normal
intracardiac, no contraindication for receiving cytostatic drugs. Thorax x-ray
examination was in normal limit. Consultation to oral health division,
otorhinolaryngology, and ophthalmology division showed no abnormality. This patient
also had tuberculin skin test and the result was 0 mm.
Patients started receiving chemotherapy on February 12th 2020 based on
Protocol of Indonesian High Risk Acute Lymphoblastic Leukemia 2016. Cerebrospinal
fluid examination result on February 17th 2020 showed that the liquid was cloudy,
leukocyte 1,000/L, PMN 10%, MN 90%, blast (+), glucose 75 mg/dL, Nonne and
Pandy test (+), erythrocyte 0-1/hpf, protein 10 mg/dL. This patient was diagnosed with
high risk acute lymphoblastic leukemia and central nervous system leukemia. The
patient’s chemotherapy protocol then replaced with Protocol of Indonesian High Risk
Acute Lymphoblastic Leukemia 2016 and Central Nervous System Leukemia with
modification. During medications, fever, pale and bone pain complaints were
subsided.
Right now, the patient didn’t have any complaint, and on his fourth week of
induction phase, the patient undergo usual laboratory examination with the laboratory
result at February 28th 2020 were hemoglobin 10.1 g/dL, hematocrit 29.7%, leukocyte
4.000/L, erythrocyte 3.19 x 106/L, platelet 124 x 103/L, MCH 28.7 pg, MCHC 35.1
g/dL, MCV 81.9 fL, ANC 1,426 cell/mm3, AST 12 U/L, ALT 3 U/L, ureum 11 mg/dL,
and creatinine 0.6 mg/dL, sodium 137 mEq/L, potassium 3.7 mEq/L, chloride 96
mEq/L, calcium 9.55 mg/dL. Patient was given supportive nutrition according to RDA
and chemotherapy was continued based on protocol.

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Examination 29/1/2020 3/2/2020 28/2/2020
Hb (g/dL) 6.4 9.4 10.1
Eri (x106/L) 2.54 3.35 3.19
Ht (%) 20.5 26.8 29.7
MCV (fL) - 28 81.9
MCH (g/dL) - 35 28.7
MCHC (pg) - 88.1 35.1
Leukocyte (/L) 62.000 48.000 4.000

Platelet (/L) 135.000 94.000 124.000

Diff.Count (%) - - 0/0/0/44/50/6

Blast (%) 55 - -

ANC (cell/mm3 ) - - 1,426

Blood Chemistry
AST (U/L) 27 - 12

ALT (U/L) 6 - 3

Ureum (mg/dL) 14 - 11

Creatinin (mg/dL) 0.6 - 0.6

Chloride (mEq/L) 100.2 - 96

Potassium (mEq/L) 4.17 - 3.7

Sodium (mEq/L) 137 - 137

Calcium (mg/dL) - - 9.55

LDH (U/L) 574 - -

PT (second) 14.6 - -

INR (second) 1.1 - -

APTT (second) 41.9 - -

Stool Exam:
Consistency: mushy
Colour: brown
Erythrocyte (-)
Epithelia (-)
Worm (-)
Bacteria (-)
Protozoa (-)
Fungus (-)

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 Urinalysis:
SG 1.020
pH 7
Epithelia 1-2/hpf
Erythrocyte 0-1/hpf
Leukocyte 0-1/hpf
Ketone (-)
Protein (-)
Nitrite (-)

Peripheral Blood Erythrocyte

Smear Normocytic, normochromic, anisocytosis (+), macrocyte (+),
(31/1/2020) microcyte (+)
Leukocyte
Leukocytosis
Differential count: eosinophil 0%, basophil 0%, stab neutrophil
5%, segment neutrophil 22%, lymphoblast 15%, lymphocyte 55%,
monocyte 3%.
Platelet
Thrombocytopenia, aggregation (-), normal morphology.
Conclusion: Suggestive of Acute Lymphoblastic Leukemia (ALL)
Suggestion: BMP, leukemia immunophenotyping

Bone Marrow Predominantly lymphoblast L2 with blast.

(5/2/2020) Compatible with ALL-L2 morphology

Immunophenotyping Gating of the blast with positive HLA-DR, CD10, CD19, CD34.
(5/2/2020) Conclusion: B-Lineage

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 Cerebrospinal Fluid Cloudy, leukocyte 1,000/L, PMN 10%, MN 90%, blast (+),
Analysis glucose 75 mg/dL, Nonne (+), Pandy (+), erythrocyte 0-2/hpf,
(17/2/2020) protein 10 mg/dL.

III. PATIENT’S DATA AND CONDITION AFTER TAKEN AS A CASE REPORT

The examination was done in pediatric hemato-oncology ward, on March 3rd 2020 at
01:00 PM

General condition: looked ill, compos mentis

Anthropometric status:
Weight : 38 kg
Height : 149 cm
Body surface area (BSA) : 1.2 m2
Nutritional status according to CDC 2000 growth chart for boys age 2 – 20 years :
 Weight / Age : 38 / 41.5 X 100% = 92% ( normal weight )
 Height / Age : 149 / 151 X 100% = 99% ( normal height )
 Weight / Height : 38 / 40 X 100 % = 95% ( good nutritional status )

Vital signs : Blood pressure 100/70 mmHg, pulse 90 bpm (regular, full
pulses), respiratory rate 24 cpm, body temperature 37°C (axilla).
Skin : Light brown colored, no efflorescent, BCG scars (+) on upper
right arm.
Head and Neck
Head and face : no deformity, normocephaly, normal, black hair, not easily
pluckable.
Eyes : no palpebral edema, anemic conjunctivae (-),
anicteric sclerae, round and isochoric pupils.
diameter 3-3 mm, reactive to light, centered eyeballs,
clear lenses, good eye movements to all directions.

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Nose : no deformities, midline septum, no secretion, no
nasal flaring.
Ears : well-curved pinna, no deformity, no fluid secretion,
tympanic membranes intact.
Mouth : no cyanosis, moist buccal mucosa and lips,
symmetrical nasolabial sulci, no caries dentis,
no stomatitis.
Throat : tonsils T1/T1 not hyperemic, pharynx not hyperemic.
Neck : centered trachea, no lymph node enlargement,
no nuchal rigidity, jugular vein pressure (JVP) not increase.
Chest : normal shape, symetrical chest expansion, no
retraction.
Heart
Inspection : ictus cordis unseen, no precordial bulging.
Palpation : ictus cordis palpable in left midclavicular line, 5th
intercostal space, no thrill.
Percussion : right border at right parasternal line, left border at left
midclavicular line, upper border at 3rd left intercostal space.
Auscultation : heart rate frequency 90 bpm, regular, no murmur.
Lungs
Inspection : symmetrical movement of breathing
Palpation : intercostal spaces not wide, symmetrical vocal
fremitus
Percussion : normal, symmetrical resonant sounds
Auscultation : normal, vesicular breath sounds, no rales, no wheezing
Abdomen
Inspection : flat, no venectation
Palpation : soft, palpable liver 2 cm below costal margin, 2 cm
below processus xyphoideus, sharp edges, smooth
surface, soft, not tender, spleen schuffner I
Percussion : tympanic, no ascites.
Auscultation : normal bowel sounds.
Vertebrae : no deformity
Genitalia : male, penis length 7 cm, testicles +/+ (5 mL)

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Puberty Scale : Tanner scale II ( G2P2 )
Extremities : warm, no cyanosis, CRT ≤ 2 seconds, no spastic, no paresis
Muscles : normal muscle tone on the fourth extremities
Neurological Status
Reflexes : normal physiological reflex, no pathological reflexes
Sensory : normal
Motoric : 5 5
5 5

Cranial nerves examination:

NI = no olfactory problem
N II = round, isochoric pupils, positives direct and indirect light
reflexes
N III, IV, VI = no strabismus, normal movements of the eyeballs
NV = no problem
N VII = symmetrical nasolabial sulci, no lagophtalmus
N VIII = no hearing or balance problem
N IX = clear articulations, can swallow well
NX = uvula is central, no deviation
N XI = can shrug shoulders and turn head against resistance
N XII = no tongue deviation

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IV. SUMMARY
The patient first admitted to hospital on January 29th 2020, patient came by
himself and his family to the hospital with chief complaint of fever. When hospitalized,
the patient had fever, looked pale, and had bone pain. On the first day in hospital, his
weight was 38 kg and height was 149 cm (good nutritional status according to CDC
2000 growth chart). The patient looked sick but his awareness was compos mentis. In
vital sign examination is found: blood pressure 110/70 mmHg, pulse 96 bpm (regular,
full pulses), respiratory rates 25 cpm, and body temperature 37,9°C. On head and
neck examination, there was anemic conjunctiva and there was multiple lymph node
enlargement around the neck, with the smallest size of lymphnode was 0.5 cm and
the biggest diameter of lymph node was 1 cm. On chest examination, heart and lung
were normal. The abdomen was flat, soft on palpation, with normal bowel movement
sound. There was liver enlargement 3 cm below costal margin (BCM) and 3 cm below
xiphoid process, with sharp edge, flat surface, soft in consistency, and spleen was
palpated measured as Schuffner II. The extremities looked pale with capillary refill time
(CRT) was <2 seconds.
On January 29th 2020 when the patient hospitalized, this patient was evaluated
with laboratory examination showed a result of: hemoglobin 6.4 g/dL, hematocrit
20.5%, leukocyte 62,000/L, erythrocyte 2.54 x 106/L, platelet 135 x 103/L, sodium
137 mEq/L, potassium 4.17 mEq/L, chloride 100.2 mEq/L, AST 27 U/L, ALT 6 U/L,
ureum 14 mg/dl, dan creatinine 0.3 mg/dl, LDH 574 U/L, PT 14.6 seconds (control
13.8 seconds), INR 1.10 seconds (control 1.13 seconds), APTT 41.9 seconds (control
32.9 seconds). In urinalysis examination was found specific gravity 1.020, pH 7,
epithelia 1-2/lpf, RBC 0-1/hpf, WBC 0-1/hpf, ketone (-), protein (-), nitrite (-) and the
result of stool examination was: mushy consistency, brown color, erythrocyte (-),
epithelia (-), worm (-), bacteria (-), protozoa (-), fungus (-).
On January 31st 2020, the peripheral blood smear examination result was
normocytic normochromic erythrocyte, anisocytosis (+), macrocyte (+), microcyte (+),
with leukocytosis, differential count: eosinophil 0%, basophil 0%, stab neutrophil 5%,
segment neutrophil 22%, lymphoblast 15%, lymphocyte 55%, monocyte 3%, with
conclusion suggestive of ALL. Following the result of laboratory examination, the
patient received a Packed Red Cell (PRC) transfusion, and was planned to have a
Bone Marrow Puncture (BMP) and immunophenotyping examination.

14
 On February 5th 2020 the patient undergo Bone Marrow Puncture (BMP)
procedure and immunophenotyping examination.
The result of BMP examination on February 5th 2020 showed predominantly
lymphoblast L2 with blast. The result of immunophenotyping showed gating on the
blast with positive with HLA-DR, CD 10, CD 19, CD 34. The conclusion was B-Lineage.
Patient was diagnosed as High risk B-cell acute lymphoblastic leukemia.
Following the BMP procedure, the patient was controlled for the laboratory
examination and the result show hemoglobin 9,4 g/dL, hematocrit 26,8%, leukocyte
48,000/L, erythrocyte 3.35 x 106/L, platelet 94 x 103/L, MCH 28.0 pg, MCHC 35.0
g/dl, MCV 88.1 fL.
The patient was planned to start his chemotherapy by first completing the
comprehensive physical examination. Echocardiography result was normal
intracardiac, no contraindication for receiving cytostatic drugs. Thorax x-ray
examination was in normal limit. Consultation to oral health division,
otorhinolaryngology, and ophthalmology division showed no abnormality. This patient
also had tuberculin skin test and the result was 0 mm.
Patients started receiving chemotherapy on February 12th 2020 based on
Protocol of Indonesian High Risk Acute Lymphoblastic Leukemia 2016. Cerebrospinal
fluid examination result on February 17th 2020 showed that the liquid was cloudy,
leukocyte 1000/L, PMN 10%, MN 90%, blast (+), glucose 75 mg/dL, Nonne and
Pandy test (+), erythrocyte 0-1/hpf, protein 10 mg/dL. This patient was diagnosed with
high risk acute lymphoblastic leukemia and central nervous system leukemia. The
patient’s chemotherapy protocol then replaced with Protocol of Indonesian High Risk
Acute Lymphoblastic Leukemia 2016 and Central Nervous System Leukemia with
modification. During medications, fever, pale and bone pain complaints were
subsided.
Right now, the patient didn’t have any complaint, and on his fourth week of
induction phase, the patient undergo usual laboratory examination with the laboratory
result at February 28th 2020 were hemoglobin 10.1 g/dL, hematocrit 29.7%, leukocyte
4.000/L, erythrocyte 3.19 x 106/L, platelet 124 x 103/L, MCH 28.7 pg, MCHC 35.1
g/dL, MCV 81.9 fL, ANC 1,426 cell/mm3, AST 12 U/L, ALT 3 U/L, ureum 11 mg/dL,

15
and creatinine 0.6 mg/dL, sodium 137 mEq/L, potassium 3.7 mEq/L, chloride 96
mEq/L, calcium 9.55 mg/dL. Patient was given supportive nutrition according to RDA
and chemotherapy was continued based on protocol.

V. DIAGNOSIS
High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous System
Leukemia Induction phase (C91.00)

VI. PROBLEM

Prognosis
- Prognosis of a 12 years 3 months old boy with High Risk B-Cell Acute
Lymphoblastic Leukemia with Central Nervous System Leukemia.

VII. MANAGEMENT PLANS

1. Treatment plans
- Chemotherapy according to Indonesian ALL Protocol 2016 with modification
for high risk and CNS leukemia
- Complete blood work up and blood chemical tests.

2. Pediatric nutritional care

A. Nutritional status assessment
12 years 3 months old boy
Actual body weight = 38 kg
Ideal body weight = 40 kg
Body height = 149 cm
Body surface area (BSA) = 1.2 m2
Nutritional status according to CDC 2000 growth chart for boys age 2 – 20
years :
• Weight / Age : 38 / 41.5 X 100% = 92% ( normal weight )
• Height / Age : 149 / 151 X 100% = 99% ( normal height )
• Weight / Height : 38 / 40 X 100 % = 95% (good nutritional status

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 B. Determination of needs based on Recommended Dietary
Allowance (RDA)
Calories : 55 kcal/kg/day = 2,200 kcal/day
Protein : 1 g/kg/day = 40 g/day
Fat : 30% x 2,200 = 660 kcal/day = 73 g/day
Fluid : 70 - 85 ml/kg/day = 2,800 – 3,400 ml/day
C. Determining the mode of administration
Nutrition were given orally
D. Determination the type of food
Given in the polymeric form
Food 3 times daily (@ 550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (40 g carbohydrate, 4 g protein, 250 kcal)
- One egg (45 g fat, 9 g protein,75 kcal)
- 100 g stir – fried spinach (5 g carbohydrate, 1 g protein, 50 kcal)
- 50 g Soybean cake (7 g carbohydrate, 5 g protein, 5 g fat, 75 kcal)
- One medium cut of beef (7 g protein, 10 g fat, 100 kcal)
Snacks 2 times daily ( @ 220 kcal, 9 g protein, 10 g fat)
- Biscuits 4 pieces (100 kcal, 40 g carbohydrate, 4 g protein)
- 1 glasses of milk 200 mL (120 kcal, 5 g protein, 10 g fat)
Mineral water 2,500 – 3,000 mL daily
E. Monitoring and Evaluation
Acceptability, food tolerance, side effects, and body weight

3. Counseling plans
 Natural history of the disease, therapy, side effects of the chemotherapy, and
prognosis
 Immunization plan after chemotherapy

4. Monitoring plans
- General state and vital signs
- Body weight monitoring
- Nutritional monitoring, fluid, and calorie everyday

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 - Monitoring of therapy, evaluation of the therapeutics response, side effects
of the therapy i.e gastrointestinal side effects and long term monitoring of the
side effects of the therapy such as hepatotoxicity, neurotoxicity, and
cardiotoxicity
- Monitoring of the development
- Supervision hygiene for parents, caregiver, and paramedics

5. Education plans
- Describes the illnesses of the patient: causes, natural history of the disease,
treatment, prognosis, complications and treatment plans.
- Educate how to give appropriate food with nutritional needs
- Educate the impact on the child's social life, and family economic situation
because of long-term treatment.
- Educate to maintain personal and environmental hygiene, and avoid
environment situation that can cause infection.

6. Nursing Care
- Vital sign monitoring
- Nutrition and growth development
- Patient’s hygiene
- Parent’s hygiene
- Input and output monitoring

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VIII. FOLLOW UP
March 4th 2020 (1st observation day)
S No pale, no fever, no joint pain, good intake, no nausea, no vomiting
O General condition : looked ill Consciousness : Compos mentis
Blood pressure : 100/70 mmHg Pulse : 88 bpm, regular
Respiratory rate : 24 cpm Temperature : 37.00C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin - xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Therapeutic:
- Methotrexate 12 mg intrathecal
- Vincristine 1.4 mg intravena
- Daunorubicine 27.5 mg intravena
- L-asparginase 6,900 unit intravena
- Prednisone 15 mg- 10 mg- 10 mg (3-2-2 tablets) orally
Nutritional care:
Food 3 times daily (@ 550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (40 g carbohydrate, 4 g protein, 250 kcal)
- 3 meat balls with clear soup (25 kcal, 8 g protein, 40 g fat)
- Two cup of stir – fried spinach (25 kcal, 10 g carbohydrate, 2 g protein)
- 50 g Soybean cake (7 g carbohydrate, 5 g protein, 10 g fat, 100 kcal)
- One medium cut of beef (7 g protein, 10 g fat, 100 kcal)
- An apple ( 50 kcal, 12 g carbohydrate)

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Snacks 2 times daily (@ 220 kcal, 9 g protein, 10 g fat)
- White bread 3 slices (100 kcal, 40 g carbohydrate, 4 g protein)
- A glass of cow milk 200 ml ( 120 kcal, 5 g protein, 10 g fat)
- Mineral Water 2,500 – 3,000 ml daily
Nursing care : same like before

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 March 5th 2020 (2nd observation day)
S No fever, no joint pain, good intake, no nausea, no vomiting
O General condition : looked ill Consciousness : Compos mentis
Blood pressure : 110/70 mmHg Pulse : 84 bpm, regular
Respiratory rate : 21 cpm Temperature : 36.90C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin-xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Therapeutic:
- Prednisone 15mg-10mg-10mg (3-2-2 tablets) orally
Nutritional care:
Food 3 times daily (@ 550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (250 kcal, 40 g carbohydrate, 4 g protein)
- 1 fried chicken egg (100 kcal, 13 g protein, 55 g fat)
- 100 g stir – fried kale (25 kcal, 5 g carbohydrate, 4 g protein)
- 50 g Soybean cake (7 g carbohydrate, 5 g protein, 5 g fat, 75 kcal)
- 2 pieces of banana (100 kcal, 24 carbohydrate)
Snacks 2 times daily (@ 220 kcal, 9 g protein, 10 g fat)
- Crackers 5 pieces (100 kcal, 40 g carbohydrate, 4 g protein)
- A glass of cow milk 200 ml ( 120 kcal, 5 g protein, 10 g fat)
- Mineral water 2,500 – 3,000 mL daily
Nursing care : same like before

21
 March 6th 2019 (3rd observation day)
S No fever, no joint pain, no pale, good intake, no nausea, no vomiting
O General condition : looked ill Consciousness : Compos mentis
Blood pressure : 110/70 mmHg Pulse : 88 bpm, regular
Respiratory rate : 24 cpm Temperature : 36.80C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin-xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Therapeutic:
- L-Asparginase 6,900 unit Intravena
- Prednisone 15mg-10mg-10mg (3-2-2 tablets) orally
Nutritional care:
Food 3 times daily (@ 550 kcal, 26 g protein, 60 g fat)
- 2 cup of noodle (40 g carbohydrate, 4 g protein, 250 kcal)
- One egg (50 g fat, 9 g protein,100 kcal)
- 200 g spinach soup (50 kcal, 10 g carbohydrate, 2 g protein)
- 2 medium sized oranges (50 kcal, 12 g carbohydrate)
- 1 medium slice of beef stew (100 kcal, 11 g protein, 10 g fat)
Snacks 2 times daily (@ 220 kcal, 9 g protein, 10 g fat)
- 1 piece steamed cassava (100 kcal, 40 g carbohydrate, 4 g protein)
- A glass of cow milk 200 ml (120 kcal, 5 g protein, 10 g fat)
- Mineral water 2,500 – 3,000 mL daily
Nursing care : same like before

22
 March 7th 2020 (4th observation day)
S No fever, no joint pain, no pale, good intake, no nausea, no vomitting
O General condition : looked ill Consciousness : Compos mentis
Blood pressure :105/70 mmHg Pulse : 86 bpm, regular
Respiratory rate : 24 cpm Temperature : 36.60C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin-xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Therapeutic:
- Prednisone 15mg-10mg-10mg (3-2-2 tablets) orally
Nutritional care:
Food 3 times daily (@ 550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (40 g carbohydrate, 4 g protein, 250 kcal)
- One hard – boiled egg (75 kcal, 9 g protein, 50 g fat)
- 100 g of stir – fried long bean (50 kcal, 5 g carbohydrate, 1 g protein)
- 50 g Soybean cake (7 g carbohydrate, 5 g protein, 5 g fat, 100 kcal)
- One medium cut of fried fish (75 kcal, 7 g protein, 5 g fat)
Snacks 2 times daily (@ 220 kcal, 9 g protein, 10 g fat)
- 1 ½ slice of white bread (50 kcal, 20 g carbohydrate, 4 g protein)
- A glass of cow milk 200 ml (120 kcal, 5 g protein, 10 g fat)
- 1 medium size apples (50 kcal, 24 g carbohydrate)
- Mineral water 2,500 – 3,000 mL daily

23
 Nursing care : same like before

March 8th 2020 (5th observation day)

S No fever, no joint pain, no pale, good intake, no nausea, no vomiting
O General condition : looked ill Consiousness : Compos mentis
Blood pressure : 100/70 mmHg Pulse : 90 bpm, regular
Respiratory rate : 23 cpm Temperature : 36.90C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin-xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
Laboratory result:
Hb : 10.1 g/dL Sodium : 136 mEq/L
Erythrocyte : 3.55 x 106 /µL Potassium : 3.77 mEq/L
Ht : 30.2% Chloride : 100.4 mEq/L
Leukocyte : 2,400/µL Calcium : 9.39 mg/dL
Platelet : 154,000/µL AST : 33 U/L
Differential count : 0/0/0/56/40/4 ALT : 26 U/L
ANC : 1,344 cell/mm3 Ureum : 11 mg/dL
Creatinin : 0.2 mg/dL
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Medical Treatment:
Therapeutic:
- Prednisone 15mg-10mg-10mg (3-2-2 tablets) orally

24
 - Vincristine 1.365 mg
- L-Asparginase 6825 U
Nutritional care:
Food 3 times daily (@550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (40 g carbohydrate, 4 g protein, 250 kcal)
- One boiled egg (50 g fat, 9 g protein,100 kcal)
- 100 g pumpkin (5 g carbohydrate, 1 g protein, 25 kcal)
- 2 piece of soybean curd (7 g protein, 75 kcal)
- 1 medium slice of beef (10 g fat, 5 g protein, 100 kcal)
Snacks 2 times daily (@220 kcal, 9 g protein, 10 g fat)
- Biscuits 4 pieces (100 kcal, 12 g carbohydrate, 4 g protein)
- A glasses of cow milk 200 mL (120 kcal, 5 g protein, 10 g fat)
Mineral water 2,500 – 3,000 mL daily
Nursing care : same like before

25
 March 9th 2020 (6th observation day)
S No fever, no joint pain, no pale, good intake, no nausea, no vomiting
O General condition : looked ill Consiousness : Compos mentis
Blood pressure : 100/70 mmHg Pulse : 88 bpm, regular
Respiratory rate : 24 cpm Temperature : 36.70C
Body weight : 38 kg Body height : 149 cm BSA : 1.2 m2
Head : normocephaly
Face : symmetric, no dysmorphic
Eyes : conjunctiva not anemic, anicteric sclera
Neck : no lymph nodes enlargement
Chest : no retraction
Heart : no murmur
Abdomen : flat, normal bowel sound, liver palpable 2-2 cm below
costal margin-xyphoid process, spleen Schuffner I
Extremities : warm, CRT ≤ 2”
Genitalia : normal
A High Risk B-cell Acute Lymphoblastic Leukemia with Central Nervous
System Leukemia Induction Phase (C91.00)
P Medical Treatment:
Therapeutic:
- Prednisone 15mg-10mg-10mg (3-2-2 tablets) orally
- Patient discharged
Nutritional care:
Food 3 times daily (@550 kcal, 26 g protein, 60 g fat)
- Rice 1 cup (40 g carbohydrate, 4 g protein, 250 kcal)
- 1 piece of chicken egg 55 gram (60 g fat, 9 g protein, 100 kcal)
- 100 g spinach (10 g carbohydrate, 3 g protein, 50 kcal)
- 2 oranges (12 g carbohydrate, 75 kcal)
- 1 small size of fish 50 gram (10 g protein, 75 kcal)
Snacks 2 times daily (@220 kkal, 9 g protein, 10 g fat)
- Crackers 5 pieces (100 kcal, 40 g carbohydrate, 3 g protein)
- A glasses of cow milk 200 mL (120 kcal, 6 g protein, 10 g fat)
- Mineral water 2,500 – 3,000 mL

26
 Nursing care : same like before
IX. PROGNOSIS

- Ad Vitam : dubia ad malam

- Ad Functionam : dubia ad malam
- Ad Sanationam : dubia ad malam

27
 Disease Course Timeline When chosen as case

January 29th, February 5th, February 12h, February 17th, February 28th, March 3rd, 2020 March 4th-7th, March 8th-9th,
2020 2020 2020 2020 2020 2019 2020

Admitted to hospital Pale (-), fever (+), Pale (-), fever (+), Pale (-), fever (-), Pale (-), fever (-), Pale (-), fever Pale (-), fever Pale (-), fever (-),
with complaints: pale, bone pain (-), bone pain (-), bone pain (-), bone pain (-), (-), bone pain (-), bone pain bone pain (-),
bone pain and fever bleeding (-) bleeding (-) bleeding (-) bleeding (-) (-), bleeding (-) (-), bleeding (-) bleeding (-)
since 1 month ago

PE: anemic conjunctiva (+),
anicteric sclera
Abdomen: liver 3-3 cm BCM-
BXP, lien Schuffner II
PE: anemic PE: anemic PE: anemic PE: anemic PE: anemic PE: anemic PE: anemic
conjunctiva (+), conjunctiva (+), conjunctiva (+), conjunctiva (-), conjunctiva (-), conjunctiva (-), conjunctiva (-),
anicteric sclera, anicteric sclera, anicteric sclera, anicteric sclera, anicteric sclera,
anicteric sclera anicteric sclera
Abdomen: liver: 3-3 Abdomen: liver: 3-3 Abdomen: liver: 3-3 Abdomen: liver: 2-2 Abdomen: Abdomen: Abdomen: liver: 2-2
cm BCM-BXP, lien: cm BCM-BXP, lien: cm BCM-BXP, lien: cm BCM-BXP, lien: liver: 2-2 cm liver: 2-2 cm cm BCM-BXP, lien:
Schuffner II Schuffner II Schuffner II Schuffner I BCM-BXP,lien: BCM-BXP,lien: Schuffner I
Schuffner I Schuffner I

Laboratory: Supportive Laboratory: Laboratory:

Supportive Laboratory:
Hb 6.4g/dL, Ht 20.5%, examination: Hb 10.1g/dL, Ht 30.2%,
examination: Cerebrospinal fluid Hb 10.1g/dL, Ht 29.7%, Diagnosis: Diagnosis:
leukocyte 62,000/uL, platelet Bone marrow leukocyte 2,400/uL,
BMP: predominance analysis: cloudy, leukocyte 4,000/uL, High Risk B- High Risk B-
135,000/uL, Blast 55% puncture and platelet 154,000/uL,
with lymphoblast L2 leukocyte 1,000/L, platelet 124,000/uL, Cell Acute Cell Acute
Blood smear: normocytic Immunophenotyping ANC 1344 cell/mm3,
morphology with ANC 1760 cell/mm3, Lymphoblastic Lymphoblastic
normochromic erythrocyte, – waiting for result PMN 10%, MN 90%, Leukemia + Leukemia + AST 33 U/L, ALT 26
blast. AST 12 U/L, ALT 3 U/L,
anisocytosis (+), nonne (+), pandy (+), U/L, Ur 11 mg/dL, Cr
Immunophenotyping: Ur 11 mg/dL, Cr 0.6 CNS Leukemia CNS Leukemia
leukocytosis, diff count: blast (+) 0.2 mg/dL, Na 136
B lineage with gating mg/dL, Na 137 mEq/L,
eosinophil 0%, basophil 0%, mEq/L, K 3.57 mEq/L,
of the blast with K 3.7 mEq/L, Cl 96
stab 5%, segment 22% Working diagnosis: Cl 100.4 mEq/L, Ca
positive HLA-DR, mEq/L, Ca 9.55 mg/dL
lymphoblast 15%, Therapy: Therapy: 9.39 mg/dL
Suspect ALL CD10, CD19, CD34.
lymphocyte 55%, monocyte Diagnosis: - High-risk ALL - High-risk ALL
3%. Conclusion: Suggestive High Risk B-Cell induction induction
ALL Acute Lymphoblastic Diagnosis: phase phase
Diagnosis:
Leukemia + CNS Indonesia Indonesia
Therapy: Diagnosis: High Risk B-Cell High Risk B-Cell
Leukemia Protocol 2016 Protocol 2016
Start chemotherapy High Risk B-Cell Acute Lymphoblastic Acute Lymphoblastic
with CNS with CNS
Working diagnosis: after completing Acute Lymphoblastic Leukemia + CNS Leukemia + CNS
Leukemia Leukemia
comprehensive Leukemia Leukemia Leukemia
Suspect ALL (Modified) (Modified)
examination Therapy: - Nutrition - Nutrition
- High-risk ALL according to according to
induction phase Therapy: RDA RDA Therapy:
Therapy: Therapy:
Indonesia Protocol - High-risk ALL - High-risk ALL
- PRC transfusion - High-risk ALL
2016 with CNS induction phase induction phase
- Nutrition according to induction phase
Leukemia Indonesia Protocol Indonesia Protocol
Indonesia Protocol
RDA (Modified) 2016 with CNS 2016 with CNS
2016
- Plan: BMP and - Nutrition according Leukemia Leukemia (Modified)
- Nutrition according
immunophenotyping to RDA (Modified) - Nutrition according
to RDA
- Nutrition according to RDA
to RDA
28
CASE ANALYSIS DIAGRAM

Male, 9 years 3 months old Physical Examination:

- Pale since 1 month before admitted - Pale
- Bone pain since 1 month before admitted - Fever
- Fever since 1 month before admitted - Hepatosplenomegaly

Hemato-oncology

Supportive - Complete blood count

Examination - Blood smear
- BMP, Immunophenotyping
- Cerebrospinal fluid examination

Diagnosis High Risk B-Cell Acute Lymphoblastic

Leukemia with CNS Leukemia

Management Curative: Supportive:

ALL High Risk chemotherapy protocol - Blood transfusion
2016 with modification for CNS Leukemia - Nutrition according to RDA

Problem - Early response Ad Vitam : dubia ad malam - Parents education

- Lab evaluation Ad Functionam : dubia ad malam - Monitoring plan
- Complication Ad Sanationam : dubia ad malam

Prognosis Pediatr Blood Cancer. 2015. Level of evidence 2b, recommendation B

J Clin Oncol. 2017. Level of evidence 2b, recommendation B
Pediatr Blood Cancer. 2017. Level of evidence 2b, recommendation B
J Pediatr Neonatal Care. 2017. Level of evidence 2b, recommendation B

29
X. CASE ANALYSIS
This is a case of 9-years-and-3-months old male, with body weight of 38 kg and height
of 149 cm. Patient was diagnosed with High Risk B-cell Acute Lymphoblastic
Leukemia with Central Nervous System Leukemia. Diagnosis of this patient is based
on anamnesis, physical examination and laboratory examination such as cytochemical
analysis from bone marrow puncture, with morphology examination based on French
American British (FAB) Classification. We also used flow cytometry / leukemia
immunophenotyping as the main diagnostic tool for classification, prognosis,
treatment, and monitoring of acute leukemia.
Acute lymphoblastic leukemia (ALL) is a malignancy of blood cell disease,
characterized by abnormal progressive infiltration of immature lymphoid cells
(lymphoblast cells) from bone marrow and lymphatic organs.1 In United States, there
are approximately 2500 to 3500 new cases of ALL diagnosed in children each year,
with an incidence of approximately 3.4 cases per 100,000.2 In Indonesia, there is about
80,000 children with ALL and age below 15 years old with peak incident at the age of
2-5 years old.3 Childhood leukemia incidence in Indonesia ranging from 2.5 to 4.0 new
cases per 100,000 children, with estimation of 2000 to 3200 new childhood ALL cases
each year.4
Many risk factors are suspected to be involved in the occurrence of leukemia,
but the exact cause until now is still unclear. Risk factors for leukemia may be genetic
predisposing and environmental factors. On genetic factors, there are some hereditary
diseases that increase the risk of leukemia, such as Down syndrome, Bloom
syndrome, ataxia-telangiectasia, and Fanconi syndrome. Family history of first or
second grade family with hematopoietic malignancy is related to the risk of leukemia
occurrence. On environmental factors, exposure of ionizing radiation, drugs, paint or
gasoline, pesticides, and high voltage electricity also shown higher risk of leukemia.
Viral infections and maternal exposure of cigarettes, alcohol, and drugs during
pregnancy can also increase the risk of leukemia.5,6
Acute lymphoblastic leukemia often occurred acutely and found from routine
blood examination on asymptomatic child, and also may found in life-threatening case
with bleeding, infection, or respiratory distress syndrome. It is usually marked with
classic symptoms relating to bone marrow infiltration which affecting to cytopenia
occurrences like fever, weakness, pale, bruise and joint/bone pain, which was

30
allegedly secondary condition as a result of periosteum or joint capsule sprawling by
infiltration of leukemic cells.7

Table 1. Signs and symptoms of ALL patient with modification7

Signs and symptoms Percentage (%)
Weakness 100
Bone pain 97,1
Pale 94,1
Fever 94,1
Lymphadenopathy 41,2
Splenomegaly 29,4
Weight loss 29,4
Hepatomegaly 20,6
Bleeding 20,6
Limb swelling 11,8
Jaundice 8,8

Clinical symptoms that mostly reported in ALL patients are weakness, followed
by prolonged moderate fever without any focus of infection found. Generally, children
with acute onset of leukemia tend to be not active and bedridden. The other common
complaints are bone pain, pale and spontaneous bleeding. Limb swellings are also
sometimes found in patient with this condition.8
Pale is the most common physical presentation in patients with anemia, which
confirmed by abnormal hemoglobin (Hb) value below normal rate according to age. 9
Pale condition in ALL patient is a result of hematopoiesis suppression in bone marrow
due to blast cell infiltration.10 Anemia is defined as a condition which hemoglobin
concentration below -2 standard deviation, according to normal population rate. 11
Anemia causes reduction of physiological oxygen transport ability in blood and
diminished oxygen supply to tissues.12
Presentation of anemia with prolonged inexplicable fever, pale, organ
enlargement, leukocytosis and thrombocytopenia will lead us to think about
malignancy process. Patient with recurrent case of anemia is indicated for bone
marrow puncture, in order to find the etiology. Fever in malignancy is thought as a

31
result of inflammatory cytokines TNF-α, IL-1, and IL-6 released by macrophages, in
response to tumor cells. Another possible etiology of fever includes infection, vaccine,
biological agent, tissue damage, tumor, hypersensitivity reaction, autoimmune
disease, metabolic / genetic disorder, and blood loss.13
On his initial hospital admission, the patient’s mother said that the patient had
recurrent fever, pale and bone pain. Moderate fever was felt since one month before
admission, accompanied with bone pain and pale which also felt since a month before
his first admission. When chosen as case, the patient looked pale, without any fever,
and his bone pain has subsided.
Physical examination on the initial diagnosis showed anemic conjunctiva,
multiple lymph node enlargement around the neck, and hepatosplenomegaly. When
chosen as case, there is no anemic conjunctiva, no lymph node enlargement, palpable
liver of 3 cm below costal margin and 3 cm below xiphoid process, sharp edge, flat
surface, no tenderness, and palpable spleen of Schuffner II.
Janus et al14 found that pale presentation on conjunctiva, tongue, palm of hand
and nail has 93% sensitivity and 57% specificity in diagnosing anemia on patient with
hemoglobin level below 5 g/dL. Peripheral blood smear examination in leukemia
usually reflects the severity of bone marrow condition, with generally low hemoglobin
and platelet count.1,15 A study by Teuffel et al16 reported mean Hb level of 8 g/dL when
diagnosed as ALL. In this patient, we found Hb level of 6.4 g/dL on his initial diagnosis.
Pale, petechiae and ecchymoses on skin and mucosal membranes are caused
by thrombocytopenia, disseminated intravascular coagulation (DIC) or combination of
both. Thrombocytopenia (platelets <100,000 /μL) is common and occurred in 80% of
ALL cases, with bleeding presentation in 10%-45% of ALL cases.17,18 In this patient
initial presentation, his platelets level was 148.000 /μL without any bleeding
presentation. Laboratory examination at the onset of diagnosis showed: hemoglobin
6.4 g/dL, hematocrit 20.5%, leukocyte 62.000/μL, erythrocyte 2.54 x 106/μL, platelet
135 x 103/μL, sodium 137 mEq/L, potassium 4.17 mEq/L, chloride 100.2 mEq/L, AST
27 U/L, ALT 6 U/L, ureum 14 mg/dl, dan creatinine 0.3 mg/dl, LDH 574 U/L, PT 14.6
seconds (control 13.8 seconds), INR 1.10 seconds (control 1.13 seconds), APTT 41.9
seconds (control 32.9 seconds). Peripheral blood smear examination showed:
normocytic normochromic erythrocyte, anisocytosis (+), macrocyte (+), microcyte (+),
with normal leukocyte count, differential count: eosinophil 0%, basophil 0%, stab

32
neutrophil 5%, segment neutrophil 22% lymphoblast 15%, lymphocyte 55%, monocyte
3%, with conclusion suggestive of ALL.
Definitive diagnosis of leukemia is based on bone marrow puncture
examination result. French American British (FAB) classified ALL morphologically into
3 types, namely L1, L2, L3.19 In this patient, bone marrow puncture examination
showed predominantly lymphoblast L2 with blast cells. Supriyadi et al20 conducted a
multicenter study to determine ALL pattern profile in Indonesia. The result showed that
83% of ALL cases in Indonesia is B-cell type. Immunophenotyping examination is
useful to determine the type of ALL cells and help to choose the management and
prognosis of the disease. Based on its immune phenotype, leukemia is divided into 3
types: pre-B cells (80% of total ALL), B cells (<5%), and T cells (15%), with T cell types
are commonly related with hyperleukocytosis, central nervous system (CNS)
involvement, mediastinal mass, males, and poor prognosis. 19 In this patient,
immunophenotyping examination showed gating on the blast with positive with HLA-
DR, CD 10, CD 19, CD 34, with conclusion of B-cell ALL.
Other supportive examinations in ALL patients include chest x-ray to determine
the presence of mediastinal mass and cerebrospinal fluid analysis to detect leukemic
cell infiltration into the CNS.21 On chest X-ray examination, there is no mediastinal
mass in this patient. Cerebrospinal fluid analysis performed simultaneously with
intrathecal chemotherapy showed cloudy liquid, leukocyte 1000/μL, PMN 10%, MN
90%, blast (+), glucose 75 mg/dL, Nonne and Pandy test (+), erythrocyte 0-1/hpf,
protein 10 mg/dL. The patient was then diagnosed with high risk acute lymphoblastic
leukemia with central nervous system leukemia.
Neurologic abnormalities in leukemia can be caused by infiltration of leukemia
cells in CNS, CNS bleeding, CNS infection, toxic effects of chemotherapy or
chemotherapy side effects. Infiltration of leukemia cells in CNS can cause CNS or
peripheral abnormalities that may worsen the prognosis. Clinical manifestations may
vary, depending on the size of leukemic infiltration, the sites and number of sites
involved. Brain localization scan cause headache, alteration of mental status, walking
abnormalities, nausea and vomiting, loss of consciousness, seizures, gait or sensory
disturbances, papilloedema. Cranial nerves localization may be associated with
diplopia, hearing and visual loss, facial numbness, dysphagia. Spinal involvement can
determine focal weakness (of legs more often than arms), paresthesias, back pain,
radicular pain, bladder, and bowel dysfunction.22 Early CNS leukemia occurred in 8%

33
of patients at the first diagnosis, whereas relapse CNS leukemia occurred in 10% of
cases.23 CNS leukemia is diagnosed by the presence of neurologic abnormalities with
or without the presence of pathological cells in cerebrospinal fluid, or the presence of
pathological cells of cerebrospinal fluid with or without the presence of neurologic
abnormalities. CNS leukemia was classified into 3 types: CNS1 when obtained <5
leukocytes /μL, no blast cells were found in cytocentrifugated cerebrospinal fluid;
CNS2 when obtained <5 leukocytes /μL, with the presence of blast cells in
cytocentrifugated cerebrospinal fluid; and CNS3 when obtained ≥5 leukocytes /μL with
blast cells in cytocentrifugated cerebrospinal fluid.23 In this patient we obtained CSF
analysis result: leukocytes 1000 /μL with presence of blast cells, so this patient was
classified as CNS3.
Associated with life expectancy, ALL is classified into standard risk and high
risk ALL. Based on national protocol, ALL patients are included in high risk category
if: age of less than 1-year-old or more than 10-years-old, leukocyte count > 50,000
/μL, presence of mediastinal mass > 2/3 diameter of thoracic cavity, central nervous
system (CNS) leukemia, T-cell leukemia, and blast cell count after 1 week of treatment
> 1,000 /mm3. This risk-based classification is also associated with treatment protocol
used.1 This patient was categorized as high risk based on: leukocyte count at the time
of diagnosis > 50.000 /μL and leukocyte + blast found in cerebrospinal fluid.
Hyperleukocytosis is defined as a peripheral leukocyte count greater than
100,000 /μL, found in 5-20% of leukemia cases in newly diagnosed children, and
known as a poor prognostic factor. Hyperleukocytosis caused by ALL is related with
early morbidity and mortality due to hyperviscosity caused by high leukocyte count. 24
On initial diagnosis was obtained the number of leukocytes 62,000 /μL, so that
hyperhydration is not indicated in this patient.
Treatment of acute leukemia includes supportive treatment and curative
therapy. Supportive treatment is essential which is including comorbidities treatment,
infection prevention and treatment, optimal nutritional support and blood component
transfusion if necessary, administration of antibiotics, granulocyte-enhancing drugs,
anti-fungal drugs, and psychosocial aspects. Curative or specific therapy aims to
eradicate leukemia cells both inside and outside of bone marrow and provide an
opportunity for the bone marrow to work normally. Curative therapy includes:
remission induction, consolidation, reinduction and maintenance phase. Generally,
initial therapy is expected to eradicate leukemia cells from the bone marrow and is

34
known as remission induction. The second phase of therapy is aimed to eradicate
residual leukemia blast cells. The third phase is reinduction phase. These three
phases are then followed by the maintenance phase. 1,3,25 For curative treatment this
patient receives chemotherapy according to the high risk ALL with CNS leukemia
Indonesia protocol 2016, which the patient is currently in induction phase.
Giving cytostatic drugs may cause side effects such as toxicity to some organs.
Common side effects including nausea, vomiting, alopecia, pain, myelosuppression
(anemia, neutropenia, thrombocytopenia), mucositis, blepharitis, immunosuppression
and side effects on organ systems affected by given cytostatic agents. 14,26
Chemotherapy protocol given to patients in induction phase are intrathecal
methotrexate, vincristine, prednisone, doxorubicin, and L-asparginase. Methotrexate
may cause adverse effects, such as nephrotoxicity, hepatotoxicity, mucositis,
blepharitis, rashes and photosensitivity.3,14 Corticosteroids used in this patient is
prednisone, where prednisone can penetrate to blood-brain barrier with the same
effect of dexamethasone, with less toxicity side effects, such as avascular necrosis,
infection, and linear growth reduction. Anthracycline used in this treatment is
doxorubicin or daunorubicin, with the same efficacy and toxicity in randomized trials. 27
L-asparaginase is a hydrolase that catalyzes the conversion of L-asparagine, an
endogenous amino acid necessary for the function of some neoplastic cells, such as
lymphoblasts. Depletion of L-asparagine from plasma by L-asparaginase results in
inhibition of RNA and DNA synthesis with the subsequent blastic cell apoptosis.
However, L-asparaginase has been associated with increased risk of adverse effects,
such as thrombosis, impaired functions of liver, kidneys or central nervous system.
Thrombotic events in L-asparaginase administration occured as a result of inhibited
synthesis of anticoagulant proteins (mainly antithrombin).28
In this patient, induction phase was started on February 12th, 2020 and still in
progress until when this patient was taken as case report. During daily observation
and evaluation, the patient didn’t show any worsening of sign and symptom. We still
need to observe any sign of relapse during bone marrow examination by the end of
induction phase. Considering there is still a chance of relapse in patient with B-cell
ALL and CNS involvement, strict monitoring is needed.
Pneumocystis jiroveci pneumonia (PCP) is an opportunistic infection in children
with cancer and is the most common cause of death in children receiving
chemotherapy. The incidence of PCP has decreased significantly since prophylactic

35
antibiotics, whereas if prophylaxis is not given, about 15-20% of children with leukemia
will have PCP. Trimethoprim-sulfamethoxazole (TMP-SMZ) / Cotrimoxazole is the
recommended drug for PCP prophylaxis, which is administered at a dose of 4 mg /
kgBW / day, twice daily, for 3 consecutive days within 1 week. Agarwal et al29
conducted a 5-year retrospective study on the administration of TMP-SMZ prophylaxis
in children with ALL therapy, which TMP-SMZ regimen for 2 consecutive days each
week has the same results as TMP-SMZ 3 consecutive days each week.
Cotrimoxazole is not yet given in this patient, because TMP-SMZ prophylaxis is
administered after the consolidation phase is finished.
The main reasons for low survival rate in patients with ALL in developing
countries are treatment rejection or treatment drop out. This may be related to the
socioeconomic status of parents. Mostert et al30 studied a number of 164 low economic
patients with ALL were found to be 35% rejected or dropped out treatment, 23%
experienced treatment-related deaths, 22% had progressive leukemia or relapse, and
only 20% had 5-year event free survival.
Counseling is given to parents and families about the things needed during the
treatment eg. nutritional care, personal and environment hygiene and cooperation
between patients, parents, family and health provider. Support from family, especially
parents is very important during the patient’s treatment period.
Treatment in patients with ALL will affect the outcome of the patient, especially
explained by Event Free Survival (EFS). Hazar et al31 showed ALL patients in
developing countries had a survival rate of 67.3% in the first 4 years after therapy and
63.2% at 8 years after therapy. Patients included in this study have mean age of 4.3
years old, with mortality rate during therapy of 17.7%. With a better life expectancy
from year to year, intensive treatment, and good family support, the life expectancy of
this patient was expected to be increasing.
Acute lymphoblastic leukemia requires a comprehensive therapy because of a
broad clinical prognosis. Prognosis is associated with host characteristics and
disease, including age, organ function, immunophenotype and karyotype of leukemic
cells, as well as leukemic cell clearance rates and complete remission achievement.
Most children with ALL are currently expected to have a long life expectancy of 80%
over 5 years. Characteristics generally believed to have a negative impact on
outcomes when diagnosed with age less than one year or more than ten years, white
blood cell count more than 50,000 /mm3, leukemia with T-cell phenotype, slow

36
response to initial therapy. Chromosomal abnormalities including hypodiploidy,
Philadelphia chromosome, 11q23 abnormalities and gene translocation t (4, 11), tend
to have a worse prognosis. The expected characteristics of good outcomes are a rapid
response to therapy, hyperliploidy, and gene fusion TEL / AML1.32,33
Permatasari et al33 conducted a study at Cipto Mangunkusumo Hospital to
determine the factors that influence the outcome of ALL treatment. Remission rate in
this research is 78.2%. The mortality rate during the induction phase at the ALL of
regular risk includes 12.3%. This is due to the lack of supportive therapy and room
isolation facilities when neutropenia is associated with infection and the high cost of
chemotherapy drugs. In this study also found that age 1-2 years had a higher life
expectancy than age 10-18 years. While in research conducted by Widiaskara et al34
in dr. Soetomo general hospital, Surabaya, found that ALL patients with high risk had
a mortality rate 2 times higher than standard risk, with the most common cause of
death was infection (76%).
Wilejto et al35 studied 19 ALL children with CNS involvement who received
intensification of CNS-directed chemotherapy by triple intrathecal chemotherapy
(84.2%), use of corticosteroid in induction (57.9%) and maintenance (66.7%), and
high-dose methotrexate (77.8%). The 5-years overall survival (OS) was 84.2±8.4%
and event-free survival (EFS) was 79.0±9.4% with a median follow-up time of 4.3 years
(range, 2.6–8.2) The cumulative incidence of CNS relapse was 5.251%. (Level of
evidence 2b, recommendation B).
A study by Winick et al36 in 8,379 patients to determine the prognostic
significance of blasts, white , and red blood cells in CSF samples at diagnosis of acute
lymphoblastic leukemia ( ALL ). CSF status was designated as follows : CNS1 ( no
blasts ); CNS2 ( 5 WBCs/ml and blasts with/without ≥ 10 RBCs/ml or ≥ 5 WBCs/ml
plus blasts, with WBCs ≥ 5 times the number of RBCs ); and CNS3 ( ≥ 5 WBCs/ml
plus blasts with/without ≥ 10 RBCs/ml or clinical signs of CNS disease ). This study
reported 5 – year event free survival ( EFS ) and overall survival ( OS ) rate of 85%
and 92.7% in CNS1, 76% and 86.8% in CNS2, and 76% and 82.1% in CNS3,
respectively ( p < o.0001 ). In children and adolescents with ALL type – B Lineage,
CNS leukemia is a poor outcome predictor and may increase the risk of relapse in
central nervous system (Level of evidence 2b, recommendation B).

37
 Hafiz et al37 in a study of 546 ALL patients were enrolled based on initial CNS
status: CNS1, CNS2, CNS3, TLP+, and TLP-. TLP+ and CNS3 status had significant
prognostic value: risk ratio (RR 2.39, 95% CI= 1.4-3.6, p=0.0005) Overall 5-year event
free survival (EFS) were found 75%. 5-years EFS found for patients in each group
were as follows: CNS1 (82 ± 2%), CNS2 (82 ± 3%), CNS3 (52 ± 6%), TLP+ (75 ± 5%)
and TLP- (85 ± 4%). Relapse rate in patients with CNS3 status was higher (35%),
compared with CNS1 (17%), CNS2 (17%), TLP+ (20%) and TLP- (12%). (Level of
evidence 2b, recommendation B).
Taskinen et al38 in a retrospective study, found that CNS involvement was a
strong independent risk factor for relapse ( HR 7.09, p < 0.001 ). They found that 5 –
year event free survival of CNS 1 – 2 was 64.1% ± 1.7 and CNS3 was 60.6% ± 6.5.
(Level of evidence 2b, recommendation B).
The prognosis of this patient is divided into prognosis ad vitam, prognosis ad
functionam and prognosis ad sanationam. Prognosis ad vitam is dubia ad malam,
because the number of event free survival rate is low, about 52%.36,37 Prognosis ad
functionam is dubia ad malam, because the patient is presented with CNS
involvement, which might cause numbers of debilitating neurological symptoms. 22,38
The prognosis ad sanationam is dubia ad malam, because although the therapy
response is good, the possibility of relapse still cannot be excluded because the
patient has not completed his chemotherapy yet.35-38
The education that can be given to this patient includes current condition of the
patient, treatment plan, and course of the illness. Ensuring parents and the patient in
this case can follow all of the planned treatment procedures. In addition, monitoring
on the growth and development also quality of life of this patient were needed. Good
knowledge is expected to create a family environment that can support the treatment
process and children can achieve optimal growth and development with a good quality
of life.

38
XI. REFERENCES
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IDG, Windiastuti E, Abdulsalam M. Buku ajar hematologi onkologi anak. 3 rd ed.
IDAI. 2010:236-45.
2. Ward E, DeSantis C, Robbins A, Kohler B, Jemal A. Childhood and adolescent
cancer statistics. CA Cancer J Clin. 2014;64(2):83.
3. UKK Hematologi-onkologi. Protokol pengobatan leukemia limfoblastik akut anak-
2013. Jakarta: UKK Hematologi-onkologi. 2013.
4. Sutaryo, Sumadiono, Suhadi, et al. Indonesian Multicentre Study Group,
Yogyakarta. Gadjah Mada University Press; 2000. The Protocol of Wijaya
Kusuma acute lymphoblastic leukemia of childhood 2000.
5. Wigle DT, Turner MC, Krewski D. A systematic review and meta-analysis of
childhood leukemia and parental occupational pesticide exposure. Environ Health
Perspect. 2009;117:1505-13.
6. Scelo G, Metayer C, Zhang L, Wiemels JL, Aldrich MC, Selvin S, et al. Household
exposure to paint and petroleum solvents, chromosomal translocations, and the
risk of childhood leukemia. Environ Health Perspect. 2009;117:133-9.
7. Lanzkowsky P, Lipton J, Fish J. Lankowzky’s manual of pediatric hematology and
oncology sixth edition. Elsevier Inc; 2016:367-71.
8. Nwannadi I, Alao O, Bazauaye G, Nwagu M, Borke M. Clinical and laboratory
characteristics of patients with leukemia in South-Nigeria. Int J Oncol. 2009;7:1-8.
9. Bernard SC, Abdelsamad EH, Johnson PA, Parvathaneni C, Parvathaneni M.
Pediatric Leukemia: Diagnosis to Treatment-A Review. J Cancer Clin Trials.
2017;2:1-3.
10. Nissenson AR, Goodnough LT, Dubois RB. Anemia. Arch Intern Med.
2003;163:1400-5.
11. Oski FA, Brugnara C, Nathan DG. A diagnostic approach to the anemia patient.
In: Nathan DG, Orkin SH, editors. Hematology at infancy and childhood. 5 th ed.
WB: Saunders, 1998:375-80.
12. Diamond CA. Anemia. In: Hastings C. The children’s hospital Oakland hematology
oncology handbook. St Louis. Mosby; 2002:161-69.
13. Cunha BA. Fever of unknown origin: clinical overview of classic and current
concepts. Infect Dis Clin N Am. 2007;21:867-915.

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14. Janus J, Moerschel SK. Evaluation of anemia in children. Am Fam Physician.
2010;81:1462-71.
15. Hutter JJ. Childhood leukemia. Pediatr rev. 2010;31:234-41.
16. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, et al. Anemia
and survival in childhood acute lymphoblastic leukemia. Haematologica.
2008;93:1652-7.
17. Hamid GA. Acute leukemia clinical presentation. In: Guenova M, Balatzenko G,
penyunting. Leukemia. Yemen: Intech. 2015.
18. Silverman LB, Sallan SE. Acute lymphoblastic leukemia. In: Nathan DG, Orkin SH,
Ginsburg D, Look AT. Nathan and Oski’s Hematology of infancy and childhood.
6th ed. Philadelphia. Saunders;2003:1135-66.
19. Morgolin JF, Rabin KR, Steuber CP. Acute Lymphoblastic Leukemia. In: Pizzo PA,
Poplack DG, penyunting. Principles and Practice of Pediatric Oncology. 6 th ed.
Philadelphia: Lippincott Williams & Wilkins;2015:519-49.
20. Supriyadi E, Widjajanto PH, Veerman AJP, Purwanto I, Nency YM, Gunawan S,
et al. Immunophenotypic patterns of childhood acute leukemia in Indonesia. Asian
Pacific J Cancer Prev. 2011;12:3381-7.
21. Pusponegoro H, Moeslichan MZ, Kaban R, Suradi R, Windiastuti E. Clinical
features and survival pattern of central nervous system leukemia in children with
acute lymphoblastic leukemia. Paediatr Indones. 2001;41:247-52.
22. Del Principe MI, Maurillo L, Buccisano F, et al. Central nervous system
involvement in adult acute lymphoblastic leukemia: diagnostic tools, prophylaxis,
and therapy. Mediterranean J Hematol Infect Dis. 2014;6:e2014075.
23. Levinsen M, Taskinen M, Abrahamsson J, Forestier E. Clinical features and early
treatment response of central nervous system involvement in childhood acute
lymphoblastic leukemia. Pediatr Blood Cancer. 2014:61:1416-21.
24. Lowe EJ, Pui CH, Hancock ML, Geiger TL, Khan RB, Sandlund JT. Early
complications in children with acute lymphoblastic leukemia presenting with
hyperleukocytosis. Pediatr Blood Cancer. 2005;45:10-5.
25. Inaba H, Greaves M, Mullighan CG. Acute lymphoblastic leukemia. Lancet.
2013;381:1-27.
26. Pui CH, Evans WE. Treatment of acute lymphoblastic leukemia. N Engl J Med.
2006;354:166–78.

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27. Cooper ST, Brown PA. Treatment of pediatric acute lymphoblastic leukemia.
Pediatr Clin North Am. 2015;62:61-73.
28. Piatkowska JB, Krawczyk-Kulis M, Giebel S, Adamczyk-Cioch M, Czyz A et al.
Use of L-asparaginase in acute lymphoblastic leukemia: recommendations of the
Polish Adult Leukemia Group. Pol Arch Med Wewn. 2008 Nov;118(11):664-9.
29. Agarwal AK, Chang PP, Feusner J. Twice weekly pneumocystis jiroveci
pneumonia prophylaxis with trimethoprim-sulfamethoxazole in pediatric patients
with acute lymphoblastic leukemia. J Pediatr Hematol Oncol. 2011;33:1-4.
30. Mostert S, Sitaresmi M, Gundy CM, Sutaryo, Veerman A. Influence of
socioeconomic status on childhood acute lymphoblastic leukemia treatment in
Indonesia. Pediatrics. 2006;118:1600-6.
31. Hazar V, Gulzun T, Uygun V, Akcan M, Alphan K, Yesilipek A. Childhood Acute
Lymphoblastic Leukemia in Turkey: Factors Influencing Treatment and Outcome:
A Single Center Experience. J Pediatr Hematol Oncol. 2010;32:317-22.
32. Pui CH, Relling MV, Downing JR. Acute lymphoblastic leukemia. N Engl J Med.
2004;350:1535-48.
33. Permatasari E, Windiastuti E, Satari HI. Survival and prognostic factors of
childhood acute lymphoblastic leukemia. Paediatrica Indonesiana. 2009;49:365-
71.
34. Widiaskara IM, Bambang P, Ugrasena IDG, Ratwita M. Luaran pengobatan fase
induksi pasien leukemia limfoblastik akut pada anak di rumah sakit umum Dr.
Soetomo Surabaya. Sari Pediatri. 2010;12:128- 34.
35. Wilejto M, Di Giuseppe G, Hitzler J, Gupta S, Abla O. Treatment of young children
with CNS-positive acute lymphoblastic leukemia without cranial radiotherapy.
Pediatr Blood Cancer. 2015;62:1881-5.
36. Jiménez-Hernández E, Jaimes-Reyes E. Arellano-Galindo J, et al. Survival of
Mexican Children with Acute Lymphoblastic Leukaemia under Treatment with the
Protocol from the Dana-Farber Cancer Institute 00-01. BioMed Research
International. 2015(1):576950.
37. Baytan B, Evim MS, Guler S, Gunes AM, Okan M. Acute central nervous system
complications in pediatric acute lymphoblastic leukemia. Pediatr Neurol.
2015;30:1-7.
38. Hafiz MG, Jamal CY, Islam A. Prognostic Significance of Cerebrospinal Fluid
Lymphoblasts at Initial Presentation with Acute Lymphoblastic Leukemia

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 Attending at Bangabandhu Sheikh Mujib Medical University, Bangladesh. J
Pediatr Neonatal Care. 2017:6(2): 00240.

CLINICAL RESEARCH REFERENCES

35. Wilejto M, Di Giuseppe G, Hitzler J, Gupta S, Abla O. Treatment of young children
with CNS-positive acute lymphoblastic leukemia without cranial radiotherapy.
Pediatr Blood Cancer. 2015;62:1881-5.
36. Winick N, Devidas M, Chen S, Maloney K, Larsen E. Mattano L, et al. Impact of
initial CSF findings on outcome among patients with national cancer institute
standard and high risk B – cell acute lymphoblastic leukemia : A report from the
children’s oncology group. J Clin Oncol. 2017; 35:1-12.
37. Hafiz MG, Jamal CY, Islam A. Prognostic Significance of Cerebrospinal Fluid
Lymphoblasts at Initial Presentation with Acute Lymphoblastic Leukemia Attending
at Bangabandhu Sheikh Mujib Medical University, Bangladesh. J Pediatr Neonatal
Care. 2017:6(2): 00240.
38. Taskinen M, Oskarsson T, Levinsen M, Bottai M, Hellebostad M, et al. The effect
of central nervous system involvement and irradiation in childhood ALL : lesson
from NOPHO ALL – 92 and ALL – 2000 protocols. Pediatr Blood Cancer 2017;
64:242-9.

42
ABBREVIATIONS

% Percent
oC Degree of Celcius

AB Antibiotics

ALL Acute Lymphoblastic Leukemia

ALT Alanine Transaminase

ANC Absolute Neurophil Count

AST Aspartate Transaminase

BW Body weight

BCG Bacillus Calmette Guerin

BCM Below Costal Margin

bpm Beats per minute

BMP Bone Marrow Dunction

BSA Body Surface Area

Ca Calsium

CDC Centers for disease Control and Prevention

Cl Chloride

CNS Central Nervous System

cm centimeter

cpm cycles per minute

CRP C- Reactive Protein

CRT Capilary Refill Time

DPT Diphtery Pertusis Tetanus

EFS Event Free Survival

F Female

fL femto Liter

43
FN Febrile Neutropenia

GFR Glomerular Filtration Rate

gr Gram

g/dL gram per deciliter

Hb Hemoglobin

Hpf high power field

Ht Hematocrit

IU/dL International unit per desiliter

K Potassium

kcal Kilo Calories

kg Kilogram

kgBW Kilograms Body Weight

LDL Low Density Lipoprotein

LTI life threatening infection

LDH Lactate Dehidrogenase

M Male

MCH Mean Corpuscular Hemoglobin

MCHC Mean Corpuscular Hemoglobin concentration

MCV Mean Corpuscular Volume

mEq/L Mili-Equivalen per Liter

mg Miligram

mg/dL Miligram per deciliter

mL Mililiter

mm Millimeter

mmHg Millimeter hydragyrum

mm3 Millimeter cubic

N Nervus

44
OS Overall Survival

pg PicoGram

RBC Red Blood Cells

RDA Recommended Daily Allowances

SD Standard Deviation

Tab Tablet

TST Tuberculin Skin Test

TT Tetanus Toxoid

U/L Unit per Liter

45
APPENDIX

PATIENT’S PHOTO

46
Nutritional Status

47
ALL Protocol High Risk + CNS Leukemia

48
49
Patient’s Chest X-Ray

50
Tanner stage

51
52
Patient’s PedsQL 4.0 Teen Report (13-18 years)

53
PATIENT’S ECHOCARDIOGRAPHY

54
 Oxford Centre for Evidence-based Medicine Levels of Evidence
Differential
Therapy /
diagnosis / Economic and
Level Prevention, Prognosis Diagnosis
symptom decision analyses
Aetiology / Harm
prevalence study

SR (with homogeneity*) SR (with homogeneity*) of SR (with

SR (with SR (with homogeneity*)
of inception cohort Level 1 diagnostic studies; homogeneity*) of
1a homogeneity*) of of Level 1 economic
studies; CDR” validated CDR” with 1b studies from prospective cohort
RCTs studies
in different populations different clinical centres studies

Analysis based on
Individual inception clinically sensible costs
Individual RCT Validating** cohort study
cohort study with > 80% Prospective cohort or alternatives;
(with narrow with good” ” ” reference
1b follow-up; study with good systematic review(s) of
Confidence standards; or CDR” tested
CDR” validated in a follow-up**** the evidence; and
Interval”¡) within one clinical centre
single population including multi-way
sensitivity analyses
Absolute better-value or
Absolute SpPins and All or none case-
1c All or none§ All or none case-series worse-value analyses
SnNouts” “ series
”””“
SR (with homogeneity*)
SR (with of either retrospective SR (with SR (with homogeneity*)
SR (with homogeneity*) of
2a homogeneity*) of cohort studies or homogeneity*) of 2b of Level >2 economic
Level >2 diagnostic studies
cohort studies untreated control groups and better studies studies
in RCTs
Analysis based on
Retrospective cohort
Exploratory** cohort study clinically sensible costs
study or follow-up of
Individual cohort with good” ” ” reference or alternatives; limited
untreated control Retrospective cohort
study (including low standards; CDR” after review(s) of the
2b patients in an RCT; study, or poor follow-
quality RCT; e.g., derivation, or validated only evidence, or single
Derivation of CDR” or up
<80% follow-up) on split-sample§§§ or studies; and including
validated on split-
databases multi-way sensitivity
sample§§§ only
analyses
“Outcomes”
Audit or outcomes
2c Research; “Outcomes” Research Ecological studies
research
Ecological studies
SR (with
SR (with
homogeneity*) of SR (with homogeneity*) of SR (with homogeneity*)
3a homogeneity*) of 3b
case-control 3b and better studies of 3b and better studies
and better studies
studies
Analysis based on
limited alternatives or
costs, poor quality
Non-consecutive study; or Non-consecutive
Individual Case- estimates of data, but
3b without consistently applied cohort study, or very
Control Study including sensitivity
reference standards limited population
analyses incorporating
clinically sensible
variations.
Case-series (and
Case-series (and poor Case-control study, poor or Case-series or
poor quality cohort Analysis with no
4 quality prognostic cohort non-independent reference superseded
and case-control sensitivity analysis
studies***) standard reference standards
studies§§)
Expert opinion Expert opinion
without explicit Expert opinion without Expert opinion without without explicit Expert opinion without
critical appraisal, or explicit critical appraisal, explicit critical appraisal, or critical appraisal, or explicit critical appraisal,
5 based on or based on physiology, based on physiology, based on or based on economic
physiology, bench bench research or “first bench research or “first physiology, bench theory or “first
research or “first principles” principles” research or “first principles”
principles” principles”

55
 Categories of Recommendations

Level

Good scientific evidence suggests that the benefits of the clinical

A service substantially outweigh the potential risks. Clinicians should
discuss the service with eligible patients.

At least fair scientific evidence suggests that the benefits of the

B clinical service outweighs the potential risks. Clinicians should
discuss the service with eligible patients.

At least fair scientific evidence suggests that there are benefits

provided by the clinical service, but the balance between benefits and
C risks are too close for making general recommendations. Clinicians
need not offer it unless there are individual considerations.

At least fair scientific evidence suggests that the risks of the clinical
D service outweighs potential benefits. Clinicians should not routinely
offer the service to asymptomatic patients.

Scientific evidence is lacking, of poor quality, or conflicting, such that

the risk versus benefit balance cannot be assessed. Clinicians should
I help patients understand the uncertainty surrounding the clinical
service.

56