CASE REPORT

ANEMIA APLASTIK

Compiled By:
Sakthy Vicknes A/P Shanmugam

110100400

Supervisor :
dr. Rina Amalina Carolina, Sp.A (K)

CHILD HEALTH DEPARTMENT

H. ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINE
UNIVERSITAS SUMATERA UTARA
MEDAN
2015

CONTENTS
CHAPTER I INTRODUCTION ..........................................................................1
1.1................................................................................................................B
ackground ..............................................................................................1
1.2................................................................................................................
Objective ...............................................................................................1
CHAPTER II LITERATURE REVIEW ............................................................2
2.1. Definition .............................................................................................2
2.2. Etiology.................................................................................................2
2.3. Classification.........................................................................................3
2.4.Pathophysiology....................................................................................4
2.5.Differential Diagnosis...........................................................................5
2.6.Diagnosis...............................................................................................6
2.7. Management.........................................................................................8
CHAPTER III CASE REPORT ........................................................................11
CHAPTER IV DISCUSSION & SUMMARY..................................................19
4.1. Discussion...........................................................................................19
4.2. Summary.............................................................................................20
REFERENCES....................................................................................................21

CHAPTER I
INTRODUCTION
1.1 Background
Aplastic anemia is defined as failure of bone marrow to producing
components of blood cells. Aplastic anemia is anemia accompanied by peripheral
blood pancytopenia caused by a primary disorder of the bone marrow in the form
of aplasia or hypoplasia of the absence of infiltration, bone marrow suppression or
displacement. Pancytopenia itself is a condition characterized by the presence of
anemia, leukopenia, and thrombocytopenia in all its manifestations.1
Aplastic anemia is a rare disease in the world. The incidence in Asia including
China, Japan, Thailand and India is higher compared with Europe and the United
States of America. The incidence of this disease varies between 2 to 6 cases per 1
million population. Research conducted The International Aplastic anemia and
agranulocytosis Study in Europe and Israel early in 1980 to get 2 cases per 1
million populasi.3
Comparison of incidence between men and women is approximately 1: 1,
although of some data showing men slightly more often affected by anemia
aplastik.3
Although aplastic anemia occurs in all age groups, a small peak in the
incidence is observed in childhood because of the inclusion of inherited marrowfailure syndromes. A second peak is observed in people aged 20-25 years
(Medscape)
1.2 Objective
The aim of this study is to explore more about the theoritical aspects on
aplastic anemia, and to integrate the theory and application of aplastic anemia
case in daily life.

CHAPTER II
LITERATURE REVIEW
2.1 Definition
Aplastic anemia is a bone marrow failure syndrome that is characterized
by peripheral pancytopenia and bone marrow hypoplasia. In aplastic anemia
decreased production of blood cells from the bone marrow, causing
retikulositopenia, anemia, granulocytopenia, monositopenia and trombositopenia.3
2.2 Etiology
Aplastic anemia is often caused by exposure to radiation and chemicals.
However, most patients the cause is idiopathic, meaning the cause is unknown.
Aplastic anemia can also be associated with viral infections and other diseases
(Table 2).
Table 2. Classification of aplastic anemia Etiology
Acquired Aplastic Anemia
Secondary aplastic anemia
Chemicals
Benzene
Insecticides
Glue
Solvents
Drugs
Cytotoxic agents
Antibiotics
Nonsteroidal anti-inflammatory drugs
Anticonvulsive agents
Gold salts

Radiation
Viruses
Epstein-Barr virus
Non-A, non-B, non-C hepatitis viral agent (?)
Human immunodeficiency virus
Immune and rheumatologic diseases
Graft-versus-host disease
Rheumatoid arthritis
Systemic lupus erythematosus
Paroxysmal nocturnal hemoglobinuria
Pregnancy
Idiopathic aplastic anemia
Inherited Aplastic Anemia
Fanconis anemia
Dyskeratosis congenital
Schwachman syndrome

2.2.1. Radiation
Marrow aplasia is a major acute sequela of radiation. Radiation damages
DNA; tissues dependent on active mitosis are particularly susceptible. Nuclear
accidents can involve not only power plant workers but also employees of
hospitals, laboratories, and industry (food sterilization, metal radiography, etc.), as
well as innocents exposed to stolen, misplaced, or misused sources. While the
radiation dose can be approximated from the rate and degree of decline in blood
counts, dosimetry by reconstruction of the exposure can help to estimate the
patient's prognosis and also to protect medical personnel from contact with
radioactive tissue and excreta. MDS and leukemia, but probably not aplastic
anemia, are late effects of radiation. (HARRISON)

2.2.2. Chemicals
Benzene is a notorious cause of bone marrow failure. Vast quantities of
epidemiologic, clinical, and laboratory data link benzene to aplastic anemia, acute
leukemia, and blood and marrow abnormalities. The occurrence of leukemia is
roughly correlated with cumulative exposure, but susceptibility must also be
important, as only a minority of even heavily exposed workers develop benzene
myelotoxicity. The employment history is important, especially in industries
where benzene is used for a secondary purpose, usually as a solvent. Benzenerelated blood diseases have declined with regulation of industrial exposure.
Although benzene is no longer generally available as a household solvent,
exposure to its metabolites occurs in the normal diet and in the environment. The
association between marrow failure and other chemicals is much less well
substantiated.
2.2.3 Drugs
In general, all drugs can cause aplastic anemia in someone with a genetic
predisposition. Drugs that commonly cause aplastic anemia is chloramphenicol.
This is caused by idiosyncratic reaction. Idiosyncratic drug reactions that arise are
not related to the pharmacological properties of the drug, with the proportion
varying dala population with no known cause. For example, doses of
chloramphenicol which more than 50 mg / kg / day with long-term use causes
idiosyncratic

reactions.

Other

drugs

are

also

frequently reported

are

phenylbutazone, compounds of sulfur, gold, and anticonvulsants, for example

cytotoxic drugs mieleran or nitrosourea.10
2.2.4 Infection

Aplastic anemia can be caused by viral infections such as viral hepatitis,

Epstein-Barr virus, HIV and rubella. Viral hepatitis is the most frequent cause.
Severe pancytopenia may occur one to two months after infection with hepatitis.
Although rarely aplastic anemia caused by hepatitis but there is a relationship
between seronegative fulminant hepatitis with aplastic.anemia Hepatitis usually
seronegative (non-A, non-B, non-C, non-G) and may be caused by a new virus
that is not detected.Fulminant hepatic failure in patients usually occurs after
infection with the virus and hepatitis seronegative marrow failure occurred more
frequently in these patients. Thus, in patients who are immunocompromised have
failed to produce neutralizing antibodies against a form of chronic hepatitis that
can form cell aplasia.Virus infection usually associated with minimal suppression
of the bone marrow, usually looks a little sparse neutropenia and
thrombocytopenia. Viruses can cause damage to the bone marrow directly, namely
by infection and cell cytolysis of hematopoiesis or indirectly through the
induction of secondary immune, the initiation of the autoimmune process that
causes a reduction in stem cells and progenitor cells or supporting stroma tissue
destruction.7

2.2.5 Aplastic Anemia in the state / Other Diseases

1. In acute lymphoblastic leukemia sometimes found pancytopenia with bone
marrow hypoplasia.
2. Paroxysmal Nocturnal Hemoglobinuria (PNH).
The disease can manifest in the form of aplastic anemia. Hemolysis
accompanied by pancytopenia may include abnormalities of PNH.
3. Pregnancy
Cases of pregnancy with aplastic anemia have been reported, but the
relationship between these two conditions is not clear. In some patients,
pregnancy exacerbates aplastic anemia, this may be due to estrogen with a
genetic predisposition, presence of inhibitors in the blood or the absence of
stimulants hemotopoesis. However, the situation would improve again

after

giving birth. In other cases, aplasia occurs during pregnancy with

recurring events in pregnancies berikutnya.5

2.3 Classification of Aplastic Anemia

Aplastic anemia is generally classified as follows:
A. Classification by cause:
1. Idiopathic: when the cause is unknown; found in approximately 50% of cases.
2. Secondary: if the cause is known, for example from radiation, drugs, chemicals,
or viruses.
3. Constitutional: abnormalities of DNA that can be derived, for example Fanconi
anemia
B. Classification by severity or prognosis (see table 1).
Table 1. Aplastic anemia classification based on severity7
Not severe aplastic anemia

Patients who do not meet the criteria

for severe aplastic anemia or severe;
with bone marrow hypocellular and
meet two of the three following
criteria:
- Neutrophil <1,5x109 / l
- Platelet count <100x109 / l
- Hemoglobin<10 g / dl

Severe aplastic anemia

- bone marrow cellularity<25% or 2550% to <30% residual hematopoietic

cells, and
- Two of the three following criteria:
neutrophils <0,5x109 / l

 platelets <20x109 / l
reticulocyte <20x109 / l
same as severe aplastic anemia except

Very severe aplastic anemia

neutrophils <0,2x109 / l
2.4 Pathopysiology
Penyebabanemiaaplastiksulitditentukan,
terutamakarenabanyakkemungkinan

yang

harusdisingkirkan.

Jikatidakditemukanpenyebab

yang

pastimakadigolongkankedalampenyebabidiopatik.Pendapatlainmenyatakanbahwa
penyebabterbanyakdarikegagalansumsumtulangadalahiatrogenikkarenakemoterapi
sitostatikatauterapiradiasi.
Kerusakan

yang

terjadipadaanemiaaplastikterdapatpadaselindukdanketidakmampuanjaringansums
umtulanguntukmemberikesempatanselindukuntuktumbuhdanberkembangdenganb
aik.

Hal

iniberkaitaneratdenganmekanisme

yang

terjadisepertitoksisitaslangsungataudefisiensiselsel stromal. Penyimpangan proses

imunologis

yang

terjadipadaanemiaaplastikberhubungandenganinfeksi

virus

atauobat-obatan yang digunakan, atauzat-zatkimia.

Hematopoesis

normal

merupakaninteraksiantara
denganlingkunganmikro

yang

progenitor

terjadi

di

dalamsumsumtulang,

hematopoetik

(microenvironment)

stem

cell

padasumsumtulang.

Lingkunganmikrotersebutmengaturhematopoesismelaluireaksistimulasiolehfaktor
pertumbuhanhematopoetik.

Sel-

selhematologikimaturdapatterlihatdenganpemeriksaanflouresent

activate

flow

citometry, yang dapatmendeteksisel antigen CD34+ danadhsesi protein kurangdari

1%padasumsumtulang

normal.

Anemiaaplastikdapatterjadisecaraheterogenmelaluibeberapamekanismeyaitukerus
akanpadalingkunganmikro,

gangguanproduksiataufungsidanfaktor-

faktorpertumbuhanhematopoetik,
dankerusakansumsumtulangmelaluimekanismeimunologis.
Limfosit

sitotoksikaktif,

memegangperan

yang

besardalamkerusakanjaringansumsumtulangmelaluipelepasanlimfokinseperti
interferon-(IFN-) dantumor necrosis factor (TNF-). Peningkatanproduksi
interleukin-2

mengawaliterjadinyaekspansipoliklonalsel

T.

AktivasireseptorFasmelaluifas-ligand menyebabkanterjadinya apoptosis sel target.

EfekIFNmelalui

interferon

adalahmenghambattranskripsi

regulatory
gen

factor

danmasukkedalamsiklus

(IRF-1),
sel.

IFN-

jugamenginduksipembentukan nitric oxide synthase (NOS), danproduksi gas

toksik nitric oxide (NO) yang mungkinmenyebabkanefektoksiknyamenyebar.
2.5.

Diagnosa Banding3
a. MyelodisplasiaHiposeluler
Untukmembedakan

anemia

aplastikdarisindrommielodisplastikhipoplastikdapatdilakukanaspirasisumsumtulan
guntukmendapatkanproporsisel-sel

CD34+.

Padasindrommielodisplastik,

ekspansiklonalmunculdariselasal CD34+, sedangkanpada anemia aplastikdidapat,

sel-selasal

CD34+merupakan

proporsisel

CD34+pada

target
anemia

sedangkanpadasindrommielodisplastik,
ataulebihtinggi.

Selainitu,

seranganautoimun.
aplastik
proporsinya

Dengandemikian,

0,3%

ataukurang

normal

(0,5%

untukmembedakan

aplastikdengansindrommyelodisplastikdapatmelaluimorfologidarah

,
1%)

anemia
yang

abnormal (misalnyapoikilositosis, granulositdengananomali pseudo-Pelger- Het),

prekursoreritroidsumsumtulangpadamyelodisplasiamenunjukkangambarandisform
iksertasideroblast
patologislebihseringditemukanpadamyelodisplasiadaripada
Selainitu,

yang
anemia

prekursorgranulositdapatberkurangatauterlihatgranulasi

danmegakariositdapatmenunjukkanlobulasinukleus
(misalnyamikromegakariositunilobuler).

aplastik.
abnormal
abnormal

b. LeukimiaLimfoblastik Granular Besar

Penyakitinijugadapatmenjadi

diagnosis

untuksumsumtulang

yang

kosongataudisplastik. Limfosit granular besardapatdikenalidarifenotipenya yang

berbedapadapemeriksaanmikroskopikdarah,
selkhususpadaflow

cytometry,

yaitupolapulasansel-

danketidakteraturanreseptorsel

yang

membuktikanadanyaekspansimonoklonalpopulasisel T.
c. Anemia aplastikdanHemoglobinuriaNokturnalParoksisimal (PNH)
Pada

PNH,

selasalhematopoetik

menurunkanpopulasiseldarahmerah,

granulosit,

abnormal

dantrombosit

yang

semuanyatidakmempunyaisekelompok protein permukaan sel. Dasargenetik PNH

adalahmutasididapatpada

gen

PIG-A

di

kromosom

yang

menghentikansintesisstrukturjangkarglikosilfosfatidilinositol. Defisiensi protein

inimenyebabkanhemolisisintravaskular,

yang

mengakibatkanketidakmampuaneritrosituntukmenginaktivasikomplemenpermuka
an.

2.6.

Diagnosis

2.6.1. Anamnesa
Anemia
atauperlahan-lahan

aplastikmungkinmunculmendadak

(dalambeberapahari)

(berminggu-mingguatauberbulan-bulan).

Keluhanpasien

anemia aplastikdapatberupapendarahan, badanlemah, pusing, jantungberdebar,

demam,

nafsumakanberkurang,

pucat,

sesaknafas,

penglihatankabur,

bahkantelingaberdengung.
Trombositopeniamenyebabkanmudahmemardanpendarahanmukosa. Neutropenia
meningkatkankerentananterhadap infeksi.3
2.6.2. PemeriksaanFisik
Hasilpemeriksaanfisikpadapasien

anemia

aplastikbervariasi.

Padapenelitiansebelumnya, keseluruhanpasien anemia aplastikditemukanpucat,

setengahnyaditemukanadanyapendarahankulit, gusi, retina, hidung, salurancerna,

atau vagina, dansedikitnyademam, hepatomegali, splenomegali.3

2.7. Treatment / Supportive Care

Transfusional support
Packed red cell transfusions must be given to maintain a safe hemoglobin,
compatible with the age and associated co-morbid conditions.1,2
Platelets must be given to prevent bleeding and are indicated if the platelet
count is < 10 109/L. Platelet sparing efforts like use of tranexamic acid in minor
mucosal bleeds and norethisterone in adolescent girls who have achieved
menarche are beneficial. Tranexamic acid is used in the dose of 2-4 g/day in 3-4
divided doses.The adverse effect of repeated blood and platelet transfusions is the
development of alloantibodies. This leads to refractoriness to platelets and febrile
reactions after blood transfusions. For those patients who subsequently undergo a
BMT, there is a greater risk of graft rejection.1,2
Ideally, leukodepleted blood and platelets should be transfused, to
minimize alloimmunization. Blood from siblings and blood relatives should be
avoided as there is a risk of fatal transfusion-associated graft versus host disease
(GVHD). For those who may undergo BMT, transfusion from family members
should be strictly avoided as alloimmunization to family antigens will increase the
risk of graft rejection.1,2,3
Immunosuppressive Therapy10
Immunosuppressive therapy consists of a combination of antithymocyte globulin
(ATG) and cyclosporine A (CsA). Response rates are about 60% at 3 or 6 months
after horse ATG. It is effective in both young and old patients.
Active infection is a contraindication. Patients should be referred early to
an appropriate center as there are different preparations of ATG with varying
dosage schedules. The following precautions are needed:
a. Admission is required
b. Corticosteroids are added to prevent serum sickness

c. Reactions during ATG transfusion are common and rarely anaphylaxis can
occur
d. Platelet support is essential, as ATG can cause a fall in platelet counts
e. Serum sickness occurs in about 40% patients in the second and third week
Cyclosporine is usually started after steroids are tapered off, usually after 3
weeks of ATG. The response with ATG/cyclosporine is seen after 3-4 months.
Cyclosporine should be tapered off very gradually after a minimum of 6 months.
If there is no response to one course of ATG, orthere is a relapse, a second or third
course may be given. Patients who show no response to twocourse of ATG are
unlikely to respond to a third course. If cyclosporine is used alone, the response
rates are about 30%.10

CHAPTER III
CASE REPORT
Name

: RZ

Age

: 1 years 4 months

Sex

: Boy

RM

: 00.62.43.99

Date of Admission

: 20 April 2015

Chief Complain

: Pale

History

RZ was admitted to RSHAM from RSUD blangkejerenwith the chief complaint is

pale. This problem has already been occurring to this patient since+ 4 months. The
patient grow paler in this +1 month , history of spontaneous bleeding (-), history
of bleeding gums (-), history defecate black (-) history of fever found+ 1 week,
fever was increasing up and down and fever decrease with the fever-lowering
medicine. Shivering was (-), convulsions is (-), history of convulsions was found
+5 months ago with frequency of 2 times (5 minute after convulsions patient
becomes conscious). Convulsions was preceded with fever, difficulty in breathing
is (-). Urinate in the normal range. Defecate in the normal range.Patients was an
old patient of hematology department with diagnosis of anemia aplastic.
History of Previous position

The patient was reference from RSUP Blangkegeren with diagnosis of congestive
heart failure ec severe anemia
Birth history: RZ was the third boy. Birth spontaneously, helped by tocologist,
cried hard. Cyanosis (-), birth weight: 3,2 kg.
Pregnancy history: mother age 34 years old, medical history (-), drug exposure (-),
herb exposure (-).

Feeding History:
From birth to 6 months: Breast feeding only,
From 6 months to 9 months : Breast milk with rice porridge
From 9 months to 1,5 years

: Breast milk with soft rice

From 1,5 years until now

: Family food

History of Growth and Development

Sitting

: 5 months

Crawling

: 8 months

Standing

: 10 months

Walking

: 18 months

Medical History: os was admitted fromRSUD

blangkejeren with differential

diagnosis of congestive heart failure ec severe anemia

Drug use history: PackedRedCell transfusion of 44 ml, inj.ceftriaxone 200 mg / 12
hours, inj. gentamicin 35 mg / 24 hours
Physical Examination:
Generalized Status:
Body weight: 7 kg
Body length: 78 cm
Body weight according to age: ( Z Score <-3 SD)
Body length according to age: (-2 < Z score < 0)
Body weight according to body length: ( Z Score <-3 SD)

BMI according to age: ( Z Score <-3 SD)

Head Circumference: 38cm (15th-50th percentile)

Presence status:
Consciousness: Compos Mentis
Heart Rate: 116 x/i regular
Respiratory Rate: 30x/i regular
Body Temperature: 37,4C
Anemic (+), icteric (-), cyanosis (-), edema (-), dyspnea (-),
Localized Status

Head: light reflexes (+/+), pupil isochoric, inferior conjuctiva pale (+/+),
fontanella open flat, icteric sclera (-/-), face edema (-), inferior and
superior palpebrae edema (-), Ear/ Nose/ Mouth: within normal limit/ O2

nasal kanal/ mucosa is pale.

Thorax: symmetricaol fusiformis, chest retraction (-) epigastric and
intercostal, breath sound: vesikular, additional sound: ronchi -/-, wheezing

(+), murmur (-)

Abdomen: soepel, peristaltic (+) Normal, liver is palpable 2 cm,spleenis

not palpable
Extremities: pulse 116 x/i , adequate pressure and volume, warm, CRT < 3

second, pitting edema (-). Hematoma (-)

Urogenital: male scrotum (+), penis (+), anus (+)

Laboratory finding
Complete blood analysis
Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil

Result
1,80
0,55
11,48
277
5,70
0,20

Unit
G%
106/mm3
103/mm3
103/mm3
%
%

Referral
11,3-14,1
4,40-4,48
6,0-17,5
217-497
37-41
1-6

Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte

0,600
43,90
47,40
7,90
5,04
5,44

%
%
%
%
103/L
103/L

0-1
37-80
20-40
2-8
1,9-5,4
3,7-10,7

absolute
Monocyte absolute
Eosinophyl absolute
Basophyl absolute
MCV
MCH
MCHC

0,91
0,02
0,07
103,60
32,70
31,60

103/L
103/L
103/L
fL
pg
g%

0,3-0,8
0,20-0,50
0-0,1
81-95
25-29
29-31

Clinical Chemistry
Test
Carbohydrate Metabolism
Blood Glucose
Electrolite
Natrium
Kalium
Cloride
Differential Diagnosis

Result

Unit

Referral

176

mg/dL

< 200

134
2,2
104

mEq/L
mEq/L
mEq/L

135-155
3,6-5,5
96-106

: Aplastic anaemia, haemolytic anaemia,

leukaemia

Working Diagnosis

: Aplastic anaemia

Management

O2 1-2 L/i
IVFD D5% NaCl 0,225% 20 gtt/i micro
Paracetamol 100 mg (as needed)
Oral prednisone 1-1-1
Folic acid1x1 mg

Follow Up
April, 21th 2015
S Swollen eyes (+), fever (-),epigastruim pain (+)
O Cons: alert, Temp: 37,4oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra

(+/+).Ear/ Nose/ Mouth: within normal limit/ within normal limit /

Neck
Thorax

:
:

Abdomen :

mucosa is pale .
Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 120x/i, regular,
murmur (-). RR: 30x/i, reguler, ronchi (-).
Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :not

palpable
Extremities: Pulse 120x/i, regular, adequate pressure and volume, warm, CRT < 3.
Genital
Male. Scrotum (+). Edema (-).
A
P

:
Aplastic Anemia
Management:
-

O2 1-2 L/i

IVFD D5% NaCl 0,225% 20 gtt/i micro

Paracetamol 100 mg (as needed )

Folic acid1x1 mg

Diet normal eating 700 kkal with 14 gram protein .

Blood transfusion PRC II 20 cc

April, 22th 2015

S Pale (+) , fever (+) , convulsion (-)
O Cons: alert, Temp: 40oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra
(-/-).Ear/ Nose/ Mouth: within normal limit/ within normal limit /within

Neck
Thorax

normal limit.
Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 116x/i, regular, murmur

A
P

Abdomen

(-). RR: 20x/i, reguler, ronchi (-).

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 116x/i, regular, adequate pressure and volume, warm, CRT < 3.

s
Genital
Male. Scrotum (+). Edema (-).
- Leukemia
- Anemia hemolytic
Management:
-

prednisone 1-1-1
Folic acid1x1 mg
Paracetamol drip 100 mg / 6 hour / iv
Blood transfusion PRC III 75 cc ( enter 100 cc , needed 260 cc )
BMP ( 24/4/15 )
Diet normal eating 700 kkal with 14 gram protein .
Consult to nutrition and metabolic .

April, 23th 2015

S
O

Pale (+) , fever (+) , cramp (-)

Cons: alert, Temp: 39.8oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (+/+).Ear/ Nose/ Mouth: within normal limit/ within normal

Neck
Thorax

limit /within normal limit.

Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 116x/i, regular,

Abdomen

murmur (-). RR: 22x/i, reguler, ronchi

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 116x/i, regular, adequate pressure and volume, warm, CRT < 3.

Genital
A- Leukemia

Male. Scrotum (+). Edema (-).

- Anemia diamond blackfan

- Anemia hemolitik
P Management:
-

prednisone 1-1-1
Folic acid1x1 mg
Paracetamol drip 100 mg / 6 hour / iv
Diet normal eating 700 kkal with 14 gram protein .
BMP + Check DL post transfusi
Blood transfusion PRC IV 75 cc ( enter 145 cc , needed 260 cc )
Blood transfusion PRC V 60 cc ( enter 200 cc , needed 260 cc )

April, 24th 2015

S
O

Pale (-) , fever (-) , cramp (-)

Cons: alert, Temp: 36,8oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-).Ear/ Nose/ Mouth: within normal limit/ within normal

Neck
Thorax

limit /within normal limit.

Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 116x/i, regular,

Abdomen

murmur (-). RR: 24x/i, reguler, ronchi

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 116x/i, regular, adequate pressure and volume, warm, CRT < 3.

s
Genital
Male. Scrotum (+). Edema (-).
A- Aplastic Anemia
P Management:
- prednisone 1-1-1
- Folic acid1x1 mg
- Paracetamol drip 100 mg / 6 hour / iv

April, 25th 2015

S
O

Pale (-) , fever (-) , cramp (-)

Cons: alert, Temp: 36,8oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-).Ear/ Nose/ Mouth: within normal limit/ within normal

Neck
Thorax

limit /within normal limit.

Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 94x/i, regular, murmur

Abdomen

(-). RR: 24x/i, reguler, ronchi

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 96x/i, regular, adequate pressure and volume, warm, CRT < 3.

s
Genital
Male. Scrotum (+). Edema (-).
A- Aplastic Anemia
P Management:
-

prednisone 1-1-1
Folic acid1x1 mg
Paracetamol 3 100 mg
Diet normal eating 700 kkal with 14 gram protein
April, 26th 2015

S
O

Pale (-) , fever (-) ,

Cons: alert, Temp: 35,6oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-).Ear/ Nose/ Mouth: within normal limit/ within normal

Neck
Thorax

limit /within normal limit.

Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 96x/i, regular, murmur

Abdomen

(-). RR: 36x/i, reguler, ronchi

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 96x/i, regular, adequate pressure and volume, warm, CRT < 3.

s
Genital
Male. Scrotum (+). Edema (-).
A- Aplastic Anemia

Management:

- prednisone 1-1-1
- Folic acid1x1 mg
- Paracetamol 3 100 mg
April, 27th 2015
S
O

Pale (-) , fever (-) , cramp (-)

Cons: alert, Temp: 35,6oC.
Body weight: 7 kg, Body length: 78 cm.
Head

Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-).Ear/ Nose/ Mouth: within normal limit/ within normal

Neck
Thorax

limit /within normal limit.

Lymph node enlargement (-).
Symmetrical fusiformis. Chest retraction (-). HR: 76x/i, regular, murmur

Abdomen

(-). RR: 36x/i, reguler, ronchi

Soepel (+),peristaltic (+) normal, liver : palpable for 2 cm, Spleen :

Extremitie

palpable S II- SIII

Pulse 76x/i, regular, adequate pressure and volume, warm, CRT < 3.

s
Genital
Male. Scrotum (+). Edema (-).
A- Aplastic Anemia
P Management:
-

prednisone 1-1-1
Folic acid1x1 mg
Paracetamol 3 100 mg
Diet normal eating 700 kkal with 14 gram protein

CHAPTER IV
DISCUSSION AND SUMMARY
4.1. Discussion
The

clinical

findings

of

aplastic

anemia

relate

to

anemia,

thrombocytopenia and neutropenia. Anemia results in pallor, easy fatigability,

headache, dyspnea, and tachycardia.1,2,3,10Thrombocytopenia manifests with
petechiae, ecchymoses, epistaxis, gum bleeding and menorrhagia. Thefundus
examination may show hemorrhages, at times suggesting an impending
intracranial bleed. Neutropenia leads to recurrent infections, oral and gingival
ulcerations.1There is no lymphadenopathy or hepatosplenomegaly in aplastic
anemia, unless this is due to some infection. Any such finding should indicate
an alternative diagnosis. In children and young adults, an active search should
be made of clinical clues which may suggest a hereditary bone marrow failure
syndrome like Fanconis anemia.1,2,3In this patient, the same clinical
manifestations based on the theories occur, such as; pallor due to severe
anemia, thrombocytopenia, leucopenia, pallor, fever, and gum bleeding.
To diagnose aplastic anemia, essential investigations should be done, such
as:

complete

blood

counts,

reticulocyte

count,

peripheral

smear

examination,bone marrow aspiration, as gold standard, and trephine biopsy (to

determine cellularity). Severity of aplastic anemia is based on these
parameters.1,2,3,4In this patient, bone marrow aspiration had been done as the
gold standard and showed hypoplasia and found many of lymphocyte and
atypical cell. The impression was hypoplasia bone marrow and he was
diagnosed with aplastic anemia.
The treatment for aplastic anemia is transfusion support, treatment and
prevention

of

infection,

hematopoiesis

stem

cell

transplant,

and

immunosuppressive therapy. 1,2,3,10,12,13,14 In this patient, the treatment that given

was Packed Red Cell transfusion, to increase the hemoglobin level, folic acid,
and prednisone.

4.2. Summary
It has been reported, an adolescent boy with the main complain of pale and was
diagnosed with anemia aplastic. The diagnose was established based on history
taking, clinical manifestation, laboratory finding, and bone marrow puncture.The
patient got PRC transfusion and still need to be followed up.