Case Report

BRONCHOPNEUMONIA

SUPERVISOR

: dr. Nelly Rosdiana, Sp. A (K)

PRESENTATOR

: Stefen Andrianus

110100009

Mutia Fri Fahrunnisa 110100071

DEPARTMENT OF CHILD HEALTH

MEDICAL FACULTY NORTH SUMATRA UNIVERSITY
H. ADAM MALIK GENERAL HOSPITAL
MEDAN
2015

ACKNOWLEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case
report,Bronchopneumonia. This case report is a requirement to complete the clinical
assistance program in Department of Child Health in H. Adam Malik General Hospital,
Medical Faculty of North Sumatra University.
We are also indebted to our supervisor and adviser, dr. Nelly Rosdiana, Sp.A (K) for
much spent time to give us guidances, comments, and suggestions. We are grateful because
without him this case report wouldnt have taken its present shape.
This case report has gone through series of developments and corrections. There were
critical but constructive comments and relevants suggestions from the reviewers. Hopefully
the content will be useful for everyone in the future.

Medan, th September 2015

Presentator

CONTENT
BACKGROUND..........................................................................................................1
LITERATURE REVIEW............................................................................................2
PNEUMONIA
2.1. Definition ..............................................................................................................2
2.2. Etiology..................................................................................................................2
2.3. Pathogenesis..........................................................................................................4
2.4. Diagnosis................................................................................................................5
2.5. Treatment and management................................................................................7
CASE REPORT...........................................................................................................8
DISCUSSION ............................................................................................................19
SUMMARY ...............................................................................................................20
REFERENCES..........................................................................................................21

BACKGROUND
1.1 Background
Each year, pneumonia kills more than 4 million people and causes illness
in millions more around the world. In developed countries, pneumonia primarily
affects elderly persons. However, half of pneumonia-related deaths worldwide
actually occur among children under age five most of whom live in developing
countries. For every child that dies from pneumonia in developed countries, more
than 2,000 children die from pneumonia in developing countries.1
Data from the World Health Organization confirm that acute respiratory
illness remains a leading cause of childhood mortality, causing an estimated 1.6
2.2 million deaths globally in children < 5 years.2,3 In North America the annual
incidence in children younger than 5 years of age is 3440 cases per 1000.4
In the UK, from 750 children assessed in hospital, incidence of CAP was
144/10 000 children per year and 338 for <5-year-olds; with an incidence for
admission to hospital of 122 and 287 respectively. Risk of severe CAP was
significantly increased for those aged <5 years and with prematurity.5
In Indonesia, Pneumonia is the 2nd most common cause of death in
children after diarrhea (15,5%). A 2007 study conducted by the Indonesia
Ministry of Health shows that 30.470 children died from pneumonia that year,
which is equal to 83 children in a day.6
This is why controlling pneumonia is essential to achieving Millenium
Development Goal (MDG) #4 - a pledge by the worlds governments to reduce
child mortality by two-thirds by 2015.1
1.2 Objective
This paper is one of the requirements to fulfill the senior clinical assistance
programs in the Pediatric Department of Haji Adam Malik General Hospital,
University of Sumatera Utara. This paper is written to report a case of a 5 months
old girl with the diagnosis of Bronchopneumonia.

LITERATURE REVIEW

2.1. Definition
Pneumonia is defined as an inflammation of lung tissue due to an
infectious agent. Commonly used clinical World Health Organization operational
definition is based solely on clinical symptoms (cough or difficulties in breathing
and tachypnoea).7 In the developing world the term Lower Respiratory Tract
Infection (LRTI) is widely used instead of pneumonia, because of poor access to
x-ray and difficulties in radiological confirmation of diagnosis.8
Depending on the place of acquisition pneumonia can be divided into: 9
a.

Community Acqiured Pneumonia (CAP)

b.

Hospital Acquired Pneumonia (HAP).

Recently a third type - Health Care Associated Pneumonia (HCAP) has
been distinguished in adult patients. 8
The significance of this classification is based on its clinical utility since in
most cases patho gens responsible for CAP and HAP are different, warranting
varying approach and empiric treatment. 8
2.2. Etiology Pneumonia
The etiology of pneumonia differs between children and adults. Because of
this, age plays a very important role in determining the cause of pneumonia in
children.9
Table 1.The etiology of pneumonia based on Age9
Age
Born- 20 days

Common Etiology
Bacteria

Less common Etiology

Bacteria

E. Coli

Anaerobic bacteria

Group B Streptococcus

Haemophilus influenza

Listeria monocytogenes

Streptococcus pneumonia
Virus
CMV

3 weeks-3 months

Bacteria

Herpes Simpleks Virus

Bacteria

Chlamydia trachomatis

Bordetella pertussis

4 months- 5 years

Streptococcus pneumonia

Haemophillus influenza

Virus

type B

Respiratory Synctial

Staphylococcus aureus

Virus

Virus

Adeno Virus

CMV

Influenza Virus
Bacteria

Bacteria

Chlamydia pneumonia

Haemophillus influenza

Mycoplasma pneumonia

type B

Streptococcus pneumonia

Staphylococcus aureus

Virus

Neisseria meningitidis

Adeno Virus

Virus

Influenza Virus

Varicella-Zoster virus

RinoVirus
Parainfluenza Virus
Respiratory Synctial
5 tahun-teenagers

Virus
Bacteria

Bacteria

Chlamydia pneumonia

Haemophillus influenza

Mycoplasma pneumonia

Staphylococcus aureus

Streptococcus pneumonia

Virus
Adeno Virus
Influenza Virus
RinoVirus
Parainfluenza Virus
Respiratory Synctial
Virus

Varicella-zoster Virus
There are several known risk factors for CAP to consider in addition to
immunization status, exposure to other children, especially preschoolers, asthma,
history

of

wheezing

episodes,

tobacco

smoke

exposure,

malnutrition,

immunological deficits, mucocilliary dysfunction (cystic fibrosis, cilliary

dyskinesia), congenital malformation of airways, impaired swallowing. 8 Tobacco

smoke exposure has been found to increase risk of hospitalization for pneumonia
in children < 5. Conditions predisposing to severe pneumonia include age <5 and
prematurity.10
2.3. Pathogenesis11
An inhaled infectious organism must bypass the host's normal nonimmune
and immune defense mechanisms in order to cause pneumonia. The nonimmune
mechanisms include aerodynamic filtering of inhaled particles based on size,
shape, and electrostatic charges; the cough reflex; mucociliary clearance; and
several

secreted

substances

(eg,

lysozymes,

complement,

defensins).

Macrophages, neutrophils, lymphocytes, and eosinophils carry out the immunemediated host defense.
Pneumonia is characterized by inflammation of the alveoli and terminal
airspaces in response to invasion by an infectious agent introduced into the lungs
through hematogenous spread or inhalation. The inflammatory cascade triggers
the leakage of plasma and the loss of surfactant, resulting in air loss and
consolidation.
The activated inflammatory response often results in targeted migration of
phagocytes, with the release of toxic substances from granules and other
microbicidal packages and the initiation of poorly regulated cascades (eg,
complement, coagulation, cytokines). These cascades may directly injure host
tissues and adversely alter endothelial and epithelial integrity, vasomotor tone,
intravascular hemostasis, and the activation state of fixed and migratory
phagocytes at the inflammatory focus. The role of apoptosis (noninflammatory
programmed cell death) in pneumonia is poorly understood.
Pulmonary injuries are caused directly and/or indirectly by invading
microorganisms or foreign material and by poorly targeted or inappropriate
responses by the host defense system that may damage healthy host tissues as
badly or worse than the invading agent. Direct injury by the invading agent
usually results from synthesis and secretion of microbial enzymes, proteins, toxic
lipids, and toxins that disrupt host cell membranes, metabolic machinery, and the

extracellular matrix that usually inhibits microbial migration.

Indirect injury is mediated by structural or secreted molecules, such as
endotoxin, leukocidin, and toxic shock syndrome toxin-1 (TSST-1), which may
alter local vasomotor tone and integrity, change the characteristics of the tissue
perfusate, and generally interfere with the delivery of oxygen and nutrients and
removal of waste products from local tissues.
On a macroscopic level, the invading agents and the host defenses both
tend to increase airway smooth muscle tone and resistance, mucus secretion, and
the presence of inflammatory cells and debris in these secretions. These materials
may further increase airway resistance and obstruct the airways, partially or
totally, causing airtrapping, atelectasis, and ventilatory dead space. In addition,
disruption of endothelial and alveolar epithelial integrity may allow surfactant to
be inactivated by proteinaceous exudate, a process that may be exacerbated
further by the direct effects of meconium or pathogenic microorganisms.
In the end, conducting airways offer much more resistance and may
become obstructed, alveoli may be atelectatic or hyperexpanded, alveolar
perfusion may be markedly altered, and multiple tissues and cell populations in
the lung and elsewhere sustain injury that increases the basal requirements for
oxygen uptake and excretory gas removal at a time when the lungs are less able to
accomplish these tasks.
2.4. Diagnosis12,13
2.4.1. Clinical Manifestation

Typical clinical symptoms of pneumonia consist of:

cough (30% of children presenting to outpatient clinic with cough, after
excluding those with wheeze, have radiographic signs of pneumonia, and
cough was reported in 76% of children with CAP). 12,13 It should be noted
that sputum production in preschool chil dren is rare, because they tend to

swallow it.
fever (present in 88-96% of children with radiologically confirmed

pneumonia).12
toxic appearance

signs of respiratory distress: tachypnoe (table 2), history of breathlessness or

difficulty in breathing chest retractions, nasal flaring, grunting, use of

accessory muscles of respira tion. Tachypnoe is a very sensitive marker of

pneumonia. 50-80% of children with WHO defined tachypnoe had
radiological signs of pneumonia, and the absence of tachypnoe is the best
single finding for ruling out the disease.12,13 In children <5 tachypnoe had
sen sitivity of 74% and specificity of 67% for radiologically confirmed
pneumonia, but its clin ical value was lower in the first 3 days of illness.
In infants < 12 months respiratory rate of 70 breaths/min had a sensitivity
of 63% and specificity of 89% for hypoxemia.8
Table 2. Tachypnoe defined according to WHO criteria8
Age
0-2 months
2-12 months
1-4 years
>5 years

Respiratory rate
>60
>50
>40
>30

2.4.2. Physical Examinations9

Typical findings on physical examinations include:
-

dullness on percussion of the chest

decreased breath sounds

additional breath sounds such as ronchi and wheeze.

2.4.3. Additional Tests8,9

a. Complete blood test
b. Chest X-ray
Chest x-ray may shows:

Interstitial infiltrate

Alveolar infiltrate, consolidation of the lungs (air bronchogram).

Bronchopneumonia, infiltrate which is equally spread in both lungs.

c. Determination of etiology microbiological investigations.

d. C-Reactive Protein (CRP)

2.5. Treatment & Management
The treatment of pneumonia in children consists of appropriate antibiotics
for the offending organisms, supportive treatment such as oxygen, iv fluid and
the correction of acid base disorder9.
a. Outpatient settings
The first line antibiotic for outpatient settings is Amoxicillin 20 mg/kg
or Cotrimoxazole (4mg/kg of Trimetoprim and 20 mg/kg of
Sulfamethoxazole)
b. Inpatient settings
The first line antibiotics for inpatient settings is Beta Lactamase group
or Chloramphenicol. Antibiotic is administered for 7-10 days.
Antibiotic must be given as soon as possible in neonates. Broad
spectrum antibiotics such as the Beta Lactamase group or third
generation of cephalosporine are recommended. Upon stabilization, iv
antibiotics can be switched to oral antibiotics and patients can be
treated in the outpatient settings.

CASE REPORT
3.1 Case
H, a 5 months old girl with a body weight of 7000 g and a body length of
61 cm was admitted to the

emergency room in Haji Adam Malik General

Hospital Medan on 9th September 2015 at 06.00 pm with a complain of shortness

of breath.
3.2 History

The patient is the youngest child in the family. The patients mother
pregnancy and delivery history was unremarkable. She was born with a birth
weight of 3000 g. The mother said that she had been noticing the shortness of
breath for the past 11 days. Her child breathlessness was not associated with
activites and weather. Productive cough was notably present for the past 2 weeks.
There was no history of hemoptysis. History of contact with others with similar
symptoms was found, which was her older sister. Her older sisters has been
experiencing chronic cough for more than 3 weeks. Intermittent fever was found,
fever subsided with antipyretics and the highest recorded temperature was 39
degree Celcius. History of urination and defecation was unremarkable. Her
mother was complaining about her child weight loss. She was losing
approximately 2 kg of body weight for the past week. She was treated in another
hospital for 8 days and was referred to RSUP HAM due to no improvement.
History of medication: Unclear
Family History: Hs sister was suffering from chronic cough for more thatn 3
weeks
History of parents medication: Unclear
History of Pregnancy: The mothers age was 38 years old during pregnancy with
a 36 weeks gestation.
History of Birth: Birth was assisted by a midwife. The patient was born
pervaginal and cried immediately after birth. Body weight at birth was 3000 gram,
body length at birth was unclear, and head circumference at birth was unclear.
History of feeding: breast fed from birth until now (5 months)
History of immunization: Incomplete immunization (polio 2 times)
History of growth and development: The patients mother reported that H grew
normally. H can now rolls from supine to prone.
Physical Examination:

Present Status: Level of consciousness: alert. Body temperature: 37,4C,

BW: 7 kg, BH: 61 cm. L/A: -2<Z<0, W/A: 0<Z<2, W/L: 1<Z<2, anemic
(-), icteric (-), dyspnea (+), cyanosis (-), edema (-).

Eye:

conjunctival pallor (-/-)

Ear: unremarkable
Nose: O2 nasal canule
Mouth: unremarkable

light

reflex

+/+,

Localized
Status

- Head: Eye: eye light reflect +/+, conjunctival pallor -/-, ear/nose/mouth:
unremarkable.
- Neck:
Jugular Vein Pressure: R+2 cm H2o
- Thorax:
Symmetric fusiform
Retractions (+) on the suprasternal and epigastric area
RR: 54x/I, regular, Ronchi (+,+) and stridor (+,+) in all lung fields
dullness to percussion was found in all lung fields
HR 144 x/I, M1>M2, T1>T2, A2>A1, P2>P1, Continous murmur grade
IV/IV
- Abdomen:
Soft, normal peristaltic, liver and spleen were both unpalpable.

- Extremities:
Pulse: 139x/i, regular, with adequate pressure and volume, warm,
CRT < 3, blood pressure: 100/60 mmHg, SaO2 : 98%
Radiography

10

Results: CTR of 56% , Aorta dilatation (-), Pulmonal artery dilatation (-),
downward apex of the heart, Congestion (+), Infiltrate (+)
Conclusion : Cardiomegaly with congestion
Echocardiography :
Large Ventricel Septal Defect and Moderate Patent Ductus Arteriosus
Laboratory Findings:
9rd September 2015
Complete blood count:
Test

Result

Unit

Reference

Hemoglobin

10.20

g%

Range
10.7-17.1

Erythrocyte

4.14

106/mm3

3.75-4.95

Leukocyte

18.25

103/mm3

6.0-17.5

Thrombocyte

311

103/mm3

217-497

Hematocrite

29.40

38-52

Eosinophil

4.10

1-6

11

Basophil

0.500

0-1

Neutrophil

25.60

37-80

Lymphocyte

50.70

20-40

Monocyte

19.10

2-8

Absolute

4.68

103/L

1.9-5.4

Neutrophil count
Absoulute

9.25

103/L

3.7-10.7

Lymphocyte count
Absolute

3.48

103/L

0.3-0.8

Monocyte count
Absolute Basophil 0.09

103/L

0-0.1

count
MCV

71.00

fL

93-115

MCH

24.60

pg

29-35

MCHC

34.70

g%

28-34

Blood Gas Analysis

Test

Result

Unit

Reference

pH
PCO2
PO2
Bicarbonate(HCO3

7.470
23.0
201.0
16.7

mmHg
mmHg
mmol/L

Range
7.35-7.45
38-42
85-100
22-26

)
Base Excess
O2 Saturation

-5.9
100.0

mmol/L
%

(-2)-(+2)
95-100

Electrolyte
Test
Calcium
Sodium
Potassium
Chloride

Result
8.8
138
3.8
100

Unit

Reference

mg/dL
mEq/L
mEq/L
mEq/L

Range
8.4-10.8
135-155
3.6-5.5
96-106

12

Peripheral blood smear morphology:

-

Erythorcyte: Microcytic hypochromic with anisocytosis.

Leukocyte

Thrombocyte : Normal

: Atypical Limfosit (+)

Differential Diagnosis:
-

Bronchopneumonia dd Bronchiolitis + Ventricel Septal Defect dd Patent

Ductus Arteriosus

Bronchiolitis + Patent Ductus Arteriosus

Diagnosis: Bronchopneumonia + Ventricel Septal Defect

Therapy:
-

O2 1 litre/i

IVFD D5% NaCl 0.225% microdrips 10gtt/i

Amoxicillin IV 350 mg q12h

Nebulized NaCl 0.9 % 2,5 cc q8h

Furosemide 7 mg PO q12h

Captopril 3.125 mg PO q12h

Digoxin 0.035 mg PO q12h

13

Follow Up:
9th September 2015
S

Dypsnea

Sensorium: alert, T: 37,4 oC, Bronchopneumoni

O2

Head: eye: light reflex +/+, a

through

conjuctival

cannula

pallor:

-/-,

mouth/nose/ear:

mg IV bid

Thorax: symmetric fusiform,

retraction (+) HR: 144x/i,
continuous murmur(+), RR:
54x/i, Ronchi +/+, Stridor +/
+
soft,

normal

peristaltic, non-tender, liver

and

spleen

are

both

unpalpable.
Extremities: Pulse: 144x/i,
regular

1-2L/i

Ceftriaxone

unremarkable.

Abdomen:

with

adequate

pressure and volume, warm,

CRT < 3, pretibial edema
(-)
Physiological

reflexes:

APR(+), KPR (+)

Pathological reflexes (-)
Meningeal sign (-)

Consult
Cardiologist.

nasal

350

14

10th September 2015

S

Dypsnea

Sensorium : alert, T : 37,0 Bronchopneumoni

O2

through

C, BP: 100/60 mmHg

Head: eye: light reflex +/+, Bronchiolitis

conjunctival

pallor:

-/-,

mouth/nose/ear:

Diapers rash
Large VSD

unremarkable.

Thorax: symmetric fusiform, Moderate PDA

retraction (+) HR: 128x/i,
continuous murmur (+), RR:
66x/i, Ronchi +/+, Stridor +/
+
Abdomen:

soft,

normal

peristaltic, non-tender, liver

and

spleen

are

both

unpalpable.
Extremities: Pulse: 128x/i,
regular

with

adequate

pressure and volume, warm,

CRT < 3, pretibial edema
(-)
Physiological

reflexes:

APR(+), KPR (+)

Pathological reflexes (-)
Meningeal sign (-)
Echochardiography result:

Mild TR

P
1-2L/i
nasal

cannula
D5%

NaCl

0,225%

IV

microdrips:
10gtt/i
Ceftriaxone

350

mg IV bid
Mizol TP q8h
Nebule

NaCl

0,9% 2,5cc tid

15

Large VSD
Moderate PDA
Mild TR

Recommendations:

consult

nutritionist and Endocrine &

Metabolic Diseases Divison

11th September 2015

S

Dyspnea(+),

Sensorium : alert, T : 36,6 Bronchopneumoni

O2

Fever (-)

through

C, BP: 100/70 mmHg

Head: eye: light reflex+/+, Bronchiolitis

conjunctival

pallor:

-/-,

mouth/nose/ear:

Diapers rash
Large VSD

unremarkable.

Thorax: symmetric fusiform, Moderate PDA

retraction (+) HR: 120x/i,
continuous murmur(+), RR:
60x/i, Ronchi +/+, Stridor +/
+
Abdomen:

soft,

normal

peristaltic, non-tender, liver

and

spleen

are

both

Mild TR

D5%

10gtt/i
Ceftriaxone

Mizol TP q8h
Nebule

NaCl

0,9% 2,5cc tid

Furosemide 7mg

regular

3,125mg

(-)

350

mg IV bid

Captopril

CRT < 3, pretibial edema

IV

microdrips:

Extremities: Pulse: 120x/i,

pressure and volume, warm,

NaCl

0,225%

PO q12h

adequate

nasal

cannula

unpalpable.

with

1-2L/i

PO

q12h
Digoxin

0,035

16

Physiological

reflexes:

mg PO q12h

APR(+), KPR (+)

Pathological reflexes (-)
Meningeal sign (-)

12th September 2015 14th September 2015

S

Improvement

Sensorium : alert, T : 36,8 Bronchopneumoni

Amoxicillin 3,5cc

in SOB

IV q8h

Fever (-)

Head: eye: light reflex +/+, Bronchiolitis

Furosemide 7mg

conjunctival

PO q12h

C, BP: 100/60 mmHg

pallor:

-/-,

mouth/nose/ear:

Diapers rash
Large VSD

unremarkable.

Thorax: symmetric fusiform, Moderate PDA

retraction (-) HR: 108x/i,
continuous murmur(+), RR:
32x/i, Ronchi -/-, Stridor -/Abdomen:

soft,

normal

peristaltic, non-tender, liver

and

spleen

are

both

unpalpable.
Extremities: Pulse: 108x/i,
regular

with

adequate

pressure and volume, warm,

CRT < 3, pretibial edema
(-)
Physiological
APR(+), KPR (+)

reflexes:

Mild TR

Captopril
3,125mg

PO

q12h
Digoxin

0,035

mg PO q12h
Nebule

NaCl

0,9% 2,5cc tid

Mizol TP q8h

17

Pathological reflexes (-)

Meningeal sign (-)

15th September 2015

S

SOB (-)

Sensorium : alert, T : 36,5 Bronchopneumoni

Amoxicillin 3,5cc

IV q8h

Fever (-)

C, BP: 110/700 mmHg

Head: eye: light reflex +/+, Bronchiolitis

Furosemide 7mg

conjunctival

PO q12h

pallor:

-/-,

mouth/nose/ear:

Diapers rash
Large VSD

unremarkable.

Thorax: symmetric fusiform, Moderate PDA

retraction (-) HR: 106x/i,
continuous murmur(+), RR:
30x/i, Ronchi -/-, Stridor -/Abdomen: Seopel, Normal
peristaltic, non-tender, liver
and

spleen

are

both

unpalpable.
Extremities: Pulse: 108x/i,
regular

with

adequate

pressure and volume, warm,

CRT < 3, pretibial edema
(-)
Physiological

reflexes:

APR(+), KPR (+)

Pathological reflexes (-)

Mild TR

Captopril
3,125mg

PO

q12h
Digoxin

0,035

mg PO q12h
Nebule

NaCl

0,9% 2,5cc tid

Mizol TP q8h

18

Meningeal sign (-)

16th September 2015

Patient was dicharged from the hospital.

19

DISCUSSION
Pneumonia causes substantial morbidity in children worldwide and is a
leading cause of death in children in the developing world. 8 The incidence of
pneumonia is highest in children under 5 years of age and in recent years the
incidence of complicated and severe pneumonia seems to be increasing.8,9
The diagnosis of pneumonia is made by the presence of respiratory distress,
such as tachypnoe, history of breathlessness or difficulty in breathing chest
retractions, nasal flaring, grunting, use of accessory muscles of respiration.
Tachypnoe is a very sensitive marker of pneumonia. 12,13 Between 50-80% of
children with WHO-defined tachypnoe had radiological signs of pneumonia,
Chest x-ray may shows: interstitial infiltrate, alveolar infiltrate, consolidation of
the lungs (air bronchogram), Bronchopneumonia, infiltrate which is equally
spread in both lungs. 8,9
The treatment of pneumonia in children consists of appropriate antibiotics for
the offending organisms, supportive treatment such as oxygen, iv fluid and the
correction of acid base disorder.9 First-line recommended therapy in previously
healthy children regardless of age is Amoxicillin, as it provides sufficient
coverage against the most common invasive bacterial pathogen, namely
Streptococcus pneumoniae. The first line antibiotics for inpatient settings is Beta
Lactamase group or Chloramphenicol. Antibiotic is administered for 7-10 days.
Antibiotic must be given as soon as possible in neonates.9
Our patient is a 5 months old baby girl brought to the emergency department
with breathlessness. Physical findings

upon admission was tachypnoe with

respiratory rate of 44x/i, retraction of epigrastic and supraclavicular region, stridor

and ronchi. The patient was diagnosed with bronchopneumonia based on her
history, physical examinations and chest X-ray. The treatments for this patient
includes oxygen 1 litre/i given through nasal canule, IVFD D5% NaCl 0.225%
microdrips 10 gtt/i, and Amoxicillin IV 350mg q12h.

SUMMARY

20

H, A 5 months old baby girl, was admitted to the emergency department due to
breathlessness and was diagnosed with bronchopneumonia and ventricular septal
defect. The diagnosis was made based on her history, physical examinations ,lab
studies, chest X-ray and echocardiography. The patients treatments consist of:

O2 1 litre/i

IVFD D5% NaCl 0.225% microdrips 10gtt/i

Amoxicillin IV 350 mg q12h

Nebulized NaCl 0.9 % 2,5 cc q8h

Furosemide 7 mg PO q12h

Captopril 3.125 mg PO q12h

Digoxin 0.035 mg PO q12h

21

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