lapkas anak

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

ii

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 wouldn’t 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

iii

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

1

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 34–40 cases per 1000.4

In the UK, from 750 children assessed in hospital, incidence of CAP was

14·4/10 000 children per year and 33·8 for <5-year-olds; with an incidence for

admission to hospital of 12·2 and 28·7 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 world’s 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.

2

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 Common Etiology Less common Etiology

Born- 20 days Bacteria

E. Coli

Group B Streptococcus

Listeria monocytogenes

Bacteria

Anaerobic bacteria

Haemophilus influenza

Streptococcus pneumonia

Virus

CMV

Herpes Simpleks Virus

3 weeks-3 months Bacteria Bacteria

3

Chlamydia trachomatis


Virus

Respiratory Synctial

Virus

Adeno Virus

Influenza Virus

Bordetella pertussis

Haemophillus influenza

type B

Staphylococcus aureus

Virus

CMV

4 months- 5 years Bacteria

Chlamydia pneumonia

Mycoplasma pneumonia


Virus

Adeno Virus

Influenza Virus

RinoVirus

Parainfluenza Virus


Virus

Bacteria


type B


Neisseria meningitidis

Virus

Varicella-Zoster virus

5 tahun-teenagers Bacteria

Chlamydia pneumonia

Mycoplasma pneumonia


Bacteria



Virus

Adeno Virus

Influenza Virus

RinoVirus

Parainfluenza Virus


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,

4

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 immune-

mediated 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

5

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.

6

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 Respiratory rate

0-2 months >60

2-12 months >50

1-4 years >40

>5 years >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

7

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

8

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 patient’s 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: H’s sister was suffering from chronic cough for more thatn 3

weeks

History of parents’ medication: Unclear

History of Pregnancy: The mother’s 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)

9

History of growth and development: The patient’s mother reported that H grew

normally. H can now rolls from supine to prone.

Physical Examination:

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

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 (-).

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%

Eye: light reflex +/+, conjunctival pallor (-/-)

Ear: unremarkable

Nose: O2 nasal canule

Mouth: unremarkable

10

Radiography

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

Range

Hemoglobin 10.20 g% 10.7-17.1

Erythrocyte 4.14 106/mm3 3.75-4.95

Leukocyte 18.25 103/mm3 6.0-17.5

11

Thrombocyte 311 103/mm3 217-497

Hematocrite 29.40 % 38-52

Eosinophil 4.10 % 1-6

Basophil 0.500 % 0-1

Neutrophil 25.60 % 37-80

Lymphocyte 50.70 % 20-40

Monocyte 19.10 % 2-8

Absolute

Neutrophil count

4.68 103/µL 1.9-5.4

Absoulute

Lymphocyte count

9.25 103/µL 3.7-10.7

Absolute

Monocyte count

3.48 103/µL 0.3-0.8

Absolute Basophil

count

0.09 103/µL 0-0.1

MCV 71.00 fL 93-115

MCH 24.60 pg 29-35

MCHC 34.70 g% 28-34

Blood Gas Analysis


Range

pH 7.470 7.35-7.45

PCO2 23.0 mmHg 38-42

PO2 201.0 mmHg 85-100

Bicarbonate(HCO3) 16.7 mmol/L 22-26

Base Excess -5.9 mmol/L (-2)-(+2)

O2 Saturation 100.0 % 95-100

12

Electrolyte


Range

Calcium 8.8 mg/dL 8.4-10.8

Sodium 138 mEq/L 135-155

Potassium 3.8 mEq/L 3.6-5.5

Chloride 100 mEq/L 96-106

Peripheral blood smear morphology:

- Erythorcyte: Microcytic hypochromic with anisocytosis.

- Leukocyte : Atypical Limfosit (+)

- Thrombocyte : Normal

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 O A P

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

Head: eye: light reflex +/+,

conjuctival pallor: -/-,

mouth/nose/ear:

unremarkable.

Thorax: symmetric fusiform,

retraction (+) HR: 144x/i,

continuous murmur(+), RR:

54x/i, Ronchi +/+, Stridor

+/+

Abdomen: soft, normal

peristaltic, non-tender, liver

and spleen are both

unpalpable.

Extremities: Pulse: 144x/i,

regular with adequate

pressure and volume, warm,

CRT < 3”, pretibial edema

(-)

Physiological reflexes:

APR(+), KPR (+)

Pathological reflexes (-)

Meningeal sign (-)

Bronchopneumonia O2 1-2L/i

through nasal

cannula

Ceftriaxone 350

mg IV bid

Consult

Cardiologist.

14

10th September 2015

S O A P

Dypsnea Sensorium : alert, T : 37,0 oC, BP: 100/60 mmHg


conjunctival pallor: -/-,

mouth/nose/ear:

unremarkable.



continuous murmur (+), RR:


+/+



and spleen are both

unpalpable.





(-)


APR(+), KPR (+)


Meningeal sign (-)

Bronchopneumonia

Bronchiolitis

Diaper’s rash

Large VSD

Moderate PDA

Mild TR

O2 1-2L/i

through 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

Echochardiography result:

Large VSD

Moderate PDA

Mild TR

Recommendations: consult

nutritionist and Endocrine &

Metabolic Diseases Divison

11th September 2015

S O A P

Dyspnea(+),

Fever (-)

Sensorium : alert, T : 36,6 oC, BP: 100/70 mmHg

Head: eye: light reflex+/+,


mouth/nose/ear:

unremarkable.





+/+



and spleen are both

unpalpable.



Bronchopneumonia

Bronchiolitis

Diaper’s rash

Large VSD

Moderate PDA

Mild TR

O2 1-2L/i

through 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

Furosemide 7mg

PO q12h

Captopril

16



(-)


APR(+), KPR (+)


Meningeal sign (-)

3,125mg PO

q12h

Digoxin 0,035

mg PO q12h

12th September 2015 – 14th September 2015

S O A P

Improvement

in SOB

Fever (-)




mouth/nose/ear:

unremarkable.


retraction (-) HR: 108x/i,


32x/i, Ronchi -/-, Stridor -/-



and spleen are both

unpalpable.





Bronchopneumonia

Bronchiolitis

Diaper’s rash

Large VSD

Moderate PDA

Mild TR

Amoxicillin 3,5cc

IV q8h

Furosemide 7mg

PO q12h

Captopril

3,125mg PO

q12h

Digoxin 0,035

mg PO q12h

Nebule NaCl

0,9% 2,5cc tid

Mizol TP q8h

17

(-)


APR(+), KPR (+)


Meningeal sign (-)

15th September 2015

S O A P

SOB (-)

Fever (-)




mouth/nose/ear:

unremarkable.


retraction (-) HR: 106x/i,


30x/i, Ronchi -/-, Stridor -/-

Abdomen: Seopel, Normal


and spleen are both

unpalpable.





Bronchopneumonia

Bronchiolitis

Diaper’s rash

Large VSD

Moderate PDA

Mild TR

Amoxicillin 3,5cc

IV q8h

Furosemide 7mg

PO q12h

Captopril

3,125mg PO

q12h

Digoxin 0,035

mg PO q12h

Nebule NaCl

0,9% 2,5cc tid

Mizol TP q8h

18

(-)


APR(+), KPR (+)


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.

20

SUMMARY

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 patient’s 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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Health: 2014. Available at http://www.jhsph.edu/research/centers-and

institutes/ivac/resources/pneumonia.html. Accessed 23.09.2015.

2. World Health Organization. The management of acute respiratory infections in

children In: Practical guidelines for outpatient care. Geneva: WHO, 1995.

3. Williams B , et al. Estimates of world wide distribution of child deaths from

acute respiratory infections. Lancet Infectious Diseases 2002;2:25–32.

4. McIntosh K . Community acquired pneumonia in children. N Engl J Med

2002;346:430–7.

5. Clark, J. e., Hammal, D., Hampton, F., Spencer, D., & Parker, L.

Epidemiology of community-acquired pneumonia in children seen in hospital.

Epidemiology and Infection, 2007. 135(2), 262–269.

http://doi.org/10.1017/S0950268806006741

6. Kementrian Kesehatan Republik Indonesia. Riset Kesehatan Dasar 2007.

Kemenkes, Jakarta: 2007.

7. World Health Organization. Pneumonia. Fact sheet No. 331. 2011. Available

at www.who.int/mediacentre/factsheets/fs331/en. Accessed 03.08.2012.

8. Banaszak, I.W., Breborowicz, A. Pneumonia in Children. Department of

Pulmonology, Pediatric Allergy and Clinnical Immunology, Poland: 2013..

Chapter 6: 54052

9. Said, M.. Pneumonia dalam Respirologi. Ikatan Dokter Anak Indonesia.

Jakarta: 2010.

10. Michelow IC, Olsen K, Lozano J, Rollins NK, Duffy LB, Ziegler T, Kauppila

J, Leinonen M, McCracken GH Jr.. Epidemiology and clinical characteristic of

community acquired pneumonia in hospitalized children. Pediatrics

2004;113:701-7

11. Bennett, N. Pediatric Pneumonia. 2015. Available at

http://emedicine.medscape.com/article/967822-overview#a3. Accessed

23.09.2015

12. Don M, Canciani M, Korppi M. Community – acquired pneumonia in

children: what’s old? What’s new? Acta paediatrica 2010;99:1602-1608

http://emedicine.medscape.com/article/967822-overview#a3

http://doi.org/10.1017/S0950268806006741

http://www.jhsph.edu/research/centers-and%20institutes/ivac/resources/pneumonia.html.%20Accessed%20September%2023

http://www.jhsph.edu/research/centers-and%20institutes/ivac/resources/pneumonia.html.%20Accessed%20September%2023

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13. Coote N, McKenzie S. Diagnosis and investigation of bacterial pneumonia.

Pediatric Respir Rev. 2000;1:8-13

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