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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
Streptococcus pneumonia
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
Streptococcus pneumonia
Virus
Adeno Virus
Influenza Virus
RinoVirus
Parainfluenza Virus
Respiratory Synctial
Virus
Bacteria
Haemophillus influenza
type B
Staphylococcus aureus
Neisseria meningitidis
Virus
Varicella-Zoster virus
5 tahun-teenagers Bacteria
Chlamydia pneumonia
Mycoplasma pneumonia
Streptococcus pneumonia
Bacteria
Haemophillus influenza
Staphylococcus aureus
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,
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
Test Result Unit Reference
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
Test Result Unit Reference
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
Head: eye: light reflex +/+,
conjunctival pallor: -/-,
mouth/nose/ear:
unremarkable.
Thorax: symmetric fusiform,
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 (-)
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+/+,
conjunctival pallor: -/-,
mouth/nose/ear:
unremarkable.
Thorax: symmetric fusiform,
retraction (+) HR: 120x/i,
continuous murmur(+), RR:
60x/i, Ronchi +/+, Stridor
+/+
Abdomen: soft, normal
peristaltic, non-tender, liver
and spleen are both
unpalpable.
Extremities: Pulse: 120x/i,
regular with adequate
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
pressure and volume, warm,
CRT < 3”, pretibial edema
(-)
Physiological reflexes:
APR(+), KPR (+)
Pathological reflexes (-)
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 (-)
Sensorium : alert, T : 36,8 oC, BP: 100/60 mmHg
Head: eye: light reflex +/+,
conjunctival pallor: -/-,
mouth/nose/ear:
unremarkable.
Thorax: symmetric fusiform,
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
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
(-)
Physiological reflexes:
APR(+), KPR (+)
Pathological reflexes (-)
Meningeal sign (-)
15th September 2015
S O A P
SOB (-)
Fever (-)
Sensorium : alert, T : 36,5 oC, BP: 110/700 mmHg
Head: eye: light reflex +/+,
conjunctival pallor: -/-,
mouth/nose/ear:
unremarkable.
Thorax: symmetric fusiform,
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
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
(-)
Physiological reflexes:
APR(+), KPR (+)
Pathological reflexes (-)
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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1. John Hopskins Public Health. Pneumonia and Children. John Hopskins Public
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
22
13. Coote N, McKenzie S. Diagnosis and investigation of bacterial pneumonia.
Pediatric Respir Rev. 2000;1:8-13
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