Pneumonia & Community – Acquired Pneumonia

Source:
1) Nelson’s Essentials of Pediatrics 8 : Chapter 110 – Pneumonia
2) Nelson’s Textbook of Pediatrics 20 : Chapter 400 – Community-Acquired Pneumonia
3) Lange Current Diagnosis & Treatment : Pediatrics, 23rd Edition, 2016
4) Panduan Diagnosis dan Terapi Edisi 5 IKA Unpad
5) WHO Pocket Book for Hospital Care of Children 2013
6) Revised WHO classification and treatment of childhood pneumonia, 2012
7) Nelson’s Pediatric Antimicrobial Therapy, 2018 (for table of Antimicrobials in bottom of page)

INTRODUCTION
 Pneumonia is an infection of the lower respiratory tract that involves the airways and
parenchyma, with consolidation of the alveolar spaces. [1]
 Pneumonia, is defined as inflammation of the lung parenchyma,[2]
 The term lower respiratory tract infection is often used to encompass bronchitis,
bronchiolitis (see Chapter 109), pneumonia, or any combination of the three.[1]
o Pneumonitis is a general term for lung inflammation that may or may not be
associated with consolidation. [1]
o Lobar pneumonia describes pneumonia localized to one or more lobes of the
lung.[1]
o Atypical pneumonia describes patterns typically more diffuse or interstitial than
lobar pneumonia.[1]
o Bronchopneumonia refers to inflammation of the lung that is centered in the
bronchioles and leads to the production of a mucopurulent exudate that
obstructs some of these small airways and causes patchy consolidation of the
adjacent lobules.[1]
o Interstitial pneumonitis refers to inflammation of the interstitium, which is
composed of the walls of the alveoli, the alveolar sacs and ducts, and the
bronchioles. [1]Interstitial pneumonitis is characteristic of acute viral infections
but may also be a chronic inflammatory or fibrosing process.[1]
 Lower respiratory tract infections are a major cause of high mortality in disadvantaged areas
of the world.[3] The infectious etiologies vary widely by geographical region and by the age
of the child.[3]
 In developed countries the majority of pneumonias are caused by viral agents and bacterial
pneumonia is a less common cause.[3] Discrimination between viral and bacterial pneumonia
is challenging as neither the white blood cell count nor differential nor the chest radiograph
are strong predictors.[3] In areas where the technology is readily available, chest radiography
is recommended to establish with certainty the presence of pneumonia.[3]

EPIDEMIOLOGY
 Penyebab utama morbiditas dan mortalitas pada anak usia <5 th di seluruh dunia, terutama
di negara berkembang.[4]
 Pneumonia is the leading cause of death globally among children younger than age 5 yr,
accounting for an estimated 1.2 million (18% total) deaths annually (Fig. 400-1).[1] The
incidence of pneumonia is more than 10-fold higher (0.29 episodes vs 0.03 episodes),
 and the number of childhood-related deaths from pneumonia ≈2,000 fold higher, in
developing than in developed countries (Table 400-1). [2] Fifteen countries account for
more than three-fourths of all pediatric deaths from pneumonia.[2]
 Immunizations have markedly reduced the incidence of pneumonia caused by pertussis,
diphtheria, measles, Haemophilus inflenzae type b, and S. pneumoniae.[1]
 Where used, bacilli Calmette-Guérin (BCG) immunization for tuberculosis has also had
some impact.[2]
 Pneumonia is the single largest contributor of childhood mortality worldwide, killing an
estimated 1 million children under 5 years of age annually.[1]
 Risk factors for lower respiratory tract infections include gastroesophageal reflux,
neurological impairment (aspiration), immunocompromised states, anatomical
abnormalities of the respiratory tract, residence in residential care facilities, and
hospitalization, especially in an intensive care unit.[1]
 Defects in host defenses increase the risk of pneumonia.[1]
 Di negara industri, epidemi RSV dan atau influenza koinsidensi dengan epidemi S.
pneumoniae.[4]
 Di negara berkembang, infeksi virus sering disertai infeksi sekunder.[4]
 Usia merupakan prediktor yang baik untuk memperkirakan patogen penyebab
pneumonia.[4]
 Virus → penyebab utama pneumonia pada anak usia lebih muda (<2 th).[4]
 Bakteri → penyebab sebagian besar pneumonia pada anak besar.[4]
 Tabel 222 menunjukkan bakteri dan virus yang umum menyebabkan
pneumonia pada anak berdasarkan usia.[4]
  Faktor risiko pneumonia pada anak meliputi malnutrisi, berat badan lahir
rendah (BBLR), tidak mendapat ASI eksklusif, tidak mendapat imunisasi
campak, polusi udara dalam rumah, dan kepadatan hunian.[4]

ETIOLOGY
1. Based on age group
Infectious agents that commonly cause community-acquired pneumonia vary by age (Table
110.1). [1]
o Streptococcus pneumonia is the most common bacterial cause of pneumonia
(particularly lobar pneumonia) and occurs in children of any age outside the neonatal
period. Other common causes include respiratory syncytial virus (RSV) in infants (see
Chapter 109), other respiratory viruses (parainfluenza viruses, influenza viruses,
human metapneumovirus, adenoviruses) in children younger than 5 years old, and
Mycoplasma pneumoniae in children older than age 5 years.[1]
o M. pneumoniae and Chlamydophila pneumonia are principal causes of atypical
pneumonia.[1]
o Chlamydia trachomatis and less commonly Mycoplasma hominis, Ureaplasma
urealyticum, and cytomegalovirus (CMV) cause a similar respiratory syndrome in
infants 2 weeks to 3 months of age, with subacute onset of an afebrile pneumonia; cough
and hyperinflation are the predominant signs.[1]

o These infections are difficult to diagnose and distinguish from each other.[1] In adults
these organisms are carried primarily as part of the genital mucosal flora.[1] Women
who harbor these agents may transmit them perinatally to newborns.[1]
o Additional agents occasionally cause pneumonia.[1]
 Severe acute respiratory syndrome (SARS) is due to SARS-associated coronavirus
(SARS-CoV).[1]
 Avian inflenza (bird flu) is a highly contagious viral disease of poultry and other
birds caused by influenza A (H5N1). [1] There were outbreaks among humans in
Southeast Asia in 1997 and 2003-2004, with high mortality rates.[1] A novel
influenza A (H1N1) of swine origin began circulating in 2009.[1]
o Other etiological agents to consider, based on specific exposure history, include
Staphylococcus aureus and Streptococcus pyogenes (especially after influenza
infection), Mycobacterium tuberculosis, Francisella tularensis, Brucella spp.,
Coxiella burnetii, Chlamydophila psittaci, Legionella pneumophila, hantavirus,
Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, and
oral flora or gram-negative bacilli (after aspiration).[1]
 o Causes of pneumonia in immunocompromised persons include gram-negative enteric
bacteria, mycobacteria (M. avium complex), fungi (aspergillosis), viruses (CMV), and
Pneumocystis jirovecii (formerly carinii). [1]Pneumonia in patients with cystic
fibrosis is usually caused by S. s aureus in infancy and Pseudomonas aeruginosa or
Burkholderia cepacia in older patients.[1]

2. Based on types and characteristics of agents

a) Infectious
Bakteri, virus, mikobakterium, dan jamur.[4] Pneumonia is caused by viruses or bacteria.[5]
Infectious agents that commonly cause community-acquired pneumonia vary by age (Table
110.1).[2]
(1) Bacterial
 Bakteri adalah penyebab utama di negara berkembang, yaitu:
o Streptococcus pneumoniae (30−50%),
o Haemophilus influenzae type b (Hib),
o Staphylococcus aureus,
o Klebsiella pneumonia.[4]
 The most common cause of bacterial pneumonia in children of all ages is S. pneumoniae.[3]
 Streptococcus pneumoniae (pneumococcus) is the most common bacterial pathogen
in children 3 wk to 4 yr of age, whereas Mycoplasma pneumonia and Chlamydophila
pneumoniae are the most frequent bacterial pathogens in children age 5 yr and
older.[1] In addition to pneumococcus, other bacterial causes of pneumonia in
previously healthy children in the United States include group A streptococcus
(Streptococcus pyogenes) and Staphylococcus aureus (see Chapter 181.1 and Table
400-2).[1]
 S. aureus pneumonia often complicates an illness caused by influenza viruses.[1]
 S. pneumoniae, H. influenzae, and S. aureus are the major causes of hospitalization
and death from bacterial pneumonia among children in developing countries, although
in children with HIV infection, Mycobacterium tuberculosis (see Chapter 215),
atypical mycobacteria, Salmonella (see Chapter 198), Escherichia coli (see Chapter
200), and
Pneumocystis jiroveci (see Chapter 244) must be considered.[1]
 The incidence of pneumonia caused by H. influenzae or S. pneumoniae has been
significantly reduced in areas where routine immunization has been implemented.[1]
 Bacterial pneumonia usually follows a viral lower respiratory tract infection.[3]
 Children at high risk for bacterial pneumonia are those with compromised pulmonary defense
systems.[3]
For example, children with abnormal mucocilliary clearance, immunocompromised children,
children who aspirate their own secretions or while eating, and malnourished children are at
increased risk for bacterial pneumonia.[3]
  Immunization status is relevant because children fully immunized against H. influenzae
type b and S. pneumoniae are less likely to be infected with these pathogens.[2]
Children who are immunosuppressed or who have an underlying illness may be at risk
for specific pathogens, such as Pseudomonas spp. in patients with cystic fibrosis (see
Chapter 403).[2]

(2) Viral
 Viral infection is a common cause of community-acquired pneumonia in children.[3]
 Viral pathogens are a prominent cause of lower respiratory tract infections in infants
and children older than 1 mo but younger than 5 yr of age.[2]
 Viral pneumonia is most common in children younger than 2 years.[3]
 Viruses can be detected in 40-80% of children with pneumonia using molecular
diagnostic methods.[2]
 Virus merupakan penyebab utama di negara maju, yaitu:
 RSV → 15–40%,
 Virus Influenza A dan B,
 Parainfluenza,
 Human metapneumovirus,
 Adenovirus.[4]
 Of the respiratory viruses, respiratory syncytial virus (RSV) (see Chapter 260) and
rhinoviruses are the most commonly identified pathogens, especially in children
younger than 2 yr of age. [2]
 RSV, parainfluenza (1, 2, and 3) viruses, influenza (A an B) viruses, an human
metapneumovirus are responsible for the large majority of cases.[3]
 However, the role of rhinoviruses in severe lower respiratory tract infection remains
poorly defined as these viruses are frequently detected in infections with 2 or more
pathogens and among asymptomatic children.[2] Other common viruses causing
pneumonia include influenza virus (see Chapter 258), parainfluenza viruses,
adenoviruses, enteroviruses, and human metapneumovirus.[2]
 Infection with more than 1 respiratory virus occurs in up to 20% of cases.[2] The age of
the patient may help identify possible pathogens (Table 400-3).[2]
 Lower respiratory tract viral infections are much more common in the fall and winter in
both the northern and southern hemispheres in relation to the seasonal epidemics of
respiratory viral infection that occur each year. [2]
 The typical pattern of these epidemics usually begins in the fall, when
parainfluenza infections appear and most often manifest as croup.[2]
 Later in winter, RSV, human metapneumovirus, and influenza viruses cause
widespread infection, including upper respiratory tract infections, bronchiolitis,
and pneumonia.[2]
 RSV is particularly severe among infants and young children, whereas influenza virus
causes disease and excess hospitalization for acute respiratory illness in all age
groups.[2]
 Knowledge of the prevailing viral epidemic may lead to a presumptive initial
diagnosis.[2]
  Severity of disease, severity of fever, radiographic findings, and the characteristics of cough
or lung sounds do not reliably differentiate viral from bacterial pneumonias.[3]
 Furthermore, viral infections may predispose to bacterial pneumonia.[3] However, substantial
pleural effusions, pneumatoceles, abscesses, lobar consolidation with lobar volume
expansion, and “round ” pneumonias are generally inconsistent with viral disease.[3]

b) Non-infectious
Although most cases of pneumonia are caused by microorganisms, noninfectious causes include
aspiration (of food or gastric acid, foreign bodies, hydrocarbons, and lipoid substances),
hypersensitivity reactions, and drug- or radiation-induced pneumonitis.[1]

The cause of pneumonia in an individual patient is often difficult to determine because direct
culture of lung tissue is invasive and rarely performed.[1] Cultures performed on specimens in
children obtained from the upper respiratory tract or sputum typically do not accurately reflect
the cause of lower respiratory tract infection.[1] With the use of molecular diagnostic testing, a
bacterial or viral cause of pneumonia can be identified in 40-80% of children with community-
acquired pneumonia.[1]

PATHOGENESIS
 Trauma, anesthesia, and aspiration increase the risk of pulmonary infection.[2]
 Viral pneumonia usually results from spread of infection along the airways, accompanied by direct injury of the
respiratory epithelium, which results in airway obstruction from swelling, abnormal secretions, and cellular
debris.[2] The small caliber of airways in young infants makes such patients particularly susceptible to severe
infection.[2] Atelectasis, interstitial edema, and ventilation–perfusion mismatch causing significant hypoxemia
often accompany airway obstruction.[2] Viral infection of the respiratory tract can also predispose to secondary
bacterial infection by disturbing normal host defense mechanisms, altering secretions, and modifying the
bacterial flora.[2]
 Bacterial pneumonia most often occurs when respiratory tract organisms colonize the trachea and subsequently
gain access to the lungs, but pneumonia may also result from direct seeding of lung tissue after bacteremia.[2]
When bacterial infection is established in the lung parenchyma, the pathologic process varies according to the
invading
organism.[2]
o M. pneumoniae (see Chapter 223) attaches to the respiratory epithelium, inhibits ciliary action, and
leads to cellular destruction and an inflammatory response in the submucosa.[2] As the infection
progresses, sloughed cellular debris, inflammatory cells, and mucus cause airway obstruction, with
spread of infection occurring along the bronchial tree, as it does in viral pneumonia.[2]
o S. pneumoniae produces local edema that aids in the proliferation of organisms and their spread into
adjacent portions of lung, often resulting in the characteristic focal lobar involvement.[2]
o Group A streptococcus infection of the lower respiratory tract results in more diffuse infection with
interstitial pneumonia.[2] The pathology includes necrosis of tracheobronchial mucosa; formation of
large amounts of exudate, edema, and local hemorrhage, with extension into the interalveolar septa;
and involvement of lymphatic vessels and the increased likelihood of pleural involvement.[2]
o S. aureus pneumonia manifests in confluent bronchopneumonia, which is often unilateral and
characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas of
cavitation of the lung parenchyma, resulting in pneumatoceles, empyema, or, at times,
bronchopulmonary fistulas.[2]
 Recurrent pneumonia is defined as 2 or more episodes in a single year or 3 or more episodes ever, with
radiographic clearing between occurrences. An underlying disorder should be considered if a child experiences
recurrent pneumonia (Table 400-4).[2]
CLINICAL MANIFESTATIONS & FINDINGS
 Age is a determinant in the clinical manifestations of pneumonia.[1]
o Neonates may have fever or hypoxia only, with subtle or absent physical examination
findings (see Chapter 65).[1]
o With a young infant, apnea may be the first sign of pneumonia.[1]
o Fever, chills, tachypnea, cough, malaise, pleuritic chest pain, retractions, and apprehension—
because of difficulty breathing or shortness of breath—are common in older infants and
children.[1]
 Physical examination findings cannot reliably distinguish viral and bacterial pneumonias, but
complete physical examination may help identify other foci of disease or associated findings to
suggest an etiology.[1]
 Pneumonia is frequently preceded by several days of symptoms of an upper respiratory tract infection, typically
rhinitis and cough.[2]
 In viral pneumonia, fever is usually present but temperatures are generally lower than in bacterial
pneumonia.[2]
 Tachypnea is the most consistent clinical manifestation of pneumonia.[2]
 Increased work of breathing accompanied by intercostal, subcostal, and suprasternal retractions, nasal flaring,
and use of accessory muscles is common.[2]
 Severe infection may be accompanied by cyanosis and lethargy, especially in infants.[2]
 Auscultation of the chest may reveal crackles and wheezing, but it is often difficult to localize the source of these
adventitious sounds in very young children with hyperresonant chests.[2]
 It is often not possible to distinguish viral pneumonia clinically from disease caused by Mycoplasma and other
bacterial pathogens.[2]
 Viral pneumonias are generally associated more often with cough, wheezing, or stridor; fever is less
prominent than with bacterial pneumonia.[1] Mucosal congestion and upper airway inflammation
suggest a viral infection.[1]
 Bacterial pneumonias are typically associated with higher fever, chills, cough, dyspnea, and
auscultatory findings of lung consolidation.[1]
 Atypical pneumonia in young infants is characterized by tachypnea, cough, and crackles on
auscultation.
 Concomitant conjunctivitis may be present in infants with chlamydial pneumonia.[1] Other signs of
respiratory distress include nasal flaring, intercostal and subcostal retractions, and grunting.[1]
Asymmetry or shallow breathing may be due to splinting from pain. [1]
 Hyperexpansion, common in asthma but also frequently accompanying viral lower respiratory
infections, may cause a low diaphragm seen on a chest x-ray.[1]
 Poor diaphragmatic excursion may indicate hyperexpanded lungs or an inability for expansion due to
a large consolidation or effusion. Dullness to percussion may be due to lobar or segmental infiltrates
or pleural fluid. [1]
 Auscultation may be normal in early or very focal pneumonia, but the presence of localized crackles,
rhonchi, and wheezes may help one detect and locate pneumonia.[1] Distant breath sounds may
indicate a large, poorly ventilated area of consolidation or pleural fluid.[1]
 Bacterial pneumonia in adults and older children typically begins suddenly with high fever, cough, and chest
pain. Other symptoms that may be seen include drowsiness with intermittent periods of restlessness; rapid
respirations; anxiety; and, occasionally, delirium.[2]
 In many children, splinting on the affected side to minimize pleuritic pain and improve ventilation is noted; such
children may lie on one side with the knees drawn up to the chest.[2]
 Physical findings depend on the stage of pneumonia. [2] Early in the course of illness, diminished breath sounds,
scattered crackles, and rhonchi are commonly heard over the affected lung field. [2] With the development of
increasing consolidation or complications of pneumonia such as pleural effusion or empyema, dullness on
percussion is
noted and breath sounds may be diminished.[2] A lag in respiratory excursion often occurs on the affected side.
[2] Abdominal distention may be prominent because of gastric dilation from swallowed air or ileus.[2]
Abdominal pain is common in lower-lobe pneumonia. The liver may seem enlarged because of downward
displacement of the diaphragm secondary to hyperinflation of the lungs or superimposed congestive heart
failure.[2]
 Symptoms described in adults with pneumococcal pneumonia may be noted in older children but are rarely
observed in infants and young children, in whom the clinical pattern is considerably more variable.
 In infants, there may be a prodrome of upper respiratory tract infection and diminished appetite, leading to the
abrupt onset of fever, restlessness, apprehension, and respiratory distress.[1] These infants appear ill, with
respiratory distress manifested as grunting; nasal flaring; retractions of the supraclavicular, intercostal, and
subcostal areas; tachypnea; tachycardia; air hunger; and often cyanosis.[2]
 Results of physical examination may be misleading, particularly in young infants, with meager findings
disproportionate to the degree of tachypnea.[2]
 Some infants with bacterial pneumonia may have associated gastrointestinal disturbances characterized by
vomiting, anorexia, diarrhea, and abdominal distention secondary to a paralytic ileus.[2]
Rapid progression of symptoms is characteristic in the most severe cases of bacterial pneumonia.[2]
 Sebagian besar pneumonia pada anak menunjukkan gambaran klinis yang ringan sampai sedang
sehingga dapat berobat jalan saja.[4]
 Hanya sebagian kecil anak mengalami pneumonia berat yang mengancam kehidupan dan
mungkin terdapat komplikasi, sehingga memerlukan perawatan di rumah sakit/[4]
 Gambaran klinis pneumonia pada bayi dan anak bergantung pada
berat ringan infeksi.[4]
 Gejala infeksi umum: demam, sakit kepala, gelisah, malaise, nafsu makan ↓, keluhan
gastrointestinal seperti mual, muntah atau diare; kadang-kadang ditemukan gejala
ekstraparu.[4]
 Pada anak dengan malnutrisi berat, demam jarang terjadi.[4]
 Gejala gangguan respiratori: batuk, sesak napas, retraksi dinding dada, takipnea, napas
cuping hidung, air hunger, merintih, dan sianosis.[4]
 Gambaran klinis pneumonia pada anak malnutrisi berat kurang spesifik dan dapat
tumpang tindih dengan sepsis.[4]
 Penelitian mengenai validasi tanda klinis WHO menunjukkan bahwa tanda klinis yang
direkomendasikan oleh WHO kurang sensitif sebagai prediktor pneumonia dibandingkan
dengan gambaran radiologis pada anak malnutrisi berat.[4]
 Pneumonia bakterial harus dipertimbangkan pada anak usia <3 th yang mengalami panas badan
>38,5 °C disertai retraksi dinding dada dan frekuensi napas ≥50×/mnt.[4]
o Pneumonia yang disebabkan Pneumoccocus spp. biasanya diawali dengan demam dan
napas cepat.[4] Gejala lain yang umum ditemukan adalah kesukaran bernapas, retraksi
dinding dada, dan anak tampak tidak sehat (unwell appearance).[4]
o Pneumonia yang disebabkan Staphylococcus spp. mempunyai gejala yang sama dengan
pneumonia yang disebabkan pneumoccocus, sering ditemukan pada bayi, tetapi dapat
ditemukan pada anak yang lebih besar sebagai komplikasi dari influenza.[4]
o Pneumonia yang disebabkan Mycoplasma spp. harus dicurigai pada anak usia sekolah
yang menunjukkan gejala demam, nyeri sendi, sakit kepala, batuk.[4]
o Meskipun penyebab pneumonia sulit ditentukan, tetapi ada beberapa gejala dan tanda
yang dapat dikenali secara klinis, yaitu:
 Staphylococcus aureus:
- Progresivitas penyakit sangat cepat dengan gejala respiratori sangat berat:
grunting, sianosis, takipnea, dan gambaran radiologis necrotizing pneumonia,
pneumonia dengan komplikasi (efusi pleura, empiema, piopneumotoraks),
perburukan klinis dan radiologis yang sangat cepat, atau pada keadaan
pascainfeksi campak (saat ini atau
4 mgg sebelumnya).[4]
- Pada kulit penderita dapat dijumpai bisul atau abses.[4]
 Streptococcus grup A:
- Penyebab tersering faringitis, tonsilitis dengan limfadenitis koli, demam,
malaise, sakit kepala, dan gejala pada abdomen.[4]
- Sering merupakan komplikasi infeksi kulit pada anak dengan varisela.[4]
- Penyakit memburuk dalam 24 jam.[4]
- Sering diikuti dengan syok septik, empiema, dan pneumatokel yang terjadi
 dalam beberapa hr sampai 1 mgg sesudah pengobatan.[4]

DIAGNOSIS
1) Anamnesis
o Demam tinggi, batuk, gelisah, rewel, dan sesak napas.[4]
o Pada bayi, gejala tidak khas, sering kali tanpa demam dan batuk.[4]
o Anak besar kadang mengeluh nyeri kepala, nyeri abdomen, disertai muntah.[4]

2) Pemeriksaan Fisis
o Manifestasi klinis yang terjadi akan berbeda-beda berdasarkan kelompok usia tertentu.[4]
o Neonatus: sering dijumpai takipnea, grunting, pernapasan cuping hidung, retraksi dinding
dada, sianosis, dan malas menetek.[4]
o Bayi yang lebih besar: jarang ditemukan grunting.[4] Gejala lain yang sering terlihat adalah
batuk, panas, dan iritabel.[4]
o Anak prasekolah, selain gejala di atas, dapat ditemukan batuk produktif/nonproduktif, dan
dispnea
Anak sekolah dan remaja, gejala lainnya yang dapat dijumpai yaitu nyeri dada, nyeri kepala,
dehidrasi, dan letargi
o Takipnea berdasarkan WHO:
- Usia <2 bl → ≥60×/mnt,
- Usia 2–<12 bl → ≥50×/mnt,
- Usia 1–5 th → ≥40×/mnt.[4]
o Takipnea terbukti memiliki sensitivitas dan spesifisitas yang tinggi dalam mendiagnosis
pneumonia.[4]
o Menurut WHO derajat berat pneumonia pada anak usia 2 bl–5 th seperti Tabel 223 di bawah
ini :[4]
 o Auskultasi → fine crackles (ronki basah halus) yang khas pada anak besar, mungkin tidak
ditemukan pada bayi.[4]
o Iritasi pleura akan menyebabkan nyeri dada; bila berat gerakan dada tertinggal waktu
inspirasi, anak berbaring ke arah yang sakit dengan kaki fleksi.[4]
o Rasa nyeri dapat menjalar ke leher, bahu, dan perut.[4]

3) Pemeriksaan Penunjang : Laboratories & Imaging Studies

a) Radiology
o Frontal and lateral radiographs are required to localize disease and adequately visualize
retrocardiac infiltrates; they are recommended for diagnosis among hospitalized children but are
not necessary to confirm the diagnosis in well-appearing outpatients.[1]
o Foto Rontgen toraks proyeksi posterior-anterior (PA) merupakan dasar diagnosis utama
pneumonia.[4]
o Foto lateral dibuat bila diperlukan informasi tambahan (tidak rutin dilakukan).[4]
o Untuk negara berkembang foto Rontgen toraks secara rutin tidak direkomendasikan
terutama pneumonia yang tidak memerlukan perawatan di rumah sakit.[4]
o Indikasi spesifik foto Rontgen toraks adalah pneumonia sangat berat, dugaan komplikasi
pneumonia (misal efusi pleura), atau tidak berespons terhadap terapi yang diberikan, dan
kecurigaan LTBI.[4]
o Indikasi tambahan lainnya adalah gejala atipikal dan pemantauan pada anak dengan kolaps
lobar atau gejala yang berlanjut.[4]
o An infiltrate on chest radiograph (posteroanterior and lateral views) supports the diagnosis of pneumonia;
the film may also indicate a complication such as a pleural effusion or empyema.[2]
 Viral pneumonia is usually characterized by hyperinflation with bilateral interstitial infiltrates and
peribronchial cuffing (Fig. 400-2).[2]
 Confluent lobar consolidation is typically seen with pneumococcal pneumonia (Fig. 400-3).[2]
o The radiographic appearance alone is not diagnostic, and other clinical features must be considered.[2]
o Repeat chest radiographs are not required for proof of cure for patients with uncomplicated pneumonia.[2]
o Pemeriksaan foto Rontgen toraks ulang hanya dilakukan bila pada foto sebelumnya
didapatkan lobar collapse, gambaran round pneumonia, atau bila gejala menetap atau
memburuk[4]
o Pada bayi dan anak yang kecil, gambaran radiologis sering tidak sesuai dengan gambaran
klinis.[4]
o Some experts suggest that a chest radiograph may not be necessary for older children with suspected
pneumonia (cough, fever, localized crackles, or decreased breath sounds) who are well enough to be
managed as outpatients.[2]
o Although there are characteristic radiographic findings of pneumonia, radiography alone cannot
provide a definitive microbiologic diagnosis.[1]
 Bacterial pneumonia characteristically shows lobar consolidation or a round pneumonia,
with pleural effsion in 10-30% of cases (Fig. 110.1).[1]
 Viral pneumonia characteristically shows diffuse, streaky infiltrates of
bronchopneumonia (Fig. 110.2) and hyperinflation.[1]
 Atypical pneumonia, as with M. pneumoniae and C. pneumoniae, shows increased
interstitial markings or bronchopneumonia.[1]
o Foto Rontgen toraks tidak dapat membedakan antara pneumonia bakteri dan pneumonia
virus.[4]
o Gambaran radiologis yang klasik dapat berupa:
  Konsolidasi lobar atau segmental disertai air bronchogram, biasanya disebabkan
infeksi Pneumoccocus spp. atau bakteri lain.[4]
 Pneumonia interstisial, biasanya karena virus atau mikoplasma; gambaran berupa
corakan bronkovaskular bertambah, peribronchial cuffing, dan overaeration; bila
berat terjadi patchy consolidation karena atelektasis.[4]
 Gambaran difus bilateral, corakan peribronkial bertambah, dan 14nfiltrate halus
sampai ke perifer.[4]
 Gambaran pneumonia
karena S. aureus biasanya menunjukkan pneumatokel.[4]
o Chest radiographs may be normal in early pneumonia, with infiltrates appearing during
treatment as hydration is restored.[1]
o Hilar lymphadenopathy is uncommon with bacterial pneumonia but may be a sign of
tuberculosis, endemic mycoses, autoimmune conditions, or an underlying malignant
neoplasm.[1]
Decubitus views or ultrasound should be used to assess the size of pleural effusions and whether
they are freely mobile.[1]
o Computed tomography (CT) is used to evaluate serious disease, lung abscesses, bronchiectasis,
and effsion characteristics.[1]
o Unusual etiologies or recurrent pneumonias require special considerations (Table 110.2).[1]
Lung abscesses, pneumatoceles, and empyema may require surgical management.[1]
 o Point-of-care use of portable or handheld ultrasonography is highly sensitive and specific in diagnosing
pneumonia in children by determining lung consolidations and air bronchograms or effusions.[2]
b) Laboratory Studies (Laboratorium)
 Bacterial flora of the upper respiratory tract do not accurately reflect flora present in lower
respiratory tract infections, and high-quality sputum is rarely obtainable from children. [1]
 In otherwise healthy children without life-threatening disease, invasive procedures to obtain
lower respiratory tissue or secretions are seldom indicated.[1]
 Serological tests are not useful for the most common causes of bacterial pneumonia.
The white blood cell (WBC) count with viral pneumonias is often normal or mildly elevated, with
a predominance of lymphocytes, whereas with bacterial pneumonias the WBC count is elevated (
>15-20,000/mm3), with a predominance of neutrophils. Mild eosinophilia is characteristic of
infant C.
trachomatis pneumonia. [1]
 Blood cultures should be performed on ill, hospitalized children to attempt to diagnose a
bacterial cause
of pneumonia. Blood cultures identify a bacterial respiratory pathogen in 5-10% of children
hospitalized for pneumonia (and 10-20% of those with pneumonia with empyema or large
effsion). Urinary antigen tests are especially useful for L. pneumophila (Legionnaires
disease).[1]
 The peripheral white blood cell (WBC) count can be useful in differentiating viral from bacterial
pneumonia.[2]
o In viral pneumonia, the WBC count can be normal or elevated but is usually not higher than
20,000/mm3, with a lymphocyte predominance.[2]
o Bacterial pneumonia is often associated with an elevated WBC count, in the range of 15,000-
40,000/mm3, and a predominance of granulocytes. A large pleural effsion, lobar consolidation, and
a high fever at the onset of the illness are also suggestive of a bacterial etiology. [2]
o Jumlah leukosit >15.000/µL dengan dominasi neutrofil sering didapatkan pada
pneumonia bakteri, tetapi dapat pula karena pneumonia nonbakteri.[4]
o Atypical pneumonia caused by C. pneumoniae or M. pneumoniae is difficult to distinguish from
pneumococcal pneumonia on the basis of radiographic and laboratory findings, and although
pneumococcal pneumonia is associated with a higher WBC count, erythrocyte sedimentation rate,
procalcitonin, and C-reactive protein level, there is considerable overlap, particularly with
adenoviruses and enteroviruses.[2]
 Viral respiratory pathogens can be diagnosed using polymerase chain reaction (PCR) or rapid
viral antigen detection, but neither can rule out concomitant bacterial pneumonia.[1]
M. pneumoniae can be confimed by Mycoplasma PCR. CMV pneumonitis can be diagnosed with
 PCR from bronchoalveolar lavage fluid. The diagnosis of M. tuberculosis is established by the
tuberculin skin test, serum interferon-gamma release assay or analysis of sputum or gastric
aspirates by culture, antigen
detection, or PCR.[1]
 The need to establish an etiological diagnosis of pneumonia is greater in immunocompromised
patients, patients with recurrent pneumonia, or those with pneumonia unresponsive to empirical
therapy. For these patients, bronchoscopy with bronchoalveolar lavage and brush mucosal
biopsy, needle aspiration of the lung, and open lung biopsy are methods of obtaining material for
microbiologic diagnosis.[1]
 The definitive diagnosis of a viral infection rests on the isolation of a virus or detection of the viral genome
or antigen in respiratory tract secretions.[2] Reliable DNA or RNA tests for the rapid detection of many
respiratory pathogens, such as mycoplasma, pertussis, and viruses, including RSV, parainfluenza, influenza,
and adenoviruses, are available and accurate.[2] Serologic techniques can also be used to diagnose a recent
respiratory viral infection but generally require testing of acute and convalescent serum samples for a rise
in antibodies to a specific viral agent.[2] This diagnostic technique is laborious, slow, and not generally
clinically useful because the infection usually resolves by the time it is confirmed serologically.[2] Serologic
testing may be valuable as an epidemiologic tool to define the incidence and prevalence of the various
respiratory viral pathogens.[2] Patient peripheral cell gene expression patterns determined by microarray
reverse transcription polymerase chain reaction is an emerging technology that may help differentiate viral
from bacterial causes of pneumonia.[2]
 When there is a pleural effusion or empyema, a thoracentesis to obtain pleural flid can be
diagnostic and therapeutic.[1]
Evaluation diffrentiates between empyema and a sterile parapneumonic effsion caused by
irritation of the pleura contiguous with the pneumonia.[1] Gram stain, bacterial culture, or
broad-range bacterial PCR may lead to microbiologic diagnosis.[1]
The pleural fluid can also be cultured for mycobacteria and fungi.[1] Removal of grossly purulent
pleural fluid reduces the patient’s toxicity and associated discomfort and may facilitate more
rapid recovery.[1] Drainage of large pleural accumulations also improves pulmonary mechanics
and gas exchange by increasing the ability of the lung to expand.[1]
 The definitive diagnosis of a bacterial infection requires isolation of an organism from the blood, pleural
fluid, or lung.[2]
 Diagnosis pasti pneumonia bakterial yaitu dengan isolasi mikroorganisme dari paru, cairan
pleura, atau darah.[4]
 Culture of sputum is of little value in the diagnosis of pneumonia in young children, while percutaneous
lung aspiration is invasive and not routinely performed.[2]
 Pengambilan spesimen dari paru sangat invasif dan tidak rutin diindikasikan dan
dilakukan.[4]
 Cold agglutinins at titers >1 : 64 are found in the blood in ≈50% of patients with M. pneumoniae
infections. [2]Cold agglutinin findings are nonspecific because other pathogens such as influenza viruses
may also cause increases.[2]
 Acute infection caused by M. pneumonia can be diagnosed on the basis of a positive polymerase chain
reaction test result or seroconversion in an IgG assay.[2] Serologic evidence, such as the antistreptolysin O
titer, may be useful in the diagnosis of group A streptococcal pneumonia.[2]
 Pemeriksaan C-reactive protein perlu dipertimbangkan pada pneumonia dengan komplikasi
dan dapat bermanfaat untuk melihat respons antibiotic.[4]
 Tidak dapat membedakan pneumonia akibat virus atau bakteri.[4]

c) Pemeriksaan mikrobiologis
o Pemeriksaan biakan darah harus dilakukan pada semua anak yang dicurigai menderita
pneumonia bakteri, pneumonia berat, pneumonia dengan komplikasi.[4]
  Hasil (+) hanya didapatkan pada 10–30% kasus.[4]
 Kultur darah hanya (+) pada 10−30% kasus.[4]
 Blood culture results are positive in only 10% of children with pneumococcal pneumonia and are not
recommended for nontoxic appearing children treated as an outpatient.[2] Blood cultures are
recommended
for those who fail to improve or have clinical deterioration, in those with complicated pneumonia (Table
400-5) and those requiring hospitalization.[2]

d) Pemeriksaan sputum
o Walaupun kurang berguna, tetapi jika anak memungkinkan untuk mengeluarkan sputum,
periksa preparat gram.[4]
o Rapid test untuk deteksi antigen bakteri mempunyai spesifisitas
dan sensitivitas rendah. Saat ini di RSHS tidak tersedia dan tidak
dilakukan.[4]

e) Pulse oxymetri
o Pengukuran saturasi O2 merupakan pemeriksaan noninvasive yang dapat memperkirakan
oksigenasi arteri.[4]
o Semua anak yang dirawat inap karena pneumonia seharusnya diperiksa pulse oxymetri.[4]
o Pemeriksaan ini sangat dianjurkan untuk negara berkembang dengan keterbatasan sarana
untuk mendeteksi hipoksemia.[4]

DIFFERENTIAL DIAGNOSIS
 Pneumonia must be differentiated from other acute pulmonary diseases, including allergic
pneumonitis, asthma, and cystic fbirosis; cardiac diseases, such as pulmonary edema caused by
heart failure; and autoimmune diseases, such as certain vasculitides and systemic lupus
erythematosus.[1]
 Radiographically pneumonia must be differentiated from lung trauma and contusion,
hemorrhage, foreign body aspiration, and sympathetic effusion due to subdiaphragmatic
inflammation.[1]

MANAGEMENT & TREATMENT

 Therapy for pneumonia includes supportive and specific treatment and depends on the degree of
illness, complications, and knowledge of the infectious agent likely causing the pneumonia.[1]
Most cases of pneumonia in healthy children can be managed on an outpatient basis.[2]
 However, children with hypoxemia, inability to maintain adequate hydration, or moderate to
severe
respiratory distress should be hospitalized.[1]
 Table 400-5 notes the indications for admission to a hospital. [2]
 Hospitalization should be considered in infants under 6 months with suspected bacterial
pneumonia, those in whom there is a concern for a pathogen with increased virulence (e.g.,
methicillin-resistant S. aureus), or when concern exists about a family’s ability to care for the
child and to assess symptom progression.[1]
 Because viruses cause many community-acquired pneumonias in young children, not all children
require empiric antibiotic treatment for pneumonia. [1]
 Recommended therapies in those without recent antibiotic exposure are listed in Table 110.1.[1]
Exceptional situations include lack of response to empiric therapy, unusually severe
presentations, nosocomial pneumonia, and immunocompromised children susceptible to
infections with opportunistic pathogens (Table 110.3).[1]
 Presumed pneumococcal pneumonia can be treated with high-dose ampicillin therapy even with
high-level penicillin resistance.[1]
 Ceftriaxone and/or vancomycin can be used if the isolate shows high-level resistance and the
patient is severely ill.[1]
 For infants 2-18 weeks old with afebrile pneumonia most likely caused by C. trachomatis, a
macrolide is the recommended treatment.[1]
 Oseltamivir or zanamivir should be used if influenza is identified or suspected, ideally within 48
hours of symptom onset.[1]
 Treatment of suspected bacterial pneumonia is based on the presumptive cause and the age and clinical
appearance of the child.[2]
 For mildly ill children who do not require hospitalization, amoxicillin is recommended. With the emergence
of penicillin-resistant pneumococci, high doses of amoxicillin (80-90 mg/kg/24 hr) should be prescribed
unless local data indicate a low prevalence of resistance.[2]
 Therapeutic alternatives include cefuroxime axetil and amoxicillin/clavulanate.[2]
 For school-age children and in children in whom infection with M. pneumoniae or C. pneumoniae is
suggested, a macrolide antibiotic such as azithromycin is an appropriate choice.[2]
 In adolescents, a respiratory floroquinolone (levoflxacin, moxiflxacin) may be considered as an
alternative.[2]
 Despite substantial gains over the past decade, in developing countries only ≈60% of children with
symptoms of pneumonia ( ≈50% in sub-Saharan Africa) are taken to an appropriate caregiver, and less than
one-third receive antibiotics. [2]
 The World Health Organization and other international groups have developed systems to train mothers
and local healthcare providers in the recognition and treatment of pneumonia.[2]
 The empiric treatment of suspected bacterial pneumonia in a hospitalized child requires an approach based
on the clinical manifestations at the time of presentation.[2] In areas without substantial high-level
penicillin resistance among S. pneumoniae, children who are fully immunized against H. inflenzae type b
and S. pneumoniae and are not severely ill should receive ampicillin or penicillin G.[2] For children who
do not meet these criteria, ceftiaxone or cefotaxime should be used.[2]
 If clinical features suggest staphylococcal pneumonia (pneumatoceles, empyema), initial antimicrobial
therapy should also include vancomycin or clindamycin.[2]
 If viral pneumonia is suspected, it is reasonable to withhold antibiotic therapy, especially for those patients
who are mildly ill, have clinical evidence suggesting viral infection, and are in no respiratory distress.
However, up to 30% of patients with known viral infection, particularly inflenza viruses, may have
coexisting bacterial pathogens.[2]
Therefore, if the decision is made to withhold antibiotic therapy on the basis of presumptive diagnosis of a
viral infection, deterioration in clinical status should signal the possibility of superimposed bacterial
infection, and antibiotic therapy should be initiated.[2]
 The optimal duration of antibiotic treatment for pneumonia has not been well-established in controlled
studies.[2] However, antibiotics should generally be continued until the patient has been afebrile for 72 hr,
and the total duration should not be less than 10 days (or 5 days if azithromycin is used).[2] Shorter courses
(5-7 days) may also be effctive, particularly for children managed on an outpatient basis, but further study
is needed.[2]
 Available data do not support prolonged courses of treatment for uncomplicated pneumonia. In developing
countries, oral zinc (10 mg/day for <12 mo, 20 mg/day for ≥12 mo) reduces mortality among children with
clinically defied severe pneumonia.[2]
 Tatalaksana Pneumonia Berat
o Rawat di rumah sakit
o Pemberian oksigen bila saturasi O2 <90%
o Tatalaksana patensi jalan napas
o Pemberian antibiotic
o Terapi demam
 Perawatan Umum di Rumah Sakit
o Terapi oksigen
 Bayi dan anak yang mengalami hipoksia mungkin tidak tampak
sianosis
 Agitasi mungkin menjadi indikasi hipoksia
 Oksigen diberikan pada penderita dengan saturasi oksigen <90%
pada udara kamar untuk mempertahankan saturasi oksigen
≥90%, dan pada penderita dengan distres napas
o Analgetik antipiretik
Anak yang terkena infeksi saluran respiratori bagian bawah akut
 umumnya mengalami pireksia dan dapat merasakan nyeri seperti nyeri
kepala, nyeri dada, nyeri sendi, nyeri perut, dan nyeri telinga.
o Terapi Cairan
 Anak yang tidak mampu mempertahankan asupan cairan akibat sesak
atau kelelahan memerlukan terapi cairan
 Pipa nasogastrik dapat memengaruhi pernapasan dan karena itu
harus dihindari pada anak yang sakit berat, terutama bayi
dengan lubang hidung yang kecil.
 Penderita yang muntah-muntah atau sakit berat memerlukan
cairan i.v.
 Bila diperlukan, cairan i.v. diberikan 80% dari kebutuhan basal
dan perlu dipantau elektrolit serum.
o Pemberian antibiotik
 Antibiotik empiris diberikan berdasarkan usia penderita dan
derajat penyakit.
 Antibiotik yang sesuai harus diberikan segera sesudah penderita
masuk rumah sakit.
 Untuk pneumonia atau bukan pneumonia berat dapat diberikan
kotrimoksazol (8 mg/kgBB/dosis trimetoprim dalam 2 dosis p.o.)
atau amoksisilin 25 mg/kgBB/dosis diberikan tiap 12 jam p.o.
(penelitian menunjukkan amoksisilin dua dosis sehari memiliki
konsentrasi dalam darah yang sama dengan amoksisilin 3
dosis/hr) selama 3–5 hr.
 Efikasi kedua obat sama, kecuali di daerah yang mengalami
resistensi pada salah satu obat.
 Antibiotik parenteral harus diberikan pada anak dengan
pneumonia berat.
 Pilihan pemberian antibiotik inisial pada pneumonia anak
Ampisilin 50 mg/kgBB/dosis i.v. atau i.m. setiap 6 jam yang
harus dipantau dalam 24 jam selama 48–72 jam pertama.
 Bila keadaan klinis berat, pengobatan inisial berupa kombinasi
ampisilin-gentamisin.
  Bayi usia <2 bl atau pneumonia sangat berat, ampisilin dosis di
atas ditambah gentamisin 7,5 mg/kgBB i.v. atau i.m. sekali
sehari.
 Pada keadaan dicurigai meningitis (malas menetek, letargis,
kejang, menangis lemah, fontanel menojol) dan septikemia,
maka obat pilihan pertama adalah sefotaksim atau seftriakson
i.v.
 Sesudah 48 jam pengobatan pneumonia sangat berat tidak
tampak perbaikan, antibiotik diubah menjadi sefalosporin
generasi ketiga, seperti seftriakson dan sefotaksim
o Pneumonia pada anak HIV
 Pada anak bukan pneumonia berat, terapi inisial dengan amoksisilin
oral (25–30 mg/kgBB/dosis, 2×/hr selama 5 hr).
 Penderita memerlukan pemantauan kondisi klinis.
 Pneumonia berat harus dirawat di rumah sakit karena risiko tinggi
cepat perburukan dan kegagalan terapi.
 Pemberian antibiotik inisial harus memerhatikan pemberian antibiotik
sebelumnya dan prevalensi resistensi antibiotik di daerah tersebut
 Ampisilin dan gentamisin dapat diberikan selama 10 hr. Bila tidak ada
respons, antibiotik dapat diganti dengan seftriakson
atau sefotaksim
 Jika diduga infeksi S. aureus dapat diberikan kloksasilin dan
gentamisin
 Pada anak usia <1 th dengan pneumonia berat dapat diterapi
secara empiris dengan kotrimoksazol i.v. (15–20 mg/kgBB/hr
komponen trimetoprim) dalam tiga atau empat dosis terbagi
diinfus dalam 1 jam selama 21 hr.
 Terapi kotrimoksazol oral diberikan pada penyakit yang ringan
atau sedang atau bila sudah terjadi perbaikan.
 Perbaikan klinis biasanya lambat, membutuhkan 5–7 hr
  Kortikosteroid sudah terbukti menurunkan ketergantungan O2
dan mortalitas penderita HIV dewasa bila diberikan dalam 72
jam pemberian terapi kotrimoksazol.
 Hal ini belum dapat dibuktikan pada anak, tetapi mungkin
efektif pada dosis 1 mg/kgBB/hr selama 7 hr dan kemudian
ditappering selama 7 hr berikutnya.
o Pneumonia pada anak malnutrisi berat
Ampisilin dan gentamisin merupakan antibiotik inisial
Terapi suportif seperti mempertahankan suhu, pencegahan
hipoglikemia, dan pemberian nutrisi yang tepat sangat penting
untuk memperoleh hasil terapi yang baik
o Pemantauan
 Sesudah pemberian antibiotik inisial, pantau dalam 24 jam
selama 48–72 jam pertama.
 Apabila kondisi klinis membaik; tidak didapatkan tanda sepsis,
empiema, necrotizing pneumonia, dan abses paru; tanda vital stabil
selama min. 48 jam; biakan darah tidak menunjukkan pertumbuhan
kuman; dan dapat makan/minum p.o. maka:
 Antibiotik i.v dapat diganti dengan antibiotik oral. Umumnya
peralihan ke antibiotik oral dilakukan sesudah 2–4 hr pemberian
antibiotik i.v.
 Selanjutnya, terapi dilanjutkan di rumah dengan amoksisilin p.o. (15
mg/kgBB/kali 3×/hr).
 Pemberian antibiotik pada pneumonia berat dilanjutkan sampai 5–7
hr atau kepustakaan lain menyatakan 7−10 hr, dan pada pneumonia
sangat berat diberikan selama 7–10 hr atau kepustakaan lain
menyatakan 10–14 hr.
o Apabila:
 Demam atau manifestasi klinis lainnya menetap sesudah 48 jam
pemberian antibiotik, atau keadaan klinis memburuk sebelum 48 jam,
atau terdapat keadaan yang berat (tidak dapat menyusu atau
minum/makan, atau memuntahkan semuanya, kejang, letargis atau
 tidak sadar, sianosis, distress pernapasan berat) maka terapi harus
dievaluasi kembali dan dipertimbangkan foto Rontgen toraks ulang.
 Tambahkan kloramfenikol 25 mg/kgBB/kali i.m. atau i.v. setiap 8 jam
atau gentamisin 7,5 mg/kgBB i.v. atau i.m. 1×/hr.
 Apabila terjadi kegagalan terapi pada penderita yang diberi
kotrimoksazol, diganti dengan amoksisilin
 Jika obat pertama yang diberikan adalah amoksisilin, maka bila terjadi
kegagalan terapi dapat ditambahkan gentamisin atau diganti dengan
amoksisilin-asam klavulanat (80−90 mg/kgBB/hr amoksisilin dalam
dosis terbagi dengan maks. 6,4 mg/kgBB/hr asam klavulanat) untuk
meningkatkan aktivitas terhadap Haemophilus influenzae penghasil β-
laktamase dan S. pneumoniae yang resisten
 Bila terjadi kegagalan terapi berikutnya, sefalosporin generasi ke-2
(sefuroksim) atau generasi ke-3 (seftriakson, sefopodoksim) dapat
digunakan untuk memperluas cakupan terhadap organisme penghasil
β-laktamase.
 Apabila diduga pneumonia stafilokokal, ganti antibiotic dengan
gentamisin (7,5 mg/kgBB i.m. 1×/hr) dan kloksasilin (50 mg/kgBB i.m.
atau i.v. setiap 6 jam). Bila keadaan anak membaik, lanjutkan
kloksasilin (atau dikloksasilin) secara oral 4×/hr sampai mencapai 3
mgg, atau klindamisin secara oral selama 2 mgg.
 Pilihan antibiotik selanjutnya berdasarkan hasil pemeriksaan
pola kepekaan antibiotic.
o Indikasi Penderita Dipulangkan
 Perbaikan secara klinis, nafsu makan membaik, bebas demam 12–24
jam,
 stabil,
 saturasi O2 >92% dalam udara ruangan selama 12–24 jam (tanpa O2),
 orangtua sudah mengerti untuk melanjutkan pemberian antibiotik
oral

Pencegahan
  Vaksinasi dengan vaksin pertusis (DTP), campak, pneumokokus, dan
H. influenza
 Vaksin influenza untuk bayi >6 bl dan usia remaja
 Untuk orangtua atau pengasuh bayi <6 bl disarankan untuk diberikan vaksin
influenza dan pertusis
 Makan bergizi
 Jaga kebersihan

Revised WHO Recommendation of Treatment

Oral amoxicillin is preferable to oral cotrimoxazole for the treatment of “fast
breathing pneumonia” and is equivalent to injectable penicillin/ampicillin in cases of “chest
indrawing pneumonia”. Hence, in a programmatic context, the distinction between
previously defined “pneumonia” (fast breathing) and “severe pneumonia” (chest indrawing)
loses its significance. The new classification is therefore simplified to include only two
categories of pneumonia; “pneumonia” with fast breathing and/or chest indrawing, which
requires home therapy with oral amoxicillin, and “severe pneumonia”, pneumonia with any
general danger sign, which requires referral and injectable therapy. Dosages for pneumonia
treatment at health facilities have been revised to reflect three age bands: 2 months up to
12 months (4–<10 kg); 12 months up to 3 years (10–<14 kg); 3 years up to 5 years (14–19
kg). Dosages and age bands for treatment of fast breathing pneumonia by community
health workers (CHWs) have not changed.
Recommendation 1
Children with fast breathing pneumonia with no chest indrawing or general danger sign should be
treated with oral amoxicillin: at least 40mg/kg/dose twice daily (80mg/kg/day) for five days. In
areas with low HIV prevalence, give amoxicillin for three days.
Children with fast-breathing pneumonia who fail on fist-line treatment with amoxicillin should
have the option of referral to a facility where there is appropriate second-line treatment.
Recommendation 2
Children age 2–59 months with chest indrawing pneumonia should be treated with oral amoxicillin: at least
40mg/kg/dose twice daily for five days.
Recommendation 3
Children aged 2–59 months with severe pneumonia should be treated with parenteral ampicillin
(or penicillin) and gentamicin as a first-line treatment.
— Ampicillin: 50 mg/kg, or benzyl penicillin: 50 000 units per kg IM/IV every 6 hours for at least
five days
— Gentamicin: 7.5 mg/kg IM/IV once a day for at least five days
Ceftriaxone should be used as a second-line treatment in children with severe pneumonia having
failed on the first-line treatment.
Recommendation 4
Ampicillin (or penicillin when ampicillin is not available) plus gentamicin or ceftriaxone are recommended as a
fist-line antibiotic regimen for HIV-infected and -exposed infants and for children
under 5 years of age with chest indrawing pneumonia or severe pneumonia.
For HIV-infected and -exposed infants and for children with chest indrawing pneumonia or severe
pneumonia, who do not respond to treatment with ampicillin or penicillin plus gentamicin, ceftriaxone alone is
recommended for use as second-line treatment.
Recommendation 5
Empiric cotrimoxazole treatment for suspected Pneumocystis jirovecii (previously Pneumocystis
carinii) pneumonia (PCP) is recommended as an additional treatment for HIV-infected and -exposed
infants aged from 2 months up to 1 year with chest indrawing or severe pneumonia.
Empirical cotrimoxazole treatment for Pneumocystis jirovecii pneumonia (PCP) is not recommended for HIV-
infected and -exposed children over 1 year of age with chest indrawing or severe
pneumonia.