Professional Documents
Culture Documents
(community or hospital)
local epidemiology
(underlying diseases,
malnutrition)
immunologic status
Mekanisme pertahanan
Saluran Napas Atas Saluran Napas bawah
o Rongga hidung o Refleks epiglotis
o Bulu hidung o Gerakan silia
o Lapisan mukus o Sekret sal napas
o Gerakan silia o Aliran limpe
o IgA Sal. napas. bronchus terminalis
o Enzim lisozim. ke bronkiolus
o Reflek batuk. o Sel fagosit alveoli
o Organ2 RES o Flora normal
Patofisiologi
Mekanisme
Kuman masuk ke
pertahanan
saluran napas atas
terganggu
Terbentuk
sekret virulen
Sekret berlebih
Inflamasi turun
ke alveoli
Stadium Inflamasi
Stadium Kongesti
o Kapiler kongesti dan melebar
Hepatisasi merah
o Terjadi reaksi jaringan yang mempermudah
proliferasi dan penyebaran kuman ke jaringan
sekitarnya.
o Bagian paru yang terkena mengalami konsolidasi
o Ditemukan kuman di alveoli
stadium inflamasi
Hepatisasi Kelabu
o Deposisi fibrin semakin bertambah
o Terdapat fibrin dan leukosit PMN di alveoli
o Terjadi proses fagositosis yang cepat
Resolusi
o Jumlah makrofag meningkat di alveoli
o Sel akan mengalami degenerasi
o Fibrin menipis
o Kuman dan debris menghilang
Asinus terisi eksudat dan infiltrasi
Sel radang kedalam alveoli
Manifestasi Klin
Sebagian besar gambaran klinis
pneumonia pada anak berkisar antara
ringan hingga sedang, sehingga dapat
berobat jalan saja
Takipnea
Ronki
Sianosis
Gejala pada Balita dan Anak lebih besa
C-Reaktive Protein(CRP)
Uji Serologis
Pemeriksaan Mikrobiologis
Pemeriksaan Radiologis
Darah Perifer Lengkap
Leukositosis :15-40 K/mm3 predominan PMN
Leukopenia :<5 K/mm3
Pada infeksi Chlamydia pneumonia kadang-
kadang ditemukan eosinofilia
Pemeriksaan DL & LED tidak dapat
membedakan antara infeksi virus dan infeksi
bakteri secara pasti
C- Reactive Protein (CRP)
Suatu protein fase akut yang disintesis
oleh hepatosit. Sebagai respons infeksi
atau inflamasi jaringan
Female infant, 0,3 y, cxr. alveolar infiltrates Male boy, 1,9 y, cxr alveolar infiltrates in
in upper right lobe ec parainfluenza and right lobe ec. S pneumoniae: IgG
human herpes virus, leucocytois 17000, ESR pneumolysin increased, leucocytosi 13.800,
8 mm/ h l, CRP 22 mg/l ESR 125/h I, CRP 332 mg/l.
Diagnosis
Prediktor paling kuat pneumonia adalah
demam, sianosis, dan lebih dari satu
gejala respiratori sebagai berikut :
o Takipnea
o Batuk
o Napas cuping hidung
o Retraksi
o Ronki
o Suara napas melemah
Sensitivity and specificity of
symptoms for identifying pneumonia
Toxic appearance 81 % 60 %
Crackles 44 % 80 %
Retractions 35 % 82 %
Flaring 35 % 82 %
Pallor 35 % 87 %
Grunting 19 % 94 %
Fast breathing
(tachypnea)
Respiratory thresholds
Age Breaths/minute
< 2 months 60
2 - 12 months 50
1 - 5 years 40
Terapi suportif
1. Cegah BBLR
2. Pemberian makanan bergizi/ gizi seimbang/
Pemberian ASI Eksklusif
3. Pemberian Imunisasi
a) Vaksin Campak
b) Vaksin Pertusis
c) Vaksin Hib
d) Vaksin Pneumokokus
Tindakan Preventif
Komplikasi
5 to 16 years old
Investigations
Management of pneumonia in children (cont)
(Alberta Clinical Practice Guideline, 2002)
Investigations
Chest X-ray is considered gold standard
Pulse oximetry for child with signs of tachypnea or hypoxemia
CBC with differential and blood cultures
Gram stain and culture of sputum (older children)
Mycoplasma IgM may be considered ( > 2 yrs old)
Cold agglutinins are limited value in the diagnosis of M pneumonia
RSV testing is not routinely recommended
No Yes
Radiographic patterns
1. Diffuse alveolar and interstitial pneumonia
(perivascular and interalveolar changes)
2. Bronchopneumonia
(inflammation of airways and parenchyma)
3. Lobar pneumonia
(consolidation in a whole lobe)
4. Nodular, cavity or abscess lesions
(esp.in immunocompromised patients)
Management of pneumonia in children (cont)
(Alberta Clinical Practice Guideline, 2002)
No Yes
General Management
Analgesic/antipyretics Decision to hospitalize and
Hydration in-patient management
Oxygen therapy
Patient with pleural effusion Out-patient management (3 mos - 5 yrs)
should be referred Amoxicillin (standard or high dose)*
Pleural empyema should Beta-lactam allergy:
be drained Azithromycin OR
Chest physiotherapy is Clarithromycin
controversial + Out-patient management (5 to 16 yrs)
Cough suppressants are NOT Azithromycin OR
routinely recommended Clarithromycin OR
Mukolitik ? Erythromycin
Follow up
In patients with uncomplicated pneumonia, repeat chest X-rays are unwarranted
In patients with pleural effusions, pneumatoceles or pulmonary abscess,
a repeat chest X-rays should be done
Antibiotic management of pneumonia: In-patient
(Alberta Clinical Practice Guideline, 2002)
In hospital 1 to 3 months pneumonitis syndrome Critically Ill
Azithromycin : 10 mg/kg PO 1st day then
Azithromycin 10 mg/kg IV (max 500 mg)
5 mg/kg/day for 4 days OR
1st day then 5-10 mg/kg/day IV
Clarithromycin 15 mg/kg/day PO
for 4 days OR
div bid for 10-14 days OR
Erythromycin 40 mg/kg/day IV div Q6h for
Erythromycin 40 mg/kg/day PO
10 to 14 days
div qid for 10-14 days
3 months to 5 years
[Cefuroxime 150 mg/kg/day IV div Q8h PLUS
Cefuroxime 150 mg/kg/day IV Erythromycin 40 mg/kg/day IV div Q6h for
div Q8h for 10-14 days 10-14 days] OR
[Cefotaxime 200 mg/kg/day IV div Q8h PLUS
Cloxacillin 150-200 mg/kg/day IV div Q6h for
10 to 14 days]
5 to 16 years
[Cefuroxime 150 mg/kg/day IV div Q8h PLUS [Cefuroxime 150 mg/kg/day IV div Q8h PLUS
Erythromycin 40 mg/kg/day IV/PO div Q6h for Erythromycin 40 mg/kg/day IV/PO div
10 to 14 days] Q6h for 10 to 14 days]
Atypical pneumonia
History:
Since Pasteur isolated S pneumoniae (1880) and Frankel
described D pneumoniae (1884) as a cause of pneumonia, the
clinical picture of pneumonia was recognized as typical:
1) sudden onset of fever and shaking chills, pleuritic chest pain and
production of rust-colored sputum and
2) radiologic evidence of segmental or lobar consolidation.
3) examination of sputum showed gram-positive diplococci in
chains, both intracellulary and extracellulary.
The typical patients evolved in recognizable result , either death
or recovered. Death was as result of crisis, during which temp rose
suddenly, reaching 39,4 to 40 oC and accompanied with severe
delirium, respiratory failure. Or patient could be recovered by lysis
mechanism: fever gradually diminished, dropping to normal
temperature and slowly regained to previous health.
Atypical pneumonia
In 1934, Gallagher described an outbreak of bronchopneumonia in
a group of 16 boys living at a preparatory school. He stressed
that these children did not have pneumococcal pneumonia but
something different something atypical.
In 1938, Reimann also described a group of eight patients with
chest infection but atypical clinical presentations and no chest
pain such as a gradual onset, a prodromal consisting headache,
photophobia, sore throat and dry cough.
Although the patients were not feeling well, they were not
critically ill. Their sputum was scanty and did not contain
pneumococci;white blood cell counts was normal and without
neutrophilic preponderance and shift to the left.
He called the term atypical pneumonia
Atypical pneumonia
1944: Eaton et al isolated a filtrable agent from a patient with
atypical pneumonia known as Eaton agent.
1960 1963 : Chanock et al were able to grow the Eaton agent
and transmit it to human volunteers.They designated the
organism as a member of a new genus and named it Mycoplasma
pneumoniae.
After that many agent were recognized causing atypical
pneumonia such as :
Chlamydia spp,
Legionella pneumophilia.
Ureaplasma urealyticum
Etc.
Atypical pneumonia
Characterized by
Insidious onset, fever, nonproductive cough, and
prominent constitutional signs ( severe headache,
malaise, myalgias)
CXR interstitial inflammation, patchy infiltrates
Less common leucocytosis
Lesser mortality, walking pneumonia
Routine culture fails to reveal microbial causes
Do not respond to common antibiotics used
Initial empirical treatment based on age
and severity of pneumonia
Outpatients
Age Inpatients (Moderate) Inpatients (Severe)
(Mild to Moderate)
Amoxicillin with or
Ceftriaxone or cefotaxime
3 - 6 mos without clavulanate Ceftriaxone or cefotaxim
+ vancomycin
Erythromycin