PNEUMONIA

K-3B

Dr. Abdul Rohman, SpP

 DEFINITION
an infection of peripheral lung
parenchyma
Suatu peradangan paru disebabkan mikroorganisme (bakteri,
virus, jamur, parasit)

Radang parenkim paru, distal bronkus terminalis

 konsolidasi jar paru dan gangguan pertukaran
gas setempat
Clinically an acute illness in which there are
signs of consolidation in the chest or new
changes on chest x-ray

Radang paru ok nonmikroorganisme (bahan kimia, radiasi, aspirasi

bahan toksik, obat-obatan, dll)  pneumonitis

infection of the central conducting

airways  bronchitis
 PATOGENESIS
Mikroorganisme Lingkungan
Host

DEFENSE
Physical, Humoral & Cellular
FAKTOR RISIKO CARA
• Alkohol • I NOKULASI langsung
•
• Merokok •
INHALASI
HEMATOGEN
• Peny. kronik: • KOLONISASI (terbanyak)
- Jantung & Paru
• Obstruksi bronkus - Red hepatization : 2 – 4 days
• Immunosupressi - Gray hepatization : 4 – 8 days
• Drug abuse - Resolution : > 8 – 10 days
Figure : Host defense in the respiratory tract
Figure : Factor that interfere with host defence of respiratory tract
 kongesti
Red hepatization
(Udara di alveolus hilang diganti
dengan eksudat yang membeku

Gray
hepatization

Resolusi
 STADIUM PATOLOGI ANATOMI KLINIK

Prodromal Alveolus terisi sekrit Tanda-tanda prodromal

(Minggu 0–1) yang terinfeksi infeksi akut

Hepatisasi Sebukan sel-sel PMN  Restriksi  Fungsi pernafasan 

(Minggu 1-3) alveolus padat, infeksi Demam  Radang menyebar ke
akut  Restriksi + pleura viscerlis Nyeri dada (tidur
demam miring kesisi yang sehat) Ekspansi
paru terhambat  sesak nafas.
Batuk  /Batuk darah +/-
Obstruksi bronkus  Wheezing
Toraks yang sakit (pernafasan
tertinggal, fremitus  suara nafas
bronkeal, ronki basah kasar)
Dehidrasi +/-
Resolusi Alveolus melunak Demam  , Batuk produktif, Ronki
(Minggu 3-) berubah menjadi dahak basah halus +/-
Table : Common Causes of Acute Pneumonia
Key Points : About the Classification of Pneumonia
 ETIOLOGY
• Jenis pneumonia

 Pneumonia komuniti (PK/CAP) : bakteri Gram positif

 Pneumonia nosokomial : bakteri Gram negatif

 Pneumonia aspirasi : bakteri anaerob

• Cara penularan

o Droplet  Steptococcus pneumoniae

o Slang infus  Staphylococcus aureus

oVentilator  P. aerugenusa dan Enterobacter

 ETIOLOGI

Pejamu  Faktor Modifikasi

Lingkungan :luar or dalam RS,
ICU atau non ICU
KEY POINTS : MOST COMMON PATHOGENS
FOR CAP
• (IN DESCENDING ORDER)

1. Pneumococcus species

2. Haemophilus influenzae

3. Atypical pathogens (coinfection possible)

4. Enteric gram-negative organisms

5. Staphylococcus aureus (especially after influenza)

 KLASIFIKASI
1. Klinis dan Epidemiologis
a. Pneumonia komuniti (community-acquired pneumonia)
b. Pneumonia nosokomial (nosocomial pneumonia) : - HAP
c. Pneumonia aspirasi - VAP
d. Pneumonia pada penderita immunocompromised. - HCAP

2. Bakteri Penyebab
a. Pneumonia bakterial/ tipikal
b. Pneumonia atipikal  penyebab: Mycoplasma, Legionella dan Chlamydia
c. Pneumonia virus
d. Pneumonia jamur  infeksi sekunder pd pend immunocompromised
3. Berdasarkan predileksi infeksi
a. Pneumonia (Pneumonia lobaris)
- Sering pada pneumonia bakterial
- Jarang pada bayi dan orang tua aspirasi benda asing

- Terjadi pada satu lobus/ segmen : sekunder  obstruksi bronkus

b. Bronkopneumonia (Pneumonia lobularis = diffuse) keganasan

- Dapat oleh bakteri maupun virus

- Sering pada bayi dan orang tua
- Pada lapangan paru & jarang dihub dgn obstruksi bronkus
c. Pneumonia interstisial
 DIAGNOSIS
• Should not be made on history & physical finding alone,
a chest X-ray should be taken
(In situations where chest x-ray is not possible, clinical
prediction rules (eg history, physical exam, presence of
fever, tachypnea, etc) may be used
• Pulmonary TB needs to be considered & rule out esp in
elderly patients
• Patients w/ HIV may present w/ PCP or pulmonary TB
 DIAGNOSIS
1. Gambaran Klinis
a. Anamnesis
- Demam, menggigil, suhu s/d > 40°C
- Batuk : kering – mukoid – purulen – kadang disertai darah
(rusty in color and frankly bloody)
- Nyeri dada pleuritik, sesak napas
b. Pemeriksaan fisis tergantung luas lesi di paru
- Inspeksi : tertinggal waktu napas
- Palpasi : fremitus suara mengeras
- Perkusi : redup
- Auskultasi : bronkovesikuler – bronkial
ronki basah halus  kasar pd stad resolusi
 These crackles and bronchial breathing were recorded posteriorly over the
consolidated left lower lung of a 16 year old boy with tuberculosis.

The respirosonogram provides a visual representation of the content of the respiratory

sound recording. Time is shown on the horizontal and frequency on the vertical axis.
Sound intensity is indicated on a color scale, ranging from red (loud) over yellow and
light green (medium) to dark green and gray (low). Calibrated air flow is displayed at
the top (I = inspiration, above zero; E = expiration, below zero).
These late inspiratory fine crackles were recorded over the right posterior lower
lung of a 55 year old woman with rheumatoid lung disease.

The respirosonogram provides a visual representation of the content of the

respiratory sound recording. Time is shown on the horizontal and frequency on the
vertical axis. Sound intensity is indicated on a color scale, ranging from red (loud)
over yellow and light green (medium) to dark green and gray (low). Calibrated air
flow is displayed at the top (I = inspiration, above zero; E = expiration, below zero).
These crackles were recorded over the right posterior lower chest of a 9 year old
boy with pneumonia.

The respirosonogram provides a visual representation of the content of the respiratory

sound recording. Time is shown on the horizontal and frequency on the vertical axis.
Sound intensity is indicated on a color scale, ranging from red (loud) over yellow and
light green (medium) to dark green and gray (low). Calibrated air flow is displayed at
the top (I = inspiration, above zero; E = expiration, below zero).
 TYPICAL SYMPTOMS OF CAP
• Fever
• New cough w/ or w/o sputum production
• Change in color of sputum in patients w/
chronic cough
• Pleutitic chest pain
• Shortness of breath
 Typical clinical features of bacterial pneumonia
Clinical features Incidence (%)

Respiratory features
cough 90
sputum 70
dyspnea 70
chest pain 65
upper respiratory tract symptoms 33
hemoptysis 13
Nonrespiratory
vomiting 20
confusion 15
diarrhea 15
rash 5
abdominal pain 5
 Typical clinical features of bacterial pneumonia
Clinical features Incidence (%)
Signs
80 – 90
fever
80 – 90
tachypnea
80 – 90
tachycardia
80 – 90
abnormal chest signs
20
hypotension
15
confusion
10
herpes labialis
 DIAGNOSIS
2. Pemeriksaan Penunjang
a. Gambaran radiologis
 Foto toraks (PA / lateral) penunjang utama diagnosis :
infiltrat – konsolidasi dg “air bronchogram”, interstisial serta gambaran kaviti.
 Foto toraks  petunjuk kearah diagnosis etiologi :
- Pneumonia lobaris  Streptokokus pneumoniae
-Infiltrat bilateral/bronkopneumonia  Pseudomonas aeruginosa

b. Pemeriksaan laboratorium
- Leukosit > 10.000 - 30.000 atau  4.500
- Hitung jenis leukosit  pergeseran ke kiri dan peningkatan LED
- Diagnosis etiologi : dahak, kultur darah, dan serologi
- Kultur darah positif : 20 -25 % penderita tidak terobati
- Analisa gas darah  hipoksemia dan hipokarbia
- Stadium lanjut  asidosis respiratorik
• Lobar pneumonia
Refers to a homogeneous radiologic density that involves a distinct anatomic segment of the lung.
Infection originates in the alveoli. As it spreads, this form of infection respects the anatomic boundaries
of the lung and does not cross the fissures. Most commonly seen with S. pneumoniae, H. influenzae, and
Legionella.

• Bronchopneumonia
The bronchopneumonia form of pulmonary infection originates in the small airways and spreads to adjacent areas.
Infiltrates tend to be patchy, to involve multiple areas of the lung, and to extend along bronchi. Infiltrates are not
confined by the pulmonary fissures. Commonly observed with S. aureus, gram-negative bacilli, Mycoplasma, Chlamydia,
and respiratory viruses.

• Interstitial pneumonia
Infection causing inflammation of the lung interstitium result in a fine diffuse granular infiltrate. Influenza and
cytomegalovirus commonly present with this CXR pattern. In AIDS patients, Pneumocystic jirovecii infection results in
interstitial inflammation combined with increased alveolar fluid that can mimic cardiogenic pulmonary edema. Miliary
TB commonly presents with micronodular interstitial infiltrates.

• lung abscess
Anaerobic pulmonary infections often cause extensive tissue necrosis, resulting in loss of tissue and formation of
cavities filled with inflammatory exudate. S. aureus also cause tissue necrosis and can form cavitary lesions.
• noduler lesions
Histoplasmosis, coccidiomycosis, and cryptococcosis can present as nodular lung lesions (multiple or single) on CXR.
Hematogenous pneumonia resulting from right-sided endocarditis commonly presents with “cannonball” lesions that
can mimic metastatic carcinoma
 PNEUMONIA KOMUNITI
(DIDAPAT DI MASYARAKAT)

ETIOLOGI
- Kepustakaan : Gram pos. & bakteri atipik
- Indonesia : Gram negatip (beberapa kota)
- Klebsiella pneumoniae 45,18 % - Pseudomonas aerugenosa 8, 56 %
- Streptococcus pneumoniae 14,04 % - Streptococcus hemolyticus 7,89 %
- Streptococcus viridans 9,21 % - Enterobacter 5, 26 %
-Staphylococcus aureus 9, 00% - Pseudomonas spp 0, 90 %
-
-
 Essential of diagnosis
• Symptoms and signs of an acute lung infection:
fever or hypothermia, cough with or without
sputum, dyspnea, chest discomfort, sweats,or
rigors.
• Bronchial breath sounds or rales are freqent
auscultary findings.
• Parenchymal infiltrate on chest radiograph.
• Occur outside of the hospital or less than 48 hours
after admission in patient who is not hospitalized
or residing in a long-term care facility for more
than 14 days before the onset of symptoms.
 DIAGNOSIS PASTI

Foto Rö : infiltrat baru atau infiltrat progresif +

2 atau lebih gejala dibawah :

 Batuk-batuk bertambah
 Perubahan karakteristik dahak/purulen
 Suhu ≥ 38 °C (aksila)/ riwayat demam
 Fisik : tanda konsolidasi, bronkial & ronki
 Leukosit ≥ 10.000 atau < 4.500
Faktor modifikasi  meningkatkan risiko infeksi
mikroorganisme patogen
spesifik

1. Pneumokokus resisten terhadap penisilin

Umur > 65 tahun
Memakai obat-obatan gol  laktam
selama 3 bulan terakhir
Pecandu alkohol
Penyakit gangguan kekebalan
Penyakit penyerta yang multipel
2. Bakteri enterik Gram negatif

Penghuni rumah jompo

Mempunyai penyakit dasar kelainan
jantung paru
Mempunyai kelainan penyakit yang
multipel
Riwayat pengobatan antibiotik
3. Pseudomonas aeruginosa

 Kelainan Struktural : Bronkiektasis

 Pengobatan kortikosteroid > 10
mg/hari
 Pengobatan antibiotik spektrum luas
> 7 hari pada bulan terakhir
 Gizi kurang ( malnutrisi )
 MODIFYING FACTORS THAT INCREASE THE RISK OF
INFECTION W/ SPESIFIC PATHOGENS
Patogen Penincillin & Drug- Enteric Gram-ve Pseudomonas
Resistant Organism aeruginosa
Pneumococcl
Factors • Age > 65 year • Cardiopulmonary • Structural lung disease
• -lactam use within • Nursing home (bronchiectasis)
the last 3 month resident • Prolonged
• Alcoholism • Multiple medical corticosteroid therapy
• Immunosuppresion comorbidities (> 10 mg
• Multiple medical • Recent antibiotic prednisolone/day)
comorbidities therapy • Broad-spectrum
• Exposure to child in antibiotic therapy > 7
daycare center days in the past month
• Malnutrition
 SKEMA LANGKAH PERTAMA RUMUS PREDIKSI PNEUMONIA :
MENDETEKSI PASIEN DENGAN KELAS RESIKO I
Pasien PK

Usia  50 Th ……………………..ya………………………………………..

Tidak

Adakah R/ ko-morbid
- Neoplasma Pasien masuk dalam kelas
- Gagal jantung kongestif ……………Ya…………………. resiko II-IV sesuai langkah
- Peny. Serebrovaskuler ke 2/ sistim skor rumus
- Peny. Ginjal prediksi
- Peny. Hati

Tidak

Adakah kelainan pd pemeriks fisik ..…… ya

- Perub. Status mental - Nadi  125x/mnt Kelas
- Pernapasan  30/mnt - Tek. Sistolik  90 mmHg.............. Tidak Resiko I
- Suhu  35°C atau  40°C
 Langkah 2 rumus prediksi pneumoni Sistem skor u/ deteksi pend dgn kelas resiko II-IV
Karakteristik penderita Jumlah poin
 Faktor demografi
• Usia : laki-laki Umur (tahun)
perempuan Umur (tahun) – 10
• Perawatan di rumah + 10
• Penyakit penyerta
Keganasan + 30
Penyakit hati + 20
Gagal jantung kongestif + 10
Peny. serebrovaskuler + 10
Penyakit ginjal + 10
 Pemeriksaan fisis
• Perub. status mental + 20
• Pernapasan ≥ 30 kali/menit + 20
• Tekanan darah sitolik ≤ 90mmHg + 20
• Suhu tubuh < 35°C atau ≥ 40° C + 15
• Nadi ≥ 125 kali/menit + 10
 Hasil laboratorium / Radiologi
• Analisis gas darah arteri : pH 7,35 + 30
• BUN > 30 mg/dL + 20
• Natrium < 130 mEq/liter + 20
• Glukosa > 250 mg/dL + 10
• Hematokrit < 30% + 10
• PO2 ≤ 60 mmHg + 10
• Efusi pleura + 10
SKOR MENURUT SISTEM PORT
(Pneumonia Patient Outcome Research Team)
 Stratification of Risk Score
Risk Risk class Based on Algorithm

I
Low II  70 total points
III 71-90
Moderate IV 91-130
High V  130
Kriteria indikasi rawat inap PK berdasarkan kesepakatan PDPI:

1. Skor PORT > 70 (Pneumonia Patient Outcome Research Team)

2. Skor PORT ≤ 70  tetap dirawat inap jika ada satu dari kriteria:

• Frekuensi napas > 30/menit

• PaO2/FiO2 kurang dari 250 mmHg

• Foto toraks paru menunjukkan kelainan bilateral

• Foto toraks paru melibatkan > 2 lobus

• Tekanan sistolik < 90 mmHg

• Tekanan diastolik < 60 mmHg

3. Pneumonia pada pengguna NAPZA

Another prognostic tool has been used to avoid overlooking a serious ill
patients. This rule named CURB-65, defines a patient as being ill (i.e.
having at least a 10 % risk of death) and probably needing
hospitalisation if at least two of five criteria are present
• Confusion
• Blood Urea > 7 mmol/L (ie blood urea nitrogen (BUN) of 19,6 mg/dL)
• Respiratory rate > 30 breaths/min
• Blood pressure of <90 mmHg systolic or <60 mmHg diastolic
• Age > 65 years

If three criteria are present, the patient is at an even greater risk of dying
and may need admission to the ICU. This rule is simple to use and is
based on clinical criteria that are generally available when the patient is
first evaluated
 CURB-65
Clinical features Score

Confusion (defined as a Mental Test Score of 8, or 1

disorientation in person, place, or time)
Uremia: blood urea > 7 mmol/L (20 mg/dL) 1

Respiratory rate: > 30 breaths/minute 1

Blood pressure: systolic < 90 mm Hg or diastolic < 60 mmHg 1

Age 65 years 1
 Penatalaksanaan berdasarkan CURB-65
Score Group Treatment Options

0 or 1 Group 1 : Low risk, consider home treatment

mortality low
(14,5%)

2 Group 2 : Consider hospital-supervised treatment

mortality
intermediate
(40%)
3 Group 3 : Manage in hospital as severe
mortality high pneumonia consider admission to
(52%) intensive care unit, especially with
CURB score of 4 or 5.
 KRITERIA PERAWATAN INTENSIF

 Minimal 1 dari 2 gejala mayor tertentu 

1. Butuh ventilasi mekanik
2. Butuh vasopresor  4 jam (syok septik)
ATAU
 2 dari 3 gejala minor tertentu 
1. PaO₂/FiO₂ < 250 mmHg
2. Foto dada : kelainan bilateral
3. Tekanan sistolik < 90 mmHg
Criteria for clinically stable:

Temperature ≤ 37,8 °C
Heart rate ≤ 100 beats/min
Respiratory rate ≤ 24 times/min
Systolic blood pressure ≥ 90 mmHg
Arterial saturation oxygen ≥ 90 % or ≥ 60 mmHg on room air
Ability to maintain intake
Normal mental status
 Anamnesis, pemeriksaan fisis, foto toraks

Tidak ada infiltrat Infiltrat + gejala klinis yg menyokong diagnosis pneumonia

Di tatalaksana sbg diagnosis Evaluasi untuk kriteria rawat jalan/ rawat inap
lain
Rawat jalan Rawat inap

Terapi empiris Pemeriksaan bakteriologis

R. Rawat biasa R. Rawat intensif

Membaik Memburuk

Terapi empiris

Terapi
Membaik Memburuk
Terapi empiris dilanjutkan kausatif
 TERAPI EMPIRIK PK
1. Sehat :  Gram  (Kota besar : ada Gram )
2. Komorbid : Gram  ditambah Gram 
3. Faktor modifikasi :
a. Pneumokokus resisten terhadap penisilin
b. Bakteri enterik Gram 
c. Pseudomonas aerogenosa

Kesemuanya dapat ditambahkan makrolid baru

(kecurigaan adanya bakteri atipik)
 PENGOBATAN
A. Antibiotika

 Berdasarkan data mikroorganisme dan hasil uji pekaan

perlu waktu relatif lama (minimal 1 minggu)
 Terapi empiris dengan syarat
- Penyakit berat dapat mengancam jiwa
- Bakteri patogen hasil isolasi belum tentu penyebab
pneumonia
- Hasil biakan bakteri perlu waktu
 Segera diberikan tanpa menunggu hasil kultur
Epidemiologis : > 4 jam  angka morbiditas & mortalitas 
Key Point : About Treatment and Outcome 0f Pneumonia
 TERAPI SULIH (SWITCH THERAPY)
• Perubahan obat : suntik  oral  obat jalan
o Masa perawatan dipersingkat
o Biaya perawatan kurang
o Mencegah infeksi nosokomial
• Ketersediaan obat iv – obat oral & efektifitas imbang
 Streamline – obat disesuaikan hasil kultur
 Sekuensial (obat sama, potensi sama) : levofloksasin, moksifloksn, gatifloksasin
 Switch over (obat berbeda, potensi sama: seftasidim iv ke siprofloksasin
 Step down ( obat sama/beda, potensi  rendah: amoksilin, sefuroksim,
sefotaksim iv ke sefiksim oral
• Obat suntik 2-3 hari  hari 4 obat oral & penderita berobat jalan
 Kriteria Terapi Sulih
• Tidak ada indikasi untuk pemberian iv lagi
• Tidak ada kelainan pada penyerapan sal
cerna
• Penderita sudah tidak panas  8 jam
• Gejala klinis membaik : frek. napas, batuk
• Lekosit menuju normal atau normal
B. Suportif

1. O₂  PaO₂ 80-100 mmHg atau SaO₂ 95-96 %

2. Nebulisasi : - humidifikasi pengencer dahak
- bronkodilator
3. Fisioterapi dada :
- batuk dan napas dalam pengeluaran dahak
- fish mouth breathing  lancarkan ekspirasi
 pengeluaran CO ₂
4. Pengaturan cairan
5. Kortikosteroid  sepsis berat
B. Suportif

6. Inotropik : gguan sirkulasi /gagal ginjal

prerenal
7. Ventilasi mekanik : - hipoksemia persisten
- gagal napas
- retensi sputum sulit
8. Drainase empiema
9. Nutrisi kalori : gagal napas diberi lemak 
CO₂ ↓
 EVALUASI PENGOBATAN
(tidak ada perbaikan 24 – 72 jam)
Penderita tidak respons dengan pengobatan empiris yang telah diberikan

Salah diagnosis Diagnosis sudah benar

• Gagal jantung
• Emboli
• Keganasan Faktor penderita Faktor obat Faktor bakteri
• Sarkoidosis • Respons penderita • Salah pilih obat • Kuman-resisten thd
• Reaksi obat tidak adekuat • Salah dosis/cara obat
• Perdarahan • Kelainan lokal pemberian obat • Bakteri patogen lain
(sumbatan benda • Komplikasi • Mikobakteria atau
asing) • Reaksi obat nonkardia
• Komplikasi • Nonbakterial (jamur
- super infeksi paru atau virus)
- empiema
 KOMPLIKASI
• Ektrapulmoner infeksius (pneumonia
pneumokokus = bakteriemia) : meningitis,
arthritis, endokarditis, perikarditis, peritonitis
dan empiema.
• Ektrapulmoner non infektious (memperlambat
gambaran radiologis paru): gagal ginjal, gagal
jantung, emboli atau infark paru dan IMA.
• ARDS, gagal organ jamak dan pneumonia
nosokomial
 Pencegahan
(pneumonia komuniti)

1. Vaksinasi influenza dan pneumokokus pada :

- orang dengan resiko tinggi
- orang dengan gangguan imunologis
- penghuni rumah jompo
- penghuni rumah penampungan peny. Kronik
- usia diatas 65 tahun
2. Pola hidup sehat : tidak merokok & alkohol
 PENCEGAHAN
(PNEUMONIA NOSOKOMIAL)

• Ditujukan pada upaya program pengawasan & pengontrolan infeksi

termasuk :
- pendidikan staf pelaksana
- pelaksanaan tehnik isolasi
- praktek pengontrolan infeksi
• Terapi pencegahan pada :
- gagal organ ganda
- skor APACHE yang tinggi
- penyakit dasar yg dpt berakibat fatal
• Beberapa faktor dapat dikoreksi
- pembatasan pemakaian slang nasogastrik atau endotrakeal
- pembatasan pemakaian obat sitoprotektif sbgi pengganti
antagonis H₂ dan antasid
 Rekomendasi Dalam Pengelolaan Faktor Resiko yang Dapat Diubah
• Faktor Inang
- Nutrisi adekuat, makananenteral dengan nasogastrik
- Reduksi/penghentian terapi imunosupresif
- Cegah ekstubasiyang tidak direncanakan (tangan diikat, beri sedasi
- Tempat tidur yang kinetik
- Spirometer incentif, napas dalam, kontrol rasa nyeri
- Menghindari penghambat histamin tipe 2 dan antasida
• Faktor alat
- Kurangi obat sedatif dan paralitik
- Hindari overdistensi lambung
- Pencabutan slang endotrakeal & nasogastrik yang terencana
- Hindari intubasi dan reintubasi
- Posisi ½ duduk ( 30 – 40 derajat )
- Jaga saluran ventilator bebas dari kondensasi
- Tekanan ujung slang endotrakeal  20 cmH ₂O (menjaga kebocoran patogen ke saluran
napas bawah)
- Aspirasi sekresi epiglottis yang kontinyu
• Faktor lingkungan
- Pendidikan
- Menjaga prosedur pengontrol infeksi oleh staf
- Program pengontrolan infeksi
- Mencuci tangan, desinfektasi peralatan
PROGNOSIS
• Pneumonia Komuniti
- Angka kematian ok pneumokokus = 5 %, meningkat pada orang
tua dengan kondisi buruk.
- Pneumonia dgn influensa = 59 %.
- Pneumonia dgn usia lanjut = 89 %.
- PK dirawat di ICU = 20 % (terkait faktor perubah)

• Pneumonia Nosokomial
- Angka kematian = 33 – 50 %  jadi 70 % terkait penyakit dasar.
Penyebab kematian biasanya ok bakteriemia - Ps. Aerugenosa
- Acinobacter spp.
 PROGNOSIS
• Umumnya : baik.
(Excelent with appropriate antimicrobial and supportive care)

penderita antibiotik

bakteri penyebab
 KOMPLIKASI

• Efusi pleura • Pneumotoraks

• Empiema • Gagal napas

• Abses paru • Sepsis

 PNEUMONIA ATIPIK
Etiologi
- Sering : Mycoplasma pneumonia, Chlamydia pneumonia, Legionella spp,
- Lain : Chlamydia psittasi, Coxiella burnetti, virus Influenza tipe A & B, Adenovirus
and RSV
DIAGNOSIS
1. Gejala : - Saluran napas : batuk non produktif
- Sistemik : demam, nyeri kepala dan mialgia
2. Fisik : rales basah tersebar, konsolidasi jarang terjadi
3. Radiologi : Infiltrat interstisial
4. Laboratorium : - Lekositosis ringan
- Gram, biakan  dahak/darah : bakteri negatif
5. Terapi : - Makrolid baru  azitromisin, klaritromisin, roksitromisin
- Fluorokuinolon, atau Doksisiklin
 THANK YOU FOR
YOUR ATTENTION
ABOUT “PNEUMONIA”
 Tanda dan Gejala Pneumonia Atipik Pneumonia Tipik
• Onset Gradual Akut
• Suhu Kurang tinggi Tinggi, menggigil
• Batuk Non produktif Produktif
• Dahak Mukoid Purulen
• Gejala lain Nyeri kepala, mialgia, sakit Jarang
tenggorokan, suara parau,
nyeri telinga
• Gejala luar paru sering lebih jarang
• Pewarnaan Gram Flora normal / Kokus Gram () or
spesifik ()
• Radiologis “patchy” atau Konsolidasi lobar
normal
• Laboratorium Lekosit N kadang Lebih tinggi
rendah
 CAP HAP
Terjadi Masyarakat Rumah sakit
Kejadian 2 days before 2 days after
Etiologi Gram positif Gram negatif
Faktor 1. Alcohol excess 1. Intubation
predisposisi 2. Cigarette smoking 2. Suppressed cough leading to
3. Chronic heart & lung aspiration (postoperatively)
disease 3. Reduced host defenses
4. Bronchial obstruction 4. Long stay in hospital
5. Immunosuppression
6. Drug abuse
Clinical features similar similar
Laboratory test similar similar
Management Out, hospitalized & ICU - Good Gram negative coverage
patients
 Pneumonia Bronko- Pneumonia
Lobaris pneumonia interstitial

Lokasi Mencakup 1 lobus Tersebar di dekat Inflamasi pada

bronkus jaringan interstitisl
paru

Insidens usia dewasa sering pada bayi dan -

orang tua

Etiologi Gram negatif? Streptococcus Virus

Virus
Staph

Gambaran Air bronchogram (+) Air bronchogram (-) - corakan

radiologis bronkovaskuler↑
- hiperaerasi
- Bercak infiltrat
 PENGOBATAN
1.Penisilin sensitif Streptococcus pneumoniae (PSSP)
 Golongan Penisilin
 TMP-SMZ
 Makrolid

2.Penisilin resisten Streptococcus pneumoniae (PRSP)

 Betalaktam oral dosis tinggi (u/ rawat jauh)
 Sefotaksim, Seftriakson dosis tinggi
 Makrolid baru dosis tinggi
 Fluorokuinolon respirasi
3. Pseudomonas aeruginosa
Aminoglikosid
Seftazidim, Sefoperason, Sefepim
Tikarsilin, Piperasilin
Karbapenem : Meropenem, Imipenem
Siprofloksasin, Levofloksasin

4. Methicillin resistent Staphylococcus aureus (MRSA)

Vankomisin
Teikoplanin
Linezolid
 PENGOBATAN
5. Hemophilus influenzae 7. Legionella Chlamydia pneumoniae
 TMP-SMZ  Doksisiklin
 Azitromisin  Makrolid
 Fluorokuinolon
 Sefalosporin gen. 2 atau 3  Makrolid
 Fluorokuinolon respirasi  Flurokuinolon
 Rifampisin

6. Mycoplasma pneumoniae 8. Chlamydia pneumoniae

 Doksisiklin  Doksisiklin
 Makrolid  Makrolid
 Fluorokuinolon  Fluorokuinolon
 Community-acquired pneumonia
Pathogenesis
Organsim enter the lungs usually having been inhaled from the environment or nasopharynx. These organism
may be eliminate by the lung’s defense mechanism (physical, humoral, and cellular defense) or they may
survive and multiply.
Factors that undermine the lung’s defense, therefore, increase the risk of pneumonia :
• Alcohol excess
• Cigarette smoking
• Chronic heart and lung diseases
• Bronchial obstruction
• Immunosuppression
• Drug abuse

The pathogen stimulates host defenses and alveolar airspaces become filled with eosinophilic edematous fluid
containing neutrophil polymorphs. The edema transport, organisms through the pores of Kohn into the alveoli.
in days 2 – 4; a red hepatization occurs; there is accumulation in alveolar spaces of polymorps,
lymphocytes, and macrophages. The alveolar exudate contains a fine network of fibrin and large numbers of
extravasated red cells. The lung is red, solid, and ariless. Red hepatization corresponds to an area of edema and
hemorrhage.
In days 4 – 8; a gray hepatization occur. Fibrinous pleurisy is present. Alveolar spaces are microscopically
distended and filled by a dense network of fibrin-containing neutrophil polymorphs. Gray hepatization
represents a zone of advanced consolidation with destruction of red and white blood cells. The lung is gray or
brown and solid.
Resolution occurs after 8 – 10 days in untreated cases. When bacteria has been eliminated, macrophages
enter and replace granulocytes. The exudate is liquefied by fibrinolytic enzymes and coughed uo or absorped.
 ETIOLOGY
S. Pneumoniae is the causative organism in 55 – 75% of cases.
Causes and features of community acquired pneumia
Organism Features of pneumonia % cases
Streptococcus pneumoniae Gram-positive alpha-hemolytic; polysaccharide capsule determines virulence and 55 - 75
is detectable serologically; responsible for a high mortality (esp. in the setting
bacteremia) unless treated appropriately; vaccine available
Mycoplasma pneumoniae Epidemics every 3-4 years usually in young patients, 50% have cold agglutinins; 5 – 18
associated with many extrapulmonary manifestations; penicillin ineffective as no
bacterial cell wall
influenzo Epidemics common; affects patients with underlying lung disease; can be severe; 8
S. aureus, S. pneumoniae, H. influenzae occur secondarily; a vaccine is available
Legionella pneumophila Gram-negative; found in cooling towers and air-conditioning; causes very severe 2–5
pneumonia with high mortality and is frequently associated with extrapulmonary
features; antigen may help in diagnosis
Chlamydia pneumoniae Headache very common; usually serological diagnosis 2–5

Haemophilus influenzae Gram-negative rod; more commonly associated with exacerbations of COPD 4–5

Viruses other than influenzae 2–8

Staphylococcus aureus gram-positive coccus; often follow flu; alcoholics and patient with mitral valve 1–5
disease are susceptible; often causes severe; often cavitating pneumonia;
commonly fatal
Klebsiella pneumoniae Gram-negative; seen in alcoholics; severe and often cavitates 1
Complications
The key of complications are:
1. Respiratory failure
2. Parapneumonic effusions
3. Empyema
4. Lung abscess
5. Pulmonary fibrosis, after resolution
Laboratory tests
• Sputum-culture and Gram stain
• Blood-full blood count, blood culture (low
sensitivity, high specificity)
• Pleural fluid-culture and Gram stain
• Chest radiography
• Bronchoscopy with BAL if diagnosis uncertain
• Assessment of oxygenation
• Other specific tests – Mycoplasma, Legionella,
and Chlamydia antibodies; pneumococcal antigen
testing by counter-immunoelectrophoresis (CIE)
of the sputum, urine, and serum.
Management
Antibiotic treatment should be started immediately, without
waiting for microbiology results.
• Empirical treatment with macrolide, doxycycline, or
fluoroquinolone (outpatients)
• Fluoroquinolone or an extended-spectrum cephalosporin
in combination with a macrolide (hospitalized patients)
• Ceftriaxone, cefotaxime, ampicillin-sulbactam, or
piperacillin-tazobactam combined with a fluoroquinolone
or macrolide (ICU patients)
• Pathogen-spesific therapy when the pathogen is identified
In addition, pleuritic pain should be relieved with simple
analgesia and oxygen therapy administered if appropriate.
Prognosis
It is important to assess the severity of CAP as this impacts
on prognosis and therefore treatment planning. Prognosis
may range from full recovery to death.
The key adverse prognostic features are:
• New mental confusion
• Urea > 7 mmol/L
• Respiratory rate ≥ 30/min
• Systolic blood pressure < 90 mmHg / diastolic ≤ 60 mmHg
Patient with two or more of these features are at high risk
of mortality and should be managed aggressively.
INDIKASI VENTILATOR MEKANIK PADA PNEUMONIA

1. Hipoksemia persisten dengan O₂ 100 % pakai masker

2. Gagal napas (asidosis resp). Henti napas, retensi sputum sulit
 Hospital-acquired Pneumonia
• Or Nosocomial Pneumonia refers to a new lower respiratory tract infection at least two days
after hospital admission
• It occurs in 1 – 5 % of admissions and is a serious cause of morbidity and mortality.

Etiology
Factors predisposing to hospital-acquired infections are:
1. Intubation
2. Suppressed cough leading to aspiration (e.g., postoperatively)
3. Reduced host defenses
4. Long stay in hospital, with associated exposure to pathogens

Pathogens
 Gram-negative bacteria (Escheruchia, Klebsiella, and Pseudomonas spp.) are the cause of
hospital-acquired pneumonia in many cases, although Staphylococcus aureus (particularly drug-
resistant strains) is also common
Clinical features & laboratory tests  similar to those described above under CAP.

Management
Good Gram-negative coverage is achieved with an aminoglycoside plus anti pseudomonal penicillin
or a third-generation cephalosporin. Most hospital-acquired pneumonia is serious, and these drugs
are frequently given intravenously.
 Pneumonia in the immunocompromised patient
1. Pneumocystis carinii pneumonia (PCP)
 Is a fungal infection that is largely confined to the lung. It is the most common
opportunistic infection in the immunocompromised.
 Infection occurs by inhalation of the organism. The patient presents with an insidious
or abrupt onset of dry cough, fever, and dyspnea. Pleural effusions  rare.

Pathology
There is an interstitial infiltrate of mononuclear cells and alveolar airspaces are filled with
foamy eosinophilic material.

Diagnosis
Bilateral pneumonia in an immunocompromised patient should raise suspicion of PCP.
Diagnosis in 90% of cases is by staining using Giemsa, methanamine-silver, Papanicocoau, or Gram-
Weigert stains with monoclonal antibodies.
Chest radiography shows diffuse bilateral alveolar and interstitial shadowing, beginning in
peripheral regions and spreading in a butterfly pattern.

Treatment
Trimethoprim-sulfamethoxazole is given, intravenously at first. Prophylaxis is recommended in
patients with low CD4 counts or where previous infection has occurred. Mortality of untreated
patients is 100%; in treated patients, mortality is 20 – 50%
 Pneumonia in the immunocompromised patient
2. Cytomegalovirus (CMV)
 Is a DNA virus in the herpes group. Of patient with AIDS, 90% are infected with CMV. CMV also occurs in
recipients of bone marrow and solid organ transplants. Only occasionally does CMV cause pneumonia.
 Usual symptoms are a nonproductive cough, dyspnea, and fever. Disseminated infection occurs, causing
encephalitis, pneumonitis, retinitis, and diffuse involvement of the gastrointestinal tract.

Pathology
• Interstitial inflammatory infiltrate of mononuclear cells
• Scattered alveolar hyaline membranes
• Protein-rich fluid in alveoli
• Intranuclear inclusion bodies found in alveolar epithelial cells.

Diagnosis
CMV infection can be diagnosed by the identification of characteristic intranuclear owl’s eye inclusions in tissue
and by direct immunofluorescence.

Treatment  by intravenous or oral ganciclovir.

3. Aspergillus
4. Cryptococcus
5. Varicella zoster
6. Kaposi’s sarcoma
 Pneumococcal pneumonia. Gross section of lung showing gray
”hepatization” of the upper lobe in right lower lobe consolidation
Pneumonia. Chest radiograph of left lower lobe pneumonia
Pneumonia. Chest radiograph of right upper lobe pneumonia
PCP pneumonia. Chest radiograph of patient with pneumocystis carinii
pneumonia
PNEUMOCYSTIS PNEUMONIA
Pneumococcal pneumonia. Gross section of lung showing gray hepatization”
of the upper lobe in right lower lobe consolidation
Pneumonia. Chest radiograph of right
upper lobe pneumonia
Pneumonia. Chest radiograph of left lower lobe pneumonia
PCP pneumonia. Chest radiograph of patient with
pneumocystis carinii pneumonia
PNEUMOCYSTIS PNEUMONIA
 Chest x-ray
 Confirm the diagnosis and detect
associated lung diseases

 Patchy airspace infiltrates to diffuse

alveolar or interstitial infiltrates

 Clearing of infiltrates can take 6

weeks
 DIFFERENTIAL DIAGNOSIS
• Pneumonia - bakterial
- viral
- aspirasi
- PCP
• Bronkitis - Sarkoidosis
• Abses paru - Tumor paru
• TB - Pneumonitis hipersensitif
• Emboli paru - Bronkiolitis,BOOP
• Infark miokard