Dr.

Abdul Rohman,
SpP
K-3B






an infection of peripheral lung
parenchyma
Clinically an acute illness in which there are
signs of consolidation in the chest or new
changes on chest x-ray
infection of the central conducting
airways bronchitis
Suatu peradangan paru disebabkan mikroorganisme
(bakteri, virus, jamur, parasit)
Radang paru ok nonmikroorganisme (bahan kimia, radiasi, aspirasi
bahan toksik, obat-obatan, dll) pneumonitis
Radang parenkim paru, distal
bronkus terminalis konsolidasi jar
paru dan gangguan pertukaran gas
setempat
DEFINITION
- Red hepatization : 2 4 days
- Gray hepatization : 4 8 days
- Resolution : > 8 10 days

PATOGENESIS
Mikroorganisme Lingkungan
Host
DEFENSE
Physical, Humoral & Cellular
CARA
I NOKULASI langsung
INHALASI
HEMATOGEN
KOLONISASI (terbanyak)
FAKTOR RISIKO

Alkohol
Merokok
Peny. kronik:
- Jantung &
Paru
Obstruksi
bronkus
Immunosupress
i
Drug abuse

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
(Minggu 01)

Alveolus terisi sekrit
yang terinfeksi

Tanda-tanda prodromal
infeksi akut

Hepatisasi
(Minggu 1-3)

Sebukan sel-sel PMN
alveolus padat, infeksi
akut Restriksi +
demam

Restriksi Fungsi pernafasan |
Demam || Radang menyebar ke
pleura viscerlis Nyeri dada (tidur
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
(Minggu 3-)

Alveolus melunak
berubah menjadi dahak

Demam + , Batuk produktif, Ronki
basah halus +/-

Table : Common Causes of Acute Pneumonia

Key Points : About the Classification of Pneumonia

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




ETIOLOGY
Pejamu Faktor Modifikasi
Lingkungan :luar or dalam RS,
ICU atau non ICU
ETIOLOGI
(IN DESCENDING ORDER)

KEY POINTS : MOST
COMMON PATHOGENS
FOR CAP
1. Pneumococcus species
2. Haemophilus influenzae
3. Atypical pathogens (coinfection possible)
4. Enteric gram-negative organisms
5. Staphylococcus aureus (especially after influenza)
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
KLASIFIKASI
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
1. Gambaran Klinis
a. Anamnesis
- Demam, menggigil, suhu s/d > 40C
- 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


DIAGNOSIS
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



If you suspect
pneumonia, ask
about alcohol
intake and
comorbidities
(especially chronic
heart and lung
disease and
diabetes mellitus);
foreign travel(risk
of legionella); and
upper respiratory
tract infection are
so common that
positive answers
are unlikely to
narrow down the
list of possible
organisms.

Typical clinical features of bacterial pneumonia
Clinical features
Incidence (%)
Respiratory features
cough
sputum
dyspnea
chest pain
upper respiratory tract symptoms
hemoptysis

90
70
70
65
33
13
Nonrespiratory
vomiting
confusion
diarrhea
rash
abdominal pain

20
15
15
5
5


Typical clinical features of bacterial
pneumonia
Clinical features Incidence (%)
Signs
fever
tachypnea
tachycardia
abnormal chest signs
hypotension
confusion
herpes labialis

80 90
80 90
80 90
80 90
20
15
10





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




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 %
-
-

PNEUMONIA KOMUNITI
(DIDAPAT DI MASYARAKAT)
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 R : 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-
Resistant
Pneumococcl
Enteric Gram-ve
Organism
Pseudomonas
aeruginosa
Factors Age > 65 year
|-lactam use within
the last 3 month
Alcoholism
Immunosuppresion
Multiple medical
comorbidities
Exposure to child in
daycare center
Cardiopulmonary
Nursing home
resident
Multiple medical
comorbidities
Recent antibiotic
therapy
Structural lung disease
(bronchiectasis)
Prolonged
corticosteroid therapy
(> 10 mg
prednisolone/day)
Broad-spectrum
antibiotic therapy > 7
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 < 35C atau > 40C


Karakteristik penderita Jumlah poin
Langkah 2 rumus prediksi pneumoni Sistem skor u/ deteksi
pend dgn kelas resiko II-IV
Faktor demografi
Usia : laki-laki
perempuan
Perawatan di rumah
Penyakit penyerta
Keganasan
Penyakit hati
Gagal jantung kongestif
Peny. serebrovaskuler
Penyakit ginjal
Pemeriksaan fisis
Perub. status mental
Pernapasan 30 kali/menit
Tekanan darah sitolik 90mmHg
Suhu tubuh < 35C atau 40 C
Nadi 125 kali/menit
Hasil laboratorium / Radiologi
Analisis gas darah arteri : pH 7,35
BUN > 30 mg/dL
Natrium < 130 mEq/liter
Glukosa > 250 mg/dL
Hematokrit < 30%
PO
2
60 mmHg
Efusi pleura

Umur (tahun)
Umur (tahun) 10
+ 10

+ 30
+ 20
+ 10
+ 10
+ 10

+ 20
+ 20
+ 20
+ 15
+ 10

+ 30
+ 20
+ 20
+ 10
+ 10
+ 10
+ 10
SKOR MENURUT SISTEM PORT
(Pneumonia Patient Outcome Research Team)
Risk Risk class Based on Algorithm

I
Low II s 70 total points
III 71-90
Moderate IV 91-130
High V > 130
Stratification of Risk Score
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
PaO
2
/FiO
2
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
disorientation in person, place, or time)
1
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 :
mortality low
(14,5%)
Low risk, consider home treatment
2 Group 2 :
mortality
intermediate
(40%)
Consider hospital-supervised treatment
3 Group 3 :
mortality high
(52%)
Manage in hospital as severe
pneumonia consider admission to
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. PaO/FiO < 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
Infiltrat + gejala klinis yg menyokong diagnosis pneumonia Tidak ada infiltrat
Evaluasi untuk kriteria rawat jalan/ rawat inap
Rawat jalan Rawat inap
Terapi empiris
Pemeriksaan bakteriologis
Memburuk
R. Rawat biasa R. Rawat intensif
Terapi empiris
Membaik Memburuk
Di tatalaksana sbg diagnosis
lain
Membaik
Terapi empiris dilanjutkan
Terapi
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)
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 |




PENGOBATAN

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

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
Kriteria Terapi Sulih
B. Suportif


1. O PaO 80-100 mmHg atau SaO 95-96 %
2. Nebulisasi : - humidifikasi pengencer dahak
- bronkodilator
3. Fisioterapi dada :
- batuk dan napas dalam pengeluaran dahak
- fish mouth breathing
lancarkan ekspirasi

pengeluaran CO
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
CO

EVALUASI PENGOBATAN
(tidak ada perbaikan 24 72 jam)
Faktor obat Faktor bakteri
Penderita tidak respons dengan pengobatan empiris yang telah diberikan
Salah diagnosis
Diagnosis sudah benar
Faktor penderita
Gagal jantung
Emboli
Keganasan
Sarkoidosis
Reaksi obat
Perdarahan
Respons penderita
tidak adekuat
Kelainan lokal
(sumbatan benda
asing)
Komplikasi
- super infeksi paru
- empiema
Salah pilih obat
Salah dosis/cara
pemberian obat
Komplikasi
Reaksi obat
Kuman-resisten thd
obat
Bakteri patogen lain
Mikobakteria atau
nonkardia
Nonbakterial (jamur
atau virus)
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
KOMPLIKASI
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 komuniti)
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 H dan antasid



PENCEGAHAN
(PNEUMONIA NOSOKOMIAL)



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 duduk ( 30 40 derajat )
- Jaga saluran ventilator bebas dari kondensasi
- Tekanan ujung slang endotrakeal > 20 cmH O (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
bakteri penyebab
antibiotik
Efusi pleura
Empiema
Abses paru
KOMPLIKASI
Pneumotoraks

Gagal napas

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

PN
EU
MO
NIA
ATI
PIK


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
tenggorokan, suara
parau, nyeri telinga
Jarang
Gejala luar paru sering lebih jarang
Pewarnaan Gram Flora normal / spesifik Kokus Gram (+) or ()
Radiologis patchy atau normal
Konsolidasi lobar
Laboratorium Lekosit N kadang
rendah
Lebih tinggi
Gguan fungsi hati Sering jarang
CAP HAP
Terjadi Masyarakat Rumah sakit
Kejadian 2 days before 2 days after
Etiologi Gram positif Gram negatif
Faktor
predisposisi
1. Alcohol excess
2. Cigarette smoking
3. Chronic heart & lung
disease
4. Bronchial obstruction
5. Immunosuppression
6. Drug abuse
1. Intubation
2. Suppressed cough leading
to aspiration
(postoperatively)
3. Reduced host defenses
4. Long stay in hospital
Clinical features similar similar
Laboratory test similar similar
Management Out, hospitalized & ICU -
patients
Good Gram negative
coverage
Faktor
modifikasi
Yes None
Pneumonia
Lobaris
Bronko-
pneumonia
Pneumonia
interstitial
Lokasi Mencakup 1 lobus Tersebar di dekat
bronkus
Inflamasi pada
jaringan interstitisl
paru
Insidens usia dewasa

sering pada bayi dan
orang tua
-
Etiologi

Gram negatif? Streptococcus
Virus
Staph

Virus

Gambaran
radiologis
Air bronchogram (+) Air bronchogram (-) - corakan
bronkovaskuler
- hiperaerasi
- Bercak infiltrat

PENGOBATAN


2.Penisilin resisten Streptococcus pneumoniae (PRSP)
Betalaktam oral dosis tinggi (u/ rawat jauh)
Sefotaksim, Seftriakson dosis tinggi
Makrolid baru dosis tinggi
Fluorokuinolon respirasi


1.Penisilin sensitif Streptococcus pneumoniae (PSSP)
Golongan Penisilin
TMP-SMZ
Makrolid
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
TMP-SMZ
Azitromisin
Sefalosporin gen. 2 atau 3
Fluorokuinolon respirasi






6. Mycoplasma
pneumoniae
Doksisiklin
Makrolid
Fluorokuinolon
8. Chlamydia
pneumoniae
Doksisiklin
Makrolid
Fluorokuinolon
7. Legionella Chlamydia
pneumoniae
Doksisiklin
Makrolid
Fluorokuinolon
Makrolid
Flurokuinolon
Rifampisin
Community-acquired pneumonia
Pathogenesis
Organsim enter the lungs usually having been inhaled from the environment or nasopharynx. These organism
may be eliminate by the lungs defense mechanism (physical, humoral, and cellular defense) or they may
survive and multiply.
Factors that undermine the lungs 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
is detectable serologically; responsible for a high mortality (esp. in the setting
bacteremia) unless treated appropriately; vaccine available
55 - 75
Mycoplasma pneumoniae Epidemics every 3-4 years usually in young patients, 50% have cold agglutinins;
associated with many extrapulmonary manifestations; penicillin ineffective as no
bacterial cell wall
5 18
influenzo

Epidemics common; affects patients with underlying lung disease; can be severe;
S. aureus, S. pneumoniae, H. influenzae occur secondarily; a vaccine is available
8
Legionella pneumophila Gram-negative; found in cooling towers and air-conditioning; causes very severe
pneumonia with high mortality and is frequently associated with extrapulmonary
features; antigen may help in diagnosis
2 5
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
disease are susceptible; often causes severe; often cavitating pneumonia;
commonly fatal
1 5
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 O 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.
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
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 owls eye inclusions in tissue
and by direct immunofluorescence.

Treatment by intravenous or oral ganciclovir.
3. Aspergillus
4. Cryptococcus
5. Varicella zoster
6. Kaposis 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