REFERAT

PNEUMONIA
PEMBIMBING : DR. HENDRA DWI KURNIAWAN, SP.PD

DISUSUN OLEH : AMANDA DAMAYANTI PABISA

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
• INHALASI
• Merokok • HEMATOGEN
• Peny. kronik: • KOLONISASI (terbanyak)
- Jantung &
Paru - Red hepatization : 2 – 4 days
• Obstruksi - Gray hepatization : 4 – 8 days
bronkus - Resolution : > 8 – 10 days
 kongesti
Red hepatization
(Udara di alveolus hilang diganti
dengan eksudat yang membeku

Gray
hepatization

resol
usi
 STADIUM PATOLOGI KLINIK
ANATOMI
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, Demam  Radang menyebar ke
infeksi akut  pleura viscerlis Nyeri dada (tidur
Restriksi + 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 basah halus +/-
dahak
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

o Ventilator  P. aerugenusa dan Enterobacter

 ETIOLOGI

Pejamu  Faktor
Modifikasi
 Lingkungan :luar or dalam
RS,
 KEY POINTS : MOST
COMMON PATHOGENS FOR
CAP ORDER)
• (IN DESCENDING

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 lobaris
- Sering pada pneumonia bakterial
- Jarang pada bayi dan orang tua aspirasi benda asing

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

b. Bronkopneumonia : 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
 file:///E:/R
TYPICAL SYMPTOMS OF CAP

• Fever
• New cough w/ or w/o sputum production
• Change in color of sputum in patients w/ chronic cough
file:///E:/Recordings.htm
• 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
- 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
 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 %
-
-
 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
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 antibiotic therapy > 7
in 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 perempuan Umur (tahun)
• Perawatan di rumah Umur (tahun) – 10
• Penyakit penyerta + 10
Keganasan
Penyakit hati + 30
Gagal jantung kongestif + 20
Peny. serebrovaskuler + 10
Penyakit ginjal + 10
 Pemeriksaan fisis + 10
• Perub. status mental
• Pernapasan ≥ 30 kali/menit + 20
• Tekanan darah sitolik ≤ 90mmHg + 20
• Suhu tubuh < 35°C atau ≥ 40° C + 20
• Nadi ≥ 125 kali/menit + 15
 Hasil laboratorium / Radiologi + 10
• Analisis gas darah arteri : pH 7,35
• BUN > 30 mg/dL + 30
• Natrium < 130 mEq/liter + 20
• Glukosa > 250 mg/dL + 20
• Hematokrit < 30% + 10
• PO2 ≤ 60 mmHg + 10
• Efusi pleura + 10
+ 10
 Pasien PK

Usia  50 tahun …………………….ya……………………………………..

Tidak

Adakah riwayat komorbid

- Neoplasma Pasien dimasukkan dalam

- Gagal jantung kongestif kelas risiko II-V

- Peny. Serebrovaskuler ……….ya………. Sesuai sistim skor rumus

- Penyakit ginjal prediksi

- Penyakit hati

Tidak

Adakah kelainan pd pemeriks. fisik

- Perubahan status mental

- Nadi  125x/menit

- Pernapasan  30x/menit …………..ya………………………

- Tekanan drh sistolik  90 mmHg

- Suhu  35°C atau  40°C

Tidak

Pasien dimasukkan dalam

Kelas resiko I

AN ALGORITHM FOR TRIAGE IN PATIENT WITH COMMUNITY ACQUIRED PNEUMONIA

SISTEM SKOR PADA PNEUMONIA KOMUNITI BERDASARKAN PORT
Karakteristik penderita Jumlah poin
Faktor demografi
• Usia : laki-laki perempuan Umur (tahun)
• Perawatan di rumah Umur (tahun) – 10
• Penyakit penyerta + 10
Keganasan
Penyakit hati + 30
Gagal jantung kongestif + 20
Peny. serebrovaskuler + 10
Penyakit ginjal + 10
Pemeriksaan fisis + 10
• Perub. status mental
• Pernapasan ≥ 30 kali/menit + 20
• Tekanan darah sitolik ≤ 90mmHg + 20
• Suhu tubuh < 35°C atau ≥ 40° C + 20
• Nadi ≥ 125 kali/menit + 15
Hasil laboratorium / Radiologi + 10
• Analisis gas darah arteri : pH 7,35
• BUN > 30 mg/dL + 30
• Natrium < 130 mEq/liter + 20
• Glukosa > 250 mg/dL + 20
• Hematokrit < 30% + 10
• PO2 ≤ 60 mmHg + 10
• Efusi pleura + 10
+ 10
• SKOR MENURUT SISTEM PORT
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
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-
85, 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
 ALUR TATALAKSANA PNEUMONIA KOMUNITI

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 Pemerikasaan

bakteriologis

Membaik Memburuk R. Rawat biasa R. Rawat intensif

Terapi empiris

Terapi empiris Terapi

Membaik Memburuk Kausatif
dilanjutkan
PENGOBATAN

A. Antibiotika

 Berdasarkan data mikroorganisme dan hasil uji pekaan

 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 
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)
PETUNJUK TERAPI EMPIRIS MENURUT PDPI

• Tanpa faktor modifikasi:

Golongan  laktam /  laktam + anti
Rawat  laktamase
• Dengan faktor modifikasi: Gol 
laktam + anti  laktamase atau
Fluorokuinolon respir (levofloksasin,
jalan moksifloksasin, gatifloksasin)
• Bila dicurigai pneumonia atipik:
makrolid baru (roksitromisin,
klaritromisin, azitromisin)
TERAPI EMPIRIS PNEUMONIA (CAP/PK)
RAWAT JALAN
PDPI
(PERHIMPUNANDOKTERPARUINDON)
• Tanpa faktor modifikasi:
Golongan  laktam /  laktam
+ anti  laktamase
• Dengan faktor modifikasi:
Gol  laktam + anti 
laktamase atau
• Fluorokuinolon respir
(levofloksasin,
moksifloksasin, gatifloksasin)
• Bila dicurigai pneumonia
PRT (PULMONARY RESP THERAPY)
• No CardioPulmDis & No Modifying Fact
Advanced macrolide (Azithromycin) or
Doxycycline
• CardioPulmoDis & Modifying Factor
- -lactam (oral cefpodoxim,cefuroxim,
high dose amoxil,amox/clav, or parenteral
ceftriaxon followed oral cefpodoxim) 
macrolide or doxycycline
- Antipneumococ fluoroquinolone
(levofloxacin,moxi-fl,gati-fl,gemi-fl) alone
- A ketolide –monoTx-no enteric Gram (-)
 • Tanpa faktor modifikasi:
- Golongan  laktam / 
laktam + anti  laktamase iv,
Rawat atau
- Sefalosporin G2, G3 iv, atau
- Flurokuinolon respirasi iv
• Dengan faktor modifikasi:
inap - Sefalosporin G2, G3 iv
- Fluorokuinolon respirasi iv
• Bila dicurigai ada infeksi
bakteri atipik ditambah
makrolid baru
 RAWAT INAP NONINTENSIF
PDPI
• Tanpa faktor modifikasi:
- Gol  laktam /  laktam +
anti  laktamase iv, atau
- Sefalosporin G2, G3 iv, atau
- Flurokuinolon respirasi iv
• Dengan faktor modifikasi:
- Sefalosporin G2, G3 iv
- Fluorokuinolon respirasi iv
• Bila dicurigai ada infeksi
bakteri atipik ditambah
PRT
• No CardioPulm Dis & Modifying Factor
- IV azithromycin alone
If allergic/intolerant Doxycycline and -lactam
- Antipneumococcal fluoroquinolone
• CardioPulm Dis & Modifying Factor
- iv -lactam (cefotaxim,ceftriaxon, ampi/sulbac or
high dose ampic)  iv or oral macrolide or
doxycycline
- iv antipneumococcal fluoroqquinolone alone
(gatifloxacine,levofloxacine, or moxifloxacine)
 Tidak ada faktor risiko infeksi
pseudomonas:
• Sefalosporin G3 iv non pseudomonas +
Rawat makrolid baru atau fluorokuinolon
respirasi iv
Ada faktor risiko infeksi pseudomonas:
inap • Sefalosporin anti pseudomonas iv atau
karbapenem iv + fluorokuinolon anti
pseudomonas (siprofloksasin) iv atau
aminoglikosida iv
intensif • Bila curiga disertai infeksi bakteri atipik
: sefalosporin anti pseudomonas iv atu
carbapenem iv + aminoglikosida iv +
makrolid baru atau flurokuinolon
respirasi iv
 RAWAT INAP INTENSIF

PDPI PRT
• No risks for Pseudomonas aeroginasa
• Tak ada faktor risiko infeks
pseudomonas: iv -lactam (cefotaxim,ceftriaxon)  either

Sefalosporin G3 iv non iv macrolide or iv fluoroquinolone

pseudomonas + makrolid baru • Risks for Pseudomonas aeroginosa

atau fluorokuinolon respirasi iv Combined therapy required
• Ada faktor risiko infeksi - Selected iv antipseudomonal -lactam
pseudomonas: (cefepim,imipenem,meropenem, or piperacilin
/tazobactam)  iv antipseudomonal quinolone
-Sefalosporin anti pseudomonas
(i.e., ciprofloxacin)
iv atau karbapenem iv +
- Selected iv antipseudomonal -lactam 
fluorokuinolon anti pseudomonas
aminoglycoside  either iv macrolide or iv
(siprofloksasin) iv atau
nonpseudomonal fluroquinolone
aminoglikosida iv
KEY POINTS : PRINCIPLES OF INPATIENTS THERAPY

1. Give the first dose antibiotics within 4 hours of arrival to the hospital
2. No beta-lactam monotherapy as emperical therapy
3. Limit macrolide monotherapy to patients without risks for drug-resistant
pneumococcus or enteric gram negative organisms
4. No quinolone monotherapy for ICU-admitted patients
5. For non-ICU patients, quinolone monotherapy is equivalent to a
beta-lactam/macrolide combination
 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 ↓
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
EVALUASI PENGOBATAN
(TIDAK ADA PERBAIKAN SELAMA 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 pend tidak • Salah pilih obat • Kuman-resisten
• Reaksi obat
adekuat • Salah dosis/cara thd obat
• Perdarahan
• Kelainan lokal beri obat • Bakteri patogen
(sumbatan benda asing) • Komplikasi lain
• Komplikasi • Reaksi obat • Mikobakteria atau
- super infeksi nonkardia
- empiema • Nonbakterial
(jamur atau virus)
 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.

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
 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, Jarang
mialgia, sakit
tenggorokan, suara
parau, nyeri telinga
• Gejala luar paru sering lebih jarang
• Pewarnaan Gram Flora normal / Kokus Gram () or
spesifik ()
• Radiologis “patchy” atau normal Konsolidasi lobar
• Laboratorium Lekosit N kadang Lebih tinggi
 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
3. Chronic heart & lung leading to aspiration
disease (postoperatively)
4. Bronchial obstruction 3. Reduced host defenses
5. Immunosuppression 4. Long stay in hospital
6. Drug abuse
Clinical similar similar
features
Laboratory similar similar
test
Management Out, hospitalized & ICU Good Gram negative
 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
 Sefalosporin gen. 2 atau3 Fluorokuinolon
 Makrolid
 Fluorokuinolon respirasi
 Flurokuinolon
 Rifampisin
6. Mycoplasma 8. Chlamydia
pneumoniae 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 airless. 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 up 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 55 - 75
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; S. 8
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 Management
Antibiotic treatment should be started immediately, without
The key of complications are:
waiting for microbiology results.
1. Respiratory failure • Empirical treatment with macrolide, doxycycline, or
fluoroquinolone (outpatients)
2. Parapneumonic effusions
• Fluoroquinolone or an extended-spectrum cephalosporin
3. Empyema in combination with a macrolide (hospitalized patients)
• Ceftriaxone, cefotaxime, ampicillin-sulbactam, or
4. Lung abscess
piperacillin-tazobactam combined with a fluoroquinolone
5. Pulmonary fibrosis, after resolution or macrolide (ICU patients)
• Pathogen-spesific therapy when the pathogen is identified

Laboratory tests In addition, pleuritic pain should be relieved with simple

analgesia and oxygen therapy administered if appropriate.
• Sputum-culture and Gram stain

• Blood-full blood count, blood culture (low sensitivity, high Prognosis

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.
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