Kul3 - Pneumonia Uby s2-2011

1
12 Maret 2011
Kuliah Farmasi UBY S2 2011
Dr. Ediyono Sp P Sub dep Paru RSAL Dr Ramelan
Penyakit penyakit Paru

NO Kelompok Penyakit
Penyakit
1. TBC 2. ( ISPA, Bronkitis, Pneumonia, Abses ) Asma Bronkiale
A Infeksi
B Allergi
C Obstruksi Nafas kronis

D Peny. Pleura E Tumor/ Kanker
PPOK
Pleuritis, Efusi Pleura, Pneumotoraks Jinak / Ganas : Primer / Sekunder
Penyakit Paru Kerja
Pneumokoniosis
Pokok Bahasan Infeksi

Definisi Penyebab ( Causa ) Penyebaran (Transmisi) Patogenesis, Patofisiologi Symptom, Sign Diagnosa Terapi
Definisi Infeksi
(Science: microbiology) invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive
metabolism, toxins, intracellular replication or

antigen antibody response.
Infeksi Saluran Nafas

Lokasi anatomis Infeksi Saluran Nafas Kuman Penyebab
Infeksi Saluran Natas Atas Infeksi Saluran Nafas Bawah Spesifik ( TBC )
Non Spesifik ( Pneumonia )
Infeksi Saluran Nafas Spesifik

TBC Non Spesifik Non TBC Bronkitis Pneumonia Abses Paru
Infeksi Saluran Nafas Atas

Rhinitis Sinusitis Pharyngitis Epiglotitis Tonsilitis Laryngitis
Bawah
Bronkitis Pneumonia Abses Paru
Pembagian Saluran nafas
Saluran Nafas Atas
Saluran Nafas Bawah
URTI (Upper Respiratory Tract Infection)

Rhinitis Sinusitis Pharyngitis Epiglotitis Tonsilitis Laryngitis Trakeitis
Rhinosinusitis
Hidung
Flora Normal
Mulut
Streptococcus sp Fusobacterium sp Actinomyces sp Leptotrichia sp Veillonella sp
Staphylococcus aureus Staphylococcus epidermidis Corynebacterium sp
Faring
Streptococcus sp Branhamella catarrhalis Corynebacterium sp Haemophyllus sp Neiserria sp Mycoplasma sp
Kulit
Staphylococcus epidermidis Propioni bacterium acnes Pitosporum ovale
Usus besar
Bacteroides fragilis Eschericjia coli Proteus mirabilis Klebsiella sp Lactobacillus sp Streptococccus sp Candida albican Clostridium sp Pseudomonas sp Enterococcus sp
`
Lactobacillus sp Streptococcus sp Candida albicans Gardnerella vaginalis
Urethra
Streptococcus sp Mycobacterium sp Escherichia coli Bacteroides sp
1. Rinitis
a) Rinitis Alergi
b) Rinitis Virus
c) Rinitis Bakteri ( Difteri , TBC, Sifilis ) d) Rinitis Jamur
Common Cold
Self limiting infection Penyebab : Rhinovirus
Influenza vurus Coronavirus Adenovirus
30 40 % 25 30 % 10 15 % 5 10 %
Parainfluenza virus Respiratory syncitial virus
5% 5%
Fishmans, Pulmonary Diseases and Disorder Vol 2, 2008
2. Sinusitis
Inflammation of paranasal sinuses Sinusitis
Sinusitis Maksilaris
Etiology of Sinusitis
70% of bacterial sinusitis is caused by:
Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis
Other causative organisms are: Staphylococcus aureus Streptococcus pyogenes, Gram-negative bacilli Respiratory viruses
Kolonisasi Kuman di Oropharyng

Streptococcus pneumoniae,
Staphylococcus aureus, Pseudomonas aeruginosa, and
Klebsiella pneumoniae
Tabel: Mikrobiologi Akut Rhinosinusitis pada dewasa
Organism 1 2 3 4 Streptococcus pneumoniae Haemophilus influenzae Streptococcus species Anaerobes
Range of Prevalence (%) 20 43 22 35 39 09
5 6
7
Moraxella catarrhalis Staphylococcus aureus

Others
2 10 08
4
Text Book of Respiratory medicine, Murray and Nadel Volume 1. 2005
Subjective Symptoms of Sinusitis

Nyeri seperti tertekan daerah sinus Nyeri terutama pagi hari, siang berkurang Lemah badan Sekret dari hidung ( Purulent / Persistent ) Postnasal drip Batuk , terutama malam hari Snoring ( mengorok ) Sakit kepala
Diagnostic Tests
Pemeriksaan : sinus radiographs ( Foto Waters), ultrasonograms, or CT scanning Laboratorium : kultur aspirasi cairan sinus.
Komplikasi Sinusitis Complications of Sinusitis
Infeksi mata
Meningitis
Abses Otak Serangan asma anak ( kambuh )
Thrombosis
Empiema subdural
Otitis media is the clinical term for a middle ear infection,
Faringitis
Nasofaring
Orofaring Laringofaring
3. Faringitis
a) Faringitis Viral b) Faringitis bakterial ( streptococcus hemolyticus ) c) Faringitis fungal
d) Faringitis gonorea e) Faringitis luetika f) Faringitis tuberkulosa
Pharyngitis
Inflammasi di pharynx Viral pharyngitis. Penyebab umumnya ok infeksi, a. Sekitar 90% disebabkan ok Virus . b. Bacterial infection c. Oral thrush (fungal candidiasis e.g. in babies) d. Irritation from agents such as pollutants or chemical substances
Streptococcal pharyngitis
Membranous pharyngitis
Pharyngitis
Pharyngitis ok bakteri ( Bacterial sore throats )
Penyebab paling sering : streptococcus.

Pembesaran & nyeri kelenjar limfe Demam, sakit kepala Nyeri tenggorokkan, Nyeri otot (myalgia) Nyeri tulang (arthralgia).
4. Tonsilitis
4. Tonsilitis
Tonsillitis : Inflammation of the Tonsil. Cause a Sore throat and fever. Symptoms : pain in the tonsil area , inability / painful swallowing. White spots may also appear on the tonsils.
Tonsillitis
Candidiasis oral
LRTI (Lower Respiratory Tract Infection) 1) Bronkitis

2) Pneumonia.
Bronkitis
Batasan
Bronchitis is an inflammation of the large breathing
tubes (airways), which causes increased

production of mucus and other changes.
Bronchitis is the inflammation of the bronchi, the main air passages to the lungs, it generally follows a viral respiratory infection. Symptoms include; coughing, shortness of breath, wheezing and fatigue
Bronkitis
Akut
BRONKITIS KRONIS:
Batuk kronik berdahak, minimal 3 bulan dalam setahun, sekurang kurangnya 2 tahun berturut-turut
Kronis
Bronkitis Akut
Symptoms of acute bronchitis : a. b. c. d. e. f. Batuk Lemah badan menggigil demam ringan nyeri otot suara serak
Bronkiektasis
Keruh ( Mukus ) Jernih ( Saliva) Keruh ( Nanah, jaringan nekrotik)
Pada kasus yang berat : Sputum banyak Bila ditampung ada 3 lapis
Kuliah Farmasi UBY 2007

Dr. Ediyono Sp P Sub dep Paru RSAL Dr Ramelan
Pokok bahasan Pneumonia

1. Pendahuluan.
2. Definisi Pneumonia.
3. Etiologi 4. Patogenesis & Patologi 5. Klasifikasi 6. Diagnosis & Diagnosis Banding
7. Penatalaksanaan Pneumonia
8. Komplikasi
Pendahuluan
Pneumonia : angka kematian tinggi ( Terutama usia
tua )
USA : Penyebab kematian ke 6 dari semua kematian Kuman penyebabnya sulit ditemukan, perlu beberapa hari untuk mendapatkan hasil.

1. Pendahuluan.
8. Komplikasi
BATASAN : Keradangan parenkim paru dimana asinus terisi dengan cairan eksudat.
* Pneumonia = keradangan ok infeksi kuman patogen (mis : bakteri, virus, fungi, parasit) * Pneumonitis = keradangan ok berbagai penyebab non infeksi (bahan kimia, radiasi, proses autoimun)
NORMAL ALVEOLI
PNEUMONIA
Definition Pneumonia ( IDSA)

Acute infection of the pulmonary parenchyma accompanied by: Acute infiltrate on CXR or auscultatory findings consistent with pneumonia . And usually two of the following: fever or hypothermia, rigors, sweats, new cough with or without sputum (or change in color), chest discomfort, dyspnea. In the elderly, more common to be afebrile/hypothermic, and altered mental status sometimes is the ONLY complaint.
IDSA = Infectious Disesases Society of America CXR = Chest X Ray
Infeksi / Keradangan Sinusitis Pharingitis Tonsilitis
Laringitis
Tracheitis
Bronchitis Bronchiolitis
Pneumonia ( Keradangan parenkhim paru )
Asinus

1. Pendahuluan.
8. Komplikasi
Etiologi Pneumonia
a. Bakteri : Gram positive, Gram Negative

b. Virus : Influenza, Avian Influenza, SARS, HIV
c. Parasit
d. Jamur e. Cacing
Table: Common causes of pneumonia

Bacteria

Streptocossus pneumoniae ( pneumococcus) Haemophilus influenzae Legionella sp Mycoplasma pneumoniae; chlamydia pneumoniae Gram negatif bacilli ( proteus sp; E.colli ) Staphylococcus aureus Moraxella catarrhalis Chlamydia psittici Coxiella burnetti Klebsiella pneumoniae Pseudomonas
Viruses

Influenza A & B Parainfluenza Cytomegalovirus Adenovirus
Fungi

Aspergillus Cadida sp Nocardia sp Cryptococcus sp Histoplasma sp Pneumocystis
Organisme penyebab pd keadaan khusus

Kondisi Patogen Penyebab
*

* Usia lanjut * Pend. Peny. Jantung

Alcoholism * Cystic fibrosis * Mech. Ventilation AIDS
Enteric gram negatif, Haemophylus influenzae, Pneumococcus Pneumococcus, gram negatif

Klebsiela pneumoniae, H. influenzae, Pneumococcus
P. aeroginosa, Staphylokokus aureus P. aeroginosa, gram negatif lainnya Pneumocystis carinii, cytomegalovirus; TB
Table : Main Pathophysiologic mechanism of Pneumonia

Mechanism Examples
Staphylococcus aureus; exstrapulmonary bacteremias
Hematogenous spreads Inhalation of aerosol
Mycoplasma pneumonia , Chlamidophyla pneumpniae, Legionella pneumophylia, Chlamidophila psittaci Streptococcus pneumoniae, haemophylus Influenza, Gram negatif bacili, anaerob Mycobacterium tuberculosis, Pneumocystis jiroveci
Aspiration of oropharyngeal secretion Reactivation of latent miroorganism

1. Pendahuluan.
8. Komplikasi
AREA STERIL !
Lower Airways
TRACHEA
MAINSTEM BRONCHI
(ADA MEKANISME PERTAHANAN PARU YANG MENJAGA AREA INI DALAM KEADAAN STERIL)
BRONCHIOLES
ALVEOLI
Mekanisme Pertahanan Tubuh

a. Filtrasi b. Reflek bersin
Bakteri
c. Reflek batuk
d. Gerakan mukosilia
1. Sel makrofag Asinus 2. Antibodi
Patogenese
Aspirasi Inhalasi
Hematogenous
Langsung
Predisposisi : influenzae alkoholisme gizi jelek / kurang
Komorbid :
Pneumonia
diabetes mellitus gagal ginjal menahun ggan imuniti PPOK pneumokoniosis
Figure 1. Neutrophils and Lung Infection
N Engl J Med 2008;358:716-27.
Sekali patogen berhasil menembus mekanisme pertahanan paru

Inflamasi
Substitusi udara di dalam alveoli (air spaces) oleh cairan eksudat (= KONSOLIDASI)
Shunting
Tgl 21 01 - 2007 jam 21.28
FiO2
Analisa gas darah
29 %
Normal
pH pCO2
7,287 45,7
41 22,1 - 5,2 73 % 250
7.35 7.45 35 45
80 - 100 22 - 24 +2 98 10
Asidosis Respiratoir
pO2 HCO3 BE SaO2
Severe Hipoxemia
Shunting
A-a DO2
Cara kuman mencapai permukaan saluran nafas
kuman
1. Inokulasi langsung 2. Hematogen
3. Inhalasi
4. Kolonisasi permukaan mukosa
Pneumonia ( Keradangan parenkhim paru )
Asinus
Gambaran Pneumonia

1. Pendahuluan.
8. Komplikasi
Pneumonia
CAP ( Community Aquired Pneumonia )
Sumber infeksi
HAP ( Hospital Aquired Pneumonia )
Aspirasi Pneumonia Immuno - compromised
Pneumonia
Bakterial
Penyebab infeksi
Atipycal
( mycoplasma, clamydia )
Virus Jamur/patogen lain
Berdasar Gambaran Foto Toraks

Pneumonia
Pneumonia Lobaris
Bronchopneumonia
Pneumonia Interstitialis
Virus, infeksi oportunistik ( Pn Carinii )
Bakteri
Bakteri - Virus
Lobus lobus pada paru
Bilateral multifocal
BRONCHOPNEUMONIA
Interstitiel Pneumonia
Beda CAP - HAP

Penampilan Klinis CAP ( Community ) HAP ( Hospital )
Terjadinya
Jenis kuman
Sebelum MRS
Gram (+) positif
2 hari setelah MRS

Gram (-) Negatif
Klinis
Perjalanan Penyakit
Gejala pneumonia
antibiotika adekuat membaik
lebih berat
Sering : sepsis gagal nafas
Beda Pneumonia Bakterial dan Atypikal

Penampilam Klinis
Bakterial
Akut ( 1 2 hari )
Atypikal
Subakut ( 3 -4 hari )
Onset Febris Batuk Manifestasi Paru Manifestasi Ekstra Paru
Panas, menggigil Kurang tinggi

Hebat dengan dahak purulen Menonjol ( Nyeri dada, Sesak nafas ) Kurang Batuk tidak produktif
Kurang
Menonjol ( Mialgia, Anoreksia, cephalgia & atralgia)
Mycoplasma
Smallest cellular microbe
Lack walls ( Tidak mempunyai dinding sel )

Not affected by antimicrobial drugs
Common cause of pneumonia Atypical
Makrolide
Struktur Bakteri
( Prokaryotic cell )
Structure Prokaryotic Cells ( Bakteri )
Struktur dinding sel bakteri Gram (+) dan Gram (-)
Gram
Gram
Struktur dinding sel bakteri Gram ( - )
Lipid A
Lipopolysacharide
Endotoxin
Toxic componen of endotoxin
Phagocyte Ingests and degrades Gram-negative bacteria and is activated by LPS to secrete cytokines
IL-1
IL-8
TNF-
Local effects
IL-6
IL-12
Activates vascular endothelium Activates lymphocytes Local tissue destruction Increases access of effector cells
Chemotactic factor for neutrophils Increases access of effector cells activates binding by 2 integrins Activation of PMNs (with TNF-)
Activates vascular endothelium and increases vascular permeability, which leads to increased entry of IgG, complement, and cells to tissues and increased fluid drainage to lymph nodes
Lymphocyte activation Increased antibody production
Activates NK cells Induces the differentation of CD4 T cells into TH1 cells
Systemic effects Fever Production of IL-6 Fever Mobilization of metabolites Shock Fever Induces acute-phase protein production
Janeway, 1999 Immuno Biology

1. Pendahuluan.
8. Komplikasi
Dx ditegakkan berdasarkan : 1. Gejala klinis 2. Pemeriksaan fisik
3. Pemeriksaan penunjang
Diagnosa Pneumonia
1
Gejala Klinis
a. b. c. d. Suhu tubuh meningkat > 40 0 C Menggigil Batuk dahak purulen / darah. Nyeri dada
Pemeriksaan Fisik Paru
Tanda Konsolidasi : Perkusi redup Suara nafas bronkovesiculer / bronkial Rhonki basah paru
Pemeriksaan Penunjang
a. b. c. d.
Foto Toraks Laborat ( Lekositosis/lekopeni ) Periksa dahak, kultur , serologi Analisa gas darah ( Kasus berat )
Tanda & Gejala

Demam mendadak, menggigil. Batuk, dahak awal putih kuning kehijauan
batuk darah.
Nyeri dada, ringan sampai berat. Gejala lain : nyeri otot, pusing, mual, muntah.
Pneumonia
Batuk dahak purulen ( kuning kehijauan )
Pemeriksaan fisik
Inspeksi / palpasi sisi hemitoraks yg sakit tertinggal
Palpasi / Perkusi / Auskultasi tanda-tanda KONSOLIDASI :

Redup Fremitus raba / suara meningkat Suara napas bronkovesikuler - bronkial Ronki basah
Pemeriksaan penunjang
1) Pemeriksaan dahak ( sputum )
2) Darah 3) Foto toraks PA / lateral
4) Analisa gas darah
Pemeriksaan dahak ( sputum )

Dilakukan pengecatan Gram ( Gram + atau - )
Dilakukan kultur dahak ( biakan kuman ) ,
sensitifitas terhadap antibiotika
Wahyuningsih, Pertamina Central Hospital
Pemeriksaan Bakteriologik
Pengambilan bahan untuk bakteriologik :
1. Non Invasif : Dahak dibatukkan, 2. Invasif : Aspirasi Transtrakeal, Sikatan Bronkus, Bronchoalveolar lavage ( BAL ) 3. Bahan lain : Darah, Cairan Pleura, Aspirasi Trans trakeal, transtorakal
Pemeriksaan darah
meningkat Bakteri
Lekosit
Normal/ rendah
Virus Mikopalsma Infeksi berat
lekopenia
Gram negatif Keganasan Gangguan kekebalan
Pemeriksaan darah
C-Reactive Protein ( CRP ) .
Procalcitonin
Kultur darah Kuman penyebab / sensitivitas antibiotika
PCP ( Pneumonia Jiroveci ) : HIV ( AIDS )
Foto Toraks Pneumonia
Pneumonia kanan
Pneumonia kanan
LOBAR PNEUMONIA
LOBAR PNEUMONIA
BRONCHOPNEUMONIA
Bilateral multifocal
BRONCHOPNEUMONIA
CT Air-bronchogram
LUNG ABSCESS
Gb. 11 : Aspiration Pneumonia

1. Pendahuluan.
8. Komplikasi
Pengobatan Pneumonia
Terapi : Antibiotika diberikan secara Empiris
( Antibiotika diberikan sebelum tunggu hasil kultur )

Terapi Empiris berdasarkan : * Pengetahuan tentang Pola kuman
* Sensitifitas dari peneliti sebelumnya

* Sifat farmakologi obat.
Alasan terapi antibiotik secara empirik :

Mortaliti pneumonia yang tinggi
penundaan pemberian antibiotik > 4 jam setelah MRS mortaliti
Sulitnya menemukan kuman patogen
30-60% kuman tidak teridentifikasi

Keterbatasan tes-tes diagnostik untuk
identifikasi kuman patogen
Bacteriologic profile of CAP

11% 16%
H. influenzae S. pneumoniae M. catharrhalis
23% 39% 11%

M. pneumoniae Miscellaneous
Weis MS, 2000
Contoh Pola Kuman CAP
Pneumonia
1. Rawat jalan
2. Rawat Inap
1. Ruang Inap biasa
2. Ruang Intesif ( ICU )
Pneumonia PORT Score

Karakteristik pasien Faktor demografik Laki-laki Perempuan Panti jompo Faktor komorbid Penyakit keganasan Penyakit hati Gagal jantung kongestif Penyakit serebrovaskuler Penyakit ginjal
PORT : Pneumonia Patient Outcome Research Team
Jumlah Skor
Umur (.th) Umur (.th) 10 + 09 + 30 + 20 + 10 + 10 + 10
Karakteristik pasien Temuan pemeriksaan jasmani Perubahan tingkat kesadaran Pernapasan 30 kali/menit Tekanan < 90 mmHg Suhu < 35 C atau 40 C Nadi 125 kali/menit
Temuan laboratorik pH < 7.35 Ureum > 30 mg/dl Natrium < 130 mEq/L Glukosa > 250 mg/dl Ht < 30% PO2 < 60 mmHg Efusi pleura
Jumlah Skor
+ 20 + 20 + 20 + 15 + 10
+ 30 + 20 + 20 + 10 + 10 + 10 + 10
Tabel 4. Stratifikasi pneumonia berdasarkan jumlah risiko, mortalitas dan jenis rawat menurut PORT
Kelas risiko
I II
Jml risiko
Tidak diprediksi 70
Mortalitas (%)
0,1 0,6
Jenis rawat
Rawat jalan Rawat jalan
III
IV
71-90
91-130
2,8
8,2
Rawat inap / rawat jalan

Rawat inap
> 130
29,2
Rawat inap
Community-Acquired Pneumonia Risiko rendah - Rawat jalan - Pemberian antibiotik P.O. Risiko sedang/berat - Rawat inap Pemberian antibiotik I.V. Evaluasi klinis dalam 48-72 jam
Klinis menetap/ memburuk

(lihat slide berikutnya)
Klinis stabil / membaik - Sulih ke terapi antibiotik p.o.(hari ke 3) Keluar rumah sakit (hari ke 4) (Strategi pemulangan pasien pneumonia rawap inap lebih dini)
EVALUASI : 48 - 72 jam
Suhu kembali normal hari 2 - 4 RHONKI (-) Hari 7 ( 60-80%)
Perbaikan klinis
Leukosit kembali normal hari 4 Perbaikan X-ray. 2 mgg ( 50.6 %) 4 mgg ( 66.7 %)
Jangan rubah Tx antibiotik < 72 jam, kecuali jika KLINIS MEMBURUK
Antibiotic Treatment CAP

( Empirical antimicrobial therapy ).
Outpatient treatment
A. Macrolide (azithromycin, clarithromycin, or erythromycin)

B. Doxycycline
Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines

( Empirical antimicrobial therapy ). Outpatient treatment
Ada Penyakit Penyerta : A. Fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin ) B. Beta-lactam plus a macrolide (High-dose amoxicillin or amoxicillin-clavulanate; alternatives include ceftriaxone, cefpodoxime, and cefuroxime doxycycline

Inpatient, Non-ICU treatment
Fluoroquinolone
Beta-lactam plus a macrolide (Preferred blactam agents include cefotaxime, ceftriaxone, and ampicillin; ertapenem for selected patients;
Fluoroquinolone should be used for penicillinallergic patients.


( Empirical antimicrobial therapy ). Inpatient, ICU treatment
b-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam) plus either azithromycin or a fluoroquinolone (For penicillin-allergic : fluoroquinolone and aztreonam are recommended.) For Pseudomonas infection, use (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus either ciprofloxacin or levofloxacin (750-mg dose) or the above b-lactam plus an aminoglycoside and azithromycin or the above b-lactam plus an aminoglycoside and an antipneumococcal fluoroquinolone (for penicillin-allergic , substitute aztreonam for the above b-lactam). For community-acquired methicillin-resistant Staphylococcus aureus infection, add vancomycin or linezolid.

Inpatient, ICU treatment b-lactam (cefotaxime, ceftriaxone, or ampicillinsulbactam) plus either azithromycin or a fluoroquinolone For penicillin-allergic :
( fluoroquinolone and aztreonam are recommended.)

For Pseudomonas infection, use (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus either ciprofloxacin or levofloxacin (750-mg dose) or the above b-lactam plus an aminoglycoside and azithromycin or the above b-lactam plus an aminoglycoside and an antipneumococcal fluoroquinolone (for penicillin-allergic , substitute aztreonam for the above b-lactam).

For community-acquired methicillin-resistant Staphylococcus aureus infection, add vancomycin or linezolid.
Terapi Antibiotika Pneumonia
Rawat Jalan
Comorbid (-)
Rawat Inap
Non ICU
Comorbid (+)
ICU
- Macrolide
- Fluoroquinolon - -lactam + Macrolide

- -lactam + Macrolide/ Fluoroquinolon
Pneumonia Nosokomial
(Hospital Aquired Pneumonia)
Pneumonia Nosokomial ( Hospital aquired Pneumonia =HAP)
a. Pneumonia nosokomial ( HAP ) :

Pneumonia yang terjadi setelah pasien 48-72 jam dirawat di rumah sakit.
b. Ventilator assosiated pneumonia ( VAP ) :

Pneumonia yang terjadi lebih dari 48 jam setelah
pemasangan intubasi endotrakeal
Common HAP Pathogens

Enterobacter spp.
11.2% 4.3% 31.5% 7.2% 4.3% 17% 4.7% 1.7% 18.1%
E. coli
K. pneumoniae
H. influenzae P. aeruginosa S. aureus Enterococcus spp. C. albicans Other
NNIS System. Am J Infect Control. 1999;27:520-532.
Etiology of VAP as documented by bronchoscopy techniques in 24 studies for a total of 1689 episode and 2490 pathohen
Pathogen Pseudomonas aeroginosa Acinetobacter spp Sternotrophomonas maltophilia Enterobacteriaceae Haemophylus sp Staphyloccocus aerius Streptococcus pneumonia Streptococcus spp Coagulase negative staphyloccoci Neiseria spp Anaerob Fungi Other ( < 1% each ) Frequency %
24,4 7.9 1,7 14,1 9,8 20,4 4,1 8,0 1,4 2,6 0,9 0,9 3,8
PATHOGENESIS HAP Sources of pathogens for HAP include healthcare devices, the environment (air, water, equipment, and fomites), and commonly the transfer of microorganisms between the patient and staff or other patients (Level II) A number of host- and treatment-related colonization factors, such as the severity of the patients underlying disease, prior surgery, exposure to antibiotics, other medications, and exposure to invasive respiratory devices and equipment, are important in the pathogenesis of HAP and VAP (Level II)
ATS/IDSA Guidelines. Am J Respir Crit Care Med. 2005;171:388-416.
PATHOGENESIS HAP
Aspiration of oropharyngeal pathogens, or leakage of secretions containing bacteria around the endotracheal tube (Level II)
Inhalation or direct inoculation of pathogens into the lower airway, hematogenous spread from infected intravenous catheters, and bacterial translocation from the gastrointestinal tract lumen (Level II)
Infected biofilm in the endotracheal tube, with subsequent embolization to distal airways, may be important in the pathogenesis of VAP (Level III) The stomach and sinuses may be potential reservoirs of nosocomial pathogens that contribute to bacterial colonization of the oropharynx, (Level II)
Buku Ajar Ilmu Penyakit Paru FK UNAIR RSUD Dr Soetomo 2004
Klasifikasi Pneumonia Nosokomial

Berdasarkan ATS, dengan melihat 3 faktor sbb : 1. Beratnya penyakit pneumonia * Ringan sedang * Berat 2. Faktor risiko 3. Onset dari penyakit pneumonia * Onset dini ( < 5 hari ) * Onset lanjut ( > 5 hari ) Kelompok I Kelompok II Kelompok III
Pneumonia ringan-sedang, onset setiap saat, tak ada faktor risiko atau pneumonia berat dengan onset dini dan tak ada faktor risiko Pneumonia ringan-sedang, onset setiap saat, faktor risiko spesifik Pneumonia berat, onset setiap saat, faktor risiko spesifik dan atau pneumonia berat dengan onset lambat dan tak ada faktor risiko
Algoritma klasifikasi Pneumonia Nosokomial

Beratnya Penyakit Ringan - sedang Faktor Risiko Tidak ada
Onset setiap saat Ada
Berat Faktor Risiko Tidak ada Onset DINI Onset LAMBAT Ada Onset setiap waktu
Onset setiap saat Kelompok II
Kelompok I
Kelompok I
Kelompok III
Kelompok III
Kelompok I : Pneumonia ringan-sedang, onset setiap saat, faktor risiko (-) atau pneumonia berat dengan onset dini & faktor risiko (-)
Patogen potensial
Streptococcus pneumoniae Haemophilus influenza Metisilin sensitif staphylococus aureus ( MSSA ) Gram negatif enterik - E coli - Klebsiella pneumonia - Enterobacter sp - Proteus spp
Antibiotika yg direkomendasikan
Sefalosporin G 3 nonpseudomonal ( Seftriakson, Sefotaksim ) Atau Betalaktam + antibetalaktamase ( Amoksisilin klavulanat )
Atau (Jika alergi Penicilin ) Quinolon ( Levofloksasin, Moksifloksasin, Gatifloksasin )
Pedoman Diagnosis & Penatalaksanaan Pneumonia Nosokomial PDPI 2005
Kelompok II : Pneumonia ringan-sedang, onset setiap saat, faktor risiko (+)
Patogen potensial
Streptococcus pneumoniae
Sefalosporin G 2/3 nonpseudomonal ( Seftriakson, Sefotaksim )
Atau
Haemophilus influenza Metisilin resisten staphylococus aureus ( MRSA ) Gram negatif enterik - E coli - Klebsiella pneumonia - Enterobacter sp - Proteus spp Jika curiga : Anaerob Jika curiga : Legionella spp Jika curiga : MRSA
Quinolon ( Levofloksasin, Moksifloksasin, Gatifloksasin )

Atau
Betalaktam + antibetalaktamase ( Amoksisilin klavulanat )
Klindamisin atau Mertronidazol Makrolid atau Fluorokuinolon Vankomisin
Jika curiga : Pseudomonas Aeroginosa
Sesuai kelompok II
Kelompok III : Pneumonia berat, onset setiap saat, faktor risiko (+) spesifik dan atau pneumonia berat & onset lambat dan faktor risiko (-)
Patogen potensial
Streptococcus pneumoniae
Haemophilus influenza Metisilin resisten staphylococus aureus ( MRSA ) Gram negatif enterik - E coli - Klebsiella pneumonia - Enterobacter sp - Proteus spp Kuman lain : Pseudomonas aeroginosa, Acinetobacter spp
Aminoglikosid dikombinasi dengan salah satu dibawah ini : @ @ @ @ @ @ Penisilin anti pseudomonas Piperasilin + Tazobactam Ceftasidin atau Cefoperazon Imipenem Meropenem Cefepim
Perbandingan Struktur Molekul Carbapenem

OH H C 3 N O OH O OH H H CH 3 S N O O OH H H N O OH O OH H N CH 3 S O O H N CH N CH O 3 3 NH H H H S H N H
Imipenem
Rentan terhadap renal DHP-I Berpotensi menyebabkan seizure
Meropenem
Stabil terhadap renal DHP-I Potensi menyebabkan seizure lebih rendah dari Imipenem Decreased gram-positive activity Stabil terhadap renal DHP-I Potensi menyebabkan seizure lebih kecil dari Mero dan Imi karena affinitas dengan GABA reseptor di CNS lebih rendah Stabilitas dalam larutan paling tinggi Paling aktif melawan P. aeruginosa
H C 3
Doripenem
N S NH 2 H
H C 3
Less alkaline side chain at position 2
Primaxin package insert. Merck & Co., Inc., West Point, Pennsylvania; 2003. Merrem package insert. AstraZeneca, Wilmington, Delaware; 2004. Data on file. Ortho-McNeil, Inc. Raritan, New Jersey.
Angka Kesembuhan Doripenem lebih tinggi daripada Imipenem dan Meropenem pada berbagai Patogen Gram Negatif
1)
80% 67%
75% 59% 50% 43%
2)
95% 79%
*
85%* 73% 75% 84%
100% 93%
P. aeruginosa
K. pneumonia
E. coli
P. aeruginosa
B. Fragilis
E. coli
K pneumonia
Doripenem Imipenem 500 mg q6h or 1000 mg q8h
Doripenem
Meropenem 1g q8h
*) Tidak Signifikan. Kriteria untuk perbedaan bermakna adalah +/- 15%
1. Adapted from Chastre et al. Clinical cure rate per patogen pada kasus Ventilator-Associated Pneumonia (VAP). 2. Adapted from Lucasti et al. Microbiological cure rate per patogen pada kasus complicated Intra Abdominal Infection (cIAI).
Doripenem lebih aman dan memiliki profil tolerabilitas setara dengan Carbapenem lainnya
Doripenem memiliki resiko minimal untuk terjadinya seizure
Doripenem adalah satu-satunya Carbapenem yang tidak diwajibkan mencantumkan class warning untuk seizure oleh US FDA Tidak terdapat kejadian seizure pada pemakaian Doripenem dalam pada uji klinis cIAI1 dan NP3
Adverse event lainnya setara dengan Imipenem

Study Drug-Related Adverse Events (1% in either arm) Patients dengan >= 1 Adverse Events Diarrhea Nausea Kenaikan hepatic enzyme Liver function abnormal Rash Vomiting Fungal infection
1. 2. 3. Lucasti et. Al 200; . Chastre et. Al Reaneto et al , CURRENT MEDICAL RESEARCH AND OPINION, VOL. 24, NO. 7, 2008, 2113 2126
Imipenem
(n = 263)
Doripenem
(n = 262)
17.5% 3.0% 2.3% 2.3% 1.5% 0.8% 0.8% 0.4%
17.2% 1.9% 1.1% 4.6% 0.8% 1.9% 1.5% 1.1%
Doripenem terbukti dapat menekan total biaya perawatan dengan kesembuhan yang lebih cepat
Medical Resource Utilization Data from VAP Study (cMITT Population)
30
P = .0102*
Doripenem 500 mg q8h Imipenem 500 mg q6h or 1000 mg q8h
25
Days (median) 20
15
10 5 0 22
27
P = .1232*
P = .0338*
12
13
7
Total LOS LOS in Primary ICU
10
Duration of MV
*The Wilcoxon P value results from the comparison of time-to-event curves, where the event was either hospital discharge, ICU discharge, or end of mechanical ventilation. 1. Merchant et al. 2008. Clinical Theurapeutics
PEDOMAN TERAPI ANTIBIOTIKA PADA HAP

Beberapa pedoman terapi HAP : 1. Mampu mencakup minimal 90% kuman patogen 2. Diberikan secara intravena. 3. De-eskalasi
4. Diberi kombinasi antibiotika

5. Janganmengganti antibiotika sebelum 72 jam, kecuali keadaan klinis memburuk 6. Penggantian antibiotika berdasarkan data mikrobial dan uji kepekaan.
Table .Survival in subsets of patients with P aeruginosa Bacteremia : combination antibiotic therapy compared with monotherapy
Patient Subset Pneumonia Critically ill Noncritically ill Malignancy All Mortality Rates Combination Therapy Monotherapy 7/20 (35) 18/37 (49) 20/106 (19) 21/66 (32) 38/143 (27) 7/8 (88) 11/12 (92) 9/31 (29) 9/19 (47) 20/43 (47) P Value 0.033 0.016 NS NS 0.023
Chest 2001; 119: 373S-384S
Strategi De-eskalasi memenuhi kebutuhan terapi awal (empirik) yang adekuat dan meminimasi munculnya resistensi bakteri1) .
Terapi awal harus broad spectrum untuk menghindari terapi yang tidak adekuat
Berdasarkan data patogen lokal Gunakan guideline dan ketahui faktor-faktor resiko Dugaan Infeksi Berat / Serius
Mulai Terapi Antibiotik Empirik dengan Antibiotik Broad Spektrum / kombinasi untuk meng-cover semua kemungkinan patogen lokal yang ada
Jangan melakukan terapi lebih lama dari yang dibutuhkan

Sesuaikan dengan data klinis dan data kultur patogen yang tersedia
Patogen Ter-identifikasi?
Yes No
De-eskalasi Antibakteri Berdasarkan Hasil Data Microbiologi Klinis Data
Lanjutkan Terapi Empirik

Nilai Kembali Setelah Kurun Waktu yang Cukup Yes
Perbaikan Klinis Bermakna setelah 48-96 Jam Terapi Antibakteri ?

No
1) Kollef MH. Drugs. 2003;63:2157-2168.
Cari Superinfeksi, Pembentukan Abses, Penyebab Noninfeksi dari Gejala, Penetrasi Jaringan yang Tidak Memadai dari Antibiotik
Hentikan Antibiotik Setelah 7-14 Hari Berdasarkan Tempat Infeksi dan Respons
Terapi Pneumonia ok Jamur

PENYAKIT
Aspergilosis
PILIHAN I
Amphotericin B +/Rifampin atau Flucytosin Amphotericin B
ALTERNATIF
Itraconazole
Zygomycosis Kandidiasis
Amphotericin B + /- Ketokonazole/itraco Flucytosin nazole/fluconazole

1. Pendahuluan.
8. Komplikasi
Batuk Darah
Efusi PleuraEmpyema
Abses Paru
Acut Lung Injure
Komplikasi Pneumonia
Gagal Nafas SepsisSeptik syok ARDS
Meninggal
Komplikasi : Gagal Nafas ( ARDS )
Penatalaksanaan Pneumonia Komunitas ( CAP )
2. Penderita Rawat Intensif : ( Pneumonia Berat ) a. Pengobatan suportif / simptomatis 1. Istirahat di tempat tidur 2. Terapi Oksigen 3. Infus untuk rehidrasi 4. Obat simptomatis, Antipiretik Mukolitik / ekspektorans
b. Pemberian Antibiotika
c. Bila ada indikasi : Dipasang Ventilator Mekanik

b-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam) plus either azithromycin (level II evidence) or a fluoroquinolone (level I evidence) (strong recommendation) (For penicillin-allergic : fluoroquinolone and aztreonam are recommended.) For Pseudomonas infection, use (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus either ciprofloxacin or levofloxacin (750-mg dose) or the above b-lactam plus an aminoglycoside and azithromycin or the above b-lactam plus an aminoglycoside and an antipneumococcal fluoroquinolone (for penicillin-allergic , substitute aztreonam for the above b-lactam). (Moderate recommendation; level III evidence.) For community-acquired methicillin-resistant Staphylococcus aureus infection, add vancomycin or linezolid. (Moderate recommendation; level III evidence.)
Duration of Antibiotic Therapy

Patients with CAP should be treated for a minimum of 5 days (level I evidence), should be afebrile for 4872 h. A longer duration of therapy may be needed if initial therapy was not active against the identified pathogen or if it was complicated by extrapulmonary infection,such as meningitis or endocarditis. (Weak recommendation; level III evidence.
Most patients with CAP have been treated for 710 days .
The presence of cavities or other signs of tissue necrosis may warrant prolonged treatment.
When to consider switch to oral therapy

Early switch to oral therapy can reduce hospital length of stay It may improve overall outcome But need an appropriate criteria :
Improvement in cough & dyspnea Afebrile ( 72 hour without fever ) WBC decrease ( Normal leucosit ) Functioning GI tract with adequate oral intake
Defining treatment failure

Early treatment failure (< 72 hours)
Hemodynamic instability Respiratory failure Need for mechanical ventilation Radiographic progression New metastatic infection foci Persistence / reappearance of fever & symptoms Hemodynamic instability Development of respiratory failure (PaO2 < 8 kPa or saturation < 90% with FiO2 of 0.21) Radiographic progression New infectious foci after 72 hours
Late treatment failure ( 72 hours)
Risk factors for treatment failure

OR (95% CI) Influenza vaccination COPD Liver disease Pleural effusion Multilobar CAP Cavitation Flouroquinolone treatment Risk class Leucopenia < 4000 / cmm Hyponatremia < 135 mEq/mL 0.3 0.6 2.0 2.7 2.1 4.1 0.5 1.3 3.7 1.6 (0.2 0.6) (0.4 0.9) (1.1 3.5) (1.8 4.2) (1.4 2.9) (1.3 13.5) (0.3 0.9) (1.1 1.5) (1.4 10.2) (1.1 2.4)
Menendez R. Thorax 2004;59:960-965
Table . Criteria for severe community-acquired pneumonia.

I.
II.
Minor criteriaa a. Respiratory rateb 30 x/min b. PaO2 / FiO2 ratiob 250 c. Multilobar infiltrates d. Confusion / disorientation e. Uremia ( BUN level, 20 mg/dL) f. Leukopeniac ( WBC count, < 4000 cells/mm3) g. Thrombocytopenia (platelet count, < 100,000 cells/mm3) h. Hypothermia ( temperature, < 360 C) I. Hypotension requiring aggressive fluid resuscitation Major criteria a. Invasive mechanical ventilation b. Septic shock with the need for vasopressors
NOTE. BUN, blood urea nitrogen; PaO2/FiO2, arterial oxygen pressure/fraction of inspired oxygen; WBC, white blood cell. a Other criteria to consider include hypoglycemia (in nondiabetic patients), acute alcoholism/alcoholic withdrawal, hyponatremia, unexplained metabolic acidosis or elevated lactate level, cirrhosis, and asplenia. b A need for noninvasive ventilation can substitute for a respiratory rate >30 breaths/min or a PaO2/FiO2 ratio < 250. c As a result of infection alone.
FAKTOR Predisposisi / risiko Pneumonia Nosokomial ( Hospital aquired Pneumonia =HAP)

a. Faktor berhubungan dg DAYA TAHAN TUBUH : 1. Penyakit kronis ( PPOK, DM, Jantung, Ginjal )
2. Perawatan di RS lama 3. Pasien koma 4. Pemakaian obat tidur 5. Intubasi endotrakeal 6. Malnutrisi 7. Usia lanjut 8. Pemakaian steroid 9. Waktu operasi lama
FAKTOR Predisposisi / risiko Pneumonia Nosokomial ( Hospital aquired Pneumonia =HAP) b. Faktor Eksogen: 1. Penggunaan antibiotika 3. Peralatan terapi pernafasan 4. Pemasangan NG Tube ( sonde ) 5. Pemberian antasida 6. Lingkungan Rumah Sakit :
a. Cuci tangan yang tidak sesuai prosedur

b. Pemasangan alkes : ventilator, selang infus, kateter, sonde makanan, penyuntikan obat
Bacterial isolates from Bronchial aspirate (Sputum) in ICU Dr. Soetomo Hospital Surabaya Jan Dec 2006
Pseudomonas aeroginosa Klebsiella pneumoniae Acinetobacter spp Enterobacter aerogenes Staphylococcus aureus Pseudomonas spp Streptococcus viridans Lain
Total
75 40 26 7 7 5 5 8 173
43.4 % 23.1 % 15.0 % 4.0 % 4.0 % 2.9 % 2.9 % 5.7 % 100.0
Fungal pathogens.
Nosocomial pneumonia ( fungi Candida and Aspergillus fumigatus ) : * Organ transplant * Immunocompromised ( DM, Steroid, HIV, Cancer ) , * Neutropenic ( leucopenia ) patients.
Nosocomial Aspergillus :associated with contaminated air

ducts or hospital construction. Isolation of Candida albicans and other Candida species from endotracheal aspirates is common, but usually represents colonization of the airways
Viral pathogens.
Incidence of HAP & VAP due to viruses is low in immunocompetent hosts. Diagnosis viral infections : by rapid antigen testing and viral culture or serologic. Pneumonia in patients with influenza A or B may be due to the virus, to secondary bacterial infection, or both. Influenza is transmitted directly from person to person when infected persons sneeze, cough, or talk.
Clinical Diagnosis of HAP

Chest radiographic abnormality
New, progressive, or persistent for >24 hours More likely if
Progressive cavitation Air space process abutting a fissure Air bronchograms Infiltrate next to an empyema
Evidence of infection (2 of the following)

Purulent sputum Temperature <36 C or >38 C Leukocyte count <5,000 or 10,000
Blood culture
Specific, but not sensitive
Higgins. Curr Treat Options Infect Dis. 1999;1:159-175.
Klasifikasi Pneumonia Nosokomial

Berdasarkan ATS, dengan melihat 3 faktor sbb : 1. Beratnya penyakit pneumonia * Ringan sedang * Berat 2. Faktor risiko 3. Onset dari penyakit pneumonia * Onset dini ( < 5 hari ) * Onset lanjut ( > 5 hari ) Kelompok I Kelompok II Kelompok III
Pneumonia ringan-sedang, onset setiap saat, tak ada faktor risiko atau pneumonia berat dengan onset dini dan tak ada faktor risiko Pneumonia ringan-sedang, onset setiap saat, faktor risiko spesifik Pneumonia berat, onset setiap saat, faktor risiko spesifik dan atau pneumonia berat dengan onset lambat dan tak ada faktor risiko
Kriteria Pneumonia Nosokomial BERAT ( ATS )

a. b. c. Di Rawat di - I C U Ada tanda Gagal Nafas ( memerlukan ventilator ) Perubahan radiologik progresif
d.
Terdapat Sepsis Berat

1. Syok ( Tensi Sistolik < 90 mmHg / Diastolik < 60 mmHg )
2. Memerlukan Vasopressor 3. Jumlah urine < 20 ml / jam / Total urine 80 ml/24 jam 4. Ada Gagal ginjal akut, perlu dialisis
Risk factors HAP

Risk factors Pathogen
Abdominal surgery, aspiration Coma, DM, renal failure Corticosteroids

Long ICU stay, corticosteroids, underlying lung dz, prior abx use
Anarobes
S. aureus
Legionella
Psuedomonas
Patogen penyebab Pneumonia berdasarkan onset timbulnya pneumonia

Pneumonia onset dini
Streptococcus pneumonia Haemophilus influenza Moraxella catarrhalis Staphyloccocus aerius Aerobic ( Gram negatif baccili )
Pneumonia onset lanjut

Pseudomonas aeroginosa Enterobacter spp Acinetobacter spp Klebsiella pneumoniae Serratia marcescens S. Aureus ( pada pasien dengan faktor risiko: termasuk MRSA )
Lain-lain
Bakteri anaerob Legionella pneumophillia Influenza A dan B Resp syncitial virus Fungi
TERAPI ANTIBIOTIKA
( Hospital aquired Pneumonia =HAP) Beberapa pedoman terapi HAP : 1. Terapi awal antibiotika diberikan secara empirik ( Harus mampu mencakup minimal 90% kuman patogen ) 2. Pemberian terapi antibiotika harus secara intravena. 3. Pemberian antiobiotika secara De-eskalasi ( harus dipertimbangkan bila ada hasil kultur ) 4. Diberi kombinasi antibiotika pada pasien dengan MDR
5. Tidak mengganti antibiotika sebelum 72 jam, kecuali keadaan klinis

memburuk 6. Penggantian antibiotika berdasarkan data mikrobial dan uji kepekaan.
HAP, VAP or HCAP suspected

Obtain lower respiratory tract (LRT) sample for culture (quantitative or semi-quantitative) and microscopy Unless there Is both a low clinical suspicion for pneumonia and negative microscopy of LRT sample, begin empiric antimicrobial therapy using algorithm and local microbiologic data
Days 2 and 3: Check cultures and assess clinical response:

(temperature, WBC, chest X-ray, oxygenation, purulent sputum, haemodynamic changes and organ function)
Clinical improvement at 4872 hours

NO
Cultures Search for other pathogens, complications, other diagnoses or other sites of infection
YES
Cultures +
Cultures Cultures +
De-escalate antibiotics, if possible. Treat selected patients for 78 days and reassess
Adjust antibiotic therapy, search for other pathogens, complications, other diagnoses or other sites of infection
Consider stopping antibiotics
Am J Respir Crit Care Med. 2005;171:388416
Empiric Antibiotic Therapy for HAP
HAP, VAP or CAP Suspected ( All disease severity ) Late Onset ( > 5 days) or Risk Factor for MDR pathogens
(Tabel 2)
No
Limited spectrum Antibiotic Therapy ( Tabel. 3 )
Yes
Broad spectrum Antibiotic Therapy For MDR pathogens ( Tabel. 4 & 5 )
Table 3. Initial Empiric Antibiotic Therapy For HAP or VAP in Patients with No Known Risk Factors for Multidrug-Resistant Pathogens, Early Onset, and Any Diseases Severity Potential Pathogen Recommended Antibiotics*
Streptococcus pneumoniae Haemophilus influenzae Methicillin-sensitive enteric gram negative bacilli Escherichia coli Klebsiella pneumoniae Enterobacter species Proteus species Serratia marcescens
Ceftriaxone or Levofloxacin,moxifloxacin,or ciprofloxacin or Ampicillin/sulbactam or Ertapenem

Am J Respir Crit Care Med 2005; 171: 388-416
Empiric Antibiotic Therapy for HAP
HAP, VAP or CAP Suspected ( All disease severity ) Late Onset ( > 5 days) or Risk Factor for MDR pathogens
(Tabel 2)
No
Limited spectrum Antibiotic Therapy ( Tabel. 3 )
Yes
Broad spectrum Antibiotic Therapy For MDR pathogens ( Tabel. 4 & 5 )
Tabel 4: Terapi antibiotika awal secara empirik untuk HAP / VAP pada pasien
dengan onset lanjut / ada faktor risiko patogen MDR ATS/IDSA 2004 )
Patogen potensial
Patogen MDR tanpa atau dengan patogen pada Tabel .1 Pseudomonas aeroginosa Klebsiela pneumonia Acinetobacter sp
Sefalosporin antipseudomonas ( Sefepim, Seftasidin, Sefpirom ) Atau Karbapenem antipseudomonas ( Meropenem, imipenem ) Atau -laktam / pengambat laktamase ( Piperasilin tasobaktam ) ditambah Flurokuinolon ( Siprofolksasin / levofloksasin Atau Aminoglikosida ( Amikasin, gentamisin / tobramicin ) Ditambah LInesolid atau vankomisin atau teikoplanin
Methicillin Resisten Staphyloccus aureus ( MRSA ) Legionella pneumophylia
Table 5 .Initial Intravenous, Adult Doses of Antibiotics for Empiric Therapy of Hospital-Acquired Pneumonia,and Healtcare-Associated Pneumonia In Patients with Late-Onset Disease or Risk Factors for MDR Pathogens
Antibiotic
Antipseudomonal cephalosporin Cefepime Ceftazidime Carbapenems Imipenem Meropenem -lactam/-lactamase inhibitor Piperacillin-tazobactam Aminoglycosides Gentamicin Tobramycin Amikacin Antipseudomonal quinolones Levofloxacin Ciprofloxacin Vancomycin Linezolid
Dosage*
1-2g every 8-12h 2g every 8h
500mg every 6h or 1g every 8h 1g every 8h
4.5g every 6h
7mg/kg per d 7mg/kg per d 20mg/kg per d
750mg every d 400mg every 8h 15mg/kg every 12h 600mg every 12h
Am J Respir Crit Care Med 2005; 171: 388-416
Table 2.
Risk factors for Multidrug-Resistant ( MDR ) Pathogens Causing

HA P, HcAP and VAP Antimicrobial therapy in preceding 90d Current hospitalization of 5d or more High frequency of antibiotic resistance in the community or in the specific hospital unit Presence of risk factors for HCAP : Hospitalization for 2 d or more in the preceding 90d Residence in a nursing home or extended care facility Home infusion therapy (including antibiotics) Chronic dialysis within 30 d Home wound care Family member with multidrug-resistant pathogen Immunosuppressive disease and/or therapy
Am J Respir Crit Care Med vol 171, pp 388-416, 2005
Recommendations for selected MDR pathogens

If P. aeruginosa pneumoniae is document, combination therapy is recommended level II If acinetobacter sp are document, the most active carbapenem,sulbactam,colistin and polymixin level II
If ESBL + Enterobacter , monotherapy with 3 rd cephalosporin

should be avoid level II Adjunctive therapy with inhaled especially in patient not improve
systemic therapy Level III

Linezolid is an alternative to vancomycin for the treatment of MRSA level II
ESBL : Extendet spectrum -lactamase
Faktor risiko MDR ( Multi drug resistant ) penyebab HAP dan VAP ( ATS / IDSA 2004 )
a. b. c.
Pemakaian antibiotika pada 90 hari terakhir Dirawat di RS > 5 hari Tingginya frekuensi resisten antibiotika di masyarakat atau di RS tersebut
d.
Penyakit immunosupresi & / pemberian imunoterapi
e.
f.
Ada faktor risiko pneumonia nosokomial

Ada terapi yang bersifat imunosupresif
Prognosis Pneumonia
Prognosa Pneumonia buruk pada keadaan :
1 2 3 4 5 Umur > 60 tahun Koma waktu masuk Perawatan di ICU Syok Pemakaian alat bantu nafas ( Ventilator )
6
7 8 9 10
Foto toraks : Infiltrat bilateral

Kreatinin > 1,5 mg / dl Penyakit yang mendasari berat ( Keganasan , DM ) Pengobatan awal tidak tepat Infeksi ok bakteri resisten
11
12
Gagal multi organ

Pemakaian obat penyekat H2 yg dapat meningkatkan ph pada pencegahan perdarahan usus
Pencegahan HAP
a. Vaksinasi
b. c. d. e. f. Pencegahan proses transmisi patogen Pencegahan terhadap terjadinya aspirasi Mengurangi penggunaan antibiotika yang tidak perlu Mempertahankan keasaman lambung Sterilisasi yang optimal terutama pada perawatan pre dan post operasi
Prevention
Infection control (hand washing) Positioning Semierect position decreases aspiration risk Prevent gastric colonization Careful use of stress ulcer prophylaxis Early enteral feeding Extubate as soon as ready Change vent circuit less frequently
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1

Penyakit penyakit Paru

C Obstruksi Nafas kronis

Penyakit Paru Kerja

Pokok Bahasan Infeksi

metabolism, toxins, intracellular replication or

Infeksi Saluran Nafas

Infeksi Saluran Nafas Spesifik

Infeksi Saluran Nafas Atas

Pembagian Saluran nafas

Saluran Nafas Atas

Saluran Nafas Bawah

URTI (Upper Respiratory Tract Infection)

Staphylococcus aureus Staphylococcus epidermidis Corynebacterium sp

Parainfluenza virus Respiratory syncitial virus

Fishmans, Pulmonary Diseases and Disorder Vol 2, 2008

Kolonisasi Kuman di Oropharyng

Staphylococcus aureus, Pseudomonas aeruginosa, and

Tabel: Mikrobiologi Akut Rhinosinusitis pada dewasa

Organism 1 2 3 4 Streptococcus pneumoniae Haemophilus influenzae Streptococcus species Anaerobes

Range of Prevalence (%) 20 43 22 35 39 09

Moraxella catarrhalis Staphylococcus aureus

Text Book of Respiratory medicine, Murray and Nadel Volume 1. 2005

Subjective Symptoms of Sinusitis

Komplikasi Sinusitis Complications of Sinusitis

Otitis media is the clinical term for a middle ear infection,

d) Faringitis gonorea e) Faringitis luetika f) Faringitis tuberkulosa

Penyebab paling sering : streptococcus.

LRTI (Lower Respiratory Tract Infection) 1) Bronkitis

tubes (airways), which causes increased

Kuliah Farmasi UBY 2007

Pokok bahasan Pneumonia

Pokok bahasan Pneumonia

Definition Pneumonia ( IDSA)

Infeksi / Keradangan Sinusitis Pharingitis Tonsilitis

Pokok bahasan Pneumonia

a. Bakteri : Gram positive, Gram Negative

Table: Common causes of pneumonia

Influenza A & B Parainfluenza Cytomegalovirus Adenovirus

Aspergillus Cadida sp Nocardia sp Cryptococcus sp Histoplasma sp Pneumocystis

Organisme penyebab pd keadaan khusus

* Usia lanjut * Pend. Peny. Jantung

Enteric gram negatif, Haemophylus influenzae, Pneumococcus Pneumococcus, gram negatif

Table : Main Pathophysiologic mechanism of Pneumonia

Hematogenous spreads Inhalation of aerosol

Aspiration of oropharyngeal secretion Reactivation of latent miroorganism

Pokok bahasan Pneumonia

Mekanisme Pertahanan Tubuh

Predisposisi : influenzae alkoholisme gizi jelek / kurang

diabetes mellitus gagal ginjal menahun ggan imuniti PPOK pneumokoniosis

Figure 1. Neutrophils and Lung Infection

N Engl J Med 2008;358:716-27.

Sekali patogen berhasil menembus mekanisme pertahanan paru

Tgl 21 01 - 2007 jam 21.28

pO2 HCO3 BE SaO2

Cara kuman mencapai permukaan saluran nafas

1. Inokulasi langsung 2. Hematogen

Pokok bahasan Pneumonia

HAP ( Hospital Aquired Pneumonia )

Aspirasi Pneumonia Immuno - compromised

Virus Jamur/patogen lain

Berdasar Gambaran Foto Toraks