6.pneumonia (new)

5/21/2018 6.Pneumonia (New)

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PNEUMONI

Dr. Abdul Rohman,

S P

K-3B


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an infection of peripheral lungparenchyma

Clinically an acute illness in which there aresigns of consolidation in thechest 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, distalbronkus terminalis konsolidasi jar

paru dan gangguan pertukaran gassetempat

DEFINITION


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- Red hepatization : 24 days

- Gray hepatization : 48 days

- Resolution : > 810 days

PATOGENESISMikroorganisme Lingkungan

Host

DEFENSE

Physical, Humoral & Cellular

CARA I NOKULASI langsung

INHALASI

HEMATOGEN

KOLONISASI (terbanyak)

FAKTOR RISIKO

Alkohol

Merokok

Peny. kronik:

- Jantung &

Paru

Obstruksi

bronkus


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Figure: Host defense in the respiratory tract


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Figure : Factor that interfere with host defence of respiratory tract


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kongesti

Red hepatization

(Udara di alveolus hilang digantidengan eksudat yang membeku

Grayhepatization

Resolusi

STADIUM PATOLOGI ANATOMI KLINIK


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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 +/-


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Table : Common Causes of Acute Pneumonia


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Key Points : About the Classification of Pneumonia


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Jenis pneumonia

Pneumonia komuniti (PK/CAP) : bakteri Gram

positif

Pneumonia nosokomial : bakteri Gram negatif

Pneumonia aspirasi : bakteri anaerob

Cara penularan

oDroplet Steptococcus pneumoniae

o

Slang infus Staphylococcus aureus

ETIOLOGY

O OG


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Pejamu Faktor Modifikasi

Lingkungan :luar or dalam RS,

ICU atau non ICU

ETIOLOGI


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(IN DESCENDING ORDER)

KEY POINTS : MOSTCOMMON 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)

KLASIFIKASI


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1. Klinis dan Epidemiologis

a. Pneumonia komuniti (communi ty-acqui red

pneumonia)

b. Pneumonia nosokomial (nosocomial pneumonia) :

- HAP

c. Pneumonia aspirasi

- VAP

d. Pneumonia pada penderita immunocompromised.

- HCAP

2 Bakteri Penyebab

KLASIFIKASI


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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


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DIAGNOSIS

Should not be made on history &

physical finding alone, a chest X-ray

should be taken

(In situations where chest x-ray is notpossible, 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 ma resent w/ PCP orDIAGNOSIS


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1. Gambaran Klinis

a. Anamnesis- Demam, menggigil, suhu s/d > 40C

- Batuk : keringmukoidpurulenkadang 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 : bronkovesikulerbronkial

ronki basah halus kasar pd stad resolusi

DIAGNOSIS

Th kl d b hi l b thi d d t i l over th


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These crackles and bronchial breathingwere recorded posteriorly overtheconsolidated 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 inspirator fine crackles ere recorded o er the right posterior lo er


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These late inspiratory fine crackleswere 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).


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These crackleswere 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).


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TYPICAL SYMPTOMS OF CAP

Fever

New cough w/ or w/o sputum

production Change in color of sputum in

patients w/ chronic cough

Pleutitic chest pain

Shortness of breath

Typical clinical features of bacterial pneumonia


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yp p

Clinical features Incidence (%)

Respiratory features

coughsputum

dyspnea

chest pain

upper respiratory tract symptomshemoptysis

9070

70

65

3313

Nonrespiratory

vomiting

confusion

diarrhea

rash

abdominal pain

20

15

15

5

5

Typical clinical features of bacterial


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Typical clinical features of bacterial

pneumonia

Clinical features Incidence (%)Signsfever

tachypnea

tachycardiaabnormal chest signs

hypotension

confusion

herpes labialis

8090

8090

8090

8090

20

15

10

DIAGNOSIS


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DIAGNOSIS

2. Pemeriksaan Penunjang

a. Gambaran radiologis Foto toraks (PA / lateral) penunjang utama diagnosis :

infiltratkonsolidasi dg air bronchogram, interstisial serta gambaran kaviti.

Foto torakspetunjuk 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 leukositpergeseran ke kiri dan peningkatan LED

- Diagnosis etiologi : dahak, kultur darah, dan serologi

- Kultur darah positif : 20 -25 % penderita tidak terobati

- Analisa gas darahhipoksemia dan hipokarbia

- Stadium lanjutasidosis respiratorik


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Lobar pneumoniaf h d l d h l d f h l


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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 abscessAnaerobic 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


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PNEUMONIA KOMUNITI


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ETIOLOGI

- Kepustakaan : Gram pos. & bakteri atipik- Indonesia : Gram negatip (beberapa kota)

- Klebsiella pneumoniae 45,18 % - Pseudomonas

aerugenosa 8, 56 %

- Streptococcus pneumoniae 14,04 % - Streptococcushemolyticus 7,89 %

- Streptococcus viridans 9,21 % - Enterobacter

5, 26 %

Staphylococcus aureus 9 00% Pseudomonas

PNEUMONIA KOMUNITI(DIDAPAT DI MASYARAKAT)

Essential of diagnosis


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g

Symptoms and signs of an acute lung infection:

fever or hypothermia, cough with or withoutsputum, 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 hospitalizedor residing in a long-term care facility for more

than 14 days before the onset of symptoms.


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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


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g

risiko infeksi

mikroorganisme

patogen spesifik

1. Pneumokokus resisten terhadap penisilin

Umur > 65 tahun

Memakai obat-obatan gol laktamselama 3 bulan terakhir

Pecandu alkohol

Penyakit gangguan kekebalan


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2. Bakteri enterik Gram negatif

Penghuni rumah jompo

Mempunyai penyakit dasarkelainan jantung paru

Mempunyai kelainan

penyakit yang multipel

Riwayat pengobatan


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3. Pseudomonas aeruginosa

Kelainan Struktural : Bronkiektasis

Pengobatan kortikosteroid > 10

mg/hari

Pengobatan antibiotik spektrum luas

> 7 hari pada bulan terakhir Gizi kurang ( malnutrisi )


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MODIFYING FACTORS THAT INCREASE THE RISK OF

INFECTION W/ SPESIFIC PATHOGENSPatogen Penincillin & Drug-

Resistant

Pneumococcl

Enteric Gram-ve

Organism

Pseudomonas

aeruginosa

Factors Age > 65 year

-lactam use withinthe last 3 month

Alcoholism

Immunosuppresion

Multiple medical

comorbidities Exposure to child in

daycare center

Cardiopulmonary

Nursing homeresident

Multiple medical

comorbidities

Recent antibiotic

therapy

Structural lung disease

(bronchiectasis) Prolonged

corticosteroid therapy

(> 10 mg

prednisolone/day)

Broad-spectrumantibiotic therapy > 7

days in the past month

Malnutrition


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SKEMA LANGKAH PERTAMA RUMUS PREDIKSI PNEUMONIA :MENDETEKSI PASIEN DENGAN KELAS RESIKO I


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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

S h 35C atau 40C

Karakteristik penderita Jumlah poinpend dgn kelas resiko II-IV


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p p

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 40C

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%

PO2 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


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(Pneumonia Patient Outcome Research Team)

Stratification of Risk Score


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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

Kriteria indikasi rawat inap PK berdasarkan kesepakatan PDPI:


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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/FiO2kurang 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


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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


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CURB-65

Clinical features Score

Confusion (defined as a Mental Test Score of 8, ordisorientation 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


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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 :mortalityintermediate(40%)

Consider hospital-supervised treatment

3 Group 3 :

mortality high(52%)

Manage in hospital as severe

pneumonia consider admission tointensive care unit, especially withCURB score of 4 or 5.


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KRITERIA PERAWATAN INTENSIF


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Minimal 1 dari 2 gejala mayor tertentu

1. Butuh ventilasi mekanik

2. Butuh vasopresor 4 jam (syok septik)

ATAU2 dari 3 gejala minor tertentu

1. PaO/FiO < 250 mmHg

2. Foto dada : kelainan bilateral3. Tekanan sistolik < 90 mmHg


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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


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Infiltrat + gejala klinis yg menyokong diagnosis pneumoniaTidak ada infiltrat

Evaluasi untuk kriteria rawat jalan/ rawat inap

Rawat jalan Rawat inap

Terapi empiris Pemeriksaan bakteriologis

MemburukR. Rawat biasa R. Rawat intensif

Terapi empiris

Membaik Memburuk

Di tatalaksana sbg diagnosis

lain

Membaik

Terapi empiris dilanjutkan

Terapi

kausatif

TERAPI EMPIRIK PK


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1. Sehat : Gram (Kota besar : ada Gram

)

2. Komorbid :Gram ditambahGram

3. Faktor modifikasi :

a. Pneumokokus resisten terhadap penisilin

b. Bakteri enterik Gram

c. Pseudomonas aerogenosa

Kesemuanya dapat ditambahkan makrolid baru

PENGOBATAN


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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 &

ey o n : ou rea men an u comePneumonia


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TERAPI SULIH (SWITCH THERAPY)


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Perubahan obat : suntik oral obat

jalano Masa perawatan dipersingkat

o Biaya perawatan kurang

o Mencegah infeksi nosokomial Ketersediaan obat ivobat oral & efektifitas

imbang

Streamlineobat disesuaikan hasil kultur

Sekuensial(obat sama, potensi sama) : levofloksasin,

moksifloksn, gatifloksasin

Switch over (obat berbeda, potensi sama: seftasidim iv

Kriteria Terapi Sulih


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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


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1. OPaO80-100 mmHg atau SaO95-96 %2. Nebulisasi : - humidifikasipengencer dahak

- bronkodilator

3. Fisioterapi dada :

- batuk dan napas dalampengeluaran dahak- fish mouth breathing lancarkan ekspirasi

pengeluaran CO 4. Pengaturan cairan

5. Kortikosteroid sepsis berat

B. Suportif


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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

(tid k d b ik 24 72 j )


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(tidak ada perbaikan2472 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 ataunonkardia

Nonbakterial (jamur

atau virus)

KOMPLIKASI


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Ektrapulmoner infeksius (pneumoniapneumokokus = 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( i k iti)


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1. Vaksinasi influenza dan pneumokokuspada :- 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

(pneumonia komuniti)

PENCEGAHAN(PNEUMONIA NOSOKOMIAL)


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Ditujukan pada upaya program pengawasan & pengontrolan infeksitermasuk :

- 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

(PNEUMONIA NOSOKOMIAL)

Rekomendasi Dalam Pengelolaan Faktor Resiko yang Dapat Diubah

Faktor Inang

- Nutrisi adekuat, makananenteral dengan nasogastrik


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, g g

- 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 ( 3040 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


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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


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Umumnya : baik.

(Excelent with appropriate antimicrobial and supportive care)

penderita

bakteri penyebab

antibiotik

KOMPLIKASI


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Efusi pleura

Empiema

Abses paru

Pneumotoraks

Gagal napas

Sepsis

PNEUMONIA ATIPIKtiologi

S i M l i Chl di i


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- 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 : bakterinegatif


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THANK YOU FOR

YOUR ATTENTIONABOUT PNEUMONIA


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Tanda dan Gejala Pneumonia Atipik Pneumonia Tipik Onset Gradual Akut

Suhu Kurang tinggi Tinggi, menggigil


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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

CAP HAP

Terjadi Masyarakat Rumah sakit

Kejadian 2 days before 2 days after

Etiologi Gram positif Gram negatif


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Etiologi Gram positif Gram negatif

Faktor

predisposisi

1. Alcohol excess

2. Cigarette smoking3. Chronic heart & lung

disease

4. Bronchial obstruction

5. Immunosuppression

6. Drug abuse

1. Intubation

2. Suppressed cough leadingto 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 Yes None

Pneumonia

Lobaris

Bronko-

pneumonia

Pneumonia

interstitial


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Lokasi Mencakup 1 lobus Tersebar di dekatbronkus

Inflamasi padajaringan interstitisl

paru

Insidens usia dewasa sering pada bayi danorang tua

-

Etiologi Gram negatif? StreptococcusVirus

Staph

Virus

Gambaranradiologis

Air bronchogram (+) Air bronchogram (-) -corakanbronkovaskuler

-hiperaerasi

-Bercak infiltrat

PENGOBATAN

1.Penisilin sensitif Streptococcus pneumoniae (PSSP)


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2.Penisilin resisten Streptococcus pneumoniae (PRSP)

Betalaktam oral dosis tinggi (u/ rawat jauh)

Sefotaksim, Seftriakson dosis tinggi

Makrolid baru dosis tinggi

Fluorokuinolon respirasi

p p ( )

Golongan Penisilin

TMP-SMZ Makrolid

3. Pseudomonas aeruginosa

Aminoglikosid


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Seftazidim, Sefoperason, Sefepim

Tikarsilin, Piperasilin

Karbapenem : Meropenem, Imipenem

Siprofloksasin, Levofloksasin

4. Methicillin resistent Staphylococcus aureus (MRSA)

VankomisinTeikoplanin

Linezolid

PENGOBATAN5.Hemophilus influenzae

TMP SMZ

7. Legionella Chlamydia

pneumoniae


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TMP-SMZ

Azitromisin Sefalosporin gen. 2 atau 3

Fluorokuinolon respirasi

6. Mycoplasma

pneumoniae

Doksisiklin

Makrolid

Fluorokuinolon

8. Chlamydia

pneumoniae

Doksisiklin Makrolid

Fluorokuinolon

pneumoniae

Doksisiklin

Makrolid

Fluorokuinolon

Makrolid

Flurokuinolon Rifampisin

Community-acquired pneumoniaPathogenesis

Organsim enter the lungs usually having been inhaled from the environment or nasopharynx. These organismmay be eliminate by the lungs defense mechanism (physical, humoral, and cellular defense) or they may


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y y g (p y , , ) y ysurvive and multiply.

Factors that undermine the lungsdefense, 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 fluidcontaining 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 ofextravasated red cells. The lung is red, solid, and ariless. Red hepatization corresponds to an area of edema andhemorrhage.

In days 4 8; a gray hepatization occur. Fibrinous pleurisy is present. Alveolar spaces are microscopicallydistended and filled by a dense network of fibrin-containing neutrophil polymorphs. Gray hepatizationrepresents a zone of advanced consolidation with destruction of red and white blood cells. The lung is gray orbrown and solid.

Resolution occurs after 810 days in untreated cases. When bacteria has been eliminated, macrophagesenter and replace granulocytes. The exudate is liquefied by fibrinolytic enzymes and coughed uo or absorped.

ETIOLOGYS. Pneumoniaeis the causative organism in 5575% of cases.

Causes and features of community acquired pneumia


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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

518

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

25

Chlamydia pneumoniae Headache very common; usually serological diagnosis 25

Haemophilus influenzae Gram-negative rod; more commonly associated with exacerbations of COPD 45

Viruses other than influenzae 28

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

15

Klebsiella pneumoniae Gram-negative; seen in alcoholics; severe and often cavitates 1

ComplicationsThe key of complications are:

1. Respiratory failure

2. Parapneumonic effusions

ManagementAntibiotic treatment should be started immediately, without

waiting for microbiology results.

Empirical treatment with macrolide, doxycycline, or

fluoroquinolone (outpatients)


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3. Empyema

4. Lung abscess5. 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 testsMycoplasma, Legionella,

and Chlamydiaantibodies; pneumococcal antigentesting by counter-immunoelectrophoresis (CIE)

of the sputum, urine, and serum.

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


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1. Hipoksemia persisten dengan O 100 % pakai masker2. 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 15 % of admissions and is a serious cause of morbidity and mortality.


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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, andPseudomonas 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 penicillinor a third-generation cephalosporin. Most hospital-acquired pneumonia is serious, and these drugsare 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.

Pneumonia in the immunocompromised patient


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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.

DiagnosisBilateral 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 2050%

Pneumonia in the immunocompromised patient2. 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.


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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


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Pneumococcal pneumonia. Gross section of lung showing gray

hepatization of the upper lobe in right lower lobe consolidation


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Pneumonia. Chest radiograph of left lower lobe pneumonia


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Pneumonia. Chest radiograph of right upper lobe pneumonia


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PCP pneumonia. Chest radiograph of patient withpneumocystis cariniipneumonia


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PNEUMOCYSTIS PNEUMONIA


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Pneumococcal pneumonia. Gross section of lung showing

gray hepatizationof the upper lobe in right lower lobe consolidation


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Pneumonia. Chest radiograph of right

upper lobe pneumonia


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Pneumonia. Chest radiograph of left lower lobe pneumonia


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PCP pneumonia. Chest radiograph of patient withpneumocystis cariniipneumonia


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PNEUMOCYSTIS PNEUMONIA


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Chest x-ray


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Confirm the diagnosis and detectassociated lung diseases

Patchy airspace infiltrates to diffusealveolar or interstitial infiltrates

Clearing of infiltrates can take 6weeks

DIFFERENTIAL DIAGNOSIS Pneumonia - bakterial


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- viral- aspirasi

- PCP

Bronkitis - Sarkoidosis Abses paru - Tumor paru

TB - Pneumonitis hipersensitif

Emboli paru - Bronkiolitis,BOOP

Infark miokard


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6.pneumonia (new)

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