Penyakit Paru Obstruksi Kronik

(PPOK/PPOM)
 COPD is a preventable and treatable disease with
some significant extrapulmonary effects that may
contribute to the severity in individual patients.
 Its pulmonary component is characterized by
airflow limitation that is not fully reversible.
 The airflow limitation is usually progressive and
associated with an abnormal inflammatory
response of the lung to noxious particles or gases.
- Ujiarus ekspirasi abnormal
- Permanen
- 3 Jenis PPOK :
1. Emfisema Paru
2. Bronkhitis Khronik
3. Penyakit Saluran nafas perifer
- Ciri khas PPOK :
- Dewasa tua / manula
- Penyakit khronik progresif
 ASTHMA COPD
Sensitizing agent Noxious agent

Asthmatic airway inflammation COPD airway inflammation

CD4+ T-lymphocytes CD8+ T-lymphocytes
Eosinophils Macrophages
Neutrophils

Completely Airflow limitation Completely

reversible irreversible
 Asthma COPD

Patho- • CD 4 lymphocytes
+ • CD 8+ lymphocytes
physiology: • macrophages
• eosinophils
chronic
• neutrophils
inflammation • mast cells

Persistent and
•Vary over time
progressive over time
and in severity

Clinical • cough
history: •cough
• sputum
symptoms • wheeze
• breathlessness
• chest tightness
• wheeze
• breathlessness
 Clinical Features That Differentiate
COPD From Asthma
Feature Asthma COPD
Course Variable progressive
Age of onset variable usually 5th-6th
decade ( -
antitrypsin early)
Role of smoking not directly directly related
related
Symptoms intermittent chronic (cough,
(dyspnea, sputum, and/or
wheeze, cough) dyspnea)
 Clinical Features That Differentiate
COPD From Asthma (cont’d)
Feature Asthma COPD
Airflow episodic chronic and
obstruction and usually persistent
reversible
Response to usually variable
bronchodilator significant
Hypoxemia episodic, chronic in
not present advanced disease
Evolution episodic slow,
progressive,
disabling
 Differential Diagnosis:
COPD and Asthma
COPD ASTHMA
• Onset in mid-life • Onset early in life (often
childhood)
• Symptoms slowly
progressive • Symptoms vary from day to day
• Long smoking history • Symptoms at night/early morning
• Dyspnea during exercise • Allergy, rhinitis, and/or eczema
also present
• Largely irreversible airflow
limitation • Family history of asthma
• Largely reversible airflow
limitation
 Risk Factors for COPD

Genes Lung growth and

Exposure to particles development
● Tobacco smoke Oxidative stress
● Occupational dusts, Gender
organic and inorganic Age
● Indoor air pollution from Respiratory infections
heating and cooking with Socioeconomic status
biomass in poorly
ventilated dwellings Nutrition
● Outdoor air pollution Comorbidities
Risk Factors for COPD

Nutrition

Infections

Socio-economic
status

Aging Populations
13
EPIDEMIOLOGI
Prevalensi di AS
- EP : 9,8/1000 penduduk
- BK : 29.5/1000 penduduk

Gangguan Aktifitas :
- EP : 37,5%
- BK : 5 %
Emphysema :
Is a pathological diagnosis, destruction of the
gas-exchange surfaces of the lung ( alveoli)

Chronic bronchitis :
Is a clinical diagnosis, the presence of cough
and sputum production for least 3 months in
each of two consecutive years.
1. EMFISEMA PARU

- Pelebaran abnormal permanen

ruang distal abronkhiolus terminalis
- Destruksi dinding alveoli
- fibrosis (-)
TYPE EMFISEMA PARU
1. Sentri Asinar
Bronkhiolus respiratorius
Perokok
Bronkhitis Khronik

2. Pan Asinar
Duktus Alveolaris, Alveoli
Defisiensi alpha 1 antitripsin
Bronkhitis Khronik ( - )

3. Distal Asinar
Sakus Alveolaris, Alveoli
Sub Pleura
Pneumotoraks/Bulla
2. BRONKHITIS KHRONIK

- Sekresi lendir/dahak >>>

- Khronik
- Setiap hari selama 3 bulan/lebih
- 2 tahun berturut-turut
1. B.K Biasa
- Batuk dahak mukoid
- Berulang
- Perokok
2. B.K Infeksi
- Dahak purulen
- Pengaruh musim hujan/dingin
- sesak nafas
3. B.K Obstruksi
- Sesak nafas permanen
- Uji faal paru terganggu
- Peradangan
- Fibrosis dinding saluran nafas
- Penyempitan
- Metaplasi sel epitel
Bronkhiolus terminalis
Bronkhiolus respiratorius

Obstruksi Arus Udara

 Inflammation

Small airway disease Parenchymal destruction

(Obstructive (Emphysema)
bronchiolitis) Loss of alveolar attachments
Airway inflammation Decrease of elastic recoil
Airway remodeling

AIRFLOW GOLD 2015

LIMITATION
 PATOFISIOLOGI :
Tahanan saluran nafas karena :
- Sempit akibat sekret (Bronkhitis Khronik)
- Elastisitas paru (Emfisema Paru)
Resistensi saluran nafas
gangguan ventilasi & difusi
PA O2 PA CO2
Kapiler Paru spasme
Resistensi Pemb. darah
Hipertensi Pulmonal
Kor Pulmonal
Pulmonary Hypertension in COPD

Chronic hypoxia

Pulmonary vasoconstriction

Muscularization
Pulmonary hypertension Intimal
hyperplasia
Fibrosis
Cor pulmonale Obliteration

Edema
Death
Source: Peter J. Barnes, MD
 Assessment of symtoms and signs
 Measurement of airflow limitation
 Assessment of severity
 Differential diagnosis
DIAGNOSIS
1. Anamnesis
2. Pemeriksaan fisik
3. Sarana bantu : - foto toraks / CT scan
- uji faal paru
- laboratorium dan EKG

1. Anamnesis : - Batuk berdahak, khronik,

dan berulang
- Sesak
- Perokok
 Chronic cough
 Chronic sputum production
 Dyspnea; progressive & persistent
 History of exposure to risk factor
 Additional symptoms in severe disease:
• Weight loss
• Anorexia
• Hemoptysis
• Cough syncope
 Diagnosis of COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
shortness of breath
indoor/outdoor pollution


SPIROMETRY
 Inspection
• Central cyanosis
• Barrel shaped chest
• Pursed lip breathing
• Resting respiratory rate more than 20 breaths
• Ankle and leg edema
 Palpation and percussion
• Difficult to detection of heart apex
• Downward displacement of the liver
 Auscultation
• Reduced breath sounds
• Wheezing
• Inspiratory crackles
2. Pemeriksaan Fisik :
- Tanda2 hyperinflasi paru
- Peningkatan kerja otot pernafasan
- Hypersonor
 Apeks jantung sulit diraba
- Batas paru hati bertambah
- Suara nafas pokok menurun
- Suara nafas tambahan : ronkhi kering
wheezing
- Contoh ekstrim COPD :
- Pink Puffer (Emfisema dominan)
- Blue Bloater (Bronkhitis khronik
dominan)
Gambar 1.Tampilan bentuk fisik pink puffer dan blue boater
 BLUE BLOATER
KOR PULMONAL
TIPE BRONKITIS
KRONIS
PROSES PROGRESIF
reaksi terhadap CO2
sudah tumpul,
hipertensi pulmonal
lebih cepat timbul dan
lebih parah
Sering jatuh dalam
gagal jantung kanan
sianosis, oedema,
hepatomegali
 PINK PUFFER
KOR PULMONAL
TIPE
EMPHYSEMA
PROSES LAMBAT

reaksi terhadap CO2

masih baik, tampak
sesak dan tidak
dijumpai sianosis
jarang gagal jantung
kanan,
hanya pada fase
terminal
 Clinical Features Differentiating
Chronic Bronchitis & Emphysema
Predominant Predominant
Chronic Bronchitis Emphysema
(‘Blue Bloater’) (‘Pink Puffer’)
General Overweight Thin, often
appearance
emaciated
Dusky Pursed-lip

Extremities breathing
Anxious
warm predominant
use accessory
muscles
Extremities
cool
 Predominant Predominant
Cont’d Chronic Bronchitis Emphysema
(‘Blue Bloater’) (‘Pink Puffer’)

Age 40-45 50-70

Onset Cough Dyspnea

Cyanosis Marked Slightly or none

Cough Very prominent Less evident

than dyspnea

Sputum Copious Scanty,

purulent clear
 Predominant Predominant
Cont’d Chronic Bronchitis Emphysema
(‘Blue Bloater’) (‘Pink Puffer’)

Recurrent Common Occasional

infection

Cor Common Only during

pulmonale exacerbation
& right or terminal
heart failure illness

Course Ambulatory Incapacitating

breathlessness
Progression to
Prolonged
right-sided
course
heart failure
3. Sarana bantu / pem. Tambahan :

a. Foto toraks, PA dan lateral :

- Hiperlusensi regional
- Corakan pembuluh darah
- Overinflasi paru dan bulla

b. Uji / tes faal paru

- Volume ekspirasi paksa detik
pertama (VEP1) menurun
- Perbandingan VEP1 / KVP menurun
Gambaran radiologis emfisema paru
Gambar
Gambaran radiologis Bronkitis Kronis
 Spirometry should be performed for patients who
have chronic cough and sputum production
 Gold standard for diagnosis and monitoring
progression of COPD
 Spirometry should measure FVC, FEV1 and ratio
FEV1 / FVC
 FEV1 < 80% predicted and FEV1 / FVC < 70 %
confirms of airway limitation
 Management of Stable COPD
Assess and Monitor COPD: Spirometry

Spirometry should be performed after the

administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
A post-bronchodilator FEV1/FVC < 0.70 confirms
the presence of airflow limitation that is not fully
reversible.
Where possible, values should be compared to
age-related normal values to avoid overdiagnosis
of COPD in the elderly. 44
Spirometry: Normal and
Patients with COPD
Stage Characteristics
0 : At Risk -Normal spirometry
-Chronic symtoms ( cough, sputum
production)
I : Mild COPD -FEV1 / FVC < 70 %
-FEV1 ≥ 80% predicted
-With or without chronic symtoms
II : Moderate - FEV1 / FVC < 70 %
COPD -50% ≤FEV1 < 80% predicted
-With or without chronic symtoms
III : Severe -FEV1 / FVC < 70 %
COPD -30% ≤FEV1 < 50% predicted
-With or without chronic symtoms
IV : very severe FEV1 / FVC < 70 %
COPD -FEV1 < 30% predicted or FEV1 < 50%
predicted plus chronic respiratory failure
c. Laboratorium :
- Polisitemia skunder
- Analisa gas darah
- Kadar alpha1 antitripsin serum
EKG : pembesaran atrium kanan
yang menjurus kearah Kor
Pulmonal
 CO2 Produksi
P CO2 = K
Ventilasi Alveoli

Ventilasi Alveoli
CO2 produksi (N)

P CO2
Gagal Nafas
 Asthma
 Congestive heart failure
 Bronchiectasis
 Tuberculosis
 Obliterative bronchiolitis
 Diffuse panbronchiolitis
 Pada prinsipnya ada 4 komponen penting dalam
penatalaksanaan
1. Pengkajian dan pemantauan penyakit
2. Usaha untuk mengurangi faktor risiko
3. Tatalaksana PPOK stabil
4. Tatalaksana PPOK eksaserbasi akut
1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD

 Education
 Pharmacologic
 Non-pharmacologic

4. Manage exacerbations
 Management of Stable COPD

Reduce Risk Factors:

Indoor/Outdoor Air Pollution

 Reducing the risk from indoor and outdoor

air pollution is feasible and requires a
combination of public policy and protective
steps taken by individual patients.

 Reduction of exposure to smoke from

biomass fuel, particularly among women and
children, is a crucial goal to reduce the
prevalence of COPD worldwide.
52
1 Terapi farmakologis
• Mengontrol gejala klinis, mencegah
eksaserbasi, mengurangi frekuensi dan
beratnya eksaserbasi serta memperbaiki
status kesehatan pasien
• Tidak dapat mencegah penurunan fungsi
paru yang berlangsung secara progresif dan
irreversibel, namun harus tetap diupayakan
PENATALAKSANAAN
- Pencegahan : stop rokok
atasi infeksi
- Atasi dahak : mukolitik, ekspektoran
minum air banyak
nebulasi
- Bronkodilator : Xanthin : aminofilin
B2 Agonis : salbutamol dll.
Antikholinergik :
ipratropium bromide
tioprotium bromide
- Kortikosteroid : prednison dll.
- Fisioterapi, mobilisasi dahak
 Terapi utama untuk mengatasi gejala PPOK.
 Terapi inhalasi lebih dianjurkan.
 Pilihan antara ß-2agonis, anti koliner gik dan
metilxantin atau kombinasi tergantung dari
ketersediaan obat, respon klinis dan efek
samping.
 Cara pemakaian : bila perlu atau rutin
 Pemberian steroid inhalasi secara reguler hanya
bermanfaat pada pasien PPOK :
 stadium III : severe COPD,
 stadium IV : very severe COPD, dan
 eksaserbasi akut
 Kombinasi: inhalasi steroid + B2 agonis (long acting)
lebih efektif dari memakai hanya salah satu
 Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe

 FEV1/FVC < 70%

 FEV1/FVC < 70%
 FEV1 < 30%
 FEV1/FVC < 70%  FEV1/FVC < 70% predicted
 30% < FEV1 <
50% predicted or FEV1 < 50%
 FEV1 > 80%  50% < FEV1 < predicted, plus
predicted 80% predicted chronic respira
tory failure
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
 α1-antitripsin: diberikan pada pasien emfisema dengan
usia muda akibat defisiensi yang berat. Obat ini agak
mahal dan belum banyak tersedia dibeberapa negara

 Mukolitik (mukokinetik, mukoregulator), contoh:

ambroxol, karbosistein, gliserol-iodida, hanya diberikan
pada keadaan eksaserbasi akut, sehingga jarang dipakai
pada keadaan rutin
 Antioksidan.
N-asetil sistein (NAC) bermanfaat untuk
mengurangi frekuensi eksaserbasi dan
diharapkan dapat diberikan pada pasien dengan
eksaserbasi yang berulang, tapi ini hanya
bermanfaat pada pasien yang tidak mendapat
therapi steroid
 Vaksinasi
• Vaksinasi terhadap influenza dapat
mengurangi morbiditas dan mortalitas PPOK
sampai 50%. Vaksin dapat diberikan 1 x
setahun
 Terapi non farmakologis
 Rehabilitasi pada PPOK
 Terapi oksigen pada PPOK
Pemberian oksigen jangka panjang (>15 jam/hari)
pada pasien dengan gagal nafas kronis dapat
meningkatkan survival, mempebaiki kelainan hemodi
namik, hematologis, meningkatkan kapasitas exercise
dan memperbaiki status mental
Terapi oksigen jangka panjang umumnya
diberikan pada PPOK stadium IV (very severe
COPD) dimana pada analisis gas darah
didapatkan:
• PaO2 < 55 mmHg atau SaO2 < 88% dengan/ tanpa
hiperkapnia
• PaO2 55-60 mmHg atau SaO2 < 89% dimana terdapat juga
hipertensi pulmonal, edema perifer akibat gagal jantung,
dan polisitemia (Ht > 55%). Target pemberian terapi O 2
adalah meningkatkan PaO2 sedikitnya menjadi 60 mmHg
dan/atau SaO2 sedikitnya menjadi 90%
 Bullectomy.
 Lung volume reduction surgery (LVRS).
 Lung transplantion.
MASALAH PPOK

1 Eksaserbasi Akut
2 Kor Pulmonal
3 Retensi O2
4 Kelelahan otot pernafasan
COPD patients are at increased risk for:
• Myocardial infarction, angina
• Osteoporosis
• Respiratory infection
• Depression
• Diabetes
• Lung cancer
COPD has significant extrapulmonary

(systemic) effects including:

• Weight loss

• Nutritional abnormalities

• Skeletal muscle dysfunction

INDIKASI RAWAT INAP

- Eksaserbasi akut
- Gagal nafas akut
- Kor Pulmonale
- Komplikasi PPOK
- Tindakan Invasif
- Tindakan Operasi
- Penyakit penyerta lain
Management COPD Exacerbations

An exacerbation of COPD is defined as:

“An event in the natural course of the

disease characterized by a change in
the patient’s baseline dyspnea,
cough, and/or sputum that is beyond
normal day-to-day variations, is
acute in onset, and may warrant a
change in regular medication in a
patient with underlying COPD.” 68
Worsening of clinical symptoms :

Cough
Sputum production
Dyspnea
As exacerbation counts as one or more symptoms from :
 dyspnoea
 sputum volume
 sputum purulence

In addition to at least one of :

• Infection of the URT within the previous five days
• Fever without other cause
 wheezing
 cough
 in either RR or HR, by 20% of baseline
 DIAGNOSTIC OF SEVERITY
COPD EXACERBATION
CLINICALY
a. Severe of exacerbation 3 symptoms
b. Moderate exacerbation 2 symptoms
c. Mild exacerbation 1 symptoms,
added with URTI > 5 days, fever,
increase cough, increase wheezing or
increase respiration frequency or pulse
frequency > 20% base line
 Management COPD Exacerbations

The most common causes of an

exacerbation are infection of the
tracheobronchial tree and air pollution, but
the cause of about one-third of severe
exacerbations cannot be identified

Patients experiencing COPD exacerbations

with clinical signs of airway infection (e.g.,
increased sputum purulence) may benefit from
antibiotic treatment

72
 Manage COPD Exacerbations
Key Points

 Inhaled bronchodilators (particularly

inhaled ß2-agonists with or without
anticholinergics) and

oral glucocorticosteroids are

effective treatments for exacerbations
of COPD 73
 HOME MANAGEMENT OF
COPD EXACERBATION
 Increasing dose and / or frequency of existing -
bronchodilator therapy, change bronchodilator inhaler to
nebulizer
 Anti cholinergic can be added
 If FEV1 < 50% predicted, glucocorticosteroid (40 mg
prednisolon/day) for 10 days
 Antibiotics if increased sputum volume and purulence
 oxygen when activity or sleeping
 Add mucolytic and expectorants
If 2 days not show improve should be refer to specialist
or hospitalized
INDICATION
MUST INCLUDE
COVERAGE :
AT LEAST 2 OF 3
- H. influenzae
FOLLOWING SYMPTOMS : - S.
pneumoniae
- Moraxella
catarrhalis
SPUTUMPRODUCTION
SPUTUM
PURULENCE
DYSPNEA
Pathogens Incidens
 Haemophilus influenzae 20-54 %
 Streptococcus pneumoniae 10-25 %
 Moraxella catarrhalis 10-30 %

Infrequent pathogens
 Enterobacteriaceae < 10 %
 Pseudomonas aeruginosa 4-15 %
 Staphylococcus aureus <5%
 Mycoplasma spp <1%
 Chlamydia pneumoniae <1%
 Klebsiella pneumoniae <1%
Classification of acute bronchial infection
and recommendation for treatment
Defenition & risk Recommended
Class Baseline first-line
clinical status factors for assesment
of severity tharapy
Acute
I Acute cough & sputum None
tracheobronchitis

Simple cronic Exacerbation in

Amoxicillin or
II bronchitis established : dyspnea  /
tetracycline
sputum =  / sputum
Class IIpurulence
plus 1 ≥ : - Fluoroquinolone
III Complicated exacerbation > 4 / year – or
chronic bronchitis comorbidity - -lactam/
age > 65 years -lactamase
– history of chronic inhibitor
bronchitis > 10 years combination
Chronic bronchial = class III, plus continuous
IV year-round production of Ciprofloxacin
suppuration
purulent sputum