OBSTRUCTIVE AIRWAY AND

PULMONARY DISEASE

• 1. ASTHMA BRONCHIALE
• 2. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE

AHMAD RASYID, dr. SpPD-KP

 ASTHMA
BRONCHIALE
 Definition of Asthma
 Asthma is a chronic inflammatory disorder of the
airways in which many cells and cellular elements play
a role (infiltration of mast cell, eosinofils and
lymphocyte)
 Chronic inflammation causes an associated increase
in airway hyperresponsiveness that leads to recurrent
episodes of wheezing, breathlessness/ shorthness of
breath, chest tightness, and coughing, symptom
varying overtime and severity particularly at night or in
the early morning
 These episodes are usually associated with
widespread but variable airflow obstruction that is
often reversible either spontaneously or with treatment
 Mechanisms Underlying
the Definition of Asthma
Risk Factors
(for development of asthma)

INFLAMMATION

Airway
Hyperresponsiveness Airflow Obstruction

Risk Factors Symptoms

(for exacerbations)
Asthma - an inflammatory disease

Normal Asthma
 PERADANGAN SALURAN NAFAS

KONSTRIKSI HIPER REAKSI

SAL. NAFAS BRONKUS

SESAK NAFAS SALURAN NAFAS

SANGAT PEKA

REVERSIBLE
SECARA SPONTAN/ “ REMODELLING” ?
PENGOBATAN
 Risk Factors that Lead to
Asthma Development
Host Factors Environmental Factors
 Genetic  Indoor allergens

predisposition  Outdoor allergens

 Atopy  Occupational sensitizers

 Tobacco smoke
 Airway hyper-
 Air Pollution
responsiveness
 Respiratory Infections
 Gender
 Parasitic infections
 Race/Ethnicity  Socioeconomic factors
 Family size
 Diet and drugs
 Obesity
Tabel : Faktor-Faktor Pencetus Serangan Asma
Faktor Alergen : Debu rumah, jamur, tepung bunga,
bulu binatang, selimut wol, kasur kapu

Faktor Emosi/stress

Faktor Infeksi : ISPA, Virus, Mycoplasma, Chlamydia,

Bakteri.

Faktor zat makanan : Udang, Susu, Telur, Ikan laut, dll

Faktor zat kimia : Obat nyamuk, asap rokok, lampu, asap

k kompor, dll.

Faktor fisik : Perubahan cuaca

Faktor kegiatan jasmani : Asma karena latihan (Exercise Induced

A Asthma)

Faktor Obat-obatan : Penisilin, Sulfa, Aspirin, dll.

 Pathogenesis of Asthma

Smooth muscle Airway

dysfunction inflammation

3 l Bronchoconstriction l Inflammatory cell

3 3 l Bronchial hyper- infiltration/activation 3
reactivity l Mucosal oedema 3 3
3 l Hyperplasia l Cellular proliferation 3
3 l Inflammatory l Epithelial damage 3
mediator release l Basement membrane 3
thickening

Symptoms \exacerbations
 Asthma Diagnosis

 History and patterns of

symptoms
 Physical examination
 Measurements of lung function
 Measurements of allergic status
to identify risk factors
 Is it Asthma?

 Recurrent episodes of wheezing

 Troublesome cough at night
 Cough or wheeze after exercise
 Cough, wheeze or chest tightness
after exposure to airborne allergens or
pollutants
 Colds “go to the chest” or take more
than 10 days to clear
 Increased loss of FEV1 in asthma
Male non-smokers
1.7

1.5
Height-adjusted FEV1 (L)

1.3
p <0.001
1.1

0.9

0.7

0.5

0.3
20 30 40 50 60 70 80
Age (years)

No asthma (n = 5480)
Asthma (n = 314)
Lange P et al, NEJM 1998
 Typical Spirometric (FEV1)
Tracings
Volume

FEV1

Normal Subject

Asthmatic (After Bronchodilator)

Asthmatic (Before Bronchodilator)

1 2 3 4 5
Time (sec)

Note: Each FEV1 curve represents the highest of three repeat measurements
 Classification of Severity
CLASSIFY SEVERITY
Clinical Features Before Treatment

Symptoms Nocturnal FEV1 or PEF

Symptoms
STEP 4 Continuous  60% predicted
Limited physical Frequent
Severe Variability > 30%
Persistent activity

STEP 3 Daily 60 - 80% predicted

> 1 time week
Moderate Attacks affect activity Variability > 30%
Persistent
STEP 2
> 2 times a month  80% predicted
> 1 time a week
Mild but < 1 time a day Variability 20 - 30%
Persistent

< 1 time a week

STEP 1  80% predicted
Asymptomatic  2 times a month
Intermittent and normal PEF Variability < 20%
between attacks
The presence of one feature of severity is sufficient to place patient in that category.
 Factors that Exacerbate
Asthma

 Allergens
 Air Pollutants
 Respiratory infections
 Exercise and hyperventilation
 Weather changes
 Sulfur dioxide
 Food, additives, drugs
 Six-Part Asthma
Management Program
1. Educate patients to develop a partnership
in asthma management
2. Assess and monitor asthma severity with
symptom reports and measures of lung
function as much as possible
3. Avoid exposure to risk factors
4. Establish medication plans for chronic
management in children and adults
5. Establish individual plans for managing
exacerbations
6. Provide regular follow-up care
 Part 3: Avoid Exposure to
Risk Factors

 Reduce exposure to indoor

allergens
 Avoid tobacco smoke
 Avoid vehicle emission
 Identify irritants in the
workplace
 Explore role of infections on
asthma development, especially
in children and young infants
 Part 4: Long-term Asthma Management

Pharmacologic Therapy

Controller Medications:
l Inhaled glucocorticosteroids
l Systemic glucocorticosteroids

l Cromones

l Methylxanthines

l Long-acting inhaled β2-agonists

l Long-acting oral β2-agonists

l Leukotriene modifiers
 Part 4: Long-term Asthma Management

Pharmacologic Therapy

Reliever Medications:
l Rapid-acting inhaled β2-agonists
l Systemic glucocorticosteroids
l Anticholinergics
l Methylxanthines
l Short-acting oral β2-agonists
 Part 4: Long-term Asthma Management
Stepwise Approach to Asthma
Therapy - Adults
Outcome: Asthma Control Outcome: Best
Possible Results

Controller:
 Daily inhaled
corticosteroid
Controller:  Daily long –  When
acting inhaled asthma is
Controller:  Daily inhaled β2-agonist controlled,
Controller: Daily inhaled corticosteroid reduce
 plus (if needed)
None corticosteroid  Daily long- therapy
acting inhaled -Theophylline-SR
β2-agonist -Leukotriene
-Long-acting inhaled
 Monitor
β2- agonist
-Oral corticosteroid

Reliever: Rapid-acting inhaled β2-agonist prn

STEP 1: STEP 2: STEP 3: STEP 4: STEP Down
Intermittent Mild Persistent Moderate Severe
Persistent Persistent

Alternative controller and reliever medications may be considered (see text).

 Emergency Department Management
Acute Asthma
Initial Assessment
History, Physical Examination, PEF or FEV1

Initial Therapy
Bronchodilators; O2 if needed
Good
Response Incomplete/Poor Response Respiratory Failure

Observe for Add Systemic Glucocorticosteroids

at least 1
hour
Good Response Poor Response
If Stable,
Discharge to Discharge Admit to Hospital Admit to ICU
Home
PENYAKIT PARU OBSTRUKTIF
KHRONIK / MENAHUN
(PPOK / PPOM)
=
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
Definition of COPD
• 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.
PPOK = PPOM = COLD
- Uji arus 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
Comparisons of asthma & COPD
Asthma COPD

Patho- • CD 4+ lymphocytes • CD 8+ lymphocytes

physiology: • macrophages
chronic • eosinophils
• neutrophils
inflammation • mast cells

•Vary over time Persistent and

and in severity progressive over time

Clinical • cough
history: •cough
• sputum
symptoms • wheeze
• breathlessness
• chest tightness
• wheeze
• breathlessness
 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 33
Biomass Fuel and COPD
Future
COPD
case

Future
asthmatic

Future COPD if
smoker

Indoor Air Pollution

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 bronkhiolus terminalis
- Destruksi dinding alveoli
- fibrosis (-)
 .
The lungs - Cont
Tracheobronchial Tree
The alveoli
Bronchioles and Alveoli
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
Bronkhitis Khronik ada 3 :
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
3. PENYAKIT SALURAN NAFAS PERIFER

- Peradangan
- Fibrosis dinding saluran nafas
- Penyempitan
- Metaplasi sel epitel

Bronkhiolus terminalis
Bronkhiolus respiratorius

Obstruksi Arus Udara

 Mechanisms of Airflow
Limitation in COPD
Inflammation

Small airway disease Parenchymal destruction

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

AIRFLOW LIMITATION GOLD 2006

 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
Diagnosis of COPD

• 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
 Symtomps
• 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
 Physical Examination
• 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)
BARREL CHEST
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
breathing
Extremities 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
 Foto toraks COPD tipe
Gambar emphisema
Gambaran radiologis Bronkitis Kronis
Pulmonary function test
• 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. 69
Spirometry: Normal and
Patients with COPD
Classification of severity of COPD (GOLD 2006)

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
Differential diagnosis of COPD

• Asthma
• Congestive heart failure
• Bronchiectasis
• Tuberculosis
• Obliterative bronchiolitis
• Diffuse panbronchiolitis
 Tatalaksana PPOK

• 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
 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.
76
 Terapi PPOK stabil
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
Bronkodilator pada PPOK stabil

• 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
 Bronchodilators
 Bronchodilator medications are central to the
symptomatic management of COPD.
They are given on an as-needed or on a regular
to prevent or reduce symptoms and exacerbations
 The principal bronchodilator treatments are:
ß2-agonists, anticholinergics & methylxanthines
used singly or in combination regular treatment
with long-acting bronchodilators, is more effective
and convenient than treatment with short-acting
80

bronchodilators
 Steroid
• 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 <
or FEV1 < 50%
50% predicted
 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
Obat-obat tambahan lainnya

• 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
Management of Stable COPD
Other Pharmacologic Treatments
 Antibiotics: Only used to treat
infectious exacerbations of COPD
 Antioxidant agents: No effect of n-
acetylcysteine on frequency of
exacerbations, except in patients not
treated with inhaled
glucocorticosteroids
 Mucolytic agents, Antitussives,
Vasodilators: Not recommended in
85
stable COPD
• 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 O2 adalah
meningkatkan PaO2 sedikitnya menjadi
60 mmHg dan/atau SaO2 sedikitnya
menjadi 90%
Tindakan pembedahan

• Bullectomy.
• Lung volume reduction surgery
(LVRS).
• Lung transplantion.
MASALAH PPOK

1 Eksaserbasi Akut
2 Kor Pulmonal
3 Retensi O2
4 Kelelahan otot pernafasan
COPD and Co-Morbidities

COPD patients are at increased risk

for:
• Myocardial infarction, angina
• Osteoporosis
• Respiratory infection
• Depression
• Diabetes
• Lung cancer
 COPD and Co-Morbidities

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
Acute Exacerbations of
Chronic Bronchitis (AECB)

Worsening of clinical
symptoms :

Cough
Sputum production
Dyspnea
 Anthonisen definition of
acute exacerbation of COPD
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
97
 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 98
 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
 Antibiotics in AECB
INDICATION
MUST INCLUDE
COVERAGE :
AT LEAST 2 OF 3
- H. influenzae
FOLLOWING SYMPTOMS : - S. pneumoniae
- Moraxella catarrhalis

SPUTUMPRODUCTION
SPUTUM PURULENCE
DYSPNEA
 Pathogens associated with AECB
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 established

Amoxicillin or
II bronchitis : dyspnea  / sputum  /
=
sputum purulence 
tetracycline
Class II 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 (oral)