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
 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
 Risk Factors that Lead to
Asthma Development
Host Factors Environmental Factors
 Indoor allergens
 Genetic
 Outdoor allergens
predisposition
 Occupational sensitizers
 Atopy
 Airway hyper-  Tobacco smoke
responsiveness  Air Pollution
 Gender  Respiratory Infections
 Race/Ethnicity  Parasitic infections
 Socioeconomic factors
 Family size
 Diet and drugs
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

 Bronchoconstriction Inflammatory cell

  Bronchial hyper- infiltration/activation 
reactivity Mucosaloedema  
 Hyperplasia Cellular proliferation 
 Inflammatory Epithelial damage 
mediator release Basement membrane 
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 80% predicted
> 1 time a week > 2 times a month
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.
 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:
 Inhaled glucocorticosteroids
 Systemic glucocorticosteroids

 Cromones

 Methylxanthines

 Long-acting inhaled β2-agonists

 Long-acting oral β2-agonists
 Leukotriene modifiers
 Part 4: Long-term Asthma Management

Pharmacologic Therapy

Reliever Medications:
 Rapid-acting inhaled β2-agonists
 Systemic glucocorticosteroids
 Anticholinergics
 Methylxanthines
 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
Controller: acting inhaled asthma is
 Daily inhaled β2-agonist
Controller: corticosteroid controlled,
Daily inhaled reduce
None Daily long-
 plus (if needed)
corticosteroid

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).

Bagaimana menilai derajat keparahan
Asma yang perlu
asma secara klinis? pengobatan di jenjang
4 atau 5 (contoh: dosis
tinggi ICS/LABA), agar
tidak menjadi “tidak
terkontrol”, atau asma
Asma yang yang tetap tidak
terkontrol dengan terkontrol meskipun
pengobatan di diobati.
jenjang 3. (contoh:
Asma yang ICS/LABA dosis
terkontrol dengan
pengobatan di
rendah) Asma
jenjang 1 atau Berat
jenjang 2
Asma
Sedang
Asma
Ringan

Global Initiative for asthma report, updated

2018
Bagaimana menilai kontrol asma untuk
pasien dewasa, remaja, dan anak ≥6 tahun?
Gejala kontrol asma Tingkat kontrol gejala asma
Dalam 4 minggu terakhir, apakah
pasien:
Kontrol Tidak
• Gejala asma di siang □ Ya □ Kontrol
Sebagian terkontrol
hari >2x/minggu? Tidak baik

• Asma menyebabkan
terbangun di malam □ Ya □
hari? Tidak
Semua 1-2 Ya 3-4 Ya
• Menggunakan pelega Tidak
untuk gejala □ Ya □
>2x/minggu? Tidak

• Pernah mengalami
kesulitan aktivitas □ Ya □
akibat asma? Tidak

Global Initiative for asthma report, updated

2018
 Emergency Department Management

Acute Asthma
Initial Assessment
History, Physical Examination, PEF or FEV 1

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.
 COPD Definition
Chronic Obstructive Pulmonary Disease (COPD) is a
common, preventable and treatable disease

that is characterized by persistent respiratory

symptoms and airflow limitation (usually progressive)
that is due to airway and/or alveolar abnormalities

usually caused by significant exposure to noxious

particles or gases.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

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
 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
Comparisons of asthma & COPD
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
 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 34
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 (-)
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 GOLD 2006

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
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

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
 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. 68
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
 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.
74
 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
78
 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 <
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
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 83
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
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
93
 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