Farmasi Ubaya S2 Mei 2014

Dr. Ediyono Sp. P

Subdep Paru RSAL Dr Ramelan
 Penyakit – penyakit Paru
NO Kelompok Penyakit
A Infeksi
B Allergi
C Obstruksi saluran nafas
kronis
D Peny. Pleura
E Tumor/ Kanker
F Gawat Darurat Paru
F Penyakit Paru Kerja
Penyakit
1. TBC
2. Bukan TBC ( ISPA, Bronkitis, Pneumonia, Abses )
Asma Bronkiale
PPOK ( Emfisema, Bronkitis kronis )
Efusi Pleura ( Empyema ), Pneumotoraks
1. Asal : PRIMER, SEKUNDER
2. Pertumbuhan : JINAK, GANAS
3. Tumor Paru, Tumor mediastinum
Batuk darah ( Hemoptoe ), Pneumotoraks,
PPOK Akut, Status Asmatikus, Oedem Paru,
gagal Nafas
Pneumokoniosis
 UPDATE 2014

GOLD
ED-AK
Kevin A
 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
 Pendahuluan
 PPOK di dunia ( WHO 1990) : urutan ke-6 penyebab
kematian.
 Indonesia : 4,8 juta pasien ( Prevalensi :5,6%)
 Th 1990 : peringkat ke 12 penyakit terbanyak di
dunia
 Th 2020 : peringkat ke 5 penyakit terbanyak
Pria : 15,6 %
didunia
 Adji Widjaja th 1993 : Wanita : 11,3%

Prevalensi PPOK di Jawa Timur :

PPOK ( Penyakit paru Obstruktif Kronik). Diagnosis dan Penatalaksanaan. PDPI Juli 2011
 COPD is projected to be the third biggest
killer worldwide by 20201

2020
1990

Ischaemic heart Cerebrovascular Lower

COPD Lower
Diarrhoeal Perinatal DisordersRoad
Trachea, traffic
COPD
disease disease Respiratory respiratory
Disease bronchus and accidents
Infections infections lung cancers

Bars are used to illustrate chronic disease ranking only and do not
1. Murray CJL et al. Lancet 1997; 349:1498-1504
represent actual values
 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
 Definition of COPD ( GOLD )

Global Initiative for Chronic Obstructive Lung Disease

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
 PPOK terdiri dari :

a. BRONKITIS KRONIS :
Batuk kronik berdahak, minimal 3 bulan dalam
setahun,
sekurang – kurangnya 2 th berturut-turut.

b. EMFISEMA:
Kelainan anatomis , ditandai adanya pelebaran
rongga
udara distal bronchioli terminal, disertai
PPOK Pedoman kerusakan
Praktis Daignosis dinding
dan Penatalaksanaan. PDPI 2004
 PPOK
Diagnosis klinis Diagnosis Patologis

1. Bronkitis Kronis 2. Emfisema

Bronkitis kronis & Emfisema tidak dimasukkan kedalam definisi

PPOK.
Keduanya tidak selalu mencerminkan hambatan aliran udara
dalam saluran nafas
ED-AK
Pink Puffer Blue boater

(Tipe A) Emfisema (Tipe B)Bronkitis Kronis

 Fig 23-1. Schema of COPD
This nonpropotional Venn diagram shows subsets of patients with chronic bronchitis,
Emphysema and asthma

Chronic Bronchitis Emphysema

1 5 2

8
3 4
2
6 7

Reversible
Asthma COPD
Non Reversible
Guzman ED, Dweik RA and Stoller JK. COPD, Asthma and related diseases.
Kevin A Egan’s Fundamental of Respiratory care 10th ed.ELSEVIER. 2013. PP 525-548
 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
Faktor Risiko
6 Efek nikotin pada susunan saraf pusat

a. Dopamin Pleasure
b. Norepinephrine Appetite supression
c. Acethylcholine Arousal,cognitive enhancement

d. Vasopressin Memory
e. Serotonin Mood modulation
f. β-endorphin Anxiety reduction
 Faktor risiko P P O K

1. Merokok ( Faktor Terpenting )

a. Riwayat Perokok : 1. Perokok Aktif
2. Perokok Pasif
3. Bekas Perokok

b. Derajat berat merokok

( Indeks Brinkman = Jumlah rata-2 batang rokok /hr X
lama merokok /th):
1. Ringan : 0 - 200
2. Sedang : 200 - 600
3. Berat : > 600
 Faktor risiko P P O K

2. Polusi udara
a. Polusi di dalam ruangan : - asap rokok
- asap kompor
b. Polusi di luar ruangan :
- Gas buang kendaranan bermotor
- Debu jalanan
c. Polusi tempat kerja ( bahan kimia, zat iritasi, gas beracun)
3. Infeksi saluran nafas berulang.
4. Defisiensi enzim alfa – 1 antitripsin ( Jarang )
5. GENETIK
 Risk Factors for COPD

Host Factors Genes (e.g. alpha1-antitrypsin

deficiency)
Hyperresponsiveness
Lung growth

Exposure Tobacco smoke

Occupational dusts and chemicals
Infections
Socioeconomic status
Hubungan Rasio FEV1 terhadap Umur
 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
CELLULAR MECHANISMS OF COPD

Cigarette smoke

? Alveolar macrophage
CD8
+
MCP-1
lymphocyte
Neutrophil chemotactic factors
Cytokines (IL-8)
Mediators (LTB4)4))

Neutrophil

PROTEASE Neutrophil elastase

PROTEASES MatrixCathepsins
INHIBITORS
- metalloproteinases

Alveolar wall destruction

Alveolar wall destruction Mucus hypersecretion
Mucus Hypersecretion
( Emphysema )
(Emphysema) ((Chronic
Chronic bronchitis)
Bronchitis )
 Pathophysiology of COPD and Asthma
Noxious Sensitizing
agent COPD Asthma agent

CD8 + Alveolar CD4 +

Mast cell
lymphocyte macrophage lymphocyte

Eosinophil Histamine
Cytokines (IL -8) Cytokines
(IL-4, IL-5, IL-13)
Mediators (LTB 4) Neutrophil
Mediators (LTD 4)

Inflammatory
Proteases mediators
Epithelial
shedding
Airway
Alveolar wall Mucus Airway
thickening
destruction hypersecretion hyperreactivity
Barnes PJ (1999; 2000)
 COPD IS NOT ASTHMA !

Dyspneu
Wheezing

a) Different causes

b) Different inflammatory cells

c) Different mediators

d) Different inflammatory consequences

 EMFISEMA

EMFISEMA
Expanded View of Etiology, Pathogenesis and
Pathology in COPD

Noxious stimulation

Chronic
inflammation

Destruction,
repair and
remodeling

Abnormal function
and symptoms
 KELAINAN SALURAN NAFAS
BRONKITIS KRONIS EMFISEMA

 Hiperplasi Kelenjar
DESTRUKSI
 Mbr Basal menebal
ALVEOLI
 Oedem Mukosa, Hipersekresi
 Perbedaan Bronkitis Kronis dan Emfisema

NORMAL

Bronkitis EMFISEMA
Kronis
 Wall thickening –
inflammation --
mucus gland
hypertrophy

Bronkitis ↑ Secretions
Bronchus kronis

Wall thickening –
inflammation –
repair --
remodeling
Loss of alveolar
Bronchiole attachments

Wall thinning -
inflammation -
elastolysis

Coalescence ↓
Elasticity
Alveoli Emfisema
Gambar Paru Perokok

dirty holes

This pattern is typical for smokers

 Bullae pada Emfisema

Bullae

large bullae apparent on the

surface of the lungs in a patient
dying with emphysema.
Bullae are large dilated
airspaces that bulge out from
beneath the pleura.
Emfisema Paru
 “Small Airways Dysfunction”
( Air Trapping )
pada Emfisema
Expiratory flow
limitation
On forced
exhalation
F
l
o
w During exercise

At rest
Volume
 EFL and Hyperinflation
Resting State

Normal COPD

Mild Obstruction, Severe obstruction,

+ mildly decreased + markedly decreased
Elastic Recoil Elastic Recoil
EFL and Dynamic Hyperinflation
Normal During COPD
Exercise

Air is trapped

Initial breathing cycle

EFL and Dynamic Hyperinflation
During COPD
Normal
Exercise

Worsening Hyperinflation

Initial breathing cycle  Next breathing cycle

Bentuk toraks
penderita
Emfisema

Barrel
Chest
 Perbedaan patogenesis Asma dan PPOK

ASMA PPOK

Bahan berbahaya
Bahan sensitif

Mediator inflamasi Mediator inflamasi

CD8 + T-Limfosit
CD4 + T-Limfosit
Makrofag
Eosinofil Neutrofil

Hambatan
Reversibel Aliran udara Irreversibel
 Perbedaan Asma – PPOK – SOPT
ASMA PPOK SOPT

1 Timbul pada usia muda ++ - +

2 Dyspneu d’effort - ++ ++

3 Riwayat merokok +/- +++ -

4 Riwayat Atopi ( Alergi ) ++ + -

5 Sesak mengi berulang +++ + +

6 Batuk kronik berdahak + ++ +

7 Hiperreaktiviti bronkus +++ + +/-

8 Reversibiliti obstruksi ++ - -

9 Eosinofil, makrofag sputum + - ?

S O P T : Syndroma Obstruksi Pasca Tuberkulosa

 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
 Diagnosis of COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
shortness of breath
indoor/outdoor pollution


SPIROMETRY
 Diagnosis P P O K
GAMBARAN KLINIS:
a. Anamnesa ( Keluhan )

- Usia tua ( > 45 th )

- Riwayat / bekas PEROKOK
- Riwayat terpajan zat iritan ( waktu lama )
- Riwayat infeksi nafas berulang, lingkungan asap
rokok
- Batuk berulang dengan / tanpa dahak
- Sesak dengan / tanpa bunyi mengi
- Sesak nafas bila aktivitas berat ( Dyspneu d’effort )
 Symptoms of COPD

• The characteristic symptoms of COPD are chronic and

progressive dyspnea, cough, and sputum production:
a. Dyspnea : Progessive, persistent and caharacteristically
worse with exercise,
b. Chronic cough : May be intermittent and maybe
unproductive,
c. Chronic sputum production ; COPD patients commonly
cough up sputum.

GOLD Revision 2011

 Diagnosis P P O K

PEMERIKSAAN PENUNJANG:

I. PEMERIKSAAN RUTIN
1. Foto Toraks ( Paru )
2. Darah rutin
3. Sputum ( dahak ): Neutrofil, makfofag

II. PEMERIKSAN KHUSUS

1. Spirometri ( Faal Paru )
2. Analisa gas darah
3. EKG
 Tanda Fisik Kelainan Paru
EMFISEMA ( PPOM)
1 Inspeksi Bentuk toraks cembung seperti Tong ( Barrel Chest ),

Iga mendatar, sela iga melebar.

Gerakan toraks terbatas, Otot bantu nafas hipertrofi

2 Palpasi Fremitus suara menurun

3 Perkusi Hipersonor seluruh hemitoraks

4 Auskultasi Suara nafas lemah, Ekspirasi lebih panjang, Krepitasi,

Wheezing.
Bentuk toraks
penderita
Emfisema

Barrel
Chest
Diameter antero-posterior
& transversal sebanding
 EMFISEMA
( PINK PUFFER )
Barrel Chest

Sela iga melebar Sela iga melebar

Scoliosis
Hipertrofi otot bantu nafas pada penderita PPOK

Hipertrofi otot bantu nafas

( Hipertrofi musc sternocleidomastoideus )

 Pola pernafasan P P O K

Pada waktu bernafas:

Ekspirasi mulut seperti bersiul
( hampir menutup )

Tekanan di rongga mulut meningkat

Tekanan intra bronkial meningkat

Lumen bronki tetap terbuka

Mencegah kolaps saluran nafas
( Air Trapping )
 Foto toraks pasien dengan EMFISEMA berat ok
defisiensi α-1 antitrypsin

hiperlucency

Diafragama letak
Rendah- datar
 Diafragma
letak
rendah
Emfisema paru
Cystic fibrosis. Bronchiectasis seen in cross section
 Pokok bahasan PPOK
1. Pendahuluan.
2. Definisi PPOK.
3. Patogenesis & Patologi
4. Faktor Risiko
5. Diagnosis & Diagnosis Banding
6. Klasifikasi
7. Penatalaksanaan PPOK
8. Komplikasi
9. Keadaan Khusus
10. Pencegahan
 Tujuan Penatalaksanaan P P O K

1. Menghilangkan gejala
2. Mencegah progresifitas penyakit
3. Meningkatkan toleransi aktivitas
4. Meningkatkan Status Kesehatan
5. Mencegah & mengobati Komplikasi
6. Mencegah & mengobati Eksaserbasi
7. Mengurangi Mortalitas
 Penatalaksanaan P P O K

2 keadaan klinis PPOK

1 2
PPOK
PPOK Stabil
Eksaserbasi Akut
Four Components of COPD Management plan:

1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD

 Education
 Pharmacologic
 Non-pharmacologic

4. Manage exacerbations
 Assessment of COPD

1. Assess symptoms

2. Assess degree of airflow limitation using

spirometry

3. Assess risk of exacerbations

4. Assess comorbidities

Source: GOLD guideline 2011 Update

 Assessment of COPD
1  Assess symptoms
Use the COPD Assessment Test(CAT)
or
mMRC Breathlessness scale

COPD Assessment Test (CAT): An 8-item measure of health status

impairment in COPD (http://catestonline.org).

Breathlessness Measurement using the Modified British Medical

Research Council (mMRC) Questionnaire: relates well to other
measures of health status and predicts future mortality risk.
 mMRC Dyspnoe scale
(modified Medical Research Council)

Tingkat Tidak terganggu oleh sesak napas kecuali

0 saat olah-raga berat.

Terganggu dengan sesak napas ketika

Tingkat
terburu-buru berjalan di tanah yang datar
1
atau mendaki tanjakan.

Berjalan lebih lambat pada permukaan

yang datar dibandingkan orang seusia
Tingkat karena sesak napas atau harus berhenti
2 untuk bernapas ketika berjalan pada
kecepatan sendiri di permukaan yang
datar.

Berhenti untuk bernapas setelah berjalan

Tingkat
90 meter atau setelah beberapa menit di
3
permukaan yang datar

Terlalu sesak untuk meninggalkan rumah

Tingkat
atau sesak saat berpakaian atau berganti
4
pakaian.
 Assessment of COPD
2 • Assess degree of airflow limitation using
spirometry
Use spirometry for grading severity according to spirometry, using

four grades split at 80%, 50% and 30% of predicted value

In patients with FEV1/FVC < 0.70:

 GOLD 1: Mild FEV1 > 80% predicted

 GOLD 2: Moderate 50% < FEV1 < 80% predicted

 GOLD 3: Severe 30% < FEV1 < 50% predicted

 GOLD 4: Very Severe FEV1 < 30% predicted

 Assessment of COPD
3  Assess risk of exacerbations

Use history of exacerbations and spirometry.

Two exacerbations or more within the last year

or an FEV1 < 50 % of predicted value are

indicators of high risk
 Combined Assessment of
COPD
• Assess symptoms

• Assess degree of airflow

limitation using
spirometry

• Assess risk of
Combine these assessments
exacerbations for the purpose of improving
management of COPD
Combined Assessment of COPD
(GOLD Classification of Airflow Limitation) 4

(C) (D) >2

(Exacerbation history)
3

Risk
Risk

2
(A) (B) 1

1 0

mMRC 0-1 mMRC > 2

CAT < 10 CAT > 10

Symptoms
(mMRC or CAT score))
Combined Assessment of COPD
Assess symptoms first

(C) (D) If mMRC 0-1 or CAT < 10:

Less Symptoms (A or C)

If mMRC > 2 or CAT > 10:

(A) (B) More Symptoms (B or D)

mMRC 0-1 mMRC > 2

CAT < 10 CAT > 10

Symptoms
(mMRC or CAT score))
 Combined Assessment of COPD
Assess risk of exacerbations next
(GOLD Classification of Airflow Limitation)

4 If GOLD 1 or 2 and only

(C) (D)

(Exacerbation history)
0 or 1 exacerbations per year:
>2
3
Low Risk (A or B)
Risk

Risk
2 1 If GOLD 3 or 4 or two or
(A) (B) more exacerbations per year:
1 0
High Risk (C or D)
mMRC 0-1 mMRC > 2
CAT < 10 CAT > 10
Symptoms
(mMRC or CAT score))
 Combined Assessment of COPD
Assess risk of exacerbations next
(GOLD Classification of Airflow Limitation)

4 If GOLD 3 or 4 or two or more

(C) (D)

(Exacerbation history)
exacerbations per year:
>2
3 High Risk (C or D)
Risk

Risk
If GOLD 1 or 2 and only
2 1 0 or 1 exacerbations per year:
(A) (B)
1 0
Low Risk (A or B)
mMRC 0-1 mMRC > 2
CAT < 10 CAT > 10
Symptoms
(mMRC or CAT score))
 Combined Assessment of
COPD
When assessing risk, choose the highest risk
according to GOLD grade or exacerbation history

Patien Characteristic Spirometric Exacerbations mMRC CAT

t Classification per year
Low Risk
A Less Symptoms
GOLD 1-2 ≤1 0-1 < 10

Low Risk
B More Symptoms
GOLD 1-2 ≤1 >2 ≥ 10

High Risk
C Less Symptoms
GOLD 3-4 >2 0-1 < 10

High Risk ≥ 10
D GOLD 3-4 >2 >2
More Symptoms
 Global Strategy for Diagnosis, Management and Prevention of COPD
Manage Stable COPD: Pharmacologic Therapy
RECOMMENDED FIRST CHOICE

C D
GOLD 4

Exacerbations per year

ICS + LABA ICS + >2
or LABA
GOLD 3 LAMA and/or
LAMA
A B
GOLD 2 SABA prn LABA 1
or or
GOLD 1 SAMA prn LAMA
0

mMRC 0-1 mMRC > 2

CAT < 10 CAT > 10
© 2013 Global Initiative for Chronic Obstructive Lung Disease
 Global Strategy for Diagnosis, Management and Prevention of COPD
Manage Stable COPD: Pharmacologic Therapy
(Medications in each box are mentioned in alphabetical order, and therefore not
necessarily in order of preference.)
Patient Recommended Alternative choice Other Possible
First choice Treatments
SABA prn LAMA or
A or LABA or Theophylline
SAMA prn SABA and SAMA
LABA
SABA and/or SAMA
B or LAMA and LABA
Theophylline
LAMA
ICS +
LAMA and LABA or
LABA SABA and/or SAMA
C LAMA and PDE4-inh. or
Theophylline
or LABA and PDE4-inh.
LAMA
ICS + LABA and LAMA or
ICS +
ICS+LABA and PDE4-inh. Carbocysteine
D LABA or SABA and/or SAMA
and/or LAMA and LABA or Theophylline
LAMA LAMA and PDE4-inh.
Source: GOLD guideline 2013
Commonly Used Formulations of Drugs in COPD
1 Beta-2 agonist  Short acting ( SABA ) Fenoterol, albuterol, terbutalin

Long acting ( LABA ) Formoterol, Salmeterol

2 Anticholinergic Short acting Ipratropium bromide

Long Acting Tiotropium

3 Methylxanthine Aminophyllin, Theophylin SR

4 Combination SABA + Fenoterol/Ipratropium,

anticholinergic
5 Combination LABA +
Glucocorticoid
6 Systemic Glucocortikoid
Salbutamol/Ipratropium
Formoterol/Budesonid
Salmeterol/Fluticasone
Prednison, Methylprednisolon
( GOLD 2006 )
Four Components of COPD Management plan:

1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD

 Education
 Pharmacologic
 Non-pharmacologic

4. Manage exacerbations
 2 Reduce risk factors

a) Stop merokok
b) Farmakoterapi ( Kecanduan rokok ) :
bupropion SR, nicotine gum, nicotine
inhaler, nicotine nasal spray, and nicotine
patch..
c) Hindari paparan “ occupational dust & chemical “
d) Hindari paparan “indoor & out door air pullution “
 Manage Stable COPD
Goal of Therapy
 Relieve symptoms

 Improve exercise tolerance Reduce

Symptoms
 Improve health status

 Prevent disease progression

Reduce
 Prevent and treat exacerbations
Risk
 Reduce mortality
GOLD Revision 2011
 Menyesuaikan keterbatasan akitifitas

Mencegah kecepatan perburukan fungsi paru

EDUKASI

Mengenal perjalanan penyakit & terapi

Melaksanakan pengobatan maksimal

Mencapai akitifitas optimal

Meningkatkan kualitas hidup

Bahan Edukasi yang harus diberikan

Penggunaan obat yang benar & tepat

Manfaat, cara penggunaan, kapan dipakai,

dosis obat, efek samping
BRONKODILATOR ANTIBIOTIKA

ANTI INFLAMASI

OBAT-OBATAN

ANTIOKSIDAN

MUKOLITIK ANTITUSIF
 Salmeterol
Budesonid
 Fenoterol
Salbutamol

budesonide and formoterol

Anticholinergic

Tiotropium
Penggunaan obat Nebulizer
 LINI 1 LINI 2
Amoksisilin Amoksisilin-asam klavulanat
makrolid Sefalosporin
Kuinolon & makrolid baru

BILA ADA INFEKSI

ANTIBIOTIKA

PERAWATAN RUMAH SAKIT

DITAMBAH
Amoksilin-klavulanat Anti Pseudomonas
Sefalosporin II & III Aminoglikoside
Kuinolon
Kuinolon oral Sefalosporin gen. IV
MENEKAN INFLAMASI METILPREDNISOLON
PREDNISON

PADA EKSASERBASI AKUT

ANTI INFLAMASI

BENTUK INHALASI TERAPI JANGKA PANJANG

UJI KORTIKOSTEROID VEP1 meningkat > 20 %

POSITIF Paska bronkodilator
 TERUTAMA KARENA
PADA MEMPERCEPAT
EKSASERBASI PERBAIKAN
AKUT EKSASERBASI

MUKOLITIK

PADA TIDAK DIANJURKAN

BRONKITIS KRONIS SEBAGAI
DENGAN PEMBERIAN
SPUTUM RUTIN
YANG VISCOUS
Mengurangi Memperbaiki
eksaserbasi Kualitas hidup

N-ASETILSISTEIN

ANTIOKSIDAN

PADA PPOK TIDAK

SERING DIANJURKAN
EKSASERBASI PEMBERIAN
RUTIN
 Management of Stable COPD
Pharmacotherapy: Vaccines

 influenza vaccines can reduce serious illness

(Evidence A).

 Pneumococcal polysaccharide vaccine :

Usia > 65 th
Usia < 65 th bila FEV1 < 40 %

90
 Meningkatkan toleransi latihan
TUJUAN
Memperbaiki kualitas hidup

INDIKASI
REHABILITASI
MEDIK Simptom pernapasan berat
Sering masuk rawat darurat
Kualitas hidup menurun
PROGRAM

1. LATIHAN FISIS
2. PSIKOSOSIAL
3. LATIHAN PERNAPASAN
 TERAPI OKSIGEN
PPOK  hipoksemia  kerusakan jaringan

Mengurangi
Vasokonstriksi Mengurangi sesak

Memperbaiki Terapi Memperbaiki

Fungsi neurupsikiatri Oksigen aktivitas

Kapan dipakai
Meningkatkan Dosis Mencegah
Kualitas hidup Efek samping komplikasi jantung
 KONDISI Kebutuhan energi meningkat
MALNUTRISI Kerja otot respirasi meningkat

Gangguan Keseimbangan
Elektrolit

NUTRISI HIPERKALEMI
HIPOFOSFATEMI
HIPOKALSEMI
TERAPI HIPOMAGNESEMI

Komposisi nutrisi seimbang

Nutrisi terus-menerus ( Nocturnal feeding )
Four Components of COPD Management plan:

1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD

 Education
 Pharmacologic
 Non-pharmacologic

4. Manage exacerbations
 Management COPD Exacerbations

Key Points
An exacerbation of COPD is defined as:

“An acute event characterized by a

worsening of the patient’s respiratory
symptoms that is beyond normal day-to-
day variation and leads to a change in
medication.”
95
GOLD Revision 2011
 Management COPD Exacerbations

Key Points

The most common causes exacerbation :

viral upper respiratory tract infection and
infection tracheobronchial tree

The goal of treatment is to minimize the

impact
of the current exacerbation and to prevent the
development of subsequent exacerbation
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GOLD Revision 2011
 Management COPD Exacerbations

Key Points
Short-acting β-2 agonist with or without short acting
anticholinergis are usually the preferred bronchodilators
for treatment of an exacerbation.

Systemic corticostreroids and antibiotics can

shorten recovery time, improve lung function (FEV1)
and hypoxemia, and reduce the risk of early relapse,
treatment failure and leng of hostipal stay.
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Consequences of COPD Exacerbations
 Komplikasi PPOK

KOMPLIKASI :
1) Infeksi berulang ( Pneumonia )
2) Pneumotoraks
3) Kor Pulmonale Kronikum ( CPC ) Kompensata
/ Dekompensata
4) Gagal Nafas
5) Meninggal
 PPOK dan Penyakit Penyerta

COPD patients are at increased risk for:

Cardiovascular diseases
Osteoporosis
Respiratory infection
Anxiety and Depression
Diabetes
Lung cancer

GOLD Revision 2011

 PPOK dan Penyakit Penyerta

COPD has significant extrapulmonary

(systemic) effects including:

Weight loss

Nutritional abnormalities

Skeletal muscle dysfunction

Komplikasi PPOK
Kor Pulmonale

Pelebaran vena di leher

Pembesaran ( hipertrofi & dilatasi )

jantung kanan
Hepar membesar
( hepatomegali )

Edema pada tungkai

Kevin. A