ASMA DAN PPOK

dr Indah Rahmawati, SpP

Blok Respirasi, 19-03-15
 DEFINISI ASMA
Asma adalah ....

gangguan inflamasi
kronik
hipersensitifitas bronkus
bronkokonstriksi yang
reversibel dengan atau
tanpa pengobatan

Ref. GINA Updated 2008

 Definition of Asthma
Asthma is a CHRONIC INFLAMATION disorder
of the airways in which many cell and cellular
elements play a role. The chronic
inflammation is associated with airway hyper-
responsiveness that leads to current episodes
of wheezing, breathlessness chest tightness,
and coughing, particularly at night in the early
morning. These episodes are usually
associated with widespread, but variable,
airflow obstruction within the lung that is
often reversible either spontaneously or with
treatment.
Ref. GINA 2010
 Gejala ASMA: hanya puncak gunung es1
Batuk
Sesak napas
GEJALA ASMA
Mengi (wheezing)
Dada rasa tertekan

Bronkokonstriksi
Edema bronkus
Obstruksi saluran napas Hiper-sekresi mukus
Keterlibatan sel-sel inflamasi
eosinofil, dll
Hiper-responsif bronkus

Inflamasi saluran napas

1. Warner O. Am J Resp Crit Care Med 2003; 167: 14651466.

 Inflamasi masalah inti pada asma

Paru normal Paru asma ringan

Epithelium
Fragile, damaged epithelium
intact
Sparsity of
bronchial
smooth
muscle Basement
membrane
relatively
thin
Thickened reticular
basement
membrane
beginnings of airway
remodelling

1. Jeffery P. Ped Pulm 2001; 21: 3-16.

 Eksaserbasi Asma
(serangan asma)

Suatu episode dari sesak napas, batuk,

mengi dan rasa tertekan di dada atau
kombinasi dari gejala-gejala tersebut
yang terjadi secara progresif dan cepat

Ref. GINA Updated 2008

 Tujuan penatalaksanaan
Asma eksaserbasi

Membebaskan obstruksi jalan napas

dan hipoksemia secepat mungkin
Mencegah kekambuhan
Catatan: makin cepat pengobatan dimulai, makin mudah mengatasi serangan .

GINA Updated 2008

 Keparahan dari Eksaserbasi Asma*
R e s p ira to ry a rre s t
M ild (rin g a n ) M o d e ra te (s e d a n g ) S e v e re (b e ra t)
GINA 2008 im m ite n t
S e sak napas B e rja la n B e rb ic a ra B e ris tira h a t
In fa n t-s o fte r; Me n a n g is B a yi b e rh e n ti m e n yu s u i
p e n d e k; S u lit m a ka n

D a p a t b e rb a rin g D u d u k le b ih n ya m a n Me m b u n g ku k ke d e p a n
B e r b ic a r a d a la m K a lim a t le n g ka p K a lim a t td k le n g ka p K a ta -ka ta
K e waspadaan Mu n g kin g e lis a h B ia s a n ya g e lis a h U s u a lly a g ita te d N g a n tu k a ta u B in g u n g
Fre k. P e rnapasan Me n in g ka t Me n in g ka t S e rin g > 3 0 /m in
F re ku e n s i p e rn a p a s a n n o rm a l d a ri a n a k-a n a k p a d a s a a t tid a k tid u r (b a n g u n ):
U s ia Frek. norm al
< b2u la
mno n th s < 6 0 /m e n it
2 -1 2 b u la n < 5 0 /m e n it
1 -5 ta h u n < 4 0 /m e n it
6 -8 ta h u n < 3 0 /m e n it
O to t B a n tu N a p a s d a n P e rg e ra ka n th o ra c o -
B ia s a n ya tid a k a d a B ia s a n ya a d a B ia s a n ya a d a
R e tr a k s i S u p r a s te r n a l a b d o m in a l p a ra d o ks a l
S e d a n g , s e rin g h a n ya p a d a
W h e e z in g K e ra s B ia s a n ya ke ra s T id a k a d a w h e e z in g
a kh ir e ks p ira s i
N a d i/m e n it < 100 1 0 0 -2 0 0 > 120 B ra d ika rd ia
P e n u n tu n b a ta s d a ri d e n yu t n a d i n o rm a l p a d a a n a k-a n a k:
B a yi 2 -1 2 b u la n - An g ka n o rm a l < 1 6 0 /m e n it
An a k b e lu m s e ko la h 1 -2 ta h u n < 1 2 0 /m e n it
An a k u s ia s e ko la h 2 -8 ta h u n < 1 1 0 /m e n it
T id a k a d a Mu n g kin a d a S e rin g a d a T id a k a d a m e n g e s a n ka n
P u ls u s p a r a d o k s u s < 10 m m Hg 1 0 -2 5 m m H g > 2 5 m m H g (d e w a s a ) ke c a p a ia n o to t p e rn a p a -
2 0 -4 0 m m H g (a n a k) s an
% AP E yg d ip r e d ik s i > 80% 6 0 -8 0 % < 6 0 % yg d ip re d iks i
s e te la h b r o n k o d ila to r (< 1 0 0 L /m e n it d e w a s a )
awal a ta u re s p o n < 2 ja m te ra kh ir
P a O 2 (o n a ir )* * N o rm a l, b ia s a td k d ip e rlu ka n > 6 0 m m H g < 6 0 m m H g ; m u n g kin s ia n o s is
d a n / a ta u
P aC O 2** < 45 m m Hg < 45 m m Hg > 4 5 m m H g :m u n g kin g a g a l n a p a s
S a O 2 % (o n a ir )* * > 95% 9 1 -9 5 % < 90%
H ip e rc a p n e a (h ip o ve n tila s i) b e rke m b a n g le b ih m u d a h p a d a a n a k-a n a k d a rip a d a d e w a s a
d a n re m a ja
* N o te : K e b e ra d a a n d a ri b e b e ra p a p a ra m e te r, te ta p i tid a k s e m u a n ya , m e n g in d ika s ika n kla s ifika s i u m u m d a ri e ks a s e rb a s i.
* * N o te : K ilo p a s c a ls ju g a d ig u n a ka n s e c a ra in te rn a s io n a l; ko n ve rs i te la h d is e s u a ika n p a d a ke a d a a n in i.

Ref. GINA Updated 2008

Managemen Asma
Jangka Pendek

ASMA AKUT
 Penanganan Asma Eksaserbasi di
Rumah Sakit
Penilaian Awal
Anamnesis, PF (auskultasi, penggunaan otot bantu napas, denyut jantung, frekuensi napas),
APE atau VEP1 , saturasi oksigen, dan tes lain yang diperlukan

Terapi Awal
Inhalasi 2-agonis kerja cepat secara terus menerus selama 1 jam.
Oksigen sampai tercapai saturasi O2 > 90% (95% pada anak-anak)
Steroid sistemik jika tidak ada respons segera, atau jika pasien sebelumnya
sudah menggunakan steroid oral atau jika derajat keparahan sudah berat
Sedasi merupakan kontra-indikasi terapi asma eksaserbasi.

Penilaian Ulang setelah 1 jam

APE, saturasi Q2, tes lain yang diperlukan

GINA Updated 2008

 lanjutan .
Penilaian Ulang stlh 1 jam

Derajat Sedang Derajat Berat

APE 60-80% dari yang diperkirakan
Pem. Fisik : gejala sedang, penggunaan
otot bantu pernapasan
Oksigen
Inhalasi 2-agonis dan anti-kolinergik
setiap 60 menit
Glukokortikosteroid oral
Teruskan terapi 1-3 jam jika ada perbaikan
APE < 60% dari yang diperkirakan
PF: gejala berat saat istirahat, retraksi dada
Riwayat faktor resiko mendekati asma yang
fatal
Tidak ada perbaikan setelah terapi awal
Inhalasi 2 -agonis dan anti-kolinergik
Oksigen
Glukokortikosteroid sistemik
Magnesium IV

Penilaian Ulang stlh 1-2 jam

Respons tidak baik Respons buruk

Respons baik
selama 1-2 jam selama 1-2 jam

Ref. GINA Updated 2008

 Respons Baik
Bertahan 60 menit setelah
terapi terakhir
PF : normal
APE > 70%
Tidak stres
Saturasi O2 > 90%
(95% pada anak-anak)
Pulangkan ke Rumah
Lanjutkan 2-agonis inhalasi
Pertimbangkan steroid oral
Pertimbangkan inhaler
kombinasi
Edukasi pasien:
Cara pakai obat yang benar
Buat rencana aksi
Follow-up teratur
Kriteria bisa dipulangkan
jika APE > 60% dari yang
diperkirakan
Kondisi tetap pada saat
terapi oral / inhalasi
Respons tidak lengkap Respons jelek
selama 1-2 jam selama 1 jam
Pasien resiko tinggi
Pasien resiko tinggi PF: gejala berat, kesadaran
PF: gejala ringan-sedang
menurun, kebingungan
APE < 70% APE < 30%
Saturasi O2 tidak membaik PCO2 > 45mm Hg
PO2 < 60mm Hg
Rawat di ICU
Rawat Rumah Sakit
Inh 2-agonis + anti-kolinergik
(acute care setting)
Steroid IV
Inh 2-agonis anti-kolinergik Pertimbangkan 2 -agonis IV
Steroid sistemik
Oksigen
Oksigen
Pertimbangkan teofilin IV
Magnesium IV
Monitor APE, saturasi O2 , nadi Intubasi dan ventilasi mekanik
jika perlu
Perbaikan Tidak membaik
Rawat di ICU
Jika tidak ada perbaikan
setelah 6-12 jam
Terapi yang tidak direkomendasi
untuk pengobatan serangan :
Sedatif (harus dihindari)
Obat Mukolitik (memperburuk batuk)
Terapi fisik dada/fisioterapi
(menambah ketidaknyaman pasien)
Hidrasi dengan cairan dalam volume yg banyak
untuk dewasa dan remaja (mungkin diperlukan
pada anak-anak dan bayi)
Antibiotik (bukan mengobati serangan tetapi
diindikasikan untuk pasien yang juga
mempunyai pneumonia atau infeksi bakteri
seperti sinusitis)
 Pengobatan Utama
Eksaserbasi Asma

Penggunaan berulang Beta 2-agonis

kerja singkat
Menggunakan kortikosteroid lebih awal
Oksigen

Ref : GINA Updated 2008

Managemen Asma
Jangka Panjang

ASMA KRONIK
 Pendekatan terapi sesuai GINA 2008

Control-driven management
to achieve and maintain control

Treating to target
Partly controlled

Controlled Not well controlled

Zain-Hamid,R; FK USU.
 Tingkatan Asma Terkontrol
berdasarkan GINA 2008 updated

Terkontrol Terkontrol sebagian

Karakteristik (muncul salah satu pada Tidak terkontrol
(semua di bawah ini) minggu tertentu)

Gejala siang hari 2 kali / minggu > 2 kali / minggu 3 atau lebih fitur
asma
Keterbatasan terkontrol
Tidak ada Ada
aktivitas sebagian
Gejala / terbangun muncul pada
Tidak ada Ada minggu tertentu
Malam hari
(kejadian
Kebutuhan obat eksaserbasi pada
2 kali / minggu > 2 kali / minggu minggu manapun
pelega
akan dinilai sebagai
minggu asma tidak
Fungsi paru < 80% prediksi atau nilai
Normal terkontrol)
(APE or VEP1) terbaik pasien tersebut

Penilaian resiko masa depan (resiko eksaserbasi, ketidak-stabilan, perburukan fungsi paru yang cepat, efek samping)
Resiko adverse event di masa depan akan meningkat pada pasien dengan fitur berikut ini :
Kontrol klinis yang jelek, eksaserbasi yang sering pada tahun yg lalu, pernah dirawat di ruang critical care di asma, VEP1
rendah, paparan asap rokok, harus sudah memakai obat dosis tinggi.
 Apa yang harus dilakukan bila Asma sudah
terkontrol ?
Setelah terkontrol 3 bulan,
turunkan dosis

Monitor
bila tetap terkontrol 3 bulan,
turunkan dosis

dan seterusnya

Obat pengontrol bisa dihentikan, jika asma pasien tetap terkontrol pada dosis obat
terendah & tidak ada gejala yg timbul selama 1 tahun

Global Initiative for Asthma (GINA): Global strategy for asthma management and prevention. Revised Edition 2008.
 Proses inflamasi
pada saluran pernapasan

Penglepasan berbagai mediator inflamasi

Kontraksi otot polos (bronkokonstriksi)

sekresi mukus
Oedema saluran pernapasan

Pembatasan aliran udara di saluran

pernapasan
 Obat pengontrol
(Anti-inflamasi)

Steroid Non steroid

budesonide (Pulmicort) sodium
(Inflamid) chromoglicate
(Intal)
beclomethasone dipropionate
(Becotide) ketotifen
triamcinolone acetonide sodium nedocromil
fluticasone (Flexotide)
Zain-Hamid,R; FK USU.
 Pengobatan Asma

Pengobatan terkontrol jangka panjang

digunakan regular kontrol gejala yang bersifat
kronik & mencegah serangan asma (terapi
pemeliharaan)
Pengobatan penghilang gejala segera
digunakan sesuai keperluan cepat, penghilang
gejala jangka pendek (selama serangan asma
berlangsung)

Zain-Hamid,R; FK USU.
 Pelega

Bronkodilator :
2 - agonist
Xanthin
Anticholinergic

Zain-Hamid,R; FK USU.
 BRONKODILATOR
SHORT ACTING 2 AGONIST (SABA)
* salbutamol/albuterol (Ventolin )
LONG ACTING 2 AGONIST
* terbutaline (Bricasma) (LABA)
* procaterol * salmoterol
* fenoterol
* formoterol
* orciprenaline, dll

ANTICHOLINERGIC XANTHINE
* ipratropium * theophylline
* tiotropium
SYMPHATOMIMETIC LAIN
* ephedrine
* adrenaline, dll Zain-Hamid,R; FK USU.
Stimulasi 2-adrenoceptor

Aktivasi enzim adenylyl cyclase

Produksi cAMP

Relaksasi otot polos

saluran pernapasan
Zain-Hamid,R; FK USU.
TERAPI INHALASI

Zain-Hamid,R; FK USU.
 Terapi Inhalasi

Cara pemberian obat pilihan pertama

untuk terapi asma

Efek samping sistemik

Mula kerja cepat
minimum
Zain-Hamid,R; FK USU.
 Terapi Inhalasi

Absorpsi obat di paru lambat

Ketersediaan hayati obat (oral) rendah

Klirens sistemik obat cepat

Indeks terapi lebih lebar (lebih aman)

Zain-Hamid,R; FK USU.
 Terapi Inhalasi

Efek samping obat (e.s.o) sistemik

Biaya tak terduga

untuk perawatan penyakit akibat e.s.o

Kualitas hidup pasien asma & keluarganya

Zain-Hamid,R; FK USU.
 Jenis inhaler
teknik penggunaan alat inhalasi

Ketersediaan hayati obat di paru

Deposisi obat di orofaring

Efek lokal terapi inhalasi di sistem pernapasan

Efek sistemik terapi inhalasi
Zain-Hamid,R; FK USU.
 PPOK
Penyakit Paru Obstruksi Kronik
The 2011 Revised Version of COPD
International Guidelines

REVISED 2011
 DEFINISI PPOK

Penyakit obstruksi saluran napas

Perlambatan aliran udara ekspirasi
Progresif lambat
Ada hipereaktiviti bronkus
Reversibel sebagian/ireversibel
 Definition of COPD
COPD: a common preventable and treatable
disease, is characterized by persistent airflow
limitation that is usually progressive and
associated with an enhanced chronic
inflammatory response in the airways and
the lung to noxious particles or gases.

Exacerbations and comorbidities contribute

to the overall severity in individual patients.

Source: GOLD guideline 2011 Update

 The difference between Asthma & COPD

COPD Asthma Severe asthma

Cells Neutrophils ++ Eosinophils ++ Neutrophils +
Macrophages +++ Macrophages + Macrophages
CD8+ T cells (Tc1) CD4+ T cells (Th2) CD4+ T cells (Th2),
CD8+ T cells (Tc1)

Key mediators IL-8 Eotaxin IL-8

TNF-, IL-1, IL-6 IIL-4, IL-5, IL-13 IL-5, IL-13
NO+ NO+++ NO++

Oxidative
stress +++ + +++

Site of disease Peripheral airways Proximal airways Proximal airways

Lung parenchyma Peripheral airways
Pulmonary vessels

GOLD guidelines, 2007

 Management of COPD the aims
Relieve symptoms
Reduce
Improve exercise tolerance symptoms
Improve health status

Prevent disease progression

Reduce
Prevent and treat exacerbations risk
Reduce mortality

Source: GOLD guideline 2011 Update

 CAUSES AND EFFECTS OF EXACERBATIONS

Wedzicha, JA, Seemungal T. Lancet 2007;370:786-96.

 MANAGEMENT OF COPD THE AIMS

Relieve symptoms
Reduce symptoms Improve exercise tolerance
Improve health status

Prevent disease progression

Reduce risk Prevent exacerbations
Reduce mortality
 Mechanisms Underlying Airflow
Limitation in COPD

Small Airways Disease Parenchymal Destruction

Airway inflammation Loss of alveolar attachments
Airway fibrosis, luminal plugs Decrease of elastic recoil
Increased airway resistance

AIRFLOW LIMITATION
GOLD Revision 2011
 Assessment of COPD

Assess symptoms
Assess degree of airflow limitation using
spirometry
Assess risk of exacerbations

Assess comorbidities

GOLD Revision 2011

 Symptoms of COPD

The Characteristic symptoms of COPD are chronic and

progressive dyspnea, cough, and sputum production.

Dyspnea: Progressive, persistent and characteristically

worse with exercise.

Chronic cough: May be intermittent and may be

unproductive.

Chronic sputum production: COPD patients commonly

cough up sputum.

GOLD Revision 2011

 Assessment of Symptoms

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.

GOLD Revision 2011

 GOLD 2011
Manage Exacerbations

An exacerbation of COPD is:

an acute event characterized by a
worsening of the patients respiratory
symptoms that is beyond normal day-to-
day variations and leads to a change in
medication.

GOLD 2013; www.goldcopd.org

 Types of exacerbation
Mild
Worse symptoms possibly requiring more reliever

Moderate
Sustained worsening of symptoms (2-3 days) eg
Cough and sputum production
Breathlessness and wheeze
Needs treatment with antibiotics and/or corticosteroids
Unscheduled hospital visit

Severe
As for moderate but requires hospitalization
 Manage Stable COPD:
Key Points
Identification and reduction of exposure to risk factors are
important steps in prevention and treatment.
Individualized assessment of symptoms, airflow limitation, and
future risk of exacerbations should be incorporated into the
management strategy.
All COPD patients benefit from rehabilitation and maintenance
of physical activity.
Pharmacologic therapy is used to reduce symptoms, reduce
frequency and severity of exacerbations, and improve health
status and exercise tolerance.

GOLD Revision 2011

 Manage Stable COPD:
Key Points
Long-acting formulations of beta2-agonists and
anticholinergics are preferred over short-acting
formulations. Based on efficacy and side effects,
inhaled bronchodilators are preferred over oral
bronchodilators.

Long-term treatment with inhaled corticosteroids

added to long-acting bronchodilators is recommended
for patients with high risk of exacerbations.

GOLD Revision 2011

 Manage Stable COPD:
Key Points

Long-term monotherapy with oral or inhaled

corticosteroids is not recommended in COPD.

The phospodiesterase-4 inhibitor roflumilast may

be useful to reduce exacerbations for patients
with FEV1 < 50% of predicted, chronic
bronchitis, and frequent exacerbations.

GOLD Revision 2011

 Manage Stable COPD:
Goals of Therapy

Relieve symptoms
Improve exercise tolerance Reduce
symptoms
Improve health status

Prevent disease progression

Prevent and treat exacerbations Reduce
risk
Reduce mortality

GOLD Revision 2011

 Manage Stable COPD:
All COPD Patients

Avoidance of risk factors

- smoking cessation
- reduction of indoor pollution
- reduction of occupational exposure
Influenza vaccination

GOLD Revision 2011

 Manage Stable COPD :
Pharmacologic Therapy
Patient First choice Second choice Alternative Choices

LAMA
SAMA prn or
A or LABA Theophylline
SABA prn or
SABA and SAMA
LAMA
SABA and/or SAMA
B or LAMA and LABA
Theophylline
LABA
ICS + LABA
PDE4-inh.
or
C LAMA and LABA SABA and/or SAMA
LAMA
Theophylline

ICS and LAMA or

ICS + LABA
ICS + LABA and LAMA or Carbocysteine
or
D ICS+LABA and PDE4-inh. or SABA and/or SAMA
LAMA
LAMA and LABA or Theophylline
LAMA and PDE4-inh.
Consequences Of COPD Exacerbations
Negative Impact on
impact on symptoms
quality of life and lung
function

EXACERBATIONS
Accelerated
Increased
lung function
economic
decline
costs

Increased
Mortality

GOLD Revision 2011

 Manage Exacerbations:
Treatment Options
Oxygen: titrate to improve the patients hypoxemia with a
target saturation of 88-92%.

Bronchodilators: Short-acting inhaled beta2-agonists with or

without short-acting anticholinergics are preferred.

Systemic Corticosteroids: Shorten recovery time, improve lung

function (FEV1) and arterial hypoxemia (PaO2), and reduce the
risk of early relapse, treatment failure, and length of hospital
stay. A dose of 30-40 mg prednisolone per day for 10-14 days is
recommended.

GOLD Revision 2011

 Manage Exacerbations:
Treatment Options

Antibiotics should be given to patients with:

Three cardinal symptoms: increased dyspnea,

increased sputum volume, and increased sputum
purulence.
Who require mechanical ventilation.

GOLD Revision 2011

 Manage Exacerbations:
Treatment Options

Noninvasive ventilation (NIV):

Improves respiratory acidosis, reduces respiratory

rate, severity of dyspnea, complications and length of
hospital stay.

Decreases mortality and needs for intubation.

GOLD Revision 2011

 Manage Exacerbations:
Indications for Hospital Admission
Marked increase in intensity of symptoms
Severe underlying COPD
Onset of new physical signs
Failure of an exacerbation to respond to initial
medical management
Presence of serious comorbidities
Frequent exacerbations
Older age
Insufficient home support
GOLD Revision 2011
 Manage Comorbidities

COPD often coexists with other diseases

(comorbidities) that may have a significant impact on
prognosis. In general, presence of comorbidities
should not alter COPD treatment and comorbidities
should be treated as if the patient did not have COPD.

GOLD Revision 2011

 Summary

Prevention of COPD is to a large extent possible and should

have high priority

Spirometry is required to make the diagnosis of COPD; the

presence of a post-bronchodilator FEV1/FVC < 0.70 confirms
the presence of persistent airflow limitation and thus of
COPD

The beneficial effects of pulmonary rehabilitation and

physical activity cannot be overstated

GOLD Revision 2011

 Summary
Assessment of COPD requires assessment of symptoms,
degree of airflow limitation, risk of exacerbations, and
comorbidities

Combined assessment of symptoms and risk of exacerbations

is the basis for non-pharmacologic and pharmacologic
management of COPD

Treat COPD exacerbations to minimize their impact and to

prevent the development of subsequent exacerbations
Look for comorbidities and if present treat to the same
extent as if the patient did not have COPD

GOLD Revision 2011

Thank You